Congestive Heart Failure Flashcards
Thiazide diuretic drugs
Chlorthalidone
Hydrocholorthiazide
Metolazone
Loop diuretic drugs
Ethacrynic acid
Furosemide
Torsemide
Thiazide description for CHF
Relieve pulmonary congestion and peripheral edema
Decrease symptoms of volume overload (orthopnea)
Decrease plasma volume -> decrease venous return (preload) -> decreased workload and O2 demand
Decrease afterload
Only give if you see edema
Loop Description for CHF
Relieve pulmonary congestion and peripheral edema
Decrease symptoms of volume overload (orthopnea)
Decrease plasma volume -> decrease venous return (preload) -> decreased workload and O2 demand
Decrease afterload
Loop vs Thiazide CHF
Loop more effective than thiazides
Thiazides: patients with hypertensive heart disease (with congestive symptoms) -ineffective by itself due to its weak diuretic effect
Aldosterone antagonist drugs
Eplerenone
Spironolactone
Sironolactone
decreases cardiac fibrosis and remodeling
Aldosterone antagonist description CHF
Prevents sodium retention, myocardial hypertrophy and potassium loss
(When combined with ACE-I’s -> decreases M & M of severe HF)
Aldosterone antagonist indication CHF
Advanced heart disease or patients with LV dysfunction after an MI (these patients have elevated aldosterone due to angiotensin stimulation and reduced hepatic clearance)
Aldosterone antagonist adverse CHF
Hyperkalemia
GI: gastritis, PUD
CNS: lethargy, confusion
Endocrine: gynecomastia, decreased libido, menstrual irregularities
Contraindicated in patients on potassium supplements
ACE-I drugs
Captopril
Enalapril
Lisinopril
ACE-I description CHF
DOC in heart failure
Dilates arterioles and veins
ACE - I mechanism CHF
Decreases PVR -> decreases BP/afterload -> increases CO
Decreases sodium and water retention -> decreases preload
Decreases long term remodeling
ACE-I indication CHF
Patients with symptomatic heart failure
Asymptomatic patients with decreased LVEF or history of MI
High risk patients: diabetes, HTN, atherosclerosis, obesity
ACE-I pk CHF
Oral- food decreases absorption
Pro-drugs except captopril
ACE-I adverse CHF
Persistent dry cough Hypotension Renal insufficiency Hyperkalemia Angioedema **Teratogenic**
ACE-I contraindications CHF
Pregnancy
Bilateral Renal artery stenosis
Hyperkalemia
ARB drugs
Candesartan
Valsartan
ARB description CHF
Losartan is used for HTN
Candesartan is used for CHF
ARB mechanism CHF
Block AT-I receptor
No effect on bradykinin
ARB Indication CHF
Intolerant to ACE-I’s
cough/angioedema
ARB adverse CHF
Same as ACE-I but no cough Hypotension Renal insufficiency Hyperkalemia Teratogenic
ARB contraindications
Pregnancy
Bilateral renal artery stenosis
Hyperkalemia
Direct vasodilator drugs
Hydralazine
Nitrates (isosorbide dinitrate)
Direct vasodilator description/mechanism CHF
Increase vasodilation -> decrease preload
Increase arterial dilation -> decrease PVR and afterload
Hydralazine dilates arterioles
Nitrates dilate the veins and venules
Give in african americans
Direct vasodilators indication CHF
Patients that are intolerant to ACE-I’s or Beta blockers or black patients with advanced HF (adjuvant Tx)
Sustained improvement of LVEF when both oral vasodilators are combined
Direct vasodilator adverse CHF
HA, dizziness, hypotension
Hydralazine can also cause tachycardia, peripheral neuritis and a lupus like syndrome
Hydralazine adverse
HA, dizziness, hypotension
Tachycardia, peripheral neuritis, lupus like syndrome
Beta blockers for CHF
Carvedilol
Metoprolol
Beta blockers description CHF
Can reverse cardiac remodeling and reduce mortality
Beta blockers mechanism CHF
Decrease HR and RAAS (-ve inotrope)
Prevents deleterious effects of NE on cardiac muscle fibers
(renin inhibition and decreased HR)
Beta blockers indication CHF
Heart disease (stage B and C) in addition to an ACE-I
Beta blockers PK CHF
Start at low dose -> gradually titrate to effective dose (to avoid sudden exacerbation of sx)
Beta blockers adverse CHF
Initial treatment can cause fluid retention
Beta blockers contraindication CHF
Use cautiously in patients with asthma or severe bradycardia
Digoxin class
Inotropic agent: Cardiac glycoside
Digoxin description CHF
+ve inotrope
-ve chronotropic
From foxglove plant
Widely used in the treatment of HF
Very narrow therapeutic window
***Decrease sx of HF and hospitalization
Increase exercise tolerance
Does NOT increase survival **
Indicated in patients with ***heart failure with A fib ** along with ACE-I and beta blocker
Digoxin mechanism CHF
Inhibits Na/K ATPase -> decreased sodium gradient -> indirect inhibition of Na/Ca2 exchange -> increased cytoplasmic calcium therefore increased contractility
Decreases SNS, RAAS, and PVR =-> decreases HR
Enhanced vagal tone -> decreased O2 demand
Decreased conduction through AV node increases the effective refractory period
Digoxin PK CHF
Widely distributed including the CSF
Accumulates in muscle -> high Vd; requires a loading dose
Sensitivity varies* between patients and may change during therapy
***Hypokalemia -> digoxin toxicity (competes with K for binding sites on ATPase)
- **Hypercalcemia or decreased magnesium facilitate digoxin action
- **High calcium increases chance atrial arrhythmia Mg does opposite
Digoxin adverse CHF
Extensive inhibition of ATPase can lead to dysrhythmias
Toxicity (very common):
Atrial arrhythmia-> slow
Anorexia, nausea, vomiting, HA, fatigue, confusion, blurred vision, altered color perception, halos on dark objects
Treatment of toxicity:
Withdraw or reduce dose
Monitor ECG, plasma concentration and K levels
V tach-treat with lidocaine and Mg or increase potassium concentration
severe- treat with digitalis antibodies
Digoxin contraindications CHF
Diastolic or right side heart failure
Uncontrolled hypertension
Bradyarrhythmias
Quinidine, Verapamil and Amiodarone and NSAIDs displace digoxin from tissue protein binding sites and compete for renal excretion
Digoxin levels affected by hyperthyroidism, hypothyroidism
Milrinone and Inamrinone CHF description
Inotropic agents
PDE-3 inhibitor (phosphodiesterase inhibitors)
Good for acute/short term in increasing CO
Milrinone and Inamrinone mechanism CHF
Inotropic agents
Increase cAMP -> +ve inotropic effects and increase CO (similar to Beta 1)
Systemic and pulmonary vasodilation -> decrease preload and afterload
Slight increase in AV conduction
Milrinone and Inamrinone Adverse CHF
Short term only, long term decreases life
Can cause thrombocytopenias
Dopamine description CHF
Inotropic agent
Used in the treatment of shock that persists after volume replacement
Stimulates both adrenergic and dopaminergic receptors
Dopamine Mechanism CHF
Inotropic agent
Low dose -> D1 dilates renal and mesenteric blood vessels
Intermediate dose -> dopaminergic and beta 1 receptors -> increase force and rate of contraction and renal vasodilation*
High dose : alpha 1 receptors -> vasoconstriction (not helpful in CHF)
Dobutamine Description CHF
Inotropic agent
Beta agonist
Recemic mixture
Used in short term management of patients with cardiac decompensation
Dobutamine Mechanism CHF
+ve inotropic effects and vasodilation
Increased cAMP [Gs] -> phosphorylation of calcium channels with increased calcium entry into myocardium -> increased contraction
Little or no effect on HR
Glucagon Description CHF
Inotropic agent
Acute cardiac dysfunction from beta blocker overdose
Glucagon mechanism CHF
Gs-> increased cAMP -> contractility (without using beta receptors)
Inotropic and chronotropic effects
Give when you gave someone too many beta blockers
Systolic failure
Want to increase volume, give inotropes
-use diuretics, beta blockers, inotropes, Spirinolactone, ACE-I, direct vasodilators
Diastolic failure
Want to slow heart, block calcium channels
Use diuretics to decrease afterload
Use Calcium blockers to slow heart and increase filling
Use Beta blockers to slowdown heart
CHF Stage A
High risk of developing heart failure (selected patients receive ACE-I’s/ARB’s)
CHF stage B
Asymptomatic heart failure (selected patients receive ACE-I’s / ARBs or beta blockers)
CHF stage C
Symptomatic heart failure (routine drugs include diuretics, ACE-I and beta blocker)
CHF stage D
Refractory end stage heart failure (end of life care or extraordinary measures)
Systolic failure definition
Contarctility and ejection fraction are reduced
Diastolic failure definition
Stiffening and loss of adequate relaxation -> abnormal ventricular filling and reduced CO even though the EF may be normal (does not respond to +ve inotropic agents)
Symptoms of heart failure
tachycardia, decreased exercise tolerance, dyspnea, peripheral and pulmonary edema
CHF
abnormal increase in blood volume and interstitial fluid leading to dyspnea and peripheral edema
Physiological compensation for CHF
Chronic activation of SNS and RAAS associated with tissue remodeling -> additional neurohormonal activation -> vicious cycle -> death
Goal of treatment of CHF
minimize the compensatory mechanisms-> reduce symptoms, slow progression and manage acute episodes
Do not use what drugs with diastolic failure?
+ve inotropic agents (increase outflow obstruction)
