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Board Exam > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q
A
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2
Q

Heparin

[half-life elimination time]

A

1 -2 hours

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3
Q

2-Chloroprocaine

[rapid onset]

A

able to use high concentrations due to its low systemic toxicitiy

  • unlike normally, does not depend on PKa, which is about 9 and thus more pronated (less likely to cross cell membrane) at physiologic pH
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4
Q

5-HT3

[receptor]

A

serotonin on platelets and GI tract

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5
Q

Adrenergic Agonists

[which 2 have the greatest increase on CO]

A

isoproterenol and dobutamien

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6
Q

Adrengergic Agonists

[which 2 cause a large decrease in renal blood flow]

A

phenylephrine and norepinephrine

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7
Q

Agents

[effect on SA node]

A

depresses SA node automaticity

  • only modest effects on AV node; explains the occurrence of junctional tachycardia when administering an anticholinergic during inhalation anesthesia
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8
Q

Agents

[effects on blood pressure]

A

decrease

  • Des, Sevo, and Iso decrease blood pressure due to a decrease in systemic vascular resistance
  • halothane depression is due to decreases in myocardial contractility and cardiac output
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9
Q

Agents

[effects on cardiac output]

A

minimal decrease

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10
Q

Agents

[effects on CVP]

A

slight increase except for Sevoflurane

  • However, around 1.5 MAC, sevo will show an increase in CVP, then drop again
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11
Q

Agents

[effects on heart rate]

A

increase heart rate

  • Sevoflurane only increases HR when MAC > 1.5
  • halothane has no effect on heart rate
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12
Q

Agents

[effects on minute ventilation]

A

decrease

  • increase respiratory rate while decreasing tidal volume
  • except for Isoflurane
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13
Q

Agents

[effects on pulmonary vascular resistance]

A

little to no effect

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14
Q

Agents

[effects on systemic vascular resistance]

A

decrease SVR

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15
Q

Agents

[ventilatory response]

A

decrease response to incrasing PaCO2

  • Desflurane above 1 MAC has the greatest effect
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16
Q

Agents

[best for ablative procedures]

A

Sevoflurane

  • no effect on AV conduction
  • Isoflurane increases the refractoriness of accessory pathways
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17
Q

Alpha Blockers

[examples]

A

prazosin

phentolamine

phenoxybenzamine

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18
Q

Alpha-1 Agonists

[cardiovascular effects]

A

vasoconstriction

leading to an increase in peripheral vascular resistance, left ventricular afterload, and atrial blood pressure

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19
Q

Alpha-1 Agonist

[mechanism of action]

A

increase intracellular [Ca2+] leading to contraction of smooth muscles

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20
Q

Alpha-2 Agonists

[cardiovascular effects]

A

reduction of sympathetic outflow

peripheral vasodilation and lower blood pressure

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21
Q

Alpha-2 Agonists

[mechanism of action]

A

inhibits adenylate cyclase activity

  • decreases the entry of calcium ions into neuronal terminal, which limits exit of norepinephrine
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22
Q

anesthetic agent with low potency and poor blood solubility

A

Desflurane

(and N2O)

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23
Q

Anti-Arrhythmic Agents

[Class I - type]

A

Na+ channel blocker

  • blocks voltage-gated Na+ channels and decreases the slope of phase 0 (Vmax)
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24
Q

Anti-Arrhytmic Agents

[Class III - examples]

A

amiodarone and sotalol

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25
Q

Anti-Arrhytmic Agents

[largest increase in QT interval]

A

amiodarone

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26
Q

Anti-Arrhytmic Agents

[best for supraventricular arrhythmias]

A

adenosine

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27
Q

Anti-Arrhytmic Agents

[class I - examples]

A

quinidine

lidocaine

phenytoin

flecainide

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28
Q

Anti-Arrhytmic Agents

[Class II - examples]

A

esmolol and metoprolol

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29
Q

Anti-Arrhytmic Agents

[class II - type]

A

beta blocker

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30
Q

Anti-Arrhytmic Agents

[class III - type]

A

K+ channel blocker

  • prolongs repolarization
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31
Q

Anti-Arrhytmic Agents

[Class IV - examples]

A

verapamil and diltiazem

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32
Q

Anti-Arrhytmic Agents

[class IV - type]

A

Ca2+ channel blocker

  • blocks slow calcium channels
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33
Q

Anticholinergics

[effects on cardiovascular system]

A

tachycardia

  • blockade of muscarinic receptors in the SA node
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34
Q

Anticholinergics

[respiratory effects]

A

decrease secretions

bronchodilation

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35
Q

Anticholinesterase

[muscarinic effects on gastrointestinal system]

A

increased spasm and salvation

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36
Q

Anticholinesterase

[muscarinic side effects on cardiovascular system]

A

decreased heart rate and bradyarrhythmias

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37
Q

Anticholinesterase

[muscarinic side effets on pulmonary system]

A

bronchospasm

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38
Q

Antimuscarinics

[3 examples]

A

atropine

scopolamine

glycopyrrolate

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39
Q

Atracurium

[metabolism]

A

ester hydrolysis and hofmann elimination

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40
Q

Atracurium

[side effects]

A

histamine release

  • avoid in severe asthmatics
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41
Q

Atropine

[anti-sialagogue IM dose]

A

0.01 - 0.02 mg/kg

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42
Q

Barbiturates

[effect on ICP]

A

greatest decrease in ICP

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43
Q

Barbiturates

[effect on seizure threshold]

A

lowers seizure threshold

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44
Q

Barbiturates

[effects on cerebral physiology]

A

decrease CMR, CBF, and ICP

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45
Q

Benzodiazepines

[effects on cerebral physiology]

A

slightly decreases CMR, CBF, and ICP

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46
Q

Benzodiazepines

[mechanism of action]

A

enhance GABA receptor affinity, but do not directly activate

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47
Q

Benzodiazepines

[pregnancy and labor]

A

crosses placenta and may lead to CNS depression

  • may increase risk of cleft lip/palate when given during first trimester
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48
Q

Bleomycin

[adverse effects]

A

pulmonary fibrosis

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49
Q

Bronchodilators

[order of effectiveness]

A

Beta agonists

glucocorticoids

leukotriene blockers

mast-cell stabilizers

theophyllines

anticholinergics

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50
Q

Bupivacaine

(marcaine)

[duration of action]

A

5 - 15 hours (anesthesia)

  • epinephrine is less effective in prolonging anesthesia because duration of action is independent of local blood flow
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51
Q

Calcium Channel Blockers

[greatest risk of SVT]

A

verapamil and diltiazem

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52
Q

Cerebral Vasospasm

[treatment]

A

Nimodipine

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53
Q

Cisatracurium

[metabolism]

A

Hofmann elimination

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54
Q

Cisplatin

[adverse effects]

A

renal impairment

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55
Q

Clomipramine

[drug class]

A

tricyclic anti-depressant

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56
Q

Clomipramine

[treatment]

A

obsessive-compulsive disorder

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57
Q

Clonidine

(catapres)

[mechanism of action]

A

alpha-2 agonist

  • less selective and longer acting than dexmedetomidine (precedex)
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58
Q

Context Sensitive Half-Time

[definition]

A

time necessary for the plasma drug concentration to decrease 50% after discontinuing a continuous infusion

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59
Q

Coronary Steal Syndrome

A

theory that coronary vasodilators that target smaller coronary vessels would redistribute blood from ischemic to nonischemic areas

  • Examples: Isoflurane, adenosine, dipyridamole, and nitroprusside
  • not clinically proven
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60
Q

Creatinine Clearance

[equation estimate]

A

[140 - age] x kg

divided by

72 x [creatinine%]

  • multiply by 85% for women
  • “Cockroft and Gault” equation
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61
Q

Cryoprecipitate

[components]

A

von willebrands

fibrinogen

factor VIII and XIII

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62
Q

Cyclosporine

[mechanism of action]

A

calcineurin inhibitor

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63
Q

Cyclosporine

[treatment]

A

immunosuppression for organ transplant

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64
Q

Anesthetic implications of decreased SVR

A
  • excess perfusion relative to oxygen needs
  • loss of body heat due to increase cutaneous blood flow
  • enhanced delivery of drugs to NMJ
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65
Q

Desflurane

[vaporizer]

A

desflurane is heated to 39oC to raise its partial pressure to 1,500 mmHg

  • ensures a constant concentration despite changes in barometric pressure or temperature
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66
Q

Desflurane

[Blood:Gas]

A

0.42

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67
Q

Desflurane

[Brand name]

A

Suprane

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68
Q

Desflurane

[MAC]

A

6.0

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69
Q

Desflurane

[vapor pressure]

A

660

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70
Q

Dexmedetomidine

(precedex)

[adverse effects]

A

antimuscarinic effects

  • dry mouth and blurred vision
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71
Q

Dexmedetomidine

(precedex)

[mechanism of action]

A

alpha-2 agonist

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72
Q

Dexmedetomidine

[receptor selectivity]

A

alpha-2 > alpha-1

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73
Q

Dextrose 5%

[osmolarity]

A

252

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74
Q

Diffusion Hypoxia

A

occurs with abrubtly ending inhalation of N2O

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75
Q

Diuretics

[3 K+-Sparing Examples]

A

Spironolactone (aldactone)

Triamterene (dyrenium)

amiloride (midamor)

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76
Q

Diuretics

[4 Loop Examples]

A

Furosemide (lasix)

Bumetanide (bumex)

Torasemide (demadex)

Ethacrynic acid (edecrin)

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77
Q

Dobutamine

[effects]

A

enhances cardiac output without changing blood pressure

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78
Q

Dobutamine

[receptor selectivity]

A

Beta-1 >> beta-2

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79
Q

Droperidol

[mechanism of action]

A

D2 Antagonist

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80
Q

Droperidol

[side effets]

A

dystonia

QT prolongation

decreased seizure threshold

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81
Q

Drugs causing decreased renal perfusion

A

NSAIDS

ACE inhibitors

IV contrast

cyclosporines

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82
Q

drugs causing direct tubular injury

A

aminoglycosides

IV contrast

heavy metals

myoglobin and hemoglobin

HIV protease

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83
Q

Edrophonium

[reversal dose of Atropine]

A

0.014 mg per mg of anti-cholinesterase

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84
Q

Effect on MAC

[hypernatremia]

A

increase

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85
Q

Effect on MAC

[alpha-2 agonists]

A

decrease

86
Q

Effect on MAC

[Cyclosporine]

A

increase

87
Q

Effect on MAC

[hyperthermia]

A

increases

88
Q

Effect on MAC

[hyponatremia]

A

decrease

89
Q

Effect on MAC

[Lidocaine]

A

decrease

90
Q

Epinephrine

[receptor selectivity]

A

Beta-1 > alpha-1 = alpha-2 = beta-2

91
Q

Esmolol

[cardiovascular effects]

A

lowers heart rate and, to a lesser extent, blood pressure

92
Q

Etomidate

[Adrenocortical Suppression]

A

inhibits converstion of cholesterol to cortisol through 11-beta-hydroxylase

  • avoid in septic or hemorrhaging patients
  • usually only seen in infusions or repeated doses
93
Q

Etomidate

[drug interactions]

A

fentanyl prolongs half-life

opioids decrease myoclonus

94
Q

Etomidate

[mechanism of action]

A

GABAA agonist

95
Q

First Pass Hepatic Effect

[which route of administration?]

A

oral

96
Q

First Pass Hepatic Effect

A

GI tract to portal venous blood to liver before entering systemic circulation

  • greatly reduces available drug
97
Q

Flumazenil

(imidazobenzodiazepine)

[contraindications]

A

tricyclic anti-depressants

patients taking benzos for control of seizures

98
Q

Flumazenil

(imidazobenzodiazepine)

[mechanism of action]

A

competitive antagonist of benzodiazepine binding site on GABAA receptors

99
Q

H1 Antagonists

[2 examples]

A

diphenhydramine (benadryl)

promethazine (phenergan)

100
Q

H2 antagonist

[gastrointestinal effects]

A

decreases gastric acid secretion from parietal cells

101
Q

Halothane Hepatitis

[risk factors]

A

female, obese, middle aged, and multiple halothane exposures

102
Q

Halothane

[cardiac risks]

A

slows conduction through SA node

  • predisoposes patients to junctional arrhythmias and bradycardia
103
Q

Histamine

[cardiovascular effects]

A

lowers blood pressure

increases HR and contractility

104
Q

Ionized Drugs

[characteristics]

A

inactive

water soluble

cannot cross BBB or undergo hepatic metabolism

can be excreted renally

105
Q

Isoflurane

[Blood:Gas]

A

1.5

106
Q

Isoflurane

[brand name]

A

Florane

107
Q

Isoflurane

[MAC]

A

1.2

108
Q

Isoflurane

[vapor pressure]

A

238

109
Q

Isoflurane

[why is emergence quicker than induction?]

A

agent continues to be absorbed by peripheral tissues dueing emergence

110
Q

Ketamine

[adverse effects]

A

increased oral secretions

myoclonic movements

increased ICP

ocular effects

difficulty to assess anesthetic depth

111
Q

Ketamine

[cardiovascular effects]

A

increases BP, HR, and CO

  • when administered with a smalld ose of benzodiazepine or Propofol, sympathetic stimulation can be blunted or eliminated
112
Q

Ketamine

[effects on cerebral physiology]

A

increase CBF and ICP

113
Q

Ketamine

[mechanism of action]

A

NMDA antagonist

114
Q

Ketamine

[ocular effects]

A

diplopia

mydriasis

nystagmus

blepharospasm

increased intraocular pressure

115
Q

Ketorolac

[contraindications]

A

kidney failure and allergy to NSAIDs

  • relative contraindications:
    • asthma, risk of hemorrhage
116
Q

Ketorolac

[equivalence to morphine]

A

standard dose of Ketorolac equals 6-12 mg of morphine

117
Q

Ketorolac

[mechanism of action]

A

NSAID that inhibits prostaglandin synthesis

118
Q

Labetalol

[cardiovascular effects]

A

lowers blood pressure without increasing heart rate

119
Q

Lactated Ringer

[components]

A

Na+, Cl-, K+, Ca2+, and lactate

120
Q

Lactated Ringer

[osmolarity]

A

273

121
Q

Lidocaine

[effects on cerebral physiology]

A

decrease CMR, CBF, and ICP

122
Q

Local Anesthetics

[cardiovascular effects]

A

depress myocardial automaticity

(spontaneous phase IV depolarization)

  • can decrease contractility and conduction velocity at high concentrations
  • inhibit nitric oxide, causing vasoconstriction
123
Q

local anesthetics

[sodium bicarb]

A

shortens onset time

  • alkinalizes drug
124
Q

Loop Diuretics

[adverse effects]

A
  • Hypo-
    • K+, Ca2+, Mg2+
  • Hyperglycemia
  • metabolic alkalosis
125
Q

Mannitol

[contraindications]

A

intracranial aneurysm

arteriovenous malformations

intracranial hemorrhage until open

126
Q

Mannitol

[dose]

A

0.25 - 1 g/kg

127
Q

Meperidine

(demerol)

[drug interactions]

A

monoamine oxidase inhibitors

  • delirium or fatal hyperthermia
128
Q

Metabolism

[4 basic pathways of metabolism]

A

oxidation

reduction

hydrolysis

conjugation

129
Q

Metabolism

[phase I reactions]

A

reduction

hydrolysis

oxidation

130
Q

Metoclopromide

[drug interactions]

A

blocked by anti-muscarinic drugs

increased side effects with droperidol

131
Q

Metoclopromide

[black box warnings]

A

tardive dyskinesia

132
Q

Metoclopromide

[contraindications]

A

GI obstruction

Parkinson’s

Pheochromocytoma

133
Q

Metoclopromide

[drug class]

A

dopamine-2 antagonist

134
Q

Minimal Alveolar Concentration

[definition]

A

concentration at 1 atm that prevents skeletal muscle movement in response to supramaximal stimulus in 50% of patients

135
Q

muscle relaxants

[effect of respiratory acidosis]

A

potentiates blockade of NDMR and antagonizes reversal

  • may prevent recovery in hypoventilating post-operative patients
136
Q

Muscle Relaxants

[effects of Magnesium]

A

potentiates blockade

  • competes with calcium at motor end-plate
137
Q

Naloxone

[adverse effects]

A

may precipitate pulmonary edema and cardiac arrest

(rare)

138
Q

Naloxone

[mechanism of action]

A

opioid antagonist

139
Q

Cerebral Palsy

[response to NDMR]

A

resistance

140
Q

Neostigmine

[onset and peak]

A

will see effects in 5 minutes

peaks at 10 min

141
Q

Nitrates

[vascular effects]

A

venodilator > arterial dilator

  • decrease preload
142
Q

Nitroglycerin

[vascular effects]

A

venous dilation > arterial dilation

143
Q

Nitrous can safely be administered in retinal reattachment surgeries as long as it is discontinued ____ minutes prior to bubble injection

A

15 minutes

144
Q

Nitrous Oxide

[Blood:Gas]

A

0.47

145
Q

Nitrous Oxide

[contraindictations]

A

COPD with blebs

venous air embolism

pneumothorax and pneumocephalus

acut intestinal obstruction

tympanic membrane

intraocular procedures

146
Q

Nitrous Oxide

[duration of analgesic effects]

A

20 minutes

147
Q

Nitrous Oxide

[effect on pulmonary vascular resistance]

A

increase PVR

  • especially in patients with pre-existing pulmonary hypertension
148
Q

Nitrous Oxide

[effect on vitamin B12]

A

inhibits vitamin B12 synthesis

  • use with caution in pregnant patients and those deficient of the vitamin
149
Q

Nitrous Oxide

[effects on right-to-left intracardiac shunt]

A

may increase shunting of blood and further jeapordize arterial oxygenation

150
Q

Nitrous Oxide

[MAC]

A

104

151
Q

NMDA Antagonists

[reason for neuroprotection]

A

during ischemia, [K+]i decreases and [Na+]i increases causing [Ca2+]i to increase

leads to release of glutamate which acts on the NMDA receptor, enhancing Ca2+ entry

152
Q

Norepinephrine

[receptor selectivity]

A

alpha-1 = alpha-2 = beta-1

153
Q

Norepinephrine

[cardiovascular effects]

A

arterial and venous vasoconstriction

  • increased myocardial contractility
  • rise in systolic and diastolic pressures
  • However, increased afterload and reflex bradycardia prevent rise in cardiac output
154
Q

Normal Saline

[osmolarity]

A

308

155
Q

Normal Saline

[components]

A

Na+ and Cl-

156
Q

Normothermic Shivering

[treatment]

A

meperidine (25-50mg)

clorpromazine (10-25mg)

butorphanol (1-2mg)

157
Q

Ondanesetron

[mechanism of action]

A

5-HT3 antagonist

158
Q

Ondanestron

[side effects]

A

dizziness, headache, QT prolongation

159
Q

Ondansetron

[brand name]

A

Zofran

160
Q

Opioids

[allergic reactions]

A

rare, although some anaphylactoid reactions may occur

  • secondary to histamine release following morphine or meperidine
161
Q

Opioids

[gastrointestinal effets]

A

decrease gastric emptying

increase biliary pressure

sphincter of Oddi spasms

162
Q

Pancuronium

[allergic reactions]

A

patients who are hypersensitive to bromides may exhibit allergic reactions

163
Q

Pancuronium

[arrhythmias]

A

predisposition to ventricular dysrhythmias

  • increased atrioventricular conduction and catacholamine release
  • avoid in combination with tricyclic anti-depressants and halothane
164
Q

Pancuronium

[side effects]

A

hypertension and tachycardia via vagal response

arrhythmias

165
Q

Phenelzine

[adverse effects]

A

decreases plasma cholinesterase activity

166
Q

Phenylephrine

[receptor selectivity]

A

alpha-1 >> alpha-2

167
Q

Phenytoin

[mechanism of action]

A

voltage-gated Na+ channel blocker

168
Q

Physostigmine

[treatment]

A

anti-cholinergic toxicity

169
Q

Plasmalyte

[osmolarity]

A

294

170
Q

Plasmalyte

[components]

A

Na+, Cl-, K+, Mg2+, gluconate, and acetate

171
Q

Propofol Infusion Syndrome

A

Prolonged high-dose infusions of Propofol that can lead to cardiac failure, rhabdomyolysis, metabolic acidosis, and kidney failure

172
Q

Propofol

[effects on cerebral physiology]

A

decreases CMR, CBF, and ICP

173
Q

Propofol

[lipid disorders]

A

due to its lipid emulsion, should be used cautiously in patients with disorders of lipid metabolism

  • examples: hyperlipidemia and pancreatitis
174
Q

Propofol

[mechanism of action]

A

GABAA agonist

  • increased chloride conductance, resulting in hyperpolarization of the post-synaptic cell membrane and functional inhibition
175
Q

Prostaglandin Inhibitors

[patent ductus arteriosus]

A

promote closure of persistent PDA

  • specifically Ibuprofen and indomethacin
176
Q

Most acidic drugs bind to _____, whereas basic drugs bind to _____.

A

albumin (acidic)

alpha-1 glycoprotein (basic)

177
Q

Proton Pump Inhibitors

[mechanism of action]

A

bind to proton-pump on parietal cells in the gastric mucosa and inhibit H+ secretion

178
Q

Pseudocholinesterase Deficiency

[drugs known to decrease activity]

A

Echothiophate

neostigmine

phenelzine

metoclopromide

esmolol

pancuronium

oral contraceptives

179
Q

Pulmonary Hypertension

[treatment]

A

nitric oxide

180
Q

“The speed in an inhalation induction is slowed by right-to-left shunting. The change in the rate of induction is LEAST pronounced when using _____”

A

Isoflurane

  • right-to-left shunting more pronounced with high blood:gas solubilities
181
Q

Which inhalational agent is most likely associated with a junctional rhythm?

A

halothane

182
Q

The rate of _____ determines the rate of induction with volatile agents

A

FA/FI

183
Q

Which of the following is most responsible
for maintenance of cardiac output during isoflurane
administration?

A

increased heart rate

  • results in maintenance of cardiac output due to preserved carotid baroreceptor reflex
184
Q

“Desflurane vaporizer dial must be set ______ at higher elevations”

(higher or lower)

A

higher

185
Q

“For intermediate-acting NDMR, a palpable post-tetanic twtich appears about _____ before spontaneous recovery of the first TOF twitch”

A

10 minutes

186
Q

“Time to recovery is prolonged in proportion to the duration of anesthesia for which agents?”

A

soluble anesthetics

(isoflourane and halothane)

187
Q

Rocuronium

[metabolism and excretion]

A

no metabolism

eliminated mostly by liver

188
Q

Second Gas Effect

A

high-volume uptake of one gas accelerates the rate of increase of the alveolar pressure of a concurrently administered “second” gas

189
Q

Seizure

[treatment]

A

Propofol (50-100mg)

phenytoin (500-1000 mg slowly)

midazolam (1-5mg)

190
Q

Sevoflurane

[brand name]

A

Ultane

191
Q

Sevoflurane

[Blood:Gas]

A

0.65

192
Q

Sevoflurane

[MAC]

A

2.4

193
Q

Sevoflurane

[vapor pressure]

A

160

194
Q

Sodium Nitroprusside

[adverse effects]

A

cyanide toxicity

  • metabolic acidosis, cardiac arrhythmias, and increased venous oxygen content
195
Q

Speed of Induction

[effects of right-to-left shunt]

A

slow induction

196
Q

Speed of Induction

[relationship to Cardiac Output]

A

inverse relationship

  • an increased cardiac output results in a rapid uptake and therefore a slower induction
  • CO mostly influeces soluble anesthetics
    • Example: Isoflurane
197
Q

St. John’s Wort

[adverse drug interactions]

A

MAO inhibitors and Meperidine

  • increased risk of serotonin syndrome
198
Q

Amyotrophic Lateral Sclerosis

[response to Succinylcholine]

A

contractures

199
Q

Myasthenia Gravis

[response to Succinylcholine]

A

resistant

200
Q

Autoimmune disorders

[response to Succinylcholine]

A

hypersensitivity

201
Q

Sulfonamides

[risks in neonates]

A

displaces uconjugated bilirubin from binding sites on albumin, leading to bilirubin encephalopathy

202
Q

Thiazide Diuretics

[adverse effects]

A
  • Hypo-
    • K+, Na+, Mg2+
  • Hyper-
    • glycemia, uricemia, lipidemia, Ca2+
203
Q

Tricyclic Anti-depressants

[drugs to avoid]

A

indirect-acting vasopressors and those with sympathetic stimulation

  • pancuronium, ketamine, meperidine, and local with epi
204
Q

Valproic Acid

(depakote)

[drug interactions]

A

benzodiazepines

  • may precipitate a psychotic episode
205
Q

Valproic Acid

[mechanism of action]

A

increases GABA and inhibitis NMDA

206
Q

Valproic Acid

(depakote or valproate)

[treatment]

A

seizures and bipolar disorder

207
Q

Vecuronium

[metabolism]

A

biliary excretion

(some renal)

208
Q

Vincristine

[adverse effects]

A

neuropathy

209
Q

volatile agents

[effect on dead space]

A

increase

  • due to the decrease in tidal volume
210
Q

volatile agents

[effects on cerebral physiology]

A

decrease CMR, but increase CBF and ICP

211
Q

volatile agents

[effects on PaCO2]

A

increase

Board Exam (5 decks)

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