Exam 3: CAD and Heart Failure Pharmacotherapy Flashcards Preview

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

Flashcards in Exam 3: CAD and Heart Failure Pharmacotherapy Deck (114):
1

Coronary blood flow at rest:

70 ml/min/100g

2

% O2 extraction by myocardial tissue beds:

70% (very high!)

3

Heart gets ____% of CO:

5%

4

Coronary blood flow increases ____x during intense exercise:

2-4x

5

Cardiac demand increases _____x during intense exercise:

4-7x

6

Systolic contraction impedes coronary filling because:

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

7

Perfusion pressure to LV =

DBP - LVEDP

8

Tachycardia during anesthesia greatly increases the chance of:

Myocardial ischemia

9

Factors (4) that ↑ myocardial O2 demand:

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

10

Factors (6) that ↑ myocardial O2 supply:

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

11

Goal HR range and indicated drugs in pts with CAD:

Slow
Indicated: β-blockers, CCBs

12

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

Isoproterenol
Dobutamine
Ketamine
Pancuronium

Sympathomimetic/vagolytic

13

Goal preload and indicated drugs in pts with CAD:

Low-normal
Indicated: NTG, diuretics

14

Therapy with negative effect on preload in pts with CAD:

Volume loading

15

Goal afterload and indicated drugs in pts with CAD:

High-normal
Indicated: Phenylephrine

16

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

Nitroprusside
High-dose volatile agents

17

Goal contractility and indicated drugs in pts with CAD:

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

18

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

Epinephrine
Dopamine

19

Summary of stable angina treatment (mnemonic):

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

20

MoA of organic nitrates:

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

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

21

Examples of organic nitrates:

NTG
Isosorbide dinitrate (Isordil)
Isosorbide mononitrate (Imdur)

22

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

Baroreceptor reflex ↑ HR

23

Describe the NO signal pathway on the endothelial cell side:

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

24

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

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

25

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

Phosphodiesterase inhibitors

26

Nitrate effects on O2 consumption:

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

27

Stronger effect of NTG: venodilation or arterial dilation?

Venodilation

28

NTG provides preferential dilation of:

Collateral vessels serving ischemic areas

29

Metabolism of nitroglycerin:

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

30

E1/2t of NTG:

1.5 minutes

31

Adverse effects of NTG:

Headaches
Postural hypotension/syncope
Methemoglobinemia

32

Tolerance issues with NTG:

Limits the efficacy, regardless of the route

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

33

Advantages of oral isosorbide mononitrate:

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

34

Drug interactions with nitrates:

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

35

Supply/demand benefit of β-antagonists in CAD:

↓ demand via ↓ CO from ↓ HR

↑ supply via longer diastolic filling time

36

Specific β-antagonists to use in CAD:

β1-selective agents: metoprolol, atenolol

Don't want to ↓ flow to peripheral vessels

37

Benefit of β-antagonists post-MI:

↓ post-MI remodeling

38

S/E of β-antagonists:

Depression
Insomnia
Masking hypoglycemia
Exercise intolerance
Bronchospasm

39

Discontinuation of β-antagonists:

Do not stop suddenly due to receptor upregulation

40

MoA of CCBs:

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

41

Effect of CCBs at the SA node:

↓ HR (negative chronotropic effect)

42

Effect of CCBs at the AV node:

↓ conductivity (negative dromotropic effect)

43

Effect of CCBs at the cardiac muscle:

↓ contractility (negative inotropic effect)

44

Effect of CCBs at the coronary vasculature:

Vasodilation

45

Adverse effects of CCBs:

AV block
Cardiac failure
Headache
Constipation
Hypotension

All "too much of a good thing"

46

Examples of dihydropyridine CCBs:

Amlodipine
Nifedipine
Nicardipine

47

Dihydropyridine CCBs more selective for:

Ca2+ channels in the vasculature (esp. arterial)

48

Adverse effect specific to dihydropyridine CCBs:

May cause reflex tachycardia

49

Examples of non-dihydropyridine CCBs:

Verapamil
Diltiazem

50

Non-dihydropyridine CCBs more selective for:

Ca2+ channels in the heart muscle

51

Adverse effect specific to non-dihydropyridine CCBs:

Heart block

52

Avoid non-dihydropryridines in combination with:

β-blockers

53

Role of ASA in CAD:

Antiplatelet activity prevents thrombus formation

54

Tx of unstable angina/N-STEMI:

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

55

Tx of STEMI:

Surgery
Thrombolytics

56

Indication for clopidogrel:

ACS pts with ASA allergy

57

Indications for GPIIb/IIIa inhibitors:

Reduce MI risk in pts w/ unstable angina
Reduce recurrent MI/revascularization in pts with NSTEMI

58

Tx for acute stable angina:

Nitrates
β-blockers
CCBs

59

Tx for acute unstable angina:

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

60

Tx for variant angina:

Nitrates
CCBs

61

Effects of aldosterone on the heart:

Insult to myocardium
Causes remodelling
Promotes atherosclerosis

62

Systolic dysfunction is EF <

EF < 40%

63

Causes of systolic dysfunction:

CAD
HTN
Valvular disease
ETOH
Thyroid disease
Cardiotoxic drugs

64

Causes of diastolic dysfuction:

Cardiomyopathies
Incomplete relaxation due to ischemia

65

Major manifestations of CHF:

Dyspnea
Fatigue
Fluid retention

66

Three physiologic goals of CHF tx:

↓ preload
↓ afterload
↑ inotropy

67

Drugs to reduce preload in CHF:

Diuretics
Aldosterone antagonists
Venodilators (NTG)

68

Drugs to reduce afterload in CHF:

ACEIs
β-blockers
Vasodilators

69

Drugs to increase inotropy in CHF:

Cardiac glycosides
Sympathomimetic amines
Phosphodiesterase inhibitors

70

Goal HR range in CHF and drugs indicated for this:

Normal-high
Indicated: dopamine, dobutamine

71

Drugs with negative effect on HR in CHF:

High-dose β-blockers

72

Goal preload in CHF and indicated therapy:

Normal
Indicated: IV fluids if needed

73

Drugs with negative effect on preload in CHF:

NTG
Thiopental

74

Goal afterload in CHF and indicated therapy:

Low
Indicated: ACEIs, nitroprusside, amrinone

75

Drugs with negative effect on afterload in CHF:

Phenylephrine

76

Goal contractility in CHF and indicated therapy:

Increased
Indicated: dopamine, dobutamine, epinephrine, amrinone

77

Drugs with negative effect on contractility in CHF:

High dose inhaled agents
High dose β-blockers

78

Important consideration before giving diuretics for CHF:

Preload status

79

Mortality benefit for thiazide/loop diuretics:

None - just QOL

80

Examples of loop diuretics:

Furosemide
Bumetanide
Torsemide

81

MoA of loop diuretics:

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

↑ excretion of Na+, K+, H2O

82

Diuretics which work on the distal tubule:

Thiazides
Metolazone
Spironolactone/eplerenone

83

Distal tubule diuretics ↑ Na+ excretion by:

5-10%

84

Loop diuretics ↑ Na+ excretion by:

20-25%

85

MoA of spironolactone:

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

Inhibits both androgen and mineralocorticoid receptors

86

S/E of spironolactone:

Gynecomastia
Impotence
Hair growth (women)

87

Spironolactone vs. eplerenone:

Eplerenone more selective with less S/E

88

Role of NTG in CHF:

Use with caution - these pts need preload!

Reduces preload and myocardial O2 demand

Alleviates ischemia to improve diastolic relaxation

89

Role of ACEIs in CHF:

Reverse RAAS-induced vasoconstriction, volume overload

Reduction of afterload also increases SV and GFR and increases diuresis

90

Drugs with proven mortality benefits in CHF:

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

91

Role of ARBs in CHF:

Reduce RAAS-induced vasoconstriction/volume overload

Lack of bradykinin-related vasodilation means less preload reduction

92

Role of β-blockers in CHF:

Inhibition of renin release
Blunting of catecholamines
Preventing of ACS

NOT for use in acute, decompensated HF!

93

Role of hydralazine + isosorbide dinirate in CHF:

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

94

MoA of digoxin:

Na-K-ATPase inhibitor
↓ SNS outflow, ↑ PSNS outflow

95

Effect on HR from digoxin:

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

96

Effect on contractility from digoxin:

Increased intracellular Ca2+; stronger contractions

97

Effect on renal aborption of Na+ from digoxin:

↓ renal absorption of Na+

98

Therapeutic levels of digoxin:

0.5 - 1.2 ng/ml

99

Onset and half-life of digoxin:

Onset: 30-60 min
t1/2: 36 hrs

100

Elimination of digoxin:

90% renally excreted

101

S/E of digoxin:

Hypokalemia
AV block
Ventricular ectopy

102

Tx for overdose of digoxin:

Digoxin immune fab

103

Drug interactions with digoxin:

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

104

MoA of phosphodiesterase inhibitors:

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

Increases intracellular Ca2+

↑ contractility
↑ art/ven dilation
↑ disastolic relaxation

105

Phosphodiesterase inhibitors a good choice for overdose of:

β-blockers

106

Onset, DOA and half-time for amrinone:

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

107

Dosing of amrinone:

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

108

S/E of amrinone:

Hypotension
Thrombocytopenia
Arrythmias

109

Elimination of amrinone:

Renal excretion

110

Amrinone vs. milrinone:

Milrinone has less tachycardia and thrombocytopenia

111

Dosing of milrinone:

50mcg/kg IV
Infusion: 0.5 mcg/kg/min

112

Half-time of milrinone:

2.7 hrs

113

Elimination of milrinone:

80% excreted unchanged via renal

114

Applications of milrinone:

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

Good for pulm HTN