Drugs for Heart Failure Flashcards
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.
Cor pulmonale
Type of heart failure in which the body’s need for cardiac output is abnormally elevated to a point beyond the heart’s capability
High-output heart failure
Causes of high-output heart failure
Hyperthyroid Pregnancy Anemia AV fistula Wet beriberi (thiamine def) Paget’s dz
2 types of left sided heart failure = systolic and diastolic. What is systolic left-sided heart failure?
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
What is diastolic left-sided heart failure (DHF)?
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!
Complications of DHF
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
Compensatory change in pts with heart failure in terms of preload and afterload
Increase in preload and afterload
Rationale for using ACE inhibitors/ARBs in heart failure
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
Prototypical ACE inhibitor(s)
Captopril
[others include enalapril, benzapril, lisinopril]
Beware of cough and angioedema AEs
Prototypical ARBs
Losartan
[others include valsartan and candesartan]
T/F: ARBs induce a more complete inhibition of the RAAS system than the ACE inhibitors
True
But ACE inhibitors usually recommended as first choice
AEs of ARBs
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]
ACE inhibitors or ARBs should be administered to ALL pts with LV systolic failure or LV dysfunction without heart failure EXCEPT in what circumstances?
Not tolerated (cough, angioedema — try ARB!)
Pregnant
Hypotensive
Serum Cr > 3 mg/dL
Hyperkalemia
What effect does heart failure have on the autonomic nervous system?
Increases sympathetic activity —> increased HR, increased myocardial contractility, increased vascular resistance
Prototypical beta blockers used in heart failure
Metoprolol, bisoprolol, carvedilol
[research suggests carvedilol works best]
MOA of carvedilol
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
Clinical applications of carvedilol in terms of heart failure
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]
Toxicities associated with carvedilol
Allergy Angina Dizziness Lightheadedness Fainting Generalized swelling Pain SOB Bradycardia Weight gain Angina/MI if abruptly stopped
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
ACE-I
MOA of ivabradine
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
Clinical use of ivabradine
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
AEs of ivabradine
Bradycardia HTN Increases risk of afib Heart block Sinoatrial arrest
MOA of spironolactone
Competitive antagonist of aldosterone receptors, decreases aldosterone-stimulated gene expression
Clinical use of spironolactone in heart failure
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]
