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Advanced Pharm Exam 2 > Week 6 Vasoactive drugs > Flashcards

Week 6 Vasoactive drugs Flashcards

1
Q

Autonomic nervous system is made of:

A

Sympathetic and Parasympathetic

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2
Q

Sympathetic preganglionic fibers are _____ and postganglionic fibers are _____

A

Short, Long
Inervated organs/target tissue are far away whereas ganglion are located directly beside the spinal cord

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3
Q

What is the goal of the autonomic nervous system?

A

Maintain homeostasis

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4
Q

Parasympathetic preganglionic fibers are _____ and postganglionic fibers are _____

A

Long, Short

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5
Q

What is the origin of SNS preganglionic neurons?

A

Thoracic & Lumbar; T1-L2

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6
Q

What is the origin of PNS preganglionic neurons?

A

Cervical & Scaral

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7
Q

What is the presynaptic neurotransmitter for SNS?

A

Acetylcholine

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8
Q

What do preganglionic fibers interact with in the Adrenal glands?

A

Chromaffin cells

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9
Q

What is the neurotransmitter for postganglionic synapses in the SNS?

A

Norepinephrine

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10
Q

What is the one exception to the postganglionic neurotransmitter in the SNS?

A

Sweat glands; Acetycholine

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11
Q

Chromaffin cells release:

A

80% Epinephrine, 20% Norepinephrine (reversed w/ pheochromocytoma)

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12
Q

When Epinephrine and Norepinephrine are secreted from the Adrenal Medulla, they are then considered

A

Hormones

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13
Q

What three substances are synthesized in nerve terminals or adrenal medulla?

A

Epinephrine, norepinephrine, and dopamine

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14
Q

What are the effects of cortisol being secreted from the adrenal cortex?

A

enhances norepinephrine conversion to epinephrine

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15
Q

What nerve is the major regulator of the parasympathetic nervous system?

A

Vagus (CNX)

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16
Q

What neurotransmitter is secreted at the postganglionic synapse of the PNS?

A

Acetylcholine

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17
Q

What are the 5 functions of the vagus nerve?

A
  1. Slow HR (negative chronotropic)
  2. Slow Conduction (negative dromotropic)
  3. Salivate
  4. Miosis
  5. Empties (bladder/rectum)
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18
Q

What 2 Na channel blockers lengthens AP?

A

procanimide
flecinide

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19
Q

What NA. channel blocker shortens AP?

A

Lidocaine

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20
Q

T/F Lidocaine is used for long term treatment of arrythmias

A

FALSE- poor oral bioavalibility

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21
Q

How do Class 1 antiarrythmic medications work? (lidocaine, procanimide, flecainide)

A

lengthens AP and Phase 0 depolarization to decrease conduction speed

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22
Q

What antiarrythmic increases pacemaker capture threshold?

A

Flecainide

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23
Q

What is the beta blocker of choice to treat tachycardia perioperatively?

A

esmolol OR labetalol for tachycardia & HYPERTENSION

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24
Q

What antiarrythmic class is Amiodarone in?

A

Class III

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25
Q

What neurotransmitter is released from ALL preganglionic auntonomic fibers?

A

Acetylcholine

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26
Q

What neurotransmitters are released in the ANS and PNS postganglionic fibers?

A

ANS: Norepinephrine OR Dopamine
PNS: Acetylcholine

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27
Q

_____ activates alpha1 which results in an ______ in blood pressure which causes ______ due to barorecptor response

A

Phenylephrine, increase, reflex bradycardia

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28
Q

What receptors does epinephrine work on?

A

Small alpha
Some beta 1 and 2

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29
Q

What receptors does norepinephrine work on?

A

Large alpha
some beta 1

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30
Q

What receptors does dopamine work on?

A

Some alpha1 and beta1, small beta2, large dopamine receptor

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31
Q

What receptors does isoproterenol work on?

A

Large beta1 and beta2

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32
Q

What receptors does dobutamine work on?

A

Large beta1 small beta2

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33
Q

What are the NATURAL catecholamines?

A

Epinephrine
Norepinephrine
Dopamine

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34
Q

What are the synthetic catecholamines?

A

Isoproterenol
Dobutamine

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35
Q

What are the synthetic noncatecholamines?

A

Ephedrine
Phenylephrine

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36
Q

What receptor does ephedrine act on?

A

some alpha1, small beta1 and 2

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37
Q

What receptor does phenylephrine work on?

A

Large alpha1

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38
Q

What sympathomimetic has both direct AND indirect effects?

A

Ephedrine

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39
Q

What are the effects of alpha 1 receptor stimulation?

A

vascular smooth muscle constriction (increased SVR), pupil dilation

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40
Q

What are the effects of alpha 2 receptor stimulation?

A

sedation, bradycardia, vasodialation

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41
Q

What are the effects of beta 1 receptor stimulation?

A

Positive chronotropic and inotropic effects
increased renin and angiotensin and cAMP

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42
Q

What are the effects of beta 2 receptor stimulation?

A

bronchodialation, vasodialation, tocolytic

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43
Q

What are the effects of dopamine receptor stimulation?

A

Increase CO and renal/mesenteric blood flow
D2: inhibits norepi release

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44
Q

What are the three mechanisms that remove neurotransmitters from the synaptic cleft?

A
  1. Uptake into presynaptic terminals
  2. Extraneural uptake
  3. Diffusion
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45
Q

What is a sympathomimetic?

A

Drug that produces same effects as catecholamines

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46
Q

What two enzymes metabolize norepinephrine?

A

COMT and MAO

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47
Q

What are the effects of beta 3?

A

lipolysis, thermogenesis in brown fat, bladder relaxation

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48
Q

What are the steps to catecholamine synthesis?

A

Tyrosine-> Dopa -> Dopamine -> Norepinephrine -> Epinephrine

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49
Q

Synthetic non-catecholamines are metabolized by

A

MAO

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50
Q

What cardiac phase does epinephrine effect?

A

Increases spontaneous phase 4 depolarization

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51
Q

What is the dose of Epinephrine push to support blood pressure?

A

2-8mcg

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52
Q

What are the lab changes caused by epinephrine?

A

Hypokalemia and hyperglycemia

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53
Q

Can epinephrine cross the BBB into the brain/CNS?

A

No, it is poorly lipid soluble

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54
Q

Why is epinephrine added to local anesthetics?

A
  1. decreased bleeding
  2. vasoconstriction to decrease absorption- thus longer effects
  3. less absorption leading to cardiotoxicity
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55
Q

What is the effect of epinephrine on diastolic blood pressure?

A

decreases it, widening the pulse pressure

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56
Q

What is the issue with giving too high of a dose of epinephrine? (10-20mcg)

A

the alpha stimulation causes an increase in afterload that may impede increases in CO

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57
Q

What is racemic epinephrine for?

A

stabilizes mast cells for severe croup (subglottic edema) and postextubation. diluted and nebulized must be observed for 2H rebound swelling

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58
Q

what is the dose for anaphylaxis Epi?

A

0.5-1.5mg

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59
Q

What should be done with 1:1,000 epi?

A

Dilute or IM for anaphylaxis

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60
Q

How much epi should be given at a time during a code?

A

1mg of 1:10,000

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61
Q

What is the concentration of “baby epi”?

A

1:100,000

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62
Q

What two drugs interact with epinephrine?

A

Halothane: arrythmias
Cocaine: block reuptake
nonselective beta blockers: alpha 1 exaggerated response

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63
Q

What are the effects of norepinephrine?

A

increased HR, conduction, contractility, SVR

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64
Q

What are 2 cautions in using norepinephrine?

A

increases O2 consumption and causes metabolic acidosis

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65
Q

What neurotransmitter is secreted from postganglionic sympathetic nerve endings?

A

norepinephrine

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66
Q

Why does norepinephrine effect drug metabolism?

A

by decreasing hepatic blood flow

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67
Q

Norepinephine should be used with caution in what patient population?

A

right sided heart failure due to increased preload

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68
Q

How do you treat pressor extravasation?

A

phentolamine 5-10mg in 10mL NS

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69
Q

What occurs with administration of dopamine at 0.5-3mcg/kg/min?

A

d1 and d2 vasodialation

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70
Q

What occurs with administration of dopamine at 3-10mcg/kg/min?

A

Beta1 and Alpha1 increases

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71
Q

What is the half life of Dopamine?

A

1-2 minutes

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72
Q

What individuals should use caution with dopamine?

A

individuals with increased intraocular pressure (increases it even more)

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73
Q

T/F the precursor to dopamine, L-dopa can cross the BBB but dopamine cannot.

A

TRUE

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74
Q

Dopamine has direct and indirect effects that:

A

Direct: vasoconstriction, inotropey
Indirect: inotrope that depends on norepinephrine for actions

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75
Q

How is dopamine metabalized?

A

MAO and COMT

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76
Q

What is the concern with high dose (10-20mcg/kg/min) dopamine?

A

vasoconstriction combats the renal perfusion effects

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77
Q

What are Dopamines effects on glucose?

A

can inhibit insulin which can cause hyperglycemia

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78
Q

Why is dopamine good for post cardiopulmonary bypass patients?

A

increases CO, dialates vascular beds, decreases SVR -> mimics balloon pump

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79
Q

What is the most potent beta sympathomimetic?

A

isoproterenol

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80
Q

how is isoproterenol metabolized?

A

COMT

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81
Q

What is the dose of isoproterenol and what is it best at treating?

A

1-5mcg/min Heart block

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82
Q

What is dobutamine good for?

A

Heart failure, weaning from bypass

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83
Q

Why do we no longer use isoproterenol for inotropic effects?

A

dobutamine and milranone are better

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84
Q

When using isoproterenol, the net increase in cardiac output is due to:

A

Increased systolic blood pressure

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85
Q

Why does isoproterenol cause a DECREASED map?

A

high risk for arrythmias
decreased coronary blood flow
increase myocardial O2 requirements

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86
Q

Is dobutamine selective or nonselective?

A

Selective Beta1

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87
Q

What is the dosage for dobutamine?

A

2-10mcg/kg/min

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88
Q

What medications must be dissolved in D5W and why?

A

Dopamine and Dobutamine- to avoid inactivation of the catecholamine in an alkaline solution

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89
Q

dobutamine infusion greater than 3 days can cause:

A

Down regulation which can cause the need to increase dosage

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90
Q

What effects does dobutamine have on the coronary arteries?

A

vasodialates

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91
Q

What are the effects of ephedrine?

A

direct: binds to alpha and beta receptors
indirect: inhibits neuronal norepinephrine reuptake and displaces more norepinephrine from storage vesicles
DOSE: 5-15mg

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92
Q

What is the dose for ephedrine?

A

5-15mg

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93
Q

How does phenylephrine work and what is the dosage?

A

alpha1 receptors, primarily venoconstriction 50-200mcg bolus

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94
Q

What is a common concern with phenylephrine?

A

reflex bradycardia due to baroreceptor response to increase in SVR

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95
Q

What is a less common effect of ephedrine?

A

anti-emetic, 0.5mg/kg IM

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96
Q

Why is the second dose of ephedrine less responsive than the first?

A

tachyphylaxis

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97
Q

What causes ephedrine tachyphylaxis?

A
  1. depletion of norepinephrine stores
  2. persistent block of receptors
  3. occupied receptor sites
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98
Q

What is the most common ephedrine supplied dose? dilution?

A

50mg/mL
dilute into 5mL NS to achieve 10mg/mL concentration
give 0.5mL at a time to give 5mg

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99
Q

What is the most common phenylephrine supplied dose? dilution?

A

10mg/mL
1. 0.1mL drug in 9.9mL NS = neo stick 100mcg/mL
2. 10mg in 100mL bag = 100mcg/mL
3. 20mg in 250mL bag = 80mcg/mL
4. 10mg in 250ml bag = 40mcg/mL

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100
Q

Does phenylephrine cause arterial or venous constriction?

A

Venous

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101
Q

How many mcg at a time should be given to support blood pressure?

A

50-200mcg

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102
Q

What is the dosage for a continuous infusion of phenylephrine?

A

20-50mcg/min

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103
Q

What receptor does dexmedetomidine work on?

A

Alpha2

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104
Q

While an alpha agonist causes reflex bradycardia, an alpha antagonist causes

A

reflex tachycardia

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105
Q

What is the dosage of a vasopressin infusion?

A

0.04-0.1unit/min

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106
Q

What is the infusion rates for norepinephrine, epinephrine, and dobutamine? (Hint: they’re all the same)

A

1-20mcg/min

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107
Q

What is the milrinone infusion dosage?

A

0.375-0.75mcg/min
with or without bolus of 37.5-75mcg/kg

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108
Q

What class of antiarrythmics greatly decreases Phase 0 depolarization?

A

Class IC
Slightly in Class IA
(blocks NA channels)

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109
Q

What occurs in phase 0 of the cardiac cycle?

A

NA channels lead to depolarization of the cell

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110
Q

How do class III antiarrythmics effect refractory period?

A

greatly increased

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111
Q

How do class III antiarrythmics effect action potential?

A

greatly increased

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112
Q

What is an example of a cardiac glycoside?

A

digoxin

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113
Q

What are indications for digoxin?

A

SVT, PAT, Afib, Aflutter, CHF

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114
Q

How does digoxin work?

A

slows conduction of impulses through AV node
positive inotrope

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115
Q

Why is digoxin not a first choice drug?

A

increases risks of sudden cardiac death from cardiac dysrhythmias

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116
Q

What is a major concern with digoxin?

A

Narrow theraputic range; Toxicity

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117
Q

What are the direct and indirect effects of digoxin?

A

direct: modify electrical and mechanical activity
indirect: evoked by reflex alteration in ANS activity

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118
Q

What ratio of individuals experiencing toxic levels of digoxin show symptoms?

A

1:5

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119
Q

What is the therapeutic digoxin level?

A

0.5-2.5ng/mL

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120
Q

What are early signs of digoxin toxicity?

A

anorexia, n/v

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121
Q

What ekg changes are associated with digoxin toxicity?

A

atrial or ventricular dysrhythmias, incomplete to complete heart block

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122
Q

How do we treat digoxin toxicity?

A

correct cause
treat dysrhythmia
pacer if needed
potassium replacement if needed

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123
Q

what drugs can cause digoxin toxicity and why?

A

diuretics from hypokalemia

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124
Q

What anesthetic drug effects cardiac glycoside levels?

A

succinylcholine

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125
Q

What sympathomimetics could cause an increased risk of dysrythmias in individuals taking cardiac glycosides?

A

Beta agonists

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126
Q

what can occur when giving IV calcium to an individual on cardiac glycosides?

A

dysrythmias

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127
Q

What is the interaction between antacids and digoxin?

A

decreased GI absorption = subtheraputic levels

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128
Q

What is the MOA of Phosphodiasterase inhibitors?

A

decreases hydrolysis of cAMP and cGMP to increase intracellular concentrations of CA in myocardium and vascular smooth muscle-> increasing intracellular calcium levels and contractility -> uptake of calcium causes smooth muscle relaxation/ decreased SVR

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129
Q

Amrinone is also know as:

A

Inamrinone

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130
Q

Why is amrinone no longer used?

A

milrinone is more potent with less side effects

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131
Q

What is a useful purpose of milrinone in arteriografts?

A

reverse vasospasm

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132
Q

What causes milrinones long half life?

A

highly protein bound

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133
Q

Which drug decreases cardiac filling pressures more: dobutamine or milrinone?

A

milrinone

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134
Q

what are side effects of milrinone?

A

decreased SVR and venous return could cause hypotension
potentially proarrythmic in CHF

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135
Q

Where in the body is calcium used?

A
  1. neuromuscular junction
  2. skeletal muscle contraction
  3. cardiac muscle contraction
  4. blood coagulation
  5. exocytosis of neurotransmitters
  6. bone component
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136
Q

What is the effect of calcium on the heart?

A

positive inotrope

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137
Q

What is the calcium dosage of inotropic purposes?

A

1000-3000mg

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138
Q

The active form of calcium is:

A

ionized

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139
Q

acidosis ______ calcium levels, whereas alkalosis ______ calcium levels

A

increases, decreases

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140
Q

What is the most common type of hypertension?

A

primary/essential

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141
Q

When should antihypertensive medications be stopped before surgery? why?

A

continue until surgery
rebound hypertension can occur with abrupt cessation

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142
Q

Metoprolol MOA, dose, onset, and half-life:

A

selective Beta1 blocker/antagonist
1-5mg IVP
1-5mins
3-7hrs

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143
Q

Labetalol l MOA, dose, onset, and half-life:

A

nonselective alpha1, beta1and2 antagonist
5-20mg IVP
1-5min
6hrs

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144
Q

Esmolol MOA, dose, onset, and half-life:

A

selective beta1 blocker/antagonist
500-1000mcg/kg
1-2min
9mins (metab plasma esterases)

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145
Q

Nicardipine MOA, dose, onset, and half-life:

A

Dihydropyridine CCB
100-400mcg
2-10mins
2-4hrs

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146
Q

Hydralazine MOA, dose, onset, and half-life:

A

arteriolar dialator
5-20mg
5-20min
2-8hr

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147
Q

Nitroprusside MOA, dose, onset, and half-life:

A

NO donor
infusion only 0.25-4mcg/kg
1-2min
<10mins

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148
Q

Nitroglycerin MOA, dose, onset, and half-life:

A

NO donor
20-400mcg
1-2min
1-3min

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149
Q

When administering a beta2 agonist, an ETT decreases MDI dose by what percentage?

A

50-70%

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150
Q

What is the purpose for selective beta blockers and some examples?

A

low-mod doses are unlikely to cause bronchospasm and mask hypoglycemia
acebutolol, atenolol, metoprolol, bisoprolol

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151
Q

What is a major concern of using beta blockers?

A

mask signs of hypoglycemia -> increases risks of coma

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152
Q

What are some examples of nonselective beta blockers?

A

propranolol, carvedilol, labetalol

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153
Q

What are some side effects of beta blocker use?

A

bradycardia
heart block
CHF, claudication
bronchospasm
sedation, impotence
angina/MI

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154
Q

What population should nonselective beta blockers be avoided in?

A

lung patients (asthma, COPD)
selective beta blockers are safe for them

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155
Q

What is an example of a Alpha1 blocker? What are the effects and side effects?

A

Prazosin
decreases SVR via vasodialation, decreases preload and CO
SE: vertigo, fluid retention, orthostatic hypotension

156
Q

What are the two most common Alpha2 blockers?

A

dexmedetomidine
clonidine

157
Q

Why does dexmedetomidine cause CNS effects while clonidine acts primarily on blood pressure management?

A

the subtype receptors dex acts on are primarily found in the CNS whereas the ones clonidine work on are in vascular smooth muscle

158
Q

What are some side effects of Alpha2 agonists?

A

bradycardia, sedation, decreased pain perception, rash, impotence, ortho hypotension

159
Q

What is the most common side effect of an ACE inhibitor?

A

Cough
minor: URI symptoms

160
Q

What is the most DANGEROUS side effect of an ACE inhibitor?

A

Angioedema- upper airway blockage = emergency

161
Q

What is the MOA of an ACE inhibitor?

A

ACE is the enzyme that converts ang I to ang II, this reaction occurs in the lungs. ACE inhibitors prevent ang I from becoming the more potent ang II

162
Q

What is the MOA of ARBS?

A

blocks the vasoconstricting effects of angiotension II without affecting ACE activity

163
Q

When should ACEs and ARBs be d/c’ed prior to surgery?

A

12-24 hours prior

164
Q

What drug might be useful intraoperatively for a patient who routinely takes ACE/ARBs?

A

vasopressin (assist in the alpha reaction to sympathomimetics)

165
Q

How do dihyrdopyridine CCBs work?

A

bind to calcium channels on vascular smooth muscle, promoting vasodilation NICARDIPINE

166
Q

How do NON dihydropyridine CCBs work?

A

block calcium channels in heart muscle, reduce Ca in cardiac cells, leading to a decrease in the heart rate and contractions DILTIAZEM

167
Q

What type of calcium channel blockers have more effect on blood vessles?

A

dihydropyridines

168
Q

What type of calcium channel blockers have more effect on the heart?

A

non-dihydropyridines

169
Q

what are the two non dihydropyridines?

A

Verapamil
diltiazem

170
Q

what are some examples of dihydropyridines?

A

nifedipine, amlodipine, nicardipine, clevidipine

171
Q

What are the three conditions dihydropyridines treat?

A
  1. hypertension
  2. prinzmetal angina
  3. raynaud’s syndrome
172
Q

What are side effects associated with dihydropyridine use?

A

reflex tachycardia, negative inotropy, hypoxemia d/t worsening VQ mismatch (shunting)

173
Q

do nondihydropyridine CCBs also have vasodilatory effects?

A

yes

174
Q

What does inhibition of PDE3 cause?

A

positive inotropy

175
Q

what does inhibition of PDE cause?

A

vascular smooth muscle relaxation

176
Q

What do PDE5 inhibitors treat?

A

Erectile dysfunction and pulmonary hypertension

177
Q

What do PDE3 treat?

A

myocardial infarction, intermittent claudication, heart failure

178
Q

What are side effects of PDE5s?

A

headache, flushing, dyspnea

179
Q

What are side effects of PDE3s?

A

Ventricular dysrhythmias, headache, hypotension

180
Q

What does inhaled nitric oxide do?

A

relaxes pulmonary arterial vasculature & improves ventilation-perfusion matching

181
Q

Is inhaled nitric approved for the adult population?

A

NO

182
Q

What is the “Off label” use of nitric oxide in adults to treat?

A

severe pHTN in the setting of right heart dysfunction/failure in heart/lung transplants

183
Q

What would occur if inhaled nitric oxide was stopped abruptly?

A

rebound pulmonary hypertension

184
Q

What is the indication for nitrates?

A

suspected MI, volume overload w/ HF, hypertension

185
Q

Do nitrates primarily dilate veins or arteries?

A

veins AND coronary arteries

186
Q

Whats the MOA of nitrates and SNP?

A

generates NO stimulates production of cGMP to cause peripheral vasodialation

187
Q

What’s the rate of a nitroglycerin gtt?

A

5-600mcg/min

188
Q

How does SNP work?

A

interacts with oxyhemoglobin leading to an increase of cGMP to inhibit Ca entry into cell and thus vascular smooth muscle relaxation

189
Q

What is a major concern associated with a nitroprusside drip and when does it become a valid concern?

A

Cyanide toxicity
+3 days of administration
>2mcg/kg/min

190
Q

Nitroprusside side effects:

A

inhibits platelet aggregation
VQ mismatch/shunting/decreased PaO2
increases ICP
tachy/decreased BP/+inotropy
Coronary steal
decreased renal function

191
Q

Nitroprusside should be used with caution in what patient population?

A

neuro peeps/ increases ICP

192
Q

What is coronary steal and what medication causes it?

A

vasodilation of a myocardial segment’s vasculature is associated with “steal” of blood from another myocardial segment
nitroprusside

193
Q

How is cyanide toxicity treated?

A

d/c SNP
100%O2
sodium bicarb
sodium thiosulfate (150mg/kg)+/ hydroxycobalamin (5mg/kg)

194
Q

What are the three things caused by cyanide toxicity?

A
  1. Anoxic tissue ischemia
  2. anaerobic metabolism
  3. Lactic acidosis
195
Q

What is methemoglobinemia?

A

an adverse effect of SNP, uncommon
dose to cause exceeds 10mg/kg

196
Q

What vessels does hydralazine work on?

A

arteries

197
Q

What are two major concerns when administering hydralazine?

A

reflex bradycardia
coronary steal

198
Q

What patient population should not receive hydralazine?

A

patients experiencing MI or CAD

199
Q

What is the sympatholytic of choice for pregnant women?

A

hydralazine

200
Q

How does hydralazine affect SVR?

A

Decreases it

201
Q

What can occur with long term use of hydralazine?

A

systemic autoimmune syndrome

202
Q

What is the dose for hydralazine?

A

2.5-5mg/5min 20mg max

203
Q

What is a common nitrate used to prevent angina and to decrease SVR in HF?

A

Isosorbide dinitrate

204
Q

How does isosorbide dinitrate work?

A

similarly to Nitro

205
Q

What is a side effect of isosorbide?

A

orthostatic hypotension

206
Q

Isosorbide dosage:

A

60-120mg

207
Q

Why would an MAOI create issues with blood pressure management?

A

MAOIs alter the break down of catacholimines

208
Q

What amino acid is the”building block” of catacolimines?

A

tyrosine

209
Q

What are the two ways neurotransmitters can be metabolized?

A
  1. reuptake
  2. metabolized by MAO into homovinellic acid
210
Q

When in the operative period is hypotension most common?

A

during induction

211
Q

What is the blood pressure goal during surgery?

A

Maintain within 20% of baseline with a map of >65

212
Q

What occurs if we do not maintain our blood pressure goals perioperatively?

A

MI
AKI
Stroke
Delirium

213
Q

When should a beta blocker be D/C’ed prior to surgery?

A

maintained until day of surgery

214
Q

When should a CCB be D/C’ed prior to surgery?

A

maintained until day of surgery

215
Q

What blood pressure necessitates postponing procedure?

A

SBP >180 or DBP >110

216
Q

What is the onset time for ephedrine?

A

2-5min

217
Q

Why isnt ephedrine used as a drip?

A

Tachyphylaxis

218
Q

What is the push dose of ephedrine?

A

5-15mg/ 1-2 doses over 5-10minutes

219
Q

What non-catacholamine sympathomimetic is resistant to COMP and MAO?

A

Ephedrine

220
Q

What happens if patients taking MAOIs receive ephedrine?

A

exaggerated hypertensive effect

221
Q

What is the push dose for phenylephrine?

A

80-100mcg

222
Q

What is the onset for phenylephrine?

A

less than a minute

223
Q

If a patient is bradycardic and hypotensive, what is the first line medication?

A

ephedrine

224
Q

If a patient is nsr-tachy and hypotensive what is the first line medication?

A

phenylephrine

225
Q

What is the ratio of baby epi?

A

1:100,000

226
Q

What is the normal push dose of baby epi?

A

2-8mcg every 1-5mins

227
Q

What is the normal push dose of norepinephrine?

A

3-12mcg/1-2mins

228
Q

Why are we less likely to give a push dose of norepinephrine?

A

higher risk of a lethal dose

229
Q

What is the push dose for vasopressin?

A

0.5-1unit

230
Q

What is the indication to give a push of vasopression?

A

hypotension in pt’s taking ACE
sepsis
shock
bypass
catecholamine resistance

231
Q

What medication can be given if vasopressin does not help hypotension?

A

methylene blue 1-3mg/kg

232
Q

What is the MOA of methylene blue?

A

interferes with NO/inhibits vasorelaxants

233
Q

Pronation and hypotension can cause what adverse event?

A

blindness

234
Q

What is our first line treatment for hypertension perioperatively?

A

increase volatile gas- probably due to ANS/gases cause vasodialation

235
Q

What physiological process causes thereputic hypertension to occur?

A

stroke

236
Q

In what setting could hydralazine cause significant hypotension?

A

in the presence of nitrates or acute ETOH intoxication

237
Q

What is the preferred antihypertensive agent for ischemia?

A

nitroglycerine

238
Q

What are the two choice drugs for severe acute hypertension?

A

nitroglycerine and sodium nitroprusside

239
Q

What are the the two choice drugs for hypertension in the setting of tachycardia?

A

Esmolol and labetolol

240
Q

What is the first choice drug for primary/essential hypertension?

A

thiazide diuretic

241
Q

What two drug classes are used to manage bradycardia?

A

anticholinergics: atropine/glyco
catecholamines: epi/ephedrine/isoproterenol

242
Q

While undergoing cardiopulmonary bypass the ______ artery is a more accurate measurement than the radial.

A

Brachial

243
Q

What is Pulsus Paradoxus?

A

decreases in systolic blood pressure during inspiration

244
Q

What has higher levels of proteins, plasma or interstitial fluid?

A

plasma

245
Q

What is Cushing’s triad?

A

hypertension
bradycardia
irregular respirations

246
Q

Cardiac output =

A

Stroke volume x Heart rate

247
Q

What is the determining factor of stroke volume?

A

venous return/preload

248
Q

What are anesthetic agents effects on cardiac output?

A

decreased

249
Q

Why should norepinephrine be used with caution in patients with right sided heart failure?

A

increase in preload can more advanced failure

250
Q

High dose dopamine can cause:

A

reflex bradycardia

251
Q

T/F dobutamine is a racemic mixture

A

True

252
Q

What plant are cardiac glycosides derived from?

A

foxglove

253
Q

What could occur with digoxin toxicity and direct current cardioversion?

A

Ventricular fibrillation

254
Q

A Frank-Sterling Curve shift to the left indicates:

A

increased inotropy/CO

255
Q

What are the effects of digoxin on EKG?

A

prolonged PR
shortened QTc
ST depression
small T wave

256
Q

T/F ekg changes related to digoxin go away once drug is cleared

A

False, EKG changes remain weeks after drug discontinuation

257
Q

What is a lusitropic state?

A

relaxation (difficult in diastolic heart failure)

258
Q

What causes milrinone to have such a long half life?

A

highly protein bound

259
Q

What does clonidine treat?

A

HTN, tremors from CNS stimulants, opioid withdrawls

260
Q

What is the dosage for dexmetatomidine?

A

0.1-1.5mcg/kg/min

261
Q

T/F dexmedetomidine can be stopped abruptly with no issues regardless of dose.

A

False, withdraw symptoms occur when at high dose for multiple days

262
Q

What is the push dose for dexmedetomidine?

A

0.25-1mcg/kg

263
Q

T/F If a patient is taking propranolol, this affects the metabolism of other drugs such as local anesthetics and fentanyl

A

True

264
Q

Whats the difference between metoprolol tartrate and succinate?

A

tartrate 1/2 life: 2-3hrs
succinate 1/2 life: 5-7hrs

265
Q

How is esmolol metabolized?

A

plasma esterases

266
Q

What is the push dose of esmolol?

A

0.5mg/kg

267
Q

What are indications for esmolol?

A

electroconvulsion therapy, phenochromocytoma excision, thyrotoxicsis, pregnancy, epi/cocaine cardio toxicity

268
Q

What would occur with absorption of cocaine or epinephrine to an individual taking a beta1 antagonist?

A

pulmonary edema, cardiovascular collapse

269
Q

Why is esmolol a painful injection?

A

It’s acidic

270
Q

What are contraindications for an esmolol push?

A

AV block, acute cardiac failure

271
Q

What is the heart rate goal when giving a beta blocker?

A

65-80

272
Q

What part of the cardiac cycle do Beta blockers work in?

A

decrease rate of phase 4 spontaneous depolarization

273
Q

How should excessive beta blockade be treated?

A

7mcg/kg atropine, 2-25mg isoproterenol
glucagon, ca cl, pacer

274
Q

What two medications should NEVER be given to a patient with excessive Beta blockade?

A

Epinephrine and dopamine

275
Q

What cardiac arrythmia does propranolol treat?

A

torsades

276
Q

What are the two mixed alpha and beta blockers?

A

Labatolol and caredilol

277
Q

What is the ratio of alpha to beta selectivity for labatolol?

A

1:7

278
Q

What are the two subtypes of CCBs?

A

Dihydropyridines and
nondihydropyridines:
phenylalkylamines (verap) and benzothiazapines (Dilt)

279
Q

How do nondihydropyridines work?

A

bind to calcium channel to maintain inactive state

280
Q

What is one thing all CCB’s treat?

A

coronary artery vasospasm

281
Q

which nondihydropyridine is a racemic mixture?

A

verapamil

282
Q

Verapamil MOA:

A

racemic mixture: dextro: slows NA channels, levo: slows calcium channels- decreasing AV conduction

283
Q

Why cant verapamil be given to a patient with WPWS?

A

could cause ventricular arrythmias

284
Q

What are the three indications for verapamil?

A
  1. SVT
  2. Angina
  3. Hypertension
285
Q

What CCB works best on cerebral vessels?

A

nimodipine

286
Q

What can occur with abrupt cessation of CCBs?

A

coronary vasospasm

287
Q

What CCB has the most profound vasodilatory effects?

A

nicardapine

288
Q

Which CCB comes in a lipid solution?

A

clevidipine

289
Q

Which CCB should not be given to patients with hyperlipidemia or pancrentitis?

A

clevidipine

290
Q

How do we treat a diltiazem overdose?

A

dopamine and calcium

291
Q

What can occur when administering volatile gases to patients on CCB’s?

A

prolonged PR interval

292
Q

What are some nonpharmalogical methods to decrease blood pressure?

A

low sodium diet, weight loss, exercise, fluid restriction

293
Q

Why arent beta blockers first line for essential hypertension management?

A

adherance/compliance isssues

294
Q

What can occur with abrupt cessation of a beta blocker?

A

angina, MI

295
Q

What is a serious side effect of beta blocker usage in diabetic individuals?

A

blunts sympathetic nervous system response to hypoglycemia

296
Q

What is an indication to give an oral alpha 1 blocker such as prazosin preoperatively?

A

resection of phenochromatoma

297
Q

What drug class does clonidine belong to?

A

alpha2 agonist

298
Q

How do treat ACE inhibitor inducted angioedema?

A

0.3-0.5mg of 1:1,000 epinephrine Subq

299
Q

What type of cardiac issue contraindicates the use of clevidpine?

A

Aortic stenosis= decreased coronary artery perfussion

300
Q

What is an example of a PDE5?

A

Sidenafil, tadalafil, vardenafil

301
Q

What is the first line medication for SVTs?

A

Diltiazem; predominantly blocks cl channels in the AV node, slowing conduction

302
Q

What calcium channel blocker should be avoided in patients with muscular dystrophy?

A

verapamil- skeletal muscle weakness

303
Q

How does CRRT affect the half-life of milrinone?

A

increases; up to 20 hours

304
Q

What is the drug of choice for fascicular VT?

A

Verapamil

305
Q

What causes nitric oxide to become toxic?

A

When it is oxidized into nitric Dioxide

306
Q

What can cause the development of cyanide toxicity to be more likely and why?

A

hypothermia/decreases enzymatic activity and greater accumulation of cyanide

307
Q

What is an administration consideration for nitroprusside?

A

must be shielded from light

308
Q

What happens with coronary steal?

A

increases ischemic area of MI

309
Q

What is an administration consideration for amiodarone?

A

needs a micron filter

310
Q

What is an administration consideration for nitroglycerine?

A

needs special non PVC plastic tubing

311
Q

Nitroglycerine infusions shouldnt be given to patients with what cardiac disease?

A

hypertrophic obstructive cardiomyopathy & AS

312
Q

What is the bolus dosage of amiodarone for VT/VF resistant to defibrillation?

A

300mg bolus

313
Q

What compound do nitrites need to be active?

A

thio-compound

314
Q

How should nitro tolerance be managed?

A

12-24 hour drug free period, rebound MI from drug free period can occur

315
Q

what two electrolyte alterations cause an increase in the occurrence of ventricular fibrillation

A

hypokalemia
hypomagnesmia

316
Q

What three things cause arrhythmias to occur?

A
  1. reentry
  2. enhanced automaticity
  3. triggered
317
Q

what rate increases risks of ventricular arrhythmias; brady or tachy?

A

brady

318
Q

how do sodium channel blockers work?

A

decrease na influx, decrease conduction and velocity of the action potential

319
Q

how to potassium channel blockers work?

A

prolong repolarization and duration of the AP/refractory period

320
Q

class IA prodrug:

A

procanimide

321
Q

class IB prodrug:

A

lidocaine

322
Q

class IC prodrug:

A

Flecanide

323
Q

class II prodrug:

A

beta blockers: metoprolol, labetolol, and esmolol

324
Q

class III prodrug:

A

Amiodarone

325
Q

What are the two prodrugs in class IV antiarrythmics?

A

verapamil and diltizam

326
Q

What cardiac phase do class I antiarrythmics work on?

A

phase 0 depolarization
+ lidocaine phase 4

327
Q

what are the effects of class I antiarrythmics on action potential?

A

classes IA and IC lengthen while class IB shortens

328
Q

What causes torsades to occur during the cardiac phase?

A

early depolarization during delayed repolarization

329
Q

what does bradycardia in the presences of a prolonged QT interval increase the risk of?

A

torsades event

330
Q

what class of antiarrythmics treat incessant ventricular tachycardia?

A

Class IA and IC slow conduction enough

331
Q

what classes of antiarrythmics treat wide complex tachycardias?

A

IC and III

332
Q

in the setting of CHF, being on amiodarone long term can cause high risks of:

A

Vfib

333
Q

what is the dosage for procanimide?

A

100mg IVP and 2-6mg/min

334
Q

what are the toxic levels of procanimide and lidocaine?

A

p: >8mcg/ml
l: >5mg/ml

335
Q

what does phenytoin treat cardiac wise?

A

decreases ventricular arrhythmias and torsades with dig toxicity

336
Q

what is the dosage for phenytoin?

A

100mg/iv

337
Q

how does phenytoin treat arrhythmia?

A

decrease automaticity and conduction

338
Q

what are side effects of phenytoin?

A

CNS disturbances

339
Q

What does flecainide treat?

A

ventricular and atrial/reenty arrythmias such as WPWS

340
Q

What antiarrythmic class prevents the risk of sudden cardiac dealth?

A

Beta blockers

341
Q

T/F the plasma level of amiodarone is higher than the level in the myocardium.

A

False, myocardial level is 10-50 times higher

342
Q

What are the major side effects of chronic amiodarone use?

A

pulmonary toxicity/pheumonitis

343
Q

What arrythmias can amiodarone cause?

A

torsades and other ventricular arrythmias

344
Q

Can amiodarine induced bradycardia be treated with atropine?

A

No, it is resistant

345
Q

Grayish blue slate skin discoloration occurs with chronic use of what drug?

A

amiodarone

346
Q

What arrythmia can solotol cause?

A

torsades

347
Q

What arrythmias do class IV treat?

A

Afib,flutter, WPWS

348
Q

What cardiac phase do class IV antiarrythmias work in?

A

Phase 2 contraction

349
Q

Verapamil dosage?

A

5-10mg

350
Q

Diltiazem dosage?

A

20mg

351
Q

What drug should never be given to a patient with WPWS and why?

A

Diltiazem, enhances conduction of accessory pathways

352
Q

What is the dosage for Digoxin?

A

0.5-1mg in two doses in 24hr

353
Q

Adenosine is an alternate to what medication for SVT?

A

CCBs

354
Q

T/F Atrial fibbrilation is an indication for adenosine.

A

False

355
Q

What is the dosage for adenosine?

A

6mg, 12mg, 12mg

356
Q

What is the MOA of adenosine?

A

stimulates Adenosine receptors in cardiac muscle that increase intracellular potassium which causes a decrease in AP duration

357
Q

What two things increase the effects of adenosine?

A
  1. dipyridamole
  2. transplanted heart
358
Q

Is adenosine safe to use in a patient with WPWS?

A

yes

359
Q

What is a frightening thing that occurs when administering adenosine?

A

transient heart block

360
Q

How long is the half life of adenosine?

A

10 seconds, necessitating RAPID IV push

361
Q

What antiarrythmic can alter thyroid function and why?

A

amiodarone, high percentage of iodine in the molecule

362
Q

What can phenytoin NOT be mixed with?

A

D5W

363
Q

What is the dose for IVP metoprolol

A

1-5mg

364
Q

What drug should not be given to an individual taking PDE5s?

A

Nitroglycerin

365
Q

What is the symatholytic of choice to use in an individual who takes PDE5s?

A

CCBs

366
Q

What is the most common dysrhythmia that occurs in surgery and what is the frequency?

A

sinus arrythmia, 70%

367
Q

What surgeries most commonly yield arrythmias?

A

cardiac and abdominal

368
Q

Which volatile gas causes less QT prolongation/less risk of arrythmias?

A

Sevoflurene

369
Q

Which inotrope is less effective in a transplanted heart?

A

dopamine

370
Q

What drug should be used in a bradycardic emergency in a transplanted heart?

A

epinephrine and isoprenaline

371
Q

What is the pneumotic that helps us remember antiarrythmic classes?

A

Some (sodium blockers)
Block (beta blockers)
Potassium (potassium blockers)
Channels (calcium blockers)

372
Q

Calcium channel blockers are a ________ inotrope and should not be used in patients with ______ heart failure

A

negative, systolic
This indicates that it prolongs repolatization

373
Q
A
374
Q

what is the cardiac moa of epi?

A

increases stimulation of the AV node and decreases the refractory period

375
Q

why does ephedrine have such a long duration or action?

A

it is resistant to MOA and COMT

376
Q

what is the ivp dose of vasopressin?

A

1-2 unit

377
Q

What is the preferred treatment for WPWS?

A

procainamide
Adenosine can be given while lidocaine cannot

378
Q

What phases of the cardiac cycle are effected by class III antiarrythmics?

A

Phase 1 and 3

379
Q

Where do class IV antiarrythmics work in the cardiac cycle?

A

mostly phase 2
phase 4 in pacemaker cells

380
Q

Why do we want to shorten the AP (contraction/depolarization) and lengthen repolarizaion period with antiarrhythmics?

A

less time for ectopic beats to occur

381
Q

where do class II antiarrythmics work in the cardiac cell?

A

Phase 4, pacemaker
phase 2, myocyte

382
Q

What phase of the cardiac cycle do class 1 antiarrythmics work on?

A

Phase 0 in nonpacemaker

383
Q

How does lidocaine work since it shortens AP while other sodium channel blockers lengthen the AP?

A

works on the conduction by decreasing conduction in the SA node to allow AV node to become the primary pacemaker at a lower rate

384
Q

What is the ACLS dosage of vasopressin?

A

20 units

385
Q

What is a contraindication for flecainide?

A

heart block

Advanced Pharm Exam 2 (3 decks)

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