Nicole's Study Guide Anes Pharm 2015 Flashcards
(157 cards)
1
Q
SVT management drugs of choice
A
Adenosine
verapamil
diltiazem
“in SVT give A,V,D”
A>D>V
2
Q
dose of adenosine in SVT
A
6 mg rapid IV push
12 mg rapid IV push second dose
3
Q
dose of verapamil in SVT
A
75-150 mcg/kg IV
= 2.5-10 mg IV
4
Q
dose of diltiazem in SVT
A
SVT 5-10 mg /2 min repeat after 5 min
75-150 mcg/kg bolus of 0.2 mg/kg /2 min repeat 0.35 mg/kg bolus after 15 min
infusion 5-15 mg/hr
5
Q
alternatives for SVT
A
Esmolol, metoprolol, amiodarone, digoxin
DAME- the first lines didn’t work!
6
Q
dose of esmolol with SVT
A
0.5 mg/kg over 1 minute
35 mg for 70 kg pt
7
Q
dose of metoprolol for SVT
A
1-2.5 mg
repeat 2.5 min double dose
8
Q
dose of amiodarone with SVT
A
150 mg IV slowly over 10 minutes
may repeat once
9
Q
dose of digoxin in SVT
A
0.5-1 mg IV
10
Q
Liver failure + asthma
drugs to avoid
A
Opiods- histamine release: morphine, codeine, meperidine
NDMB- atracurium and mivacurium- histamine
non-selective BB- timolol, propranolol, labetalol
esterLA’s- PABA allergic reactiosn
Succ- histamine (OK WITH RSI) give benadryl or famotidine- H1/H2 respectively
11
Q
asthma pateint questions
A
asthma severity
hospitilizations
intubations in last 6 months
12
Q
pre-treat asthmatic pt with…
A
beta-agonist (albuterol)
steriods
13
Q
drugs to use with asthma + liver failure
A
Ketamine- bronchodilator
propofol- bronchodilator
fentanyls- no histamine
NMB- pancuronium, Vec, Roc, Cisatracurium - no histamine
*if also liver NO Panc or Vec
maintenance of Cis @ 0.03 mg
14
Q
how does liver failure affect drug PD/PK
A
increases Vd decreased plasma protein binding of drugs decreased clearance BLEEDING- caution renals heptopulmonary or hepatorenal pathology encephalopathy decreased plasma pseudocholineserases
15
Q
liver failure and benzos
A
metabolism impaired
prolonged elimination
16
Q
liver failure prolongs the elimination of what drugs?
A
benzos lidocaine meperidine morphine phenobarbitol
17
Q
liver failure delays the metabolism of which induction agents
A
vecuronium (50-60%) biliary)
rocuronium (70-90% biliary)
Succ- d/t decreased psudocholinesterases
18
Q
which drugs are highly protein bound that liver failure effects
A
opiods
benzo
increased free drug with hypoalbuinemia
19
Q
drugs preferred for induction with liver failure and asthma
A
etomidate
propofol
iso
cisatracurium (metabolism independent of liver may need larger dose because Vd is increased - use PNS)
20
Q
plan for liver failure induction with asthma
A
Versed 1-2 mg lidocain 1 mg/kg fentanyl 1mcg/kg propofol 1-1.5 mg/kg succs 1-1/5 mg/kg cisatracurium for maintenance NMB 0.03mg/kg sevo 2% reverse *fentanyl * albumin
21
Q
what can cross the BBB
A
water- unpolarized CO2- small O2-small lipid-soluble free forms of steroids glucose- via GLUT1 transporters Thyroid hormones organic acids choline nucleic acid precursors neutral, basic, and acidic amino acids in BBB
22
Q
CAN NOT cross BBB
A
protiens polypeptides ionized/charged water soluble drugs- lipophilic large molecules highly protein bound
23
Q
are NMB lipophilic or hydrophilic
A
hydrophilic- degree of ionization determined by dissociation constatnt pKa of agent and its pKa gradient HIGHLY ionized
24
Q
what affects/can alter the BBB
A
being a neonate- immature uremia head trauma infections tumors strokes seizures- sustained
25
do local anesthetics pass the BBB?
they can- unbound lipophilic drugs
26
what 5 factors contribute to crossing the BBB
serum concentration (passive diffusion)
active transport ("in" or "out")
lipophilicity (predisposition to dissolve in fat vs water)
the electrical charge (polarity)
molecular size and configuration (bulk not purely molecular weight but also the way the molecule aligns)
27
which anticholinergics cross the BBB?
ONLY tertiary amines- atropine, scopolamine (have CNS effects)
glycopyrolate does NOT quaternary amine
28
which Ach-ase-Inhibitors cross the BBB?
ONLY physostigmine to reverse anticholinergic effects too
| AChase- Inhibitors: neostigmine and edrophonium have quarternary ammonium structure
29
where does parkinson's affect the CNS
dopamine containing neurons of the substantial nigra
| neurodegenerative disease`
30
EPS symptoms of Parkinson's
extrapyramidal motor dysfunction
tremor (pill rolling)
rigidity
hypokinesis
31
what is the goal of treatment with parkinson's
increase dopamine in the basal ganglia (not periphery)
| decrease s/e of Ach on neurons
32
what drugs are patients with Parkinson's likely taking?
levodopa
MAO-B Inhibitors (selegiliine, rasagiline)
SSRI- concern with 5Ht3 blockers risk seratonin syndrome
33
what medications should be avoided with a pt with parkinson's
Ephedrine b/c MAO-B -I use
antidopaminergics (butyrophenones = haloperidol and droperidol) butyrophenones, phenothiazines, phenergan metoclopramide - all reverse dopamine effects at the basal gaglia
34
Which anti-emetics can be used in Parkinsons?
5HT3 antagonists = -onsetron
i.e. ondansetron 4 mg 30 minutes before emergence
H1 antagonist diphenhydramine- (10-50 mg IV) Benadryl 25 mg
NK1 receptor blocker - 5-HT blocker of substance P- 3 hours before ages- 8-12 hours active chemo drug = Aprepitant
steriod = Dexamethasone 2.5-10 mg IV 4 mg!
35
anti emetics to AVOID with Parkinsons
Promethazine
Droperidol- no antidopaminergic drugs
Metoclopramide - Reglan- antagonizes central and peripheral dopamin receptors
36
considerations with N/V
make sure adequate volume recitation
37
What are the systemic clinical effects of repeated dosing of narcan?
```
discomfort
withdrawl
reversal of RD
catecholamine release
pulmonary edema
sudden death
```
38
What are the systemic side effects of repeated dosing of narcan?
```
HTN
CV instability
increased HR
pulmonary edema
nausea
vomiting
sweating
tachycardia
seizures
pulmonary edema
arrhythmias
```
39
how does RD compare to analgesia with opiods- how does this effects narcan dosing?
RD from opiods occurs at higher receptor occupancy rates than analgesia
Analgesia is NOT compromised with CAREFUL titration of naloxone
40
what is the opoid overdose dose of narcan/naloxone
0.4-2 mg/dose
titrate SLOWLY 0.1-0.2 mg to start
q 2-3 incremental increases * usually no more than 0.2 needed
dilute 0.4mg in 9mL NS = 0.04mg/mL and give 0.5-1mcg/kg q 3-5 min
41
what are the s/e of rapid withdrawal or unmasking of pain by narcan
```
catecholamine replease!
pain
htn
sweating
agitation
irritabilty
vomiting
```
42
MOA of naloxone
derivative of oxymorphone
small structural change converts to pure ovoid antagonist
NO agonist properties
43
onset of naloxone
1-3 minutes
44
duration of naloxone
60 minutes
CAUTION- may have to redoes d/t renarcotization
caution with liver failure
RAPIDLY metabolized by the liver
45
Demerol:morphine potency
0.1x
46
morphine:morphine potency
1x
47
hydromorphone:morphine potency
8x
48
alfentanil:morphine potency
10x
49
fentanyl:morphine potency
100x
50
remifentanil:morphine potency
100 (some sources say 200)x
51
sufentanil:morphine potency
1000x
52
where is epidural location?
Outside the dura mater
| contains blood vessels nerve roots fat connective tissue
53
where is the spinal space located
Spinal-intrathecal- subarachnoid
= between arachnid and piamater
baths the spinal cord- CSF is here
54
which opiods are hydrophilic?
Morphine
Hydromorphone
meperidine
55
which opiods are LIPOphilic
```
Fentanyls love FAT
Fentanyl
sufentanil
alfentanil
remifentanil
```
56
rank the fentanils in order of lipophiliciry
sufentenil (1600 x's MS04)
fentanyl (800x MSO4)
Alfentanil
Remifentanil least- rapidly off b/c of ester hydrolysis
57
what property of the drug does lipophilic/hydrophilic affect the most?
PEAK
58
how is the peak affected by lipophilicity?
Morphine is hydrophilic- SLOWER peak
| fentanyl is the least lipophilic of the fentanils and still peaks in only 20 minutes
59
what is the peak of sufentanil
6-8 minuts
60
what is the peak of morphine and why is it this time?
1-4 hours
| because it is hydrophilic and peaks slower- slower to cross the dura
61
what is the greatest risk of opiods intrathecally?
Respiratory depression
62
how is the RD different for the hydrophilic vs. the lipophilic drugs
Neuroaxial opioid RD occurs in 2 way
1- early phase- systemic absorption with parenteral dosing- similar with all fentanyls- lipophilic
2- insidious depressoin- 8-12 hours
rostral flow of CSF delivery of morphine to the brainstem
63
describe the properties of lipophilic opiods epidural/intrathecal doses
```
Fentanyls
rapid absorbed into the spinal tissues
FASTER onset
Smaller area of distribution
more limited area of analgesia
faster clearance of the drug out of the epidural and intrathecal space
shorter duration of action
higher blood concentrations of the opioid
GOOD for selective anesthesia
```
64
asthmatic treatment with Des v. Iso v. Halothane
Des- pungent-airway irriatant- bronchodilator
Iso- less pungent than des-
halothane-bronchodilator but hepatotoxic
65
Vapor pressure and MAC of Des, Iso, Halothane
Halothan- 243/0.75
Iso- 240/1.2
Des- 669/6
Sevo- 160/2
66
local anesthetics are weak-
bases
67
infected tissue is…
acidic
68
weak base in acid =
Ionization increases
water soluble
-locals loose their effect when they are more ionized
it is the LIPID soluble- NON-ionized portion of the local that takes effect
69
-locals loose their effect when..
they are more ionized
it is the LIPID soluble- NON-ionized portion of the local that takes effect
can not cross fatty nerve sheeth- NOT effective
70
what determines the degree of ionization for an individual drug?
pKa of the agent
AND
its pKa gradient across the membrane
71
acids are…
proton donors
72
bases are…
proton acceptors
73
where do local anesthetics act
uncharged form crosses the neuronal cell membrane
| acts on the Na channel INSIDE
74
what does the ability to counteract a non depolarizing blocking agent depend on?
the amount of spontaneous recovery before the administration of a reversal drug
75
how much time is required for several of anticholinesterse take?
15-30 minutes
76
when should you reverse with anti cholinesterase drugs?
alway
| 4 hours or less and even 4/4 twiches still may have unto 75% blocked
77
what else could be affecting prolonged blockade after NMDA
```
overdose
inadequate reversal dose
adjunctive agents contributing to the pt weakness
metabolism of relaxant decreased
excretion of the relaxant slowed
acid-base status
temp
age
drug interactions
```
78
what is the MAX DOSE of neostigmine?
0.07 mg/kg
| 5 mg total
79
what diseases affect neuromuscular blockade reversal with a ACHE-Inhibitor
Myasthenia Gravis
| over treatment with ACH can precipitate cholinergic crisis
80
when should reversal agent not be given for a NMBA
when 0-2 twitches are present
TOF stimulation 2 or less may have prolonged recovery
do not attempt until T1 > 25%
```
0 twitches- 95% ACh receptor blocked
90% = 1 twitch
80% = 2 twitch
75= 3 twitch
4 twitch STILL can have just under 75% blocked!!
```
81
when TOF > 0.9 how long is the block typically
15 minutes
82
all acetecholinesterase- Inhibitors all experience
a ceiling effect
lower doses may be just as effective
overdose in fact may lead to ACh on muscarinic and nicotinic receptors in PNS- leading to bradycardia, prolonged QT, systole
MUST maintain airway- Sp02, CV monitor, BP, CRNA to stay with pt
Reintubate if needed
83
intermediate active NMBA
vecuronium
rocuronium
cisatricurium
atracurium
84
what drug interactions prolong NMBA
halogenated agents
when continued after neostigmine administration
prolong time to full reversal
EVEN when d/c at time of reversal that is OK- b/c of wash out
aminoglycosides
Mg
85
what happens if you exceed the max dosage of reversal agent of a NMBA?
choACh accumulates in sufficient amounts at the NMJ
ACh is sustained
block develops just as it would with Sch.
86
what are the s/s of excessive Anti-cholinesterase activity?
```
cholinergic overactivity
bradcardia
increased secretions
Abdominal cramp
n/v
resp distress
miosis
skeletal muscle paralysis
weakness
```
87
what do you give to treat overdose of anti-cholinesterase drugs?
Atropine
88
electrolyte imbalance that may prolong paralysis
Hypomagnesium
hypokalsemia
hypophosphatemia
hypocalcemia
89
what electrolyte is affected by Succinylcholine?
Potassium
0.5-1 mEq/L increase
within 3 minutes
for 10-15 minutes
90
why does K increase with Succ administration?
When the muscle depolarizes-
Na influx and K efflux occurs
this efflux = potassium release during normal muscle
do influx back of K slow to enter back into cell
signaling and the response to Succ
91
What pathologic states result in an up-regulatoin (increase) of AChRs spreading throughout the muscle membrane
```
Upper or lower motor denervation
infection
direct muscle trauma
muscle tumor
muscle inflammation
burn injury
immobilization- disuse atrophy
prolonged chemical denervation by muscle relaxants, drugs or toxins (NDMR, Mg, clostridial toxin)
muscular dystrophies
```
92
where are AChR in the normally innervated mature muscle
only in the junctional area
93
what depolarizes the nicotinic actylcholine receptors in the muscle that leads to hyperkalemia?
ACh
Succ
AND choline
94
when are ACh receptors up-greulated after a burn and Succ is unsafe to give?
24-48 hours
95
when is it ok to use Succ in a post-burn victim?
NEVER
96
how do you treat hyperkalemia from Succ- emergently?
promote the cellular uptake of K
insulin with glucose
catecholamines
sodium bicarbonate
97
what are the most common causes of delayed awakening during emergence?
prolonged action of anesthetic drugs
metabolic causes
neurologic injury
98
what is the most common cause of delayed awakening?
prolonged action of anesthetic drugs
99
why does prolonged action of anesthetic drugs occur?
secondary to alterations in drug PK/PD
pt status
hypoventilation
combo anesthsia- opiods, IV anesthetics, inhalational agetns
100
PK alterations leading do delayed awakening
changes in drug distribution secondary to
mobilization of drugs from body tissue stores
redistribution
decreased protien binding
changes in metabolism
excretion secondary to renal or hepatic dysfunction
101
PD alterations leading to delayed awakening
increased pt sensitivity to drug effects b/c of extremes of age
hypothermia
concomitant alcohol or drug use
102
who is at risk for delayed awakening?
pre-existing cognitive or psych disorders
chronically take sedatives
intoxicated etoh/drugs at the time of induction
physically exhausted prior to surgery
103
how does hypoventilation affect inhalational drugs
hypoventilation limits exhalation
prolongs elimination of inhalational agents \
CO2 narcosis
104
how do benzodiazepines affects delayed awakening?
long-acting benzos (lorazepam and diazepam) may contribute to delayed awaking
esp. in elderly
105
what herbal supplements affect emergence?
delayed: kava kava, St. John's wart, valerian
106
metabolic causes of delayed awakening
Hypoglycemia *monitor diabetics peri and post ob BG!
hyperglycemia
electrolyte imbalance - Na, Ca, Mg
107
what electrolyte imbalance occurs post TURP that leads to delayed emergence?
dilutional hyponatremia
transurethral prostate resection
sedation, coma, hemiparesis
108
conditions that lead to HHNK
```
BG > 600 mg/dL
can lead to sedation post-op/delayed emergence
type 2 DM
severe dehydration (esp old)
uremia
pancreatitis
sepsis
pneumonia
CVA
large surface burns
```
109
hypocalcemia post parathyroidectomy can lead to
delayed awakening
110
hyperMg from prolonged MgSO4 during labor with pre-eclamptic pt may result in
sedation, muscle weakness after general/regional
111
what are potential causes of neurologic injury responsible for delayed awakening?
```
RARE
CVA
Intracranial hemorrhage
IICP
HTN uncontrolled
air/fat emboli
HypoTN uncontrolled esp if previously a HTN pt with carotid disease
```
112
how to manage a pt on a BB post op bradycardia
| given succs, propofol, and vec
1) perfusion, pulses, blood pressure, O2
2) baseline HR- consider 12 lead EKG for underlying rhythm/electrolyte disturbances
3) hold next dose of atenolol
4) if stable monitor, cardiology, fluids
5) if hypotensive, SOB, CP, diaphoresis, decreased pulses
- O2/ventilate if needed, - glyco 0.2 mg or atropine 0.5 mg if severe, Ephedrine 5-10 mg, Epi 10-20 mcg's or infusion of epi 2-10 mcg/min or transcutaneous pace until cards can place temporary pacing wires
113
during a lap chili- pneumoperitoneum is created- bradycardia and dropping actions include:
```
Ask surgeon to release pressure
admin 100% O2
increase IV fluids to increase preload
assess for 4 possible complications
consider medications
transcutaneous pacing? @ 80 bpm
ABG, hemoglobin, lytes
EKG troponins
```
114
Intra-abdominal pressure
increased venous return
increased CO
hypertension
115
Intra-abdominal pressure > 15 s/e
decreased venous return
decreased CO
hypotension
116
bradycardia during intrabdominal surrey causes:
IIAP
vagal stimulation- trochar CO2 emboli, mesentary stretch
reduced lung volumes, PAP increased, V/Q mismatch, pneumothorax
IICP
decreased blood flow
117
4 possible complications of pneumoperitoneum
pneumomediastinum
pneumopericardium
pneumothorax
CO2 gas embolism
118
what medications to give in bradycardia post pneumomediastinum lap chile?
BP and pulse check
Ephedrine 5-10 mg
glycopyrolate 0.2 mg or atropine 0.5 mg
ACLS doses if PEA/Asystole
119
max dose of atropine
3 mg
120
infusions to consider during unstable bradycardia
dopamine 2-20 mcg/kg/min
| epinephrine 2-10mcg/min
121
PEA arrest steps
1) call for help
2) CPR 100/min >2 in deep ETCO2 >10
3) turn off agent 100% FiO2
4) 10 breaths/min NO over vent
5) IV good, IO?, Art?
6) Epinephrine 1 mg 3-5 min
7) vasopressin 40 units x1
8) rhythm check Vt/Vf shockable
9) causes- Hemorrhage, anesthetic overdose, septic shock, shock, auto PEEP, anaphylaxis, med error, high spinal, pneumo, local anes tox, vagal stimulation, PE
H &T
122
causes of PEA arrest
```
Hemorrhage
anesthetic overdose
septic shock, shock
auto PEEP
anaphylaxis
med error
high spinal
pneumo
local anes tox
vagal stimulation
PE
```
123
Pt has a spinal and now BP is 80/40 hypotensive- how would you treat this?
sympathetic blockade in1) Fluids
2) Ephedrine is bradycardia 5-10 mg
3) Phenylephrine is normal/tachy - 10-20 mcg (may decrease CO because increased SVR)
4) dopamine? low dose consider
5) vassopression 2-4 units consider if RAAS depressed
124
why does hypotension occur with neuroaxial blockade?
sympathetic blockade -> arterial vasodilation
decreased SVR
venous pooling
reduction in venous return
125
a high block can cause what CV complication?
T1-T4 blockade = sympathetic innervation of the heart is blocked
cardiac accelerators anesthetized
vagal fibers and heart rate slows leading to HYPOTENSION
126
what factors are involved in the cardiovascular response to neuroaxial anesthesia?
baroreceptor reflex
volume receptor reflexes
decreased central sympathetic outflow
-loss of ability to handle normal CV stresses and normal CV homeostatic reflexes
127
what is allowable decrease in BP?
20%
| *previously HTN or elderly with CA disease
128
pre-treating with fluids for hypotension induced by spinal
15mL/kg of glucose free crystalloid or colloid solutions
15 minutes pre-op
including post-op deficits by NPO status
129
which vasoactives are more effective for spinal induced bradycardia?
alpha and beta adrenergic active- IE ephedrine
phenylephrine is only an alpha agonist- will not increase HR
130
```
lap chole
DM
hx- PONV
hx- spontaneous pneumothorax
what gas would you not give and why not?
```
Nitrous:
PONV - activation of chemoreceptor trigger zone and the vomiting center in the medulla
potential for pneumo
N2O can expand a pneumothorax to double or triple its site in 10 to 30 minutes respectively
expansion of air filled structures/bubbles
131
what is the property of N2O that allows it to worsen pneumothorax?
greater solubility in blood compared to nitrogen
diffuses into air-containing cavities more rapidly than nitrogen is absorbed by the blood spream
N20 delivered to a patient diffuses from the blood into these closed gas spaces easily- until the partial pressure equals that of the blood and alveoli
complaint spaces will expand until sufficient pressure is generated to oppose N20
132
how much more soluble is N20 than nitrogen in the blood?
35 X
*N20 is insoluble compared to other inhalation agents
133
how would you induce a pt with open globe emergently- intoxicated, smokes, MJ
succ- rapid sequence full stomach is more of the concern!
IOP will increase, but aspiration is more likely
-research does not support extrusion of ocular contents
-coughing must be avoided also
*modified RSI with >1 mg/kg (0.6-1.2)of Roc approaches the onset of Succ
K replacement
decrease mac d/t etoh decrase opioids and benzos
134
how much dose such increase IOP and for how long
5-10 mmHg
| for 5-10 minutes
135
what induction/anesthetic agents increase IOP or should be avoided?
Succ
and ketamine- unclear by how much
etomidate- risk of myoclonus
136
what drugs and dose for induction with open globe?
lidocaine 1.5 mg/kg to blunt the response to laryngoscopy
opioid other option-
remifentanil 0.5-1 mcg/kg
alfentanil 20 mcg/kg
propofol- rapid onset but does not blunt sympathetic response to DL
fentanyl 1-3 mcg/kg
esmolol 0.5-1 mg/kg
137
how should you manage open globe with full stomach
```
NO NG- may make them cough/gag IIOP
metoclopramide 10mg
Ranitidine 50 mg
cimetidine 300 mg
famotidine 20 mg
all options
must give anti-emetic before extubation need to avoid vomiting IIOP
```
138
If you give Succ what should you give also with an open globe injury on induction
defaciculating dose of Rocuronium
| atropine or glyco- decrease oculocardiac reflex
139
How to treat a bronchospasm
1) 100% 02
2) I:E to allow for adequate exhalation 1:3
3) deepen agent- use sego
4) rule out maintop, kink, secretions
5) Beta 2 agonist- albuterol, ipratropium
6) Consider epinephrine @ 10 mcg IV increase PRN
7) Ketamine 0.2-1 mg/kg IV
8) hydrocortisone 100 mg IV
9) nebulized racemid epinephrine
10) R/u anaphylaxis
11) ABGs
140
s/sx of bronchospasm
1) increased peak airway pressure
2) wheezing on lung exam
3) increased expiratory time
4) increased ETCO2- UPSLOPING
5) decreased tidal volumes if pressure control
141
How do you sedate a pt with multiple allergies
1) ASK QUESTIONS- egg allergy- do you eat them, do you eat products with eggs cooked in it- what happens- do you get a flu shot- if YES then proposal OK
2) pre-med for allergic rxn.
142
how do you treat a beta blocker overdose?
```
ABC #1 stabilize airway breathing circulation
bolus of IV fluids
atropine 1 mg IV unto 3 doses #1 for brady/hypotension
IV glucagon-
IV calcium slats
vasopressor
IV high dose insulin (with glucose)
IV lipid
```
143
s/sx of BB overdose?
hypotension and bradycardia
Electrocardiogram - show PR prolongation or any bradydysrhythmia
hyperkalemia
hypoglycemia
144
IV glucacon dose in BB overdose
5 mg IV bolus
145
dose of calcium chloride in BB overdose
10-20 mL of 10% solution or
146
calcium gluconate IV dose in BB overdose
30-60 mL of 10% solution
147
high-dose insulin and glucose dose in BB overdose
1 unit/kg bolus IV regular insulin short acting THEN
continuous infusion 0.5 units/kg per hour
titrate until hypotension is corrected
MAX 2 units/ kg
148
which vasopressor to use for BB overdose
ephedrine 5-10 mg
149
lipid emulsion dose in BB overdose
1. 5 mg/kg over 2 minutes
| 1. 5 mL/kg infusion over 60 minutes
150
Carotid endarterectomy hypotension and bradycardia considerations:
```
Carotid sinus baroreceptors
cerebral perfusion
no less than 20% change
Ephedrine with brady
phenylephine with tacky
Fluids- crystalloi/colloid depending on comorbidities
```
151
AA male HTN peri-op how to treat this
no > 20% increase
ok to start case if chronic
```
Increase sedation- gas
give proposal
pain medication
give esmolol 10-20 mg or gtts
nipride gtts
```
152
Characteristics of depolarizing NMB
ACh agonist
binds to nicotinic ACh receptors
generate AP
Phase 1 block : depolarize NMB NOT degraded by Achase
NO FADE- Na inactivated- confirmational change- BOTH subunits bound
Phase 2 block: resembles NDNMB - FADES
153
characteristics of Non-depolarizing block
ACh antagonists binds to nicotinic ACh receptors
no conformational change- JUST block
only 1 alpha subunit bound for blockade
FADE in PNS
prejunctionally also block ACh receptors
decreasing mobilization of ACh and this is seen with contraction fade
154
which induction drugs should you avoid with renal failure?
pancuronium
| vecuronium
155
B1 selective Beta blockers
Atenolol
Metoprolol
Esmolol
156
Asthma avoid…. MAST drugs
Mivacurium
Atricurium
Succs
Temolol (B non selective drugs)
157
contraindications with Succ
persons with personal or familial history of malignant hyperthermia
skeletal muscle myopathies
known hypersensitivity to the drug.
patients after the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury,
because succinylcholine administered to such individuals may result in severe hyperkalemia which may result in cardiac arrest
