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Anesthesia Pharmacology > ANS- Cardiovascular > Flashcards

ANS- Cardiovascular Flashcards

1
Q

what is Cleviprex

A

Clevidipine

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2
Q

Clevidipine

class/ categorie, uses

A

Class/Category: Dihydropyridine Calcium-Channel Blocker

Uses: HTN

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3
Q

Clevidipine

MOA

A

Calcium-Channel Blocker: Inhibits Ca2+ influx into cardiac muscle and vascular smooth muscle

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4
Q

Clevidipine

onset, peak, duration

A

Onset: 1-3 min

Peak: 2-10 min

Duration: 5-15 min

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5
Q

Clevidipine

metabolism

A

plasma esterases

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6
Q

clevidipine

CV effects

A

↓ BP, ↑ HR, ↓ SVR, ↔ preload, ↓ afterload, ↓/↔ inotropy
May experience reflex tachycardia or baroreceptor reflex

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7
Q

Clevidipine

CNS effects

A
  • May ↑ CBF, moderate cerebral vasodilator
  • CO2 reactivity maintained
  • HA
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8
Q

Clevidipine contraindications

A

Allergy to soybeans, soy, eggs, or egg products; defective lipid metabolism

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9
Q

Clevidipine relative contrainidations

1

A

severe aortic stenosis

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10
Q

What conditions should you avoid using clevidipine for

3

A
  • Avoid in heart failure with reduced EF,
  • hyperlipidemic states,
  • acute or chronic pancreatitis
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11
Q

Does clevidipine cause tachyphylaxis OR rebound HTN

A

NO, not associated with tachyphylaxis or rebound HTN upon stopping

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12
Q

clevidipine effect on renal blood flow

A

Increases renal blood flow

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13
Q

What condition prolongs the effects of clevidipine?

A

Effect prolonged if pseudocholinesterase deficiency

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14
Q

what is EmerPhed

A

Ephedrine

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15
Q

Ephedrine

class/ category

A

Synthetic/Non-Catecholamine Adrenergic Agonist; Sympathomimetic

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16
Q

Ephedrine

use

A

Treatment of hypotension

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17
Q

Ephedrine

MOA

A

Adrenergic Agonist: Indirect&raquo_space; Direct effects (α1, β1, and β2)

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18
Q

Ephedrine

dose

A

5-25 mg IV in 5-10 mg incremental doses

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19
Q

Ephedrine

onset, peak, duration

A

Onset: <1 min

Peak: 2-5 min

Duration: 10-60 min

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20
Q

Ephedrine

elimination

A

renal

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21
Q

Ephedrine

CV effects

A
  • ↑ BP, ↑ HR, ↑ CO
  • ↑ SVR may be offset by β2-induced vasodilation
  • ↑ myocardial O2 consumption
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22
Q

Ephedrine

Pulm effects

A

Bronchodilation (β2)

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23
Q

Ephedrine

CNS effects

A
  • Crosses BBB, CNS excitation
  • Mydriasis
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24
Q

What does ephedrine do to renal and splanchnic blood flow?

A

Decreases renal and splanchnic blood flow

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25
Q

What does repeat dosing with ephedrine cause?

A

Tachyphylaxis with repeat dosing (due to depleted NE stores), may require increasing doses

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26
Q

Ephedrine does what to MAC requirements

A

Increases MAC requirements

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27
Q

Ephedrine may interact with which medications and cause what?

A

May interact with MAO-inhibitors → hypertensive crisis or serotonin syndrome

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28
Q

use this medication cautiously with questionable coronary perfusion

A

ephedrine

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29
Q

What is Adrenalin

A

Epi

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30
Q

Epinephrine

class/ category, uses

A

Class/Category: Adrenergic agonist

Uses: Cardiac arrest; anaphylaxis; bradycardia; bronchospasm; cardiogenic or vasodilatory shock

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31
Q

Epi

MOA

A

Adrenergic Agonist: Direct-acting α1, β1, β2

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32
Q

Epi

dose-infusion

A

Infusion:
β effects: 0.01-0.03 mcg/kg/min
β & α effects: 0.03-0.15 mcg/kg/min
α effects: 0.15-0.3 mcg/kg/min

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33
Q

Epi

bolus dose-cardiac arrest

A

Cardiac arrest (pulseless):
1 mg IV/IO or 2-2.5 mg ETT (diluted in 5-10 mL Sterile Water), may repeat every 3-5 min
01 mcg/kg IV/IO or 0.1 mg/kg ETT; may repeat initial dose up to 10x, repeating every 3-5 min
IV/IO/ETT doses up to 0.2 mg/kg may be effective[

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34
Q

Epi

dose-anaphylaxis

A

Anaphylaxis:
5-10 mcg IV bolus, if hypotension, titrate to effect[2]
1-1 mg IV bolus, if CV collapse[2]
Infusion 5-10 mcg/min (0.01 mcg/kg/min),[2] may increase up to 20 mcg/min[4]
If laryngeal edema without hypotension, administer SubQ[2]
Avoid IV administration if normal BP

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35
Q

Epi

Dose-bradycardia

A

Bradycardia:
01 mg/kg IV/IO or 0.1 mg/kg ETT

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36
Q

Epi

Peds-cardiac arrest and vasoactive doses

A

Cardiac arrest: 0.01-0.02 mg/kg
Vasoactive (α & β effects) 0.05-2 mcg/kg/min

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37
Q

Epi

Peds bronchospasm and bradycardia doses

A

Bronchospasm: 5-10 mcg/kg IV/SQ
Bradycardia (neonatal): 0.01-0.03 mcg/kg IV or 0.05-0.1 mcg/kg ETT (1:10k)

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38
Q

Epi

onset, peak, duration

A

Onset: < 1 min

Peak: 1-2 mins

Duration: 5-10 min

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39
Q

Epi

Metabolism

A

Enzymatic degradation by COMT and MAO

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40
Q

Epi

CV effects

A
  • ↑ HR, ↑ CO, ↑ contractility, ↑ conduction velocity, ↑ ventricular relaxation
    Initial ↑ HR → ↓ HR (baroreceptor reflex)
  • ↑ BP, ↑ SVR, ↑ preload, ↑ afterload
  • ↑ myocardial O2 demand; possible ↓ myocardial O2 supply, may → myocardial ischemia
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41
Q

Epi

pulm effects

A

Bronchodilation
May ↑ PAP

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42
Q

Epi

CNS effects

A
  • Cerebral arteriolar vasoconstriction
  • Risk for stroke and cerebral hemorrhage
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43
Q

Epi’s effects on hepatosplanchnic, renal blood flow and what does it cause to tissue O2 exchange and lactate clearance?

A

↓ hepatosplanchnic and renal blood flow → ↓ tissue O2 exchange and ↓ lactate clearance

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44
Q

epi does what to renin secretion

A

↑ renin secretion

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45
Q

Epi is not recommended for what type of medication overdose

A

Not recommended for β-blocker overdose

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46
Q

T/F epi can cause hyperglycemia and mydriasis?

A

True

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47
Q

Caution use in epi for what condition?

A

pulm HTN

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48
Q

what could a supratherapeutic does of Epi cause?

A

Supratherapeutic dose may → acute heart failure, pulmonary edema, arrhythmia, HTN, myocardial ischemia

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49
Q

T/F Epi causes tachyphylaxis

A

False, no tachyphylaxis

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50
Q

what is Brevi-Bloc

A

Esmolol

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51
Q

Esmolol

class/ category

A

Selective Adrenergic Antagonist; Class II antiarrhythmic

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52
Q

esmolol

uses

A

HTN, dysrhythmia, myocardial ischemia, β-blockade continuation; blunt SNS response to noxious stimuli

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53
Q

esmolol and metoprolol

MOA

A

Adrenergic Antagonist: β1 (cardioselective)

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54
Q

Esmolol

dose (bolus and infusion)

A

Bolus: 0.5-1 mg/kg over 1 min

Infusion: 50-300 mcg/kg/min

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55
Q

Esmolol

onset, peak, duration

A

Onset: 1-2 min

Peak: 5 min

Duration: 10-15 min

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56
Q

Esmolol

metabolism

A

Non-specific plasma esterases

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57
Q

Esmolol and metoprolol

CV effects

A
  • ↓ BP, ↓ HR, ↓ contractility, ↓ conduction velocity, ↑ ventricular relaxation
  • ↓ myocardial O2 demand
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58
Q

Esmolol and metoprolol

GI effects

A

N/V/D

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59
Q

T/F esmolol and metoprolol might mask signs of hypoglycemia

A

True

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60
Q

T/F esmolol does not cause pain on injection

A

FALSE, pain on injection

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61
Q

what happens with large doses of esmolol or metoprolol

A

Large doses may have β2 antagonist effect

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62
Q

esmolol and metoprolol are not recommended for treatment what overdose

A

Not recommended for treatment of Phenylephrine overdose

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63
Q

T/F to avoid esmolol or metoprolol if sinus brady,
what could occur?

A

TRUE! Avoid if sinus brady, cardiogenic shock

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64
Q

Relative contraindications for esmolol and metoprolol

A

Relative contraindication: Reactive or obstructive airway disease (especially if high dose)

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65
Q

contraindications for esmolol and metoprolol

2-cardiac

A

Preexisting AV block (greater than 1st degree), acute/ uncompensated HFrEF

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66
Q

what is apresoline

A

hydralazine

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67
Q

hydralazine

class/ category and uses

A

Class/Category: Antihypertensive

Uses: Treatment of hypertension

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68
Q

hydralazine

MOA

A

Mechanism of Action:
* Not well understood
* Direct systemic vasodilator arterial > venous relaxation

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69
Q

hydralazine

dose

A

Bolus: 2.5-20 mg IV

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70
Q

Hydralazine

onset, peak, duration

A

Onset: 2-20 min

Peak: 10-80 min

Duration: Up to 12 hr

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71
Q

esmolol

metabolism and elimination

A

Metabolism: Hepatic

Elimination: Renal

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72
Q

hydralazine

CV effects

A
  • ↓ BP, ↑ HR, ↑ CO, ↓ SVR, ↑ contractility
    Stimulates baroreceptor → reflex vagal activity, may include bradycardia
  • May cause CHF, angina
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73
Q

hydralazine

pulm effects

A

May alter reactivity of pulmonary vasculature

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74
Q

hydralazine

CNS effects

A
  • ↑ CBF, ↑ ICP (unless MAP markedly reduced)
  • Inhibits CBF autoregulation
  • HA, dizziness, tremors
75
Q

hydralazine

GI effects

A

nausea

76
Q

what type of blood flow does hydralazine effect and what does it do?

A

↑ coronary, cerebral, renal, and splanchnic blood flow

77
Q

hydralazine reversal agent

A

Phentolamine

78
Q

T/F hydralazine may cause lupus-like syndrome (usually with renal involvement)

A

TRUE!

79
Q

hydralazine is not recommended for patients with what disease and what could that cause?

A

Not recommended for patients with coronary artery disease, myocardial ischemia

80
Q

what is Trandate

A

Labetolol

81
Q

Labetalol

class/ category and uses

A

Class/Category: Non-Selective Adrenergic Antagonist

Uses: HTN, tachycardia

82
Q

Labetolol

MOA

A

Adrenergic Antagonist: Combined, α1 (selective), and β1 & β2 (non-selective)

83
Q

Labetolol

dose

A

Bolus:
2.5-10 mg IV bolus over 2 min, then 5-20 mg every 10 min until desired response (typically 5-20 mg)

84
Q

Labetolol

onset, peak, duration

A

Onset: 1-5 min

Peak: 5-10 min

Duration: 2-6 hr, dose dependent

85
Q

Labetolol

metabolism

A

hepatic

86
Q

Labetolol

CV effects

A
  • ↓ BP, ↓ HR, ↓ SVR, ↔ CO, ↓ Contractility
  • May cause reflex tachycardia
  • CHF
  • Heart block
87
Q

Labetolol

Pulm effects

A

Bronchospasm

88
Q

T/F Labetolol can cause orthostatic hypotension

A

TRUE!

89
Q

what condition should labetolol be avoided with?

A

Avoid with symptomatic asthma

90
Q

labetolol effects and ratio

A

Β:α effects, 7:1 by IV route

91
Q

what is lopressor

A

metoprolol

92
Q

metoprolol

class/ category and use

A

Class/Category: Selective Adrenergic Antagonist

Uses: HTN, myocardial ischemia, β-blockade continuation

93
Q

metoprolol

dose

A

Bolus: 1-5 mg IV, every 2-5 min until desired response, up to 15 mg

94
Q

metoprolol

onset, peak, duration

A

Onset: 1-5 min

Peak: 20 min

Duration: 1-4 hr

95
Q

metoprolol

metabolism

A

hepatic

96
Q

what is Cardene

A

Nicardipine

97
Q

Nicardipine

class/ category and use

A

Class/Category: Dihydropyridine Calcium-Channel Blocker

Uses: HTN, perioperative BP management

98
Q

Nicardipine

MOA

A

Calcium-Channel Blocker: Inhibits Ca2+ influx into cardiac muscle and vascular smooth muscle

99
Q

Nicardipine

Dose (bolus and infusion)

A

Bolus: 100-400 mcg IV

Infusion: 2-5 mg/hr IV, up to 15 mg/hr IV (1-2 mcg/kg/min, increased to 7.5 mcg/kg/min as needed)

100
Q

Nicardipine

onset, peak, duration

A

Onset: 1-3 min

Peak: 5-10 min

Duration: 30-60 min

101
Q

Nicardipine

metabolism

A

Hepatic CYP3A4

102
Q

Nicardipine

CV effects

5

A
  • ↓ BP, ↑/↔ HR, ↓/↔ CO, ↓ afterload, ↓/↔ contractility
  • May experience reflex tachycardia or baroreceptor reflex
  • Moderate to no myocardial depression
  • Marked coronary artery and peripheral artery dilation
  • Marked peripheral artery dilation
103
Q

Nicardipine

CNS effects

4

A
  • ↑ CBF, ↑ CBV
  • Moderate cerebral vasodilator
  • CO2 reactivity maintained
  • HA
104
Q

what type of edema does nicardipine cause

A

peripheral edema

105
Q

nicardipine increases blood flow where

A

Increases renal blood flow

106
Q

Nitroglycerin

class/ category and MOA

A

Class/Category: Nitrovasodilator

Mechanism of Action: Generates Nitric Oxide (NO)

107
Q

Nitro

uses

A

Uses:
Myocardial ischemia; Heart failure with reduced EF; Controlled hypotension

108
Q

Nitro

dose-bolus

A

Bolus: 5-100 mcg

109
Q

Nitro

infustion dose

A

Infusion:
Start at 5 mcg/min, increase by 5 mcg/min every 3-5 minutes until desired effect; if no response at 20 mcg/min, may increase by 10-20 mcg/min every 3-5 min

110
Q

Nitro

onset, peak, duration

A

Onset: 2-5 min

Peak: 1-2 mins

Duration: 5-10 min

111
Q

Nitro

metabolism

A

Hepatic

112
Q

Nitro

CV effects

A
  • ↓ BP (↓ preload),↑ HR, ↓ CO
  • Stimulates baroreceptor
  • Coronary artery vasodilator, improves myocardial supply-demand balance
113
Q

Nitro

pulm effects

A

May ↓ PaO2
↓ PAP

114
Q

Nitro

CNS effects

A
  • ↑ CBV
  • ↑ ICP (but less than SNP)
  • HA
115
Q

T/F nitro inhibits platelet aggregation

A

TRUE!

116
Q

Do not use Nitro with in how many hours of what type of medications AND what could it cause?

A

Do not use within 24 hours of erectile dysfunction drugs (PDE5 inhibitors)
May result in
* significant hypotension,
* myocardial ischemia,
* myocardial infarction,
* death

117
Q

Avoid in patients with what SBP, HR, and what?

A

Avoid in patients with SBP < 90 mmHg, HR < 50 or > 100, or RV infarction

118
Q

Nitro is not recommended in what type of patients?

A

Not recommended for patients with hypertrophic obstructive cardiomyopathy, or in the presence of severe aortic stenosis

119
Q

Nitro should be used cautiously in what type of patients and what could it cause?

A

Caution in hypovolemic patients, severe hypotension may compromise coronary perfusion pressure

120
Q

what could nitrite metabolites cause?

A

Nitrite metabolite may oxidize ferrous ion in hemoglobin to methemoglobin → methemoglobinemia (especially in patients with hepatotoxicity or receiving high doses)

121
Q

T/F Nitro and nitroprusside is methemoglobin-inducing

A

True!

122
Q

what is Nipride/ SNP

A

Sodium Nitroprusside

123
Q

Nitroprusside

class/ category

A

Nitrovasodilator; Nonselective peripheral vasodilator

124
Q

Nitroprusside

Uses

A

Hypertensive emergency; controlled hypotension; aortic/cardiac surgery; cardiogenic shock

125
Q

Nitroprusside

MOA

A

Nitric Oxide (NO) donor, Direct-acting

126
Q

Nitroprusside

Dose (infusion/ duration)

A
  • Infusion: Start at 0.3 mcg/kg/min and increase up to 10 mcg/kg/min
  • Duration of 10 mcg/kg/min infusion not to exceed 10 min
127
Q

Nitroprusside

onset, peak, duration

A

Onset: Seconds

Peak: 2 min

Duration: 1-5 min

128
Q

Nitroprusside

metabolism and toxic metabolites

A

Metabolism: Interacts with oxyhemoglobin, dissociating immediately to methemoglobin, releasing cyanide and NO

Toxic metabolites: Cyanide, thiocyanate (especially in renal disease)

129
Q

Nitroprusside

CV effects

A
  • ↓ BP(↓ Preload, ↓ Afterload), ↑ HR, ↑ contractility
  • Stimulates baroreceptor
  • ↑ myocardial O2 demand
  • ↓ coronary perfusion pressure
130
Q

Nitroprusside

Pulm effects

A
  • ↓ PaO2, ↑ pulmonary shunt
  • ↓ PVR
131
Q

Nitroprusside

CNS effects

A
  • ↑ CBF, ↑ CBV
  • ↑ ICP, may be offset by slowing infusion
132
Q

T/F nitroprusside contains cyanide

A

TRUE

133
Q

Is Nitroprusside associated with coronary steal?

A

YES!

134
Q

What does Nitroprusside do to platelet aggregation

A

Inhibits platelet aggregation

135
Q

Nitroprusside increases bleeding time at what rate?

A

↑ bleeding time at > 3 mcg/kg/min

136
Q

what are possible nitroprusside antidotes

3

A
  • Sodium thiosulfate,
  • Hydroxocobalamin,
  • Sodium nitrite
137
Q

Nitropruside relative contraindication?

hint: cardiac

A

Relative contraindication: Acute myocardial ischemia

138
Q

What is levophed

A

Norepinephrine!

139
Q

Norepi

class/ cateory

A

Adrenergic agonist

140
Q

Norepi

uses

A
  • Vasopressor
  • Septic, cardiogenic, or refractory shock
  • Distributive shock
  • Anaphylaxis
141
Q

Norepi

MOA

A

Adrenergic agonist; Direct-acting α1, β1, β2 agonist

142
Q

Norepi

Dose

A

Infusion: 1-20 mcg/min(0.01-0.2 mcg/kg/min)

143
Q

Norepi

onset, peak, duration

A

Onset: < 1 min

Peak: 1-2 mins

Duration: 2-10 min

144
Q

Norepi

metabolism

A
  • Primary adrenergic reuptake
  • secondary enzymatic degradation by COMT and MAO
145
Q

Norepi

CV effects

A
  • ↑ HR, ↑ contractility (less than Epi); ↑ conduction velocity, ↑ ventricular relaxation
  • ↑ BP, ↑ SVR (more than Epi); ↑ venous return, ↑ afterload
  • Arrhythmogenic potential (less than Epi)
  • ↑ myocardial O2 demand; possible myocardial ischemia if flow-limiting stenosis
146
Q

Norepi

pulm effects

A

↑ PAP

147
Q

Norepi effects on which bloodflow (2), less than what medication, and effect on tissue O2 and lactate

A

↓ hepatosplanchnic and renal blood flow (less than Epi) → ↓ tissue O2 exchange and ↓ lactate clearance

148
Q

Norepi could cause what type of vasoconstriction and what could it cause?

A

Renal artery vasoconstriction may → oliguria, renal failure

149
Q

T/F Norepi is okay to use with RV dysfuction/failure

A

FALSE, caution with RV dysfunction/failure

150
Q

T/F concern for end-organ hypoperfusion and ischemia with norepi

A

TRUE!

151
Q

what is Neo-Synephrine?

A

Phenylephrine

152
Q

Phenylephrine

class/ category

A

Synthetic/Non-catecholamine Adrenergic Agonist; Sympathomimetic

153
Q

Phenyl

use and MOA

A

Uses: Treatment of hypotension

Mechanism of Action: Adrenergic Agonist: Direct α1

154
Q

Phenyl

dose (bolus and infusion)

A

Bolus: 40-200 mcg bolus

Infusion: 20-200 mcg/min or 0.15-0.75 mcg/kg/min

155
Q

Phenyl

onset, peak, duration

A

Onset: <1 min

Peak: 1 min

Duration: 15-20 min

156
Q

Phenyl

metabolism

A

hepatic

157
Q

Phenyl

CV effects

A
  • ↑ BP, ↑ SVR, ↑ Preload, ↑ Afterload
  • Stimulates baroreceptor → reflex vagal activity, may include bradycardia
  • ↓ CO
158
Q

phenyl

Pulm effects

A

↑ PAP

159
Q

reversal agent for phenylephrine

A

Phentolamine

160
Q

Phenylephrine does what to renal, splanchnic, cutaneous, mesenteric, and skeletal muscle blood flow

A

Decreases

161
Q

T/F Tachyphylaxis with infusions may require upward titration of infusion dosing of phenylephrine

A

True

162
Q

what is phenylephrine NOT recommended for treatment of?

A

Not recommended for treatment of septic shock, unless serious arrhythmia with norepinephrine, high CO, or require salvage therapy

163
Q

How does phenylephrine effect vessel constriction?

A

Venoconstriction > arterial constriction

164
Q

what is Vasostrict?

A

Vasopressin

165
Q

vasopressin

class/ category and uses

A

Class/Category: Nonadrenergic Vasopressor

Uses: Treatment of hypotension, shock

166
Q

Vasopressin

MOA

A

Nonadrenergic Agonist; Direct acting, V1

167
Q

Vasopressin

dose (bolus and infusion)

A

Bolus: 1-2 units IV (perioperative hypotension)

Infusion: 0.01-0.1 units/min (shock states)

168
Q

vasopressin

onset, peak, duration

A

Onset: 1-5 min

Peak: 5 min

Duration: 10-30 min

169
Q

Vasopressin

elimination

A

hepatic/ renal

170
Q

vasopressin

CV effects

5

A
  • ↑ BP, ↔ HR, ↔ Contractility, ↓ CO,↑ SVR
  • ↑ Myocardial O2 consumption
  • Arrhythmias
  • Coronary artery vasoconstriction → angina pectoris, EKG changes suggestive of myocardial ischemia, MI
  • Risk for cardiac arrest
171
Q

Vasopressin

CNS effects

A

↑ CBF, ↔ ICP

172
Q

vasopressin

GI effects

A

↑ peristalsis → abdominal pain, N/V

173
Q

vasopressin does what to splanchnic, renal, coronary, and peripheral vascular beds and what is the risk associated?

A

Vasoconstricts splanchnic, renal, coronary, and peripheral vascular beds → ischemia risk

174
Q

where does vasopressin shunt blood?

A

Shunts blood to cerebral, cardiac, and pulmonary vascular beds

175
Q

what does vasporession do to cutaneous vessels and the symptoms seen?

A

Cutaneous vasoconstriction → pallor

176
Q

what does vasopresson do to uterine smooth muscle?

A

uterine smooth muscle contraction

177
Q

T/F caution with CAD with vasporessin

A

True

178
Q

prolonged use of vasopresson can cause what?

A

Prolonged use may decrease effect

179
Q

Vasopression is not recommended for the treatment of what?

A

not recommended for the treatment of LAST

180
Q

what is the most potent arterial vasoconstrictor?

A

Vasopressin

181
Q

V1-what G coupled receptor and action

A

V1 (Gq) – Vascular smooth muscle → Arterial vasoconstriction

182
Q

V1-what G coupled receptor and action

A
183
Q

V3-what G coupled receptor and action

A

V3 (Gq) – Anterior pituitary → Corticotropin release

Anesthesia Pharmacology (5 decks)

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