CHF - Chap 13

Question 1

what is the result when c/o is inadequate for the needs of the body?

Answer 1

heart failure

Question 2

what are the 3 groups of drugs used to treat heart failure?

Answer 2

v/d, positive inotropic drugs, and miscellaneous for chronic failure

Question 3

what are the two major manifestations (think symptoms) of heart failure?

Answer 3

dyspnea and fatigue

Question 4

when heart failure is due to systolic failure, what is really the problem?

Answer 4

reduction in cardiac contractile force and ejection fraction.

Question 5

what happens when heart failure is as a result of diastolic failure?

Answer 5

stiffening or changes in the ventricles that prevent them from filling properly/prevent adequate filling during diastole (EF may be normal)

Question 6

the homeostatic response by the body to decreased c/o is mediated how? (think of what systems are involved)

Answer 6

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.

Question 7

what is the irony of the compensatory responses to cardiac failure?

Answer 7

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

Question 8

current clinical evidence suggest that acute heart failure should be treated with what specific class of drugs? what if the case is very severe?

Answer 8

loop diuretics; beta agonist or phosphodiesterase inhibitor and vasodilator (these will all optimize filling pressure and bp)

Question 9

chronic cases of heart failure should be treated with what combo of drugs?

Answer 9

diuretics (loop) plus ace inhibitor and if tolerated beta blocker

Question 10

which drug is used in cases where there is prominent systolic dysfunction?

Answer 10

digitalis

Question 11

drug that is a recombinant form of brain natriuretic peptide and has v/ding and diuretic properties.

Answer 11

nesiritide

Question 12

“digitalis” is really a short way of calling which drugs? what is the prototype?

Answer 12

cardiac glycosides; digoxin

Question 13

what is the MOA of digitalis?

Answer 13

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.

Question 14

what is the effect of increased contractility evoked by digitalis? (meaning on ejection, end-diastolic size, c/o and renal perfusion)

Answer 14

increased ventricular ejection, decreased end-systolic and end diastolic size, increased c/o, and increased renal perfusion

Question 15

the benefits of digitalis in its ability to increase contractility of the heart has what effect on the compensatory sympathetic tone?

Answer 15

it decreases the compensatory sympathetic tone which reduces heart rate, preload and after load which in effect allows the heart to work more efficiently.

Question 16

what do cardiac glycosides do to the PR interval on the EKG and why?

Answer 16

increased the interval caused by decrease in AV conduction velocity - note, these drugs will also flatten the T wave.

Question 17

what drug can you give to block the effects of cardiac glycosides (for exam dig)

Answer 17

atropine b/c the effects on the atria and AV nodes are p/s and mediated by the vagus.

Question 18

what is the effect of digitalis on ventricular rate?

Answer 18

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

Question 19

what is one of the most important manifestations of cardiac glycoside toxicity? Hint: think specifically about the MOA

Answer 19

increased automaticity (due to increased ITC calcium levels) - basically you are at very high risk of extraystoles, tachycardias, or fibrillations

Question 20

when pvbs (extra systoles) are coupled to normal beats in a 1:1 fashion, what is this rhythm called?

Answer 20

bigeminy

Question 21

although dig is the DOC for CHF, does it really have an affect on prolonging life?

Answer 21

NO - diuretics, ACE inhibitors, and v/d are much better at this.

Question 22

how would you describe the half life of cardiac glycosides as a class?

Answer 22

they are SUPER LONG which is why dosing regimens must be carefully designed and monitored b/c they can accumulate significantly.

Question 23

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?

Answer 23

ccb and beta blockers are negative inotropes while cardiac glycosides are positive

Question 24

what are the two things you want to do in terms of treatment for afib or aflutter? (think, immediate action)

Answer 24

reduce the conduction velocity and increase the refractory period of the AV node

Question 25

in terms of drug-drug interactions with digitoxin, what is well known to cause increase in serum digitoxin?

Answer 25

quinidine - class I antiarrhythmic agent

Question 26

digitalis toxicity is increased by what type of levels (IOW, high or low) of the following in your blood: potassium, magnesium, and calcium?

Answer 26

hypokalemia, hypomagnesium, hypercalcemia

Question 27

how does digitalis induced vomiting make matters worse in terms of precipitating digitalis toxicity?

Answer 27

b/c by vomiting you deplete serum magnesium levels.

Question 28

the major signs of digitalis toxicity are vomiting, arrhythmias, ___ and _____

Answer 28

nausea and diarrhea - note, chronic intoxication is an extension of the therapeutic effect of the drug and is caused by excessive calcium accumulation in cardiac cells

Question 29

true or false: acute intoxication caused by OD of digitalis will result in cardiac depression.

Answer 29

true - it will lead to cardiac arrest NOT tachycardia or fibrillation

Question 30

what is typically the first step in treating digitalis toxicity?

Answer 30

correcting the potassium or magnesium levels; this can often be managed by omitting 1 or 2 doses of digitalis and giving oral or parenteral k+ supplements - NOTE however in severe ACUTE toxicity, you don’t want to give these supplements b/c hyperkalemia is often the problem.

Question 31

in terms of increase automaticity with digitalis toxicity what are the two anti-arrhytmic drugs that are best to use?

Answer 31

lidocaine and phenytoin - why? b/c these drugs do not severely impair cardiac contractility.

Question 32

what does severe acute digitalis overdose do to cardiac pacemakers?

Answer 32

inhibits them all!

Question 33

true or false: b1 selective sympathomimetics are often used in heart failure

Answer 33

true - other drugs include beta blockers, diuretics, ace inhibitors, phosphodiesterase inhibitors, and v/d.

Question 34

what is often the first line of therapy for both systolic and diastolic failure?

Answer 34

diuretics

Question 35

what is the drug (by name) most useful for immediate reduction of pulmonary congestion and edema associated with acute heart failure?

Answer 35

furosemide - loop diuretic

Question 36

which class of diuretics are known to have significant long term benefits and can reduce mortality in chronic heart failure?

Answer 36

aldosterone antagonists - specific examples include spironolactone and eplerenone

Question 37

what class of drugs along with diuretics are becoming a part of the first line choice of drug to treat CHF?

Answer 37

angiotensin antagonists

Question 38

what class of drug is losartan?

Answer 38

angiotensin receptor blocker

Question 39

what class of drug do inamrinone and milrinone belong to?

Answer 39

phosphodiesterase inhibitors

Question 40

the use of these drugs is based on reduction in cardiac size and improved efficiency that can be achieved with proper adjustment of venous return (aka ____) and reduction of impedance to ventricular ejection (aka ____)

Answer 40

vasodilators; preload and afterload

Question 41

to which class of drugs does nesiritide belong?

Answer 41

vasodilators - note this drug has severe renal toxicity

Question 42

what is the one class of drugs that are of NO real value in heart failure?

Answer 42

ccbs