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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
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

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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