Primary 1 Flashcards

1
Q

Alfent reason for speed of elimination

A

decreased Vd–>increased elimination

Elim=Cl/Vd

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2
Q

Paediatric Vd

A

increased BV and ECF–>increased Vd

of CO lower percentage to brain–>increased V2

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3
Q

sevo Resp

A
1 CO2 drive
2 hypoxic drive 
3 RR increased
4 TV decreased
5 MV decreased
6 ciliar
7 HPVC
8 BD
9 mech-decreased FRC below CC-->atelectasis -->decreased comp-->increased WoB
10 airway reflexes decreased to tolerate LMA
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4
Q

DKA

A

unopposed action of glucagon
(antiinsulin)
-decreased insulim–>decreased glucose uptake
-increased glycolysis
-increased GNG
-increased lipolysis–>fatty acid for ketones and Glycerol for GNG (KETONES MEANS LESS GNG REQ SO MUSCLES NOT BROKEN DOWN)
-increased protein catabolism–>AA–>GNG

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5
Q

Fasting patient

A

glycolysis then GNG then KG

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6
Q

Immune reaction PRBC
#viralTAG
i forget TAG

A

A-Anaphylaxis
B-TRALI

mild reaction
ABO incomp
non ABO incomp
immunomodulation
Graft vs Host

Viral/protozoan Infection
-hep C, HIV, Malaria

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7
Q

Non-immune PRBC reaction

A

Ms VET
microaggregates
sepsis

Vol
Electrolytes- iron, hyperkalaemia, Citrate–>decreased Ca and Mg
Triad: cold, acid, coagulopathy

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8
Q

PRBC contains (additives)

A
160g/L Hb
saline
glucose 
mannitol
adenosine

42 days

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9
Q

2 types of Dose response curves

A

Quantal-population binary eg MAC

Graded-individual continuous eg fentanyl

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10
Q

justify afterload line rationale

A

max wall tension for a given preload

ideally would be peak but corner easier

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11
Q

Pressure in RV

A

Systole 25 diastole 0-8

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12
Q

potassium channel in myocyte AP

A

Kito Phase 2-3
Kiro phase 3 rapid
Kiso phase 3 slow
Ki1 inwardly rectifying potassium channel
-most important for RMP
-activated at -40->-70 to efflux K
-with experimental hyperpolarisation in dead->INWARD potassium!

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13
Q

why platue

A

K vs Ca

  • ->refractory period
  • —->avoid tetany of heart
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14
Q

winkessel effect

A

elastic aorta maintain a narrowed pulse pressure

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15
Q

alveolar time constant

CORE RV

A

Comp.RESISTANCE

NOT! COMP.RADIUS

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16
Q

capnography-why platue gradient rises

A

slow time constants empty last.
these are the ones that are the most compliant and biggest (mostly basal) with low VQ hence higher conc of CO2.
APEX DOES NOT EMPTY LAST

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17
Q

Vd calc and risk

A

equal dispertion–>overdose

1 compartment
vd=conc x loading dose

3 compartment
Vss=V1 +V2 +V3

Non compartmental model for Vss
Vss = Cl.MRT

use AUC to find clearance
AUC time vs conc
-AUC=dose/cl
-hence AUC–>calc clearance

AUC.time on x axis give vs time –>AUMC (area under moment curve)

AUMC/AUC–>MRT (mean residence time)

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18
Q

N2O CBF

A

increases CBF and CMR and ICP

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19
Q

Volatile coronaries

A

VD due to volatile vs decreased DO2 VC

in isolated hearts, volatile increased Supply and decreases demand
(MAP decrease controlled)

Coronary steel

anaesthetic preconditioning

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20
Q

Mech of Vd volatile

A

Direct Sm
OPEN KATP Ch–>hyperpol–>decreased Ca influx at VGCC (MILLERS SAYS mech unclear but i just remember it this way)
decreased Ca release from SR
inhibit PLC (GPCR second messager that increases Ca)
unrelated to NO

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21
Q

coronary steal

A

iso (now evidence it doesn’t occur)

  • CorVD–>less blood flow to subendocardium of stenosed artery–>ischaemia
  • not an issue if CorPP maintained
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22
Q

Anaesthetic preconditioning

A

decreased infarct size
attenuated in anyone that needs it ha (old, DM, cardiomeg, fat)

improve supply (open KATPase) and decrease demand
improved NO release in isolated ischaemic hearts
reduce excess Ca influx on reperfusion
protect against neutrophil action on ischaemic tissue

bitemporal protection

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23
Q

Pulm VR

A

Picture a ICOPDe

  • LRTI
  • barrel chest
  • hypoxic
  • hypercapnic
  • acidotic
  • standing up
  • hypovolaemic on fluids
  • tachycardic
  • PEEP applied
  • sevo gassing down
Patient
FRC
low O2
high CO2 
Acid
interstital fluid
gravity
low blood volume

Proceedure
PEEP eg valsalva

Anaesthetic
volatiles–>decreased TV–>increased Pulm VR (miller)
catechol, SNS, Ca

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24
Q

HPVC and volatiles

A

mech of HPVC-MILLER DOSEN’T KNOW
end result is less Ca release and and changed K ch.

Volatile dose dependent blunt HPVC

  • Net: less Ca, less sens to Ca
  • VD effect is small and relatively offest by decreased CO to maintain prior perfusion
  • direct VD by increasing SR Ca release
  • but indirect inhibit K mediated VD (by increasing Katp opening) hence net not much VD at 1 MAC but is present
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25
Hepatic BF
30% CO 75% portal vein 50% DO2 by each HABR (semireciprical interrelationship) - decreased PV flow-->increased HA flow (x2) - decreased PVF-->increased adenosine-->HA VD HA - autoreg of HA - F=P/R P=Hep Art- Hep Venous hence in CCF-->hep flow increased VO2-->increased OER ******P+K decreased PV-->adenosine increase-->hep vasoDILATES (THIS IS THE OPPOSITE TO RENAL TG FEEDBACK WHERE ADENOSINE CAUSES VC)-BLOODY RIDICULOUS
26
Uterine autoreg
maximally dilated hence cant dilate more no autoreg | volatile -->decreased MAP-->decreased PP (F=P/R)
27
Metabolism phase | CORE R/V
``` Midaz Phase I -1-Hydroxymidazolam Phase II -1-hydroxymidazolam glucoronide ``` Morph - predom phase II - Morphine 3 glucorinide or M6G Paracetamol - Phase I-->NAPQI - Phase II (not a flow on of phase one products)-->glucoridine conjugates and sulfate conjugates Phase I - alter to expose or add charge or reactive group - oxidation, reduction, hydrolysis - eg cytp450 hydroxylation (OH- addition) MAO in mitochondria - more water sol Phase II - conjugation: add a large polar group eg glutathion by S-glutathionase - so cant cross membrane so can be actively transported Both make it more polar so more water soluble for urine and bile excretion (P+H p20) LF-->phase I effected most
28
local anaesthetic VD vs VC
pek and hill VD at low and VC at high
29
ester vs amide LA
PC PD PK different linkage between lipophilic aromatic ring and hydrophilic group Esters - comparatively unstable - high allergy due to met para-aminobenzoate - rapidly hydrolysed by butrylcholinesterase - mid PrB-->smaller Vd amides - have a shelf life of 2 years - met in liver
30
CNS/CVS
bup 3 lig 7
31
PrB LA
Increased tissue protein binding-->remain at axon longer Increased acidity locally eg seziure -->increased unbound-->increased risk of toxicity bind A1acid glycoproteint-->saturated at clinical doses -->albumin
32
LA ionization
bases ionise below hence acid decrease unionised. low pKa increases unionized. primary determinant of onset Lig pKa 7.9 bupiv pkA 8.1
33
LA def | and MoA
temporary blockade of neurotransmission when applied to a nerve fibre Block VGSC from inside axon in ionized form (crossed unionized) Higher affinity to open and inactive vs resting state
34
Henderson Haschelbah
pH=pka +log A-/AH pH=pka +log B/BH+ proton acceptor ie base on top in both equations
35
Fowlers method why does apex fill first
Wests p 118 At FRC base is ideal compliance and fills most. at RV bases is at very bottom of PV compliance curve and apex is on steep rise-->most compliant-->fill first Hence the took in deed space volume high in N2 and low in O2 hence CC flick when dependant alveoli close and higher Nitrogen percentage open Note N2 vs Volume to calculate volume (not time)
36
Alv half time
=R.C | basal are bigger and more compliant s apex
37
O2 cascade missing elements
Dead space and MV (note DS not a sig Cx)
38
NMDA rec tutorial
Voltage dependant ligand gated transmembrane cation channel. A delta or C fibers stim glutamate release C fibres are polymodal and with wind up non-nociceptive stimuli-->pain initially glut stim AMPA slower is NK1 buy substance P eventually Mg plug removed-->excitation of post gang nerve ketamine bind PCP rec
39
pulmonary circ
#sydney course desk top additionally less intermedia CO2-->VC in lungs
40
COPD
decreased calibre due to loss of elastin with less radial traction
41
CSF | prod and vol and pressure and content
``` #50ml:50ml 500ml/day 15mmHg SPIDER sucks it up Rb Na:KATP ``` active secretion + ultrafiltrate produced in choroid plexus of ventricles and SAS tight junction of choroid epithelium ATPase pumps Na in and takes K out water and anions follow passively glucose actively transported (60% glucose level of plasma) 60+60ml total brain and CSF replace 4x per day (500ml) absorbed in arachnoid villi Pressure 11mmHg due to production-->drive Mg and Cl increased Na normal everything else decreased (K, glucose, protein etc) Power and Kam - REAB INCREASES IN RAISED ICP - SECRETION constant until CPP is less than 70mmHg
42
PO half life vs IV
same!
43
half life
Vd/Cl
44
``` reynolds number CORE CORE CORE CORE ```
In normal airways, the flow is mainly laminar (turbulent flow is localised to the upper airways) "derranged phys #INERTIA is key viscoisty maintains flat sliding sheets inertia ripples them into turbulent waves hence reynolds number =2r.inertia/viscosity =2r. density X velocity / viscosity more inertia -->more tubulent large radius-->space for eddies etc lamina flow-->hagen poisel F=P/R turbulent not the same! R=8nl/pi.r2 note n=viscosity Derranged phys viscosity increase lamina R to slow! density increase likelyhood of turbulent therefore-->slow! density of turbulent flow-->decreased flow -Oxygen pushes bobbin higher than less dense He density of lamina flow-->do change -eg low flow rotameter same viscosity O2 and He -->same flow pushing bobbin Turbulent flow Flow is proportional to the square root of driving pressure. For turbulent flow, resistance is relatively large. That is, compared with laminar flow, a much larger driving pressure would be required to produce the same flow rate. Because the pressure-flow relationship ceases to be linear during turbulent flow, no neat equation exists to compute its resistance. , and cannot be described using the traditional Hagen-Poiseuille equation. Pressure = K.(flow)^n where K is an empirical constant which, for the human respiratory tract, appears to be 0.24 ( when the pressure gradient is expressed in kPa), and n=1.3 Density is the most important determinant of whether or not flow will be turbulent, all other things being equal. This is where helium becomes useful, i.e. by decreasing the density of the inspired gas mixture helium improves the likelihood of laminar flow occurring in narrowed airways, and this decreases the resistance to flow.
45
FA/Fi O2
starts not at zero Alv O2 is 100mmHg hence 60% of inspired RA
46
antiHTN
``` Central * Clonidine * Methyldopa Cardiac * Beta blockers Vasc * Alpha blocker * Acei ARB * CCB * Direct * CCB * N * K ch Renal * Diuretics * Renin inhib ```
47
catechol SF
Q1- - 2 OH—>COMT met AND increase POTENCY - OH group position ie any B2 activity. (The ones that can be boluses routinely are not potent and last longer eg metaramino, phenylephrine and ephedrine) Q2 -beta chain size—>lipid insol and potent Q3 -alpha chain alteration—>MAOi hence longer and can have an indirect action Q4 - small—>alpha (note even a methyl in my understanding increases beta eg Norad has nothing but Adrenaline and a methyl group—>more beta. Same with metaraminol vs ephedrine-noting that ephedrine also has no benzyl hydroxyl groups) - bigger—>beta and MAOi
48
volatile structure function
substituted Hydrocarbons(methyl (2C) ethyl (1C) ethers (O connecting to alkanes) except Halo-->alkane 5 changes 1) low MW, and polarity-->lower BP and higher Vapour pressure (as less bonds to hold together in my mind) 2) Flouride - decrease flam - decrease sol in blood and lipid - decrease potency 3) Br or CL - retain or increase potency 4) CHF2 - react with soda lime to liberate CO 5) chain length - max potency above and below
49
Boyles perfect gas law
think boiling water with temp constant Constant temp: decreased volume-->increased pressure
50
Charles perfect gast law
Think Charles Charted a Hot air balloon of Chitwan National Park at a fixed pressure: Increased temp-->increased volume
51
Gay lussax
Think Gays need to blow of steam partying on a gay train at a constant Volume: increased temp-->increased pressure
52
Henry's law
Henry scuba diving at a constant temp and at equilibrium: PP is proportional to ammount dissolved
53
Dalton's law
In a mixture of non-reactive gases the PP exerted is equal to the sum of the PP of the individual gases #doesnt apply to volatiles just gases
54
anaemia threshold
men 130 women 12O g/L target >75 TRICC
55
PRBC blood gas
``` acidotic hyperkalaemic low Ca high glucose (added) CO2, O2 lactate ```
56
Absolute humidity H20 37C HME
44mg/L HME - condense due to cooling air - ->Latent heat of condensation warms water - evaporates on insp due to heating - ->Latent heat of vapourisation-->cool 70% efficient at 30C Coiling heat wire in water bath-->maitain temp
57
pasteur point
O2 PP at which oxidative phosphorylation ceases 1mmHg
58
23 DPG
naturally exist in RBC binds more avidly to deoxy to shift OHDC down ie right to release O2 in tissues increased in Altitiude and CCF as acidosis and hypoxaemia inhibit the enzyme that break it down and stim those that make it. Increased in Preg to offload oxygen to fetus decreased sens in fetus to take up mums oxygen Stored blood has DECREASED DPG-->poor offloading of oxygen for 24 hours
59
VIVA right side down patient with right pulmonary contusion and PTx
spont breathing awake - dependant becomes base with increased perfusion and increased ventilation - fat-->worsen VQ GA - decreased volume - ->changed position on compliance curve-->upper like apical becomes most compliant (worsen V:Q)
60
temp and pressure compensation for vapouriser
1) copper sink-high specific heat capacity 2) metal with high thermal conductivity conducts heat: enviro to bottle (no insulation) 3) splitting ratio altered eg Bimetalic strip Pressure 1) baffles 2) one way valves 3) long serpantine
61
variable bipass isoflurane
SVP=1/3 atmp | for 3.3% inhaled need 10% to vapouriser and 90% bipass
62
roc metabolism
MAINLY EXCRETED UNCHANGED in bile and to a lesser extent in urine. a little bit of de-acetylated metabolites prolonged in liver and renal failure
63
Cis atrac vs atrac met
"BOTH ARE INDEP OF LIVER AND RENAL FUNCTION" P+H Cisatrac UNIQUE - Hoffman elimination (enzyme indep degen) - no direct hydrolysis by non specific esterase as per P+H - -but ester hydrolysis of metabolite laudenosine-->harmless Atrac UNIQUE - Hoffman - spontaneous BD at normal pH and temp -->laudenosine - hydrolysis by non-spec plasma esterase-->laudenosine Laudenosine-->seizure in doses above what is ever seen clinically
64
R quotient
O2=CO2/0.8 ie for each O2 0.8 CO2s (less CO2 than O2) | 1:1 for car met
65
Shunt Equation
Aagradient/AVgradient Berggren equation CcO2-CaO2/CcO2-CvO2 Above is per L for each unit therefore ratio is end result. CcO2 is presumed to be maximal (100*Hb*1.34) If Aa is zero then no shunt If AV is massive then no shunt NOT CO2!!! CAPILLARY OXYGEN ``` Gold standard Role vs PaO2 -factors in low mixed venous O2 Role vs PaO2/FiO2 -Partial pressure isn’t as meaningful as content ```
66
Venous admix
Calculated amount of venous blood that would be needed to be added to pulmonary end capillary blood to give the PaO2 seen. issues: don't know the exact volume or PO2 of all the venous blood. Hence it's an estimate
67
Glomerular charge selectivity
Positive penetration Roc is excreted in liver and to a lesser degree kidney UNCHANGED
68
Gpcr
GDP-->GTP with activation then breaks down to GDP HENCE name GPCR
69
Thio
thio decreases SVR as per OCHB update hand notes and decreased resp to hypercarbia and BC no uterine change decreased renal BF
70
Deadspace
Physiological DS - anatomical - alveolar Apparatus DS
71
Shunt
``` Anatomical -thesbian, bronchioli, coronary veins -cardiovasc fistulas/malformations Alveoli -V:Q mm ``` No CO2 Rise due to increased MV in response
72
Calculating DS
Anatomical -fowelers N2 VS Vol curve Alv - bohrs eqn for physiological DS (all DS) Minus Fowler's anatomical = alv DS BOHR eqn -all CO2 is from alveoli. More DS more diluted capno like in an arrest! Vd/Vt= PACO2-PmixedCO2/PACO2 alv CO2 (assume PaCO2) - mixed end tidal CO2 / alv CO2 Presume alv CO2 = PaCO2 #DEAD SPACE DEAD MAN CPR ETCO2
73
Adrenaline dose and response
Beta predome at low dose alpha predominantly at high dose 0.01-0.1mcg/kg/min-->beta >0.1mcg/kg/min-->alpha ``` #MAP can be unchanged! #NSWhealth ```
74
Adrenaline PD
``` A-decrease oedema B-BD, small increase TV *increase Pulm VR C- HR, rhythm Vaso and veno changes ino work, VO2 AL D *increase MAC E -alpha decreases insulin release, -stims glucagon, Glycolysis, GNG, lipolysis -K+ driven intracell B2 # salbutamol *increased lactate F -RAAS -direct Na reab -decreased RBF G -BSL ```
75
Windkessel
stretch of aorta to buffer SBP and DBP to smooth
76
Infrared Capno
* Infrared absorbed by molecules that have 2 or more different atom types (not O2) * CO2, N2O, iso * Beer * Amount absorbed proportional to conc of infrared absorbing substance * Analyser * Infrared source, chamber, analyser * Different gases absorb different wavelengths * Hence to measure CO2 emit infrared at 4.25micrometer wavelength (doesn’t cross over with N20 absorption) * Must be a narrow band to avoid absorption by other gases * Chamber * Fixed size * No infrared absorption * Detector * Low CO2—>high IR detected—>low visual display of CO2 on capnograph * Collision broadening * Collision of different gases—>broader IR absorption pattern—>potential error source—>measure O2 and N2O to compensate * Mainstream vs sidestream * sidestream * compirse * suction * Recycle * comparison * Transit time * Minimal weight at patient end non bulky * In Paeds 150ml/min suction may be significant * Block and kink * Condensation—>error—>water trap * delay * Response time= transit time +rise time * Transit time for Co2 to arrive at detector * Rise time=time for display value to rise from baseline to max eg 0.2s * Quicker with smaller chamber
77
La Place
tension=p.r in a cylinder | note AL=tension/wall stress so p.r/thickness
78
Obesity PGx
SVR INITIALLY DECREASED!!!! due to parallel vasculature #adipokines Leptin (KEY ON ALL FRONTS except coag) - VC - cardiac remodel-->LVH - myocyte impaired contractility - leptin resistance-->DM Plasminogen activator inhibitor (NOT PLATELET) Angiotensinogen Resistin (think of a fat resistance army being strong) -Myoctye impaired contractility-->hypertrophy adipokines impaired neural control of resp system in sleep-->OSA (and fatty pharnyx)
79
Cardiac model structure
``` BP=COxSVR #work #ECG #REFLEXES!!!!!! #AL=valves #coagulopathy #exercise ```
80
Obesity CVS
>30kg/m2 morbid obesity >35 with comorb or >40 #hyperdynamic ciculation #distributive change(decreased %to brain-absolute maintained) HR generally unchanged increased preload (50ml/kg vs 70ml/kg non obese) -due to RAAS and polycythemia -MAP unchanged wide pulse pressure due to to increased SV -AL initially decreased due to parrallele and concentric hypertrophy DILATED NOT REALLY A THING ITS HYPERTROPHY
81
Resp model structure
``` Consumption req and Work of breathing Trigger Mech-Flow=P/R #resistance #CW and LC VQ-->Aa Diff Pulm VR Carriage ``` Dx Measurement clinical imp 9Cs 1. consumption 2. control 3. compliance 4. comparison 5. capillaries 6. carriage 7. Crisis 8. Calculation 9. Clinical implications
82
OSA OHS
fatty pharynx leptin resistance-->impaired CO2 resp drive sensitivty OHS -awake hypovent
83
Elderly CVS change
``` CO decrease 1% per year over 30 years HR 220-AGE impaired contractility->increased reliance on frank starling curve two maintain CO HR not sig changed #hypertrophy-->increased demand #atrial kick (30%vs 5%) ```
84
Obesity resp
#restrictive picture - abdo fat - CW fat - increased pulm BV Airway resistance "↓Lung volumes → ↓radial traction → ↓airway diameter" ↓Lung compliance ↑Pulmonary blood volume → stiffer lungs ↓Lung volumes → operating on flatter part of compliance curve ↓Chest wall compliance ↑Weight of adipose tissue surrounding thoracic cage supply demand -decreased TV, increased RR net increase MV to meet demand decreased 1% FRC for every unit BMI >30 BMI 40 FRC =1L (normal is 2.5L) ↓FEV1 and FVC FEV1/FVC remains normal
85
elderly
WHO 60-75y.o old=75-90 ``` #GRAPES AND RAISENS BV decreased-->decrease loading ```
86
3 compartment model
central compartment (effectively plasma)
87
Propofol BP reduction
15% decrease CO 15% decreased SV 15% decrease SVR -due to reduced SNS-->decreased Ca in, increased K out, NO stim
88
NDMR intubation doses CORE
``` sux 1 roc 0.6 (this is 6x less potent faster acting derive of Vec!) atrac 0.5 cisatrac 0.15-0.2 (3x more potent) vec 0.1 panc 0.1 tube at 2 min for 45min ``` Note Roc and Vec and tubocurarine are Monoquaternary rest and Bisquaternary Mono is less potent and faster acting (hence why we use roc while cisatrac is so slow)
89
Lactic acid production
glucose-->pyruvate-->LA or Acetyl CoA (oxygen path) 1. Glycolysis (ADD) - ADP-->ATP NAD-->NADH 2. NAD recycle (Subtract)
90
Venturi | fixed vs variable performance
Bendenoili effect
91
PaCO2
proportion to prod/AV | normal produ=200ml/min
92
ED95 NDMR
This is not the conc required to have an effect of 50% in 95% of the pop. It is in fact then ED50 for a 95% reduction in twitch height TOFC MENTAL!
93
pulse ox
SeXy DARL Six hundred ie red deox absorbs CO same ab as oxygenated Hb in red light and no light absorbed at 900 nm ISOBESTIC point ab equal deox and ox
94
detecting Alv DS
diluted ETCO2 vs PaCO2 all CO2 from alv
95
why a shunt is compensated to a degree
high PP diluted with low PP-->some dexocygenated HB get loaded up. Hence why platue is useful that a decrease PP can still have fair sats before the drop
96
Gate theory
stim of Ab ascending touch fibers increase inhbitory interneruons-->along with desc inhib pathway stop ascending pain fibre Ad and C
97
Adelta C fibre
mechanothermal | mechanothermal +polymodal
98
ascedning tract
Lissauer's tract up or down 2 levels
99
Central sensitization
Polymodal C fibers transmit non noxious stim as painful (allodynia) glial inflam-->substance P neutrophils Nitric oxide-->alter Ca homeostasis 3 key features - decreased threshold - increased magnitutude (hyperalgesia) - increased zone
100
METS
1 met is BMR ie VO2 of 3.5ml/kg/min
101
Diathermy
Cut-like a jigsaw high current low volt continuous Clot-like a rotating fan heater high volt low current interupted
102
NDMR structure
quaternary ammonium compounds, are structurally related to acetylcholine. synthetic alkaloids Stoelting and P+H don't go beyond aminosteroid-steroid structure rigid and big BQ-long flexible chain
103
LASER
Light AMPLIFIFICATION by Stimulated Emmission Radiation 1. spontaneous emission excited-->base 2. stimulated emission when excited struck-->2 photons in phase, direction, wavelength-->chain reaction Ho:yag-->mild IR-->lithotripsy (Hodoor was built like a stone) CO2-->deep IR-->Cut Coag aRgon-->Retinal Risk 1) ETT Dx 2) fire in O2 and N2O 3) eyes and tissues
104
LASER
Light AMPLIFIFICATION by Stimulated Emmission Radiation 1. spontaneous emission excited-->base 2. stimulated emission when excited struck-->2 photons in phase, direction, wavelength-->chain reaction #monochromatic, coherent, collimated Ho:yag-->mild IR-->lithotripsy (Hodoor was built like a stone) CO2-->deep IR-->Cut Coag aRgon-->Retinal Risk 1) ETT Dx 2) fire in O2 and N2O 3) eyes and tissues
105
Inductance
a conductor in motion in an EM field-->current | ->transform and generator
106
Macro shock
though body 100mA-->VF
107
Microshock
through PICC or pacing wire to heart 0.1mA-->VF due to current density! Prevented with EES +/-more (CHECK!)
108
Electical safety principles
Shock req 1) potential diff 2) closed circuit Cx 1) fault-->expose a connection to active circuit 2) leak-->(present in all equipment even without fault) - -casing of other conductive component of equip - --due to capacitive coupling-->*****stray capacitance***** active-->resistor-->neutral with a neutral to earth touch active wire-->shock person as path of least resistance is through you and not the resistor touch neutral wire is fine as path of least resistance is through neutral wire
109
Capacitors and capacitive coupling and stray capacitance | CORE REVIEW
Capacitor -2 electrical conductors separated by an insulator Capacitance - the ability of a capacitor to store electrical charge - DC - -voltage pushes electrons from negative end to capacitor and build up on this negative side (cant cross due to insulator) on the other side electrons are release -->current flows until voltage on other side is equal to voltage of battery (then current=zero) - AC - -flick back and forth on one side-->back and forth on other (sustained current) Capacitive coupling -transfer of ALTERNATING SIGNAL on one site causing alternating signal on the other Stray capacitance -unintentional unavoidable capacitive coupling due to proximity of 2 conductors with an insulator and an AC current
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RCDs
not volts #Red! Residual Current Devices -an active and a neutral wire pass through a toroidal (coil of wire) detector -compare current difference in each to identify leak (due to a parralel path not through neutral wire) --if >5-10mA detected-->disruct power in 40ms ``` Short falls If 1st fault... 1) for 40ms risk of shock 2) power gets cut off Not ok for anaesthetic machine or bipass therefore need Isolated Power Systemie floating circuit ```
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IPS electrical and LIM
``` #blue plug for IPS #green and orange gauge for LIMD ``` Isolated Power System ie Floating circuit - no connection to earth - ->first fault doesnt connect to earth to create a circuit - can touch the line line and not get shocked! primary circuit-->isolation transformer-->secondary circuit isolation transformer is required to create a floating circuit (primary circuit is earthed while secondary is not) to shock need -2 faults or connections Line Isolation Monitor -monitors secondary circuit to confirm that it remains isolated from ground -->ALARM if the PROSPECTIVE HAZARD CURRENT >5mA --actually doesn't measure current but resistance Flow=V/R R=V/I -attempts to inject 5mA into pre and then post socket line of secondary circuit - if resistance reduced (due to parallels circuit) then flows -doesn't actually determine if current flowing just if it had potential to flow if 1 fault occurred
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EES electrical
#green test button Equipotential Earthing System earthing wires at different powerpoints have different electrical potentials due to different resistance in wires EES-->large diameter Cu wire to connect all earthing wires prevents microshock
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equipment classes electrical
1-earthing wire due to metal casing eg fridge 2-double insulated so no earth eg hair drier 3-low voltage or battery eg mobile phone no earth as no risk of macroshock
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Applied PARTS electrical/ 3 levels of shock protection
``` B body unprotected -no additional protection #man BF Body floating - F #maninbox eg NIBP lead --macro CF cardiac Floating #heartinbox -eg ECG leads --micro ```
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Treatment areas electrical
Body protection area -RCD or floating with LIM Cardiac protected area - RCD or Floating with LIMD and EES (RCH and ANZCA power point confirm RCD is acceptable-this confuses me as 40ms to switch off is a risk of shock but ok) (it appears mane role for floating then is for uninteruptable supply eg Bipass or anaesthetic machine
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earthing wire
to protect supply if struck by lightening has an alternative path to flow. eg Class I device eg kettle. Fault-->shock you-->ground-->blow fuse. if no earthing wire ie IPS can touch active wire without shock as no circuit
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fatties not slower to wake up
time constant=sol.vol/filling as filling is flipping slow don't even come close to equilibrium especially with newer insol agents
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alv half time
=vol.sol/filling increased MV-->increased filling increased CO-->effective increase vol (insufficient time to hit equillibrium before ripped away)
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half time
0.693.Vd/Cl =vol.sol/filling VRG has smaller Vd and more filling so shorter halftime
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green whistle
methoxyflurane so lipid soluble impossible to knock out without N2O hence safe for ambos! lipid sol-->accumulate-->long DoA for analgesia
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Halogen
group 7 periodic table-->unfilled outer ring-->reactive-->strong bond-->inflammable, low volatility (unchangable), high boiling point Br and Cl increase potenecy Fl decreases potency but increases stability
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Vapour and volume change
not a gas-->no gas laws | no pressure change simply more in liquid form
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ED50 vs EC50
ED50 dose required for 50% of pop eg roc #quantal DR curve | EC50 conc required for an individual to experience 50% of max effect #graded DR curve
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Schild eqn
Ag vs antag equilibrium equation | Ag conc with antag/Ag conc if along minus 1=antag conc/dissocation constant #derrangedpharm
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non comp antag
decrease Emax without affecting affinity at rec hence EC50 remains same
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receptor theory old vs new
Kd=dissociation constant=point at which 50% rec occupied. old theory 100% occupied-->100% respon yet spare rec shows max resp and lower % eg NMJ 75% full-->full response at 75% occupancy of AcH
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GPCR types
GiPCR M2A2D2 2s MAD 2s GqPCR HAVE 1 M and M H1A1V1e M1 M3 GsPCR The rest
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LA onset lipid sol
slow-->perineural trapping
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pulse ox
beer lambet unreliable due to scatter-->patient calibration pulation therefore CHANGE in ab measured
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``` Isolated Power System IPS why no shock #how equipment works #shock free ! ```
No connection Neutral to earth in isolated system. shock cannot cross transformer either Hence neither way can a circuit be closed
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Osmorec
VOLT SFO IN HYPOTHAL! P+K normal osmolarity 280-300 if Blood loss then increased osmolarity-->>280-->increased ADH 280=R.M.O give too much hypertonic solution
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hypovol-->oliguria
overview-->compensation Early autoreg of RBF--> preserve GFR then fail Sensors 1. osmorec #280 2. low pressure baro-->ADH and decreased ANP 3. high presure baro-->RAAS 4. renal Baro JGA-->R ``` Effector hormones ADH ->increase water, sodium and urea reab Renin -due to SNS, intrarenal baro of the JGA (not MD!), MD due to Na conc! , ATII, baro AT -->VC-->decrease peritubular capillary pressure-->increased reab increased SNS-->MAP -->VC afferent and efferent and reduce filtration coeff-->decreased GFR Ald in CD SNS-->Renin and VC afferent and efferent ANP -normally-->diuresis --block Renin and ADH --block Na reab in CD --increase GFR by VD aff and VC eff and increasing filtration coeff ```
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BP control due to renal mechanism
Renin | -due to SNS, intrarenal baro of the JGA (not MD! Just pressure), MD due to Na conc! , ATII, baro
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CSF ph
7.33 due to CO2
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why IT morphine risks delayed resp dep but not fent
Fentanyl diffuses away rapidly primarily due to higher lipid sol (600x) -->rapid ab into perineural tissue, ED veins etc D=Sol.A.P/MW.T pH 7.33 in CSF-->both are more ionized-->trapping not sure how legit this is
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full breathe
vital capacity breath
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preoxygenation
nitrogen washout curve | time constant for washout reduced with increased MV hence 3x VC breath
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Time constants and wash out
``` 1 time constant-->63% complete 3 time constant to be 95% complete T=0.693xsol.vol/flow T=1/k T=R.C for alveoli ```
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preoxygeneation GOLD
nitrogen washout as lung is only decent potential O2 reservoir safe apnoic period ie time to SaO2 < 88% 21% FiO2 2.5L FRC-->450ml O2--> <2min 100% sig higher O2 optimal ETO2 is 90% airway occlusion-->atelectasis and shunt LITFL 3 minutes of tidal breathes or 8 VC breaths half-time for exponential change in FAO2with a step change in FIO2is 0.693 × VFRC/V̇A for a non-rebreathing system With VFRC equal to 2.5 l, the half-time is 26s and 13s when V̇A= 4.0 and 8.0 l/min, respectively Thus, most of the oxygen that can be stored in the alveolar and arterial spaces can be brought in by hyperventilation with FIO2= 1.0 for a short period of time this is the basis for the 4-deep-breath-within-30-seconds method of preoxygenation However the4DB/30 sec method still submaximally preoxygenates and leads to more rapid desaturation because: it does not allow enough time to maximally oxygenate tissue and venous compartments, and FiO2 may be decreased if the oxygen flow rate is insufficient for the rate of alveolar ventilation (due to entrained air)
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sux met
butryl cholinesterase hetro -->double homo A-->4-8 home F-->several hours
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sux and burns
``` aabgd dystophy burns demylination-stroke GBS, prolonged immob, paraplegic -->lethal ```
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sux anaphylaxis
anaphylaxis 1:10K fo GA with 1/3 due to MR even on first exposure 60% cross reac DMR and NDMR
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sux ICP
small and offset by benefit of not tubing paralysed patient | offset by NDMR
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sux IGP
due to abdo m not gastric m contraction--><30cmH20
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sats probe error Rb
CO-->normal sats dye-->false low like nail polish too small-->compress or not full finger
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hep met phases | CRITICAL
1. eg morphine to Normorphine 2. ADDITION OF LARGE POLAR MOL eg morph-->M3G (70%) and M6G 10% (active and 3x potent) #SX-->trouble but adding glucorinide by glucorinde transferase
147
Nor
methylated
148
why do we care about clearance rather than elim and why is it ml/hr?
Clearance is constant but elimination decreases with decreasing conc. Conc=IMD/Cl (conc=x/Vd so conc=change x over change Vd is IMD over Cl!!!!) AUC=dose/Cl
149
p in pKa and pH Ka in pKA
p is -log10 Ka=equilib constant acid:base Ka= Proton acceptor [H][A-]/proton donator [AH] at equilib
150
Boiling point
Not at all simply liquid-->vapour instead of evaporation from surface from liquid to vapour. boiling point is when SVP is as great as the external pressure on the liquid. hence bubbles can form in rather than just at the surface (as just as much pressure to fight against either way!) - vapour pressure > or equal to enviro pressure - so on everest this boiling point is lower! so in a closed system liquid and vapour form an equilibrium adding heat above boiling point-->no increase in temp but change in equillibrium with higher vapour pressure until critical temp reached (above which no compression to liquid so no equilibrium)-->gas boiling point is pressure dependant (low P-->low boiling point) crit temp vapour-->gas
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VIE
handy features 1. insulated 2. pressure gauge - decreased use-->no LHV-->increased temp-->increased P-->let off-->cool and decrease pressure 3. evaporator (extenal pipeline) No power supply req -use-->vapour drawn off-->more liquid to vapour-->LHV-->cool Critical temp of O2 -116C Boiling point (liq-->vapour -183C) system -180C--160C -liquid:vapour in euquilibrium Pros - cheap on mass vs gas - no power req Cons - set up cost and waste - back up - fire and explosion
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Vec SE
critical illness myopathy met liver-->active met-->renally cleared -->accum biliary clearance
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roc SE and mets
vec derivative with decreased potency-->increased SoO mild vagolytic anaphylaxis NO METS (<5%) biliary clearance unchanged mild renal clearance #suggamadex
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Panc
vagolytic due to SA MAch stim +/- SNS stim met in liver to active mets-->biliary excretion unchanged elim in kidney
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Atrac
``` Histamine-->BS and VD critical illness myopathy uniqu met -hoff -non spec plasma esterases-->laudenosine ```
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Mivacurium
BENZYLISOQUINOLINIUM butryl cholinesterase histamine release
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defib | how equ works: search "Summary of biphasic defibrillator sequence"
high capacitance-->high storage -hence increase SA by coiling 1. build up on either side of capacitor to charge 2. connect alternative circuit to defib - 4 switches for biphasic shock (two paths-->forward then back with transition time inbetween to avoid short circuit - truncation (cut off) occurs to avoid low current-->arrhythmia - achieve by intensional short circuit-->dissipated energy as heat - twitches for above dictated by computer based on oscilloscope reading ``` #transformer-->12V-->2000V -since high voltage-->increase capacitance storage=capacitancexVoltage squared/2 #AC-->DC in machine ```
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defib | how equ works: search "Summary of biphasic defibrillator sequence"
high capacitance-->high storage -hence increase SA by coiling 1. build up on either side of capacitor to charge 2. connect alternative circuit to defib - 4 switches for biphasic shock (two paths-->forward then back with transition time inbetween to avoid short circuit - truncation (cut off) occurs to avoid low current-->arrhythmia - achieve by intensional short circuit-->dissipated energy as heat - twitches for above dictated by computer based on oscilloscope reading ``` #transformer-->12V-->2000V -since high voltage-->increase capacitance storage=capacitancexVoltage squared/2 #AC-->DC in machine ```
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Heparin vs lmwh moa
Both bind ATIII ATIII CONNECTED TO II AND X II has binding site requiring binding achieved by Heparin not LMWH X DOESN'T HENCE SHORT LMWH ACHIEVES EFFECT
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Hit vs HITTS
HIT JUST LOW NUMBER HITTS 1% mortality ``` <100 3-14 days 50% drop Clot ?sepsis and dic ```
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atropine glyco structure
tertiary vs quarternary amine
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oxytocin MoA and SE
oxytocin rec GqPCR -->PLC-->IP3 and DAG-->Ca increase amp and freq with normal relaxation between ``` CVS = vasodilatation ! ↓MAP ! reflex ↑HR; ↓coronary perfusion RENAL = mild ADH effect ! fluid retention ± volume overload MATERNAL = ↑uterine contraction (esp. in multigravid) ! possible uterine rupture FETAL = ↓uterine blood flow ! possible fetal distress ```
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Ergometrin
ergot alkaloid 500 IU IM agonist at A1, DA, 5HT increase basal tone and force of contraction A1-->VC and decreased coronary perf DA-->CTZ and CNS-->N+V headache seizure
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Prostaglandin
misoprostol PGE2 -coordinated contraction, increased basal tone and cervical relaxation -induction, PPH, abortion decrease MAP, increase HR BS, increased RR Given PO, SL, PV, PR - i have seen it given PR 4x200mg tabs (up2date) - onset gastro inhib of secretion in 30 min and DoA 3 Hr also given to Mx NSAID induced GI ulcers
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tocolytics
1. NSAID (prost) 2. Salbutamol or terbutaline (b2) 3. Mg 4. nifedipine 5. GTN 6. volatile (not N2O) 7. atosiban (oxytocin antag)
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oxytocin MoA and SE
oxytocin rec GqPCR -->PLC-->IP3 and DAG-->Ca increase amp and freq with normal relaxation between ``` CVS = vasodilatation ! ↓MAP ! reflex ↑HR; ↓coronary perfusion RENAL = mild ADH effect ! fluid retention ± volume overload MATERNAL = ↑uterine contraction (esp. in multigravid) ! possible uterine rupture FETAL = ↓uterine blood flow ! possible fetal distress ```
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Ergometrin
ergot alkaloid 500 IU IM agonist at A1, DA, 5HT increase basal tone and force of contraction A1-->VC and decreased coronary perf DA-->CTZ and CNS-->N+V headache seizure
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Prostaglandin
PG rec misoprostol PGE2 -coordinated contraction, increased basal tone and cervical relaxation -induction, PPH, abortion decrease MAP, increase HR BS, increased RR
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tocolytics
1. NSAID (prost) 2. Salbutamol or terbutaline (b2)-tachy 3. Mg--limp baby and resp distress for baby 4. nifedipine 5. GTN 6. volatile (not N2O) 7. atosiban (oxytocin antag)-->yes hypotension and nausea
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terbutaline
b2 ag for tocolytics
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lignocaine and Li and Ach
both stop post synaptic NaCh
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gent and Mg and CCB and Ach
block presynaptic Ca Ch
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botuline and tetanus
block Ach vescicle release disrupts docking protien SNARE
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hemicolinium
block choline channel for reab
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lignocaine and Li and Ach
stop post synaptic NaCh
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gent and Mg and Ach
block presynaptic Ca Ch
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Volatiles and Ach
block presynaptic NACh-->reduce positive feedback
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physiological changes that prolong NM block for both NDMR and DMR
cold acidotic Mg K (NDRM yet shortens sux)
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PTC
increased mobilization, production of Ach and increased Ca
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NM monitoring | Hz = units per second 1 Hert is 60bpm
tetany= 50Hz x for 5s Single twitch=1Hz PTC= tetany then 1Hz 3s later (many twitches #PTC twitch of 9=TOFC of 1) -effect of tetany-->mobilization lasts 6min-->TOFC falsely raised -post tetanic fascilitation -useful for deep block req eg retinal surgery "A Post-Tetanic Count (PTC) of 2 by palpation suggests no twitch response for about 20-30 minutes, PTC of 5 about 10-15 minutes" TOFC=2Hz x 0.1ms x4 DBS=(50Hz x 0.2ms x 3 20ms appart)x2 separated by 75 ms "the second burst is lost as the third twich of TO4 is lost; the first burst is lost a little after you lose all response to TO4" DBS of 2 is reversible DBS less useful to assess depth of block but has a potential roll in confirming lack of residual block post reversal Summary: burst and tetany intense PTC chilled TOFC chilled Tetany 50Hz x1 PTC 1 Hz x many (5-->10-15min TOFC1) TOFC 2Hz x 4 DB 50Hz x3x2
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DTS
role: qualitatively say if 1=2 then no clinically sig residual block (less sensitive when quantified manually)
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suggamadex SE and MOA
picture -preganant donut with breast CA vomiting after taking ABx with a bogan heart tatoo and a strange rash PONV >1% OCP progesterone ineffective hypersens reaction severe brady rare may have slower action with IV fusidic acid (Abx) and ERModulator-->release the wrapped up roc. negatively charge hydrophilic center binds charge Quaternary amine (a modified gamma cyclodextrine)
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mat fetal blodd gases
uterine artery - O2 100mmhg - CO2 30mmHg Uterine Vein - 40mmHg - CO2 45mmHg umbi artery - O2 15mmHg - CO2 55mmhg Umbi Vein - O2 30mmHg - CO2 40mmhg
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o2 cascade
end capillary 40mmHg venouns 60mmhg mitochonidria 4-22mmHg
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Spiro obstructive VC breathe
FEV1 decreased more than VC is decreased but both are decreased restrictive normal FEV1 and markedly decreased FVC
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respiratory compliance combined curve x axis
-ve on left and +ve on right which is bloody different to every other lung PV curve! makes no sense if you get this wrong
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Cardaic PV loop in ischaemia
right lean systole-->early ventricular LENGTHENING (bulging of ischaemic muscle) DIASTOLE-->postsystolic shortening ie elastic recoil in severe ischameia
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CPP limits
normal 80-matey 70-sats drop due to increased extraction 40->fucked
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CMRo2 brain
3ml/100g 1.5kg not 3.5ml/kg is total body so close to 10x normal body req 20% of bodies o2
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resp quotient
is PC | Prod CO2/Consumed O2
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Shunt equation derivation (CORE STUFF)
Qt.CaO2= Qs.Contentmixedvenous +(Qt-Qt).Contentendcap several steps--> Qs/Qt=CcapO2-CaO2/CcapO2-CmixedvenousO2
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pulse pressure AR AS
wide AR narrow AS
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wiggers
Twave end is MV open (end of isovol relaxation)!!!!!
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ECG time interval (for wiggers)
5mm=0.2s cycle is 1s for 60bpm PR 0.2s QTinterval <540ms
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HS for wiggers
1 AV close 2 Aortic and pulm close 3 Filling in diastole 4 filling of stiff ventricle post atrial contraction before S1
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AP of myoctye vs nerve/skeletal M
ARP of 250ms vs 1ms due to platue due to L-type CaCh | higher RMP for myocyes -70mv vs -90mv
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PWP swanganz from insertion to end CV physiology
PWP is literally occluding the PA and letting pressure drop then pressure wave transfused from LEFT atrium to PV to PA hence looks like CVP trace but with pressure 6-10mmHg CVP 0-5 RV due to valve 25/0 PA due to valve 25/10 PAWP looks like CVP at 6-12mmHg
198
valsalva changes in path
baro rec defect in Autonomic neuropathy or quad - excessive BP drop in p2 - no overshoot or brady in phase 4 CCF -increased blood vol-->increased venous pressure-->maintain venous return then ITP translated to ITP -->raised MAP -SQUARE WAVEFORM! (ELEVATED NOTE DROPPED) -think of how PEEP-->improved frank starling in CCF (not exactly the same but close (or maybe the exact same?)
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Afterload line
arterial elastance line
200
preload line
EDVP relationship (elasatance line (not compliance))
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contractility line
ESDVP relationship
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BOWDITCH: force frequency contractility
increased HR-->increased Ca-->increased force of contraction
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Anrep effect
increased afterload-->increased wall tension-->increased contractility
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HR and SV
increase one the other drops
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Bain bridge
Bainbridge | Atrial stretch—>baro—>decreased HR
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contractility changes
1. SNS 2. catechol 3. drugs +ve or neg 4. pH, oxygen, CO2 5. electrolytes 6. MI 7. reflexes - Anrep increased AL-->increased Contract - Force frequency Contraction
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normal LVEDP
8mmHg
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VR and CO intercept
at RAP of zero | frank starling curve starts at RAP -2 ish
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VR determininants
MSFP-RAP/Restistance to filling resistance to filling is note venous tone! - increased venous tone with SNS improves venous return - ->shift MSFP - resistance to filling is dictated by organ autoreg - ->in exercise decreased resistance-->increased VR - ---->pivot gradient
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radial vs aortic
1. delay 2. wider PP-less compliant 3. narrower- less compliant 4. decreaed MAP 5% 5. distorted shape - reflection - resonance - damping - various pressure waves at different velocities 6. loss of incisur due to damping 7. diastolic hump due to reflection and resonance Changes with age -narrower PP and less distortion in non compliant arteries
211
Art line physics | nat freq def and eqn
the freq at which the system would oscillate at if stimulated then left undisturbed eg for BV 1Hz eg for artline system >24Hz (8th harmonic of 3Hz) Nat freq=square root of r squared.stiffness/density.length
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fundamental wave form and harmonics
the complex wave (ie 1Hz pulse) that is being broken down into 8 by fouriers analysis harmonic eg 2Hz, 3Hz, 4Hz 8 harmonics to appreciate dicrotic notch
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resonance
amplification of sine wave when natural frequency of measuring system is close to fundamental freq of that being measured not if it overlaps with the 8th harmonic-->resonance but 8th harmonic is high freq LOW AMP-->minimal impact
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damping def and reason why whe want some
the absorption of energy of oscilations req to damp resonance
215
frequency response | damping coeff
(flat range) range of frequencies for which minimal change in amplitude due to resonance ie the range of frequencies for which natural frequency of the artline system does not cause significant resonance frequency: response ie freq:resonance ie how much can i increase freq before i get resonance Damping Coef of 0.7 -index of the system to resist oscillation Flat range influenced by natural frequency of the artline - if the artline system has a low nat frequency eg 7Hz then very high chance of resonance with 7th Harmonic and no amount of damping could fix this - if artline system was 70Hz this is well above the 8th harmonic and resonance very minimal hence no damping even required - the flat range would be a over a large number of frequencies before resonance amplified the signal damping reduces the amplitude-->increased the flat range a bit damping also slightly increases the nat freq of the system! #derranged phys. sine wave squeeze down alot and pushed to the right a little.
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damping Cx
narrowing 1/r^3
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underdamped
reverb-->amplify
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nat freq of art line and fast flush test
most 10-25 Hz ideal NOT SIMPLY >24 Hz BUT A FLAT RANGE>24HZ simplistically people say 24Hz how to measure Fast flush test -freq of once per 30ms-->33Hz-->flat range >24 Hz-->set to go
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info from artline #DoD GOLD
HR. SV-area from upstroke to incisura Preload contract SVR sup- area below diast Diastolic Pressure time index demand-area below systole Tension Time index art compliance Swing-PEEP-->decreased systolic
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depol last
Last part of ventricle to depolarise → epicardial surface of LV wall at base of heart RV depols first as thinner
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fastest conduction
perkinji fibers
222
ECG scale
25mm/sec 1mc/cm
223
Hyperkalaemia
peaked T waves P wave flat PR prolonged -harder to pushout K-->less neg-->excitable muscle but suppresses conducting tissue
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ECG positive and negative ends
positive electrode-->upstroke RA-->LA LA +ve LA-->LL LA is -ve etc
225
torsades trigger
prolonged Qtc hence increased risk in brady
226
PR interval defin
start of p to start of QRS not R!
227
SAN phase o
Tca-->Lca
228
funny current
CV phys says Na influx | wiki says K and Na influx
229
aortic vs pulm artery opening and closing
Pulmonary opens first as PA pressurePaP | Splitting AP greater on insp as pulm VR decreased-->even later close of Pulm
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Ficks principle | CORE and GOLD
Consumed=CO.Ca-CO.Cv | Consumed/AV diff=CO !!!!!!!!!
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first to contract
septum
232
art baro rec afferent effect
-->NTS-->inhibitory GABA interneurons to vasomotor center in ventrolateral medulla
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morphine met CORE
phase ii M3G-potentially a mu antag M6G 13x more potent! -Six is Strong! both excreted in urine
234
glut rec
1 RBC and brain 2 panc liver and kidney 4 fat and skeletal four fatties flexxed while eating glucose
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exercise and resp changes | Wests
can increase MV 15x theory unknown 1) not CO2, O2 or pH 2) muscle spindle play a role 3) oscillating CO2 and O2 may play a role 4) central chemorec threshold may change 5) temp may have a role
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CBF and CPP and CO2 and O2
y axis % of normal x CPP 50-165mmHg Co2 20-80 O2 flick up at 50
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monroe kelly pressures
normal 10mmHg comp to 20 focal 20-45 general >45
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atrial action potential
minimal platue-->RAF possible as decrease ARP
239
thermo reg changes graph spinal
phase 2 is 1-4 hrs | temp change is from -1.5->-2.5
240
Ductus venosis
umbi vein - 1/3-->DV-->bipass liver straight to IVC - 2/3-->liver-->portal vein-->IVC
241
fetal circ % blood flow and Sats
``` definitely! flow 3/4 from IVC 2/3 RV-->90%DA 10% lungs 1/3 LV-->2/3 head 1/3 lower ``` sats umbi and DV 80% (call it 3/4) IVC 2/3% SVC 1/3% ascending aorta 2/3% as from IVC (small water down) PA essential from SVC with some extra O2-->50%
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Intrapleural pressure vs ITP vs transpulmonary pressure vs transmural CORE R/V
IPP and ITP are the same!!!!!! IPP: pressure in pleura TPP: Alv-IPP TPP is the same as TMP intra inside the pleura trans is outside to insude
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glucose handling graph
x axis is plasma glucose mmol/L y axis is glucose flux mg/min at 11mmol max reab of 300mg/min
244
capno flat line
machine to patient 1. electronic issue 2. sampling line 3. ETT lumen 4. ETT placement in eosophagus 5. resp obstruction 6. resp arrest 7. cardiac arrest
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capno upslope
partial obstruction patient or tube
246
info from capno
1. CO2 level (and site) 2. RR 3. patency/obstruction 4. curare sign 5. rebreathing (not same as breath stacking)
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Wheat stone bridge circuit Wiki! CORE R/V
Artline saline collumn-->move diaphragm-->change resistance-->measured with WBC must see wiki image 2 sets of parallel resistors left side known and variable right side known and an unknown gauge between left and right ABCD clockwise NULL DEFLECTION:when galvanometer is zero the bridge is balance with no flow. This is because the ratio of the bottom sides is equal to the top sides on both sides resistance electronically converted into SBP, MAP , DBP and displayed
248
Carotid body vs sinus
sinus has baro rec hence a sinus for pressure | body has chemo rec
249
afteload line
arterial elastance line ESP to EDV P/SV not perfect representation but is indep of preload and afterload so used as a surregate
250
contractility line
ESPVR line
251
resistance unit
mmHg/ml/sec of dynes/sec/cm^5
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EDV and ESV of RV
minimal more than left ESV right 50-70ml still!
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empty ventricle reflex
bezold jarish
254
coronary dominance
most are RIGHT ie right -->PDA-->inferior IVS
255
mixed venous O2 sampling
pulmonary artery
256
VIP
vasoactive intestinal peptide-->VD
257
cGRP
VD
258
neuropeptide Y
VC
259
affinity graph CORE RV
KD | -conc at which 50% of available rec occupied
260
dose response curve graded vs quantal and shape options
both can be drawn as either a sigmoid log or a non log (kinda inverse exponential function) EC is for individual graded ED is for pop quantal log conc x axis non lg y axis
261
STP unionized at pH
acid with a pKa of 7.6 -obviously because acidosis goes to huge change in vial is basic to make ionized to dissolve-->necrosis if extravesates
262
alfent pka fent | lig and bup
alften 6.5-->90% UI fent 8.4-->10% UI lig 7.9%-->25% UI bup 8.1%-->17% UI
263
exponential function math
y=e^kx y=e^-kx (negative to zero) y=1-e^-kx (washin with asymptote at 1)
264
BG PC sevo
0.58 halo 2.4
265
resp volatile compartments
VRG muscle fat
266
triexponential function of propofol CORE RV
log conc y axis and normal x axis ie a semi-log plot my initial understanding was wrong!!!!!!!.. NOT: first is V1-V2 THEN second is V1-V3 THEN third is elimination balance against redistribution back into V1 P+H uses 2 exponential: distribution and elim clinical aneasthesia uses 2 exponentials millers says nothing derrange phys uses 3 1. distrib 2. elim 3. terminal elim (rate that it is eliminated in the final phase as redistribution flattens gradient) https://derangedphysiology.com/main/cicm-primary-exam/required-reading/pharmacokinetics/Chapter%202.0.1/single-and-multiple-compartment-models-drug-distribution
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fentanyl onset peak and DoA
onset 3-5 min peak 5-10 DoA <3mcg/kg is 30-60min Doa at 50mcg/kg is 5 hours
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STP infusion
1) ZERO ORDER KINETICS at infusion 2) active met 3) hang over
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ph and H conc
ph=-logH 7.4=40nmol.L 7=100nmol 8=10 (not 1/10th of ph of 7)
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pKa and strength of acid
HA-->H+A- (k1) backwards is K2 K1/K2=K high Ka means stronger acid-->LOWER PKA (a negative log!!!!! like pH)
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pKa and strength of acid
HA-->H+A- (k1) backwards is K2 K1/K2=K high Ka means stronger acid-->LOWER PKA (a negative log!!!!! like pH)
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H2CO3 buffer system pKa and explain
pKA 6.1 (good for acids) | note H+-->shift left-->resp center-->out
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C anydrase loc
rbc lung renal tubule | eyes and gastric mucosa
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acid Mx 3 parts
1. buffer (instant) 2. comp (slower) eg resp and renal CO2/HCO3 changes 3. Correction
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acid Mx 3 parts buffer etc
1. buffer (instant) 2. comp (slower) eg blowing off Co2 ???? 3. Correction of underlying problem eg COPD, haemorrhagic shock, sepsis. #P+K
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plasma protein buffers
Carboxyl group pKa 2-->little effect ECF but more effect for ICF amino group pka 9
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renal comp CORE RV
max net loss 300mmol H+ secretion per day 70mmol of fixed acid produced per day 4321mmol per day for recapture of HCO3 renal comp 1) H secretion to recapture HCO3 -secrete H-->H2CO3-->CO2-->into cell-->HCO3-->system -90% PCT -against conc gradient -5% in DCT intercalated cells secrete H+ and can increase H conc 900 fold 2) secretion of tritratable acids H++HPO4-->H2PO3 also includes sulfate once HCO3 reabsorbed any further H+-->H2PO3 3) excretion of ammonia (75% of daily metabolic acid secreted this way) PCT: glutamine-->2NH4+ +2HCO3 -->HCO3 reab DCT NH3 secreted (lipid sol)-->H++NH4+ charged and not reab
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BE types
BE: amount of acid need to be added to 1L of blood to restor pH to 7.4 with normal CO2 and temp Standard BE: if Hb 50
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BE
amount of acid need to be added to 1L of blood to restor pH to 7.4 with normal CO2 and temp
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HCO3 types and derrivation ABG
CO2 is MEASURED (ITS EASY TO MEASURE) HCO3 is CALCULATED -actual HCO3 calculated from HHE -standard caclulate is HHE had a normal CO2 ----if standard HCO3 is normal then shift in pH is due to changed CO2 and not any metabolic process
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Balance IVF solultion CORE RV BRILLIANT
SID in body is 42 140+4-102 giving non albumin product with dilute albumin down so HCO3 increase (in general-it is a balance of dilution vs SID number) to avoid ALKALOSIS SID needs to be reduced to 27 to have neutral effect on pH note hyperchloaemia facted in to this SID of 27 (shit tone of Cl--->decreased SID-->decreased HCO3 hyperchloraemic MA Plasma has osmolarity of 296mosmol/L Na 140 Cl 102 NaCl 150-150=SID of ZERO-->hyperchloaraemic acidosis -osmol 300 CSL 131+5+2-112=SID 28-->neutral -osmol 276 -has lactate-->HCO3-->further alk i believe Plasmalyte (no colloid) 140+5+1.5-98=SID 50-->alkylosis 4% albumin is iso-oncotic with same alb conc as blood and SID of 42-->no change in pH
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temp and pH
increased temp--> increased energy so more sol (picture hot water absorbing more salt increased temp-->increased dissociation of H20-->H and OH-->increased acidity
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alphastat vs pH stat | R/V RV
temp not corrected assumed 37C - fine for adults - -1) ICF pH unchanged by temp due to imadozole temp dependant intracellular buffering system
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CO2 prod
20,000mmol/day
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RTA to acidosis
cant secrete H to reab bicarb | -->NAG MA!
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shock | CORE
acute circulatory failure with inadequate perfusion to meet tissue metabolic demand resulting in generalised tissue hypoxia (BMJ)
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EEG BIS and entropy R/V CORE
summation of inhibitory and excitatory action potentials of cortical pyrimidal cells ***UNPROCESSED ALPHA THEN BETA THEN DELTA FROM AWAKE TO ASLEEP AND FROM HIGH FREQ TO LOW*** awake- high freq low amplitude asynchronous - alpha predom when awake with increased amp when eyes closed ALPHA >8 HZ - sedation Beta predome >13Hz - anaesthetised delta shift <4Hz (4 looks like a d) low freq high amp SPINDLE WAVES - deep anaesthesia burst sup-->isolectric line ``` PROCESSED BIS or entropy -3 point, frontotemperal -fouviers analysis -detect interference and compensate -proprietery algorythms -for hypnotics NOT OPIOIDS ``` BIS (FFFFFFF) ***BFF***read's my mind. Bi is single - Freq and phase analysis - single number Entropy (FT) (this world and it's entropy is ***F't*** ENtropy is 2 - RE - SE - Freq and Time analyse -->entropy (degree of disorder)
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heat vs temp | CORE RV
``` # evernote #contrasting SI units #eg of specific heat capacity ``` heat is energy measured in joules (both KINETIC AND POTENTIAL) Temp is measured in Kelvin and related to how fast the molecules of a substance are moving ie their kinetic energy but does not factor in their potential energy heat can be added to a substance and either increase temp or change state (potential energy added) as in LHoV an equal amount of heat energy can be add to two different substance of differing SHC-->different change in temp - SHC of water 4200J - SHC of Hg is 140J SHC is the amount of energy to increase 1kg 1K J/kg/K
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temp measure CORE RV
non electric - mercury/ETOH-->delay - bimet coild - volatile-->Boudan (BOW DOWN) gauge thermometer electric - Resistance thermometers eg old ventilators! - -platenum-->Galvonometer in Wheatstone bridge - -INCREASED RESITANCE LINEARLY WITH TEMP - --->bulky - Thermisters (therma resistors) - -ceramic or metal oxides beads in series with a circuit - -increased temp-->EXPONENTIALLY increase in resistance - --->small-->swanganz catheters - --->overheat-->messed callibration eg in sterilization - IR - -IR-->pyroelectric sensors (yes pyro not piso)(crystals that become electrically polarised by EMR eg IR radiation)-->charge-->changed capacitance-->measured-->displayed
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neonatal airway and resp differences
https://www.wfsahq.org/components/com_virtual_library/media/ 324d4c30cd8e5bc6473f988dec984d25-7-Paediatric-anatomy---physiology-and-the-basics-of-paediatric-anaesthesia.pdf airway forgettables - mandible - funnel - narrowest at cricoid vs vocal cords - nasal Dx easy. oedema is big consequence - larynx is both ant and high - epiglottis is large and stiff yet flops Breathing forgettables 1) consumption 2) drive-apnoea, RR 40, 3) mech #CC #diaphram #CW compliance-->decreased FRC
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neonatal circ changes CORE RV
``` #insp-->increased Pulm BF-->increased LAP #decreased hpvc -->decreased RAP ``` #cord clamp-->increased SVR -->increased LAP YES P+K small fry - high O2 constricts DA - increasing O2 and decreasing CO2 decrease pulm VR A then Ovale then V seconds minutes hours Duo weeks Forament 5 weeks Vino hour seconds: DA-narrow with first breath phys close 14 hours anatomical closure 14 days minutes FO-functional close minutes perm at 5 weeks hours DV-hours
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RESP CHANGES AT BIRTH CORE RV | P+K
stim-->Reticular formation-->resp centre stim vaginal birth 35ml squeeze from thorax to pulm cap-->reab O2 falls 30--15mmHg CO2 rises 55--60mmHg centeral and peripheral chemo rec become more sensitive (likely due to increased BF to them) FRC 20ml/kg at birth -->30ml/kg at 1 hours -80cmH20 first insp
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DS average
2.2ml/kg=150ml
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body composition neonates vs adults
increased ECF and TBW TBW 75% vs 60% ECF 40% vs 20% ICF 35% vs 40% adult 70kg-->42L 28L ICF 14L ECF 11 IF 3 plasma (2L of RBC)=5L of blood
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fetal transfer roc
F:M 0.16 | sux is zero
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tocolytics
``` Rb Mg (apparently not on new evidence #anzca course- yet royal womens has diagram with i...) Rb CCB ```
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oxytocin met and SE
met by oxytocinase | VD-->reflex tachy
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ergometrin Moa and SE CORE CORE CORE CORE R/V #MELBOURNE COURSE (or maybe sydney)
ergot alkaloid from fungus DIRECT Sm stim-yet no VD as blocks vasomotor component onset 40s for 2-3H little known about PK note also VC uterine artery increases SVR and CVP and BP CORONARY ARTERY SPASM, MI STROKES, PULMONARY OEDEMA
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misoprostol and carboprost CORE R/V
prostaglandin rec-->increased SR release of Ca bronchoconstriction NV+D severe VC uterine rupture
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nifedipine tocolytic
1st line for preterm
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indomethacin tocolytics
DO NOT USE FOR ACUTE - close PDA - renal - gut
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GTN tocolytic
IN 400mcg or 100mcg IV
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physiological tocolytics
hypoxia and acidosis
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neonatal glucose control P+K
decreased glycogen stores increased req glucose main source then fat once insufficenet N BSL is 3 at term
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neonatal PK (NEED MORE) https://www.fda.gov/media/100219/download
decreased conjugation for first 70 days decreased albumin initially volatiles - increased resp rate and decreased FRC - increased CO and ECF-->increased uptake (slower onset) and decreased % to brain ``` A -RR and FRC -slow gastric emptying -imature biliary secretion-->decreased AB lipid sol -less acidic stomache-->change ionization -less GI enzymes -percutaneous ab increased D -alb -ECF -less body fat 10 vs 20% vs 1 year old -low Prbinding alpha 1 and alb -->increased free Phenytoin -BBB immature M -liver phase 1 and 2 normal at 2 years -non linear mcg/kg morphine req peak at 3yo E -renal GFR decreased up to 2 years-non liner -Tubular secretion and reab also reduced for 2 years ```
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uptake of volatile | CORE RV
Uptake=Q˙×𝜆b/g×(Palv−PMV)
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vomiting
#evernote Rb labyrinth -->Vest-->CNVII-->CRTZ VC ach rec GI 5HT-->NTS CRTZ has 2 names and 2 feed ins Victoria Cross has 4 points steroids at 5HT GI
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``` aerobic metabolism #khan academy image and Dr pod ```
Rb pyruvate oxidation-->CO2 and NADH not ATP kerb prod only 2 ATP and CO2 ETC 32 ATP glycolysis-->2ATP+NADH pyuvate oxidation-->acetyl CoA (CO2 +NADH) kreb cycle: acetyl coa cycles with prod of CO2, ATP, NADH, FADH2 Oxidative phosphorylation. electrons carried to electron transfer chain by NADH. with O2 as electron acceptor. electrons taken from high potential to lower. and ADP-->ATP glycolysis in cytosol pyruvate oxidation and kreb cycle exclusively in mitochondira electron transfer chain -the membrane of the mitochondira glycolysis occurs without oxygen everything else requires oxygen (definitely!)
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IC vs EC electrolytes and nernst potential | CORE RV
Gold Cats K high IC-->negative Nernst 150conc vs 5conc Cl low IC-->negative nernst 10 vs 125 Na low IC-->positve nernst 15 vs 150 calc E=58log(o/i) Goldman-Hodgkin-Katz E=58log Ko+Nao+Cli/Ki+Nai+Clo 0 is Over I is Inferior bellow
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nunns O2 vs CO2 for severity of resp Dx
O2 is severity | CO2 is DDx of ventilatory failure vs shunting
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Nunns response time to change AV Co2 vs O2 changes
on room air - small store of O2 so decreased AV-->half time of 30s - large store of CO2 so decreased AV-->half time 16 min practically we can preoxygenate and desat much quicker than building up CO2 with hypovent hence accutely desat is earlier warning of vent failure than CO2 (could erroniously mislead practitioner to believe it is a shunt as CO2 not yet risen)
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STP SF CORE RVish
barbituate with sulfur added at C2 hence "thio" at C5 substitution of central pyridimine ring-->"pentone" --phenyl at C5-->anticonvulsant --Methal at C1-->excitation TAUTOMERISM KETO-LIPID SOL ENOL-WATER SOL contains sodium (hence STP) salt N2 and NaCO3 -->basic-->enol 80% PrB pka 7.6
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midaz tautomerism
not enol, keto but closing of ring above ph of 4
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volatile SF relationship CORE R/V CORE CORE
substituted HCs all methyl ethyl ethers except halothane which is an ethane sub and sevo-->propyl methyl ether forgetables - CF3-->stable (3=tripod=stable) - CHF2-->react with sodalime-->CO (2=two soda and lime) - C next to O without halogen-->metabolised eg sevo! (no halo=no angel=no protection)
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sympathomimetic SFR CORE R/V
benzyl hydroxyl groups - 2 for max affinity eg Adr and Na but also BD by COMT and now too polar to cross BBB - just site 4-->alpha selective - -note metaraminol and ephedrine just have 4 (weak and long lasting-->good as bolus) beta chain - DECREASES LIPID SOL and increases potency - eg NA and A alpha chain -addition-->MAOi eg metaraminol and ephedrine. phenylepherine doesnt have addition-->direct action only with no indirect action amine - methyl-->alpa and MAOi - large-->Beta eg dobutamine
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isomers CORE CORE CORE R/V
same formular different structure A)structural with diff bonds A1 static iso vs en ethyl group arrangment of Cl vs F A2 is dynamic B)stereo same bonds diff 3D space B1 optic ie enantiomer (mirror) B2 diastereoisomer (non mirror) B2x is configurational (can't be converted by rotation around a single bond) B2y geometric eg cis and trans around double bond
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ANP
NATURETIC=DIURETIC VD affenent VC efferent and increase filtration coefficient blocks ADH, ATII, Ald
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macula densa in hypovol
less Na-->increased renin less Na-->NO more Na-->adenosine
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Gibbs-Donnan effect | CORE RV derranged phsyiology
Key role in cellular stability due to osmotic forces and albumin having astronger oncotic effect in plasma (RMB contribution small) describes the fact that uneven distribution of charged particles near a semipermeable membrane will form in the presence of impermeant charged particles Kerry brandis-->until chem and electrical gradient equal BUT THEN osmotic pressure-->distort things double gibbs donnan 1) large colloids Pr and PO4 IC pull H20 in -Cl pushes out to offset negativity and join Na outside 2) Na impermeant (would rush in if it could)--> EC Na high pulls H2O out -->balance ####if Na:K also pumps Na out and if this was blocked the cell would fill with h20 and burst # brandis note therefore high NaCl outside and high PO4 and Pr inside small Role 1) cell stability 2) increased plasma effective oncotic pressure 3) small contribution to RMB - vast vast majority comes from K+ permeability-->changed potassium conc (not exactly the same process) derranged phsyiology - DOES NOT CONTRIBUTE significantly RMB - "if the Gibbs Donnan equillibrium was unnopposed RMB would be -20mv (goldman-Hodgekin-Katz" - COMPLETELY PASSIVE is the effect (it is compensated for with active N:K ATPase to ensure not too osmotic inside-->burst) - in contrast RMB is set up because if because of different perm of potassium vs Na GOLDISH So, we are now at the Gibbs-Donnan equilibrium: the products of diffusible ion concentrations must be the same on both sides, and on each side of the membrane electrical neutrality is preserved. However, the presence of non-diffusible protein makes the total concentration of intracellular molecules much higher than the concentration of extracellular molecules:
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Colligiate properties
dep on particle conc. BP FP SVP osmotic pressure
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Specific heat capacity H20 LHV H20 Absolute humidity at 37 and SVP of H20 at 37C CORE RV
4.2Kj/Kg/C 2.2Kj/kg 44mg/L 47mmHg
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compatability blood testing CORE RV
key is that for X match you mix patient plasma with what could cause a big reaction (the donor RBC) -name is IDAT step 1 is forward and back 1. ABO (what Antigens are present on RBC) (including Rhesus which in on the RBC no in the plasma) 1. Forward test 1. Recipient RBC vs control 2. Backward test (confirm forward) 1. Recipient plasma vs control RBC 2. Screen for non ABO antigens (these are not on RBC! So patients serum is tested for antigens!!!!!) 1. Recipient plasma vs control RBC 3. Xmatch 1. Is screen and Hx negative for ABs then 2 options 1. Algorithm based on data—>choice 2. Immediate saline spin (check screen really right with real donor sample) 1. Recipient plasma vs donor RBC 2. Screen positive or sig hx 1. Indirecirect Antiglobulin test (IDAT) to see if ABO and other antigens present 1. Incubation of recipient plasma and donor RBC 2. Wash this combo to remove any plasma Ig not bound to RBC (this would react with the anti-human immunoglobulin about to be added 3. Glutination-add anti-human-IG to bind the Ig that is bound to antigens—>little clumps—>positive result
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universal FFP compatability
AB FFP because no antigens
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blood products that can be given and if they need testing
PRBC PL-ABO preferable but can give incompat (as ABO antigen-->minor reaction) FFP- i presume same as cryo... -all factors eg DIC, liver Dx warfarin but not if a more specifc therapy available. Cryo ABO preferable but can give incompat -high in fibrinogen, 8, vWF
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Dead space calculation
``` Bohr eqn is all DS Fowler is Anat DS (CC is not alv DS) Alv DS is Bohr-fowler Bohr eqn =PACo2-PexpiredCO2/PACO2 (PA is changed to Pa as minimal difference) ```
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anatomical DS
vol of conducting airways from insp to arrival at Alv ducts (respiratory zone)
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DS DDx kinda
Massive shunt or a shunt in a GA'd patient can look like DS as PaCO2 builds up and
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PaCO2-ETCO2
dead space 5mmHg normal
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hepatic blood flow and anaesthetics and spinal
spinal and epidural -decrease HBF due to MAP and PV Volatiles decrease HBF (ER at anaesthetic conc AR maintianed for sevo...Hm) - halo has severly impair HABR-->dropped HA and PV - newer agents have better maintianed HABR-->increased HA for decreased PV-->net decrease yet enough with increased OER to maintain oxygenation GA - decreased CO-->decreased map and venous congestion - impaired HABR
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HEP ROLE | CORE
``` synth met Rb protein cat and anabolism (AA to build or release for KG) Rb FFA for KG and prod of LDL from FFA exc ab immune reservoir rb ADEK, glycogen excretes and regulated hormones ammonia-->urea-->urine ```
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bili liver function
liver converts biliverdin to bili and then conj that bili total increased if excess BD, inefficient conj or obstruction - increase conj if obst - increased unconj if cant conj fast enough
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LFTs CORE
AST>2xALT-->SLab of beers S>L AST in hep and mitchondria so increased in Dx muscle of heart or skel (System) ALT in liver alone (L) ALP-bile duct bones GI renal CA GGT-bili duct ALP and GGT>AST and ALT then obstructive
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coag and liver Dx
PDreams and BJA suggest INR and PT (INR is derived for PT!-not aPTT) -all coag factors except 8 produced in liver so i think aPTT also relevant-some reasearch articles entertain this. coags in liver failure DO NOT CORRELATE WITH BLEEDING RISK as decreased coags yes but decreased anticoags too!
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NaCHR
Na rushes in and K out
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skeltal m vs sm muscle
1. Diffuse spread of NMJ 2. Visceral sm—>1 nerve actives multiunit sm connected by gap junctions 3. Tiny SR vs skeletal 4. Slower contraction as no troponin instead Ca:Calmodulin—>Myosin LC kinase—>phosphorylate ie activate myosin to bind 5. Plagued action potential for this 6. Kinase req to end contraction 7. Slow onset sustained powerful 8. Trigger: nerve, stretch hormone eg VC
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skeletal NMJ transmission CORE
In my memory 1. NACHR 2. Na in 3. Local depol 4. Ttubule (cardiac and Sk-more important for cardiac as has less developed SR vs Sk) 5. L-type VGCC (for cardiac most critical, and skeletal #guyton) ie DHPR-dihydropyridine 6. DHPR:Ryanodine rec interaction (for cardiac and skeletal #guyton) 7. SR Ca release(most dev in sk. less in cardiac, tiny in SM) 8. Trop change—>tropmysin change 9. Myosin binding site on actin exposed—>cross bridge—>shortening of myofibril unit
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``` sleep #P+K ```
necessary state associated with decreased reactivity to surroundings or level of consciousness, easily reversible with sensory stim progression to deep sleep awake-alpha dyssynch low freq high voltage 1. alpha from awake-->theta 2. spindles 3. delta 4. delta synchronous high voltage low freq sync non rem - restful - inhib midbrain - decreased BMR, decrease ANS REM 15min Q90min - retic and sleep centre - high freq, low amp, dysynch like awake - BMR increased 20% - dream, move, necrease muscle tone - GCorticoid prod increased - increased HR and BP - decreased pharyngeal tone-->OSA no sleep -impaired cog, mood, changed BP, BMR ``` CNS CVS RESP ENDO note core temp Renal-ADH ```
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brain fuel | CORE
glucose and ketones no fat
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fasting RV
glucose mainstay for brain, neural, RBC, renal maintain 3.5-6 glucose store plasma and IF 2 hours glycogen store 4: sk m vs hep 12 hours fluid req 30ml/kg/day <6 - ADH, Adr, decreased insulin - very minor role of GNG >6 - increased glucagon, adren, ADH, cortisol - GNG source is AA, glycerol, lactate, pyruvate (cori cycle) - ketogen DONT FORGET - acid effect of hypovol and KB - vol resp - electrolyes - glucagon
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ketogen and GNG RV CORE
both use fat and muscle!! GNG from AA and TG ketone is most classically from FFA from fat - trying to take away protein catabolism from GNG path - some AA still go to ketogen ``` KG FFA-->(betaoxidation) -->acetyl CoA-->if Acetyle CoA in excess what kreb cycle can use (oxaloacetate is depleted in fasting state) then Acetyl coA diverted to KG via acetoacetyl CoA enzyme and BMG-CoA--> acetone B-hydrybutyrate acetoacitate ``` used in brain, cardiac and sk m.
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cori cycle
lactic acid cycle | glucose-->p-->lactate
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spinal cord BS R/V
the single ant posted two posts and got a radical response descending from level of foramen magnem 1. Single Ant (2 vert arteries supply) - ->ant 2/3 2. dual post (Post inf cerebellar Art) - ->post grey and white tracts single anterior is Supplimented with radicular arteries that enter through the intervertebral foramen and follow ventral and dorsal nerve root these radicular arteries are from the spinal branches of the cervical, intercoastal, lumbar and sacral arteries. Nil ANASTOMOSES
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Spinal cord perfusion pressures
MAP-ISP or CVP dura is indistensible so injury-->swell-->monroe kelly doctrine req is SCPP of >90 vs CPP >75 Rx with raised MAP vent and manitol doesn't work on SC
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glut rec | RV
``` Glut 1 brain and rbc Glut 2 -liver for GNG glycolysis control -panc beta cells -gut for absorp Glut 3 neural glut 4 fat and muscle ``` Two trigger Four Fat
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measure BMR | RV
indirect calorimetry - heat indrectly related to O2 consumption and CO2 producution - wait until CO2 and ET at steady state then crunch then numbers ``` Resting energy exp related to (Fio2-VeO2) plus VeCO2 with a few other constants #weir eqn ```
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factors influencing Metabolic rate (Note BMR!)
affected by: Age BMR decreases as age increases. Neonates have a BMR twice that of an adult Children have an increased BMR relative to that of an adult BMR declines by 2% for each decade of life Body Composition Lean muscle has a greater energy requirement than fat. Higher body fat percentage results in a lower BMR Females have a lower BMR for this reason - when adjusted for lean mass there is no difference Diet Digestion increases BMR by ~10% due to the energy required to assimilate nutrients This is known as the specific dynamic action of food. Protein > carbohydrate > fat Note that the Specific Dynamic Action for each macromolecule is not related to the respiratory quotient for that food type. Starvation decreases the BMR Exercise Skeletal muscle is the largest and most variable source of energy consumption Environment Cooler environments increase BMR Temperate environments decrease BMR up to 10% Physiological states Pregnancy increases BMR up to 20% in 2nd and 3rd trimester Lactation increases BMR Catecholamines increase BMR Corticosteroids increase BMR Disease states Malignancy increases BMR Sepsis increases BMR Hyperthyroidism increases BMR
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Kelvin SI | CORE
triple point of water is 273K - ice, liquid, vapour all present at equilibrium - this is zero degrees!!!!!! =O degrees celcius! - boiling point of water (conveniently not by design) is 100C - -SVP=atm p-->bubble
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1mol
atoms in 12g of C12
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SI
meter-related to speed of light second-related to period of a specific atom oscilating kg (only one with a physical prototype) candela-about the light from a standard candel Current=amp=based on force of attraction between parralell wires Kelvin=triple point of water (frozen, liquid, vapour in equilibrium at same time) =273K 0K is absolute zero no movmenet mole=about in 12g of C12 #SMMACKK ``` Derived Newton=kg/m/s2 pressure= Pa=N/m2 energy=J=n.m power=J/s ``` Non SI units
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paramagenetic O2 analyser CORE #check equipment book to see if this is sufficent
O2 has a strong magnetic susceptability EMField present-->attract O2-->pressure-->move flow meter-->callibrated to O2 content Oxygen, nitric oxide, and nitrogen dioxide alone among the common gases exhibit paramagnetic proper- Nitrogen as reference gas
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freezing point
triple point equal part liquid, solid, vapour liquid to solid=0 degrees with water at atm pressure
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harmonic freq
Fundamental freq=n (Hz) Harmonics 2nHz 3nHz 4nHz etc (multiples of fundamental freq)
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optimal damping
optimal damping coefficient of a system therefore depends on the natural frequency one overshoot and one undershoot Damping coeff 0.64 over damp high number eg 1.5-->alot of damping underdamped 0.03-->hardly any damping
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Ach met and prod
acetate and choline choline gets recycled cholineacetyl transferase AcetylCoA+Choline-->Ach
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neo organophos and edro CORE
Neo reversible covalent bond to esteratic site -->carbamylated (NH2-CO-) complex --->slowly hydrolysed Organophosphate - broard group with PO4 in industry and insect - irreversible covalent binding of esteratic site Edrophonium - weak reversible electrostatic bond - QuAternary end binds Anionic site - OH-binds esteratic site (Ammino acidand OH is the esteratic site)
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mono quaternary and bisquartnerary
mono is faster and less potent
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ENANTIOMER EXAMPLE CORE ish
ENANTIOMERS -TRAMADOL —+ (S) 5HT RUI (S for seretonin S for SUM) — - NA RUI (R for reduce) ``` Ketamine S (+) -potent -faster off -less neg ino -less psych severity (not freq) R(-) -BD ``` ``` # sinister (left) # rectus (right) ```
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NDMR SE
AS - Vec-->CIM. hep met to active-->renal - roc-->mild Vagolytic anpahyl-->95% unchanged 5% liver-->biliary and renal exc - Panc-->vagolytic-->hep met to active-->bili and renal exc ``` BIQ -histamine Atrac -->CIM. met hoff and NSE laudenosine Cistatrac-->hoff and mets-->NSE Mivac-->Butyrlcholinesteras!!!! ```
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thermodilute calculation and rationale CORE GOLDEN CORE CORE CORE
Equipment book: utilise Fick's Principle CO=uptake/Ca-Cv -FICKs prinicple-->dose/AUC ``` CO=Clearance (clears the cooled blood) AUC=dose/Cl Cl=dose/AUC dose=density.Vol.SHC.difference in temp density and SHC assumed same as blood CO=Vol of injection.difference in temp/ Integration of temp vs time ie AUC ``` constant.thermal capacity of injectate. / constnat.AUC
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PO4 buffer
HPO4+H pkA 6.8
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bohr effect and buffering CO2 mech | CORE RV
CO2-->H2O+CO2-->H2CO3-->HCO3+H (HCO3 pushed in to plasma) | H+ KHbO2-->HHb +K+O2 (O2 released)
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urine titratable acidity
refers to amount of H bound to buffers in urine. | the amount of base needed to be added to equal pH 7.4
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H+ secretion
PCT Na/H pump Na from Na:Katpase active H+ produced by CA from CO2+H2O DCT H+ secreted alone by intercalated cells and also by HATPase
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HCO3 PRODUCTION
1. H+HPO4-->H2PO4 and 1 HCO3 added to peritubular capillary #P+K (is this production) 2. glutamine-->2NH4+2HCO3 in PCT
365
Counter current LoH | CORE
counter current - simultaneous movement of 2 substances in different dirrection across a membrane - in context of vasarecta 1 current down the other current back up Goal: concentrated hyperosmolar medulla to reabsorb from CD if ADH present only small amount of H20 reab itself note dilute 100mosmol/kg exit LoH (NOT CONCENTRATED) 1. Thick ascending loop active reab Na (imperm to H20) (exit LoH dilute water osmol 200-->100 with repeat) 2. creates hyperosmolar IF 400-->magnified to 1400 at hairpin with repeat 3. hence H20 reab into IF in desc loop (impermeable to NaCL #P+K)(causing hyperosmolar tubular fluid osmol 400-->500 with repeat) this reabsorbs water in LoH but more importantly creates gradient for CD NOTE medullary gradient 50% due to CC and 50% due to urea trapping. LoH, DCT, CD imperm to urea
366
Counter Current Vasrecta CORE
role:minimise medullarly conc washout perm to NaCL and H20 the whole way slow flow H20 sucked out on descent and Nacl drawn in. then highly osmolar tubuleare solution draws H20 back in on ascent and Nacl leaks out.
367
WZ4
Pa>Pi>Pv low lung vol-->increase Pi as less radial traction. also increased in pulmonary oedema. occurs at bases Pa:Pv steady and irrelevant and Pa:Pi governs flow
368
Co2 carriage | CORE
Arterial 5% dissolved 5% carboamine 90% HCO3 Venous STC #Vascular STEAK!!!!! 10% dissolved 30% carboamine 60% HCO3
369
hypoxia hypoxaemia Cxs | CORE
Hypoxia O2flux eqn 1. Hypoxaemia 2. Cardiac output 3. Hb-anaemia or CO poisoning 4. Histotoxic (eg cyanide-stop OP process Rx nitrate) (also diffusion) ``` Hypoxaemia Normal Aa -PiO2 -MV -increased req Abnormal Aa -diff -V/Q-->shunt ```
370
measuring humity and definitions CORE
water vapour in a gas Absolute Mg/M3 relative=VP /SVP ie absolute/max Measure 1. Hair hygrometer (relative) - hair wrapped around spool that turns dial. - humid-->lenthen-->turn 2. Wet and dry bulb hygrometer (relative) - wet thermometer vs dry thermometer - wet is constantly kept in a wet surrounding-->evaporation. - increased humidity-->less evaporation-->less temp change between them 3. Regnauld Relative and ab - shiny metal plate temp dropped until precip 4. electrical - metal with changed capacitance or resistance with humidiity
371
ITR TNZ CORE
ITR 36.9-7.1 (Millers) ie normal is 37 core temp - millers GA drops threshold 2-3C widens a fraction above - miller "This range is bounded by the sweating threshold (P+K says VD) at its upper end and by vasoconstriction at the lower end. " - poikilothermic in the ITR TNZ 27-31 naked P+K ambient lower limit is critical temp
372
humitidy 20C
20C-->20mmHg-->20mg/L
373
heat loss graph
note evap platues at crit temp (horse shit but whatever) | others have a brief platue at crit temp (no logic but sure)
374
``` antihypertensives #katzung ``` CORE
Rb methyldopa central dexmedatom Rb monoxidil K chan openiner yes (physioten) Rb prazosin ALPHA BLOCKER Rb phentolamine alpha blocker betablockers work at a) heart b) block b1 rec in JGA-->block renin stim
375
propanolol
old school non selective B1 and B2 negative ino and blocked renal B1 rec main action also VD B1 SE brady HB B2 asthma, ischaemia in PVD, Diabetic BSL*** rebound on WD #katzung ``` --------------------- P+H High lipid sol -T/2 4H -hep met-->ACTIVE MET -membrane stablilers ``` indic: T4
376
metop and atenolol
selectiv B1 ++ (not complete) | hypertension MORE?????
377
labetalol
``` 4 isomers 1 alpha blocker 1 beta blocker IV PO 3:1 B:A ``` great for phaemochromocytoma and emergency hypertensive (alpha with stopped reflex tachy)
378
Carvidelol
isomers with alpha beta | indic: heart failure with HTN
379
esmolol
B1 selective rapid met by hydrolysis by RBC esterase half life 10min load 1mg/kg then 100mcg/kg/min and titrae indic: hypertensive crisis with tachy or periop indic: risk of tox of other bb in heart failure
380
betablocker indic\ CORE
``` HTN angina peri MI phaechromocytoma T4 HOCM anxiety migraine glaucoma suppress tachy on laryngospasm ``` Head down - brain and psych - eyes - thyroid - heart - -HTN, IHD, HOCM - adrenal
381
BB division
selectivity - BD generally unwanted-->BC and VD - Met, aten, esmolol (AME like AIM=selective) intrinsice Sympathomimetic activity ie partial ag - good for mild HF-->reduce severe brady - CI in severe as any neg inotrope bad membrane stabilizers -little clinical sig
382
BB effect CORE
Cardiac and vasc Chrono automaticity-class ii antiarrhythmic ino B2 block-->VC!!!!! and BC-->cold hands brady-->increased supply and reduced demand -outways the harm of B2 blockade-->VC of CorArt Resp -all will eventually cause BC Metabolic - BSL complex alpha and beta rec and many hormones - B2 block-->unable to raise BSL in hypoglycaemia but baseline increased in DM - B mask Sx - increased TG lipids CNS -lipid sol-->CNS Sx (Metop and propran) #fat PM -->hallucination, depression, nightmare, fatigue Occular -decreased prod of AH GI -dry mouth and GI disturb (like PSNS override)
383
BB PK | CORE
lipid sol-main low - atenolol - ->poor GI ab, little hep met, excreted unchanged in urine - ->T/2 7 H - sotalol - ->half life 15 hours and renal exc ``` High -well ab -extensive hep met -short T/2-->freq dosing -Cross BBB-->CNS SE #labetalol is highly lipid sol yet used in maternity ``` High cont - Labetalol - ->short T/2 5H and hep met - Metop - ->T/2 3-6H hep - Esmolol - ->T/2 10 min - ->RBC esterase - Propanolol - T/2 4H hep - TImolol - -T/2 4H Hep and renal PrB is variable for high and low
384
SNP CUPADORSETDAME
``` P+H p235 # evernote ```
385
B2 agonist
VD and BD
386
alpha 2 ag
moxonidine physioten VD
387
ATII arteriols and ACEi
EFFERENT VC to maintain glomerular perfusion in hypotension in shocked patient ACEi-->
388
ACEi indication
``` HTN MI CCF DM atherosclerotic CVDx CKD ``` ``` Prevents cardaic remodelling improve supply (CorVD) and reduc demand (HR,Pre, contract, AL) minimise endothelial Dx ```
389
ACEi and renal Dx CORE #AFP and AHA
CKDx -usually improves renal blood flow (RBF) and sodium excretion rates in CHF and reduces the rate of progressive renal injury in chronic renal disease AKI risk ARF is most likely to occur when renal perfusion pressure cannot be sustained because of substantial decreases in mean arterial pressure (MAP) or when glomerular filtration rate (GFR) is highly angiotensin II (Ang II) dependent. -ATII normal VD efferent to MAINTAIN GLOM PERFUSIONPRESSURE so ellimination of efferent VD +hypotension -->ischaemia
390
Magnesium everything RV #stoelting P+H and OxCH CHECK KERRY BRANDIS FOR MORE DETAILS
C-inorganic cation U -A-attentuate SNS response to laryngoscopy -B-BD. attenuate (reduce HPVC) -C-VD (Cor, periph, cerebral, pulm), prolong SA, PR, AV conduction, torsade, peri MI -D-CNS dep-->anticonvulsant. solumn increased effect of hypnotics. CCB-->weak and increased DoA of Muscel relaxants (give 1/3 muscle relaxant) analgesia-blocks NMDA. inhibit release of Adr. decreases (Mx phaemochromocytoma) AcH release at NMJ worsen MGx minimise BBB disruption in TBI-->decreased cerebral Oedema -E electrolyte-CCB. modulate Na, K flow at NACHR and ion pumps, enzyme cofactor for 300+ and ATP, DNA, Pr -F renal VD-->diuresis -GI osmotic laxative -H-CCB-->increased clotting time -Interaction MR and CNS. deduce K release with Sux and reduce fasciculation and myalgia after. -M. cramp Rx -Uterine relaxant for preterm labour and PETx P -10ml of 20mmol CCS Dose 4g ie 8ml of 0.5mg/ml neat solution then diluted down R-IV or IM D 99% ICF A ileum passive ab M E-renal (95% reab -mostly LoH) Hypomagnesaemia vomiting, weakness, convulsions, tetany, fasciculations, as well as electrocardiogram (ECG) abnormalities (prolonged PR and QT intervals, diminished T-wave morphology, torsades de pointes, and others) and accompanying hypokalemia and hypocalcemia.
391
SNP CUPADORSETDAME
P+H p235
392
GTN CUPA
#evernote
393
neonatal first breath graph
note: breath 1,2,3 all create a volume greater than the normal TV peak. i guess the negative pressure overcomes and overshoots
394
neonatal PD (NEED MORE) https://www.fda.gov/media/100219/download
``` A B C D E -hypothermia F G H -less Vik K ddep clotting I -poor immunity ```
395
COPD to CO2 and O2 changes | https://bjaed.org/
air trapping and atelectasis-->VQ mm narrow-->Alv hypovent Dx-->impaired gas transfer
396
potassium intracell why
binds to Pr- !!!!!!!
397
anti arrhytmic classes | CORE
1 P.S Naaaaaa a) prolong refract (Procainamide) b) shorten (lignocaine and phenytoin) c) no change (flecanide) 2. BB 3. K CH eg amiod 4. CCB Verap and Dilt
398
lig use arrhytmia | CORE
VT -especially reentry of MI reduce rate of rise 0 and threshold and reduce ARP #evernote
399
amiodarone CUPA | CORE
``` #evernote note phlebitis note interaction ctyp450 inhibitor PrB QTc (TCA) AV block BB CCB A -variable OBA 20-80% D large Vd 98% PrB M-CYP450 metabises to active mets E-1% renal 99% all biliary ET/2=days ``` Dose adjust not req in renal (OxCHB) Interaction - PrB—>bump plus CYP450 inhibition—>effects - digoxin, warfarin, BB
400
CYTOCHROME P450 inhibitors
``` amiodarone erythromycin clarithyromyc fluconazole Diltiazem and verap grape fruit imatinib cimetidine ```
401
CYP450 inducers
``` Phenytoin, barbituates Carbemazepine st johns wart rifampicin ETOH ```
402
metabolised by CYTp450 https://www.aafp.org/afp/2007/0801/p391.html GOLDEN CORE
#evernote Phase 1 hepatic met (MUCH BETTER FROM COURSE warfarin is a substrate metoprolol CYP2C9 amiodarone/flucon/bactrim-->inhibit-->decreased met of NSAIDs and ARB and carvidelol-->hypotension, renal injury and bradycardia phenytoin/carbemazepine/phenobarbital/rifampicin induces-->ineffective analgesia, HTN and tachycardia NOTE THAT PHENYTOIN IS AN INDUCER (and also a substrate) like a terrorist destroying himself and others
403
zero order kinetics
phenytoin just above theraeputic range STP infusion ETOH
404
Cardiac output measure | CORE GOLDEN RV
1. Thermodilution dose/auc - gold standard but dangerous 2. USS - AoCSA.Veloc=flow - errors wrong angle. technically difficult 3. Pulse contour analysis -computer algorythm -requires calibration with a TD test on that patient first hence PiCCO (Pulse Contour Cardiac Output) -->CVC cold flush -->artiline with thermister calibrated then CO=K (constant from thermodilution). integration of factors such as...P, SVR, compliance, change in P/time 4. throracic electrical impedence - outdated - size changes with diastole vs systole relative to SV NOTE THAT swing alone is hypovol not cardiac output
405
dex vs clonidine guy tut
both increase hypotension dex is worse if given as a bolus or high dose dex is the only one to cause sig brady dex reduces sig tachy and sig HTN
406
flow meter | CORE
turbulent in all devices except roatmeter at low flow ``` turbulent Re: r.inertia/viscosity F proportional to square of pressure change increased flow-->increased Res Increase Density-->decreased flow ``` Method 1. a) Orifice with U shaped manometer around (no flow through manometer at all (filled with water) THINK OF THE ORIFACE AS A THIN PIPE Pressure is less of other side vs where blast has come from change pressure is proportional to Q2 constant orifice-->change pressure causing changed flow b) same principle with rotameter but constant p-->variable orifice ie variable flow Method 2 Bernoilli principle venturi draw in=lamina so linear so more accurate upstream mean veloicty need to be continued through narrowing kinetic energy increased at expense of potential energy. reopen-->low pressure --entrail
407
reynolds turb lamina the lot | effects of density and res with bobbin example
In normal airways, the flow is mainly laminar (turbulent flow is localised to the upper airways) "derranged phys #INERTIA is key viscoisty maintains flat sliding sheets inertia ripples them into turbulent waves hence reynolds number =2r.inertia/viscosity =2r. density X velocity / viscosity more inertia -->more tubulent large radius-->space for eddies etc lamina flow-->hagen poisel F=P/R turbulent not the same! R=8nl/pi.r2 note n=viscosity Derranged phys viscosity increase lamina R to slow! density increase likelyhood of turbulent therefore-->slow! density of turbulent flow-->decreased flow -Oxygen pushes bobbin higher than less dense He density of lamina flow-->do change -eg low flow rotameter (decreased radius and decreased velocity) same viscosity O2 and He -->same flow pushing bobbin Turbulent flow Flow is proportional to the square root of driving pressure. Resistance increases in proportion to flow rate, and cannot be described using the traditional Hagen-Poiseuille equation. Pressure = K.(flow)^n where K is an empirical constant which, for the human respiratory tract, appears to be 0.24 ( when the pressure gradient is expressed in kPa), and n=1.3 Density is the most important determinant of whether or not flow will be turbulent, all other things being equal. This is where helium becomes useful, i.e. by decreasing the density of the inspired gas mixture helium improves the likelihood of laminar flow occurring in narrowed airways, and this decreases the resistance to flow.
408
venturi effect reworded | GOLDEN CORE
fixed volume flow -->mean upstream velocity this velcoity must be maintained so increased flow through narrowing increased kinetic energy with decreased potential energy open up-->decreased Pressure bernoulli equn for hydrollics changed P=V^4
409
venturi appature
venturi smaller appetur-->less oxygen #mari
410
daltons law
Pt=P1+P2 | the partial pressure exerterted by each gas would be the same if it were the only gas in the volume
411
thermister graph
relatively linear over measured range # eqbookyes semiconductor
412
bimetal therdsmometer | CORE
thermocoupling -diff temp-->electrolytic cell-->voltage and current-->non-lineraly proportional to diff in temp between the ends (not temp diff between metals)
413
measure vol
spirometry | not VC or hence TLC
414
flow with hot wire
anemometry - cooling of wire related to SHC and gas flow - wheatstone bridge change temp-->change res due to changed flow (in ICU vents)
415
flow USS
dopper | -send and receive (lower freq if running away)
416
``` FRC measurement (including RV) CORE ```
He dilution (funny and simple and only disolved ventilated RV not collapse air trapped) bag and tube=C1V1 end of normal tidal breath then inspire. equilibrate with lung with several Tidal breaths now whole system C2.(V1+v2) V2=FRC
417
FRC CORE
body plethysmograph (not fun but covers everything including trapped gas) try breathe in after normal exhalation against obstructed tube V1.P1=P2.(V1-changed V) in telephone box V3.P3=P4(V3+change in V) in lungs first equation determines change in V second equation uses this to solve V3=FRC
418
plethysmograph
refers to both the O2 trace and to volume change in body plethsmograph study of FRC
419
antipschotics
all block DA in BG and limbic and CRTZ also block alpha and hist Typical D2 Drop, halo and chlorpromazine (NOT PROCHLORPERAZINE=STEMETIL) Atypical D2 and 5HT-->less EPSE, less prolactin, dissociate before tardives can dev olanzapine 1st line less sedation, minor hypotension, no QTc change.
420
Typical antipsych SE
``` Neuroleptic Malig Sx -RF=dehydration and illness 1. hyperthermia 2. hypertonic m. 3. Unstable ANS (arrhythmia, changing BP and HR) 4. Changing LoC -30% mortality -Cx not known (DA ag—>Rx hence likely related) -Rx supportive —Dantrolene—>m relax —DA agonist amantadine -DDx -MHx (NDMR DONT RELAX IN MH but do in NMSx), antichol Sx ``` ``` Prolactin increase (disinhibited)—>gynaecomastia Weight gain Amenorrhoea Decreased CrH Some impair insulin ``` Sedation -due to alpha blocker, antichol, and hist Poikilothermic Decreased seizure thresh Interaction -decreased response drive interact with anaesthetic drugs Halo—>longer vs drop and doesn’t block alpha to cause hypotension ``` SE “Resemble the others above” -The outwardly calming effect of droperidol may mask an overwhelming fear of surgery. -CI in PDx -rare laryngospasm ``` Decreased CBF but CMR nil change—>risk ischaemia No reticular activating system depression No amnesia Mild pull and systemic SVR drop “A cardiac antidysryhtmic—>protect against Nad induced arrhythmia” Large doses >0.2mg/kg—>decreased conduction—>reentry tacky in WPW Prolong QTc -delayed vent repol (slow K efflux) -Droperidol is capable of prolonging the QTc interval on the ECG.[70],[71],[72],[73] Although the QTc prolongation effect peaks 2 to 3 minutes following IV administration of droperidol, the effects may persist for several hours Furthermore, droperidol should be administered with caution to patients who may be at risk for development of prolonged QTc syndrome (congestive heart failure, bradycardia, hypokalemia, elderly, concomitant administration of other drugs known to prolong the QTc interval). Resting ventilation and the ventilatory response to carbon dioxide are not altered by droperidol.[78] Furthermore, droperidol administered IV augments the ventilatory response evoked by arterial hypoxemia, presumably by blocking the action of the inhibitory neurotransmitter dopamine at the carotid body A D 2L/kg M Liver: High HER so Cl=hep BF E ET/2 2H
421
flow meter. change lamina to turbulent how does flow estimate change CORE R/V
lamina F=P/R Turbulent F proportional to square root of pressure so big drop in pressure due to turbulence misinterpretted as high flows. ie overestimation
422
PK of antipsych
all are lipid sol and cross BBB and placenta all are completely met in liver and excreted in urine all have long half life for OD dosing
423
flow measurement in vent | RV
Pneumotachogram 1) laminia F=Pressure grad/res errors 1) changed resistance R=8nl/piR2 - different viscosity requires diff calibration 2) temp-->cold-->condense-->increase res hot-->altered res 3) NONLAMINA FLOW 4) extremes of flow - too low reistance - too high (too small pressure diff to appreciate Types 1) fleisch (pipes) 2) lilly (gauze) 3) pitot
424
flow measurement machine | CORE CORE CORE CORE
ROTAMETER peak expiratory flow meter (in anaesthetic machines) blow-->spin a rotating door reistened by coild spring with annular orifice to exit
425
rotameter errors and safety
1) static or dirt-->stick 2) crack 3) non verticle safety 1) rotameters in series and mixes with other gases(from other rotameters last to avoid hypoxic mix #14.11
426
capnography measurement | CORE CORE CORE
IR SPECTROMETERY errors 1) collision braodening hence measure O2 and N20 to compensate 2) WATER VAPOUR-->WATER TRAP
427
beer-Lambet law eqn
Ab=e.L.C e= extinction coefficient SUPPLIMENT FORM EQUIPMENT BOOK P226 Chopper wheel—>intermittent IR Reference tube separated from testing tube with diaphragm—>different pressure from heating (with oscillation from intermittent IR—>change electrical conductance—>display (Some modern use photocells instead) Errors 1 CO2 CO and N2O all very close together in wavelength absorbed 2. Collision broadening 3. ethanol 4. acetone 5. Can’t detect different volatiles unless informed 6. BASE ON NUMBER OF MOLECULE IE partial pressure not conc! 1. PSV, narrow bore sampling or altitude —>increased pressure. Hence re calibration 7. Water condense (absorbs IR -can be measured) and blocks line) water trap
428
mass spectrometry
mass and charge any gas if known to be in mix errors unexpected gas eg acetone or propellant from BD pump vacuum failure loose two electrons instead of one (appear to have mass halve as much) 1) sampling inflow 2) vaccum ionization chamber (lose electgron-->positive charge) 3) accelerated into final chamber by negatively charge plate with slit 4) now all charge wih one ion lost and attracted to magnetic field (negative) hence Charge:mass now just mass-->heavy--->less deviation--> detected by ion detecting plate 5) for same mass eg N20 and CO2-->fragmented by ionization-->measure consituent parts.
429
plenum safety
Propofol dreams forgot 1) max conc 2) antispil mech 3) vol of bipass=vapouriser so increased temp causes equal change in pressure to avoid back flow 4) state different volatilies-->diff SVP 5) flow compensation 6) removable eg in MH 7) low pressure leak test
430
RCD coil name and fault cut time | amps
toroidal 40ms 5-10mA
431
micro mac
0.1mA and 100mA
432
LIM current
prospective hazard current>5mA
433
equipment class
1 earthing wire 2 no earthin as double insulated 3 no earthing as small voltage
434
Applied parts
B BF CF
435
P+K SNS kidney | CORE
NOT AUTOREG AS AUTOREG IS INTRINSIC VC Aff and Eff-->decrease RBF alot and GFR just a little
436
AUC conc time
AUC=x/Cl INDEP OF Vd!!!!!!!!!!!!!!!!!!!!!!!! Elimination=Cl/Vd so AUC=x/(Elim.Vd) but as Vd changes Elim changes the same so actually indep of Vd!!!
437
Vd calc multicompartment (3 options) GOLD CORE HARRY
1) extrapolate from terminal elim on Logconc vs time -->small estimate of conc at time zero-->overestimate volume (vd=x/conc at time zero based on term elim) 2) Varea -Elimination=Cl/Vd so Vd=Cl/elimination (P+H p 65) -AUC-->calc clearance -Beta rate constant from term ellimination -assume rate constant for terminal elimination is average of all (which it isn't-->underestimate elim-->overestimate volume) 3) Vss Vss=Cl.MRT conc.time vs time-->First moment curve AUMC/AUC=MRT
438
determinants of Vd
low MW uncharged lipid sol tissue binding | CCF, renal, hep Dx, fat, dehyd, aging
439
assumptions of loading dose
x=conc.Vd if Vd single compartment then assumes instant equal mixing if Vdss then in my mind also assumes instant mixing
440
Vd calc fixed vs changing
ITS DYNAMIC!!! | smallest at bolus then bigger at Vss and platues at final max at terminal elim
441
Vd EN
must same that Vd can be bigger than body weight and use the term APPARENT Vd marks for drugs eg and reasons marks for pathology
442
CBF EN | CORE
importance of stable CBF (high MRO2 nil anaerobic option) P+K 50-150 MAP linear increase 3%/mmHg CO2 due to H+-->VD-->steal Sx O2-->double flow at 30mmHg due to hypoxia and LAcid 10% CMRO2 per degree temp-->parralel CBF drop
443
Mg role (1 word)
NNa:K aTP
444
NEOSTIG
reversible covalent bond at esteratic site of acetylcholinesterase
445
inuslin reg
stim TK rec
446
liver prod...
no ATIII | yes vWF
447
brain ketones
glucose primary but can use a bit of ketones
448
raman spectroscopy
light reflects with a tiny proprotion losing energy and changing wavelength determined by the reflecting material. laser with mirrors bounces back and forth light reflected changes wavelength this change in frequency is proportional to conc of that gas cons -lots of power, noisy pros no alteration to gas-->return to circuit
449
M1 and M3 | RV
M1 is brain (1 tracked mind) | M3 is lungs and lung and BV VD 3 for the tree
450
platelet steps CORE CORE CORE CORE HARRY
1. adhere (Gp1a=collagen of GP1b with collagen:vwF 2. activate (by collagen, TXA, 5HT, Adren, IIa-->Phospholipase a-->PKC-->Ca and sphere to disc 3. aggregate (bind by Gp2b3a and Fibrinogen) 4. PL plug stabilization by fibrin from fibrinogne
451
O2 prod
fractional distillation of atm | (can also be done by hydrolysis of 2H2O-->4H and 2O2
452
VIE safety | and if demand EXCEDES SUPPLY
additional note - outside - caged - cylinders in reserve - weighing scales MORE DEMAND-->pull liquid from bottom-->heat-->vapour store -160C (below cirt temp of -118C) at 100Bar ie 1000kpa
453
cori cycle ie lactic acid cycle | CORE
P+H is ++ brief on it glucose-->LA in m-->liver-->GNG-->glucose with production of HCO3 that is matched by H+ in this closed system but giving lactate in CSL-->addition of HCO3
454
indomethacin
nonselective COXi
455
Clonidine
Tachy is not much of a thing | Dex it is especially if given as a bolus due to a1 stim prior to alpha 2 onset
456
ADH ant or post
Post-Pooo (Oxytocin)
457
ADH ant or post
Post-Pooo (Oxytocin)
458
``` GABA rec #wikik ``` CORE
GABAB gamma alpha beta alpha beta (sounds like kebab) GABA rec at AB junction x2 BNZ at GA junction
459
``` GABA rec #wikik ``` CORE
GABAB gamma alpha beta alpha beta (sounds like kebab) GABA rec at AB junction x2 BNZ at GA junction
460
CBF and MAC
EN. AUTOREG PRESERVED at 1 mac of sevo low mac decrease CMR-->DECREASED CBF! high MAC-->uncouple MILLERS - if MAP controlled with vasopressor then yes as above - if MAP allowed to drop then CBF drops at 1 MAC 40%=same drop in CMR so OK
461
CBF and MAC
EN. AUTOREG PRESERVED at 1 mac of sevo low mac decrease CMR-->DECREASED CBF! high MAC-->uncouple
462
CBF CO2 | CO2 response unchanged with volatiles (Miller's)
CO2 response is depressed by up to 70% during the administration of volatile anesthetics. slope is depressed.
463
LA charge
tertiary amine yes
464
cyclizine MoA
central M and H antag
465
H1 antag CORE
THE 1 DRUG I TAKE 1st gen Phenergen-->cross BBB - antihist, anticholinergic - AE, sed, antihist - SE from antichol and sed from hist 2nd gen Fexofenadine-->no BBBB - anti hist and antichol - no AE or sed
466
H2 antag | CORE
Cimetidine-->inhibit p450 and has antiandrogen effects Rinitidine-->no inhibition of P450 and more powerful and no antiandrogen-->preffered both can cause brady due to H1 rec -->AV slow conduction-->arrhythmia
467
H secretion gut #evernote chief
Gcell-->gastrin-->ECL-->histamine-->H2 rec GPCR at parietal-->acid parietal and G also stim by Ach from vagus and inhibited by Prostaglandin rec eg misoprostol vs NSAID
468
PPi MoA PK and SE | CORE
Omeprazole - prodrug in capsule to avoid stomach acid-->BD - activated in parietal cell - blocks final common pathway SE - inhibit P450-->decreased activation of clopidogrel (a prodrug)-->clots! - change stomache pH-->changed ab of things
469
antacid
al and mg salts-->diarrhoea and constipation-->complex things-->change ab sodium citrate and NaHCO3 water sol-->systemic ab rapid onset (10min prior) and HCO3-->CO2-->belch
470
transdermal ab EN forgettables CORE
ionization-->ab thicker epidermis on back vs chest BF-->ab hence thorax and abdo more than limbs Pros NO FIRST PASS MET!!!!!! P+H eg GTN NBM relatively constant ``` CONS slow offset variability dermatitis not possible for most drugs ```
471
EMLA
eutectic - mix-->one set of physical features - decreased melting point-->liquid instead of crystal 2. 5+2.5 prilocaine and lig
472
decreased respons to NDMR
MoA Measurement Effect -on, off, depth, SE Patient - phys Rb CO and m mass and Alkylosis - path Rb burns Drug - type, conc - interaction - -Phenytoin up reg hep met - -nil volatile
473
Propofol PrB
98%
474
sevo vs prop offset and CVS and CNS | CORE
overall similar offset HR and contractility reduced in prop!!!! HR and contractility maintianed in sevo (mild decrease ino Miller) (no change in HR P+H vs des and ison increased to responde to hyotnesion) QTc prolonged by sevo! CNS propofol - increased res, decreased CBF decreased ICP hence NSx - rb excitation
475
Sevo met
C next to O without halogen-->met
476
Prop mech of VD
SNS, Ca, K, NO # millers
477
Volatiles CVS millers | CORE
blunted barorec in sevo (des and iso presserved) minor neg ino VD-VGCaCH (not mentioned in millers) maybe less SNS too- (P+H direct sm relax) preserved CO
478
prop cor BF
DECREASED
479
Prop HR | CORE
P+H tachy is rare due to reflex blunted and decreased SNS-->BRADY
480
prop CNS effects EVERs and MAY | CORE CORE
in Vitro -->VD ``` in Vivo decreased CMRO2 decreased MAP decreased CBF decreased ICP "autoregulation maintained" CO2 cerebral vascular response unchanged ``` good for NSx -controversial if protective or not (as supplyvs demand not really changed)
481
Prop resp effects
blunt reflexes blunt CO2 and O2 response (and decrease CO2 prod from met) Bronchodilator
482
Prop CVS supply demand | CORE
millers "Thus, global myocardial oxygen supply-to-demand ratio is likely preserved." CorBF decreased
483
prop brain and heart supply demand | CORE GOLDEN
both supply decreased and demand decreased without a change in ratio
484
sevo MoA MUST MUST MUST READ MORE
The exact mechanism of the action of general anaesthetics has not been delineated.[7] Sevoflurane acts as a positive allosteric modulator of the GABAA receptor in electrophysiology studies of neurons and recombinant receptors.[8][9][10][11] However, it also acts as an NMDA receptor antagonist,[12] potentiates glycine receptor currents,[11] and inhibits nAChR[13] and 5-HT3 receptor currents.[14][15][16] Myer Overton Protein rec target
485
Prop mech of VD
SNS, Ca, K, NO # millers
486
Volatiles CVS millers | CORE
blunted barorec in sevo (des and iso presserved) minor neg ino VD-VGCaCH (not mentioned in millers) maybe less SNS too- preserved CO
487
prop cor BF
DECREASED
488
Prop HR | CORE
P+H tachy is rare due to reflex blunted and decreased SNS-->BRADY
489
prop CNS effects EVERs and MAY | CORE CORE
in Vitro -->VD ``` in Vivo decreased CMRO2 decreased MAP decreased CBF decreased ICP "autoregulation maintained" CO2 cerebral vascular response unchanged ``` good for NSx -controversial if protective or not (as supplyvs demand not really changed)
490
Prop resp effects
blunt reflexes blunt CO2 and O2 response (and decrease CO2 prod from met) Bronchodilator
491
Prop CVS supply demand | CORE
millers "Thus, global myocardial oxygen supply-to-demand ratio is likely preserved." CorBF decreased
492
prop brain and heart supply demand | CORE GOLDEN
both supply decreased and demand decreased without a change in ratio
493
sevo MoA MUST MUST MUST READ MORE
The exact mechanism of the action of general anaesthetics has not been delineated.[7] Sevoflurane acts as a positive allosteric modulator of the GABAA receptor in electrophysiology studies of neurons and recombinant receptors.[8][9][10][11] However, it also acts as an NMDA receptor antagonist,[12] potentiates glycine receptor currents,[11] and inhibits nAChR[13] and 5-HT3 receptor currents.[14][15][16] Myer Overton Protein rec target
494
``` Dr Pod stats Variation calc stardard deviation CORE p256 ```
``` find mean mean minus every result square all of these so they are positive now square root them now divide by degree of freedom ie number of observations-1 ``` variation=sum of (mean-indidiual)squared/n-1 standard deviation= square root of variation within 1 STD of mean=68% within 2 is 95 3 is 99
495
T test CORE RV
for continuous data ,2 groups that are parameteric use either paired or unpaired difference in mean/SEM SEM=SD/squareroot of (n-1) t score translate to p value with table
496
NDMR monitoring device
Acceleromyography was developed as a more convenient method of monitoring evoked responses in the operating theatre. The principle is similar to MMG; however, instead of measuring force of contraction directly, acceleration of the contracting muscle is measured. Force can then be calculated using Newton's second law of motion: force = mass × acceleration. Acceleration is measured by a piezoelectric ceramic wafer that is strapped to the thumb. When the adductor pollicis is stimulated, the thumb will move and the attached transducer will produce a voltage, which is proportional to its acceleration. The voltage can then be converted into an electrical signal and displayed as a twitch response. For accurate measurement, the accelerating digit must be free to move.
497
neostigmine TOFC indication
BJA at least 3
498
TOFC timing adductor pollicis
larynx high BF so acts as central m.-->rapid paralysis and rapdi reversal (blocked and reversed quicker than adductor pollicus)
499
non adducto pollicus | CORE
orbicularis oculi - eyebrow from temporal nerve reflects diaphragm blockade more accurately as both resistant to blockade but can directly stimulate muscle-->false impression of reversal
500
CYTp450 interaction | GOLDEN CORE
#evernote Phase 1 hepatic met (MUCH BETTER FROM COURSE picture is cardiac transplant with cylclospirin and tacrolymus immunosup on CCB(VD) and amiodarone and fluconazole and statin and antidepressent (fluoxetine) has a seizure 1) PrB of pheny and carb 2) inducers pheny and carb 3) inhibitors amiodarone, CCB, fluconazole 4) competition for cyp450-->statin-->decreased met of both
501
power | CORE
``` 1-beta beta is FN rate so power of 1=nil FNs 0.8 is the standard 20% FN is acceptable pv p value of 0.05 5% FP is standard ```
502
histamine rec
H1 GqPCR-->variable effects -increased Ca in bronchi-->BC -VD due to increased NO H2GsPCR-->increased cAMP H1 first gen-promethazine (phenergen) Rb -AE effect mild -BD and decrease secretions
503
CSHT figures | CORE RV ABSOLUTE CORE CORE
Conclusion simplification (rounded ++) - prop at 30min -5 4H-10 Vss-20 - sevo/des 5,8,8 - iso 10, 20, +++ - propofol 5 in short 9 in long - sevo 5 in short 8 in long to clinically relevant pseudo awake point propofol 10min -->5min 180min-->9min Vdss-->20min STP 10min-->4min 180min-->85min Fentanyl 10min-12min 180min-->70min Remifent 10min-->3min 180min-->3min Sevo 90% decrement time MILLERS*** below time to MAC awake from MAC 1.2 (approx 75% decrement 1.2-0.3) Iso NOTE SEVO -30min-->9min -4hrs-->20min Des - 30min-->5min - 4hrs-->6min Note difference between sevo and des is clinically very small SEVO FIGURES NOT AVAILABLE IN MILLERS STOELTING **** "For example, the 80% decrement times of desflurane and sevoflurane are <8 minutes and do not increase!!!!!!!!!!! significantly with the duration of anesthesia, whereas 80% decrement times for enflurane and isoflurane increase significantly after about 60 minutes, reaching plateaus of approximately 30 to 35 minutes." "The major differences in the rates at which desflurane, sevoflurane, isoflurane, and enflurane are eliminated occur in the final 20% of the elimination process." (WHICH IS CLINICALLY NOT Very RELEVANT!!!!!!)
504
IJV #anatomy text | GOLD CORE
Quartad to consider 2 vessels 2 nerves 1) IJV-in carotid sheath 2) Carotid-internal then common-in carotid sheath 3) vagus nerve (BETWEEN IJ and CA)-in sheath 4) cervical sympathetic chain POST 5) Cervical chain lymph node-in sheath CLOSE to IJ - ->htoracic duct on right 6) pleural dome 2.5cm above medial 1/3 of clavicle Path 1) jugular foramen from sigmoid sinus - at first superficial in anterior triange. superficial to pulsating external carotid 2) vertically down neck 3) joined by external JV 4) dive deep to SCM 5) descends through groove of two SCM heads 6) join Subclavian to become brachiochepalic post to junction of clavicle and sternum CVC technique aim ipsilateral nipple head down aspirating 1) high-midpoint of SCM between mastoid join and sternal join 2) low-middle of triangle formed by 2 heads of SCM (sternum and clavicle) and clavicle
505
ANS NTs EN R/V CORE ISH
remember sweat glands ******* -SNS Ach-->M rec Fibers from parasympathetic ganglia release, VIP (Vasodilate), nitric oxide (NO) and the neurotransmitter acetylcholine (ACh). Fibers from sympathetic ganglia release neuropeptide Y (vasoconstrict) (NPY), and the neurotransmitters noradrenaline (NA) and adenosine triphosphate Note that ion channels has faster response for shorter duration note exicte or inhib Note onset time of gene transcription change (PKA from cAMP!!!!)
506
GsPCR
GDP-->GTP amplication 1) 1rec-->multiple Gproteins 2) cell signalling amplication due to Gprotien stimulating multiple second messengers-->stim more messengers
507
GPCR CORE CORE CORE
interact with AC or PLC OR ION CHANNEL eg opiates (GiPCR)-->block VGCaCh "The cAMP so formed acts by stimulating protein kinase A, which has two regulatory (R) and two catalytic (C) units. cAMP binds to the R unit, revealing the active C unit, which is responsible for the biochemical effect, and it may cause either protein synthesis, gene activation or changes in ionic permeability."
508
GPCR offset
phosphorlyation of GTP:alpha-->allows arrestin to bind | agonist-->phsoporylation-->>tachyphylaxis
509
ANS NTs EN R/V CORE ISH
remember sweat glands ******* -SNS Ach-->M rec Fibers from parasympathetic ganglia release, VIP (Vasodilate), nitric oxide (NO) and the neurotransmitter acetylcholine (ACh). Fibers from sympathetic ganglia release neuropeptide Y (vasoconstrict) (NPY), and the neurotransmitters noradrenaline (NA) and adenosine triphosphate Note that ion channels has faster response for shorter duration note exicte or inhib Note onset time of gene transcription change (PKA from cAMP!!!!)
510
GsPCR
GDP-->GTP amplication 1) 1rec-->multiple Gproteins 2) cell signalling amplication due to Gprotien stimulating multiple second messengers-->stim more messengers
511
GPCR CORE CORE CORE
interact with AC or PLC OR ION CHANNEL eg opiates (GiPCR)-->block VGCaCh "The cAMP so formed acts by stimulating protein kinase A, which has two regulatory (R) and two catalytic (C) units. cAMP binds to the R unit, revealing the active C unit, which is responsible for the biochemical effect, and it may cause either protein synthesis, gene activation or changes in ionic permeability."
512
GPCR offset
phosphorlyation of GTP:alpha-->allows arrestin to bind | agonist-->phsoporylation-->>tachyphylaxis
513
define neurotransmitter
wiki endogenous chemical messenger that allows transmittion of a chemical message across a synaps from a nerve to a target nerve, mucle gland etc
514
CNS/CVS ratio
7 4 3 There is a decrease in the duration of action potential and refractory period Bupivocaine has highest affinity for NaCh-->most toxic
515
LA tox patient group
extremes of age hypovol and elderly decreased vd preg-->increased sens-->increased risk (but also increased Vd renal Dx-->longer conductive and IHD Dx-->myocardium more sens CCF-->long half life "Reduced hepatic blood flow or hepatic dysfunction can decrease amide metabolism." P+H liver Dx-->long half life BB CCB-->increased risk of arrhytmia/conduction
516
LA absorption volume
eg epidural vol-->increased SA
517
LA tox drug type | and drug interaction
Rb S enantiomers safer eg of bup Drug Interactions 1. Competition for protein binding AAG → ↑free fraction → ↑risk toxicity - Opioids 2. Inhibition enzyme systems → ↓metabolism → ↑duration of action - Phenytoin
518
LA tox age
changed Vd | increased sens of mycocytes
519
LA tox patient group
hypovol and elderly decreased vd preg-->increased sens-->increased risk (but also increased Vd renal Dx-->longer conductive and IHD Dx-->myocardium more sens CCF-->long half life "Reduced hepatic blood flow or hepatic dysfunction can decrease amide metabolism." P+H liver Dx-->long half life BB CCB-->increased risk of arrhytmia/conduction
520
LA toxicity EN CORE CORE
"This question requires an understanding that systemic toxicity is due to an excess in the plasma concentration of local anaesthetic, which is dependent on the rate of absorption into the systemic circulation, drug distribution and clearance."
521
PrB LA | CORE CORE CORE
Binding to plasma proteins alters drug distribution, affinity for receptor proteins affects dwell time and binding to tissue proteins affects release of drug into the systemic circulation P+H e amides are more extensively bound (bupivacaine > ropivacaine > lidocaine > prilocaine) in the plasma. α1-Acid glycoprotein binds local anaesthetic with high affinity although albumin binds a greater quantity due to its relative abundance. When protein binding is increased.
522
lignocaine clearance
90% of mets-->urine excretion 10% unchanged in urine
523
ester mets
plasma cholinesterases and other esterases Para-aminobenzoate is one of the main metabolites and has been associated with hypersensitivity reactions especially in the atopic patient. This rapid hydrolysis results in a short elimination half-life. Cocaine is the exception, undergoing hepatic hydrolysis to water-soluble metabolites that are excreted in the urine
524
Head down anaestheis cerebral changes
TRICKY BUGGERS-want discussion of effects of GA and also head down
525
prop and STP CNS blood flow | CORE
"The effects of propofol (2,6-diisopropylphenol) on CBF and CMR are similar to those of barbiturates." Because blood flow and metabolism coupling are preserved, CBF is decreased. MILLERS In general, autoregulation and CO 2 responsiveness are preserved during the administration of intravenous anesthetic drugs.! ceiling of 50-60% decrease in CMRO2 for bar and prop as baseline met req During deep pentobarbital anesthesia, autoregulation is maintained at mean arterial pressures as low as 60 mm Hg. CO 2 responsiveness also persists.
526
ketamine CBF
increased CMRO2 and CBF | N2O increased CBF
527
opiates CBF
Inconsistencies can be found in the available information, but narcotics likely have relatively little effect on CBF and CMR in the normal, unstimulated nervous system. When changes do occur, the general pattern is one of modest reductions in both CBF and CMR.
528
benzo CBF
Benzodiazepines cause parallel reductions in CBF and CMR in humans.
529
volatile CBF and CO2 autoreg
CO 2 responsiveness is well maintained during anesthesia with all volatile anesthetics. MILLER As with all vasodilators, CBF is preserved up to lower MAP values during the administration of volatile anesthetics with no evidence of differences among the various anesthetics. Direct comparisons of CBF with isoflurane, desflurane, and sevoflurane anesthesia during hypotension are not available. By contrast, autoregulation of CBF in response to increasing arterial blood pressure is impaired, which is most apparent with the anesthetics that cause the most cerebral vasodilation and are dose related. Sevoflurane may cause less impairment of autoregulation than other volatile anesthetics.
530
NAcH fetal
aabgd | adult is aabge
531
NaCHR pharm EN
Na in POTASSIUM OUT!!!--HYPERKALAEMIA central neuro is different NaCHR strucutre 2alphas3betas vs nα3mβ4 (n+m=5) vs 2abge NMJ SO GANGLION BLOCKERS dont cause NMJ blockade
532
alv transit time
0.75s
533
isobologram
synergy dose x and y req
534
compound A
20ppm but required 150ppm
535
Halothane hepatox | CORE
stoelting It is likely that the more common self-limited form of hepatic dysfunction following halothane is a nonspecific drug effect due to changes in hepatic blood flow that impair hepatic oxygenation. -reactive metabolites (trifluroacetylated adduct-->Dx Conversely, the rarer, life-threatening form of hepatic dysfunction characterized as halothane hepatitis is most likely an immune-mediated hepatotoxicity -Ig in 70% found #reexposure
536
He use
airways diving measure
537
USS priniciples Dopper formula freq wavelength
speed 1.5km/s in soft tissue V=wave.freq doppler change=2costheta. change in velocity. original freq/USS velocity
538
insulator resistance
high res
539
impedence resistors capacitors iducotrs
resistors yes capacitors - increased freq-->decreased impedence (as flow) - ideally zero Inductors - increased freq-->increased impedence - ideally zero
540
methaemoglobin pulse ox
85% sats | -strongly absorbs both 660 and 990nm wavelength
541
Circuit sampling insp BJA and position structure
O2 volatile and N2O detector on insp limb just before Y piece O2, volatile agents, and N2O monitoring, with samples taken from the patient end of the system, is obligatory Fuel cell. It reads either the inspiratory or expiratory oxygen concentration. It is usually positioned at the common gas outlet of the anaesthetic machine (inspiratory). FGF supply downstream of the CO2 absorber,
542
pulse ox response time finger ear
6s ear | 24s hand
543
bili and pulse ox
Fetal haemoglobin and bilirubin introduce no significant error,
544
fuel cell
4e+O2+H2O-->4OH Pb+2HO- -->PbO+H20+2e- gold cathode (neg charge terminal) lead anode (positive charge) (silver looks like lead) KCl electrolyte fill O2permeable membrane -->current proprotional to O2 100% and 21% O2 as references no power supply life of 1 year until exhausted delay20s accurate +/-3% will a cumulate nitrogen in the presence of N2O Results in an under-reading of PO2 Diffusion is linearly dependent on the partial pressure gradient, but is also temperature dependent, and the current rises about two to three percent per kelvin rise in temperature. A negative temperature coefficient resistor is used to compensate, and for this to be effective it must be at the same temperature as the cell.
545
Circuit sampling insp BJA and position structure
O2 volatile and N2O detector on insp limb just before Y piece As FGF is reduced, it becomes a significantly smaller part of the gas being delivered to the patient, the majority of which is recirculated gas. With low FGF, the gas concentrations received by the patient bear considerably less resemblance to those delivered by the anaesthetic machine.7 Measured concentrations depend on the rate of uptake and excretion of any gas at a given moment. There is a dynamically changing relationship between what the patient inspires and expires, what is measured, and what is delivered in the FGF. This degree of uncertainty means that O2, volatile agents, and N2O monitoring, with samples taken from the patient end of the system, is obligatory FGF supply downstream of the CO2 absorber,
546
apparatus dead space
Two breathing tubes carry gases to and from the patient. Each tube connects to a port on the absorber at one end and the Y-piece at the other. The dead space in the system extends from the Y-piece to the patient. The length of the tubes does not affect the amount of dead space or rebreathing because the gas flow is unidirectional. A Y-piece with a septum will decrease the dead space. When exhalation or inhalation starts, the gases in the breathing tubes move in the opposite direction from their usual flow until stopped by a closed unidirectional valve.
547
Capno expiratory volatile expiratory *emailed guy jan 19
I presumre just distal the Y piece in exp limb?????or is The sampling chamber can either be positioned within the patienťs gas stream (main-stream version, Fig. 10.16 ) or connected to the distal end of the breathing system via a sampling tube (side-stream version, Fig. 10.17 ).
548
fuel cell | final days
#oxidation reduction reaction LEAD ME TO GOLD Pb+2HO- -->PbO+H20+2e- gold cathode (neg charge terminal) Pb anode (positive charge) KCl electrolyte fill O2permeable membrane -->current proprotional to O2 100% and 21% O2 as references no power supply life of 1 year until exhausted delay20s accurate +/-3% insp limb
549
polarographic O2 analyser | CORE
PS i love u Plat-->silver ``` platenum anode silver cathode electolytes teflon O2 perm memb potential difference created by power source O2 -->cathode donating 4e to anode CURRENT at constant voltage is proprotional to PP 600mV (linear voltage-->O2) ``` ``` lasts 3 years temp compensation (increased diffusion with increased temp-measure and correct for ``` "Many candidates omitted a description of methods of calibration and factors affecting accuracy and limitations. These included the effects of temperature, consumption of oxygen by the electrode, problems with the membrane (e.g. holes, proteins), non-linearity of voltage and current."
550
safety O2 analysers
1. Regular calibration of the analysers is vital. 2. Paramagnetic analysers are affected by water vapour therefore a water trap is incorporated in their design. 3. The galvanic and the polarographic cells have limited lifespans and need regular service. 4. The fuel cell and the polarographic electrode have slow response times of about 20–30 seconds with an accuracy of ± 3%. 5. The positioning of the oxygen analyser is debatable. It has been recommended that slow responding analysers are positioned on the inspiratory limb of the breathing system and fast responding analysers are positioned as close as possible to the patient.
551
define CCF
Heart failure is a condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure. systolic diastolic mixed The term 'congestive heart failure' (CHF) is reserved for patients with breathlessness and abnormal sodium and water retention resulting in oedema.
552
Rx of chornic LVHF
yes nitrates and hydralazine PO
553
prazocin | CORE
alpha blocker with phentolamine
554
moxonidine | CORE
sounds like clonidine | alpha agonist
555
Rx of chronic LVF structure answer
``` def heart failure syst and diast ``` comp-->worsen preload #frankstarlin!!!! contractility afterload digoxin too
556
diuretics
Thiazide blocks Na/Cl in DCT | K sparing eg amiloride blocks Na reab DCT and CD
557
O2 measurement
polarographic (blood or gas sample) fuel cell parmagnetic
558
sevo maintainance inspired dose SAQ structure
``` def MAC and MAC awake goal -immob, aware, SE Patient -phys --Rb, low O2, Na, temp, bp -path Drugs Procedure-surgical and regional block ``` Insp>exp and gap changes with low FGF MONITOR WITH BIS and titrate
559
simple analgesia in neuropathic pain
``` Simple analgesics, including nonsteroidal anti-inflammatory drugs and paracetamol are usually not effective, unless a component of the pain is due to nociceptive stimulation. ```
560
GABAPENTINOIDS MoA and SE and metabolism CORE
CCB not NaCH!!!!!!--> prevent subsequent release of excitatory neurotransmitters NMDA antag central and presynaptic Shane warn at the GABA eating Shells (Ca) ->seizure and Erectile dysfunction gabapentin - first order-->zero order - slow ab with less absorbed at higher % - non linear plasma conc to dose - TDS dose Pregabalin - reliable fast absorption - linear increase in plasma with intake - 1 order kinetics - OD or BD Both drugs are met in liver then excreted renally, with elimination half-lives of approximately 6 hours Gabapentin TDS pregabalin OD or BD
561
TCA MoA CORE
SNRI block H1, Ach, alpha 1 #alpha dog NASH until put on 3 antidpressents
562
neuropathic pain
remember Lignocaine and carbemazepine
563
ketamine SE
rb salivation
564
clonidine MoA as analgesia | CORE
Clonidine hyperpolarizes nerve cell membranes, blocks the conduction of nerve induce enkephalin-like substance release at peripheral sites. Clonidine primarily activates presynaptic autoreceptors in the locus coeruleus (midbrain) and reduces norepinephrine release and turnover. give epidurally
565
NMDA rec
GLYCINE!!! BINDING SITE found at most excitatory synapses -DH, central
566
single twitch vs tetany CORE ish recommended text
1Hz-->uniform lower amplitude in NDMR and DMR (see evernote) use - define supramaximal - flat-->intubate Neg - need a control - return to normal is not safe for extubation - cant distinguish NDMR from DMR - It can be used (in conjunction with a tetanic stimulus) to monitor deep levels of NMB [the posttetanic count (PTC), discussed below]. Twitch: a short duration (0.1–0.2 ms) square wave stimulus of a frequency of 0.1–1 Hz (one stimulus every 10 seconds to one stimulus every 1 second) is applied to a peripheral nerve. When used on its own, it is of limited use. It is the least precise method of assessing partial neuromuscular block. Tetanic stimulation: a tetanus of 50–100 Hz is used to detect any residual neuromuscular block. Fade will be apparent even with normal response to a twitch. Tetanus is usually applied to anaesthetized patients because of the discomfort caused.
567
neuromuscular monitoring recommended text
Current, not voltage, is the determining factor in nerve stimulation. Because skin resistance may change, only a stimulator that automatically adjusts its output to maintain a constant current can ensure constant stimulation with changes in skin resistance.
568
TOFC benefit and negs recommended text
A control is not necessary. The main disadvantage of TOF is its poor performance at both extremes of NMB, deep relaxation, or near complete recovery.
569
tetany CORE recommended text
decreased amp for MR fade with NDMR but not Sux 5s 50Hz A significant disadvantage of tetanic stimulation is that it is very painful and should be avoided in the conscious patient.
570
DBS recommended text
Douuble-burst stimulation (DBS, minitetanus) consists of two short bursts of 50-Hz tetanic stimuli separated by 750 milliseconds. DBS DBS has been used mainly to detect residual NMB. Studies show that fade (response to the second burst weaker than that to the first) is more readily detected with DBS than with TOF using visual or tactile monitoring. It has also been used for intraoperative assessment of NMB Another use of DBS is to assess deep block, since the first twitch in double burst can be detected at deeper block levels than the first twitch in TOF.
571
WPW antiarrhytmic CI
Digoxin or calcium-channel blockers should not be used in pati
572
HYdromorph vs morphine
more rapid on offset similar hydromorph has no active mets hydromorph mets neuroexcitatory so caution in seizures hydromorph nephrotoxic mets accum in renal failure
573
dexmed Doa Vs clonidine
1-2H vs 4-7H
574
STP dose for delivery COPE MIllers
Sodium thiopental 4 to 6 mg/kg intravenously is still used in many countries for induction of anesthesia and was previously the most commonly used drug for induction of anesthesia within the United States (see also Chapter 30 ) increased Vd but dcreased PrB
575
propofol dose crash LSCS CORE millers
Propofol administration does not affect neonatal Apgar scores with typical intravenous induction doses (2.5 mg/kg),
576
oxytocin SE and Moa and onset offset
onset 1 min for 45 min Rb oxytocin rec GqPCR Rb reflex tachy and decreased Cor P and increased Pulm VR-->pulmonary oedema
577
Ergometrin MoA and DoA
Rb alpha, 5HT and DA agonist Rb Pulmonary oedema, IHD DoA 45 min MIMS onset 1 min
578
carbeprostal
PG rec agonist--> quicker onset vs misoprostol
579
CORE Vd relation formula to Cl
Vss=Cl.MRT | MRT=AUMC/AUC
580
Nat freqeqn bubbles ruler
related to r squared. stiffness/density.length
581
damping factors
inversely proprotional to radius cubed | bubble-->damping (will cusion oscillation)
582
Triexponential decay Dr Pod CORE HARRY
1) V1-2 2) V1-3 3) terminal ellimination
583
Vd calc CORE CORE CORE CORE HARRY
the word clearance only related once 1) single comp C=x/Vd Vd=x/C 2) Extrap use terminal elim to back tract to determine conc at time zero then Vd=x/Cattimezero 3)Varea -T/2=0.693.Vd/Cl hence Vd= halfline. Cl=Cl.1/beta 4) Vss=dose.AUMC/AUC
584
bupivocaine S enantiomer | CORE
Levobupivocaine less VD hence...!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! - dont need to add Adr -longer DoA -less systemic uptake -less CNS and CVS toxicity-->larger dose can be given 13% less potent hence slower onset !!!!!!!!!!!!!!
585
maintainance infusion | CORE HARRY
in=elim=cl.c not simply clearance as the infusion would need to be higher to maining a higher conc due to high elim while clearance stable
586
PROP TCI max rate
1200ml/hr
587
VIE | temp and why
vaccum insulated evaporator - 160C - BELOW CRITICAL TEMP so can be condensed - above boiling point so vapour is forming effectively
588
RR mode forgetable
RR
589
diastole stages
dont forget isovol, e, l, atrial kick | relate to valves!
590
diastolic heart failure and atria
increased LVEDP-->decreased gradient to fill-->increased dep on atrial contraction
591
AF poorly tol in who
old and CCF | cant comp
592
TNZ vs ITR
TNZ is the ambient 27-31 for minimal ITR 36.9-37.1 of no ANS
593
Affinity graph
Kd shifts right if low affinity
594
pH and H conc
7. 4 40nmol/L 7. 1 80nmol 6. 4 400nmol
595
HHassel
pH=6.1 + log HCO3/paCO2.0.003
596
HCO3 buffer pka
6.1
597
RBC buffer pka
6.8 hence very effective #histadine reisdue
598
Pr buffer
intracell due to pKa of 2.8
599
renal HCO3 prod
prox CT and thick asc glutamine-->2NH4+2HCO3 CD NH3 secreted
600
ephedrine Stoelting
direct B agonist and indirect NAd release met by MAO in liver slowly (MAOi) 40% renal excretion unchanged nil hyperglycaemia
601
indirect sympathomimetics CORE
uptake 1 via transporter protein at presynaptic nerve terminal - ->reuptake inhibitor of catechol - ->displace NAd vesciles - ->inhibit MAO-->decrease BD in cleft Uptake 2 occurs at postsynaptic and peripheral cells to prevent the neurotransmitter from diffusing laterally.
602
pethidine P+H
synthetic opioid deisgned initially as an anticholinergic -also SSRI mech. Use-labour onset- more rapid due to lipid sol offset-2H R-PO IV IM S -active metabolite with long ellimination half life (norpethidine)-->renal excretion-->accumulate -fetal accumulation as crossed placenta then metabolised to less lipid so norpeth -peak in fetus four hours post IM maternal dose -Seretonin reuptake inhibitor-->CI with MAOi-->seretonin syndrome small amount eliminated in urine unchanged T -NOT REVERSED WITH NALOXONE! (YES TRUE)
603
NSAID PATH | CORE
PLM via PLA2 AA-->Cycloperoxidase via COX which then produces TXA2, and prostaglandins AA-->5HPETE (via LOX)-->leukocytes that produce leukotreines
604
NSAID with stable PL effect
Naproxen has a stable biological antiplatelet effect similar to aspirin.
605
esmolol CORE
``` Peak effect 6-10min ET/2 10min DoA 20min extravesation-->necrosis irritates veins can precip CCF mostly inactive met (1 weak B antag)-->urinary excretion RBC esterase-->hydrolysis Vd 3.6L ``` CAUTION IN RENAL FAILURE DUE TO METS
606
Triexponential decay Dr Pod
1) V1-2 2) V1-3 3) terminal ellimination
607
Vd calc CORE CORE CORE
the word clearance only related once 1) single comp C=x/Vd Vd=x/C 2) Extrap use terminal elim to back tract to determine conc at time zero then Vd=x/Cattimezero 3)Varea -T/2=0.693.Vd/Cl hence Vd= halfline. Cl=Cl.1/beta 4) Vss=dose.AUMC/AUC
608
Elim calc | CORE CORE CORE CORE
Cl.c NOTE Vd
609
maintainance infusion
in=elim=cl.c not simply clearance as the infusion would need to be higher to maining a higher conc due to high elim while clearance stable
610
dose freq
wide therapeutic range then.... 1st dose-->into TR a half life later 2nd dose-->TR if didn't dip below therapeutic range in t/2 then dose freq=elimination half life Simplified freq=T/2
611
half life with double the dose
``` #derranged phys first order kinetics-->increase by one half life as after once halflife it is the same as half the dose! ``` zero order double dose-->double duration
612
Half life freq dosing and SS source This viva is relevant to Section B(v) of the 2017 CICM Primary Syllabus, which expects the exam candidate to "describe the concepts of effect-site and context sensitive half time". GOLDEN CORE HARRY
dose every T/2-->increasing dose BUT Elim is conc dep so increases by decreasing amount so rise is by half of prior ie after 1 T/2=50 after 2T/2=75, 87 92 etc
613
liitations of T/2
It may be irrelevant if the effect of the drug has little relationship with its plasma concentration It usually refers to β half-life, which has less relevance for widely and rapidly distributed drugs
614
``` propofol contains HARRY CORE CORE CORE CORE ```
``` 1% propfol 10% soya bean oil to disslove prop 1%purified egg phospholipid from yoke (nil albumin-->allergy) to emulsify soyabena oil glycerol for tonicity Na EDTA fo bacteria NaOH for base ```
615
``` opiate classification CORE CORE CORE CORE CORE ```
fing and throne on heroin Phenanthrene Phenylpipperadine (Funnel pipe high) 1) endogenous 2) opiates -morph and codeine Phenanthrene derive 3) semi synth -smal change to morph-->oxycodone or heroine 4) synthetic (not a change but a construction) phenylpipperadine derive -fent, su, remi, alf
616
opiate structure
morphine-3 phenanthrene rings and tertiary amine ionized
617
non nervous system sites of opiate action
immune cells VD cardioprotective
618
opiate rec
#evernote
619
sterilization vs decontamination
Decontamination renders an item or material safe to handle. The level of microbial contamination is reduced enough that it can be reasonably assumed free of risk of infection transmission. Sterilization, disinfection, and antisepsis are forms of decontamination. disinfection and antiseptic used interchangably in stoelting
620
``` chlorhex vs iodine #evernote ```
evernote
621
ED95
In anaesthesia, the term ED95 is also used when referring to the pharmacology of neuromuscular blocking drugs. In this context, it is the dose which will cause 95% depression of the height of a single muscle twitch, in half of the population. Put another way, it is the ED50 for 95% reduction in twitch height.
622
Respiratoyr centre
evernote
623
CVS baro rec loop
evernote
624
sinus big
max also Rb nasal septum
625
role nose
rb eustacian tube and decrease water loss
626
treachea length and flat
trachealis m. 10-12cm neanoate is 4cm ring only anteriorly
627
right bronchus
short straight wide divides
628
drug-->effect
physiochem, enzyme inhib, rec
629
GABA subunit
GABAB
630
BP HR SVR changes with different inotropes approach-to-the-patient-with-hypotension-and-hemodynamic-instability
google
631
Volatile CBF
note if MAP maintained its simple as you know if map not compensated then 40% decrease CBF with 1MAC CO2 VD response unchanged (MILLERS)
632
PV curve top and bottom core core and you keep getting confused CORE HARRY
apex most negative IPP due to gravity-->over distent (-10-->too high up curve) -2.5 at base-->ideal shift
633
vertebral anatomy
articular facet
634
midazolam PK
``` pH 3.5 tautomerism at 4 pka 6.5 mets as known then renal excretion <5% to active oxazepam T/2 1-4 Hrs met same p450 as alfent -->prolong 95% PrB ```
635
endocrine kidney
renin EPO vit D active also GNG (not strictly endo)
636
GFR calc CORE HARRY
if freely absorbed and no secretion or reab then... amount filtered=amount in urine plasma c. GFR=urine c.v INULIN INULIN INULIN INULIN INULIN 5500 Daso is freely filtered. In addition it is not reab• sorbed, secreted, metabolised or synthesised in the kidney Creatinine is released at a steady state from skeletal muscle eel.ls. It is freely filtered and not reabsorbed. A smaU amount is secreted into the tubules; however, this only introduces a small error and ilie error is constant.
637
Renal blood flow calc
Paramino hippuric acid -freely filter and secreted-->all renal art content-->urine [p].RPF=[u].vol RBF=RPF/(1-HCT) so is piss all HCT then RPF=RBF
638
``` SID IVF and body CORE CORE CORE CORE ``` HARRY
SID in body is 42 141+4-103 27=neutral IVF due to alb dilution
639
Measuring airway resistance CORE
1) full body plethysmograph - can figure out TLV and then with boyles law p.v=p.v - F=P/R so flow measured and resistance calculated 2)eosophageal balloon-->estimate intrapleural pressure IPP is caused by recoil of lungs in vs spring of chest out AND resistance to air and tissue recoil can be calc from compliance curve the IPP less recoil-->resistance HENCE BALLOON DOESNT WORK IF COMPLIANCE INCONSISTENT eg with variable time constants in COPD -
640
Causes of increased airway res wests Ch7
LUNG VOL due to radial raction. smallers-->increased res Hist, PSNS SNS-->dilate density-->increased turbulence (medium size is site of most res)
641
density vs viscosity resistance | CORE
lamina R=8nl/pir4 n is viscosity He is low DENSITY so won't help lamina flow (viscoisty s higher) but will decrease turbulent fraction via reynolds number the fact that He helps deep see divers is evidence than medium sized conductive airways are not purely laminia #wests
642
hypervent and ICP SAQ EN
Rb - hagen poisel r and R and flow - impact of hypotension and hypoxia -->VD cerebrally -->raise ICP so hypervent can be protective against this rise.
643
Ketamine onset route CVS effects
30s OxCHB Rb PO PR IT ED note intrinsic neg ino
644
ketamine CNS mech dissociate and other
``` dissociative anaesthesia (break thalamolimbic connection) DO NOT FORGET RAISED ICP, CBF, CMRO2 CPP ```
645
CORE HARRY RV CORE CORE CORE Time to LoC litfl
PK including drug effects fill circ circ to al -----Rb MV, second gas, deadspace alv to blood----B:G, CO, compare washins blood to brain---O:G compare mac # myer overton PD septic old etc
646
NSAIDS P+H aspirin CORE CORE CORE
``` #phospholipase A2 #cyclic endoperoxidases -PL, vasc endo, widespread ``` NOTE: ASPIRIN SELECTIVELY INHIBITS PL COX! without effecting COX of Prostaglandins or prostacyclin. IRREVERSIBLE (aspirin induced bronchoconstriction from leukotreins) NSAIDS - PGE2 PGF2alpha - -->inflam Renal perf PGE2 and PGI2 COX1 constitutive COX 2 inducible -COX2 PRODUCES PROSTACYLCIN: block-->PL clot and VC! but less GI ulcer Rb haemorrhage with aspirin ? with others? Hep Dx
647
NSAIDS GI RISK Comparison | CORE
COX2 lower risk celoxib paracoxib Nonselective -high risk=ketoralac, piroxicam -low risk=ibuprofen, diclofenac, naproxen
648
NSAID clot risk
COX2>non selective but both MI yes Stroke not statistically sig yet listed by AMH NSAIDS can cause gastric ulcer-->bleed but don't otherwise cause bleeds
649
WoB def | CORE
energy in Joules expended to insp and exp in one resp cycle 3% of MBR =area under PxV curve #dynamic PV curve!!! =Restistive +elastic elastic -surface tension (surfactant) + tissue (PF, empyema) remeber active expiration if ++ resistance eg emphysema
650
WOB and RR | CORE Harry
#evernote elastic vs frictional changes EN: parks for % contribution insp elastic: 70% surface tension and 30% tissue
651
PV loop resp x and y axis
-5-->-10 | 1L above FRC # wests
652
Work of breathing calculation and O2 cost CORE
diffucult to measure unless paralysed in iron lung so... 1) measure O2 cost then assume efficiency to be 5-10% in healthy and plug formula efficiency (5%)=useful work/O2 cost.x100 to find useful work ie WoB effciency O2 cost is 5% of Baseline o2 req in COPD cost is up to 30% and limits exercise
653
SENS SPEC Core | HARRY
Sensitivity -proportion of people with disease who have positive test Spec -The specificity of a test (also called the True Negative Rate) is the proportion of people without the disease who will have a negative result Sensitivity and specificity are independent of prevalence of outcome in population!!!!!!!!!! Spec= TN/TN+FP so rare will have high FP and high TN in proportion! PPV=TP/TP+FP so rare-->high FP and low TP-->marked drop in PPV!!!
654
Difficult inutbation odds EN
1:1000 Outcomes with low prevalence ! reduce PPV and increase NPV of test ! more likely to have false positives (type I error) and less likely to have false negatives (type II error) potentially serious consequences if unpredicted note only useful if representative ie obstetrics not the gen pop
655
Stats | flow chart
numerical or catagorical if numerical - cont or discrete - para vs non para - paired - group >2 if catagorical >2 or not expected >5 or not
656
t test | CORE
numberical continuous parametric paired or unpaired difference in mean/SEM SEM=sample SD/square root of N so t test is increased if big diff in mean and small SEM (due to small SD and large study)
657
Wilcox signed ranked
``` numerical continuous nonparametric PAIRED #WILCOX IS MEAN signed summed from mean and add up the negs ```
658
Mann-whittney U test
numerical continuos non parametric unpaired | left=right
659
Chi squared
numerical discrete 2 or less with expected >5 in each sum of all (O-E/E)^2
660
resp system in obese
Rb anatomical
661
LBW calc
LBM = 1.1(weight)−1.28(weight/height)2
662
IBW calc
Ideal body weight (kg) = height (cm) - 100
663
obesity resp vols and Cx | figures
everything! TLC, FRC, TV, ER, VC Cx -abdo chest and increased pulm blood FRC decrease 1% per unit BMI over 30 FRC>CC-->atelectasis
664
obesity compliance
decreased lung comp due to decreased vol | decreased CW com due to fat
665
obesity resistance
decreased vol-->increased res
666
OSA and OHS
OSA 5x10s/hr chronic hypercapnia-->decreased CO2 resp OHS leptin-->decreased resp CO2 resp
667
obesity resp clinical imp
↓Time to desaturation during apnoea Hypoventilation during supine, spontaneous breathing Prone to getting atelectasis Low threshold for RSI, intubation, IPPV with PEEP
668
transpleural intrapleural etc
IPP and ITP are the same!!!!!! IPP: pressure in pleura TPP: Alv-IPP TPP is the same as TMP intra inside the pleura trans is outside to insude
669
consequence of intermittent PPV
PPV is air driven in in inspiration-->Positive ITP-->effect on heart lungs vessels
670
Afterload formula | CORE
AL=p.r/2T
671
PRESSURE Alv | CORE
la place P=2T/r essentially the afterload eqn rewritten with AL=1
672
CORE HARRY | Intermittent positive pressure
PD model answer spont-->neg IPP, ITP, TTP PPV-->positive TTP-->exert force on heart, lungs, great vessels insp 1) left vent early and late 2) right vent early and late Exp reversed note: laplaces afterload left preload up then down right preload decrease (++ with hypovol or high PPV or PEEP) right afterload increased-->raised RAP-->ventricular interdependance-->bulge-->impair diastole and systole splinting impair diastole in both ``` # frank starling in young-->decreased CO (EN) ```
673
CORE central neuraxial block
spinal OR epidural ``` #vasomotor centre #renal #sacral ```
674
AS haemodynamic goals
fixed CO so cant comp for drop in SVR! AS-->LVH-->diastolic failure-->reliance on atrial kick for 40% of preload slow N HR for long diastole sinus High, N AL adequate preload
675
RBF | CORE
P+K SUmmary: AR then everything else you can think off (afferent is RBF A:E is GFR) The main resistance vessels in the renal circulation are the afferent and efferent arterioles, and contraction of either reduces renal blood flow. !!!!This autoregulation of renal blood flow is produced by changes in the contraction of afferent arteriole smooth muscle in response to changes in perfusion pressure (the efferent arteriole is not involved).!!!! THIS OCCURS IN ISOLATED KIDNEY YES other things effect renal BF -SNS VC aff and eff-->reduced RBF and mild decrease GFR -RAAS --SNS-->direct stim a and b rec in JGA-->renin-->ATII --ATII-->VC aff and eff-->reduce RBG and moderate decrease GFR since also contracts mesangial cells-->decrease filtration coeff --PG Prostacyclin and prostaglandins PGI2 and PGE2 are locally active renal vasodilators produced by the kidneys in clinical states associated with high concentrations of circulating vasoconstrictors. In such clinical states, inhibition of prostaglandin production by the administration of cyclo-oxygenase inhibitors can reduce renal blood flow and impair kidney function -ANF increases glomerular hydrostatic pressure and GFR by dilating the afferent arteriole while constricting the efferent arteriole. 20% CO P+K OER 10% MENTION FUCKING GFR IS PARRALELLED regional (cortex more than medulla)
676
T piece original CORE | HARRY
Low FGF—>expired air High FGF—>no dilution with expired air (1.5-2.5xMV achieves this) Hence 20kg TV= 140mlx RR20=2.8L 2.8Lx2.5=7L Hence any bigger than 20kg get less and less benefit Mapelson E-->longer reservoir Mapelson F has bag and is used in current practice
677
``` MAPLESON AND T piece #evernote ```
Summary Tots EF'D As! * T piece * E #ET make a longer reservoir tube * FGF close to mouth flushes exp out so high FGF 3xMV for no dilution * F ad a bag (Frequently used) * FGF close to mouth flushes exp out so high FGF 3xMV for no dilution * D changes bag to a exp valve (with scavanger) * FGF close to mouth flushes exp out so high FGF 3xMV for no dilution * A-a grade * FGF from distal fills bag then breathed in. Expiration of DS doesn’t spill out but after DS sufficient pressure to open exp valve close to mouth (with scavenger) * 0.7*MV req for no dilution * Lack * Modified A * B is Bannished * C is Crap
678
``` MAPLESON AND T piece #evernote ```
Summary Tots EF'D As! * T piece * E #ET make a longer reservoir tube * FGF close to mouth flushes exp out so high FGF 3xMV for no dilution * F ad a bag (Frequently used) * FGF close to mouth flushes exp out so high FGF 3xMV for no dilution * D changes bag to a exp valve (with scavanger) * FGF close to mouth flushes exp out so high FGF 3xMV for no dilution * A-a grade * FGF from distal fills bag then breathed in. Expiration of DS doesn’t spill out but after DS sufficient pressure to open exp valve close to mouth (with scavenger) * 0.7*MV req for no dilution * Lack * Modified A * B is Bannished * C is Crap
679
ionization charge protonation | CORE
ionizated is charged | protonation is uncharged for an acid and charged for a base
680
PrB LA
plasma PrB separate from Rec affinity and dissociation rate | bup has highest for both-->long and toxic
681
LA tox CVS mech comparison CORE
myocardial depressent slows phase zero rise -->DECREASED action potention--> shorten refractory prolong QRS and PR -OXCHB AND P+H First, bupivacaine exhibits a much stronger binding affinity to resting and inactivated Naþ channels than lidocaine [72]. Second, local anesthetics bind to Naþ channels during systole and dissociate during diastole. Bupivacaine dissociates from Naþ channels during cardiac diastole much more slowly than lidocaine. Indeed, bupivacaine dissociates so slowly that the duration of diastole at physiologic heart rates (60–180 beats per minute) does not allow enough time for complete recovery of Naþ channels and bupivacaine conduction block accumulates (Fig. 36.4). In contrast, lidocaine fully dissociates from Naþ channels during diastole and little accumulation of conduction block occurs [73]. Thus, enhanced electrophysiological effects of more potent local anesthetics on the cardiac conduction system may explain their increased potential to produce sudden CVS collapse through cardiac dysrhythmias.
682
uterine blood flow
10%
683
Mg Rx and SE | GOLD
ANTICONVOLSANT no coma essentially CCB-->VD, brady, Bronchodilator, anticonvulsant, renal VD-->diuresis, prolong clotting small so crosses placenta so Rx CCB with Cagluconate! enhanced NMB and CNS dep
684
metaraminol effect
some indirect-->NA release and OXCH Adr | increases SVR due to arterial VC (OXCHB doesnt mention veno or preload)
685
facial nerve muscle monitor
orbicularis oculi | orbi eye
686
GOLD CORE HARRY | PK changes obese
Increased - Tot Body water - ECF (as fat is mostly extracell water) - -early distribution, low peak con-->increase load - increased BV - increased RBF--increased renal clearance - increased LBW-->increased CO and increased clearance in muscle - -faster offset - decreased % CO to brain - -slower onset?????? (i think) - increased fat - ->Vd doesn't increase in proportion to % fat - --Propofol Vd obese is same per kg as non obese! -increased alphaacidglycoproteirn yet opiates decreased due to risks LBW - STP - prop load - LAs-decrease epidural as epidural veins compressed TBW - prop - sux due to increased butryl cholinesterase and LBW and CO
687
roc DoA and half life
DoA 40min elim T/2 100min redistribution half life 2 min (uptodate) giving double the dose adds a half life but roc 1.2 doesn't feel 100min longer (i think this is because elimination half life is not the same as the half life)
688
``` amiodarone # evernote ```
``` Forgetables -QTc, AV, AP, refractory, CHB -decreased HR—>increased Cor BF Active met Biliary excretion ```
689
meth Hb pulse ox graph
smile with 940 ab> 660 ab=same as deox
690
The term SpO2vs SaO2 (EN)
The term SpO2 means the SaO2 measurement determined by pulse oximetry.
691
fent vs morph PCA T/2Keo and peak and DoA CORE HARRY
T/2Keo 4.5 min vs 4.5hrs (CORRECT IN 2 sources) peak 4min vs 20min-->stacking of morph DoA 30-60min (Small dose-note large dose 3-4H OxCHB) vs 3-4H Morphine similar Vd 3.5-4L and clearance 20ml/kg/hr and terminal elim #fent fall asleep-->pain Thus, if a patient administered five doses of morphine to achieve an analgesic level (ignoring the potential contribution of the active metabolite, morphine-6-glucuronide, see below) that will allow him or her to fall asleep, the effect-site concentration would remain elevated for more than 3 hours after the last morphine dose Hydromorphone is associated with less nausea, one of the major opioid-related side effects that decreases patient satisfaction. In addition, plasma hydromorphine concentrations remain elevated for a long time, which may result in prolonged analgesia. However, without knowing hydromorphone PDs, it is difficult to predict the effects of a given PK profile on the effect of the drug accurately
692
Hydromorph stoelting | CORE GOLD
onset 10-20min vs 20min of morph offset (Anesthetic Pharmacology says slower vs morph) -Potentially the ideal agent for quick onset-->decreased risk of stacking before peak. and long DoA so can sleep It is less hydrophilic than morphine, leading to faster onset of analgesia. This opioid produces somewhat more sedation and evokes less euphoria than morphine. Because of rapid elimination and redistribution, oral dosing every 4 hours is needed to maintain adequate plasma concentrations for analgesia. Hydromorphone is an effective alternative to morphine in the treatment of opioid-responsive moderate to severe pain.[170] The uses and side effects of hydromorphone are the same as those of morphine, although histamine release is less prominent with hydromorphone. Up2date - glucorination-->inactive mets-->renal excretion (decrease in hep failure - 7% excreted unchanged in urine so avoid in severe CKD
693
opiate half lives
plasma conc of all drops by >50% in less than 5 min
694
CO and loading dose and CBF
Higher CO -->larger apparent Vd -->larger induction dose required "The effect of cardiac output on the apparent volume of distribution was poorly understood with most discussions being exclusively devoted to the effect on the duration of onset of action." Higher CO and CBF  faster onset and offset  may need larger induction dose "Total CBF was significantly higher in children compared with adults" A common misconception made was that alterations in clearance and metabolism affect induction doses. They do not. Many candidates asserted that an elderly patient would have a significantly reduced cardiac output. This is not the case in an elderly patient without co-morbidities.
695
septic prop dose
slowly and titrated to effect due
696
neonatal changes
articulate decreased PVR-->increased RAP and increased LAEDV-->LAP
697
ductus venosis
lost of umbivein flow-->decreased flow-->functional close in minutes Functional closure occurs within minutes of birth. Structural closure in term babies occurs within 3 to 7 days. The ductus venosus is open at the time of birth and is the reason why umbilical vein catheterization works
698
CVS change at birth
#RAP change normal changes dont occur if... hypoxia, prostaglandins-->PDA high RAP-->PFO
699
delta gap
* Calculate the delta gap (or delta ratio) to identify the possibility of a mixed disorder ie HAGMA +NAGMA (ANZCA MELBOURNE SAYS DO THIS IF Chloride is abnormal) * Delta gap = Delta AG – Delta HCO3 * Delta gap = (AG – 16) – (25 – [HCO3]) * -6 to 6 mmol/L = isolated RAGMA * < -6 mmol/L = excess HCO3 loss, therefore also a NAGMA present * > 6 mmol/L = excess HCO3 present, therefore also a respiratory acidosis or metabolic alkalosis present
700
TEG | RV
``` #evernote C3HFP ``` R,A,K,MA
701
Dynamic vs static compliance and contributers to WoB
``` #evernote (great formulas for Elastic res etc) ```
702
total resp compliance curve CORE
CW at small volume really negative pressure due to spring out. CW at normal volume less spring. CW at overdistended actual recoils back in hence a positive pressure Lung. increased positive pressure-->increased vol
703
COPD lung vol | CORE CORE CORE
increased FRC and TLV
704
DS total calc
PACO2-PeCO2/PACO2
705
FRC with age and CC | CORE
FRC doesn't decreased with age as per the classic graph of age FRC and CC! CC>FRC-->V:Q mm and shunt
706
Pulm VR and extra alv cap | CORE
extra alv are right outside alv. | capillaries are further away
707
increase and decreased FRC CORE HARRY LITFL
Patient, Procedure, Anaesthetic, position ``` Decreased -patient: decreased CW or lung compliance eg restrictive lung Dx (TRUE), abdo pressure, atelectasis -procedure raised intraabdo pressure -Anaesthetic -GA -supine ``` Increased - patient: increased compliance eg emphysema - anaesthetic: PEEP emphysema, FRC is increased, because the lungs are more compliant and the equilibrium between the inward recoil of the lungs and outward recoil of the chest wall is disturbed.
708
Role of FRC CORE CORE
``` A)-decrease airway res B) Compliance-WoB (comp and res) B) reservoir B) gas exchange in exp B) vol>CC-->avoid V:Q mm C) optimise PulmVR-->decrease RV AL ```
709
PENDELUFT CLINICAL SIG and capno
alpha angle of capno plateu reflects V:Q status due to this! pendelluft. In pendelluft, distribution of inspired gas is dependent on respiratory rate As respiratory rate increases, the proportion of the tidal volume that is delivered to the region with a long time-constant decreases Fast alveoli are preferentially inflated, causing V/Q scatter or shunt in the unventilated slow alveoli. Dynamic compliance will decrease as respiratory rate rises and be markedly different from static compliance
710
Avagadros law | CORE
vol of gas is directly proportion to the number of molecules of that gas
711
types of MAC
MAC50, MAC95 =1.3x MACBAR 1.7 MACAWAKE=0.3 | MACHours
712
HCT
volume percentage (45%) Hematocrit is usually lower in the smaller vessels in tissue than in the large veins or arteries from where the blood samples are withdrawn. The spleen is an exception; hematocrit in splenic blood is usually almost two times higher than in arterial blood. -i believe decreased in capillaries because RBC volume is reduced to squeeze through caps
713
Hamberger effect derranged phys CORE R/V
Venous CO2 diffuses into RBC. CA HCO3+H. RBC allow HCO3 out for Cl in. reverse true in pulm cap. The chloride shift has signficant effects for the organism: It mitigates the change in pH which would otherwise occur in the peripheral circulation due to metabolic byproducts (mainly CO2) It increases the CO2-carrying capacity of the venous blood It increases the unloading of oxgyen, because of the allosteric modulation of the haemoglobin tetramer by chloride (it stabilises the deoxygenated T-state)
714
CORE CVS volume change in preg | P+H
Estrogen->renin and Angiotensin Prostaglandin and progesterone-->VD BMR increased 20%
715
cartilage
3 paired -arytenoid-pyramid -cuneform (isolated flake of cartilage within the margin of the aryepiglottic fold) -corniculate (Corn means horn-ontop of arytenoid) 3 unpairded -thyroid -cricoid-signaturi ring with signaturi post -epiglottis arytenoid at post, sup, lat aspect of cricoid corniculate is the horn on top
716
laryngeal m. anatomy book GOLD CORE HARRY
SET for CT (sup ext tensor Cricothroid) Cartilage 3 paired -arytenoid-pyramid -cuneform (isolated flake of cartilage within the margin of the aryepiglottic fold) -corniculate (Corn means horn-ontop of arytenoid) 3 unpairded -thyroid -cricoid-signaturi ring with signaturi post -epiglottis arytenoid at post, sup, lat aspect of cricoid corniculate is the horn on top Muscles The actions of the intrinsic laryngeal muscles can be summarized thus: 1 abductors of the cords: posterior cricoarytenoids; 2 adductors of the cords: lateral cricoarytenoids, interarytenoid; 3 sphincters to vestibule: aryepiglottics, thyro-epiglottics; 4 regulators of cord tension: cricothyroids (tensors), thyroarytenoids (relaxors), vocales (fine adjustment). Nerves Vagus (ipsilateral)—>sup laryngeal and recurrent laryngeal Sup laryngeal—>small external—>motor Critcothroid—>sole TENSOR—>Hoarse—>compensate -SLN close to sup thyroid art and vein—>dx in T4 surgery Sup laryngeal—>large internal branch—>sens to VC and above. Runs deep to piriform fossa (cavity lateral to cords—>easy to block with topical LA) Recurrent Laryngeal Nerve Right: loop under subclavian artery. Associated with inf thyroid art and vein—>Dx in surg or malignancy, cervical lymph malignancy, rarely in goitre Left: loop under AoA: associated with same in addition to Dx in lung, oesophagus malignancy, Aortic arch aneurism. Both—>sensation below VC Sx—>vocal cord paralysis—>midline and inf. If unilateral—>hoarse—>compensate Bilateral—>valve like obstruction worse on insp—>stridor —>wow
717
Diffusion vs perfusion limitation
CO-->diffuses easily across alv into RBC-binds avidly to Hb. So soluble that no appreciable increase in PP established to create back pressure. so it is not flow but diffusion that determines amount t/f to blood. N2O (not nitrogen) rapidly crosses and as doesn't react with Hb rapidly establishes a PP that within 1/10 of transit equals alveoli so uptake ceases. hence perfusion is the only thing that will increase uptake.
718
ketogen vs GNG substrates
AA+Glycerol-->GNG | AA+FFA-->Ketogen (less m. break down vs GNG)
719
steroid rec
The glucocorticoid effects relevant to this discussion are initiated by interaction of the drugs with specific intracellular glucocorticoid receptors nuclear receptor superfamily with action at nucleus-->changed gene transcription This suggested that in addition to controlling gene expression within the nucleus, the liganded receptor itself could initiate important signal transduction events while still in the cytosolic compartment (there may even be a subpopulation of receptors that reside there permanently). One such effect seems to be interaction of the receptor with the regulatory complex, NF-κB (see Fig. 34.6 and Ch. 3 ) and other important interactions may involve protein kinases/phosphatase signalling systems.
720
lost slides CORE
google CVP wave form atrial contraction-->tricuspid bulge X-relax and ventricle tugs down-->vacuum Venous filling followed by opening of TV-->drop—>atrial S3 increased blood vol in ventricule as in CCF or athlete S4 atrial contraction int stiff ventricle-->pathological eg CCF or AS LV -diastole 10mmHg RV - systole 15-25mmHg - Diastole 0-8mmHg CONTRACTILITY AND AFTERLOAD SHIFTS up and down evernote " vasoconstriction CO “ CO is independant and on X axis technically max CO when RAP sig neg mutation genetic mutation of skeletal isoform sarcomer is the muscle fibre util sarcolemna membrane AP travels Goldman-hodgkins, Katz calc E=58log(o/i) E=58/log150/5=K RMP Goldman-Hodgkin-Katz E=58log Ko+Nao+Cli/Ki+Nai+Clo Absolute 200ms due to NaCH inactive RRP 50ms as some Nach have transitioned to resting more Na perm-->unstable resting less Inward rect K cha-->further from Nerst potential-->high baseling membrane potential SA -65mv-->T-->L (phase 0 at -40mv)-->K (triggered by positive Memb pot Mycotye-90 ``` NO...FIRMTITS Please #heparin ``` Hb is a metabolloprotein with 4 polypeptide globin chains each with an associated haem (1Fe each) in its pocket As Hb acts as an oxygen carrier, the globin chains slide on each other. e α1 β 1 and α2 β 2 contacts stabilize the Hb molecule when oxygen reacts with Hb (in the Relaxed form). When O2 is unloaded, the β-chains are pulled apart so that 2,3-diphosphoglycerate (2,3-DPG) !enters! the molecule and decreases the affinity of the Hb molecule for oxygen MELBOURNE COURSE deox-->stabilized in Tense form oxy-->stabilized in Relaxed form Wiki Each heme group contains one iron atom, that can bind one oxygen molecule
721
Soda lime vs newer and reaction | CORE HARRY
Co2+H20-->H2CO3 H2CO3+NaOH-->Na2CO3+H20+heat Na2CO3+Ca(OH)2-->CaCO3+2NaOH strong base --> react-->CO des>iso CF2H (cant f 2 hard) strong base-->compound A for sevo Newer absorber is Amsor nil strong base CaOH and CaCl H20 and pH indicator and setting agents
722
NMB monitor thumb thingo
acceleromyography
723
DBS role
Double-Burst Stimulation Double-burst stimulation (DBS, minitetanus) consists of two short bursts of 50-Hz tetanic stimuli separated by 750 milliseconds. DBS P.506 should not be repeated at intervals of less than 12 seconds. Caution should be exercised when switching between double-burst and TOF stimulation. Up to 92 seconds may be required before these responses stabilize. DBS has been used mainly to detect residual NMB. Studies show that fade (response to the second burst weaker than that to the first) is more readily detected with DBS than with TOF using visual or tactile monitoring. It has also been used for intraoperative assessment of NMB. Another use of DBS is to assess deep block, since the first twitch in double burst can be detected at ###!deeper block levels than the first twitch in TOF.!#### DBS causes more discomfort than TOF stimulation but less than tetanic stimulation. It can be used at submaximal currents. This causes less discomfort and, in most cases, is more reliable than testing with supramaximal stimuli.
724
aging def
time dep phys process-->decreased cellular function and reserve
725
afterload CORE
laplace A=p.r/t AS, SVR increase Pressure!!! dilated heart-->increased radius
726
OER
V/D 25% normal 70% is max
727
fasting PD | HARRY
DO NOT FORGET RAAS ``` goal why reservers 2 months 2H glucose 10H glycogen requirement -1ml/kg/hr fluid -2500kcal ``` REMEMBER decreased consumption with lethergy, hunger, thirst rb Cori
728
Antiglycaemic CORE
1) biguanide metformin Rb renal excreted unchanged LA in renal Dx inhibit GNG, GI uptake, increased sens 2) sulfonylurea - eg gliclazin!!!!!!!!!!!!!!!!!!! LICK - increased release and sens. renal excretion unchanged and hep met 3) DPP4i eg sitagliptin (SITTING DUCK FOR A fuck up) normal BD GLP-->less GLP-->more insulin ``` 4) gliflozins SODIUM GLUCOSE TRANSPORTER 2inhibitor in PCT UTI, osmotic diureses UKA high PRb ``` 5) acarbose INHIBIT ALPHA GLUCOSIDASE
729
pain pathways nerves and drugs that block pain
C fibres are demylinated and synaps at 1,2, laminae A delta are myelinated an I,II, V laminae Desc Higher centers-->PAG-->DH Transduction-capsaisin transmission-LA, everything else Perception modulation Rb with NMDA anatag ad N2O and Mg with tapentadol add TCA
730
Ketamine met
active met NorKet (demethylated) conj-->inactive renal exc
731
paracetamol R/V
NAPQI
732
paracetamol R/V
NAPQI
733
Ketamine SoA
predom DH stoelting
734
Gabapenting SoA | core
IT doesnt do shit so it is a CCB centrally (stoelting) also reduces glutamate release at DH (stoelting)
735
KG
FFA-->(betaoxidation) -->acetyl CoA-->if Acetyle CoA in excess what kreb cycle can use (oxaloacetate is depleted in fasting state) then Acetyl coA diverted to KG via acetoacetyl CoA enzyme and BMG-CoA--> acetone B-hydrybutyrate acetoacitate
736
KG
FFA-->(betaoxidation) -->acetyl CoA-->if Acetyle CoA in excess what kreb cycle can use (oxaloacetate is depleted in fasting state) then Acetyl coA diverted to KG via acetoacetyl CoA enzyme and BMG-CoA--> acetone B-hydrybutyrate acetoacitate
737
PCWP
12/8
738
adenosine
adensosine 1 rec at SA and AV adensosine sensitive K channel open-->hyperpol-->neg chrono GiPCR-->decreased camp-->neg ino
739
hamburger effect and HCT
deoxy As a result of the shift of chloride ions into the red cell and the buffering of hydrogen ions onto reduced haemoglobin, the intercellular osmolarity increases slightly and water enters causing the cell to swell. This can be measured as an increase in mean corpuscular volume (MCV).
740
what drive Nernst for K to be high intracell
The typical resting membrane potential of a cell arises from the separation of potassium ions from intracellular, relatively immobile anions across the membrane of the cell
741
HArry Core staring forces
Cp=60mmHg Gp=15mmHg Co=21-->33 average 27 59-15-27=19=180L/day
742
Harry osmolarity
R is retardable so arithmatic | 2Na+glucose+urea
743
tonicity topic HARRY
Tonicity is the measure of the osmotic pressure gradient between two solutions. (Derranged phys) Dextrose and urea are the main ineffective osmoles. In a diabetic patient, dextrose can still be an effective osmole. An iso-osmolar solution can be hypotonic if the solute is able to penetrate the cell membrane. For example, an iso-osmolar urea solution is hypotonic to red blood cells, causing their lysis. This is due to urea entering the cell down its concentration gradient, followed by water. The osmolarity of normal saline, 9 grams NaCl dissolved in water to a total volume of one liter, is a close approximation to the osmolarity of NaCl in blood (about 290 mOsm/L). Thus, normal saline is almost isotonic to blood plasma. Neither sodium nor chloride ions can freely pass through the plasma membrane, unlike urea. or 5% dex isoosmolar but hypotonic in plasma-->tissues
744
osmolality | derranged phys
Osmolality is the same in the ICF and the ECF. 290mosmol/kh
745
glom charge
neg - - - - - - - - - -
746
interstitial pressure
slightly neg due to active lymphatic pump ``` structure function control of lymph ```
747
Pulse pressure | CORE HARRY
Pulse pressure is the difference between systolic and diastolic blood pressure Pulse pressure depends on stroke volume, arterial compliance and run-off –is increased if: • Stroke volume increases –exercise, aortic regurgitation • Arterial compliance is reduced –elderly with stiff arteries • Run-off is increased –artero-venous shunt, aortic regurgitation • Compare this to hypovolaemia/cardiogenic shock: low SV/pulse pressure
748
resistance to VR vs MSFP
res is arterioles | MSFP is based on venous tone
749
conductor insulator conductor
capacitor capacitance=storage
750
Renal blood flow calc | HARRY CORE
#PAH if Plasma flow=clearance as 100% cleared then [p].vol/time=[u].vol/time so clearance=[u].vol/[p] and RBF=Plasmaflow/(1-HCT)
751
hep blood flow measure HARRY CORE
Indocyanine green has a fixed HER of 0.74 and no clearance elsewhere Cl=x/auc HBF= Cl/HER
752
HARRY CORE | ficks principle
Consumed=CO.Ca-CO.Cv | Consumed/AV diff=CO !!!!!!!!!
753
CO measurement harry core
USS CSA.VTI V=c/fo. fd/costheta c=USS velocity f0= emitted freq fd=doppler shift theta=angle https://link.springer.com/content/pdf/bbm%3A978-1-84882-336-5%2F1.pdf
754
CBF measure HARRY
``` Ficks prince N20 or xenon PET USS bulb So2 Once inserted blood can be sampled for p02 and oxygen saturation, lactate and other substances. These measurements can give an indication of the adequacy of CBF. Lower val-ues suggest a greater uptake by the brain and therefore decreased blood flow, providing there is no change in oxygen consumption and that it is uniform throughout the brain tissue. ```
755
PiCCO
thermodilution to calibrate then pulse contour analysis Other measures generated include: — preload: global end-diastolic blood volume (GEDV) and intrathoracic blood volume (ITBV) — extravascular lung water (EVLW) which is a sensitive indicator of pulmonary oedema. — arterial BP, HR, stroke volume (SV), systemic vascular resistance (SVR), and cardiac function index (CI). -ve severe AR -->inaccurate thermodilution can't use with Aortic balloon pump
756
viscosity
frictional force between sliding layers of fluid apparent viscosity decreases with reduced radius and increased flow
757
barorec FUCKING CORE CORE HARRY FINAL DAYS
Cvs barorec loop evernote
758
resp centre CORE HARRY | FINAL DAYS
#EVERNOTE
759
pressure diuresesis CORE RV
CORTICAL NEPHRONS are auto reg increased BF-->VC-->decreased renal BF juxtaMEDULLARY nephrons and vasa recta are not autoreg increased BF-->washout conc grad-->diuresis -->exponential curve RAAS alters this curve
760
CNS prop vs sevo CORE final days
sevo - uncouple above 1MAC - CO2 responsivness to VD preserved Propofol - CMRO:CBF maintained - CO2 responsiveness maintained
761
Propofol and sevo CVS | final days
Prop every mech you can think of 15% decrease CO 15% decreased SV 15% decrease SVR no reflex tachy and can reset barorec and Brady -due to reduced SNS-->decreased Ca in, increased K out, NO stim Sevo VD due to direct sm relax blunts barorec reflex (no change in HR), minor neg ino (changed Ca sens and decreased ICC due to L type CCh, preserves CO, cardioprotective Cor VD
762
regional bf
google heart, brain, liver, kidney regional blood flow normal values ml/100g
763
glom tubular balance CORE CORE CORE HARRY final days
increased filtration-->increased sodium reab 1) increased Na filtered also means increased glucose and AA filtered-->reab together 2) increased GFR-->increased oncotic p in peritubular cap-->increased reab TBFB -high flow-->high Na-->Adenosine-->VC-->decreased GFR
764
Pulm VR and flow
flow decreases resistance (never reaches overdistention) | 1) recruit then distend (both decrease res)
765
IR gas analyser pros and cons CORE
IR analyzers are based on the principle that gases with two or more dissimilar atoms in the molecule (nitrous oxide, CO2, and the halogenated agents) have specific and unique IR absorption spectra. Oxygen and nitrogen cannot be measured. There is interference from other gases, such as oxygen in high concentrations, although this can be compensated for by most new monitors. Water vapor can absorb IR light.
766
Paramagnetic | CORE
O2 is attracted because of the fact that it has two electrons in unpaired orbits. When introduced into a magnetic field, some substances locate themselves in the strongest portion of that field. These substances are termed paramagnetic. Oxygen is the only paramagnetic gas that is important in anesthesia. When a gas that contains oxygen is passed through a switched magnetic field, the gas will expand and contract, causing a pressure wave that is proportional to the oxygen partial pressure. They are very accurate and highly sensitive. The analyser should function continuously
767
Sux CVS SE moa FUCKING CORE HARRY
mimics Ach at M2-->brady at ganglionic NaCH-->tachy
768
HCO3 prod PCT
glutamine NH4+HCO3
769
pKa H20+Co2-->H2CO3
6.1 hence better for acid buffer but so big and open its good for both
770
aldosterone core
Cortical CD principle cells and Type A intercalated cells increased Pr prod including NaKATPase pumps and Na and K ch. The release of the steroid hormone aldosterone from the zona glomerulosa of the adrenal cortex is stimulated by angiotensin II, increased plasma potassium concentration and adrenocorticotrophic hormone. Aldosterone acts in the renal cortical collecting duct where it stimulates sodium reabsorption and potassium secretion by the principal cells, and hydrogen secretion by the type A intercalated cells. Aldosterone is the main determinant of tubular sodium reabsorption and controls the reabsorption of over 500 mmol of sodium, which is more than the normal dietary intake. Aldosterone induces the production of proteins in the cortical collecting duct cells, including the basolateral membrane Na/K-ATPase pump and sodium and potassium channels in the luminal membrane. Aldosterone similarly increases sodium reabsorption from the gut, sweat and salivary glands.
771
Glucocorticoids SE | CORE
1) met 2) antinflam - block PL-A - ->decreased PG, leukotriens 3) immune - inhibit T lymphocytes and macrophages - decreased antibody production and interleukin 4) fetal lung 5) mania, insomnia
772
CO2 absorber
amsor
773
Xenon
PC - non reactive with sodalime - odourless PK -nil diff hypoxia PD - nil neg ino - MAC 71%-->decreased max FiO2 - raised CBF - PONV - dense and viscous - MV unchanged - nil MH
774
CORE HARRY muscle group onset and sens to roc
Diaphragm and laryngeal m. are resistant (req higher conc to block) BUT BF is higher so onset and offset are faster vs Add. P Upper airways are more sens vs Add.p so diaphragm -->breathes, Add.p appears normal but swallowing ineffective-->aspirate with normal TOFR<0.9 vs >0.9
775
roc onset
Millers "When doses lower than those required to cause 100% neuromuscular block are administered, the time required to reach maximum effect is a function of the NMBD and blood flow to the muscles. It is independent of the dose administered. However, if the administered dose is high enough to cause 100% neuromuscular block, the time required for maximum block will depend on the dose of NMBD administered. Larger doses will, up to a certain point, produce a faster onset of effect. " "The maximal effect of either 0.25 or 0.5 mg/kg of rocuronium at the laryngeal muscles occurs after 1.5 minutes.:
776
why is sux quick Millers
Makes no sense The times to 95% blockade at the adductor pollicis after administration of the ED 95 dose of succinylcholine, rocuronium, vecuronium, atracurium, mivacurium, and cisatracurium are shown in Figure 34-10 . 114133135 The illustration shows that the most potent compound, cisatracurium, has the slowest onset, and the least potent compound, rocuronium, has the most rapid onset. 114133135 Bevan also proposed that rapid plasma clearance is associated with a rapid onset of action. 137 The fast onset of succinylcholine’s action is related to its rapid metabolism and plasma clearance.
777
muslce to monitor
The pattern of blockade (onset, depth, and speed of recovery) in the corrugator supercilii is similar to that in the larynx, 119 the diaphragm (eye brow) The onset of maximal blockade in the larynx also corresponds with the point at which the adductor pollicis begins to show palpable evidence of weakening.
778
Roc DoA 0.6 vs 1.2
Increasing the dosage of rocuronium from 0.6 mg/kg (twice the ED 95 ) to 1.2 mg/kg (four times the ED 95 ) shortens the onset time of complete neuromuscular block from 89 seconds to 55 seconds but essentially doubles the clinical duration of action of the compound (the recovery of the first twitch of TOF [T1] to 25% of baseline values) from 37 minutes to 73 minutes.
779
roc DoA obses
With larger doses, when administration is based on TBW, recovery occurs during the elimination phase when plasma concentration decreases more slowly than during the distribution phase. 312 The pharmacokinetics of rocuronium is not altered by obesity. In the same way, the duration of action of rocuronium is significantly prolonged when the dose is calculated according to TBW. In contrast, when rocuronium is dosed according to ideal body weight (IBW), the clinical duration is less than half.
780
NMBA and pka
They are therefore usually completely ionized at 7.4 pH and are poorly bound to plasma proteins.
781
NMDA and renal function
Only atracurium, cisatracurium, and, to some extent, vecuronium are independent of renal function. Succinylcholine elimination is mainly independent of kidney function However, succinylcholine is metabolized by plasma cholinesterases, and concentrations may be slightly decreased in patients with severe renal failure ( Table 34-10 ). The decrease in plasma cholinesterase activity is always moderate (30%) and does not result in prolongation of succinylcholine-induced neuromuscular block. Succinylcholine induces a transient increase in plasma K + concentration (<0.5 mmol/L). Therefore, succinylcholine is not contraindicated in severe renal failure when plasma K + concentrations are within the normal range. Consequently, the duration of action of NMBDs may be prolonged in patients with renal failure.
782
hep dx and NMBA
In comparison with renal elimination, liver function is a modest determinant of the pharmacokinetics of nondepolarizing muscle relaxants (see also Chapter 73, Chapter 74 ). The influence of hepatobiliary disease on the pharmacokinetics of NMBDs can be complex because of the different types of liver failure ( Table 34-11 ). Cirrhosis is associated with an increased extracellular water compartment, edema, and often kidney dysfunction. Cholestasis induces decreased biliary excretion but is not associated with significant liver failure, contrary to acute hepatic failure.
783
``` SAQ shift roc DR curve Millers CORE CORE CORE CORE Final days ```
ED5095=0.3 Ed9595=0.45 intub 0.6 (2xED5095) ED5050=0.15 stoelting left shift with volatile, Mg, hypothermia, aminoglycocides, LA right shift with chronic anticonvulsants -->upreg of Nicotinic achR, increased clearacnce and increased binding to A1aGP. increased Ca with hyperparathyroidism NOTE this is not the same as onset or offset but similar key points Diaphragm and laryngeal m take more but have higher BS (this would be a different y axis) IM probably has incomplete BA decreased dose req (defs is explicitly. non defs is unexplicit) 1) other NDMR (defs) 2) volatile (defs) 3) Mg, CCB (defs) 4) LA, low Ca, Tamoxifen, Lith, aminoglyco increased dose req 1) paeds No change in load -oldies-more ECF but less Ach release (increased DoA-->decreased maintainance DoA hypothermia (millers doesnt define onset) liver failure (complex) renal Dx Onset faster with NDMR, Volatiles, aminoglycosides, Ma, low ca, CCB, li, LA, Slower LF-->increase ECF
784
Sux MoA | COre
NONCOMPETETIVE | partial agonist
785
NMBA duration of action definition
time to first twitch (T1) becoming 25% of control twitch | ie time for 25% of rec to become available again
786
phase I and II block
I sux | II NDMR
787
Mitocondira resp #khan academy
2 +2 +32=36 from 1 glucose ``` Structure IC organelle outermembrane inner membran high H between membranes ribosomes for protein synth DNA tRNA cristae are inner membrane folds to increase SA and ATP prod Proton pump out ATPsynthase-->H flows back in ``` not present in RBC (Quora) - as needs to squueze through small space - not use up O2 just glycolysis - fit more Hb
788
Pain lecture sydney
C fibres are demylinated and synaps at 1,2, laminae A delta are myelinated an I,II, V laminae in lamina 5 polymodal C and Abeta (touch) fibers synapse with Wide Dynamic Range Neurons. WDRN sensitized by inflam--> transmit non-noxious as pain ``` Central Sens NMDA glutamate sub P NO-after NMDA stim-->increased NO-->nerve Dx-->hyperalgesia neurotrophins ``` silent nociceptors which can become active
789
Sydney pain talk | ascending pain pathway
1. Spinothalamic DH to thalamus to cortex. Sensory discriminative aspects of pain 2. Spinoreticular and spinomesencephalic (= Spinoparabrachial) To medulla and midbrain: arousal, homeostatic, autonomic To cortex: anterior cingulate cortex, insular and prefrontal cortex= affective and motivational components of pain
790
Desc pain pathway | sydney lecture
one or a series of neurons projecting down Periaqueductal Gray: Enkelpahin, GABA Locus Coeruleus: NorAdrenaline VRM: Nucleus Raphe Magnus: Serotonin
791
referred pain
Convergence. Referred pain is felt in the cutaneous area corresponding to the DH neurons on which visceral affernts converge. This is accompnied by allodynia and hyperalgesia in the skin area. Peripheral visceral afferents branch with considerable overlap in the territory of individual roots Viseral hyperalgesia
792
neurpathic pain
Sites of ectopic discharge in the damaged primary afferent nerve Spont firing neuroma Demyelination and production of ectopic impulses Sensitivity of DRG: Increased sensitivity to nordrenaline Upregulation of NGF and BDNF (Brain derived neurothrophic factor): peripheral and central effects
793
peripheral sensitization | CORE HARRY
Tissue Dx, SNS, inflam--> soup-->sensitize the PRIMARY AFFERENT REC PERIPHERAL H+, K, histamine, NAd, PG, leukotreines, -sensitize rec, VD and increased perm-->more inflam mediators sensitizing HENCE NO GLUTAMATE or sub P INVOLVED! central sensitaztion is at dorsal horn 1) glut and sub P-->NMDA -->ca in-->second mesengers-->rec upreg and gene transcription --> NO-->effect 2) Wide dynamic range neurons Abeta and polymodal C in context of inflam and central sensitization 3) neurotrophins and glial inflam CENTRAL SENSITAZTION-->allodynia, hyperalgesia, windup (resolves rapidly), long term potentiation (persists up to months)
794
how GA works
This requirement could indicate that either hydrophobic sites on proteins (the interior of soluble proteins or the membrane-spanning regions of membrane proteins) or lipid membranes could be the target sites of anesthetic action. The absence of apparent structure–activity relationships for anesthetics coupled with the Meyer–Overton relationship, led to the “unitary theory of anesthesia,” which posited that all anesthetic agents act by a common molecular mechanism Indeed, the changes in membrane biophysical properties produced by clinical concentrations of anesthetics are similar to those produced by a 1 C change in temperature There are a number of volatile compounds that deviate from the Meyer–Overton correlation. These include compounds, referred to as “transitional compounds,” that are less potent than predicted by their oil/gas partition coefficients, as well as “nonimmobilizers,” compounds that do not produce immobility despite being highly soluble in olive oil (and lipid) Photoaffinity labeling experiments have identified specific protein binding sites for a few anesthetics ( Site-directed mutagenesis has shown that anesthetic actions on specific target proteins can be eliminated with single amino acid changes in protein sequence; subsequent generation of transgenic animals has confirmed that these specific target protein modifications can dramatically and selectively alter anesthetic potency
795
GA define
A more useful definition of anesthesia is as a collection of component behaviors including: (1) sedation (2) immobilization in response to a noxious stimulus (3) amnesia (4) attenuation of autonomic responses to noxious stimulation (5) analgesia
796
Barbituate SF activity
add hydrophobic side chain-->sedation make that chain longer-->more lipid sol and more potents swap position 2 O2 for sulfur-->more potent
797
Thios | final dasy
R/V ``` KETO-->ENOL how it is kept alkaline minimal neg ino (VD-->decrease preload) induces CYP450 #dynamic equiplib #porphyria crisis -inducible and non-inducible genetic condition -block enzyme that converts haem precurer into haem -->Sx ```
798
volatiles MoA
Meyer overtone-->amount in lipiphilipd membrane-->expand-->block poor BUT temp-->same expansion enantiomers and o:gxMAC not a constant gene mutation of protein-->change effect lipid potency alone inadequate variable effects of different agents at different sites
799
sulfonylurea rec site and action
bind to ATP sens K ch-->depol, ca, insulin
800
metformin moa cellula
active AMP sens protein kinase
801
thiazolidenidiones
``` rosiglitazone PARR gamma inhibit -->increase glucose ut -->decrease hep glucose prod -->increased sens ```
802
acarbose moa
inhbit alpha glucosidase
803
DPP4 i
sitagliptin inhibit BD of GLP1 less hypos
804
resp prev vol
TV increased VC normal all else decreased
805
o neg draw backs
``` bombay gp (nil H antigen) Minor RBC antigens Kell-->sensitize for next time # minimal plasma in PRBC ```
806
serum vs plasma
Serum is solo without coags | Plasma eg FFP has coags
807
PL and coagulation cascade
adhere, activ, agg initiation, amplification, propogation of coag cascade PL plug with fibrinogen is stabilized by coag cascade that converts fibrinogen to fibrin and then cross bridge with XIII. TXA VC and act 5HT VC and act ADP activate only
808
Opiate Elim half life | FInal days
``` P+H Morphine Vdss 4L Cl 15ml/L/min Elimination half life =3 hours ``` FENT IS ESSENTIALLY THE SAME - so at ss both equal - after bolus very different 1hr vs 3-4 hours DoA
809
oxycodone IV CORE FINAL DAYS
onset of fent and doa of morph! Onset 5-8min Doa 4 hours Met CYP2D6-->active oxymorphone (n-alk of this is naloxone!) -->variable oxycodone -CYP2D6 is the genetic polymorph --Poor 10 --intermed 10 --Extensive 70 --Ultrafast 10 -codeine prodrug-->variable met to morphine -Tramadol prodrug-->desmethyltramadol 10% don't get it CYP3A4-->inactive Noroxycodone
810
oxycodone IV CORE FINAL DAYS
onset of fent and doa of morph! Onset 5-8min Doa 4 hours Met CYP2D6-->active oxymorphone (n-alk of this is naloxone!) -->variable oxycodone -CYP2D6 is the genetic polymorph --Poor 10 --intermed 10 --Extensive 70 --Ultrafast 10 -codeine prodrug-->variable met to morphine -Tramadol prodrug-->desmethyltramadol 10% don't get it CYP3A4-->inactive Noroxycodone
811
Pethidine | CORE R/V
P+H synthetic phenylpiperadinee anitcholinergic-->SE SSRI--> Seretonin Sx with MAOi opiate-->SE more lipid sol vs morph-->rapid onset DoA 2Hrs met to inactive me plus 50% active Nor-pethidine (via N demethylation) NP is less lipid sol and has longer half life and eliminated renally it accumulates in the fetus where it is eliminated even slower not reversible with naloxone
812
Delta ratio
NAG is a Neg quality Delta gap = (AG – 16) – (25 – [HCO3]) * -6 to 6 mmol/L = isolated RAGMA * < -6 mmol/L = excess HCO3 loss, therefore also a NAGMA present * > 6 mmol/L = excess HCO3 present, therefore also a respiratory acidosis or metabolic alkalosis present
813
CORE AF! | HCO3 and CO2
as CO2 goes up H2CO3 buffer system response is increased HCO3 then with time more HCO3 created Met acidosis HCO3 drops and CO2 drops in response (move in PARALLEL)
814
Base excess and HCO3
#evernote "Abg presentation anion gap Aa alveolar gas eqn" the "actual ie what it is" HCO3 as calculated by the HH eqn will alter with change in CO2. "standard ie standardise condition" with normal CO2 because if the CO2 was normal is there a metabolic process that was masked. BE is similar to standard HCO3 but factors in Hb into its complex eqn as this buffers CO2 Standard BE is with Hb of 50
815
Base excess and HCO3
#evernote "Abg presentation anion gap Aa alveolar gas eqn" the "actual ie what it is" HCO3 as calculated by the HH eqn will alter with change in CO2. "standard ie standardise condition" with normal CO2 because if the CO2 was normal is there a metabolic process that was masked. (dual process) BE is similar to standard HCO3 but factors in Hb into its complex eqn as this buffers CO2 Standard BE is with Hb of 50
816
sigaard
evernote siggaard anderson GOLDEN
817
Afterload and pressure
Intraventricular pressure so AS or raised SVR-->raised intraventricular P to overcome this PPV reduces afterload as the transmural pressure is less and the gradient from ventricle to aorta is less.
818
Afterload and pressure
Intraventricular pressure so AS or raised SVR-->raised intraventricular P to overcome this PPV reduces afterload as the transmural pressure is less and the gradient from ventricle to aorta is less.
819
P+H IMD infusions etc CORE R/V beautiful
derranged phys is perfect! Css in=out mg/hr in=target conc.clearance Conc of infusion. rate of infusion= Conc of plasma.Clearance so rate of infusion=target conc.cl/conc of infusion
820
isomers | final days
isomers A)structural with diff bonds A1 static iso vs en ethyl group arrangment of Cl vs F A2 is dynamic B)stereo same bonds diff 3D space B1 optic ie enantiomer (mirror) B2 diastereoisomer (non mirror) B2x is configurational (can't be converted by rotation around a single bond) B2y geometric eg cis and trans around double bond
821
alfent met
CYP450 | CYP3A4-->compete with midaz
822
PO4 vs NH4
NH4 greater capacity | (think of it as 2 mechanisms>1
823
circle system review
APL just distal to reservoir bag to titrate bag filling. | APL on ex limb so spill weak shit not strong shit.
824
volatile structures
``` ChF2 not present on sevo or halo sevo has lots of F too so weak halo small (just alkyl) Des is covered in F so very weak Iso and En have Cl and a CHF2 ``` #CHF2 is CO risk
825
soda lime | CORE
Overall: CO2 + Ca(OH)2 -->CaCO3 + H2O
826
phenyleph
as only 1 hydroxyl on benzyn ring-->nil COMT but as nothing at alph MAO does break down metaraminol lasts longer as nil COMT or MAO
827
propofol preparation action and toxic effect MoA CORE
potentiate action of glycine and GABA may reduce NaCh opening time ``` 26dipp 1% 10%soya bean oil (proteins removed so safe) 1% egg Phosphatide (not protein so safe) glycerol-tonicity OH-alk ``` propofl infusion syndrome - met acid, rhabdo, MOF - quinol met-->green urine and hair distribution T/2=4 min (note CSHT at 10 min is 5min) inactive mets via glucorination or met to a quinol no effect in renal or hep Dx
828
prop vs sevo CSHT etc | final days
Conclusion simplification (rounded ++) - prop at 30min -5 4H-10 Vss-20 - sevo/des 5,8,8 - iso 10, 20, +++ - propofol 5 in short 9 in long - sevo 5 in short 8 in long to clinically relevant pseudo awake point propofol 10min -->5min 180min-->9min Vdss-->20min STP 10min-->4min 180min-->85min Fentanyl 10min-12min 180min-->70min Remifent 10min-->3min 180min-->3min Sevo 90% decrement time MILLERS*** below time to MAC awake from MAC 1.2 (approx 75% decrement 1.2-0.3) Iso NOT SEVO -30min-->9min -4hrs-->20min Des - 30min-->5min - 4hrs-->6min Note difference between sevo and des is clinically very small SEVO FIGURES NOT AVAILABLE IN MILLERS STOELTING **** "For example, the 80% decrement times of desflurane and sevoflurane are <8 minutes and do not increase!!!!!!!!!!! significantly with the duration of anesthesia, whereas 80% decrement times for enflurane and isoflurane increase significantly after about 60 minutes, reaching plateaus of approximately 30 to 35 minutes." "The major differences in the rates at which desflurane, sevoflurane, isoflurane, and enflurane are eliminated occur in the final 20% of the elimination process." (WHICH IS CLINICALLY NOT Very RELEVANT!!!!!!)
829
ketamine moa
Rb R vs S ischaemic precond NDMA antag NaCHB NAchB opioid rec onset not in one arm brain 90s P+H doa 10min IM onset 5 min for 20 min 5-10mg procedural 0.2mg/kg active met--.conj-->inactive no change to SVR
830
H secretion
all luminal have H-ATPase PCT and thick asc H:Na Type A IC in DC have K/H ATPase
831
wo of sevo compartment halflife
B:G 0.69 VRG 2 min VPG 70 min fat 30 hours due to diff BS and sol patient facotr circuit anaesthetic -depth, duration, conc, second gas fat is short case-->speed up awakening due to distribution
832
SNP met and MoA
art and venous VD
833
GTN moA
venous VD >>>art-->decreased preload decreased wll tension-->increased cor BF to subendocardial regions GTN-->nitrate-->NO Elim T/2 1 min OCH onset SL 3min and last for 30-60min
834
phentolamine OXCH and P+H
``` 1mg onset 1min for 10min alpa 1 block-->decreased SVR alpha 2 blockade presynaptically-->increased NAd release-->positive inotrope, chronotrope increase Cor BF increased insulin-->hypoglycaemia ```
835
hydralazine
active GC->increase cGMP-->decrease Ca -->VD art>venous onset 10min for 5 hrs
836
moxonidine
alpha 2 ag physioten sounds like clonidine
837
minoxidil
K ch opener katzung #mink seksy KKK
838
Venturi Bernoulli principle
FOR LAMINA Pressure + potential energy (graivty.dens.height) + density.Vsquared dive by 2=a constant so increase P-->decrease V increase V-->decrease P-->draw air in
839
pitot
The pressure difference between the ports is proportional to the square of the flow rate.
840
derranged phys efficacy vs affinity | CORE CORE CORE
Efficacy (Emax) is the maximum effect which can be expected from this drug (i.e. when this magnitude of effect is reached, increasing the dose will not produce a greater magnitude of effect) Intrinsic activity is the drug's maximal efficacy as a fraction of the maximal efficacy produced by a full agonist of the same type acting through the same receptors under the same conditions
841
spare rec theory CORE RV
"A pharmacological system has spare receptors if a full agonist can cause a maximum response when occupying only a fraction of the total receptor population
842
partial agonist mechanism | derranged phys
This maximal efficacy thing is related to several possible mechanisms. Perhaps the partial agonist occupies all the receptors (i.e. achieved full receptor occupancy), and interacts with them in a manner identical to the full agonist, but for some of the receptors it inexplicably fails to activate the ligand binding site or secondary messenger system. The obvious extension of this is where the drug, while binding avidly to the receptors, somehow fails to activate any of them - in which case it is said to be an antagonist. Alternatively, a drug may be a partial agonist because it produces a different distinct structural change in the receptor - for example, an ion channel might open incompletely with a partial agonist, with ionic conductance reduced thereby. The latter effect is observed in the effect of different partial agonists on the acetylcholine receptor
843
lignocaine pH
5 to ionize and dissolve
844
1
22
845
chemo rec moa
decrease O2 tension - ->glomus cell in preriph CR - ->decreased ATP - ->block ATP sens K ch - ->depol - ->Ca in - ->NT release - ->AP - ->medullar resp centre stimulated Raised Pco2 also stimulates glomus cell neurotransmitter release, perhaps by raising intracellular hydrogen ion concentration
846
O2 resp Q | CORE
``` CO2 vs O2 (High and low!) O2 vs CO2 glomus cells CNs reflex ```
847
static vs dynamic
is is the change in volume of the lung produced by a unit pressure change, the ow of gas having ceased. For example, a subject can inspire a known volume of gas and then relax against a closed airway for as long as possible, while intrapleural pressure is measured (usually by observing oesophageal pressure). Lungs with a high compliance have a steep slope in their pressure–volume curves. us, a small change in distending pressure will cause a large change in lung volume. Compliance is the inverse of elasticity or elastic recoil. Dynamic compliance is a measure of the volume and pressure changes that occur during normal breathing, without any breath holding. e calculation of dynamic compliance is made from the volume and pressure values at times of no gas ow at the mouth at the end-expiratory and end-inspiratory points.
848
m of resp
``` insp at rest -diaphragm-phrenic C3,4,5 -EIC -angelled down and forward #AP LAT (spinal nerves at that level) -scale-oppose -ve ITP pulling ribs in accessory -sternomastoid lift ribs 1,2, sternum AP LAT -traps etc -nares ``` Exp forceful -IIC pull closed -Ab rect, EO,IO, TA
849
why do I care about pendeluft
increased RR-->exaggerate-->overdistend and underdistend -->VQ mm worsend dynamic compliance as change in pressure -->flow between alveoli and not in and out-->decreased TV for same pressure widen gap between static and dynamic compliance pendelluft. In pendelluft, distribution of inspired gas is dependent on respiratory rate As respiratory rate increases, the proportion of the tidal volume that is delivered to the region with a long time-constant decreases Fast alveoli are preferentially inflated, causing V/Q scatter or shunt in the unventilated slow alveoli. Dynamic compliance will decrease as respiratory rate rises and be markedly different from static compliance
850
Peak vs platue P CORE GOLDEN FINAL DAYS
airway pressure = flow x resistance + alveolar pressure so zero flow simple alv pressure alveolar pressure = (volume/ compliance) + PEEP so High alveolar pressures can be due to excessive tidal volume, gas trapping, PEEP or low compliance as shown by this relationship: Static compliance is measured in the absence of gas flow, and is based on plateau pressure: Cstat = Vt/(Pplat – PEEP) Dynamic compliance is measure in the presence of gas flow, and is based on peak pressure: Cdyn = Vt/(Ppeak – PEEP) Remember these three scenarios to understand how compliance curves will change: Pulmonary emboli do not change resistance or compliance, so both compliance curves are unchanged. Plugging or bronchospasm increases airway resistance (Raw) and peak pressure, so dynamic compliance curve shifts to the right and flattens. Plateau pressure and static compliance are unchanged. Tension pneumothorax, atelectasis, pulmonary edema, pneumonia, bronchial intubation cause reduced lung compliance which increases both peak pressure and plateau pressure, so both static and dynamic compliance fall.
851
resistance
yes turb changes res!
852
turbulent and flow
flow proportional to. square root of Pressure increased flow -->increased res ie more P req for same flow
853
Peak vs platue P CORE GOLDEN FINAL DAYS
airway pressure = flow x resistance + alveolar pressure so zero flow simple alv pressure alveolar pressure = (volume/ compliance) + PEEP so High alveolar pressures can be due to excessive tidal volume, gas trapping, PEEP or low compliance as shown by this relationship: Static compliance is measured in the absence of gas flow, and is based on plateau pressure: Cstat = Vt/(Pplat – PEEP) Dynamic compliance is measure in the presence of gas flow, and is based on peak pressure: Cdyn = Vt/(Ppeak – PEEP) Remember these three scenarios to understand how compliance curves will change: Pulmonary emboli do not change resistance or compliance, so both compliance curves are unchanged. Plugging or bronchospasm increases airway resistance (Raw) and peak pressure, so dynamic compliance curve shifts to the right and flattens. Plateau pressure and static compliance are unchanged. Tension pneumothorax, atelectasis, pulmonary edema, pneumonia, bronchial intubation cause reduced lung compliance which increases both peak pressure and plateau pressure, so both static and dynamic compliance fall.
854
resistance
yes turb changes res!
855
bohr vs haldane
bohr - CO2-->push O2 out and Cl in - more CO2-->increase T stabilization-->more effective CO2 buffer haldane deoxy more effective buffer more O2-->drive the following to the right->CO2 release H+ +HbO-->HbH +O (this eqn also represents the bohr effect
856
fuel cells Final days
4e+O2+H2O-->4OH Pb+2HO- -->PbO+H20+2e-
857
collision broadening
CO2 on capnograph * Collision broadening * Collision of different gases—>broader IR absorption pattern—>potential error source—>measure O2 and N2O to compensate
858
bohr vs haldane
bohr - CO2-->push O2 out and Cl in - more CO2-->increase T stabilization-->more effective CO2 buffer haldane deoxy more effective buffer more O2-->drive the following to the right->CO2 release H+ +HbO-->HbH +O (this eqn also represents the bohr effect
859
hadlane and bohr | P+K
Bohr Hydrogen ions bind to the α-amino and imidazole groups of haemoglobin and alter the allosteric conformation of haemoglobin, which reduces the anity of oxygen to haem. Carbon dioxide binds to the N-terminal amino acid residues, and this reduces the accessibility of the haem groups to oxygen and causes the oxyhaemoglobin curve to shi to the right. 2,3-Diphosphoglycerate binds to the β chains of one tetramer of deoxyhaemoglobin, causing a conformational change in the haemoglobin molecule, which reduces oxygen anity. Haldane e attachment of oxygen to haem reduces the capacity of haemoglobin to carry carbon dioxide. Oxygen increases the ionization of nitrogen groups, reducing the capacity of the globin chain to carry carbon dioxide as carbamino compounds. erefore, deoxyhaemoglobin can carry more carbon dioxide in the form of carbamino compounds, which account for about one-third of the arterial venous dierence of carbon dioxide carried in blood. In addition, deoxyhaemoglobin is more basic and therefore has an increased buering capacity for carbon dioxide.
860
phentolamine
1mg 1min 10min BC due to reaction increased insulin release-->hypoglycaemia
861
STP in container
NaCO3-->NaCO3 +H20-->Na + OH +NaHCO3
862
STP tautomerism | CORE
enol in vile | keto in body
863
phentolamine
1mg 1min 10min
864
protamine
neg ino, hypotension brady | anaphylaxis
865
decreased butyrl cholinesterase
live, renal CCF, hyperthyroidism, preg | neostigmine
866
dipyridamole | CORE
inhibit PL reuptake of adenosine to increase conc in plasma to keep stimulating receptors PDEi to decrease BD of camp-->PKA-->block activation, aggregation and also-->VD
867
enoxaparin onset
up2date | 3-5hrs for 12 hrs
868
HITS MX
Fondaparinux
869
HIT types
non-immune - PL recover without ceasing heparin - day 1-4
870
Carbon monoxide
shift OHDC far left (can't release O2) Wiki: Because of the increased affinity between hemoglobin and oxygen during carbon monoxide poisoning, little oxygen will actually be released in the tissues. The affinity between hemoglobin and carbon monoxide is approximately 230 times stronger than the affinity between hemoglobin and oxygen so hemoglobin binds to carbon monoxide in preference to oxygen The traditional understanding is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen-carrying capacity of the blood and inhibits the transport, delivery, and utilization of oxygen by the body.
871
CO2 is perfusion vs diffusion
Both oxygen and carbon dioxide exchange is perfusion-limited. Diffusion of gases reaches equilibrium one-third of the way through the capillary/alveolar interface diagram google: is co2 diffusion or perfusion limited mak95
872
O2 perf diff
Elite Athlete |  ↑↑CO → ↓red cell transit time (<0.25s) preventing equilibration b/n PAO2
873
O2 diffusion perfusion at altitidue
1) ficks law decreased P change-->decreased diffusion rate-->slower-->diffusion limited 2) deoxygenated patient lower on OHDC so O2 in alv taken into Hb avidly so Partial pressure doesn't increase as fast vs a well oxygenated patient whose Hb are quickly filled and pressure spills over into plasma - ->longer to equilibrate
874
VQ lateral
awake -dep gets more vent and Q-->10% better VQ than supine anaesthetised -dep gets less vent one lung - surgical lung up - bottom lung has even worse compliance as IPP that was holding mediastinum up is lost - ->sig decrease vent and - ->increased Q due to HPVC of surgical upper lung ?????is this right (as per melbourne it is)
875
disinfection
decontaminate - clensing to remove micro - include sterilization and disinfection Sterilization -kill all forms including spores-heat radiation, pressure etc Disinfection -apply to surface to kill (doesnt kill spores) Decontamination renders an item or material safe to handle. The level of microbial contamination is reduced enough that it can be reasonably assumed free of risk of infection transmission. Sterilization, disinfection, and antisepsis are forms of decontamination. disinfection and antiseptic used interchangably in stoelting
876
phenylbutazone
anitinflam high PrB aplastic anaemia so just for severe arthritis
877
misoprostol
PG analgoe at EP3 rec parietal cel inhibit H+ sec surface cell-->increase mucous secretion
878
H2 anatgonists
cimetidine (only one to inhibit cyp450) ranitidine famotidine
879
pethidine
less neonatal resp dep
880
raman spectroscopy
less commonly used can measure O2, CO2, N2O, volatiles 1. Raman spectroscopy: the anaesthetic gas sample is illuminated by an intense argon laser. Some light energy is simply reflected but some energy stimulates the sample molecules, causing them to scatter light of a different wavelength from that of the incident light energy (Raman scattering). This scattered light is detected at right angles to the laser beam and the difference in energy level between the incident and reflected light is measured. All molecules in the gas/volatile phase can be identified by their characteristic spectrum of (Raman) scattering.
881
chlorpropramide
sulfonulyruea-renal excretion unchanged
882
placenta t/f
>6000daltons dont cross increase t/f later in preg as less Alb to bind PrB drugs
883
domperidone
D2 antag for N+V doesnt cross BBB so no tardives | does cause prolactinaemia
884
why log the dose response curve
This is traditionally converted to a semi-logarithmic plot because:  The doses from smallest measureable response to maximum response usually spans several orders of magnitude (Evers and Maze) The hyperbola can be transformed into a sigmoid which:  Expands the scale at the low concentrations where effect is rapidly changing and compresses it at high concentrations where the effect is changing slowly  usually linearizes the the dose-response range of interest  20% - 80%.
885
tolerance evers and maze p501 CORE RV
1st desens: Phosphorlation of GPCR-->functional uncoupling of rec and effector systme 2nd internalisation phosphorlyation of GPCR-->arrestin 3rd down reg with rec degradation slower AC upreg NMDA rec activation !!!!!!! VGCCH and K chan sens change
886
dissociation constant for drugs
D + R-->DR DR--D+R Kd=D+R/DR
887
affinity
how avidly it binds eg high affinity antagonist
888
drug action
1. phsyiochem 2. rec 3. enzyme 4. ion Ch eg LA 5. other
889
Isomers CORE final days
Structural: In structural isomers, the atoms in each isomer are connected, or bonded, in different ways Stereo: In stereoisomers, the atoms in each isomer are connected in the same way but differ in how they are oriented in space. Enantiomers are stereoisomers that are non-superimposable mirror images of each other with chiral centre Diastereomers are any stereoisomers that are not enantiomers.
890
CVP wave | FINAL days
fucking hell man
891
PV cardiac loops AVR tricky MR tricky
https://www.cvphysiology.com/Heart%20Failure/HF005
892
Radial vs aortic
``` delay systolic hump wider as diff waves at diff speeds PP greater as less compliant decreased MAP 5% ``` #more compliance radial looks like aortic as faster and less distortion from stretch
893
pressure wave contour analysis
``` HR and rhytm SV area under curve from contraction to incisur Contractility is up AL is down angle and incisure higher up if high SVR swing is preload index of supply is area under dias index of demand is area under syst MAP etc ```
894
SA node phase 3
depol-->Kch open-->hyperpolarisation (4)– closing of K channel-->funny current
895
sevo CBF autoreg
x
896
nerve AP
nil CCh so no plateu
897
noninvasive BP | CORE
https://academic.oup.com/bjaed/article/7/4/122/466759 #evernote
898
avagadros law
at a set P, T equal volumes contain same number of moles
899
dopamine antage P+H
#evernote
900
anticholinergic meds
#everntoe
901
AE antihistamine
cyclizine motion sickness, RT, PONV block H1 and Ach -->antichol Sx
902
ondans
brady, flush, HA, constipation OBA 70% hydroxylation-->conj-->inactive decrease in hep Dx
903
VIE
Critical temp of O2 -116C . 120 Boiling point (liq-->vapour -183C) . 180 system -180C--160C 160 -liquid:vapour in euquilibrium
904
vomiting centre
Rb labarynth-->Vestibular n.-->CN 8 Ach and H1 CRTZ 5HT and DA EC Ach
905
Outline the factors that determine the rate of recovery from nondepolarising neuromuscular block CORE
#propofl dreams
906
VIE
Critical temp of O2 -116C . 120 Boiling point (liq-->vapour -183C) . 180 system -180C--160C 160 -liquid:vapour in euquilibrium
907
HYPOTHALAMUS ROLE | CORE
#EVERNOTE
908
aspirin OD vs paracetamol OD
150 vs 200mg/kg both have active mets salycilate--> resp acidosis renal K and H dump ETC block-->MA NAPQI-->oxidative Dx ``` Mx PK A D M E ``` PD electrolyes salycilate Liver synth paracetamol Psych Charcoal salicylate-->NaCO3-->increased urine ion trapping both can be taken off with dialysis
909
M3
bronchial tree
910
severe asthma attack
Rb theophyline PDEi and adrenlaine
911
metoprolol
``` onset 10-20min (uptdate) NOT A SALLY so is highly lipid sol so 1) extensive absorption 2) large Vd 3) cross BBB ``` Exc-90% in urineunchanged (this is the exception to the rule that high lipid sol-->hep met like bisoprolol) DoA dose dependant t/2 20mg 6hrs atenolol - Lowlipid sol-->poor GI ab--> - No IV formular - onset 1hr peak 3 DuO 24hrs - met
912
cisatrac
Critical illness myopathy (OXCH) incompatable with fent, midaz, propofol ``` 1 of 10 stereoisomers 2mg/ml 2.5mg onset ED5095 is 0.05 tube at 2min 905 Twitch height reduction at 2.6min peak at 3.5min ```
913
catecholamine
benzyl group with 2 hydroxyl groups attached, alpha, beta and amine SO PHENYLEPHERINE metarminol, ephedrine ARE NOT CATECHOLAMINES
914
Obese Washo
iso will be longer in obese x y z short case can be quicker vs long-->longer MELBOURNE COURSE Note: OHS-->resistance to leptin and letin involved in resp drive so decreased resp to high CO2. accentuated with GA Increased sens to CNS dep drugs -->resp dep
915
ASepisi etc
Sterilization, disinfection, and antisepsis are forms of decontamination. disinfect-disrupt nonpor sterilise-kill all asepsis prevent contam
916
LASER
light amplified Stimulated emmision of radiation stim by light or electricity Spont decay stim emmision amplification
917
diathermy
cut like a saw
918
laryngoscopy view | HARRY
see book
919
obese
Both fat and lean body mass increase in the obese individual, although there is a relative decrease in lean body mass; water content and blood flow per gram of fat tissue are reduced in obese patients compared with non-obese subjects.4–7 For these reasons, obesity is likely to increase the degree of importance of partition coefficients (λblood/gas, λoil/gas) of inhaled drugs as total body weight and duration of anaesthesia increase.
920
IBW
Ideal body weight = 22 × H squared (m).
921
Obese Washo
iso will be longer in obese x y z short case can be quicker vs long-->longer MELBOURNE COURSE Note: OHS-->resistance to leptin and letin involved in resp drive so decreased resp to high CO2. accentuated with GA Increased sens to CNS dep drugs -->resp dep
922
Leptin
lipton iced tea - ->VC - ->heart remodels and gets weak - ->IT DOESN'T MAKE YOU RETAIN WATER
923
RESISTIN
the resistance are just contracts-->decrease contractility and remodel
924
AoA
1. Brachiocephalic 2. Left CC 3. left SC
925
laryngoscopy view | HARRY
see book
926
IJ
Quartad to consider 2 vessels 2 nerves 1) IJV-in carotid sheath 2) Carotid-internal then common-in carotid sheath 3) vagus nerve (BETWEEN IJ and CA)-in sheath 4) cervical sympathetic chain POST 5) Cervical chain lymph node-in sheath CLOSE to IJ - ->htoracic duct on right 6) pleural dome 2.5cm above medial 1/3 of clavicle Path 1) jugular foramen from sigmoid sinus - at first superficial in anterior triange. superficial to pulsating external carotid 2) vertically down neck 3) joined by external JV 4) dive deep to SCM 5) descends through groove of two SCM heads 6) join Subclavian to become brachiochepalic post to junction of clavicle and sternum CVC technique aim ipsilateral nipple head down aspirating 1) high-midpoint of SCM between mastoid join and sternal join 2) low-middle of triangle formed by 2 heads of SCM (sternum and clavicle) and clavicle
927
LP
rb supraspinous interspinous lig flav
928
trachea m.
trachealis m
929
chest drain
Pec M Lat Dorsi 5th ICS (nipple) axillar apex note vascular nerve bundle under rib
930
prostaglandins
F-flex E-easy and ebate eating is complex prostaglandins evernote
931
AoA
1. Brachiocephalic 2. Left CC 3. left SC
932
anticubital fossa final days
Prop dream (better than text-misc zone)
933
Opiate classification
Evernote
934
absorber
amsor
935
Paco2 | HARRY
evernote
936
Cough
Afferent -CNX Control Medulla: POns and Brainstem Efferent CNX phrenic spinal
937
eicosanoids
PG and TXA and leukotreins icosanoids are signaling molecules made by the enzymatic or non-enzymatic oxidation of arachidonic acid
938
prostaglandins
Katsung prostaglandins evernote
939
ATII CORE AF FINAL DAYS HARRY
RBF=P/R!!!!!!!!!!!!! Decreased RBF-->decreased Na-->renin from MD VC afferent and efferent - ->decrease RBF and GFR - ->mesangial contraction decrease filtration coef ATII rec in SFO and VOLT-->thirst VC eff>aff-->decreased RBF deu to afferent VC yet preserve GFR in hypotension due to efferent VC (and mesangial contraction SNS aff and eff -->decrease RBF but as Pressure hydrostatic increased GFR minimally dropped
940
Metabolic rate
(MR) = amount of energy liberated by catabolic processes in the body
941
ion ch R/V HARRY
sens, channel, gate pot diff-->conf change imperm if not open -->selective perm various arrangements of subunits around central poor Resting active inactive NaCH CCh -rianodine, NT release KCh changes with drugs
942
tuffiers line
superior aspect of the illiac crest
943
propanolol
angina, HTN, T4, phaemo NOT FOR AF. weakly active met CYP2D6
944
esmolol
weakly active met renally excrete
945
O2 trasport from alv
remeber fick law diffusion vs perfusion limited
946
1L CSL
load distributed through ECF in 15min. peed out by 6hrs sepsis-->leak even less IV vol. 1) osmo 276 but water into cells and electrolytes out -->no change 2) Na net 0.3mmol/L rise CL 1.5mmp;/L rise 3) SID, 4) lactate-->met to CO2 and H20 and consumes a H 5) 1:4 IV to EC and 9:1 ECF: ICC-->225ml IV-->outside A 5%–10% change in blood volume is required before ADH secretion is stimulated.threshold for bar rec change (derranged phys) -->increase Preload-->increa CO and BP 6) TG balance -diluted alb-->decreased reab-->urine (i believe insufficient to alter other renal system-probs some pressure diureses and medulla RBF not autoreg)
947
ATII CORE AF FINAL DAYS
RBF=P/R!!!!!!!!!!!!! Decreased RBF-->decreased Na-->renin from MD VC afferent and efferent - ->decrease RBF and GFR - ->mesangial contraction decrease filtration coef SNS aff and eff -->decrease RBF but as Pressure hydrostatic increased GFR minimally dropped
948
IVF response framework
``` osmo tone vol ONSET and OFFset oncotic UEC and BSL SID baro renal ```
949
conduction speed
dromotropy peledrome drome=speed
950
volatile safety
visualise - max dial - mount - interlock - pressure check - size of 2 chambers
951
vol vs osmo threshold
Baroreceptors are less sensitive (but more potent) than the osmoreceptors. The threshold of the volume receptors for causing changes in ADH secretion is an 8 to 10% change in blood volume
952
GT balance | RV
increase AA and glucose increase pertibular ONCOTIC PRESSURE -->more reab A constant fraction of filtered sodium and water is reabsorbed from the proximal tubule despite changes in GFR; this is called glomerulotubular balance
953
lactate in CSL
The lactate in Hartmanns is a conjugate base, the anionic part of lactic acid, in which the role of the hydrogen ion is played by sodium. However. The lactate anion is what the ABG machine measures
954
1L CSL
load distributed through ECF in 15min. peed out by 6hrs sepsis-->leak even less IV vol. 1) osmo 276 but water into cells and electrolytes out -->no change 2) Na net 0.3mmol/L rise CL 1.5mmp;/L rise 3) SID, 4) lactate-->met to CO2 and H20 and consumes a H 5) 1:4 IV to EC and 9:1 ECF: ICC-->225ml IV-->outside 8% threshold for bar rec change (derranged phys) -->increase Preload-->increa CO and BP 6) TG balance -diluted alb-->decreased reab-->urine (i believe insufficient to alter other renal system-probs some pressure diureses and medulla RBF not autoreg)
955
osmorec threshold
280-295mosmol
956
IVF response framework
``` vol osmo oncotic UEC SID baro renal ```
957
5% dex
This one time, Lobo et al infused some healthy volunteers with 2 litres of dextrose over 1 hour. The average BSL at the end of this hour was around 15. At the end of the second hour, it had already dropped to normal (actually, on average it was slightly low).
958
Paeds MAC | COREish
3.3% sevo peaking in term neonate-->2.5% at older than 6month require deep plane narrower margin of safety immature CVS system -->risk
959
Neo nat PK PD Millers
evernote
960
paeds PK PD
CORE >2yo-->Increased CO with increased % to kidney and liver that are heavier per Kg-->more rapid met and elim vs adult! <2yo-->immature hep and renal In general, most medications will have a prolonged elimination half-life in preterm and term infants, a shortened half-life in children older than 2 years of age up to the early teenage years, and a lengthening of half-life in those approaching adulthood. The response of infants and children (particularly neonates) to medications is modified by many factors: body composition, protein binding, body temperature, distribution of cardiac output, functional organ (heart, liver, kidneys) maturity, maturation of the blood-brain barrier, the relative size of the liver and kidneys, and the presence or absence of elevated intraabdominal pressure (gastroschisis or omphalocele closure) or congenital malformations because the neonate has less fat, a drug that depends on the redistribution into fat for the termination of its action will have a long clinical effect; and (3) a drug that redistributes into muscle may have a long clinical effect (e.g., fentanyl, for which, however, saturation of muscle tissue has not been demonstrated).
961
mapelson
Tots EF'DA T E F D add pressure valve Mapelson A a grade
962
mapelson A spont vs controlled
spont - exp: DS into tubing the FGF pushes Alv gas out - insp nice conc gas Controlled 1) expiration is low pressure APL doesnt open DS and Alv fill tubing 2) insp: PPV-->Alv rebreathed shit goes back into patient with some blasted out with FGF-->++ wasteful.
963
paeds Anaesthetic risk volatile
Perhaps the most important factor influencing the potential for anesthetic overdose in neonates is the number of MAC multiples that can be delivered by the vaporizer; for example, a halothane vaporizer can deliver up to 5.75 MAC multiples versus 2.42 MAC multiples for a sevoflurane vaporizer
964
paeds sevo vs halo
sevo better in everything except excitation on awakening
965
propofol MILLERS reaction
It should be avoided in children with anaphylactic reactions to eggs. dose larger in infants than kids
966
ketamine paeds millers
Contraindications to the use of ketamine in children include the presence of an active upper respiratory infection (URI), increased intracranial pressure, open-globe injury, and a psychiatric or seizure disorder. Ketamine does not preserve the gag reflex and thus should not be used as the sole anesthetic for children with a full stomach or a hiatal hernia.
967
alfent CORE CORE CORE
Rb smaller Vd-->increased Elim despite smaller Cl Rb CYP3A3/4-->compete with madaz
968
Sux paeds | Millers
Succinylcholine is highly water soluble and rapidly redistributes into the extracellular fluid volume. For this reason, the dose required for intravenous administration of this depolarizing muscle relaxant in infants (2.0 mg/kg) is approximately twice that for older children (1.0 mg/kg). IM -->double the dose
969
roc IM
1mg/kg
970
sugamadex
Sugammadex is a cyclodextrin whose endoskeleton forms a water-soluble complex with the exoskeleton of rocuronium; because sugammadex is made of sugars, the potential for adverse side effects would appear to be minimal. can be given in paeds yes
971
midaz met
CYP450 CYP3A3/4 | met inhib by CCB grapefruit juice erythromycin
972
Midaz PD | CORE FINAL DAYS
decrease SVR-->reflax tachy-->decrease MAP 5% TV decreased, RR increased MV stable decreased response to CO2 -my patients desat: atelectasis? decrease CO2 resp?
973
clonidine CORE FINAL DAYS
alpha 2 GiPCR PARTIAL agonist-->less potent with ceiling - Lat reticular n.-->decreased SNS - SNS presynaptic neg feedback - DH-->opiate release - Loceus ceruleous-->analagesia 100% OBA nil sig resp dep P+H nil change in CO nil sig neg ino 50% EXCRETED UNCHANGED IN URINE
974
Dexmed CORE FINAL DAYS
1600:1 extensive hep met-->fine in CKD unpredictable OBA severe brady decrease MAC 90% 94% PrB
975
Prevention of excess clot
P+K 1) Proteases C (5,8), S, Antithrombin (2,10), plasmin C cuts S Supports C C is stimulated by thrombomodulin when thrombin binds to endothelial surface proteases inhib by antitrypsin and antiplasmin virchows triad
976
Plasmin control
Endothelium release tPA Plasminogen always circulating (prod in liver) - bind to clot or endothelial tPA or urokinase or XIIa or XIa - ->activated to plasmin-->BD fibrin and fibrinogen to D-dimer products
977
Hypersens classification
evernote
978
allergy and histamine
Haemaccel causes direct histamine release from mast cells without complement activation or IgE production
979
IgG IgM IgE
IgM in milk-primary immune response vs bacteria #milk IgG crosses placenta-secondary immune # igG rhesus antibody crosses #goes IgE mast cell
980
histamine release morphine
The mechanism of this opiate response has remained unclear, although it is known to be non-immunological in nature. Immunoglobulin E antibodymediated immediate hypersensitivity reactions to the drugs are not often encountered.
981
lactate in CSL
1)cori cycle lactate-->pyruvate-->GNG-->glucose-->pyruvate-->lactate 2) conjugate Base of lactic acid - met to CO2 and H20 consuming 1 H - effectively 1HCO3 produced
982
plasmalyte
acetate 27 | vs CSL lactate 28
983
colloids
However, in large randomized studies, colloids have no superiority over crystalloids in terms of major outcome measures such as mortality. 5556 They are more expensive than crystalloids and can have unfavorable side effects. gelofusine-hydolysed end product of collagen 80% IV vol expansion (more leak vs albumin) T/2 in IV 6Hrs vs Alb 24hrs anaphylaxis nil renal issues not a sig procoagulant
984
albumin
Albumin is transported back to the circulation system via the lymphatic system. Albumin 5% expands plasma volume by 80% of the infused volume In critically ill patients, there is increased leakage of albumin and supplementation of more albumin only contributes to peripheral edema (i.e., “albumin trapping”). Despite excellent volume-expanding efficacy of albumin, randomized clinical trials have found no superiority over crystalloids.
985
Dextran
Dextran molecules are excreted by the kidneys or metabolized by endogenous hydrolase (dextranase) to carbon dioxide and water. Dextrans have been associated with anaphylactic reactions.
986
hetastarch
Hetastarches are synthetic colloids consisting of polysaccharides prepared from either grain or corn. The older hetastarch solutions and pentastarches have been associated with considerable side effects such as renal and coagulation problems.
987
CORE | GD therapy
Definition. Goal directed therapy (GDT) is a term used to describe the use of cardiac output measurement to guide intravenous and inotropic therapy, to ensure adequate tissue perfusion and cellular oxygenation
988
GFR and arterioles
A reduction in renal perfusion normally results in dilatation of the afferent glomerular arteriole and constriction of the efferent arteriole so that the GFR is kept constant. However, if mean arterial pressure falls below 70 mm Hg (the kidney autoregulatory threshold), renal perfusion pressure and GFR fall, leading to oliguria.
989
fluid responsiveness
Response to Fluid Challenge An important concept for guiding rational fluid administration is the use of the Frank-Starling curve for cardiac performance ( Fig. 41.5 ). In most clinical circumstances, a basic assumption is that the patient is on the ascending part of the Starling curve and has a submaximal cardiac output. When the subject reaches the flat part of the curve, more fluid administration has little effect on cardiac output/stroke volume and will only increase tissue edema. Although this concept applies to healthy volume-depleted patients, less than half of critically ill patients might respond to a fluid challenge.
990
CVP
CVP is influenced by many factors unrelated to actual fluid balance, such as venous tone, intrathoracic pressure, and left and right ventricular compliance. Consequently, there is poor correlation between CVP and the right ventricular end-diastolic volume,
991
PCWP
Pulmonary Artery Occlusion Pressure The pulmonary artery catheter (PAC) is used to measure pulmonary artery occlusion pressure or pulmonary capillary wedge pressure, which is intended to reflect left ventricular preload. 69 However, pulmonary artery occlusion pressure is not a good indicator of preload. 7071 The catheter measures pressure and not volume, the relationship is not direct but curvilinear, and clinical benefit is highly doubtful. 7273 Left ventricular compliance is dependent on filling of the right ventricle, which means that the PAC has the same limitations as the central venous catheter.
992
echo
Transesophageal Echocardiography Widely used in cardiothoracic surgery, transesophageal echocardiography has not proved a reliable predictor of fluid responsiveness in critically ill patients. There are conflicting results for use of the left ventricular end-diastolic area as a good predictor because it is a static measurement. 7475 Continuous measurements, such as positive-pressure ventilation, induced changes in vena cava diameter, and aortic flow velocity/stroke volume assessed by echocardiography, all have limitations.
993
Thermodilution
Transpulmonary thermodilution is a method that uses a cold bolus as a single indicator for determination of the assessment of the largest volume of blood contained in the four heart chambers, called the global end-diastolic volume. It requires the use of a specific thermodilution arterial catheter (pulse contour cardiac output monitoring) that measures temperature changes after the injection of the bolus through a central vein catheter (normally the central vein catheter is placed in the neck, the arterial line in the femoral artery). It does not appear to be a good predictor of fluid responsiveness according to available studies.
994
PPV swing GOLD
Changes in RV and LV stroke volume are greater when the ventricles work on the steep part of the Starling curve Thus change in LV stroke volume is an indicator of biventricular preload dependence. According to a large systematic review, pulse pressure variation (PPV) and stroke volume variation (SVV) predict with a high degree of accuracy (receiver operating curve 0.94 and 0.84, respectively) patients who are likely to respond to a fluid challenge limited by arrhythmias and the requirement for mechanical ventilation. They are less reliable in critically ill patients receiving ventilatory support. Furthermore, PPV is a direct measurement, whereas SVV is an indirect calculation from pulse contour analysis. PPV can be affected by the tidal volume, with the recommendation that tidal volume should be at least 8 mL/kg.
995
PPressure
Pulse pressure = stroke volume / arterial compliance
996
PLR
Passive Leg Raising Test Passive leg raising (PLR) represents an endogenous volume challenge that can be used to predict fluid responsiveness. This procedure rapidly returns 150 to 200 mL of blood from peripheral veins in the lower extremities to the central circulation. When ventricular preload is increased, cardiac output is augmented according to the degree of preload reserve. 86 A PLR test can be used in patients with spontaneous or assisted breathing and irregular cardiac rhythm; therefore it can be a more useful test of fluid responsiveness in critically ill patients. 87 PLR is a simple test in which the legs are elevated by 45 degrees above the bed, but to be reliable it must be accompanied by cardiac output monitoring. Because of the ease of use, simplicity, and high diagnostic accuracy, PLR is the preferred method to assess fluid responsiveness.
997
Water deficit
TBW.(Na-140/140) TBW 50% male Current sodium x Current (unknown water)=ideal sodiumxideal water ie 0.5*wt—>derivation of above formula
998
osmolarity
2Na +g +U makes perfect sense
999
osmolarity measure
Freezing-point depression osmometry is the most commonly used method for measuring the changes in colligative properties of a solution. It is based on the principle that the addition of solute molecules lowers the temperature at which a solution freezes.
1000
osmolarity measure
Freezing-point depression osmometry is the most commonly used method for measuring the changes in colligative properties of a solution. It is based on the principle that the addition of solute molecules lowers the temperature at which a solution freezes. membrane osmometers not used much (not referenced in text) only wiki
1001
albumin
does more to interstitial fluid! 20% alb =20g in 100ml 100mmol/L Na T/2 in vasc=24 hrs-->interstital fluid then degraded after 2 days From this we can extrapolate that in our healthy cylinder model, the 20g of albumin will attract about 220ml of water into the intravascular space (increased onc pressure) with the expansion maximal at 30 minutes post infusion, and petering out rapidly afterwards (suggesting that in septic ICU patients the transcapillary escape rate is increased by as much as 200%, to 10% per hour).
1002
HCT for estimated blood volume
EPV = [0.065 X wt(kg)] X [1-Hct]. since BVE and 65 mL/kg RBC volume, mL = total blood volume, mL × hematocrit / 100 Plasma volume, mL = total blood volume, mL × ( 1 – hematocrit / 100 ) Example: adult male, height = 180 cm, weight = 70 kg, Hct = 25% ``` Total blood volume, L = [ 0.3669 × (height, m)3 + 0.03219 × (weight, kg) + 0.6041 ] = [ 0.3669 × (180 / 100)3 + 0.03219 × (70) + 0.6041 ] = 2.1398 + 2.2533 + 0.6041 = 5.0 L (4,997 mL) Red blood cell volume, mL = (4,997 mL) × (25% / 100) = 4,997 mL × 0.25 = 1,249 mL Plasma volume, mL = 4,997 mL × [1 - (25% / 100)] = 4,997 mL × 0.75 = 3,748 mL ```
1003
Midaz IM
same dose as IV 10mg for seizure
1004
sufent | RV
12x more potent than fent as more affinity (IA same obviously) highly lipid sol-->fast onset and offset after bolus ET/2 between fent and alfent high PrB-->smallish Vd CSHTweakly active desmethyl sufentanil (n-dealkylation)
1005
suction
evernote diagram To ensure good flow, the maximum vacuum and the shortest possible length of tubing should be used, the internal diameter of tubings, connectors, and the suction catheter should be as large as possible, and the vacuum system should not leak. The outlet from the vacuum system is on a roof Filter for bacteria, liquid, solid, condensation and smoke ``` Additionally note Nozzle-soft with multi openings Tubing is flex but strong Receiver is not too big or small Vacuum source is electric pump with pneumatic pumps—>neg pressure 500mmHg—>generate flow of 25L/min pithing 10s of switch ``` Test before use Titrate suction req to effect High P low flow (vs scavenger system)
1006
gauge pressure
Vacuum is usually stated in gauge pressure, the difference between the measured pressure and ambient atmospheric pressure (which is zero on the gauge).
1007
risk of suction
evernote ``` A #cough and laryngospasm and Dx B C D Exposure to infection ``` Inadequate tip to wall 1. tip 2. Tubing-intra luminal or extra 3. receiver 4. Filter 5. Pressure
1008
final days
http://www.partone.lifeinthefastlane.com/inhalational-anaesthetics.html Pka Rat LaM O:G sevo 50:1 SVP of iso 33kpa
1009
methoxyflurane
BGPC 15 vs 0.69—>slow—>can’t knock self out with N20 OG 950 vs 50—>to fat—>prolonged effect above analgesic level 70% hepatic met—>Fl ions—>high output renal failure Neg ino, catechol sensitisation Raised ICP if PP sustained Same Resp SE vs others Nil tocolytic—>good for labour
1010
WZs west zones
Zone 1 conditions are generally said to be absent from the normal lung under physiological conditions.
1011
OLV nunns
Finally, the addition of PEEP to the ventilated lung during OLV seems like a logical response to its reduced lung volume and propensity to develop atelectasis, but PEEP will also increase the pulmonary vascular resistance of the dependent lung and potentially worsen the shunt The suggested ‘protective ventilation’ strategy requires pressure-controlled ventilation, low tidal volume (6 ml.kg −1 predicted body weight) and low levels of PEEP (5 cmH 2 O). This strategy has been shown to improve oxygenation during OLV, reduce the systemic inflammatory response associated with OLV 56 and improve postoperative lung function. Non vent lung CPAP5-10 Fio2 100% recruite or clamp or squeeze if needed Vent lung 0.7%Fio2 PCV
1012
quzze
z
1013
Grey matter | CORE
picture what is darker in brain outside is grey in SC inside is grey
1014
ANS GOLD | RV
Nerve systems 1. Cerebrospinal brain, SC, peripheral nerves 2. ANS (contort of nonskeletal to reg internal enviro) Higher centres influence ANS ANS - SNS-efferent cell bodies in lateral grey column and in peripheral ganglion of T1-L2 - PSNS-efferent Brainstem CNs 3,7,9,10 and sacral primary rami—>pelvic splanchnic nerves Exit as myelinated the ganglia then unmyelinated Ganglia 2.5cm from midline for SNS and very close to organ for PSNS SNS-mass effect - exit lat grey column—>white rami communicans 3 options in the Sympathetic trunk 1. Synapse at that ganglion in white rami communicans 2. Travel upon down trunk to ganglions above # cervical ganglion 3. Pass through and synapse with a more distal ganglion - therefore blocking or stimulating one white rami communicans segment—>wide effect on many organs at many levels above and below SNS 2 segments -somatic—>skin—>VD, sweat, piloerector -visceral—>organs (from ganglia to organ) —enteric: ganglia more distal and stimulated by splanchnic nerves (autonomic nerves) —adrenals —>preganglionic—>chromaffinc cells of medulla
1015
final days CORE airway anatomy lochi
corniculate corn is horn on top of arytenoid posterior is aryepiglottic fold attaches to epiglotis VC-->vestibular (Channel) fold-->false VC nares have vestibule (Channel) too
1016
data types | CORE RV final days
catagorical vs numerical catagorical-->binary, nominal, ordinal numerical-->cont vs discrete cont-->interval (zero is just a number celcius) or ratio (kelvin)
1017
TNR
vs Metabolic rate | MnM
1018
colligative
colligative properties are those properties of solutions that depend on the ratio of the number of solute particles to the number of solvent molecules in a solution, and not on the nature of the chemical species present
1019
CORE AS FUCK FINAL DAYS | CO2
CO2prod=AV.PaCO2 .k | AV=CO2 prod/PaCO2 .k
1020
CORE AS FUCK FINAL DAYS | CO2
CO2prod=AV.PaCO2 .k | AV=CO2 prod/PaCO2 .k
1021
core AF | physiological DS
Anatomical+alv
1022
core AF | physiological DS
Anatomical+alv
1023
Bohr eqn | FINAL DAYS
PACO2-PETCO2/PACO2 | NOT CONTENT
1024
shunt eqn CORE AF | FINAL DAYS
Qs/Qt = (CcO2 - CaO2) / (CcO2 + CvO2) Aa/AV
1025
phenanthrene
finger ann on throne while doing heroin
1026
phenylpiperadine
rb
1027
gaba rec
pre and post synaptic GABA binding at AB AB a gamma is for benzo aaaaayyyyyy B-barb-allosteric volatile and prop also act at B at sep site to Barb ``` If a benzodiazepine increases the frequency of channel opening by 300%, and a barbiturate increases the duration of their opening by 300%, then the combined effects of the drugs increase the channels overall function by 900%, not 600%) #BarbD BenF ```
1028
allosteric
In biochemistry, allosteric regulation is the regulation of an enzyme by binding an effector molecule at a site other than the enzyme's active site. #conformational change
1029
nonshivering thermogen
non mech Lipolysis -->glycerol and FFA FFA-->acetylcoa-->recycled back to FFA with release of Heat and consumption of ATP increase BMR x2
1030
thermo reg | CORE FINAL DAYS
Cold: BoK in dermis fires over wide range (max 40C) with peak at 25C Adelta mylin BoR 30-46 peaking at 44 C unmyelin both LSTT-->RAS and medulla and HT ``` increased firing from cold-->stimulate Post Thal-->VC and shiver #poles are cold ``` increased firing from hot and local warm blod -->ant pit increased firing-->sweat and VD Shiver increase BMR x1 shunt -artioventous shunt cap venous plexu1.5L -VD-->decreased SVR-->increased CO-->flood plexus and heat loss BFincrease x30
1031
thermo reg | CORE FINAL DAYS
Cold: BoK in dermis fires over wide range (max 40C) with peak at 25C Adelta mylin BoR 30-46 peaking at 44 C unmyelin both LSTT-->RAS and medulla and HT ``` increased firing from cold-->stimulate Post Thal-->VC and shiver #poles are cold ``` increased firing from hot and local warm blod -->ant pit increased firing-->sweat and VD Shiver increase BMR x1 shunt -artioventous shunt cap venous plexu1.5L -VD-->decreased SVR-->increased CO-->flood plexus and heat loss BFincrease x30
1032
CYP450 HARRY
EVERNOTE
1033
MAC of des
6.6
1034
Halothan
trifluroacetic acid , Br and Cl
1035
Sevoflurane CORE AS FUCKING FUCK Harry
5% hepatic met CYP450-->inorganic F- additionally reacts with sodalime-->compound A -more when dry, low flow, (only with strong base) additionally if not enough water in storage tank-->lewis acid -->hence 300ppm water
1036
onset of sevo Millers GOLD
#bulk exchange process time constant for circuit equilib Vol/FGF -conc of FGF will not change the time constant but set a higher equilib point V circ = 6 L and FGF = 6 L/min, the exponential time constant will be 1 minute with delta p/t= FGF/Vol.chang in circ P - Uptake into lung time constant for alveoli equilib (if no uptake) FRC/Alv vent with delta P/t= Alv vent/FRCxPressure grad circ to alv time for alv to blood uptake=Sol.Vol/blood flow tim constant is the same time constant from for tissue equilib Vol.sol/flow -brain has high flow ans small vol so short fast time constant ``` VARIABLES ARE circ vol.sol, FGF, conc vol of alv, Alv vent (Deadspace i.e., ventilated but not perfused pulmonary regions, reduces effective alveolar ventilation thus slows anesthetic uptake), CO (and shunt) Sol of drug irritant drug ```
1037
MV effects and lipid sol | Millers
However, the relative size of the ventilation effect is greater for soluble agents ``` Low MV for Low lipid sol low problem as will saturate quickly anyhow #sevo you can just chill. ```
1038
Shunt effects lipid sol | millers
shunt-->50% cant participate in exhcange-->slower rise of arterial PP-->slower onset effect lipid sol more (same logic)
1039
sevo time to MAC 1.2 | core
Evernote
1040
bendenouli CORE got it wrong before
in order to maintain a constant flow, a fluid must increase its velocity as it flows through a constriction This is achieved despite the patienťs respiratory pattern by providing a higher gas flow than the peak inspiratory flow rate. P+12𝜌𝑣2=𝜅 P is pressure p is density Because of the high fresh gas flow rate, the exhaled gases are rapidly flushed from the mask, via its holes. Therefore there is no rebreathing and no increase in dead space. calibrate For example, a 24% oxygen Venturi mask has an air : oxygen entrainment ratio of 25 : 1. This means an oxygen flow of 2 L/min delivers a total flow of 50 L/min, well above the peak inspiratory flow rate. These masks are recommended when a fixed oxygen concentration is desired in patients whose ventilation is dependent on their hypoxic drive, such as those with chronic obstructive pulmonary disease. However, caution should be exercised as it has been shown that the average FiO 2 delivered in such masks is up to 5% above the expected value. 2. The Venturi mask with its Venturi device and the oxygen delivery tubing is often not well tolerated by patients because it is noisy and bulky. Anaesthetic breathing systems are other examples of the fixed performance devices. The reservoir bag acts to deliver a fresh gas flow that is greater than the patienťs peak inspiratory flow rate.
1041
HFNP | RV
"fixed performance device" PEEP of 5 " It is thought that it produces a reduction of anatomical dead space" The above can lead to reduced work of breathing, improved oxygenation and ventilatory efficiency. 4. Such systems enhance patient comfort and tolerance compared with other oxygen delivery systems Contraindicated in recent nasal surgery and severe epistaxis. 2. Base of skull fracture and/or cerebrospinal fluid (CSF) leak.
1042
HFNP | RV
"fixed performance device" PEEP of 5 " It is thought that it produces a reduction of anatomical dead space"-as nasopharynx and traceha and conducting airways-->reservoir?? The above can lead to reduced work of breathing, improved oxygenation and ventilatory efficiency. 4. Such systems enhance patient comfort and tolerance compared with other oxygen delivery systems Contraindicated in recent nasal surgery and severe epistaxis. 2. Base of skull fracture and/or cerebrospinal fluid (CSF) leak.
1043
simple FM
its tiny effective reservoir is air in front of face. expired air pushout out faster resp rate -->breathing in expired ie rebreath High FiO 2 delivered Low FiO 2 delivered Low peak inspiratory flow rate High peak inspiratory flow rate Slow respiratory rate Fast respiratory rate High fresh oxygen flow rate Low fresh oxygen flow rate Tightly fitting face mask Less tightly fitting face mask
1044
NP
The nasopharynx acts as a reservoir!! Mouth breathing causes inspiratory air flow. This produces a Venturi effect in the posterior pharynx entraining oxygen from the nose.
1045
Benzo PrB
95%
1046
benz class
short int long | <12 <24 >24 half life
1047
gastric motility
evernote
1048
gastric motility
evernote
1049
fasting
 Reflux & Regurgitation:passive processes  Reflux:relaxation of lower oesophageal sphincter and passage of gastric contents into oesophagus  Regurgitation: relaxation of upper oesophageal sphincter and passage of gastric contents into pharynx  Aspiration:gastric contents reach tracheobronchialtree when airway reflexes are obtunded and protective gag and cough reflexes don’t occur
1050
PPi
irreversible covalent bond most potent CYP450 inhibitors some benzimidazole derivative
1051
barrier for GI med
Sucralfate
1052
H pylori Rx
ACE amox clarythm esomeprazole
1053
Prostaglandin rec in stomach
GiPCR-->decrease camp-->decreased H secretion parietal at mucosal cell-->HCO3 and mucous
1054
metoclop as prokinetic CORE
DA antag in GI stim Ach rec ``` SE extrapyramid Prolactin porphyria inhibit bytylcholinesterae NEUROLEPTIC MALIGNANT SYNDROME ``` Met conj and excretion with sig amount unchanged
1055
SUCRALFATE
gut coating | decreased ab of some drugs warf and phenytoin etc
1056
flecainide
1c amide LA slows Na rise, increase pacing threshold, slow AV conduction good for AF, VF, WPW neg ino junctional arrhytmia dizzy headache active met renal excretion of unchanged
1057
Sotalol
1,2,3 nil Ca so SVT AF and VT -->prolong Qt-->torsades low lipid sol (so nil met but defies rule and good absorption) nonselective
1058
phenytoin
``` class I antiarrhytmic depresses pacemaker activity but allow good conduction so Rx digoxin toxicity (slowed conduction) ```
1059
lignocaine
1b slow rate of rise raise pacing threshold REDUCE AP and ARP SE AV block neg ino met amidase
1060
Digoxin
evernote
1061
Verapamil
nondihydro CCB slow AP and conduction neg ino cor VD Rx SVT precip by WPW risk of VT due to accessory pathway instead risk brady in other AV blockers in CCF will cause decreased CO
1062
amiodarone
active met
1063
MoA of triple whammy
evernote
1064
ephedrine
evernote
1065
anaesthetic machine
If the anaesthetic machine incorporates a gas flowmeter bank, oxygen must be the last gas to enter the common gas manifold at the top of the flowmeter tubes. The oxygen flow knob must be the first from the left on the rotameter, relative to other flow knobs. Vaporisers with mechanical adjustment dials, when used in high pressure circuits, must increase the delivered anaesthetic vapour concentration when the dial is rotated in an anti-clockwise direction.
1066
scavenger
active and passive positive and negative relief valves on either side of a reservoir bag-->protect if it collapses with neg pressure risk of rebreath A receiving system (reservoir bag) can be used. Two spring-loaded valves guard against excessive positive (1000 Pa) in case of a distal obstruction or negative (–50 Pa) pressures in case of increased demand in the scavenging system. 1. passive model - when pressure exceeds APL-->out and driven by patietn expiration of PPV - ->out to atmosphere (not recylced) problems Connecting the scavenging system to the exit grille of the theatre ventilation is possible. Recirculation or reversing of the flow is a problem in this situation. 2. Excess positive or negative pressures caused by the wind at the outlet might affect the performance and even reverse the flow. 3. The outlet should be fitted with a wire mesh to protect against insects. 4. Compressing or occluding the passive hose may lead to the escape of gases/vapours into the operating theatre and thereby polluting it. The disposal hose should be made of non-compressible materials and not placed on the floor. Active A bacterial filter situated downstream and a visual flow indicator positioned between the receiving and disposal systems can be used. A reservoir bag with two spring-loaded safety valves can also be used as a receiving system The active disposal system consists of a fan or a pump used to generate a vacuum The reservoir is designed to prevent excessive negative or positive pressures being applied to the patient. Excessive negative pressure leads to the collapse of the reservoir bag of the breathing system and the risk of rebreathing. Excessive positive pressure increases the risk of barotrauma should an obstruction occur beyond the receiving system.
1067
CO2 Ab
Barylime, which consists of barium hydroxide (80%) and calcium hydroxide (20%), is widely used in the United States. Another absorber is Amsorb that consists of CaCl 2 and Ca(OH) 2 .
1068
sodalime CORE RV! HARRY
base neutralizing an acid!!!!! The acid is carbonic acid formed by the reaction of carbon dioxide with water. The end products are water and a carbonate. Heat is liberated in the reaction NaOH and KOH-->(if dry)-->carbon monoxide (exothermic) Absorbents no longer contain potassium hydroxide Compound A, formaldehyde, and methanol can be formed with sevoflurane Their capacity to absorb carbon dioxide is decreased by decreased moisture, and they adsorb anesthetic agents more when dry Newer types of soda lime have a low concentration of a zeolite added. This helps to maintain the pH at a high level for longer and retains moisture so improving carbon dioxide absorption and reducing the formation of carbon monoxide and compound A. Disintegrated granules increase resistance to breathing. Because of this, silica (0.2%) is added to harden the absorbents and reduce powder formation. Colour changes can be from white to violet/purple (ethyl violet dye), from pink to white (titan yellow dye) or from green to violet 7. The size of soda lime granules is 4–8 mesh. Strainers with 4–8 mesh have four and eight openings/in, respectively. Therefore, the higher the mesh number, the smaller the particles are. Recently produced soda lime made to a uniform shape of 3–4-mm spheres allows a more even flow of gases and a reduction in channelling. This results in a longer life with lower dust content and lower resistance to flow: 1 kg can absorb more than 120 L of CO 2 .
1069
amsor
CaOH!!!!!!!!!!!!! Alkali-free absorbents consist mainly of calcium hydroxide, with small amounts of other agents added to accelerate carbon dioxide absorption and bind water. With these absorbents, there is no evidence of carbon monoxide formation with any anesthetic agent, even if the absorbent becomes desiccated. There is little or no compound A or formaldehyde formation with sevoflurane even with low fresh gas flows and desiccated absorbent. The indicator in these absorbents changes color on drying. Once exhausted, these absorbents do not revert to their original color. The carbon dioxide absorption capacity of these absorbents is less than that of absorbents containing strong alkali but does not deteriorate when moisture is lost.
1070
preg analgesia
antenatal Concentrations of morphine in the colostrum of parturients receiving patient-controlled analgesia with morphine are low and it is unlikely that significant amounts of drug will be transferred to the breast-fed neonate Systemic opioids including those used in patient-controlled intravenous analgesia cross the placenta and may reduce fetal heart rate variability. However, there is no evidence that this is detrimental to the fetus.
1071
elderly opiate
Electroencephalographic studies of subjects treated with fentanyl, alfentanil, sufentanil, and remifentanil support a 50% dose reduction for elderly patients. Creatinine clearance is reduced with advancing ag
1072
fent origin
Fentanyl is a phenylpiperidine-derivative synthetic opioid agonist that is structurally related to meperidine
1073
N demethylation
phase I | eg Adr-->norad
1074
fent elim
Despite the clinical impression that fentanyl has a short duration of action, its elimination half-time is longer than that for morphine A prolonged elimination half-time for fentanyl in elderly patients is due to decreased clearance of the opioid because Vd is not changed in comparison with younger adults.[87] This change may reflect age-related decreases in hepatic blood flow, microsomal enzyme activity, or albumin production, as fentanyl is highly bound (79% to 87%) to protein. For these reasons, it is likely that a given dose of fentanyl will be effective for a longer period of time in elderly patients than in younger patients Vd not changed in elderly for fent!
1075
aging
#unpredictable theoretical Body composition Dec lean body mass and TBW, contracted blood volume Inc body fat (relative) Inc serum conc and dec Vol distribution of water soluble drugs Inc duration of action lipid soluble drugs Vd not changed in elderly for fent! (MILLER)
1076
midaz
active phase metabolite then renal excretiondecrease dose as per AMH if CrCl<10
1077
hep enceph cx
The underlying mechanism is believed to involve the buildup of ammonia i
1078
mivacurium met
butyrl cholinesterase | decreased in LF, RF, CCF, thyrothoxicosis, preg
1079
s
In general, severe liver disease predictably alters the metabolism of drugs with large extraction ratios, such as lidocaine and meperidine, in which clearance primarily depends on hepatic blood flow or portosystemic shunting. Conversely, the metabolism of low-extraction drugs, such as the benzodiazepines, is influenced mainly by protein binding, in which unbound drug is available for elimination, and by intrinsic hepatic clearance and metabolism, which are reduced in accordance with the severity of hepatocellular dysfunction.
1080
SIRS
T T T Leuk
1081
Crit pressure
pressure to liquify at exactly the critcal temp
1082
O2
black body white shoulders
1083
Entenox
blue and blue and white
1084
N20
blue and blue THE ONLY USED VAPOUR (CO2 ALSO BUT RARE)
1085
RA
black body and Back+W
1086
CO2
Grey
1087
Safety features
1) non corrosive 2) strong 3) melting valve block attachement 4) pin index (yoke vs cylinder) 5) colour coding 6) N2O Filling ration 3/4 or 2/3 (weight vs if water) - crit temp 36C - verticle 7) thermostat reg for N2O 8) washer (bodok seal) 9) 5 year check 10) entenox - ->horizontal >5C as at -6C poynting effect - ->dipper - ->multiple to share cooling of LHV
1088
PIn index
O2 RaF 2 5 N2O at TaFe 3 5 RA is SaFe 1 5 CO2 if SiC 1 6
1089
He
brown and brown
1090
N20 | CORE
vapor exerts 4.4Kpa pressure will only drop once all liquid used therefor wiegh it! s the liquid is less compressible than a gas, the cylinder should be only partially filled.
1091
entenox | CORE
poynitng-->O2 gas N2O liquid-->under dose early then hypoxic late
1092
bottle
thin-walled seamless molybdenum steel. Internally endoscopic examination is carried out to look for cracks and defects in the inner surface. Each cylinder is then subjected to high pressures, much higher than their normal working pressure, of normally approximately 22 000 kPa. This pressure is then stencilled on the valve block. One out of every 100 cylinders undergoes tensile testing, where it is cut into strips and it is stretched to assess the yield point. Bending, flattening and impact tests are also performed on 1 in every 100 cylinders
1093
pipeline safety
reg pressures The pipelines are made of special high quality alloyed carbon which prevents the break-down of the gases it carries and also has bacteriostatic properties. Outlet sockets are found throughout the hospital and the gas supplied is identified by name, shape and colour-coding. Colour-coded hoses connect the outlet socket to the anaesthetic machine; these hoses have a quick connect/release Schrader valve, with an indexing collar for each gas. A singie hose and tug test should be performed to check for misconnection or cross-connection. The hoses should be permanently attached to the anaesthetic machine with a non-interchangeable screw thread.
1094
boyles law for O2 cylinder
E cylinder is 10L 144Bar-->1440L
1095
N20 core ABSOLUTELY MUST REVIEW HARRY
EVERNOTE
1096
phenylepherine
100mcg/ml 1ml bolus (i believe)
1097
atropine DoA
30 vs 60 of glyco ish
1098
hyosisne
DOES CROSS BB SO ANTICHOLSYNDROME +++ AND CONFUSOIN AND SEDATION AND URINARY RETENTION
1099
glyco doesnt cross
quarternary not teritary
1100
CHF2
Sodalime
1101
N20 SE
methiothione
1102
sevo
DOSE NOT CAUSE CO WITH SODALIME! increase CBF>1mac
1103
HALO
INCREASED CBF DESPITE DECREASED CMRO2
1104
anaesthetic precond
sevo des and iso | K+ Ch.
1105
sevo MoA
The exact mechanism of the action of general anaesthetics has not been delineated.[7] Sevoflurane acts as a positive allosteric modulator of the GABAA receptor in electrophysiology studies of neurons and recombinant receptors.[8][9][10][11] However, it also acts as an NMDA receptor antagonist,[12] potentiates glycine receptor currents,[11] and inhibits nAChR[13] and 5-HT3 receptor currents.[14][15][16] Myer Overton Protein rec target
1106
ischaemic precond
Ischemic preconditioning occurs in two phases – the first takes place 1-2 hours after the conditioning episode, the second takes place 24-72 hours later and is dependent on ATP-sensitive mitochondrial K+ channels – this second mechanism is fundamental to anesthetic agents’ ability to enhance ischemic preconditioning and/or provide myocardial protection decreased infarct size attenuated in anyone that needs it ha (old, DM, cardiomeg, fat) improve supply (open KATPase) and decrease demand improved NO release in isolated ischaemic hearts reduce excess Ca influx on reperfusion protect against neutrophil action on ischaemic tissue bitemporal protection
1107
sevo
Sevo VD due to direct sm relax blunts barorec reflex (no change in HR), minor neg ino (changed Ca sens and decreased ICC due to L type CCh, preserves CO, cardioprotective Cor VD All inhaled anesthetics prolong the QT interval (clinical significance unclear), but sevoflurane should be avoided in patients with long QT syndrome [Miller].
1108
sevo prop | SO FUCKING CORE
Prop every mech you can think of 15% decrease CO 15% decreased SV 15% decrease SVR no reflex tachy and can reset barorec and Brady -due to reduced SNS-->decreased Ca in, increased K out, NO stim Sevo VD due to direct sm relax blunts barorec reflex (no change in HR), minor neg ino (changed Ca sens and decreased ICC due to L type CCh, preserves CO, cardioprotective Cor VD All inhaled anesthetics prolong the QT interval (clinical significance unclear), but sevoflurane should be avoided in patients with long QT syndrome [Miller].
1109
Glut rec
4 for MOOOOR-fat | 2- trigger
1110
GLUT2
glucose in. increased ATP-->close K channel-->depol-->ca
1111
Insulin
binds to insulin rec (transcellular)-->internalisation-->beta subunit activation-->TK activation-->second messenger -->GLUT4 internalisation, and gene transcriptioin and other effects complex with Zn or protamine or crystalise-->less lipid sol-->less ab-->longer
1112
liver Dx
Whereas the phase I reaction involving CYP enzymes may be impaired in liver disease, the phase II reaction (glucuronidation) seems to be affected to a lesser extent, although both phase I and phase II reactions in drug metabolism are substantially impaired in patients with advanced cirrhosis
1113
metoprol tramadol tapentadol flow meter
evernote
1114
ECG
1MV is height of QRS
1115
prolong PR
BB CC digitalis Adenosine (very transient) hypokalamia LITFL Hyperkalaemia LITFL Hypermagnesaemia essentially CCB Fibrosis, MI Vagal or acetylcholinesterase inhibitor—>increased Ach #neostigmine! Role: in my mind - max rate of ventricular contraction in AF - atria contract pause for atrial dump and only when that is complete does ventricle contract
1116
ADH source
post pit for post partum
1117
Ipratropium
instant effects