Primary 1 Flashcards
Alfent reason for speed of elimination
decreased Vd–>increased elimination
Elim=Cl/Vd
Paediatric Vd
increased BV and ECF–>increased Vd
of CO lower percentage to brain–>increased V2
sevo Resp
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
DKA
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
Fasting patient
glycolysis then GNG then KG
Immune reaction PRBC
#viralTAG
i forget TAG
A-Anaphylaxis
B-TRALI
mild reaction ABO incomp non ABO incomp immunomodulation Graft vs Host
Viral/protozoan Infection
-hep C, HIV, Malaria
Non-immune PRBC reaction
Ms VET
microaggregates
sepsis
Vol
Electrolytes- iron, hyperkalaemia, Citrate–>decreased Ca and Mg
Triad: cold, acid, coagulopathy
PRBC contains (additives)
160g/L Hb saline glucose mannitol adenosine
42 days
2 types of Dose response curves
Quantal-population binary eg MAC
Graded-individual continuous eg fentanyl
justify afterload line rationale
max wall tension for a given preload
ideally would be peak but corner easier
Pressure in RV
Systole 25 diastole 0-8
potassium channel in myocyte AP
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!
why platue
K vs Ca
- ->refractory period
- —->avoid tetany of heart
winkessel effect
elastic aorta maintain a narrowed pulse pressure
alveolar time constant
CORE RV
Comp.RESISTANCE
NOT! COMP.RADIUS
capnography-why platue gradient rises
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
Vd calc and risk
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)
N2O CBF
increases CBF and CMR and ICP
Volatile coronaries
VD due to volatile vs decreased DO2 VC
in isolated hearts, volatile increased Supply and decreases demand
(MAP decrease controlled)
Coronary steel
anaesthetic preconditioning
Mech of Vd volatile
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
coronary steal
iso (now evidence it doesn’t occur)
- CorVD–>less blood flow to subendocardium of stenosed artery–>ischaemia
- not an issue if CorPP maintained
Anaesthetic preconditioning
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
Pulm VR
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
HPVC and volatiles
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