Congestive Heart Failure Flashcards
define positive inotropy, positive chronotropy, positive dromotropy, positive lusitropy
positive inotropy - increase in cardiac contractility
positive chronotropy - increase in HR
positive dromotropy - increase in conduction velocity
positive lusitropy - increase in rate of relaxation
what type of drugs have been shown to decrease cardiac remodeling hence attenuating disease progression
drugs that reduce ventricular wall stress or inhibit the RAAS system (like ACEIs, ARBS, aldosterone antagonist etc)
drugs to treat heart failure: given to reduce blood volume
diuretics: thiazide diuretics, loop diuretics, aldosterone antagonists
drugs to treat heart failure: given to reduce peripheral resistance
vasodilator: inhibitors of angiotensin (ACEIs, ARBS, renin inhibitors) and direct vasodilators
drugs to treat heart failure: given to reduce heart rate and contractility
cardioinhibitory drugs: beta blockers and calcium channel blockers
drugs to treat heart failure: to stimulate contractility (inotropic agent)
inotropic agent: digoxin
drugs to treat heart failure: inotropic agents used in acute heart failure
dopamine, dobutamine, inamrinone, glucagon, milrinone
DDIG M
when are diuretics recommended for heart failure patients
if there is evidence of fluid retention (because they do not alter disease progression or prolong survival)
mechanism of action of diuretics in HF patients
- reduce venous pressure and ventricular preload
- reduce pulmonary and/or systemic congestion or edema
- and associated symptoms –> dyspnea
what do ACEIs do in HF patients
- reduce peripheral resistance hence reduce afterload (resistance against which left ventricle must eject its volume of blood during contraction)
- reduce Na and H2O retention thereby reducing preload (volume of blood in ventricle after diastole)
- reduce sympathetic activity by reducing NE release
ARBs approved by FDA for the use of HF
candesartan and valsartan
concurrent use of these drugs have been shown to produce sustained improvement in left ventricular ejection fraction
hydralazine and nitrates (isosorbide dinitrate)
mechanism of action for hydralazine and isosorbide nitrate
- hydralazine is a vasodilator that reduce peripheral resistance in arterial SM and increases stroke volume and cardiac output –> decrease afterload
- isosorbide nitrate is a venodilator that reduces preload
adverse effect of combination therapy of hydralazine and isosorbide dinitrate
hypotension
reflex tachycardia
sodium and water retention
headache, dizziness, and GI disturbances
drugs used to treat systolic HF
diuretics spironolactone inhibitors of angiotensin direct vasodilators beta blockers inotropic agents
drugs used to treat diastolic HF
diuretics
beta blocker
calcium channel blockers
what are the beta blocker used for HF
carvedilol
metoprolol
mechanism of beta blockers in HF
they block excessive sympathetic influence on the heart –> slows/reverses ventricular remodeling, improve LV systolic function, decreasing heart rate and ventricular wall stress thereby reducing myocardial oxygen demand, and inhibiting plasma renin release
clinical application of digoxin
decrease symptoms of HF, increase exercise intolerance, decrease rate of hospitalization
DOES NOT INCREASE SURVIVAL
when should digoxin be used?
patients with HF and supraventricular tachyarrhythmias such as atrial fibrillations
mechanism of digoxin
- positively inotropic (increases contractility of heart by increasing cytoplasmic calcium)
- negatively chronotropic (decreases HR)
- enhanced vagal tone (decreased oxygen demand)
- decreased conduction through AV node increases the effective refractory period
adverse effects of digoxin
- cardiac arrhythmias esp atrial tachycardias and AV block
- alteration of color perception and other CNS effects
- hypokalemia (enhance therapeutic and toxic effect of digoxin)
- hypercalcemia
- hypomagnesia
drug interaction of digoxin
Digoxin is QueeN of VA
quinidine, NSAID, verapamil, and amiodarone compete with digoxin for binding sites and depress renal clearance of digoxin
diuretics can indirectly react with digoxin because of ability to cause hypokalemia
contraindications of digoxin
- pts with diastolic or right sided HF –> outflow obstruction
- uncontrolled hypertension
- bradyarrhythmias
- non responders or intolerance
- hypokalemia
tx of digoxin toxicity
- withdraw drug or lower dose
- adjust electrolyte status (increase K and Mg and reduce Ca)
- lidocaine and/or Mg for ventricular tachyarrhythmias
- if real severe, give digitalis antibodies
what are the phosphodiesterase III inhibitors and how do they work
inamrinone
milrinone
inhibit myocardial phosphodiesterase –> increase in cAMP activity –> positive inotropic activity and arterial and venous vasodilating effects
clinical use of phosphodiesterase III inhibitors (name them again)
iniamrinone and milrinone
short term therapy in people with intractable heart failure
adverse effects of PDE III Inhibitors
PDE HAT
Hypotension
Arrhythmias
Thrombocytopenia
when is dopamine used for HF
in treatment of shock
mechanism of dopamine in HF
activates dopaminergic and beta 1 receptors –> increase force and rate of contraction and renal vasodilation
adverse effect of dopamine
cardiac arrhythmias
use of dobutamine in HF
it is a beta 1 agonist so it is used to increase cardiac output in acute management of HF
mechanism of dobutamine in HF
increase in cAMP via Gs –> phosphorylation of calcium channels with increased calcium entry into myocardium –> increased contraction
positive inotropic effects and vasodilation
use of glucagon in HF
cardiac stimulant in management of severe cases of beta blocker overdosage
mechanism of glucagon in HF
increase in cAMP via Gs leads to increased contractility without using beta receptors
positive inotropic and chronotropic effects
