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Cardiovascular Exam II > Drugs for Heart Failure > Flashcards

Drugs for Heart Failure Flashcards

1
Q

Term for right-sided heart failure NOT due to left-sided heart failure, but caused by things like COPD, interstitial lung dz, pulm HTN, thromboembolic dz, OSA, etc.

A

Cor pulmonale

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2
Q

Type of heart failure in which the body’s need for cardiac output is abnormally elevated to a point beyond the heart’s capability

A

High-output heart failure

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3
Q

Causes of high-output heart failure

A 
Hyperthyroid
Pregnancy
Anemia
AV fistula
Wet beriberi (thiamine def)
Paget’s dz
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4
Q

2 types of left sided heart failure = systolic and diastolic. What is systolic left-sided heart failure?

A

Failure of the pump function of the heart (EF < 45%), typically d/t dysfunction or deestruction of cardiac myocytes or their molecular components

Usually progressive chamber dilation with eccentric remodeling

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5
Q

What is diastolic left-sided heart failure (DHF)?

A

Occurs when ventricular capacitance is diminished and/or when the ventricle becomes “stiff” and cannot fully reslax during diastole; abnormal diastolic function usually with concentric remodeling or hypertrophy

Dx is fairly common among older women; causes include ventricular hypertrophy d/t chronic HTN and CT diseases such as amyloidosis

~normal LVEF with ~normal EDV

Dx is one of exclusion — consider diastolic heart failure when there is heart failure with PRESERVED EF!

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6
Q

Complications of DHF

A

DHF —> poor tolerance of Afib d/t loss of atrial contraction and decreased ventricular filling

DHF —> poor tolerance of tachycardia d/t shorter duration of diastole — limits time for relaxation and filling

DHF is worsened by increased MAP, especially if abrupt or severe

Worsening of DHF by ischemia raises left atrial pressure —> angina, wheezing, SOB, pulmonary edema

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7
Q

Compensatory change in pts with heart failure in terms of preload and afterload

A

Increase in preload and afterload

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8
Q

Rationale for using ACE inhibitors/ARBs in heart failure

A

Decrease angiotensin II —> less vasoconstriction (decreased afterload), less aldosterone secretion and less sodium/water retention (decreased preload), decreased cell proliferation and remodeling

Note that high doses are required

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9
Q

Prototypical ACE inhibitor(s)

A

Captopril

[others include enalapril, benzapril, lisinopril]

Beware of cough and angioedema AEs

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10
Q

Prototypical ARBs

A

Losartan

[others include valsartan and candesartan]

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11
Q

T/F: ARBs induce a more complete inhibition of the RAAS system than the ACE inhibitors

A

True

But ACE inhibitors usually recommended as first choice

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12
Q

AEs of ARBs

A 
Hypotension
Fatigue
Dizziness
Fever
Hypoglycemia
Hyperkalemia
Diarrhea
Gastritis
Nausea
Weight gain
Anemia
Weakness
Joint pain
Cough, bronchitis, nasal congestion

[common with valsartan = hypotension, hyperkalemia, increased serum Cr]

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13
Q

ACE inhibitors or ARBs should be administered to ALL pts with LV systolic failure or LV dysfunction without heart failure EXCEPT in what circumstances?

A

Not tolerated (cough, angioedema — try ARB!)

Pregnant

Hypotensive

Serum Cr > 3 mg/dL

Hyperkalemia

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14
Q

What effect does heart failure have on the autonomic nervous system?

A

Increases sympathetic activity —> increased HR, increased myocardial contractility, increased vascular resistance

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15
Q

Prototypical beta blockers used in heart failure

A

Metoprolol, bisoprolol, carvedilol

[research suggests carvedilol works best]

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16
Q

MOA of carvedilol

A

Nonselective beta and alpha blocker with no intrinsic sympathomimmetic activity

In CHF, decreases pulmonary capillary wedge pressure, pulmonary artery pressure, HR, systemic vascular resistance, right atrial pressure —> increased stroke volume index

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17
Q

Clinical applications of carvedilol in terms of heart failure

A

If clinically stable, carvedilol (or bisoprolol or metoprolol) is recommended for all with recent or remote hx of MI or ACS and reduced EF (<40%), or just those with reduced EF to prevent symptomatic heart failure

Used to prevent down-regulation of the beta1 adrenergic receptors in the heart as aresult of excess sympathetic stim during heart failure — keeps heart responsive to sympathetic drive, protects against dysrhyhtmias, reduces renin secretion, reduces myocardial O2 consumption, limits heart remodeling and reduces necrosis and apoptosis of myocardial cells

[NOTE should only be administered to clinically stable pts]

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18
Q

Toxicities associated with carvedilol

A 
Allergy
Angina
Dizziness
Lightheadedness
Fainting
Generalized swelling
Pain
SOB
Bradycardia
Weight gain
Angina/MI if abruptly stopped
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19
Q

Unless there are contraindications, carvedilol should also be given along with ______ to all pts with left ventricular systolic dysfunction caused by MI to reduce mortality

A

ACE-I

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20
Q

MOA of ivabradine

A

Selective and specific inhibition of the HCN channels (f-channels) within the SA node of cardiac tissue

Disrupts “funny” current to prolong diastole and slow HR

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21
Q

Clinical use of ivabradine

A

Tx of resting HR >70 bpm in pts with stable, symptomatic CHF wtih left ventricular EF <35% who are in sinus rhythm with:

  • Maximally tolerated doses of beta blockers (or)
  • Contraindications to beta-blocker use
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22
Q

AEs of ivabradine

A 
Bradycardia
HTN
Increases risk of afib
Heart block
Sinoatrial arrest
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23
Q

MOA of spironolactone

A

Competitive antagonist of aldosterone receptors, decreases aldosterone-stimulated gene expression

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24
Q

Clinical use of spironolactone in heart failure

A

Decreases myocardial fibrosis

Reduces early morning rise in HR

Reduces mortality and morbidity in pts with severe heart failure

[other range of benefits includes decreased Na and water retention, decreased K+ and Mg loss, prevents reduction of baroreceptor reflex, decreases ischmia, decreases sympathetic activation]

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25
AEs of spironolactone
``` Hyperkalemia Amenorrhea Hirsutism Gynecomastia Impotence Tumorigenic ```
26
Spironolactone and eplerenone are approved for tx of symptomatic heart failure with reduced systolic function, but are the most underutilized of all classes, primarily because of potential complication of _______
Hyperkalemia
27
MOA of furosemide
Blocks Na/K/2Cl cotransporter Indirectly inhibits paracellular reabsorption of Ca and Mg by TAL d/t loss of K backleak responsible for lumen + transepithelial potential Causes increased excretion of water, sodium, potassium, chloride, magnesium, and calcium
28
Clinical use of furosemide (or torsemide, bumetanide, ethacrynic acid) in heart failure
Management of edema associated with heart failure Decreases preload —> treats acute pulmonary edema; rapid dyspnea relief
29
Toxicities of furosemide
``` Hypokalemia Hyponatremia Hypocalcemia Hypomagnesemia Hypochloremic met.alkalosis Hyperglycemia Hyperuricemia Increased cholesterol and TAGs ``` Ototoxicity Sulfonamide — so risk of hypersensitivity
30
MOA of HCTZ
Inhibits Na reabsorption in DT via blockade of NaCl cotransporter Increases urinary excretion of Na, H2O, K, and Mg
31
Clinical use of HCTZ (or other thiazides - chlorothiazide, chlothalidone, metolazone) in heart failure
Relief of congestion — gets rid of excess volume and returns ventricular fiber length to more optimal range Note that LOOP diuretics are used first, K+ sparing diuretics next, and if STILL needing more diuresis, thiazides are used
32
Toxicities of thiazides
``` Orthostatic hypotension Hypokalemia Hypomagnesemia Hyponatremia Hypochloremic metabolic alkalosis Hypercalcemia Hyperglycemia Hyperuricemia ``` Sulfonamide— so risk of hypersensitivity
33
Vasodilators used for chronic HF
Isosorbide dinitrate (to dilate veins, decrease preload) + Hydralazine (to dilate arteries, decrease afterload)
34
The combination of vasodilators isosorbide dinitrate + hydralazine is especially useful in _____ ____, caucasians fail to respond for unknown reasons. It is also a good drug to consider in pts who cannot tolerate ______
African Americans; ACE-I
35
MOA of nitroglycerin
Forms free radical with NO, which increases cGMP —> smooth muscle relaxation Produces vasodilation in peripheral veins and arteries (more potent in veins) Primarily reduces cardiac O2 demand by reducing preload, may modestly reduce afterload, dilates coronary arteries
36
Clinical applications of nitroglycerin in terms of heart failure
Tx or prevention of angina pectoris Acute decompensated heart failure (especially when associated with AMI)
37
Toxicities associated with nitroglycerin
Reflex tachycardia, flushing, hypotension, orthostatic hypotension, peripheral edema, syncope, bradycardia HA, dizziness, light headedness, N/V, xerostomia, paresthesia, weakness, dyspnea, pharyngitis, rhinitis, diaphoresis
38
MOA of hydralazine
Not completely understood Endothelium dependent, hyperpolarizes, requires activation of COX, mediated by PGI2 receptor Effect is direct vasodilation of arterioles with little effect on veins —> decreased systemic resistance
39
Clinical application of hydralazine in terms of heart failure
Used off-label for: - HF with reduced EF if intolerance to ACEI or ARB - HF with reduced EF class III-IV
40
Toxicities associated w/ hydralazine
Angina pectoris, flushing, orthostatic hypotension, palpitations, peripheral edema, tachycardia Pruritis Drug-induced lupus-like syndrome [Tons more]
41
MOA of digoxin
Inhibition of Na/K ATPase pump in myocardial cells Results in increased contractility, direct suppression of AV node conduction, positive inotropic effect, enhanced vagal tone, and decreased ventricular rate to fast atrial arrhythmias
42
Clinical applications of digoxin
Control of ventricular response rate in adults with chronic afib Tx of heart failure in adults and pediatrics to increase myocardial contractility Used in pts with left ventricular systolic heart failure in combo with diuretics, beta-blockers, and ACEI Especially useful in pts with afib d/t prolongation of effective refractory period at AV node
43
Digoxin is administered _______; its half life is 36-48 hr, but this is increased as CO and renal function decrease, so needs a ______ dose; it is widely distributed and crosses the placenta but it has long hx of being safe in pregnant women with _______
Orally; loading; SVT
44
Toxicities associated with digoxin
Accelerated junctional rhythm, asystole, atrial tachycardia with or without block, AV dissociation, heart block, PR prolongation, PVCs, ST depression, Vtach, Vfib Dizziness, mental disturbance, HA, apathy, anxiety, confusion, delirium, depression, fever, hallucinations Rash, N/V, diarrhea, abd pain, anorexia, weakness, blurred or yellow vision, laryngeal edema
45
Digoxin has positive inotropic effect on heart, what does this mean?
Increases force of ventricular contraction
46
Hemodynamic benefits of digoxin
Increased cardiac output —> decreased sympathetic tone, increased urine production, decreased renin release
47
Electrical effects of digoxin
Increases firing rate of vagal fibers, alters electrical properties of the heart — increases responsiveness of SA node to ACh
48
Effects of digoxin on ECG
At therapeutic levels: depression of ST segment, longer PR interval Toxicity: AV dissociation, ectopic ventricular beats
49
Drug interactions with digoxin
Diuretics —- bc diuretics cause hypokalemia which leads to increased digoxin binding, which leads to increased risk of toxicity ACEI and ARBs can increase K levels, decreasing digoxin effects Sympathomimmetics - beneficial interaction on contractility, detrimental effect on arrhythmias Quinidine, spironolactone, verapamil, propafenone, and alprazolam interfere with clearance of digoxin Cholesterol-binding resins block its absorption
50
Which drugs show no evidence of benefit for diastolic heart failure?
Nitrates PDE5 inhibitors Digoxin
51
Drugs used to tx acute decompensated heart failure (ADHF)
Diuretics (loop>K+sparing>thiazide) Vasodilators: nitroprusside, nitroglycerin Discontinue carvedilol or other beta blockers
52
MOA of nitroprusside
Forms free radical with NO, increases cGMP —> smooth muscle relaxation Causes peripheral vasodilation by direct action on venous and arteriolar smooth muscle; reduces peripheral resistance Increases CO by decreasing afterload
53
Clinical applications of nitroprusside
Management of hypertensive crisis ADHF Used for controlled hypotension to reduce bleeding during surgery
54
Toxicities associated with nitroprusside
Tachycardia, ECG changes, flushing, hypotension, palpitation, substernal distress, increased ICP Apprehension, dizziness, HA, rash Metabolic acidosis secondary to cyanide toxicity [many others]
55
Drug approved for acute decompensated CHF, but not effective in chronic cases
Nesiritde
56
Inotropic agents
Catecholamines PDE inhibitors Cardiac glycosides
57
Examples of sympathomimetics used as inotropic agents
Dobutamine (synthetic catecholamine that selectively activates B1 and B2 adrenergic receptors) Dopamine (catecholamine, activates B1, increases HR and contractility, also stimulates alpha receptors at higher doses)
58
Prototypical PDE inhibitor (type III)
Milrinone Results in vasodilation and inotropic effects with little chronotropic activity
59
Clinical applications of milrinone
Inotropic therapy for pts unresponsive to other acute heart failure therapies (e.g., dobutamine) Outpatient inotropic therapy for heart transplant candidates Palliation of sx of end-stage HF not eligible for transplant Perioperative support for heart transplant recipients
60
Toxicities of milrinone
Arrhythmia Hypotension Angina/CP HA
61
Drugs to avoid in heart failure
Class I antiarrhythmics — some are negative inotropes; all can cause arrhythmias Calcium channel blockers — directly suppress myocardial contractility NSAIDs — impair renal salt and water excretion which can exacerbate HF

Cardiovascular Exam II (11 decks)

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