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Pharm Flashcards

1
Q

Halothane:

  • B:g
  • MAC
  • MAC-awake
  • SVP
A
  • b:g - 2.4
  • MAC - 0.76%
  • MACawake - 55% of MAC
  • SVP - 244
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2
Q

Isoflurane:

  • B:g
  • MAC
  • MAC-awake
  • SVP
A
  • B:g - 1.4
  • MAC - 1.17%
  • MAC-awake - 38% of MAC
  • SVP - 240
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3
Q

Desflurane

  • B:g
  • MAC
  • MAC-awake
  • SVP
A
  • B:g - 0.42
  • MAC - 6.6%
  • MAC-awake - 34% of MAC
  • SVP - 669
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4
Q

boiling point of des

A

22.8 degrees C

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5
Q

Sevoflurane:

  • B:g
  • MAC
  • MAC-awake
  • SVP
A
  • B:g - 0.69
  • MAC - 1.8%
  • MAC-awake - 34% of MAC
  • SVP - 170
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6
Q

Nitrous Oxide:

  • B:g
  • MAC
  • MAC-awake
  • SVP
  • critical temperature
A
  • B:g - 0.46
  • MAC - 104%
  • MAC-awake - 64% of MAC
  • SVP - 44,000
  • critical temp - 35.5 degrees C
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7
Q

halothane’s chemical name

A

2-bromo-2-chloro-1,1,1-trifluoroethane

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8
Q

isoflurane chemical name

A

1-chloro-2,2,2-trifluoroethyl-difluoromethyl ethyl ether

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9
Q

desflurane chemical name

A

1-fluoro-2,2,2-trifluoroethyl difluoromethyl ether

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10
Q

sevoflurane chemical name

A

2,2,2-trifluoro-1-trifluoromethyl ethyl ether

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11
Q

which volatile is not stable in moist soda lime

A

sevo

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12
Q

main advantage of increased fluorination

A

decreased solubility

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13
Q

factors that decrease MAC

A
  • Age (decreases 6% per decade)
  • decreased body temp
  • pregnancy
  • decreased CNS sodium
  • depressant drugs (opioids, benzos, barbiturates, propofol, acute ETOH)
  • IV lidocaine
  • N2O
  • clonidine & precedex
  • some beta blockers & CCBs
  • PaO2 < 38 mmHg
  • BP < 40 mmHg
  • bypass
  • adenosine
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14
Q

Decreased MAC:

infants > children > neonates > adults

A

:)

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15
Q

for every 10 degree C decrease in temp, MAC of des decreases by:

A

almost ½

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16
Q

why does pregnancy decrease MAC

when does it normalize?

A

increased progesterone

normalizes 12-72 hrs postpartum

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17
Q

how do clonidine and precedex affect MAC?

A

decrease by decreasing CNS catecholamines & hyperpolarizing cell membranes in CNS

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18
Q

factors that increase MAC

A
  • red hair (excess pheomelanin)
  • increased CNS catecholamines (cocaine, ketamine, amphetamine)
  • hyperthermia
  • hypernatremia
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18
Q

factors that increase MAC

A
  • red hair (excess pheomelanin)
  • increased CNS catecholamines (cocaine, ketamine, amphetamine)
  • hyperthermia
  • hypernatremia
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19
Q

things that do not alter MAC

A
  • gender
  • duration of anesthesia
  • PaO2 > 50
  • PaCO2 < 80
  • Hct > 10%
  • BP > 40 mmHg
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20
Q

how is MAC-awake affected by age?

how is the ratio of MAC:MAC-awake affected?

A

MAC-awake decreases with age

ratio of MAC/MAC-awake is not affected by age as both decrease

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21
Q

what does a high MAC-awake:MAC ratio indicate?

A

poor amnestic and fast recovery

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22
Q

how do low-dose opioids affect MAC-awake and ratio of MAC-awake:MAC?

A

minimally affect MAC-awake

decreases MAC - increases MAC-awake: MAC and awakening should happen quicker

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23
Q

what is MAC-TE?

A

MAC at which there’s no coughing/bucking during suctioning, no movement or coughing within 1 min of extubation, and no breath-holding or laryngospasm after extubation

“MAC-intubation”

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24
Q

what is MAC-bar?

A

MAC that blocks autonomic responses to surgical stimulation

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25
Q

Meyer-Overton Hypothesis

A
  • direct correlation between anesthetic potency and lipophilicity
  • suggests inhaled agents site of action is lipid portion of membrane
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26
Q

according to the Meyer-Overton hypothesis, what’s the relationship between MAC and oil:gas partition coefficient

A

indirect relationship

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27
Q

possible site of action for amnestic effect of inhaled agents

A

RAS

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28
Q

MAC assoc. with hyperalgesia

A

0.1

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29
Q

respirations in Guedel’s Stage 2

A

irregular breathing, breath-holding

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30
Q

respirations in Guedel’s stage 3 planes I-III

A

I: shallow

II: deep

III: shallow

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31
Q

signs of light anesthesia

what signs are the best indicators?

A
  • lacrimation
  • tachycardia, HTN
  • sweating
  • reactive, dilated pupils
  • movement*
  • laryngospasm*

*best indicators

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32
Q

how do volatiles affect CMRO2/CBF coupling

A
  • no uncoupling < 1 MAC
  • uncoupling > 1 MAC = decreased CMRO2 at the same time CBF is increased
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33
Q

how do volatiles affect CBF

A

dose-dependent increase

iso = des > sevo

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34
Q

how does MAP affect increase in CBF seen with volatiles?

A

doesn’t - CBF increases within minutes independent of MAP

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35
Q

neuro effects of N2O

A
  • significantly decreased cerebral vascular resistance
  • increased CBF
  • increased CMRO2
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36
Q

how do volatiles affect CMRO2

A

dose-dependent decrease

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37
Q

how do volatiles affect cerebral vascular reactivity to CO2

A

des, sevo, and iso maintain at < 1 MAC

halothane eliminates autoregulation

at 1.5 MAC, sevo preserves autoregulation better than iso

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38
Q

intervention to counter increased ICP caused by volatiles

A

hyperventilation to decrease PaCO2 to 30 mmHg

  • halothane: hyperventilate before agent
  • others: hyperventilate with start of agent
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39
Q

iso, des, sevo, and N2O effects on CSF

A
  • iso: increased reabsorption
  • des: may increase or not change
  • sevo: decreases production
  • N2O: no change
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40
Q

how do volatiles affect EEG

A
  • ~1 MAC = increased voltage, decreased frequency
  • 1.5 MAC = burst suppression
  • 2 MAC = isoelectric
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41
Q

volatile that has been associated with sz activity

what things might increase this risk?

A

sevoflurane

increased with sustained > 2 MAC, hypocarbia (doubles), repeated auditory stimulation, preexisting sz disorder

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42
Q

how does MAC affect temperature regulation

A

dose-dependent impairment

threshold between shivering and vasoconstriction decreases as MAC increases

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43
Q

dose-dependent ventilatory effects of volatiles

A
  • breathing pattern
  • response to CO2
  • airway resistance
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44
Q

alveolar ventilation and minute ventilation with volatiles

A

minute ventilation may not change

alveolar ventilation decreases with deadspace ventilation

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45
Q

how does substituting a portion of MAC with N2O affect PaCO2

A

substitution attenuates increase in PaCO2

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46
Q

how do volatiles affect PaCO2

A

increases proportionately with concentration of volatile

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47
Q

how do inhaled anesthetics affect response to hypoxemia

A

depressed response when PaO2 < 55mmHg

not dose-dependent

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48
Q

what factors increase likelihood of airway irritability with des

A

> 6% concentration

smoker

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49
Q

how to blunt airway irritability of des

A
  • premed with 1.5 mcg/kg fentanyl or 0.1 mg/kg morphine
  • increase slowly
  • avoid inhalation induction
  • humidify inspired gases
  • add N2O
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50
Q

how do volatiles affect HPV?

A

concentrations used clinically do not prevent

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51
Q

how do volatiles affect MAP

A

all have dose-dependent decrease

halothane d/t decreased contractility

others d/t decreased SVR

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52
Q

how do volatiles affect CO, contractility, and O2 demand?

A

all cause dose-dependent myocardial depression

increased HR may offset decreased CO

decreased contractility = dose-dependent decrease in O2 demand

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53
Q

how does N2O affect CO

A

increased (mild sympathomimetic effects)

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54
Q

how do inhaled agents affect RAP

A

all increase except sevo (d/t decreased SV)

N2O increases d/t increased PVR

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55
Q

which volatile decreases SVR the most?

A

iso

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56
Q

how does N2O affect pulmonary vasculature

A

increases PVR - exaggerated in pts with preexising pHTN

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57
Q

how do volatiles affect HR

A
  • sevo: increases only > 1.5 MAC
  • iso & des: increase at lower concentrations
  • halothane: bradycardia
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58
Q

how do volatiles affect the baroreceptor reflex

A

dose-dependent depression (no reflex increased HR when BP decreases)

  • des: attenuates response, doesn’t abolish
  • iso: maintained at 1 MAC, depressed at 2 MAC
  • sevo: increasing to 4% (~2 MAC) decreases response
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59
Q

MAP that prevents coronary steal from happening

A

> 60

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60
Q

risk factors for halothane hepatitis

A
  • female
  • middle age
  • obese
  • multiple halothane exposures
  • potential genetic factor
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61
Q

metabolism of N2O

A

0.004% metabolized by normal flora in the gut (none by liver)

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62
Q

renal effects of volatiles & how to attenuate

A
  • all cause dose-related decreased RBF
  • decreased GFR & UOP
  • attenuated by preop hydration
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63
Q

adverse effects of compound A

A
  • high output renal failure
  • inability to concentrate urine
  • decreased response to vasopressin
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64
Q

how to decrease risk associated with compound A formation

A
  • min. flows 2 L/min if case > 2 hours, 1 L if < 2 hours
  • lower concentrations of sevo
  • avoid KOH and NaOH in absorbent
  • avoid increased temp in absorbent
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65
Q

how do volatiles affect skeletal muscles?

TOF?

A

dose-dependent skeletal muscle relaxation

the higher the MAC multiple, the greater the fade on tetanus

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66
Q

how do volatiles affect nondepolarizing NMBs

which has the biggest effect

A

enhanced neuromuscular blockade

des (specific study - effect on Roc)

des > sevo > iso > TIVA

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67
Q

how do volatiles affect uterine smooth muscle & effects at different MACs

A

dose-dependent relaxation

0.5 MAC = modest relaxation

> 1 MAC = significant

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68
Q

how does N2O affect uterine contractility

A

no effect

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69
Q

max. MAC to use in a pregnant mom having a non-labor procedure

why?

A

1.5

volatiles decrease uterine blood flow

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70
Q

what might trigger the antibody response that leads to halothane hepatitis?

A

TFA produced by degradation of halothane, iso, and des

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71
Q

immune effects of halothane

A

depresses defense against infection

oxidative burst response of neutrophils

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72
Q

how does iso affect CO?

A

preserved by increased HR (baroreceptor reflexes partially preserved)

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73
Q

which volatiles has mild beta adrenergic properties?

A

isoflurane

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74
Q

how does iso affect conduction?

A

slows rate of SA node discharge

increases refractoriness of accessory pathways & AV conduction system

prolongs QT in healthy pts

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75
Q

why is iso used for deliberate hypotension?

A

decreased O2 demand when used for deliberate hypotension

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76
Q

which volatile requires a preservative

A

halothane (thymol)

*sevo has water added

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77
Q

adverse effect of rapidly increasing des concentration to > 6%

A

SNS stimulation - increased BP/HR

can double HR and BP with change from 4 to 8% in < 1 minute

(returns to normal within 5 minutes)

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78
Q

does N2O attenuate SNS stimulation that occurs with rapidly increasing des?

A

nope

but apparently does help blunt airway irritability

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79
Q

is coronary steal seen with CAD pts when des is used

A

nope

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80
Q

which volatile has less of an effect on hypoxic drive

A

desflurane

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81
Q

why is des used for deliberate hypotension

A

rapid titratability

reduced CMRO2 and CPP

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82
Q

at what MAC is autoregulation maintained with des

A

1

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83
Q

which volatile is the least metabolized

A

des (0.02%)

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84
Q

which volatile is assoc. with the greenhouse effect

A

des

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85
Q

how does sevo affect CO

A

decreased at 1-1.5 MAC, recovered at 2 MAC

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86
Q

how to treat bradycardia that occurs with sevo

A

decrease concentration

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87
Q

how does sevo affect conduction

A

may prolong QTc in pts with preexisting long QTc syndrome

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88
Q

change in SVR with iso vs. sevo

A

iso: dose-dependent, gradual reduction in arteriolar resistance
sevo: abruptly decreases resistance via aortic arch (at higher concentrations)

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89
Q

which volatile preserves the baroreceptor reflex to a greater extent than with other agents

A

sevo

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90
Q

which volatile has the least degree of airway irritation among available agents

A

sevo

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91
Q

volatiles assoc. with platelet aggregation

A

sevo, halothane

(sevo more)

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92
Q

which volatile suppresses arachidonic acid

A

sevo

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93
Q

how much sevo is metabolized

what is the metabolite and is it significant

A

5-8% metabolized to inorganic fluorides

no evidence of clinically significant renal failure

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94
Q

is N2O organic or inorganic

A

inorganic

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95
Q

which inhalation agent supports combustion

A

N2O

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96
Q

CV effects of N2O & pts more prone to these changes

A
  • direct myocardial depression
  • SNS stimulation, increased SVR - more in young/healthy pts
  • increased PVR - more in preexisting elevation
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97
Q

how does N2O affect NMBs

A

no effect on non-depolarizing

potentiates succs

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98
Q

which inhaled agent is assoc. with rigidity with opioids

A

N2O

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99
Q

why is N2O assoc. with analgesia

A

increased enkephalins

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100
Q

why does N2O cause polyneuropathy

A

oxidizing effect on cobalt atom of vitamin B12

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101
Q

which inhaled agent inhibits methionine synthetase & thymidylate synthetase?

what is the significance?

A

N2O

necessary for myelin and DNA - prolonged exposure can result in bone marrow suppression, pernicious anemia, and peripheral neuropathies

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102
Q

pts at increased risk for cobalamin deficiency with N2O

A

nutritional disorders: elderly, vegans, alcoholics

malabsorption: prolonged PPIs/H2 antagonists, pernicious anemia, atrophic gastritis, postgastrectomy, Whipple, ileal resection, Crohn’s

infection, tapeworm

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103
Q

absolute contraindications to N2O

A

known deficiency of enzyme or substrate in methionine synthetase pathway

emphysema, PTX, middle ear surgery, pneumocephalus, air embolus, bowel obstruction

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104
Q

relative N2O contraindications

A
  • increased ICP
  • pHTN
  • prolonged anesthesia (>6 hrs)
  • 1st trimester (teratogenic?)
  • high risk PONV
105
Q

how to avoid diffusion hypoxia assoc. with N2O

A

supplemental O2 for first 5-10 min after N2O discontinued

106
Q

what is the second gas effect

A

theoretical - admin of high concentrations of N2O will cause increase in alveolar concentration of 2nd gas

107
Q

where do SNS nerves arise

A

T1-L2

108
Q

preganglionic vs. postganglionic fiber lengths

A

SNS: short preganglionic, long postganglionic

PNS: long preganglionic, short postganglionic

109
Q

where do PNS nerves arise

A

CN III, Vi VII, IX, X from sacral spinal cord

110
Q

neurotransmitter secreted by all preganglionic fibers

A

ACh

111
Q

when do postganglionic fibers release ACh

A

all PNS postganglionic

some SNS (Sweat glands, some blood vessels)

112
Q

what do most SNS postganglionic fibers release?

A

norepi

113
Q

ANS fibers that go to adrenal medulla

A

only preganglionic

114
Q

what is responsible for termination of action of norepi

A

reuptake

115
Q

what metabolizes ACh

A

acetylcholinesterase (not pseudocholinesterase)

116
Q

how does alpha 1 stimulation affect smooth muscles

A

vasoconstriction r/t increased intracellular calcium

117
Q

how does alpha 1 stimulation affect insulin

A

inhibits secretion and lipolysis

118
Q

how does alpha 2 stimulation affect norepi

A

inhibits release (negative feedback loop)

119
Q

effects of postsynaptic alpha 2 receptors in CNS

A

hyperpolarization = sedation, decreased MAC, decreased SNS outflow

120
Q

CV effects of beta 1 stimulation

A

inotropy, chronotropy, dromotropy

121
Q

how does beta 2 stimulation affect muscle and vasculature

A

relaxation of respiratory, uterine, and vascular smooth muscles

vasodilation of skeletal muscle vasculature

122
Q

effects of D1 receptor agonism

A

vasodilation of renal, mesenteric, coronary, and cerebral blood vessels

123
Q

effects of D2 receptor agonism

A

presynaptic inhibition of NE release

N/V

124
Q

where are nicotinic cholinergic receptors located

A

within ANS ganglion and at NMJ

125
Q

how is the adrenal medulla mediated by the ANS?

A

innervated by preganglionic fibers directly from spinal cord

126
Q

function of NE and epi once secreted from adrenal medulla

A

hormones, not neurotransmitters

127
Q

does chronic treatment with albuterol cause upregulation or downregulation

A

downregulation

128
Q

patients who may not have desired response with indirect acting sympathomimetics

A

denervation (heart transplant)

neurotransmitter depletion (sepsis)

129
Q

receptors activated at > 0.15 mcg/kg/min of epi

A

alpha1, beta1, beta2

130
Q

effect of a beta blocker + epi

A

bronchoconstriction (especially with non-selective)

131
Q

which catecholamine has the most significant metabolic effects

A

epi (increased blood sugar)

increased glycogenolysis and lipolysis

alpha 2 inhibits insulin release

131
Q

receptors agonized by norepi

A

alpha1 = alpha2

beta1 >>>> beta2

132
Q

how does high-dose norepi gtt affect HR

A

decreased d/t baroreceptor reflex (may be offset by beta1-mediated increased HR)

133
Q

when should norepi gtt be avoided

A

cardiogenic shock/failing LV

134
Q

how does dopamine have indirect sympathomimetic effects

A

increased NE release via beta 1 stimulation (but the ANS ppt says D2 inhibits NE release so idk)

135
Q

how do dopamine vs dobutamine affect myocardial O2 supply and demand

A

dopamine: can make demand > supply
dobutamine: less imbalance (coronary vasodilation increases supply & balances increased demand)

136
Q

respiratory effects of dopamine

A

inhibits ventilatory response to arterial hypoxemia and hypercarbia

137
Q

which catecholamine inhibits HPV

A

dobutamine

138
Q

use of dobutamine

A

increase CO In CHF pts

139
Q

most potent beta agonist

A

isoproterenol

140
Q

good and bad uses of isoproterenol

A

good: increase HR in heart block or denervated heart, induce arrhythmias in cath lab, chemical pacemaker

bad: CAD

141
Q

direct & indirect actions of ephedrine

A

direct: stimulates alpha and beta
indirect: stimulates NE release or prevents is reuptake

142
Q

main effect of ephedrine

A

increased contractility (beta 1)

143
Q

effect of ephedrine + beta blocker

A

resembles alpha agonist

144
Q

how does ephedrine affect SVR

A

might not change d/t vasoconstriction (alpha1) and vasodilation (beta2)

144
Q

how does ephedrine affect SVR

A

might not change d/t vasoconstriction (alpha1) and vasodilation (beta2)

145
Q

DBP in epi vs. ephedrine

A

epi may decrease

ephedrine increases

146
Q

how does ephedrine affect MAC

A

increases (CNS stimulation)

147
Q

how does phenylephrine affect CO

A

decreased d/t decreased afterload or reflex bradycardia

148
Q

drug of choice for treatment of hypotension in CAD

A

phenylephrine

149
Q

phenylephrine preserves uterine blood flow

A

cool

150
Q

MOA of clonidine & precedex

A

centrally acting alpha agonist (Alpha2 > alpha 1 >>>> beta)

decreased SNS outflow from CNS

precedex is 7x more selective for alpha2

151
Q

how does clonidine affect MAC

A

can decrease 50% d/t hyperpolarization of CNS cell membranes

152
Q

CV effects of clonidine

A

dose-dependent decreased BP, HR, CO

rebound HTN if abruptly stopped

153
Q

how to treat bradycardia with clonidine

A

decreased NE release (alpha 2) = decreased catecholamine levels = may require anticholinergic for decreased HR

154
Q

use of clonidine in neuraxial techniques

A

inhibits spinal substance P release, blunts perception of noxious stimuli

prolongs effects

155
Q

adverse effect of rapid precedex injection

A

HTN

156
Q

how does precedex affect MAC

A

decreases > 90%

157
Q

conditions that are contraindications to digoxin

A
  • WPW (30% develop Vfib)
  • hypertrophic CM: increased contractility = increased obstruction
  • acute MI: increased O2 demand
158
Q

conditions that are contraindications to digoxin

A
  • WPW (30% develop Vfib)
  • hypertrophic CM: increased contractility = increased obstruction
  • acute MI: increased O2 demand
159
Q

MOA of digoxin

A

inhibits Na-K-ATPase which increases Na, affects Na-Ca exchange, and increases Ca inside the cell

= increased contractility

160
Q

CV effects of digoxin

A

increased contractility

increased CO

161
Q

EKG changes seen with digoxin

A
  • prolonged PR
  • short QTc
  • ST depression
  • small/inverted T wave
162
Q

most common cause of digoxin toxicity

A

renal dysfunction

163
Q

every 10 mmHg decrease in PaCO2 = serum K decreases by ____

A

0.5 mEq/L

164
Q

correctable causes of digoxin toxicity

A

hypokalemia

hypomagnesemia

arterial hypoxemia

165
Q

meds that cause dysrhythmias when given with digoxin

A

halothane, beta agonists, pancuronium, calcium

166
Q

drugs that cause increased automaticity with digoxin

A

fentanyl

isoflurane

167
Q

effect of increased cAMP in the myocardium vs vascular smooth muscle

what drug class does this

A

myocardium: increased intracellular Ca and increased contractility
muscle: decreased intracellular Ca, smooth muscle relaxation/vasodilation

PDE3 inhibitors

168
Q

use of milrinone

what class is this?

A

PDE3 inhibitor

acute LV dysfunction after surgery, weaning from CBP

169
Q

things that enhance and slow metabolism of theophylline

A

decreased/slowed: alcoholism, cimetidine, age extremes

enhanced: smoking

170
Q

CV effects of alpha blockers

A

vasodilation

reflex tachycardia

orthostatic hypotension

hypoglycemia

171
Q

uses of phentolamine

A

acute HTN emergencies, preop pheo

PIV norepi infiltration (should restore perfusion immediately)

172
Q

how does phenoxybenzamine affect BP

A

increased CO despite decreased BP

orthostatic hypotension with preexisting HTN or hypovolemia

173
Q

vasculature effects of beta blockers

A

blocking beta 2 = alpha 1 predominates = vasoconstriction

174
Q

does prolonged use of beta blockers cause upregulation or downregulation

A

upregulation

175
Q

which beta blockers are not recommended for diabetics? why?

A

nonselective (propranolol, timolol)

mask s/s hypoglycemia (HR), glycogen can’t be broken down

176
Q

contraindications to beta blockers

A
  • AV heart block
  • hypovolemia (eliminates compensatory tachycardia)
  • COPD
  • diabetic
  • PVD, raynaud’s
  • alpha agonist use
177
Q

treatment for beta blocker overdose

A

avoid epi and dopamine

1st: atropine, then glucagon

CaCl, isoproterenol (nonselective), dobutamine, pacemaker, iHD (minimally protein bound, renally excreted)

178
Q

when can withdrawal be seen with beta blockers

A

within 24-48 hours (d/t upregulated beta receptors)

179
Q

symptoms of beta blocker withdrawal

A

profound HTN

tachycardia

increased contractiltiy

180
Q

which antagonist can dcrease its own metabolism

A

propranolol (via decreased hepatic blood flow)

181
Q

how does propranolol affect myocardial O2 supply and demand

A

decreased o2 requirement > coronary blood flow

182
Q

how does propranolol affect fentanyl

A

decreases pulmonary uptake (more circulating)

183
Q

when should metoprolol be held

A

HR < 60 or SBP < 100

184
Q

most selective beta 1 blocker

A

atenolol

185
Q

which antagonist provides better protection than fentanyl or lidocaine against tachycardia/HTN from DL

A

esmolol

186
Q

MOA of labetolol

A

selective alpha 1 block, nonselective beta block

intrinsic beta 2 agonism

187
Q

CV effects of labetolol

A

decreased SVR

unchanged CO

vasodilation (alpha 1 block, beta 2 agonism)

188
Q

HR with labetolol

A

no reflex tachycardia - attenuated by beta 2 block

189
Q

adverse effects of labetolol

A

orthostatic hypotension (most common)

bronchospasm (offset by alpha 1 block?)

CHF, bradycardia, heart block

190
Q

MOA of carevedilol

A

alpha 1 + nonselective beta block

191
Q

how do pts on antihypertensives respond to direct sympathomimetics

A

exaggerated response (no counter-balancing beta 2 activity)

192
Q

how do ACE inhibitors affect aldosterone

A

decreased (decreased Na, H2O retention, increased K retentioN)

193
Q

when are ACE inhibitors contraindicated

A

pts with renal artery stenosis

194
Q

ideal HTN treatment in diabetics

A

ACE inhibitors (no metabolic effects)

195
Q

how to treat angioedema from ACE inhibitors

A

IM epi

TXA

icatbiant

FFP

196
Q

most common side effect of ACE inhibitors

A

cough

197
Q

periop complication to expect if pt takes ACE inhibitor DOS

A

hypotension

198
Q

how do calcium channel blockers affect vessels

A

arterial vasodilation

little effect on venous circulation

199
Q

uses of CCBs

A

coronary artery spasm

unstable or chronic stable angina

essential HTN

200
Q

how do CCBs affect NMBs

A

potentiate like mycin antibiotics

201
Q

effect of verapamil + dantrolene

A

hyperkalemia, CV collapse

202
Q

how does verapamil effect contractility, HR, and conduction through AV node

A

all decreased

203
Q

effect of CCBs + volatiles

A

additive myocardial depression, especially if preexisting LV dysfunction

204
Q

why shouldn’t nifedipine be stopped abruptly

A

abrupt stop assoc. with coronary artery vasospasm

205
Q

which CCB has the greatest vasodilating effects

A

nicardipine

(especially coronaries)

206
Q

when is nicardipine contraindicated

A

advanced aortic stenosis

207
Q

which CCB is metabolized by esterases

A

clevidipine

208
Q

use of nimodipine

A

treat vasospasms r/t SAH

209
Q

which produces more NO - arteries or veins

A

arteries

210
Q

how does NO affect smooth muscles

A

NO = increased cGMP = smooth muscle relaxation

211
Q

NO has antithrombotic effects

A

kewl

212
Q

how do NO synthase inhibitors affect MAC

A

dose-dependent reduction

213
Q

MOA of Nipride

A

direct-acting arterial and venous vasodilation & smooth muscle relaxation

reacts with hgb to form methemoglobin and releases cyanide & NO

214
Q

dose of nipride assoc. with cyanide toxicity

A

> 2 mcg/kg/min

215
Q

symptoms of cyanide toxicity with Nipride

A

tachyphylaxis

increased MvO2

metabolic acidosis

seizures

216
Q

how to treat cyanide toxicity

A

stop gtt

100% O2

sodium bicarb

sodium thiosulfate

217
Q

how does Nipride affect ICP?

A

increased d/t increased CBF & CBV

increase is maximal if MAP decreases less than 30%

>30% decrease in MAP = ICP at awake levels

218
Q

contraindications to Nipride

A

increased ICP and inadequate CBF

carotid artery stenosis

219
Q

how does Nipride alter HPV

A

alters and causes shunting

more with healthy lungs

treat with PEEP

220
Q

MOA of nitroglycerin

A

produces NO

venous dilation (arterial dilation at high doses)

221
Q

how does nitroglycerin affect venous return

A

decreases

222
Q

how does nitroglycerin affect CO in a normal heart vs. failing heart

A

normal: decreases CO
failing: increases, relieves pulmonary congestion

223
Q

HR with nitroglycerin

A

baroreceptor-mediated reflex tachycardia

224
Q

condition nitroglycerin is bad for

A

CAD

increases inotropy, which increases demand and decreases supply

225
Q

nitroglycerin = better blood flow to ischemic areas

A

vs nipride which can cause coronary steal

226
Q

MOA of hydralazine

A

interferes with calcium ion transport

direct systemic arterial vasodilator

227
Q

how does hydralazine affect coronary perfusion

A

may decrease

(Decreases DBP > SBP)

228
Q

how can hydralazine cause MI

A

baroreceptor-mediated direct increase in HR + increased SV & CO can affect supply/demand

229
Q

which vasodilator is assoc. with a lupus-like syndrome

A

hydralazine

230
Q

elimination ½ time of adenosine

A

0.6-1.5 seconds

231
Q

BP goals in deliberate hypotension

A

SBP 80-90 mmHg

MAP 50-60 mmHg in normotensive pts

(best definition: 30% reduction)

232
Q

contraindications to deliberate hypotension

A

severe anemia

untreated HTN

233
Q

how to reduce rebound HTN with use of nipride gtt for deliberate hypotension

A

pretreat with propranolol or captopril

234
Q

spinal blockade that prevents tachycardia

A

T1-T4

235
Q

PaO2 and PaCO2 in deliberate hypotension

A

increased PaCO2 (increased dead space)

decreased PaO2 (increased shunt) - seen with Nipride not iso, in normal lungs not COPD lungs

236
Q

at what MAP does CBF no longer respond to changes in PaCO2

A

< 50 mmHg

237
Q

MAP at which GFR is reduced

A

< 75 mmHg

238
Q

SBP guideline for deliberate hypotension

A

don’t decrease to < preop DBP

239
Q

what determines FI (inspired gas concentration)

A

FGF

breathing circuit volume

circuit absorption

240
Q

vessel rich group:

what’s included?

body mass?

% CO?

A

brain, heart, liver, kidneys, endocrine

10% mass

75% CO

241
Q

what determines FA (alveolar gas concentration)

A
  • uptake
  • alveolar ventilation
  • concentration effect
  • 2nd gas effect
242
Q

lean muscle group:

what’s included?

body mass?

% CO?

A

muscle, skin

50% body mass

18% CO

243
Q

fat group:

what’s included?

body mass?

% CO?

A

fat, duh

20% body mass

5% CO

244
Q

vessel poor group:

what’s included?

body mass?

% CO?

A

bone, ligament, cartilage

20% mass

2% CO

245
Q

which of the 4 compartments in the 4 compartment model is slowest to equilibrate

A

vessel poor

246
Q

Factors determining partial pressure gradient from machine to alveoli (input):

A
247
Q

how does alveolar ventilation affect induction

A

increased alveolar ventilation = more rapid induction

more evident with more soluble anesthetics

248
Q

how to prevent inhaled anesthetic overdose in inhaled induction

A

maintain spontaneous ventilation (potential for OD with controlled ventilation)

249
Q

what is a time constant?

A

L / L/min

minutes required for 63% turnover of gas within a container

250
Q

how many time constants until equilibrium is reached

A

4

251
Q

Factors determining rate of transfer of agent from alveoli to arterial blood (Uptake)

A
  • Solubility
  • CO
  • Alveolar to venous partial pressure gradient
252
Q

Factors determining rate of transfer of agent from alveoli to arterial blood (Uptake)

A
  • Solubility
  • CO
  • Alveolar to venous partial pressure gradient
253
Q

how does b:g affect PA/PI

A

lower b:g = lower solubility = faster rate of rise

254
Q

how does CO affect inhalation induction

A

increased CO = slowed induction (increased uptake, slower rise in alveolar partial pressure)

255
Q

how does V/Q mismatch affect inhalation induction

A

slowed induction

poorly soluble more affected

(dilutional effect)

256
Q

Factors determining the transfer of agent from arterial blood to brain (uptake)

A
  • Brain:blood partition coefficient
  • Cerebral blood flow
  • Arterial-to-venous partial pressure difference
257
Q

methods to increase elimination

A
  • high FGF
  • low anesthesia circuit volume
  • low absorption by anesthesia circuit
  • decrease solubility
  • high cerebral blood flow
  • increased alveolar ventilation

Finals (2 decks)

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