CHF 61/62 Flashcards
Digoxin (Lanoxin)
Digitalis Glycoside
inotropic agent
(Digitoxin not available in US anymore)
Digoxin Immune Fab (DigiFab)
Digitalis Glycoside antidote
not a drug “per say” but goes in body and binds up digitalis (Digibind)
Dobutamine
Non-Glycoside Inotropic Agent (± Vasodilator Activity)
synthetic β 1 -agonist (cardioselective) given
only IV in intensive care to treat severe, refractory congestive heart failure
causes increased CO mainly by increased ventricular β 1 -receptor action (positive inotropic effect)
tolerance can develop to all effects
Dopamine
Non-Glycoside Inotropic Agent (± Vasodilator Activity)
endogenous catecholamine given only IV in intensive care
to treat severe, refractory congestive heart failure.
positive inotropic effect due to direct activation of heart β1 receptors. Increases HR and oxygen demand more than dobutamine.
At certain doses (low to intermediate), can increase renal BF thru vasodilation, may enhance Na+, H2O excretion
Inamrinone
Non-Glycoside Inotropic Agent (± Vasodilator Activity)
phosphodiesterase inhibitors
Milrinone
Non-Glycoside Inotropic Agent (± Vasodilator Activity)
phosphodiesterase inhibitors
Captopril (Capoten)
ACE inhibitor
NOT a prodrug
Enalapril (Vasotec)
ACE inhibitor
prodrug, needs good liver function (may be less predictable in CHF congestion)
Fosinopril (Monopril)
ACE inhibitor
prodrug, needs good liver function (may be less predictable in CHF congestion)
Quinapril (Accupril)
ACE inhibitor
prodrug, needs good liver function (may be less predictable in CHF congestion)
Losartan (Cozaar)
ARB
Valsartan (Diovan)
ARB
Candesartan (Atacand)
ARB
Hydrochlorothiazide (Microzide)
diuretic
Furosemide (Lasix)
diuretic
Epleronone (Inspra)
diuretic
Spironolactone (Aldactone)
diuretic
Hydralazine
Direct Vasodilator
Primarily Afterload Reduction
Nitroprusside (Nitropress)
Direct Vasodilator
Preload and Afterload Reduction
raise IC cGMP–>vasodilation
IV only
SE: cyanide toxicity
Nitroglycerin (Minitran)
Direct Vasodilator
Primarily Preload Reduction
Isosorbide Dinitrate (Isosordil)
Direct Vasodilator
Primarily Preload Reduction
Nesiritide (Natrecor)
Direct Vasodilator
Preload and Afterload Reduction + diuretic (natriuretic peptide)
raise IC cGMP–>vasodilation of both arterial and venous sm. muscle
promotes natriuresis
IV only
Bisoprolol (Zebeta)
B-blocker
Carvedilol (Coreg)
B-blocker
antioxidant and alpha-blocker as well as a beta blocker
Metoprolol (Toprol-XL)
B-blocker
Conivaptan (Vaprisol) FYI
Vasopressin Antagonists (Vaptans) V-1a and V-2 receptor antagonist approved for IV treatment for hospitalized pts with hyponatremia/excessive water retention
Tolvaptan (Samsca) FYI
Vasopressin Antagonists (Vaptans) only a V-2 antagonist and is available orally for hyponatremia/water retention; often as an adjunct to standard diuretic therapy in CHF
CASE: 58 yr old man, SOB and weight gain
dyspnea on exertion after one flight of stairs, orthopnea, and ankle edema
nonproductive cough, nocturia (2-3 times/night) and more signs of edema.
tachycardia
complicated??
Low Output or Congestive Heart Failure (CHF)
most common, gradual, typ. chronic (not acute like cardiogenic shock)
ventricles unable to pump out all the blood normally being returned to them because either they (1) fail to relax properly and fill with enough venous blood during diastole (diastolic failure) or (2) fail to contract with enough force during systole (systolic failure), or both. Either way SV (therefore CO) is reduced
blood back up–>systemic/pulmonary congestive conditions
- underperfused kidneys retain* large amounts of sodium and water which adds to the congestion
- LHF*(LV fails first) then RHF, almost always combined HF eventually (LHF most serious)
Causes
of Left Ventricular CHF (Also called Forward Failure)
MI (most common)
Coronary HD (atheroslerosis)
HTN related cardiac enlargement
LVH with inc. stiffness due to chronic primary HTN
less common: valvular disease, dilated cardiomyopathy, congenital heart diseases, cardiac infections and rheumatic heart disease.
s/s of LV CHF
respiratory wheezing ("cardiac asthma")-1st indication nonproductive cough DOE rest dyspnea orthopnea PND nocturia Fatigue, Weakness and Exercise Intolerance LVH and tachycardia (to compensate)
when considering drugs to tx LV CHF
determinants of CO
-contractility* where most problems lie
Ca2+ role in HF
increase in free IC Ca2+ for contraction
remove to relax
SR has powerful SR pump
allows contractile proteins to relax during diastole
can be stimulated by B-receptors: NE–>cAMP–>influx of Ca2+
contractile proteins impaired in CHF (cardiac musc. remodeling, assoc. with hypertrophy), do not get good strong contraction
also impairment of Ca2+ reuptake, not enough for during contraction
dec. B-receptors in membrane, so stimulation via NE is compromised (dec. due to high NE from sympathetic overaction
SV as a function of preload
Preload: filling force of venous blood returning to the ventricles
CHF pts: high preload (congested), but low output (SV, CO) due to decreased ventricular performance
suppressed output–>congestion in lungs, diff breathing, fatigue
mechanism of digoxin is to raise curve to try to bring up to normal (output)
SV as function of afterload
no compromise in HTN pts
CHF: SV (and CO) decreases dramatically as afterload increases
to compensate for low CO, inc. SNA and Ang II levels, which inc. PVR–>FURTHER increasing afterload
meds to dec. afterload