CHF - Chap 13 Flashcards
what is the result when c/o is inadequate for the needs of the body?
heart failure
what are the 3 groups of drugs used to treat heart failure?
v/d, positive inotropic drugs, and miscellaneous for chronic failure
what are the two major manifestations (think symptoms) of heart failure?
dyspnea and fatigue
when heart failure is due to systolic failure, what is really the problem?
reduction in cardiac contractile force and ejection fraction.
what happens when heart failure is as a result of diastolic failure?
stiffening or changes in the ventricles that prevent them from filling properly/prevent adequate filling during diastole (EF may be normal)
the homeostatic response by the body to decreased c/o is mediated how? (think of what systems are involved)
by sns and renin-angiotensin-aldosterone - system (this increase in BV leads to edema and pulmonary congestion - this also contributes to increased end-diastolic fiber length) - remember, this response is GREAT when the heart is working normally - not so much when the heart is currently failing.
what is the irony of the compensatory responses to cardiac failure?
that they at first do improve cardiac output; but also in the long run will increase load on heart which leads to further cardiac failure
current clinical evidence suggest that acute heart failure should be treated with what specific class of drugs? what if the case is very severe?
loop diuretics; beta agonist or phosphodiesterase inhibitor and vasodilator (these will all optimize filling pressure and bp)
chronic cases of heart failure should be treated with what combo of drugs?
diuretics (loop) plus ace inhibitor and if tolerated beta blocker
which drug is used in cases where there is prominent systolic dysfunction?
digitalis
drug that is a recombinant form of brain natriuretic peptide and has v/ding and diuretic properties.
nesiritide
“digitalis” is really a short way of calling which drugs? what is the prototype?
cardiac glycosides; digoxin
what is the MOA of digitalis?
inhibits the NA+K+ pump of the cell membrane which leads to small increase in Na+ ITC concentration which leads to less calcium being removed from the cell; this “extra” calcium is now stored and upon release can increase contractile force.
what is the effect of increased contractility evoked by digitalis? (meaning on ejection, end-diastolic size, c/o and renal perfusion)
increased ventricular ejection, decreased end-systolic and end diastolic size, increased c/o, and increased renal perfusion
the benefits of digitalis in its ability to increase contractility of the heart has what effect on the compensatory sympathetic tone?
it decreases the compensatory sympathetic tone which reduces heart rate, preload and after load which in effect allows the heart to work more efficiently.
what do cardiac glycosides do to the PR interval on the EKG and why?
increased the interval caused by decrease in AV conduction velocity - note, these drugs will also flatten the T wave.
what drug can you give to block the effects of cardiac glycosides (for exam dig)
atropine b/c the effects on the atria and AV nodes are p/s and mediated by the vagus.
what is the effect of digitalis on ventricular rate?
it slows it down - remember, high ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate
what is one of the most important manifestations of cardiac glycoside toxicity? Hint: think specifically about the MOA
increased automaticity (due to increased ITC calcium levels) - basically you are at very high risk of extraystoles, tachycardias, or fibrillations
when pvbs (extra systoles) are coupled to normal beats in a 1:1 fashion, what is this rhythm called?
bigeminy
although dig is the DOC for CHF, does it really have an affect on prolonging life?
NO - diuretics, ACE inhibitors, and v/d are much better at this.
how would you describe the half life of cardiac glycosides as a class?
they are SUPER LONG which is why dosing regimens must be carefully designed and monitored b/c they can accumulate significantly.
in terms of force of contraction of the heart muscle, what is the basic difference between cardiac glycosides and drugs like ccbs and beta blockers?
ccb and beta blockers are negative inotropes while cardiac glycosides are positive
what are the two things you want to do in terms of treatment for afib or aflutter? (think, immediate action)
reduce the conduction velocity and increase the refractory period of the AV node
