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Anesthesia Pharm Oral Exam > Adjuncts 1: catecholamines, noncatecholamines, beta blockers, CCBs, alpha blockers, vasodilators, antiarrythmics > Flashcards

Adjuncts 1: catecholamines, noncatecholamines, beta blockers, CCBs, alpha blockers, vasodilators, antiarrythmics Flashcards

1
Q

Epinephrine: class

A

Endogenous catecholamine and nonselective adrenergic agonist at a1, a2, b1, b2

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2
Q

Epinephrine: MoA

A

Binds to adrenergic receptors, stimulating G-coupled proteins, adenylate cyclase, and cAMP.

Low doses = stimulation of beta2 = vasodilation, bronchodilation, decreased histamine release

Higher doses = stimulation of alpha1 = peripheral, renal, splanchnic vasoconstriction and decrease in bronchial secretions

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3
Q

Epinephrine: PK

A

Onset 1-2 mins IV
DOA 5-10 mins
E 1/2t = 30 secs
Small Vd = poor lipid solubility

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4
Q

Epinephrine: AE

A 
Tachycardia and severe HTN
Arrhythmias
Cerebral hemorrhage
Hyperglycemia 
Hypokalemia
Increased IOP
Periph vascular insufficiency

Headache, nervousness, tremor

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5
Q

Epinephrine: CI

A 
Non-anaphylactic shock
Cardiac arrhythmias
Severe hypertension
Pheochromocytoma
Active labor
Cerebral or coronary artherosclerosis
Glaucoma
Renal insufficiency
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6
Q

Epinephrine: dosing

A

2-8mcg IV for hypotension
10mcg/kg for resuscitation

Continuous infusion:
1-2mcg/min beta2
4-5mcg/min beta 1
10-20mcg/min alpha 1 + beta

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7
Q

Norepi class:

A

Endogenous catecholamine
Direct acting nonselective adrenergic agonist
Alpha and B1&raquo_space;»> B2

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8
Q

Norepi MoA:

A

Binds to alpha and beta1 adrenergic receptors, stimulating C-coupled proteins, adenylate cyclase, and cAMP.

Low doses = increased CO (inotrophy and chronotrophy) and increased blood pressure.

High doses = potent alpha1 effects outweighs beta –> arterial constriction and decreased vital organ blood flow.

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9
Q

Epinephrine: metabolism

A

COMT and MAO in the blood, liver, kidneys; metabolites excreted in urine

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10
Q

Norepi: PK

A

Rapid onset
Limited DOA
E1/2t = 2.5 mins

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11
Q

Norepi: metabolism

A

COMT and MAO in the blood, liver, kidneys; metabolites excreted in urine

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12
Q

Norepi: AE

A

Usually a result of intense vasoconstriction…

HTN
Severe bradycardia
End organ ischemia
Hemorrhagic stroke or ischemia of cerebral vessels
Renal vasoconstriction + oliguria

Anxiety and headache

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13
Q

Norepi: CI

A

HTN
Extreme hypovolemia
Mesenteric or PVD

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14
Q

Norepi: dosing

A

0.01-0.1mcg/kg/min or 4-16mcg/min

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15
Q

Isoproterenol: class

A

Synthetic catecholamine

Selective beta adrenergic receptor agonist (beta1&raquo_space; beta 2)

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16
Q

Isoproterenol: MoA

A

Stimulates beta adrenergic receptors, stimulating g-coupled protein receptors, further stimulating adenylate cyclase and cAMP within the cell.

Beta 1 = increases inotropy and chronotropy of the heart

Beta 2 = Vascular, GI, pulmonary and uterine relaxation

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17
Q

Isoproterenol: PK

A

Immediate onset
DOA 5-10mins
E1/2t = 2.5-5mins

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18
Q

Isoproterenol: metabolism

A

COMT in liver and lungs

40-50% unchanged in urine

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19
Q

Isoproterenol: AE

A

Tachycardia, dysrhythmias
MI and increased O2 consumption
Decreased CBF
Peripheral vasodilation and hypotension

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20
Q

Isoproterenol: CI

A

HAT
Hypersensitivity
Angina/CAD
Tachycardia

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21
Q

Isoproterenol: dosing

A

0.5 - 10 mcg/min

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22
Q

Dobutamine: class

A 
Synthetic catecholamine (analog of isoproterenol)
Direct acting selective beta 1 adrenergic receptor agonist with some beta 2 activity at clinical doses
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23
Q

Dobutamine: MoA

A

Binds with beta1 adrenergic receptors, stimulating G-coupled proteins, adenylate cyclase, and cAMP within the cell causing influx of Ca+ and promoting cardiac muscle contractility

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24
Q

Dobutamine: PK

A

Onset 1-2mins

Peak effect in 10 mins

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25
Q

Dobutamine: metabolism

A

COMT and MAO in blood, liver, kidneys, GI tract

Metabolites excreted in urine

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26
Q

Dobutamine: AE

A 
Dyspnea
Tachycardia, SVT
Thrombocytopenia and platelet inhibition
Phlebitis
Down regulation of beta receptors after 3 days of tx = tolerance

Fever, headache, nausea
Paresthesia

TOXICITY = anorexia, NV, tremor, head, SOB, angina, chest pain, anxiety

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27
Q

Dobutamine: CI

A

Hypersensitivity
Hypovolemia
CAD without CHF
Caution in pregnancy

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28
Q

Dobutamine: dosing

A

Start at 0.5-1mcg/kg/min; titrate every few minutes to 2-20mcg/kg/min

Max dose 40mcg/kg/min

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29
Q

Dopamine: class

A

Endogenous catecholamine

Alpha, beta adrenergic, and dopaminergic receptor agonist

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30
Q

Dopamine: MoA

A

Low doses – agonize dopaminergic 1 receptors in coronary, renal, and mesenteric vascular smooth muscle cells to stimulate G-CP, AC, cAMP

Medium doses – agonize beta 1 adrenergic receptors in cardiac myocytes to increase contractility = +inotrope = ↑CO and HR

High doses – agonize alpha1 in GU, GI, heart, liver and vascular smooth muscle

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31
Q

Dopamine: PK

A

Rapid onset

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32
Q

Dopamine: metabolism

A

MAO and COMT
Beta hydroxylated to norepinephrine, then methylated to epinephrine in liver and plasma
Eliminated in urine

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33
Q

Dopamine: AE

A 
Limb ischemia if extravasated
Tachycardia, angina, palpitations
Dyspnea
Increased IOP
Hyperglycemia

Headache, N/V

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34
Q

Dopamine: CI

A 
Right heart failure d/t increase pulm art pressure
MAOIs
Sulfa allergy
V-fib
Pheochromocytoma
Cocaine use (exaggerated response)
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35
Q

Dopamine: dosing

A

0.5 to 2mcg/kg/min low dose
2-5mcg/kg/min medium dose
>10mcg/kg/min large dose

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36
Q

Vasopressin: class

A

Exogenous antidiuretic peptide and vasopressor

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37
Q

Vasopressin: MoA

A

Stimulates V1 receptors on vascular smooth muscle, glomerular mesangial cells, and vasa recta causing potent vasoconstriction

Stimulates V2 receptors on basolateral cell membrane of renal collecting ducts to ↑ water reabsorption and constricts glomerular efferent arteriole to maintain GFR

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38
Q

Vasopressin: PK

A 
Onset = nasal 1hr
DOA = nasal 3-8hrs
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39
Q

Vasopressin: metabolism

A

Metabolized by tissue peptidases
Rapid oral inactivation by trypsin
E1/2t 10-20min

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40
Q

Vasopressin AE:

A 
Coronary artery vasospasm, angina, MI
Vasoconstriction and HTN 
Increased peristalsis, N/V, and abd pain
Decreased PLTs
Tremor, headache, fever, diaphoresis
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41
Q

Vasopressin: CI

A

Hypersensitivity

Caution w/ NSAIDs, carbamazepine (inc AVP effect)

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42
Q

Vasopressin: dosing

A

Refractory cardiac arrest: 40 units IV push
Esophageal varicies: 20 units over 5 mins
Hemorrhagic/septic shock: 0.04 units/min
DI: 100-200mU/hr IV

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43
Q

Ephedrine: class

A

Synthetic non-catecholamine
Indirect alpha 1 and beta 2 agonist
Direct beta 1 agonist

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44
Q

Ephedrine: MoA

A

Indirectly: increases NE release from post ganglionic SNS nerve, activating receptors
Directly: binds to receptors and activates G protein, activates or intracellular enzyme adenylate cyclase to cAMP and phospholipase C

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45
Q

Ephedrine: PK

A

Rapid onset
DOA 1 hr
E1/2 t 3hrs

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46
Q

Ephedrine: metabolism

A

COMT, though inefficiently; 40% unchanged in the urine

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47
Q

Ephedrine: AE

A 
Tachyphylaxis
Arrhythmias
HTN
MI
CNS stim
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48
Q

Ephedrine: CI

A 
Hypersensitivity
Severe HTN
Arrhythmias
CHF
Glaucoma
MAOIs
Cocaine use (be cautious)
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49
Q

Ephedrine: dosing

A

5-25 mg IV

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50
Q

Phenylephrine: class

A

Synthetic non-catecholamine

Selective alpha 1 adrenergic agonist

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51
Q

Phenylephrine: MoA

A

Binding to alpha1 receptor causes direct stimulation of g-protein coupled receptor, increases adenylate cyclase, and cAMP, leading to an influx of calcium on systemic VENOUS vascular smooth muscle and vasoconstriction

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52
Q

Phenylephrine: PK

A

Onset

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53
Q

Phenylephrine: AE

A

Reflex bradycardia
Hypertension and decreased CO d/t increased afterload
Decreased renal, splanchnic, cutaneous blood flow
Decreased UO
Metabolic acidosis

Anxiety, HA, nervousness, weakness, paresthesia
Rebound nasal congestion

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54
Q

Phenylephrine: CI

A 
Hypersensitivity
Glaucoma
Severe HTN and tachycardia
Arrythmias
Caution in elderly, heart blocks, HTN, bradycardia
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55
Q

Phenylephrine: dosing

A

50-200mcg IV bolus Q5mins

20-180mcg/min to start with maintenance at 10-60mcg/min

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56
Q

Esmolol: class

A

Selective beta 1 adrenergic antagonist

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57
Q

Esmolol: MoA

A

Reversibly binds to beta 1 adrenergic receptor antagonists to inhibit the binding of NE, EPI, and other beta agonist, preventing the stimulation of G-coupled protein receptors, adenylate cyclase, and cAMP

Slows SA rate and conduction through the AV node and decreases contractility, reducing cardiac O2 demand

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58
Q

Esmolol: PK

A 
Onset: 30-60 sec
DOA = 10-15mins
E1/2t = 9 mins
High Vd
55% PB
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59
Q

Esmolol: metabolism

A

Plasma esterases and excretion in the urine

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60
Q

Esmolol: AE

A 
Severe bradycardia
Hypotension
Heart block
CHF and pulmonary edema
POI d/t propylene glycol

Syncope/dizziness
Headache

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61
Q

Esmolol: CI

A 
Hypersensitivity
CHF
Concurrent CCB (= complete heart block)
Sick sinus syndrome
Severe hypotension
HR dependent
Asthma and COPD (in high doses)
Pregnancy
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62
Q

Esmolol: dosing

A

5-10mg IV Q3-5mins to total dose of 80mg

300-500mcg/kg/min

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63
Q

Labetalol: class

A

Beta 1, beta 2, alpha1 adrenergic antagonist

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64
Q

Labetalol: MoA

A

Reversibly binds to beta1, beta2, alpha1 adrenergic receptor antagonists to inhibit the binding of NE, EPI, and other beta agonist, preventing the stimulation of G-coupled protein receptors, adenylate cyclase, cAMP.

Slows SA node rate (beta 1), slows conduction through the AV node (beta 1), decreases contractility (beta 1), and causes peripheral, cerebral, and coronary vasodilation (alpha 1)

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65
Q

Labetalol: PK

A 
Onset = 3-5 mins
Peak effect 5-10mins (redose 5-10mins)
E1/2t = 5-8hrs
Vd 7L/kg
50% PB
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66
Q

Labetalol: metabolism

A

Hepatic microsomal enzymes

Eliminated in urine 50% - fecal 50%

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67
Q

Labetalol: AE

A 
Bronchospasm*
Fluid retention*
Hypoglycemia*
Severe bradycardia
Hypotension
Heart block

Syncope/dizziness
Headache

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68
Q

Labetalol: CI

A 
Hypersensitivity
Asthma/COPD
Severe CHF
Concurrent CCB use (= complete heart block)
Severe hypotension or bradycardia
Sick sinus syndrome
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69
Q

Labetalol: dosing

A

5-10mg IV Q5-10mins up to 300mg total

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70
Q

Metoprolol: class

A

Selective beta 1 adrenergic antagonist

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71
Q

Metoprolol: MoA

A

Reversibly binds to beta 1 adrenergic receptor antagonists to inhibit the binding of NE, EPI, and other beta agonist, preventing the stimulation of G-coupled protein receptors, adenylate cyclase, and cAMP

Slows SA rate and conduction through the AV node and decreases contractility, reducing cardiac O2 demand

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72
Q

Metoprolol: PK

A

Onset Rapid
E1/2 life = 3-7hrs
12% PB

73
Q

Metoprolol: metabolism

A

Hepatic metabolism

Renal excretion

74
Q

Metoprolol: AE

A 
Bradycardia
Cardiac failure/asystole
Dyspnea
Heart block
Peripheral edema
Arterial insufficiency
75
Q

Metoprolol: CI

A 
Hypersensitivity
Sick sinus syndrome
Concurrent CCB use (= complete heart block)
Asthma and COPD (in high doses)
HR dependent pts
76
Q

Metoprolol: dosing

A

1.25-5mg IV Q2-5mins to max of 15mg

77
Q

Propranolol: class

A

Beta 1 and beta 2 adrenergic antagonist

78
Q

Propranolol: MoA

A

Reversibly binds to beta 1 adrenergic receptor antagonists to inhibit the binding of NE, EPI, and other beta agonist, preventing the stimulation of G-coupled protein receptors, adenylate cyclase, and cAMP.

Slows SA rate and conduction through the AV node and decreases contractility, reducing cardiac O2 demand.

Causes peripheral, cerebral, and coronary vasodilation.

79
Q

Propranolol: PK

A

Vd 4L/kg
90%PB
E1/2t = 4hrs

80
Q

Propranolol: metabolism

A

1st pass effect & pulmonary uptake
Active metabolite: hydroxypropanolol
Excreted in the urine

81
Q

Propranolol: AE

A 
Bronchospasm*
Hypoglycemia* 
Severe bradycardia
Severe hypotension
Heart block
Rebound tachycardia with rapid withdrawal

Syncope/dizziness

82
Q

Propranolol: CI

A 
Hypersensitivity
Asthma/COPD
Heart block
Concurrent CCB (= complete heart block)
PVD
DM
Pregnancy
83
Q

Propranolol: dosing

A

0.25-0.5mg IV titrate to 1mg/min IV

84
Q

Nifedipine: class

A

Dihydropyridine calcium channel antagonist

85
Q

Nifedipine: MoA

A

Competitive binds to calcium channels in vascular smooth muscle to maintain them in the INACTIVATED CLOSED STATE, preventing the influx of calcium through slow L-type voltage gated Ca++ channels , preventing the contraction of vascular smooth muscle cells

86
Q

Nifedipine: PK

A

Onset 1-3 mins
Peak 1-3 hrs
E1/2t = 3-7 hrs
90% PB

87
Q

Nifedipine: metabolism

A

Hepatic CYP450 metabolism

Renal excretion

88
Q

Nifedipine: AE

A

Reflex tachycardia
Hypotension
MI d/t decreased afterload
Skeletal muscle weakness

Flushing
Vertigo
HA

89
Q

Nifedipine: CI

A

Hypersensitivity
Heart failure
Hypotension
Concomitant with grapefruit juice

90
Q

Nifedipine: dosign

A

5-15mcg/kg

91
Q

Verapamil: class

A

Non-dihydropyridine calcium channel antagonist

Class IV antiarrythmic

92
Q

Verapamil: MoA

A

Competitively binds to calcium channels in cardiac muscle tissues to maintain them in the INACTIVATED CLOSED STATE, preventing the influx of calcium through slow L-type voltage gated Ca++ channels in cardiac muscle cells.

Primarily inotropic/chronotropic effects, not blood pressure.

93
Q

Verapamil: PK

94
Q

Verapamil: metabolism

A

CYP 450 enzymes
Active metabolite: norverapamil
70% unchanged in urine

95
Q

Verapamil: AE

A

Heart failure
Peripheral edema
Increased K+ with blood products

Gingival hyperplasia
Dizziness

96
Q

Verapamil: CI

A 
Hypersensitivity
Renal failure
Wide QRS V-tach
Heart failure
WPW, SSS, bradycardia, or heart block (conduction abnormalities)
97
Q

Verapamil: dosing

A

2.5-5mg IV over 2 mins

Then 5-10mg in 15 to 30 mins as needed

Max 20mg

98
Q

Diltiazem: class

A

Benzothiazipine antiarrythmic

99
Q

Diltiazem: MoA

A

Competitively binds to calcium channels in cardiac muscle tissues, and ARTERIOLAR vascular smooth muscle tissue maintaining them in INACTIVATE CLOSED STATE, preventing the influx of calcium through slow L-type voltage gated Ca++ channels and preventing the contraction of both vascular smooth muscle and cardiac muscle cells.

100
Q

Diltiazem: PK

101
Q

Diltiazem: metabolism

A

1st pass effect

CYP450 and 30% unchanged in the urine

102
Q

Diltiazem: AE

A

Bradycardia
AV block
Heart failure
Edema

HA, flushing
Dizziness/syncope

103
Q

Diltiazem: CI

A

Hypersensitivity

104
Q

Diltiazem: dosing

A

SVT 0.25mg/kg over 2 mins + 0.35mg/kg prn

Pheo 3-10mcg/kg/min

105
Q

Nifedipine: drug interactions

A

Potentiates NMB
Decreases anesthetic reqs
Use w/ BBs can cause heart block

106
Q

Verapamil: drug interactions

A

Decreases anesthetic reqs

Use w/ BBs can cause heart block

107
Q

Diltiazem: drug interactions

A

Potentiates NMB

Use w/ BBs can cause heart block

108
Q

Phenoxybenzamine: class

A

Long acting, non-selective alpha adrenergic receptor antagonist

109
Q

Phenoxybenzamine: MoA

A

Irreversibly binds to the alpha 1 and alpha 2 adrenergic receptors preventing the binding of NE, Epi, and other alpha agonists, preventing the stimulation of G-coupled proteins, adenylate cyclase, and cAMP.

Blocks alpha mediated vasoconstriction.

It also antagonizes Ach, Histamine, 5HT

110
Q

Phenoxybenzamine: PK

A

Slow onset – Prodrug
60mins to peak
E1/2t 24 hrs

111
Q

Phenoxybenzamine: metabolism

A

Hepatic metabolism

Renal and biliary excretion

112
Q

Phenoxybenzamine: AE

A 
Reflex tachycardia
Hypotension
Seizures
Palpitations
Sedation with chronic use (alpha 2)
Hypoglycemia

Flushing/syncope
Impotence
Nasal stuffiness
Dry mouth

113
Q

Phenoxybenzamine: CI

A

Hypersensitivity
Hypotension
Hypovolemia

114
Q

Phenoxybenzamine: dosing

A

10mg BID up to total 120mg/day oral – started 2-3 weeks pre op

115
Q

Phentolamine: class

A

Short acting, non-selective alpha adrenergic receptor antagonist

116
Q

Phentolamine: MoA

A

Competitively but REVERSIBLY binds to alpha 1 and alpha 2 adrenergic receptors, preventing the binding of NE, Epi, and other alpha agonists, preventing the stimulation of G-coupled proteins, adenylate cyclase, and cAMP.

Blocks alpha mediated vasoconstriction.

117
Q

Phentolamine: PK

A

Onset =2-5 mins
DOA = 10-15 mins
E1/2L = 19 mins

118
Q

Phentolamine: metabolism

A

Hepatic metabolism

10% excreted unchanged in urine

119
Q

Phentolamine: AE

A 
Tachycardia – reflexive
Severe hypotension
Arrhythmias
MI
Hypoglycemia
Dizziness
Flushing
Impotence
Nasal stuffiness
Abd cramps
120
Q

Phentolamine: CI

A 
Hypersensitivity
CAD, MI
Pregnant moms
Renal impairment
PUD
121
Q

Phentolamine: dosing

A

30-70 mcg/kg IV to decrease BP from transient stimulation

Max 20mg

Extravasation = 10mg injected into affected site.

122
Q

Prazosin: class

A

Selective alpha 1 adrenergic antagonist

123
Q

Prazosin: MoA

A

Competitively binds to alpha 1 adrenergic receptors preventing the stimulation of G-coupled proteins, adenylate cyclase, and cAMP causing vasodilation of arterial and venous vasculature.

Leaves the inhibiting effect of alpha 2 activity on NE release intact = less likely to have reflex tachycardia

124
Q

Prazosin: PK

A

Peak 3 hrs

E1/2 t = 3-4 hrs

125
Q

Prazosin: metabolism

A

Hepatic metabolism, elimination via bile and feces NON RENALLY!!

126
Q

Prazosin: AE

A 
Hypotension
Fluid retention
Anticholinergic effects
N/V
Palpitations
Drug-induced lupus
Hepatotoxicty
Flushing/dizziness
Syncope
HA
Dry mouth
Nasal congestion
127
Q

Prazosin: CI

A

Hypersensitivity
BB use (refractory hypotension)
Pregnant

128
Q

Prazosin: drug interactions

A

Additive effects with diuretics/other BP meds

129
Q

Prazosin: dosing

A

1mg PO at bedtime (max daily 20mg in divided doses)

130
Q

Clonidine: class

A

Selective alpha 2 adrenergic antagonist

131
Q

Clonidine: MoA

A

Inhibits sympathetic outflow from the medulla = decreased HR and contractility and vasomotor tone.

Enhance antinociceptive state by inhibiting release of spinal substance P.

Inhibit central thermoregulatory control to decrease vasoconstriction and shivering.

Also affects the function of K+ channels in the CNS = making cell hyperpolarized = decreased anesthetic requirements

132
Q

Clonidine: PK

A 
Onset 30-60mins
Peak 60-9mins
DOA 8 hrs PO
E1/2t 9-12hrs
30% PB
2L/kg
133
Q

Clonidine: metabolism

A

50% metabolized in liver, 50% excreted unchanged

134
Q

Clonidine: AE

A 
Bradycardia
Heart failure
Hepatotoxicity
Sedation
Postural hypotension
Rebound hypertension with abrupt withdrawal
Sodium and water retention

Dry mouth
Skin rash
Impotence

135
Q

Clonidine: CI

A

Pregnant women
Prior to surgery
Hypersensitivity

136
Q

Clonidine: dosing

A

0.2mg-0.3mg/day

Epidural and SAB = 150-450mcg

137
Q

Hydralazine: class

A

Direct acting vasodilator

138
Q

Hydralazine: MoA

A

Activates guanylate cyclase which leads to membrane hyperpolarization, K+ channel activation, inhibition of calcium release from SR in vascular smooth muscle.

Can trigger reflexive tachycardia.

139
Q

Hydralazine: PK

A 
IV onset 5-20mins 
Peak 15-20mins
E1/2t = 4 hrs (4x in renal dz)
E1/2L = 100hrs d/t strong binding to smooth muscle 
90% PB
140
Q

Hydralazine: metabolism

A

Metabolized in the liver with extensive first pass effect

141
Q

Hydralazine: AE

A

Anemias, hepatotoxicity

Increased ICP, head ache, fever, chills, anxiety, disorientation, depression and coma

RA, lupus like syndrome, cramps, weakness, tremors, neuritis

Tachycardia, angina, orthostatic hypotension, dizziness, palpitations,

Nasal congenstion, dyspnea

Anorexia, NV, diarrhea, constipation, ileus

Impotence, difficult micturition

142
Q

Hydralazine: CI

A

Hypersensitivity
Dissecting aortic aneurysm
CAD
Mitral valve rheumatic heart disease

Prolonged onset should be considered before redosing

143
Q

Hydralazine: dosing

A

2.5 - 20 mg IV Q4hrs

144
Q

Nitroglycerin: class

A

Organic nitrate and venodilator

145
Q

Nitroglycerin: MoA

A

Generates Nitric Oxide to stimulate production of cGMP to cause peripheral and smooth muscle vasodilation.

Increased venous capacitance decreases the preload to the right side of the heart = decreased right and left end diastolic pressure = decreased myocardial demand.

146
Q

Nitroglycerin: PK

147
Q

Nitroglycerin: AE

A 
Reflex tachycardia
Tachypnea
Increase in ICP with decreased intracranial compliance 
Increased bleeding time
Dizziness, lightheadedness, syncope
N/V
148
Q

Nitroglycerin: CI

A 
Hypertrophic obstructive cardiomyopathy
Severe aortic stenosis
Hypotension, shock or MI with low left ventricular filling pressures
Increased ICP
Glaucoma
Severe anemaia
Cardiac tamponade
Restrictive cardiomyopathy or pericarditis
149
Q

Nitroglycerin: metabolism

A

Metabolism results in nitrate metabolite capable of producing methemoglobin by oxidation of ferrous ion in hgb

150
Q

Nitroglycerin: dosing

A

5-200mcg/min IV

151
Q

Milrinone: class

A

Phosphodiesterase inhibitor vasodilator

152
Q

Milrinone: MoA

A

Selectively inhibits phosphodiesterase III which is a heart specific enzyme responsible for degradation of cAMP, which increases calcium and thus increases contractility and inotropic effects. Increased cAMP also works in vascular smooth muscle to cause vasodilation and decrease peripheral vascular resistance. This all increases cardiac output.

153
Q

Milrinone: PK

A 
Onset 5-15mins
Peak after 5 mins
E1/2time = 2.5hrs
Vd = 0.4L/kg
70% PB
154
Q

Milrinone: metabolism

A

80% unchanged in the urine

155
Q

Milrinone: AE

A 
Cardiac dysrhythmias, ventricular arrhythmias, and supraventricular arrhythmias
Hypotension
Angina
Headaches
Hypokalemia, tremor, thrombocytopenia
156
Q

Milrinone: CI

A

Hypersensitivity

Acute MI

157
Q

Milrinone: dosing

A

50mcg/kg IV over 10mins + 0.375mcg/kg/min maintenance infusion

158
Q

Adenosine: class

A

Antiarrythmic, endogenous nucleoside consisting of adenine and pentose sugar

159
Q

Adenosine: MoA

A

Adenosine acts on adenosine A1 receptors in the cardiac conduction system that are linked to acetylcholine activated G-coupled potassium channels (Kach). This leads to slowing of cardiac conduction tissue, slowing SA node conduction, and a delay in AV node conduction.

160
Q

Adenosine: PK

A

E1/2 life = 10 sec; immediate onset, must be IV pushed very fast

161
Q

Adenosine: metabolism

A

Intracellular enzyme metabolism. No hepatic/renal involvement.

162
Q

Adenosine: AE

A 
Headache, dizziness, parasthesia
Palpitations, chest pain
Hypotension
Dyspnea
Chest pressure
Numbness
163
Q

Adenosine: CI

A 
Hypersensitivity
2nd or 3rd degree heart block
SSS without pacer
Bronchospastic and restrictive lung disease
(not effective in afib, aflutter, VT)
164
Q

Adenosine: dosing

A

SVT: 6mg IV, if not effective give 12mg, if not effective give 18mg

Controlled hypotension: 220mcg/kg/min

165
Q

Amiodarone: class

A

Class III antiarrhythmic (with Class I, II, IV effects)
Benzofurane derivative containing iodine
Atrial and ventricular dysrhythmic

166
Q

Amiodarone: MoA

A

Alters lipid membrane where ion channels are located, particularly the K+ channels responsible for repolarizations

Also blocks Na+ and Ca++ channels, as well as alpha/beta receptors

167
Q

Amiodarone: PK

A 
Onset – IV is rapid
Vd 66L/kg
96% PB
E1/2t = 29days
Duration after d/c therapy = 7-50days
168
Q

Amiodarone: metabolism

A

CYP450 microsomal enzymes with biliary excretion

Active metabolite: DEA

169
Q

Amiodarone: AE

A

Hypotension
Bradycardia
AV block, prolonged QTc and VT, torsades,
Decreased response to catecholamines
Pulm fibrosis, alveolar pneumonitis, ARDS (2% of pts)
Hyper/hypothyroidism, photosensitivity

170
Q

Amiodarone: CI

A

Hypersensitivity
Cardiogenic shock, bradycardia, 2nd or 3rd degree heart block
Pregnancy

171
Q

Amiodarone: drug interactions

A

Inhibits CYP450 enzymes = increased conc of warfarin, procainamide, digoxin

Fentanyl = cardiac arrest, bradycardia, hypotension

172
Q

Amiodarone: dosing

A

A-flutter, Stable VT/SVT: 150mg IV over 10 mins, 1 mg/min over next 6 hrs, then 0.5 mg/min over next 18hrs

Pulseless VT/VF: 300mg IVP, then 150mg IVP, then gtt

173
Q

Digoxin: class

A

Antiarrythmic

Cardiac glycoside

174
Q

Digoxin: MoA

A

Directly inhibits Na+/K+/ATPase pump, which increases Na+ in cardiac myocytes, which decreases Ca++ outflow by Na+/Ca++ pump, which increases available calcium for cardiac muscle contractions.

Also decreases sympathetic tone and increases vagal tone to slow conduction through SA and AV nodes

175
Q

Digoxin: PK

A 
Onset = 5-30mins IV
Peak 1-5 hrs
E1/2life = 30-48hrs
Vd 7L/kg
25% PB
176
Q

Digoxin: metabolism

A

Hepatic metabolism

50% excreted by kidneys unchanged.

177
Q

Digoxin: AE

A

EKG changes: prolonged PR interval, ST depression, T wave changes
Dysrhythmias
Heart block

Blurred vision
NV, diarrhea, headache, fatigue

178
Q

Digoxin: CI

A

Vfib, v-tach, heart block
IHSS
Renal impairment (decrease dose)
Hypokalemia, hypomagnesemia or hypercalcemia can lead to toxicity

179
Q

Digoxin: dosing

A

Loading dose = 0.75-1.5mg PO or 0.5-1.0mg IV
Maint dose = 0.125-0.5mg PO or 0.25mg IV

Therapeutic level 0.5-2.0ng/mL

Anesthesia Pharm Oral Exam (5 decks)

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