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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 3: CAD and Heart Failure Pharmacotherapy > Flashcards

Exam 3: CAD and Heart Failure Pharmacotherapy Flashcards

1
Q

Coronary blood flow at rest:

A

70 ml/min/100g

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2
Q

% O2 extraction by myocardial tissue beds:

A

70% (very high!)

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3
Q

Heart gets ____% of CO:

A

5%

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4
Q

Coronary blood flow increases ____x during intense exercise:

A

2-4x

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5
Q

Cardiac demand increases _____x during intense exercise:

A

4-7x

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6
Q

Systolic contraction impedes coronary filling because:

A

Intramural pressure increases, redistributes blood from subendocardial to subepicardial layers, compresses vessels

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7
Q

Perfusion pressure to LV =

A

DBP - LVEDP

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8
Q

Tachycardia during anesthesia greatly increases the chance of:

A

Myocardial ischemia

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9
Q

Factors (4) that ↑ myocardial O2 demand:

A

Tachycardia*
High afterload (↑ SVR)
High preload
↑ contractility

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10
Q

Factors (6) that ↑ myocardial O2 supply:

A 
Hgb concentration
O2 saturation
Bradycardia (w/in reason)
↑ DBP
Low-normal preload
↓ contractility
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11
Q

Goal HR range and indicated drugs in pts with CAD:

A

Slow

Indicated: β-blockers, CCBs

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12
Q

Drugs (4) with negative effect on HR in pts with CAD:

A

Isoproterenol
Dobutamine
Ketamine
Pancuronium

Sympathomimetic/vagolytic

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13
Q

Goal preload and indicated drugs in pts with CAD:

A

Low-normal

Indicated: NTG, diuretics

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14
Q

Therapy with negative effect on preload in pts with CAD:

A

Volume loading

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15
Q

Goal afterload and indicated drugs in pts with CAD:

A

High-normal

Indicated: Phenylephrine

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16
Q

Drugs (2) with negative effect on afterload in pts with CAD:

A

Nitroprusside

High-dose volatile agents

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17
Q

Goal contractility and indicated drugs in pts with CAD:

A

Normal-low

Indicated: β-blockers, CCBs, high-dose volatile agents

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18
Q

Drugs (2) with negative effect on contractility in pts with CAD:

A

Epinephrine

Dopamine

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19
Q

Summary of stable angina treatment (mnemonic):

A 
A: ASA/anti-anginals
B: BP control
C: cholesterol, cigarettes
D: diet, diabetes
E: education, exercise
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20
Q

MoA of organic nitrates:

A

Release NO after metabolism which ↑ NO concentration in smooth muscle cells

Relaxes coronary arteries to increase supply, decrease demand (↓ preload?)

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21
Q

Examples of organic nitrates:

A 
NTG
Isosorbide dinitrate (Isordil)
Isosorbide mononitrate (Imdur)
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22
Q

Nitrates are not good long-term antihypertensives d/t:

A

Baroreceptor reflex ↑ HR

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23
Q

Describe the NO signal pathway on the endothelial cell side:

A

Endothelial cell: bradykinin activates GPCR, which ↑ Ca2+ and triggers calmodulin, which activates eNOS to turn arginine into NO, which diffuses out

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24
Q

Describe the NO signal pathway on the vascular smooth muscle cell side:

A

NO diffuses in and activates guanylyl cyclase to ↑ cGMP, which leads to decreased Ca2+ and vasodilation

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25
Q

Enzyme that converts (active) cGMP to (inactive) GMP:

A

Phosphodiesterase inhibitors

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26
Q

Nitrate effects on O2 consumption:

A

Reduces it via ↓ preload (venodilation) and ↓ afterload (arterial dilation)

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27
Q

Stronger effect of NTG: venodilation or arterial dilation?

A

Venodilation

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28
Q

NTG provides preferential dilation of:

A

Collateral vessels serving ischemic areas

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29
Q

Metabolism of nitroglycerin:

A

90% degraded by liver to inactive metabolites; sublingual/transdermal bypass first pass effect

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30
Q

E1/2t of NTG:

A

1.5 minutes

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31
Q

Adverse effects of NTG:

A

Headaches
Postural hypotension/syncope
Methemoglobinemia

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32
Q

Tolerance issues with NTG:

A

Limits the efficacy, regardless of the route

Must have nitrate-free intervals (usually at night, when O2 demand is lower)

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33
Q

Advantages of oral isosorbide mononitrate:

A

High bioavailability
Long t1/2
High levels during day, low levels at night

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34
Q

Drug interactions with nitrates:

A

Phophodisterase inhibitors (sildenafil, tadalafil, vardenafil) - additive effect w/ nitrates

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35
Q

Supply/demand benefit of β-antagonists in CAD:

A

↓ demand via ↓ CO from ↓ HR

↑ supply via longer diastolic filling time

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36
Q

Specific β-antagonists to use in CAD:

A

β1-selective agents: metoprolol, atenolol

Don’t want to ↓ flow to peripheral vessels

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37
Q

Benefit of β-antagonists post-MI:

A

↓ post-MI remodeling

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38
Q

S/E of β-antagonists:

A 
Depression
Insomnia
Masking hypoglycemia
Exercise intolerance
Bronchospasm
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39
Q

Discontinuation of β-antagonists:

A

Do not stop suddenly due to receptor upregulation

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40
Q

MoA of CCBs:

A

Bind the α1 subunit of the L-type calcium channel in mode “0”, the state where channel will not respond to depolarization

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41
Q

Effect of CCBs at the SA node:

A

↓ HR (negative chronotropic effect)

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42
Q

Effect of CCBs at the AV node:

A

↓ conductivity (negative dromotropic effect)

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43
Q

Effect of CCBs at the cardiac muscle:

A

↓ contractility (negative inotropic effect)

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44
Q

Effect of CCBs at the coronary vasculature:

A

Vasodilation

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45
Q

Adverse effects of CCBs:

A 
AV block
Cardiac failure
Headache
Constipation
Hypotension

All “too much of a good thing”

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46
Q

Examples of dihydropyridine CCBs:

A

Amlodipine
Nifedipine
Nicardipine

47
Q

Dihydropyridine CCBs more selective for:

A

Ca2+ channels in the vasculature (esp. arterial)

48
Q

Adverse effect specific to dihydropyridine CCBs:

A

May cause reflex tachycardia

49
Q

Examples of non-dihydropyridine CCBs:

A

Verapamil

Diltiazem

50
Q

Non-dihydropyridine CCBs more selective for:

A

Ca2+ channels in the heart muscle

51
Q

Adverse effect specific to non-dihydropyridine CCBs:

A

Heart block

52
Q

Avoid non-dihydropryridines in combination with:

A

β-blockers

53
Q

Role of ASA in CAD:

A

Antiplatelet activity prevents thrombus formation

54
Q

Tx of unstable angina/N-STEMI:

A

Anti-anginal drugs
Heparin/ASA
GPIIb/IIIa antagonists
Clopidogrel

55
Q

Tx of STEMI:

A

Surgery

Thrombolytics

56
Q

Indication for clopidogrel:

A

ACS pts with ASA allergy

57
Q

Indications for GPIIb/IIIa inhibitors:

A

Reduce MI risk in pts w/ unstable angina

Reduce recurrent MI/revascularization in pts with NSTEMI

58
Q

Tx for acute stable angina:

A

Nitrates
β-blockers
CCBs

59
Q

Tx for acute unstable angina:

A 
Nitrates
β-blockers
CCBs
ASA/clopidogrel
Heparin/thrombolytics
GPIIb/IIIa inhibitors
60
Q

Tx for variant angina:

A

Nitrates

CCBs

61
Q

Effects of aldosterone on the heart:

A

Insult to myocardium
Causes remodelling
Promotes atherosclerosis

62
Q

Systolic dysfunction is EF <

63
Q

Causes of systolic dysfunction:

A 
CAD
HTN
Valvular disease
ETOH
Thyroid disease
Cardiotoxic drugs
64
Q

Causes of diastolic dysfuction:

A

Cardiomyopathies

Incomplete relaxation due to ischemia

65
Q

Major manifestations of CHF:

A

Dyspnea
Fatigue
Fluid retention

66
Q

Three physiologic goals of CHF tx:

A

↓ preload
↓ afterload
↑ inotropy

67
Q

Drugs to reduce preload in CHF:

A

Diuretics
Aldosterone antagonists
Venodilators (NTG)

68
Q

Drugs to reduce afterload in CHF:

A

ACEIs
β-blockers
Vasodilators

69
Q

Drugs to increase inotropy in CHF:

A

Cardiac glycosides
Sympathomimetic amines
Phosphodiesterase inhibitors

70
Q

Goal HR range in CHF and drugs indicated for this:

A

Normal-high

Indicated: dopamine, dobutamine

71
Q

Drugs with negative effect on HR in CHF:

A

High-dose β-blockers

72
Q

Goal preload in CHF and indicated therapy:

A

Normal

Indicated: IV fluids if needed

73
Q

Drugs with negative effect on preload in CHF:

A

NTG

Thiopental

74
Q

Goal afterload in CHF and indicated therapy:

A

Low

Indicated: ACEIs, nitroprusside, amrinone

75
Q

Drugs with negative effect on afterload in CHF:

A

Phenylephrine

76
Q

Goal contractility in CHF and indicated therapy:

A

Increased

Indicated: dopamine, dobutamine, epinephrine, amrinone

77
Q

Drugs with negative effect on contractility in CHF:

A

High dose inhaled agents

High dose β-blockers

78
Q

Important consideration before giving diuretics for CHF:

A

Preload status

79
Q

Mortality benefit for thiazide/loop diuretics:

A

None - just QOL

80
Q

Examples of loop diuretics:

A

Furosemide
Bumetanide
Torsemide

81
Q

MoA of loop diuretics:

A

Inhibit Na+/K+/2Cl- cotransporter in Loop of Henle

↑ excretion of Na+, K+, H2O

82
Q

Diuretics which work on the distal tubule:

A

Thiazides
Metolazone
Spironolactone/eplerenone

83
Q

Distal tubule diuretics ↑ Na+ excretion by:

84
Q

Loop diuretics ↑ Na+ excretion by:

85
Q

MoA of spironolactone:

A

↓ K+/Na+ exchange in distal tubule (sheds Na+, spares K+)

Inhibits both androgen and mineralocorticoid receptors

86
Q

S/E of spironolactone:

A

Gynecomastia
Impotence
Hair growth (women)

87
Q

Spironolactone vs. eplerenone:

A

Eplerenone more selective with less S/E

88
Q

Role of NTG in CHF:

A

Use with caution - these pts need preload!

Reduces preload and myocardial O2 demand

Alleviates ischemia to improve diastolic relaxation

89
Q

Role of ACEIs in CHF:

A

Reverse RAAS-induced vasoconstriction, volume overload

Reduction of afterload also increases SV and GFR and increases diuresis

90
Q

Drugs with proven mortality benefits in CHF:

A 
Aldosterone antagonists
ACEIs
ARBs
β-blockers
Hydralazine + isosorbide dinitrate together in African-American pts
91
Q

Role of ARBs in CHF:

A

Reduce RAAS-induced vasoconstriction/volume overload

Lack of bradykinin-related vasodilation means less preload reduction

92
Q

Role of β-blockers in CHF:

A

Inhibition of renin release
Blunting of catecholamines
Preventing of ACS

NOT for use in acute, decompensated HF!

93
Q

Role of hydralazine + isosorbide dinirate in CHF:

A

Vasodilators (hydralazine arterial, ID venous) - used when pts cannot tolerate ACEIs

94
Q

MoA of digoxin:

A

Na-K-ATPase inhibitor

↓ SNS outflow, ↑ PSNS outflow

95
Q

Effect on HR from digoxin:

A

↓ conduction velocity and ↑ AV refractory period leads to ↓ HR

96
Q

Effect on contractility from digoxin:

A

Increased intracellular Ca2+; stronger contractions

97
Q

Effect on renal aborption of Na+ from digoxin:

A

↓ renal absorption of Na+

98
Q

Therapeutic levels of digoxin:

A

0.5 - 1.2 ng/ml

99
Q

Onset and half-life of digoxin:

A

Onset: 30-60 min

t1/2: 36 hrs

100
Q

Elimination of digoxin:

A

90% renally excreted

101
Q

S/E of digoxin:

A

Hypokalemia
AV block
Ventricular ectopy

102
Q

Tx for overdose of digoxin:

A

Digoxin immune fab

103
Q

Drug interactions with digoxin:

A

Risk of AV block w/ β-blockers
↓ contractility from β-blockers, CCBs
Abx ↑ absorption
Verapamil, quinidine, amiodarone ↑ digoxin levels

104
Q

MoA of phosphodiesterase inhibitors:

A

Inhibit degradation of cAMP/cGMP in myocytes, vascular smooth muscle

Increases intracellular Ca2+

↑ contractility
↑ art/ven dilation
↑ disastolic relaxation

105
Q

Phosphodiesterase inhibitors a good choice for overdose of:

A

β-blockers

106
Q

Onset, DOA and half-time for amrinone:

A

Onset: 5 minutes
DOA: 2 hrs
E1/2t: 6 hrs

107
Q

Dosing of amrinone:

A

0.5 - 1.5 mg/kg IV
Infusion: 2-10 mcg/kg/min
Max dose 24 hrs: 10mg/kg

108
Q

S/E of amrinone:

A

Hypotension
Thrombocytopenia
Arrythmias

109
Q

Elimination of amrinone:

A

Renal excretion

110
Q

Amrinone vs. milrinone:

A

Milrinone has less tachycardia and thrombocytopenia

111
Q

Dosing of milrinone:

A

50mcg/kg IV

Infusion: 0.5 mcg/kg/min

112
Q

Half-time of milrinone:

113
Q

Elimination of milrinone:

A

80% excreted unchanged via renal

114
Q

Applications of milrinone:

A

Acute managment, not long-term; long-term use increases M&M

Good for pulm HTN

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