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Advanced Pharm > Exam 2 Material > Flashcards

Exam 2 Material Flashcards

1
Q

What enzyme metabolizes phenylephrine?

A

MAO

Monoamine oxidases

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2
Q

Which adrenergic agonist is NOT arrhythmogenic?

A

Phenylephrine

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3
Q

Which selective alpha 2 agonist is more highly protein bound?

A

Dexmedetomidine

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4
Q

Name the endogenous sympathomimetics

A

Norepinephrine
Epinephrine
Dopamine

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5
Q

Define chronotropy

A

Affects heart rate

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6
Q

What receptors does clonidine work on?

A

-alpha 1 and alpha 2 adrenergic receptors
-acts as an anti hypertensive

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7
Q

Why is clonidine use in PNB?

A

Extends life if PNB

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8
Q

What receptor does dexmetomidine work on?

A

Central acting alpha 2

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9
Q

What is dexmetomidine used for intra-operatively?

A

Sedative
Proanesthetic

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10
Q

Dexmetomidine blunts central ____ response

A

Sympathetic

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11
Q

What 5 things does dexmetomidine reduce in patient intraop

A

-opioid muscle rigidity
-reduces post op shivering
-little respiratory depression
-hemodynamically stabilizing effect
-reduced opioid requirements

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12
Q

Dexmetomidine can cause a _____ in HR

A

Decrease

Alpha 2 may lead to hypotension when combined with other anesthetics

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13
Q

What is a sympathomimetic

A

Stimulates adrenergic receptors

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14
Q

what is the protype drug for sympathomimetics

A

epinephrine

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15
Q

what receptor relates to vasculature

A

alpha 1

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16
Q

what receptor relates to heart rate

A

beta 1

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17
Q

what receptor relates to bronchiole smooth muscle

A

beta 2

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18
Q

what drug is an agonist for all adrenergic receptors?

A

epinephrine

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19
Q

what does alpha 1 stimulation do

A

-arteriolar vasoconstriction
-pulmonary artery vasoconstriction

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20
Q

What does beta 1 stimulation do

A

-increase HR
-increase myocardial contractility
-increased CO

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21
Q

what does beta 2 stimulation do

A

-vasodilation in airway smooth muscle
-vasodilation of skeletal muscle
-increase cAMP

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22
Q

what is mydriasis

A

contraction of iris= dilation

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23
Q

what are the metabolic effects of epi

A

hypokalemia
hyperglycemia

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24
Q

norepinephrine has ___ alpha 1 than epi

A

greater

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25
Q

norepinephrine has ___ B2

A

NO

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26
Q

when compared to epi, norepi has ___ effect on SVR, systolic/diastolic BP, and MAP.

This is due to its affect on the ___ receptor

A

greater
alpha 1

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27
Q

what is the first line vasopressor for septic shock

A

norepinephrine

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28
Q

how much metabolic effect does norepi have

A

limited (not as much K or blood sugar effect)

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29
Q

what systems does dopamine help regulate

A

-cardiac
-vascular
-endocrine
-central nervous system
-peripheral nervous system

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30
Q

what receptors does dopamine affect

A

D1 D2 alpha and beta

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31
Q

what are the effects of D1 stimulation

A

-vasodilation of renal, mesenteric, coronary and cerebral

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32
Q

what are effects of D2 stimulation

A

inhibits norepi release

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33
Q

what is the reward mechanism in the brain

A

dopamine

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34
Q

what receptors are activated at dopamine rate 0.5-3 mcg/kg/min? What is its effect?

A

D1 and D2

vasodilation, decreased arterial BP, increased renal and splanchnic blood flow

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35
Q

what receptors are activated at dopamine rate 3-10mcg/kg/min

A

B1
alpha 1 increase

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36
Q

what does an increase in dopamine dose put a patient at risk for

A

arrhythmias

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37
Q

what is the half life of dopamine

A

1-2 min

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38
Q

what 6 things does dopamine increase

A

-myocardial contractility
-renal blood flow
-GFR
-Na excretion
-Urine output
-intraocular pressure

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39
Q

what are two synthetic catecholamines

A

isoproterenol
dobutamine

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40
Q

what is isoproterenol used for

A

heart blocks
B1 B2 agonist

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41
Q

what are the effects of isoproterenol

A

-increased HR
-increased contractility
-decreased SVR through skeletal muscle vasodilation

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42
Q

what is dobutamine?

A

-synthetic catecholamine
-racemic mixture of isoproterenol

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43
Q

what receptor is dobutamine specific for?

A

B1, weak B2 effects

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44
Q

does dobutamine have alpha effects

A

yes at high doses

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45
Q

does isoproterenol have alpha effects?

A

NO

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46
Q

what is dobutamine used for?

A

heart failure
weaning from bypass

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47
Q

what are the effects of dobutamine?

A

increased contractility
decreased afterload

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48
Q

what are two synthetic noncatecholamines

A

ephedrine
phenylephrine

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49
Q

what is the indirect acting sympathomimetic

A

ephedrine- must go through metabolism

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50
Q

what receptor does ephedrine work on

A

alpha and beta

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51
Q

which synthetic noncatecholamine mimics epi

A

ephedrine

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52
Q

what is benefit of ephedrine over epi

A

less intensity
lasts longer

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53
Q

what happens when you keep giving ephedrine

A

tachyphylaxis, effect diminishes have to give higher doses

catecholamine depletion at the synapse

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54
Q

which synthetic noncatecholamine mimics norepi

A

phenylephrine

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55
Q

what receptor does phenylephrine act on

A

alpha 1

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56
Q

what kind of vessel does phenylephrine constrict

A

venous and arterial

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57
Q

what is a reflex effect of phenylephrine

A

baroreceptors reflex vagal from elevated BP, bradycardia

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58
Q

what is the effect of selective B2 adrenergic agonist

A

relax bronchioles and uterine smooth muscle

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59
Q

what is the protype drug for beta 2 agonist

A

albuterol

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60
Q

what are the routes of admin for B2 agonists

A

inhaled most common
oral and subq

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61
Q

what happens when you put inhaler through ETT

A

decrease dose by 50-70%

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62
Q

what is calcium used as in anesthesia

A

inotrope

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63
Q

when is ionized Ca used to treat cardiac depression

A

-volatile anesthetics
-citrate infused blood products
-post bypass

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64
Q

what has effect on heart: ionized Ca or total plasma calcium

A

ionized

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65
Q

acidosis ___ ionized Ca

A

increases

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66
Q

alkalosis ___ ionized Ca

A

decreases

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67
Q

infusion dose for isoproterenol

A

0.015-0.15mcg/kg/min

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68
Q

how is isoproterenol metabolized

A

rapidly by COMT

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69
Q

what is infusion dose of dobutamine?

A

2-20mcg/kg/min

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70
Q

IV dose of ephedrine

A

5-25mg

IM dose up to 50mg

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71
Q

ephedrine is a ___ inotrope and ____ O2 demand with CAD

A

positive, increase

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72
Q

what potent alpha agonist is the chemical precursor of epinephrine?

A

norepinephrine

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73
Q

an FDA Black Box warning is attached to what B2 selective agents?

A

salmeterol and formoterol

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74
Q

which adrenergic receptor agonist is metabolized by the liver?

A

ephedrine

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75
Q

which synthetic catecholamine is derived from dopamine?

A

isoproterenol

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76
Q

what is the precursor of norepinephrine

A

dopamine

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77
Q

How does labetalol possess intrinsic sympathomimetic activity (ISA)?

A

Partial stimulation (agonist) action at the beta adrenergic receptor while blocking endogenous catecholamines from binding to the beta receptor

Less potent than catecholamines and other beta agonists

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78
Q

Concerns with beta antagonists

A

-brandy arrhythmias
-obtunding the cardiovascular response to hypovolemia
-progressive heart block
-HF
-bronchoconstriction

Abrupt d/c can cause rebound HTN and tachycardia

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79
Q

What can happen to the selectivity of a selective beta blocker if dose increases

A

The degree of selectivity is diminished

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80
Q

What is the ratio of beta to alpha block for labetalol

A

7 (beta) : 1 (alpha)

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81
Q

What receptors does labetalol effect

A

Alpha 1
Beta 1 and beta 2

Non selective beta antagonist

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82
Q

Half life and metabolism of labetalol

A

Half life: 6 hrs

Metabolized in liver, eliminated by kidneys

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83
Q

Propranolol’s use as an anti-dysrhythmic is best related to its:

A

Membrane stabilizing ability (MSA)

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84
Q

Administration if a B2 receptor antagonist to a patient with COPD may trigger?

A

Bronchoconstriction

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85
Q

Which beta blocker has intrinsic sympathetic activity (ISA)

A

Labetalol

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86
Q

Which beta receptor antagonist undergoes renal metabolism

A

Atenolol

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87
Q

What’s the most common side effect of prazosin

A

Orthostatic hypotension

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88
Q

Which beta blocker is metabolized by non specific esterases?

A

Esmolol

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89
Q

What substance is a an agonist of acetylcholine

A

Nicotine

Nicotine is a cholinomimetic

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90
Q

What effect does diltiazem have on the AV node?

A

Negative dromotropic

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91
Q

Define dromotrope

A

-A dromotropic agent affects the conduction speed (the magnitude of delay) in the AV node of the heart
-influences the rate of electrical impulse propagation in the heart

Negative- prolongs AV node conduction
Positive- shortens AV node conduction

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92
Q

CCBs produce greater relaxation of ___ vs ____

A

Arterial than venous smooth muscle

Many CCBs induce coronary artery vasodilation and inhibit coronary artery vasospasm

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93
Q

Verapamil and diltiazem are class ____ antiarrhythmics that______

A

Class 4

That depress electrical impulses in the SA and AV nodes

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94
Q

Effects of CCBs on O2 supply and demand

A

Demand:
-decrease after load
-decrease preload
- decrease contractility
-can decrease or increase Hr

Supply:
- increases diastolic perfusion
-decreases vasoconstriction
-decreases arterial spasms

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95
Q

How do CCBs work?

A

Block the biochemical pores preventing the movement of ions across the membrane

Targets L form ca channels

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96
Q

What are CCBs used to treat

A

HTN
Arrhythmias
Peripheral vascular disease
Cerebral vasospam
Angina

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97
Q

Rank the CCBs (highest to lowest) ability to impair contractility

A

Verapamil

Nifedipine (Procardia)

Diltiazem

Nicardipine (Cardene)

Example: In a patient with decreased contractility you would choose Diltiazem over verapamil

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98
Q

Which CCB better control HR?

A

Verapamil and Diltiazem

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99
Q

Which CCB is the only one proven to reduce morbidity and mortality from cerebral vasospasm?

A

Nimodipine

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100
Q

CCBs preserve ____ while reducing ____

A

Preserve preload
Reduce LV after load

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101
Q

Which type of calcium channel do CCBs target

A

L type

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102
Q

Which CCBis often prescribed for Raynaud’s disease?

A

Nifedipine

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103
Q

What drug is a nitric oxide donor with great effect on venules than arterioles

A

Nitroglycerin

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104
Q

Which specific PDE inhibitors prevent platelet aggregation

A

PDE 3 inhibitors

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105
Q

Which specific receptor (subtype) mediates cardiovascular effects of vasopressin?

A

V1 receptor

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106
Q

Which PDE inhibitor is useful in inflammatory states?

A

PDE 4 inhibitors

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107
Q

Which PDE inhibitor selectively increases cGMP

A

PDE 5 inhibitors

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108
Q

The dry cough associated with an ACE-inhibitor is most likely due to

A

Accumulation of bradykinin

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109
Q

What are the best agents to augment the heart rate in a patient after heart transplant?

A

Epinephrine
Isoproterenol

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110
Q

what messenger does beta 1 stimulate

A

cAMP

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111
Q

what is an alpha 2 agonist

A

sympatholytic

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112
Q

what is the MOA of alpha 2 agonists

A

competitively bind to alpha 2 receptors inhibiting the neurotransmitter NE release

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113
Q

what can happen with ending of alpha 2 agonists

A

rebound HTN and tachycardia from increase in sympathetic flow

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114
Q

what are examples of alpha 2 agonists

A

clonidine and dexmetomidine (precedex)

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115
Q

where does dexmetomidine act

A

locus ceruleus

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116
Q

what are the benefits of dexmetomidine

A

blunts sympathetic response
airway reflexes remain unchanged
minimal resp depression
reduction of opioid requirements
use in awake intubations

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117
Q

what are side effects of dexmetomidine

A

bradycardia and hypotension

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118
Q

what can happen with large doses of dexemetodine

A

transient hypertension due to the crossover stimulation of alpha 1

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119
Q

what are withdrawal symptoms of dexmetomidine

A

HTN
tachycardia
anxiety

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120
Q

what is dosing for dexmetomidine

A

IV 0.1-1.5 mcg/kg/min

loading dose 1mcg/kg

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121
Q

where are alpha 2 receptors located

A

pre-synaptic neurons

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122
Q

what is the MOA of alpha antagonists

A

inhibit the effects of catecholamines and sympathomimetics on the heart and vasculature

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123
Q

what are effects of alpha antagonists

A

decreased BP
decreased BPH effects

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124
Q

what are side effects of non selective alpha antagonists

A

reflex tachycardia (baroreceptor mediated from vasodilation)

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125
Q

what medication do we use for pheochromocytoma

A

phenoxybenzamine (labetalol, prazosin)

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126
Q

what are examples of non selective alpha antagonists

A

phentolamine
phenoxybenzamine

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127
Q

what is the onset and half life of phenoxybenzamine

A

onset 1 hr

half life 24 hrs (due to covalent bond)

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128
Q

what happens with hypotensive patients and non selective alpha antagonists

A

vasodilation and more hypotension

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129
Q

what are examples of selective alpha 1 adrenergic antagonists

A

terazosin
prazosin
tamsulosin

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130
Q

what is the alpha 2 selective antagonist

A

yohimbine

used for some htn

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131
Q

what are uses of selective alpha antagonists

A

BPH and HTN

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132
Q

what does happens with beta 1 stimulation

A

increased contraction
increased HR
increased conduction rate through AV node

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133
Q

what are the effects of beta blockers

A

decreased HR
decreased AV conduction
decreased contractility
decreased myocardial oxygen consumption
relaxation of the heart
increased airway resistance

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134
Q

why are beta blockers used in CABG patients

A

decrease incidence of afib

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135
Q

what medication do you NOT use in asthma patients

A

non selective beta blockers (like propanolol)

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136
Q

what beta blocker is highly protein bound

A

propanolol

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137
Q

what are examples of selective beta blockers

A

metoprolol
atenolol
esmolol

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138
Q

what receptors are selective beta blockers selective for

A

beta 1

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139
Q

what kind of beta blockers are better with airway diseases or asthma

A

cardioselective

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140
Q

what is the risk of non selective beta blockers

A

more side effects
risk of bronchospasm

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141
Q

should patients stop beta blockers in periop period

A

no, continue to avoid rebound effect

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142
Q

what kind of beta blocker is best for diabetic patients

A

atenolol

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143
Q

what are anesthesia considerations for Beta antagonists

A

myocardial depression
airway resistance
changes in metabolism
increased extracellular potassium
anesthesia interactions
nervous system effects
fetal bradycardia
hypotension

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144
Q

what are the side effects of beta blockers

A

MYOCARDIAL DEPRESSION
bradycardia
hypotension
cardiogenic shock

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145
Q

how do you treat beta antagonist overdose

A

glucagon and maybe calcium chloride

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146
Q

what are the side effects of beta blockers

A

airway resistance (more likely with propanolol)
masks symptoms of hypoglycemia (tachy, palpitations, tremors anxiety)
increased extracellular K (nonselective)

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147
Q

what kind of beta blockers are not recommended in diabetic patients

A

non selective (propanolol)

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148
Q

how does propanolol effect local anesthetics

A

slows clearance of local amides
decreases pulmonary uptake of fentanyl (2-4x in circulation)

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149
Q

how does timolol interact with inhaled anesthetics

A

profound bradycardia

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150
Q

what beta blocker can cross the BBB and what are the effects

A

propanolol (lipid soluble)

causes lethargy and fatigue

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151
Q

what beta blockers can cross the placenta and what is the effect

A

propanolol and labetalol- cause hypotension and bradycardia

still the first line therapy for acute onset or emergent HTN in pregnancy

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152
Q

what receptors does labetalol work on

A

alpha 1 and non selective beta antagonist

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153
Q

what is the MOA of labetalol

A

alpha 1 blockade: lowers systemic BP by decreasing SVR

beta nonselective blockade: lowers reflex tachycardia by vasodilation

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154
Q

what are the clinical uses of labetalol

A

HTN emergencies
rebound HTN
pheochromocytoma

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155
Q

what are common side effects of labetalol

A

orthostatic hypotension
bronchospasm
CHF
bradycardia
heart block

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156
Q

what are uses of CCBs

A

HTN
cardiac arrhythmias
angina pectoris

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157
Q

what are the pharmacological effects of CCBs

A

decreases HR
decreases myocardial contractility
decreases SA node activity
decreases cardiac conduction through the AV node
decreases systemic BP
relaxes smooth muscle
vasodilation

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158
Q

what are two types of CCBs

A

dihydropyradines
non-dihydropyradines

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159
Q

what do dihydropyradines effect

A

vessels

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160
Q

what are examples of dihydropyradines

A

nifedipine
nicardipine
amlodapine
nimodipine

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161
Q

what do non dihydropyridines effect

A

heart

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162
Q

what are the divisions of non dihydropyridine CCBs

A

phenylalkylamines (verapamil)

benzothiazepines (diltiazem)

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163
Q

what vessels does nimodipine mostly work on

A

cerebral vessels

think arterial vasospasm

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164
Q

what vessels do nifedipine and nicardipine work on

A

arteriolar beds

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165
Q

what is the effect of nifedipine

A

coronary/peripheral arterial vasodilator
no effect on SA/AV
increases in HR from baroreceptors
angina pectoris

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166
Q

what are side effects of nifedipine

A

flushing, vertigo, head ache

may have: peripheral edema, hypotension, paresthesias, skeletal muscle weakness

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167
Q

what happens when you abruptly d/c nifedipine

A

coronary artery vasospasm

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168
Q

where does nimodipine work?

A

cerebral arteries

highly lipid soluble

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169
Q

what are uses for nimodipine

A

cerebral vasospams
cerebral protection after MI

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170
Q

what is contraindication for any BB or CCB

A

heart block

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171
Q

what does verapamil do

A

negative chronotropy on SA
depresses AV
negative inotrope
cardiac muscle vasodilates coronary arteries

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172
Q

what does verapamil treat

A

SVT
angina pectoris
essential HTN
hypertrophic cardiomyopathy

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173
Q

what are side effects of verapamil

A

HF
bradycardia
SA dysfunction
AV block
ventricular dysrhythmias
WPW syndrome

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174
Q

what does diltiazam do

A

blocks ca channels and Na-K pump
inhibits calcium calmodulin binding

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175
Q

what does diltiazem treat

A

SVT and HTN

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176
Q

what is a contraindication for CCBs

A

heart blocks
conduction abnormalities

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177
Q

can you continue CCBs through surgery

A

yes

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178
Q

how can you reverse CCB overdose

A

IV calcium or dopamine

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179
Q

how do CCBs affect NMB

A

increase effects

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180
Q

how do CCBs effect K levels

A

hyperkalemia
especially with K and verapamil

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181
Q

how do CCBs effect platelet function

A

Interfere with platelet functions

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182
Q

how do CCBs effect digoxin

A

increases the plasma concentration

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183
Q

how do CCBs effect H2 antagonists

A

cimetidine and ranitidine increase CCB plasma concentrations

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184
Q

name some other outcomes from CCBs

A

prevent ischemic reperfusion injury
decreased effect of nephrotoxic drugs/contrast media
increases renal blood flow and GFR

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185
Q

what is stage 1 HTN

A

130/80-139/89

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186
Q

what is stage 2 HTN

A

> =140 sys and >= 90 dias

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187
Q

what is the most common type of HTN

A

primary/essential HTN

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188
Q

what are causes of secondary HTN

A

OSA
renal disease
renal artery stenosis
pheochromocytomac
cushings
hyper/hypo thyroid
oral contraceptives
chronis NSAID use
antidepressants
ETOH
aortic coarctacion

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189
Q

what are risks of HTN

A

atherosclerosis
HF
stroke
renal disease
death

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190
Q

what are lifestyle changes for HTN

A

change diet
smoking cessation
weight loss
exercise
lower salt intake
medication

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191
Q

what is initial therapy for essential htn

A

thiazide diuretics then dihydropyridine CCB, ace or arb

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192
Q

should antihypertensive therapy be continued through surgery

A

YES

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193
Q

what are the adrenergic receptors

A

alpha 1 alpha 2 beta 1 beta 2

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194
Q

alpha 1 stimulation causes

A

vasoconstriction
increase in peripheral resistance
increase in BP
mydriasis
increase closure of bladder sphincters

NE>EPI

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195
Q

alpha 2 stimulation causes

A

inhibits norepi release
inhibits Ach release
inhibits insulin release

EPI>NE

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196
Q

beta 1 stimulation causes

A

increased HR
increased lipolysis
increased myocardial contractility
increased renin

EPI= NE

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197
Q

beta 2 stimulation causes

A

vasodilation
decreased peripheral resistance
bronchodilation
increased glycogenolysis (muscle and liver)
increased glucagon release
relaxes uterine smooth muscle

EPI» NE

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198
Q

what are examples of nonselective BB

A

propanolol, carvedilol, labetalol

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199
Q

what is MOA of metoprolol

A

B1 blocker

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200
Q

what is MOA of labetalol

A

A1 B1 and B2 blocker

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201
Q

what is MOA of esmolol

A

B1 blocker

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202
Q

what is class of CCB is nicardipine

A

dihydropyridine CCB

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203
Q

what is mechanism of hydralazine

A

arteriolar dilator

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204
Q

what is mechanism of nitroprusside

A

NO donor

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205
Q

what is mechanism of nitroglycerin

A

NO donor

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206
Q

what receptor do selective BB attach to

A

B1

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207
Q

what is MOA of alpha 1 antagonists

A

lower BP by blocking alpha 1 receptors so they cant constrict

dilate venous and arterial vessels

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208
Q

what is the protype drug for alpha 1 blockers

A

prazosin

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209
Q

what are side effects of alpha 1 antagonists

A

vertigo
fluid retention
orthostatic hypotension

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210
Q

what type of drugs interfere with prazosin anti HTN effects

A

NSAIDS

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211
Q

if a pt is on alpha 1 antagonist what alpha agonist would you use?

A

epi

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212
Q

what anesthesia procedure can cause hypotension when pt is on alpha 1 antagonist

A

spinal/epidural

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213
Q

what receptor does clonidine work on

A

alpha 2 agonist

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214
Q

what are desired effects of clonidine

A

vasodilation
decreased BP
decreased HR
decreased CO

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215
Q

what are side effects of clonidine

A

sedation
dry mouth
skin rashes
impotence
orthostatic hypotension

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216
Q

how do you stop clonidine use

A

gradually decrease over 7 days

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217
Q

what can happen with abrupt d/c of alpha 2 antagonist

A

rebound HTN

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218
Q

advantage of using clonidine and dexmetomidine together

A

induced sedation
decreased anesthetic requirements
improved perioperative hemodynamics

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219
Q

what is the MOA ace inhibitors

A

decreased angiotensin 2 production leading to decreased vasoconstriction

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220
Q

how does angiotensin 2 produce vasoconstriction

A

leads to increased release of Ca from sarcoplastic reticulum to produce vasoconstriction

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221
Q

what is MOA of ARBs

A

block binding of angiotensin 2 to AT1 receptor blocking angiotensin 2 from causing vasoconstriction

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222
Q

what are side effects of ACE inhibitors/ ARBs

A

ACE:
cough
angioedema

BOTH:
congestion
rhinorrhea
allergy like symptoms

223
Q

what is the only IV ACE inhibitor

A

enalaprilat

224
Q

do you continue ace and arbs intraop

A

no

leads to hypotension, D/C 12-24 hours before surgery

225
Q

what dietary constraints do you needs with CCBs

A

none, patients can have Na

226
Q

what is MOA of CCBs

A

block Ca influx through L type Ca channels in vascular smooth muscle

227
Q

what type of CCB is nifedipine

A

dihydropyridine

228
Q

what type of CCB is nicardipine

A

dyhydropyridine

229
Q

what do dihydropyridine CCBs mostly work on

A

vessels (vasodilate)

230
Q

side effects of Dihydropyridines

A

reflex tachycardia
negative inotropy
hypoxemia due to V/Q mismatch (vasodilation)

231
Q

what type of CCB is verapamil

A

non dihydropyridine

232
Q

what type of CCB is diltiazem

A

non dihydropyridine

233
Q

where do non dihydropyridines mostly work

A

heart, antiarrythmic

234
Q

what are nondihydropyridine used for

A

negative chronotropy
negative inotropy
antiarrhythmic

235
Q

what is the MOA of phosphodiesterase inhibitors

A

increase cGMP and cAMP which reduced intracellular Ca which causes smooth muscle relaxation (vasculature, lungs, penis, bowels)

236
Q

what is effect of inhibition of PDE3

A

positive inotropy

237
Q

what are examples of PDE3 inhibitors

A

amirinone
milrinone

238
Q

what are common PDE5 inhibitors

A

sildenfil
tadalafil
vardenafil

239
Q

what are side effects of PDE3 inhibitors

A

head ache
ventricular arrythmias
hypotension

240
Q

what are side effects of PDE5 inhibitors

A

nasal congestion
dyspepsia (indigestion)
flushing
priapism

241
Q

what are PDE5 inhibitors used for

A

ED
pulm HTN

242
Q

what are PDE 3 inhibitors used for

A

MI
intermittent claudication

243
Q

what are PDE4 inhibitors used for

A

asthma
COPD
inflammatory conditions

244
Q

where does nitric oxide cause vasodilation

245
Q

what is nitric oxide used to treat

A

VQ mismatch only approved in peds lung injury

off label:
pulm htn with R heart dysfunction
heart lung transplant

246
Q

why do you d/c NO slowly

A

rebound pulm HTN

247
Q

what is side effect of nitroprusside (SNP) or any nitric oxide

A

methemoglobin
cyanide toxicity
NO release

248
Q

how does SNP effect heart, renal hepatic cerebral pulm and hematological

A

heart: decrease BP, tachycardia, increased contractility, increase CO
renal: decrease function
Hepatic: no changes
cerebral: increased cerebral blood flow, increased ICP
pulm: decreased PaO2
heme: inhibits platelet aggregation

249
Q

what drug causes cyanide toxicity

A

SNP / nitroprusside

250
Q

when do you expect cyanide toxicity in nitroprusside

A

increasing dose, pt no longer responsive to previous dose
PEDs have accelerated toxicity

251
Q

signs and symptoms of cyanide toxicity

A

tachyphylaxis-needing to go up on gtt
metabolic acidosis
increase PvO2
altered mental status
seizures

252
Q

treatment for cyanide toxicity

A

d/c nitroprusside
100% FiO2
-sodium bicarb for acidosis
sodium thiosulfate
hydroxycobalamin (B12a) (red discoloration of skin)
sodium nitrate for severe toxicity

253
Q

where do nitrates work to cause vasodilation

A

large coronary arteries
arterial relaxation

254
Q

examples of nitrates

A

nitroglycerin

255
Q

MOA of nitrates

A

generate NO, stimulate cGMP, vasodilation

256
Q

what do nitrates require to work

A

thio containing compounds

257
Q

when do we use nitrates

A

suspected MI
volume overload HF
HTN
controlled hypotension

258
Q

what does hydralazine do

A

direct arterial vasodilator
afterload reduction

259
Q

side effects of hydralazine

A

SNS stimulation
increased HR and contractility

260
Q

what type on patient is hydralazine not recommended in

A

myocardial ischemia
CAD

261
Q

what condition is hydralazine often used for

A

pregnancy HTN

262
Q

what is onset of hydralazine

263
Q

what can long term use of hydralazine lead to

A

systemic autoimmune disease (lupus)

264
Q

what messenger does beta 1 stimulate

265
Q

where are alpha 1 receptors located

A

blood vessels
bladder (urinary retention)
pupils (dilation)
ejaculation

266
Q

what do alpha 2 receptors do

A

negative feedback for NOREPI release

267
Q

Parasympathetic affects which nerves

A

Cranio sacral

Cranial nerves: 3 7 9 10

Pelvic splanchnic nerve

268
Q

what are epi drip dosing and receptors it stimulates

A

1-4mcg/min stimulates B2

10-20 mcg/min stimulates both alpha and beta ; more alpha than beta

269
Q

how does nifedipine affect SVR and heart rate?

A

decreases SVR and reflex increase in HR

270
Q

when would you use sublingual nifedipine?

A

used to treat intraoperative myocardial ischemia when hemodynamics are normal

271
Q

describe the actions of epinephrine on skeletal muscle blood flow

A

Beta 2 effects of epinephrine increase blood flow to skeletal muscles

272
Q

what happens to CO and SVR with low dose epi? what receptors produce the effects

A

CO increases secondary to stimulation of cardiac Beta 1 receptors which increase HR and myocardial contractility
SVR decreases secondary to stimulation of vascular beta 2 receptors, most in skeletal muscle vasculature

273
Q

what happens to systolic, diastolic, pulse pressure, and MAP with low dose epi?

A

sys increases due to B1 increase in CO
dias decreases due to B2 mediated vasodilation
pulse pressure increases
MAP generally increases, but could decrease or remain unchanged
the change in MAP depends on how much sys increases and diastolic decreases

274
Q

at what concentration of epi will effects of bronchodilation predominate

A

lower doses
(0.25 to 0.50 mcg/min) primarily causes bronchodilation

275
Q

at low dose epi (0.25 to 0.50 mcg/kg) theres bronchodilation, what physiological responses occur as the dose of epi increases

A

epi doses >0.5mcg/kg cause increase in inotropy, chronotropy, and vasoconstriction

as dose increases stroke volume may fall as SVR increases
significant tachycardia, dysrhythmias and myocardial ischemia may limit usefulness of epi

276
Q

what two enzymes metabolize catecholamines in the body? what are these enzymes located and where are the enzymes specifically concentrated?

A

MOA and COMT

MOA concentrated in the mitochondria of presynaptic nerve terminal along with COMT found in the blood, liver and kidneys

COMT found in post synaptic nerves and in high concentration in the liver

277
Q

by what mechanism does cocaine alter sympathetic function

A

cocaine blocks reuptake of norepinephrine

278
Q

what is the drug of choice for treating the hypotensive cocaine addict? what drugs for be avoided and why?

A

direct acting agents are most effective

avoid indirect acting agents such as ephedrine

cocaine inhibits the reuptake of epinephrine and norepi thereby potentiating responses to exogenous/endogenous released catecholamines, result may be remarked pressor response.

279
Q

Inotrope

A

Force of contraction

280
Q

Chronotrope

A

Heart rate

281
Q

Dromotrope

A

Conduction velocity through AV node

282
Q

Give dopamine doses and the receptors that are activated at each

A

1-4 mcg/kg/min dopamine receptors

5-10mcg/kg/min beta receptors (elicits release of norepi via B1 stimulation)

11-20mcg/kg/min alpha receptors

283
Q

Why is dopamine not used in gram negative sepsis?

A

Because sensitivity of beta receptors is diminished due to down regulation

284
Q

How does dopamine affect aldosterone

A

Inhibits aldosterone causing increase in sodium excretion and urine output

285
Q

What enzyme metabolizes dopamine

A

MAO and COMT

caution pts with MAOI can have prolonged effects of dopamine

286
Q

How do antidepressants effect sympathomimetics

A

MAOI can prolong effects

Tricyclic can augment the effects

287
Q

What is Isoproterenol mostly used for

A

Treatment of bradycardia with heart block

Torsades de pointes

Chronotropic support after heart transplant

288
Q

What are three factors that limit the use of Isoproterenol

A

Excessive tachycardia
Induction of myocardial ischemia
Arrhythmias

289
Q

Why is dobutamine used in cardiogenic and septic shock

A

Positive inotrope with lack of chronotropy and maintenance of normal BP (nahelhout 180)

290
Q

Where is vasopressin stored and released from

A

Stored in Posterior pituitary gland
Released from neurons of the hypothalamus

291
Q

What’s the function of vasopressin

A

Controls osmoregulation- release is stimulated by increased osmolality and hypovolemia

292
Q

Vasopressin selectively dilates 3 things?

A

Renal afferent arterioles
Pulmonary arterioles
Cerebral arterioles

293
Q

Why do we use phenylephrine over ephedrine in pregnant patients?

A

Ephedrine produces increases in fetal metabolic rate leading to fetal acidosis due to beta stimulation

294
Q

What drug is used in pts with pheochromocytoma to decrease the response to endogenous catecholamines?

A

Phenoxybenzamine

Start 1-3 weeks before surgery

295
Q

Phenylephrine stimulates what receptors? Describe the cardiovascular action of phenylephrine

A

Activates alpha 1 and alpha 2
Greater venoconstriction than arterial constriction
Elevates BP by increasing SVR and increased venous return with reflex decrease in Hr and CO

296
Q

What is the important clinical response to blockade of the autonomic ganglia? What division of the ANS mediates this?

A

Hypotension secondary primarily to venodilation but also some arterial dilation

Response occurs because transmission of sympathetic impulses is blocked

297
Q

Norepinephrine stimulates what adrenergic receptors?

A

Alpha 1 alpha 2 and beta 1 with little effect on beta 2

298
Q

What adrenergic receptors are stimulated by epinephrine?

A

Alpha 1, 2 Beta 1,2

299
Q

Which adrenergic receptors, alpha or beta, are most sensitive to epi?

A

Beta

Think low dose epi stimulates beta receptors

300
Q

How does Epi increase Bp?

A

-venoconstriction and increased venous return
-arterial constriction and increased SVR
- increased myocardial contractility

301
Q

What are the side effects of phenylephrine

A

-reflex bradycardia
-decreased CO
-increased myocardial oxygen requirements

302
Q

What is the rationale for giving phenylephrine to the patient who becomes hypotension and shows sign of myocardial ischemia?

A

It will increase coronary perfusion by increasing arterial Bp

303
Q

Ephedrine stimulates what adrenergic receptors? are the effects direct, indirect or both?

A

Ephedrine stimulates indirectly and directly alpha 1 and 2, beta 1, 2

It triggers the release of norepinephrine from nerve terminals producing indirect effects, also directly stimulates adrenergic receptors

304
Q

Describe cardiovascular actions if ephedrine

A

Produces venoconstriction greater than arterial construction which leads to improved venous return and CO.

Beta stimulation increases Hr and CO

Alpha and beta effects result in modest and predictable increases in BP

Ephedrine is “weak” epi

305
Q

What is the clinical use of ephedrine? What are side effects?

A

Used to treat hypotension (5-10mg IV)

Tachycardia and cardiac dysrhythmias possible

306
Q

What is a proposed mechanism for the tachyphylaxis associated with the use of an indirect acting sympathomimetic?

A

It may develop because of depletion of norepinephrine from sympathetic post ganglionic nerve terminals

307
Q

What receptors are stimulated by dobutamine?

A

Predominantly beta 1 but some beta 2 and alpha receptors

Increases contractility more than increase Hr

308
Q

Dobutamine affects the cardiovascular system in what ways?

A

Increases CO by improving stroke volume with minimal increases in Hr and BP and only small decreases in SVR

309
Q

Drugs that stimulate what receptors have both positive inotropic and positive chronotropic properties?

A

B1 stimulation have both positive inotropic and positive chronotropic

310
Q

Isoproterenol stimulates what receptors and what are 3 cardiovascular actions of it?

A

Stimulates B1 and B2

Increases CO by enhancing HR and myocardial contractility (B1 effect)

Increases conduction through AV node (B1 effect)

Reduces SVR and after load by dilating skeletal muscle blood vessels (B2 effect)

311
Q

What may be the most important clinical use of Isoproterenol

A

Used temporarily as a chemical pacemaker in complete heart block

312
Q

What is the most frequent cause of death from digitalis toxicity

313
Q

What herbs increase bleeding tendencies

A

Garlic
Ginger
Ginkgo biloba
Ginseng

314
Q

Herbs that reduce MAC (have increased GABA effect)

A

Kava kava
Valerian

315
Q

What are some complications of ephedra containing compounds?

A

-SNS effects
-Catecholamine depletion
-Increased risk of serotonin syndrome when given with MAOIs

316
Q

what are side effects of isoproterenol

A

-increase myocardial O2 consumption
-may descrease myocardial O2 delivery due to decreased coronary artery blood flow

317
Q

what is the most common uses of dopamine?

A

positive inotrope effect in pts with poor cardiac contractility

318
Q

where in the CV system are B2 receptors predominantly located? what happens when these are stimulated?

A

-primarily found in the smooth muscle of the vasculature of skeletal muscles
-stimulating in vascular walls causes vasodilation
-SVR decreases when B2 stimulated

319
Q

at what dopamine dose do you see effects on the dopamine receptor, beta receptor and alpha receptor

A

dopamine 0.5-3 mcg/kg/min *promotes renal vasodilation
beta 3-10 mcg/kg/min
alpha >10 mcg/kg/min

320
Q

what is a sympatholetic?

A

blocks the outflow of sympathetic impulses from the CNS or inhibits release of NOREPI from peripheral sympathetic post ganglionic nerve terminals

321
Q

what are two major CV actions of competitive alpha adrenergic antagonists

A

-decrease bp secondary to vasodilation
- reflex tachycardia

322
Q

what receptors are inhibited by phentolamine

A

nonselective antagonist of alpha 1 and alpha 2 receptors

323
Q

what is the major pharmacologic action of phentolamine?

A

-produces peripheral vasodilation which decrease BP

324
Q

how does phentolamine produce tachycardia

A

reflects release of norepi from sympathetic post ganglionic nerve terminals owing to alpha 2 blockade

325
Q

how does alpha 2 blockade of sympathetic nerve terminals by an alpha adrenergic antagonist alter release of norepi?

A

presynaptic blockade of alpha 2 adrenergic receptors increases the release of norepi

326
Q

what kind of drug is prazosin and phenoxybenzamine and how is it used in anesthesia

A

phenoxybenzamine- long acting alpha adrenergic antagonist (1 and 2)
prazosin- selective alpha 1 antagonist
-used to control bp to remove pheochromocytoma

327
Q

what are 5 side effects of beta blockers

A
  • heart block
    -worsening heart failure
    -bronchospasm
    -coronary artery constriction
    -hypoglycemia
328
Q

signs and symptoms of beta receptor antagonist overdose

A

hypotension
bradycardia
prolonged AV conduction times
wide QRS
seizures
depression
hypoglycemia
bronchospasm

329
Q

what is the treatment of adrenergic antagonist overdose

A

epinephrine
glucagon

330
Q

how does propanolol decrease myocardial O2 consumption?

A

-decreasing HR and myocardial contractility

331
Q

what is the purpose of giving beta blocker to angina patients

A

prevents increase in HR which keeps O2 requirements reduced and prevents angina

332
Q

what are 3 manifestations of abrupt beta blocker withdrawal

A

tachycardia
hypertension
angina

333
Q

why do tachycardia and HTN develop after abrupt beta blocker withdrawal

A

beta receptors are upregulated as a result of chronic BB use, they are highly sensitive to catecholamines

334
Q

how is esmolol eliminated and what is the primary use?

A
  • metabolized by plasma esterases
    -used for rapid and short term reductions in HR and BP
335
Q

6 contraindications/ cautions for esmolol

A

-sinus bradycardia
-AV heart blocks
-COPD
-hypotensive
-cardiogenic shock
-heart failure

336
Q

anesthesia considerations for pt with cocaine abuse

A

-paranoid delusions preop
-hypertensive
-labile BP
-difficult vascular access
-depression following withdrawal
-acute toxicity seizures vfib and sudden death

337
Q

what are two alpha 2 agonists

A

clonidine
dexmetomidine

338
Q

where does alpha 2 agonist work to produce their therapeutic effect

A

stimulation of alpha 2 receptors of inhibitory neurons in the vasomotor center of the medulla in the brain stem inhibits SNS outflow, this decreases BP

339
Q

how do alpha 2 agonists antagonist the SNS

A

-alpha 2 receptors found peripherally in the surface membrane of the norepi containing presynaptic nerve terminals,
-stimulation of these receptors decrease the release of norepi,
-decreased release of norepi contributes modestly to clonidine decrease in BP

340
Q

6 clinical uses of clonidine

A
  • preanesthetic med
    -prolong effects of regional anesthesia
    -diagnose pheochromocytoma
    -treat opioid withdrawal
    -treat shivering
    -protect against perioperative myocardial ischemia
341
Q

how much does pretreatment of clonidine decrease MAC

A

decreases MAC of inhalation agents by up to 50%

342
Q

3 common side effects of clonidine

A

-sedation
-bradycardia
-dry mouth

dont d/c abruptly bc rebound hypertension may occur 8-36 hrs after last dose

343
Q

how should life threatening hypertension from clonidine withdrawal be treated

A

-reinstituting clonidine therapy
-administering vasodilating drugs (hydralazine or nitroprusside)

344
Q

should beta blockers be given during clonidine withdrawal

A

no, may exaggerate the magnitude of rebound HTN by blocking B2 vasodilating effects of catecholamines, can also cause HF

345
Q

what drugs can cause exaggerated rebound HTN of clonidine withdrawal

A

BB
trycyclic antidepressants

346
Q

anesthesia consideration for chronic clonidine therapy

A

clonidine likely to promote perioperative hypotehermia
clonidine and precedex alter central thermoregulation control

347
Q

name 3 vasodilators that decrease BP by direct effects on vascular smooth muscle independent of alpha or beta receptors?

A

hydralazine
nitroprusside
nitroglycerin

348
Q

how do nitrovasodilators relax smooth muscle? what substance produced? what enzyme and second messenger are involved?

A

-nitroprusside and nitroglycerin donate NO
-NO activates the enzyme soluble guanylate cyclase which increases cGMP
-cGMP (second messenger) relaxes vascular smooth muscle, promoting vasodilation and deccreasing BP

349
Q

how does nitroprusside work to decrease BP

A

decreases both preload and SVR
both lower arterial blood pressure

350
Q

what is the acceptable dose range for nitroprusside?

A

0.3-10mcg/kg/min

351
Q

what are three ways Cyanide ions can react

A

1) binding to methemoglobin to for cyanomethemoglobin
2) reaction with thiosulfate in the liver to produce thiocyanide, catalyzed by rhodanese
3) binding to tissue cytochrome oxidase which interferes with normal O2 utilization by the tissues (prevents the formation of ATP)

352
Q

4 hallmark signs of cyanide toxicity

A
  • metabolic acidosis (base deficit)
    -cardiac arrhythmias
    -increased venous oxygen content due to inhibition of cytochrome oxidase and cells ability to use O2
    -tachyphylaxis (having to titrate your drip up)
353
Q

how do you know when tachyphylaxis of nitroprusside has occured?

A

if patient is resistant to titrate drip up to 10mcg/kg/min for no longer than 10 min

354
Q

if tachyphylaxis occurs with nitroprusside, after dc drip how do you treat cyanide toxicity?

A

-100% fiO2
1 amp sodium bicarb
give sodium thiosulfate

sodium thiosulfate acts as a sulfur donor and converts cyanide to thiocynate

355
Q

what else can be given to treat cyanide toxicity?

A

b12- binds to cyanide to form cyanocobalamin
sodium nitrate- converts hemoglobin to methemoglobin which acts as an antidote by converting cyanide to cyanomethemoglobin

356
Q

where is nitroglycerins site of action?

A

acts primarily on venules, which decreases venous return due to venodilation

357
Q

what is the cardiac benefit for nitroglycerin in treatment of myocardial ischemia?

A

-reduces myocardial workload decreasing myocardial O2 consumption
-decreases preload, decreases stroke volume, decreases CO to lower BP

358
Q

how does hydralazine lower BP

A

its a direct relaxant on vascular smooth muscle
-works by hyperpolarizing smooth muscle and direct activation of guanylyl cyclase to produce vasodilation

*dilation greater in arterioles than veins**

359
Q

what can occur in 10-20% of pts treated chronically with hydralazine

A

systemic lupus erythematosus

360
Q

how can hydralazine cause angina

A

causes barorecptor reflex increase HR, contractility and CO in response to the lowering of BP; increased myocardial O2 consuption can cause angina

361
Q

how can nitroprusside cause angina?

A

coronary steal can occur
-its the appearance of ischemic changes on the ECG, decreases in DBP and coronary blood flow produced by nitroprusside can contribute to myocardial ischemia

362
Q

what are class I anti arrhythmic drugs and their subclasses

A

class I- membrane stabilizers that work by inhibiting fast sodium channels; block sodium channels
ClassIA: quinidine and procainamide
Class IB: lidocaine, tocainide, phenytoin
ClassIC: flecainide and propafenone

363
Q

class I antidysrhythmics used to treat what 3 conditions?

A

acute and chronic SVT dysrhythmias
slow atrial rate in atrial fib
suppress tachydysrhytmias associated with WPW

364
Q

what are class II antidysrhythmics and what do they do

A

-they are beta adrenergic antagonists
-they depress automaticity (decrease HR by decreasing spontanous phase 4 depolarization in nodal tissues) and decrease conduction speed of cardiac impulses

365
Q

class III antidysrhythmics and what they do?

A

-they prolong repolarization by blocking voltage gated potassium channels
ex: amiodarone and sotalol
-prolong the effective refractory period in the SA and AV node, atria, ventricles, and His-Purkinje fibers

366
Q

what are class IV antidysrhythmics and what are they used to treat?

A

-slow calcium channel blockers
-ex: verapamil diltiazem
-used to treat paroxysmal surpaventricular tachydysrhythmias and control ventricular rates in pts with afib/aflutter

367
Q

List 3 general locations of alpha 2 adrenergic receptors in the body

A

Presynaptic
Postsynaptic
Nonsynaptic

368
Q

Alpha 2 receptor stimulation on platelets causes

A

Increased platelet aggregation

369
Q

What effects are produced by alpha 2 stimulation of the locus coeruleus

A

Sedation and hypnosis

370
Q

Rapid administration of dexmedetomidine can stimulate peripheral postsynaptic alpha 2 receptors in the circulation leading to

A

Vasoconstriction and hypertension

371
Q

What beta blockers have membrane stabilizing activity?

A

Propranolol
Carvedilol

372
Q

What beta blocker has intrinsic sympathomimetic activity

A

Carvedilol
Labetalol

373
Q

What is intrinsic sympathomimetic activity (ISA)

A

A beta blocker with ISA exerts a partial stimulating agonist action at the beta receptor while at the same time blocking endogenous catecholamines from binding to the receptor

374
Q

What is membrane stabilizing activity (MSA)

A

The inhibition or abolition of action potential propagation across the cell membrane

BB with MSA act as antiarrhythmics

375
Q

Esmolol IV and infusion dose

A

IV 10-80mg

Infusion 50-300mcg/kg/min

376
Q

Metoprolol IV and max dose

A

IV 2.5-5mg

Max dose 15mg

377
Q

phenylephrine bolus and infusion dose

A

IV bolus 40-100 mcg

infusion 0.15-0.75mcg/kg/min

378
Q

dexmedetomidine iv bolus dose and infusion dose

A

IV bolus 1mcg/kg

infusion 0.2-0.8 mcg/kg/hr

379
Q

Blood pressure goals in anesthesia

A

-within 20% of patients baseline
-map>65 systolic >100

380
Q

Which calcium channel blocker does NOT produce negative chronotropic and inotropic effects

A

Clevidipine

381
Q

What class is phenoxybenzamine and what is it used for

A

Non selective noncompetitive alpha antagonist

Used almost exclusively in the preoperative management of pheochromocytom to normalize bp and prevent episodic HTN

382
Q

what tissues does lidocaine work on the heart

A

-delays the rate of spontaneous stage 4 depolarization of ventricular cardiac cells and the His-Purkinje system by preventing or diminishing the gradual decrease in potassium ion permeability during this phase

383
Q

which antidysrhythmic is drug of choice for treatment of ventricular dysrhythmias?

A

lidocaine

valley memory master

384
Q

verapamil and diltiazem slow heart rate by working on what phase in the sino atrial action potential

A

slowing phase 4 depolarization of the sinoatrial node action potential

385
Q

name 5 drugs or treatments for cardiac dysrhythmias due to digoxin toxicity

A

-lidocaine
-atropine
-phenytoin
-propanolol
-pacemaker for complete heart block

386
Q

what antidysrhythmic drugs are not local anesthetics but have local anesthetic activity

A

class I drugs produce sodium channel blockade

386
Q

what 4 drugs should be avoided in a patient being treated with digitalis

A

-any drug that decreases serum K
-oral antiacids and digoxin increase cardiac glycosides
-beta adrenergic agonists- may increase cardiac dysrhythmias
-IV calcium which may precipitate cardiac dysrhythmias

386
Q

what two drugs are used to treat heart block

A

atropine or isoproterenol

387
Q

how does adenosine work

A

blocks conduction of impulses through the AV node by hyperpolarizing the AV nodal cells.
-hyperpolarization occurs because adenosine binds to A1 purinergic receptors which then open potassium channels in these cells and increases the efflux of K from nodal cells, this decreases excitability

388
Q

what is the metabolism and elimination of adenosine

A

rapidly eliminated by enzymatic clearance (less than 1 min) or via the RBCs and vascular endothelial cells

389
Q

what are ways afib can be treated in anesthesia if required

A

-if patient stable- amiodarone, beta blockers (propanolol) digitalis
-if pt unstable- synchronized cardioversion withcalcium channel blockers, beta blockers

390
Q

what are the cardiovascular actions of glucagon

A

it increases myocardial contractility (has positive inotrope effect) and heart rate which increases CO

391
Q

glucagon MOA

A

binds to glucagon receptors which promotes the formation of cAMP

392
Q

name 5 situations glucagon might be beneficial hemodynamically

A

-low CO following cardiopulmonary bypass
-low CO with MI
-chronic congestive HF
-anaphylactic shock with refractory hypotension
-excessive adrenergic blockade

393
Q

3 cardiac effects of digitalis

A

-enhances myocardial contraction
-decreases heart rate
-slows impulse propagation through the AV node

394
Q

what are two uses of digoxin

A

-treat CHF
-control supraventricular dysrhythmias

395
Q

how does digitalis produce positive inotrope effect

A

it inhibits the sodium potassium pump

when Na-K pump inhibited Na accumulates in the cell which inhibits the sodium calcium exchange system. Ca accumulates in cardiac cell so contractility increases

396
Q

what phase in cardiac cycle does digitalis work

A

phase 4
-decreases automaticity and lowers HR

397
Q

what 3 electrolyte disturbances enhance digitalis toxicity

A

-hypokalemia
-hypercalcemia
-hypomagnesia

398
Q

why does hypokalemia enhance digitalis toxicity

A

it allows increased binding of digitalis to Na-K ATPase pump in cardiac cells resulting in excessive drug effect

399
Q

why should hyperventilation be avoided during anesthesia for the pt taking digitalis

A

hyperventilation causes hypokalemia which causes increase risk of digitalis toxicity

400
Q

what are 5 uses of calcium channel blockers

A

-treat supraventricular tachy dysrhytmias
-treat essential HTN
-treat coronary vasospasm
-treat angina
-treat cerebral vasospasm

401
Q

how does verapamil effect SVR and HR

A

decreases both SVR by relaxing vascular smooth muscle and HR

402
Q

what actions does verapamil potentiate in anesthesia drugs

A

potentiates the actions of nondepolarizing and depolarizing muscle relaxants

403
Q

what 4 patient groups is verapamil contraindicated

A

-wolff parkinson white syndrome
-sick sinus syndrome
-AV block
-heart failure

404
Q

why is verapamil a poor drug choice for patient with WPW

A

it may increase conduction velocity in the accessory tract and increase HR excessively

405
Q

what drugs partially reverse CCB overdose

A

IV calcium and dopamine

406
Q

What are some examples of alternative medicine

A

Acupuncture
Massage therapy
Meditation
Aromatherapy
Relaxation therapy
Reflexology
Float pool
Herbal medicines

407
Q

What is the current federal organization that does research on herbal medication

A

National Center for Complimentary and Integrative Health

408
Q

What are two ASA recommendations for all herbal meds

A

-d/c two weeks before surgery
-all anesthesia providers should be aware of herbal medications and potential perioperative interactions

409
Q

Anesthesia implications for herbal meds

A

-direct and indirect health effects
-intrinsic pharmacological effects
-pharmacodynamic interactions
1. Alteration of drug receptors
2. Pharmacokinetic interactions altering absorption/metabolism/elimination of anesthetic meds
-more meds=more potential drug interactions

410
Q

What are direct health effects of herbal meds

A

-direct impact on physiology
-drug-herbal interaction
-allergic reactions
-hypertension (ephedra)
-coagulopathy (ginkgo)

411
Q

What 11 supplements have anesthesia implications

A

-Dong Quai
-Echinacea
-Ephedra
-feverfew
-garlic
-ginger
-ginkgo biloba
-ginseng
-kava
-papain
-saw palmetto
-st johns wort
-valerian

412
Q

what direct effect does ephedra have on pt health

413
Q

what direct health effect does ginkgo biloba have

A

coagulopathy

414
Q

what if the effect of herbal meds on CYP450

A

can inhibit or induce leading to alerted metabolism

415
Q

what is dong quai used for

A

migraines
anemia
HTN
menstrual cramps
menopausal symptoms

416
Q

what drug is dong quai related to

A

coumadin derivative

417
Q

what is echinachea used for

A

viral bacterial and fungal URI
chronic wounds
arthritis
decrease effects of chemo

418
Q

what does echinachea stimulate

A

macrophages
NK cells

419
Q

adverse effects of echinachea

A

GI upset
headache
dizziness
unpleasant taste

REJECT RENAL TRANSPLANT
INHIBITS CYP450
antagonizes immunosuppressants
>8wks causes immunosuppression

420
Q

what is ephedra used for

A

weight loss
energy
bronchodilator
URI
asthma
bronchitis
aphrodisiac

421
Q

what are active metabolites of ephedra

A

ephedrine
psuedoephedrine
methylephedrine
norepinephrine

422
Q

what does prolonged use of ephedra lead to

A

catecholamine depletion
hemodynamic instability
tachyphylaxis

423
Q

adverse effects of ephedra

A

palpitations
htn
tachycardia
hyperthermia
seizures
STROKE and MI
cardiomyopathy
severe vasoconstriction
cerebral&coronary artery vasospasm
myocardial hypersensitivity

424
Q

effects of MAOI and ephedra

A

hyperpyrexia
HTN
coma

425
Q

what is feverfew used for

A

migraines
fever
menstrual irregularities

426
Q

what is feverfew contraindicated in

A

allergies to chamomile ragweed and yarrow
warfarin use (increased inhibition of platelet activity)

427
Q

what is ginger used for

A

nausea and vomiting
motion sickness
anti-inflammatory ( arthritis)

428
Q

side effects of ginger

A

inhibits platelet aggregation (bleeding)
arrhythmias
cns depression
potentiation of CCBs

429
Q

what is garlic used for

A

infection
tumor
DM
HTN
HLD
atheroschlerosis

430
Q

what does garlic inhibit

A

biosynthesis of cholestrol

431
Q

what are adverse affects of garlic

A

nausea
hypotension
allergy
bleeding
decreased blood sugar

432
Q

what drugs does garlic interact with

A

anticoags like coumadin, ASA and NSAIDS

433
Q

what is ginseng used for

A

stimulant
tonic
diuretic
immunomodulation
mood elevation
hypoglycemia
may lower cholesterol
increased stress tolerance
increased vitality

434
Q

what drugs interact with ginseng

A

phenelzine (nardil)
warfarin
heparin
ASA
NSAIDs
caffeine

435
Q

what conditions are contraindicated for ginseng

A

bipolar
psychosis
cardiac disease
HTN
caffeine use
stimulant use

436
Q

what is gingko biloba used for

A

Alzheimer disease
dementia
memory loss
vasodilator
decreases fibrinogen
inhibits platelet aggregation
bronchodilator
increased coronary blood flow
increased cardiac contractility

437
Q

how does ginkgo biloba improve vascular conditions

A

vasodilation
decreased viscosity

438
Q

what are adverse effects of ginkgo biloba

A

gi upset
headache
bleeding

439
Q

what are drug interactions with ginkgo biloba

A

anticoagulants
NSAIDs
ASA
warfarin
heparin

440
Q

what is kava kava used for

A

anxiety
sedative
sleep enhancer
anticonvulsant
central muscle relaxant

441
Q

how does kava kava effect anesthesia

A

increased anesthetic dose with long term

442
Q

how does kava kava affect sodium/calcium channels

A

inhibits them
leading to a decrease in SVR

443
Q

what are adverse effects of kava

A

increased effects of ETOH, barbituates/benzo pyschopharmacologics
prolongs anesthetics

444
Q

what is papain used for

A

treat dyspepsia
inflammatory disorders
hemorrhoids
intestinal worms
diarrhea
tumors
resp infections

topical for psoriasis, ringworm, wounds, ulcers and infections

445
Q

what drug is papain contraindicated for concurrent use with

446
Q

what is saw palmetto used for

A

BPH
diuretic
urinary antiseptic

447
Q

what is an adverse effect of saw palmetto

A

potentiation of barbituates

448
Q

what is st johns wort used for

A

anxiety and depression

449
Q

what are adverse effects of st johns wort

A

GI upset
fatigue
dizziness
confusion
headache
photosensitivity

450
Q

what can st johns wort interact with

A

tricyclic antidepressants
MAOIs
digoxin

451
Q

how does st johns wort affect metabolism

A

induces CYP450 which decreases coumadin effectiveness
delays emergence from anesthesia

452
Q

what does valerian root treat

A

anxiety
restlessness
sleep aid

453
Q

what drug is in almost all herbal sleep aids

A

valerian root

454
Q

what are adverse effects of valerian root

A

stomach upset
tremor
headache
cardiac disturbances
PROLONGED ANESTHESIA EMERGENCE

455
Q

how does curcumin longa (tumeric) effect metabolism

A

inhibits CYP450 decreasing metabolism

456
Q

how does tumeric effect antacids

A

interferes with action by increasing stomach acid

457
Q

what is garcinia cambogia used for

A

weight loss
DM
HLD

458
Q

how does garcinia combogia effect metabolism

A

induces CYP450 increasing metabolism

459
Q

what herbal drugs delay emergence from anesthesia

A

valerian root
ginger
st johns wort
saw palmetto
kava kava

460
Q

what herbal drugs increase bleeding

A

dong quai
feverfew
ginger
garlic
echinachea
ginkgo biloba
tumeric
saw palmetto
ginseng
papain
valerian root
kava kava

461
Q

what herbal drugs have CV effects

A

ephedra
ginkgo biloba
ginger
kava kava
garcinia cambogia

462
Q

atropine - plant derived and use

A

atropa belladona

anticholinergic

463
Q

curare- plant derived and use

A

chondrodendon tomentosum

neuromuscular blockers

464
Q

digoxin- plant and use

A

foxglove

anti arrhythmic

465
Q

ephedrine- plant and use

A

ephedra sinica

CNS stimulant

466
Q

morphine plant and use

A

poppy

analgesic

467
Q

scopolamine- plant and use

A

datura metel

anti-emetic

468
Q

caffeine- plant and use

A

camelia sinesis

CNS stimulant
bronchodilator

469
Q

cocaine- plant and use

A

erythoxylon coca

local anesthetic

470
Q

what herbal drugs induce CYP450

A

st johns wort
garcinia cambogia
Garlic in some isoforms
Ginseng

471
Q

What neurotransmitters can increase neuronal excitability and seizure activity

A

Glutamate
Aspartate

472
Q

How do we think anti-epileptics work?

A

By decreasing neuronal excitability or enhancing the inhibition of neurotransmitters

  1. Altering electrical activity in the neurons by affecting ion currents like (Na, K, and Ca) in the cell membrane
  2. Altering chemical activity of neurotransmitters like GABA in synapse
473
Q

Carbamazepine (Tegretol) MOA and effective uses

A

MOA: sodium ion channel blockage

Effective uses:
-convulsive and nonconvulsive seizures
-trigeminal and glossopharyngeal neuralgia

474
Q

Anesthesia specific considerations for carbamazepine

A

-hepatic enzyme inducer-accelerates the metabolism of lipid soluble drugs (ex: higher doses of prop needed

-creates resistance to NDMB/may need higher doses roc/vec

-plasma protein bound medication- pts with altered protein states/albumin like liver failure and malnutrition

475
Q

Most Side effects of neuropsych drugs

A

Sedation
Vertigo/dizziness
Diplopia
Hyponatremia/electrolyte imbalance
GI disturbances
Headache
Ataxia
Weakness

476
Q

MOA of phenytoin

A

Blocks voltage gated Na channels (membrane stabilization)

477
Q

MOA of carbamazepine

A

Blocks voltage gated Na channels (membrane stabilization)

478
Q

MOA of gabapentin

A

Inhibits the alpha 2 delta subunit of voltage gates Ca channels in the CNS

479
Q

6 side effects of phenytoin

A

Dysrhythmias
Gingival hyperplasia
Aplastic anemia
Cerebral vestibular dysfunction
Steven Johnson syndrome
Birth defects

480
Q

Do gabapentinoids produce respiratory depression

A

They can exacerbate respiratory depression when combined with an opioid

481
Q

Which anticonvulsants do not induce hepatic enzymes?

A

Gabapentinoids

482
Q

What effect does Diltiazem have on the heart?

A

Negative dromotrope

Prolongs AV node conduction

Used to treat afib a flutter and supraventricular tachycadia

Is a negative chronotrope at SA node and negative inotrope in cardiac muscle

483
Q

which group of drugs interfere with the metabolism of adrenergic neurotransmitters?

A

MAOI bind to and inhibit monoamine oxidase

the result is an increase in the levels of adrenergic neurotransmitters in brain, heart, intestines and plasma

484
Q

name 4 non selective MOAI

A

isocarboxazid
phenelzine
moclobemide
selegiline

485
Q

what drugs are prohibited in pt taking MAOI

A

tricyclic antidepressants
opioids (especially meridipine)
indirect acting sympathomimetics (ephedrine)
fluoxetine
ketamine
nasal decongestants
epi in local anesthetics

all these can cause severe HTN, CNS excitation, seizures and death

486
Q

what effect does st johns wort have on the liver?

A

induces cyp450, doubling its activity

487
Q

what are two perioperative drugs levels may be altered in patient taking st johns wort

A

warfarin
NSAIDs

488
Q

why do you want to check lithium levels in a patient

A

toxic levels >1.5mEq/L

check sodium levels before surgery because they could be decreased and avoid diuresis in these patients

489
Q

what are three major mechanisms that cause arrythmias

A

enhanced automaticity
re entry
triggered

490
Q

explain enhanced automaticity

A

when any cell outside of the SA node (includes AV node/purkinje fibers) become more excitable and generates an action potential at a rate faster than our normal cardiac pacemaker cells

could be due to increased sympathetic tone or abnormal electrolyte concentrations

491
Q

explain re-entry arrythmias

A

the cardiac arrhythmia occurs in the presence of a re entry circuit in the heart; the electrical signal follows a circular pathway repeatedly which perpetuates abnormal rhythms

492
Q

key factors of re-entry arrhythmias

A

-loop/circuit of electrical activity
-unidirectional blocks
-presence/risk of abnormal conduction pathways

examples of these are aflutter, AV re-entry tachycardia, AV nodal re-entry tachycardias, vtach, WPW

493
Q

explain triggered arrhythmias

A

we trigger or an outside triggers an arrhythmia

ex: inhaled anesthetics, IV meds, reaction to meds related to anaphylaxis

494
Q

what are the most common causes of arrhythmias in anesthesia

A

-hypoxemia
-certain drugs
-bradycardia
-altered sympathetic nervous system activity
-myocardial ischemia
-acid/base abnormalities
-electrolyte imbalances

495
Q

MOA of class 1 antiarrhythmics and examples

A

sodium channel blockers
MOA: blocks Na channels in the cardiac cell membrane inhibiting the influx of Na ions during the depolarization phase of an action potential

ex: procainimide (class 1A) moderate Na and K channel blockade
Lidocaine (1B) weak Na channel blockade
flecainimide (1C)- marked Na channel blockade but minimal effect on repolarization

used to treat ventricular arrhythmias and atrial arrhythmias

496
Q

MOA of Class 2 antiarrhythmics and examples

A

beta blockers

MOA: block adrenergic receptors which leads to decrease in effects of sympathetic stimulation; blocks effects of catecholamines norepi/epi

Ex: metoprolol and esmolol (decreases rate of depolarization)

used to reduced HR and treat atrial and ventricular arrhythmias

497
Q

MOA of class 3 antiarrhythmics and examples

A

potassium channel blockers

MOA: work by blocking K channels prolonging the action potential of the duration of the refractory period;

ex: amiodarone

used to treat atrial and ventricular arrhythmias, used when other classes not effective

498
Q

MOA of class 4 antiarrhytmics and examples

A

calcium channel blockers

MOA: inhibits slow calcium channels (L type); blocks ca channels, reduces influx of Ca ions during the depolarization phase of an action potential

ex:
class A: effects atrial tissue- Verapamil
class B: effects ventricular tissue- diltiazem

used to treat supraventricular arrhythmias, afib and aflutter

499
Q

what phase does sodium channel blockers (class 1) work on

A

atrial/ventricular phase 0 ( depolarization)

slow conduction and suppress maximum upstroke velocity of cardiac action potential

500
Q

what phase does beta blockers (class 2) work on

A

phase 4 SA/AV node

501
Q

what phase does potassium channel blockers (class 3) work on

A

myocyte and SA/AV node phase 3 (repolarization)

prolong repolarization by increasing duration of cardiac action potential and refractory period; prolongs QT

502
Q

what phase does calcium channel blockers (class 4) work on

A

phase 0 and 4 of SA/AV

503
Q

how does procainimide work

A

lengthens the action potential duration and refractory period by Na channel inhibition; prolongs repolarization

treats: WPW, PVCs, paroxysmal vtach

504
Q

how does lidocaine work

A

shortens action potential duration and refractory period; delays rate of spontaneous phase 4 depolarization by preventing or diminishing the gradual decrease in K ion permeability

treats: ventricular arrhythmias and reentry cardiac arrhythmias

not effective in treating supraventricular tachyarrhythmias

505
Q

What is the first line drug for myoclonic seizures

A

Benzodiazepines

Midazolam

506
Q

What is the first line treatment for status epilepticus

A

Midazolam

2.5-5mg IV up to 15mg

IV, intranasal, buccal

507
Q

What is the management for status epilepticus

A

-upper airway management
-IV access
-drug therapy benzodiazepines
-continuous infusion of AED med to stop seizure activity

508
Q

Why does cardiac muscle not contract during MH crisis?

A

RYR1 receptor is only on skeletal muscles and not cardiac muscles

509
Q

What herbal drugs inhibit cyp450

A

Echinacea
Curcumin longa (tumeric)
Ginkgo biloba
Garlic in some isoforms
Ginger
Valerian root
Kava kava

510
Q

What antiarrrhythmic do we not use in WPW

511
Q

MOA of opioid agonist

A

Bind to opioid receptors coupled to G proteins that inhibits adenyl cyclase
-inhibits voltage gated Ca channels
-activates and opens k channels
>intracellular k increases which decreases neutrotransmission

Opioid receptors are mu, kappa, delta

512
Q

Explain Mu receptors and their subtypes

A

Mu: primary receptors for analgesia and adverse effects

Mu1: analgesia

Mu2: respiratory depression, bradycardia, dependence

513
Q

Define kappa pain receptors

A

-inhibit neuro transmission via type Ca channels

-responsible for dysphoria and diuresis

514
Q

Define delta receptors

A

Modulate Mu receptor activity

Is the receptor for endogenous opioids (endorphins etc)

515
Q

How does class 1A effect
-depolarization phase 0
-conduction velocity
-effective refractory period
-action potential duration
-automaticity
-p-r duration
-QRS duration
-QTc duration

A

think slow ventricles

-depolarization phase 0: ⬇️
-conduction velocity: ⬇️
-effective refractory period:⬆️⬆️⬆️
-action potential duration⬆️
-automaticity⬇️
-p-r duration✖️
-QRS duration⬆️
-QTc duration⬆️⬆️⬆️

516
Q

How does class 1B effect
-depolarization phase 0
-conduction velocity
-effective refractory period
-action potential duration
-automaticity
-p-r duration
-QRS duration
-QTc duration

A

think small spaces out action potentials

-depolarization phase 0✖️
-conduction velocity✖️
-effective refractory period⬇️
-action potential duration⬇️
-automaticity⬇️
-p-r duration✖️
-QRS duration✖️
-QTc duration✖️or ⬇️

517
Q

How does class 1C effect
-depolarization phase 0
-conduction velocity
-effective refractory period
-action potential duration
-automaticity
-p-r duration
-QRS duration
-QTc duration

A

think long slow ekg

-depolarization phase 0⬇️⬇️⬇️
-conduction velocity⬇️⬇️⬇️
-effective refractory period⬆️
-action potential duration⬆️
-automaticity⬇️
-p-r duration⬆️
-QRS duration⬆️⬆️⬆️
-QTc duration⬆️

518
Q

How does class 2 effect
-depolarization phase 0
-conduction velocity
-effective refractory period
-action potential duration
-automaticity
-p-r duration
-QRS duration
-QTc duration

A

think slow electricity

-depolarization phase 0 ✖️
-conduction velocity⬇️
-effective refractory period⬇️
-action potential duration⬆️
-automaticity⬇️
-p-r duration✖️ or ⬆️
-QRS duration✖️
-QTc duration⬇️

519
Q

How does class 3 effect
-depolarization phase 0
-conduction velocity
-effective refractory period
-action potential duration
-automaticity
-p-r duration
-QRS duration
-QTc duration

A

think long ekg and long refractory action potentials

-depolarization phase 0 ✖️
-conduction velocity⬇️
-effective refractory period⬆️⬆️⬆️
-action potential duration⬆️⬆️⬆️
-automaticity⬇️
-p-r duration⬆️
-QRS duration⬆️
-QTc duration⬆️⬆️⬆️

520
Q

How does class 4 effect
-depolarization phase 0
-conduction velocity
-effective refractory period
-action potential duration
-automaticity
-p-r duration
-QRS duration
-QTc duration

A

think short APs, long PRs

-depolarization phase 0✖️
-conduction velocity✖️
-effective refractory period✖️
-action potential duration⬇️
-automaticity✖️
-p-r duration✖️ or ⬆️
-QRS duration✖️
-QTc duration✖️

521
Q

What is the pro type drug for class 1a

A

Procainamide

522
Q

What is the pro type drug for class 1B

523
Q

What is the pro type drug class 1C

A

Flecainide

524
Q

What is prodrug class 2

A

Beta blockers
Metoprolol and esmolol

525
Q

Protype drug for class 3

A

Amiodarone

526
Q

Protype drug class 4

A

Diltiazem- ventricle
Verapamil- atrial

527
Q

What anti arrhythmic effects thyroid function

A

Amiodarone

528
Q

Anesthesia consideration for nitroglycerin

A

Not recommended for aortic stenosis and hypertrophic cardiomyopathy

529
Q

Which type of sympathomimetics have greatest effect on beta receptors

A

Synthetic catecholamines

530
Q

Which type of sympathomimetics have the least effect on alpha receptors

A

Synthetic catecholamines

531
Q

Which synthetic non catecholamine has the greatest affinity for alpha receptors

A

Phenylephrine

532
Q

What is the first step if a patient has sudden elevated HR and BP

A

-check monitors/equipment
-deepen anesthetic
-treat pain

533
Q

How do you treat concurrent increased HR and BP

534
Q

What medication can you use to treat a short painful stimulation that is non opioid

A

Esmolol- can be used for intubation/DL

535
Q

What happens if you give dantrolene and verapamil

A

Hyperkalemia
Myocardial depression
Hypotension

536
Q

What channels do local anesthetics block

537
Q

What can happen if pt on sildenafil doesn’t stop use before periop

A

Sudden irreversible loss of vision
Severe hypotension (treat with pressors)

Stop med 7 days before surgery

538
Q

What are beta blocker contraindications

A

Vasospasm
Toxic with cocaine
Heart block
Catecholamine induced HTN/tachy

539
Q

What does digitalis inhibit

540
Q

4 Ps of CCB

A

Platelets inhibited

Pressure decreased

Paralytics increased

Potassium increased

541
Q

What neuropsych drugs are hepatic enzyme INDUCERS

A

Carbamazepine
Lamotrigine
Phenobarbital
Phenytoin

542
Q

What neuropsych drugs DO NOT induce hepatic enzymes

A

Levetiracetam
Gabapentin

543
Q

Formula for MAP

A

MAP=COxSVR

MAP=(SBP+2DBP)/3

544
Q

Formula for MAP

A

MAP=COxSVR

MAP=(SBP+2DBP)/3

545
Q

When is phenytoin used as an antiarrhythmics

A

To suppress ventricular arrhythmias due to digitalis toxicity

546
Q

Does valproic acid induce or inhibit liver enzymes?

547
Q

What is the first line benzo for myoclonic seizures

A

Clonazepam

548
Q

What antiemetics are contraindicated for Parkinson’s patients

A

Prochlorperazine
Metoclopramide
Promethazine

549
Q

Is levadopa stopped in the perioperative area?

A

NO, abrupt dc of levadopa may result in parkinsonism hyperpyrexia syndrome

S/s: rigidity, pyrexia, autonomic instability, decreased LOC
looks like MH

550
Q

Ginseng proposedMOA

A

-augmentation if adrenal steroidogenesis
-increased IgGand IgM production
-increased interferon production
-enhancement of cell mediated immunity
-enhancement of natural killer cell activity

551
Q

Ginseng proposedMOA

A

-augmentation if adrenal steroidogenesis
-increased IgGand IgM production
-increased interferon production
-enhancement of cell mediated immunity
-enhancement of natural killer cell activity

552
Q

Which anesthesia meds are seizure inducing

A

Ketamine
Etomidate
Methohexital
Inhaled: sevo, nitrous oxide
Meperidine

Advanced Pharm (4 decks)

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