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101 Cards in this Set
- Front
- Back
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What does heart failure mean?
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That the heart FAILS to supply the tissues of the body with adequate blood flow.
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What are the cardinal symptoms of heart failure?
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Dyspnea, fatigue and fluid retention.
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What are the main causes of heart failure?
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Arteriosclerotic heart disease, myocardial infacrtion, hypertensive heart disease, valvular heart disease, dilated cardiomyopathy and congenital heart disease.
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Why is heart failure often called "congestive" heart failure, CHF?
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Because the heart failure is often accompanied by fluid overload which leads to a dilated heart and pulmonary edema etc.
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What is THE most common cause of heart failure?
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70% of heart failures are due to left systolic dysfunction as a result of longstanding coronary artery disease. (atherosclerosis)
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Why is the number of patients with heart failure increasing?
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Because more individuals now survive a myocardial infarction.
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Why does the heart failure progress due to physiologic compensatory mechanisms?
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Because a failing heart causes an chronic activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system which further increases the work of the heart and causes a progressive decline in its function.
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What are the progressive changes in the heart?
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Loss of myocardial cells, hypertrophy of a chamber, and fibrotic changes. The heart becomes less elliptical and more spherical.
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What are the goals in the therapy of heart failure?
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The goals of treatment of heart failure is to alleviate symptoms, decrease the rate of progression and improve survival rates.
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What are the six classes of drugs which have been shown effective in the treatment of heart failure?
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1. inhibitors of the renin-angiotensin system
2. beta blockers 3. diuretics 4. inotropic agents (cardiac glycosides) 5. direct vasodilators 6. aldosterone antagonists |
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Why is myocardial hypertrophy bad for the failing heart?
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Initially, stretching of the myocardium provides for a stronger contraction. However, excess elongation of the muscle fibers result in weaker contractions, and the geometry diminishes the ability to efficiently eject blood.
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What is the name of the decreased ability to eject blood from the heart?
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Systolic failure
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What is then diastolic failure?
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The inability of the ventricles to relax and accept quantities of blood.
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Which is more common, the systolic or diastolic failure?
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Systolic failure.
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Which patients are especially prone to diastolic heart failure?
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The elderly women.
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What does compensated heart failure suggest?
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That the heart is failing but that increases in sympathetic activity, renin angiotensin system and increased dilation of the heart compensates for the failure.
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What does decompensated heart failure mean?
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That the compensation mechanisms are no longer sufficient for restoring sufficient blood flow and the patient thereby shows symptoms of heart failure.
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What are the means of treating heart failure besides pharmacological treatment?
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Decreased levels of physical activity, low dietary sodium intake, treating comorbid conditions.
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Which drugs may precipitate or exacerbate heart failure?
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NSAIDs, alcohol, calcium channel blockers and some antiarrhythmics.
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What are the two mechanisms by which renin is released in response to heart failure?
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1. Decreased renal blood flow.
2. Sympathetic activation. |
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Which are the agents of choice in HF?
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The ACE inhibitors
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Which are the ACE inhibitors?
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Enalapril, Captopril, Fosinopril, Lisinopril, Quinapril, Ramipril
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What are their mechanism of action?
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They block the angiotensin converting enzyme in the lungs which normally converts circulating angiotensin I into angiotensin II.
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What is an additional function of the angiotensin converting enzyme?
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It normally degrades circulating bradykinin.
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What effect does bradykinin possess on the blood vessels?
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It is a potent vasodilator.
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So what are the physiological effects of the ACE inhibitors?
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The ACE inihibitors cause vasodilation (less angiotensin II and more bradykinin), and decrease the secretion of aldosterone thus leading to lower levels of fluids.
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How has the ACE inhibitors affected the treatment of heart failure?
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The use of ACE inhibitors has significantly reduced morbidity and mortality of HF.
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When may ACE inhibitors be considered for single therapy?
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When patient presents with mild dyspnea and no signs of fluid overload. It is also effective in decreasing HF in asymptomatic patients who have an ejection fraction of less than 35%. Also patients who've had a recent MI may benefit from ACE inhibitors.
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What patients shows the greatest benefits from ACE inhibitor therapy?
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The patients with the lowest ejection fractions.
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When after myocardial infarction should therapy be initiated?
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Immediately after a myocardial infarction.
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How about oral adminnistration of ace inhibitors?
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All of the ace inhibitors are adequately but incompletely absorbed on oral adm.
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What may decrease the absorption of ace inhibitors?
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Food, and thus the ace inihibitors should be taken on empty stomach.
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Are ACE inihibitors immediately effective?
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No, the ace inhibitors are prodrugs which require hydrolysis in the liver before being active.
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Which ace inhibitor is an exception and does not require hydrolysis for initiation of activity?
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Captopril
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What is the route of elimination of the ace inhibitors?
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Renal, except for fosinopril
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What are the plasma hallf-lifes of the ace inhibitoors?
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Between 2 and 12 hours.
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Does the inhibition of ACE correlate with the drugs half life?
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No, the inhibition of ACE may last much longer.
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Which compounds are the newer ones and require only once a day dosing?
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Fosinopril and Ramipril
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What are the adverse effects of the ACE inhibitors?
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Postural hypotension, renal insufficiency, hyperkalemia, angioedema, and a persistent cough.
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In what patients are ACE inhibitors contraindicated?
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In pregnant women as the ace inhibitors may be fetotoxic.
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Why is postural hypotension part of the side effects of the ace inhibitors?
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Because they cause vasodilation.
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Why is renal insufficiency part of the side effects of the ace inhibitors?
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Decreased renal BF?
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Why is hyperkalemia part of the side effects of the ace inhibitors?
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Because decreased action of aldosterone can cause potassium sparing.
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Why is angioedema part of the side effects of the ace inhibitors?
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Because bradykinin is not only a vasodilator but also increases the permeability of the vessels.
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Why is cough a side effect of ace inhibitor therapy?
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Because bradykinin apparently causes cough, as evidenced by the absence of cough when using the angiotensin-receptor blockers.
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What side effect may require the patient to be monitored?
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The symptomatic hypotension.
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Which is the prototypical angiotensin receptor blocker?
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Losartan
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Which are the rest of the angiotensin receptor blockers?
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Candesartan
Telmisartan Valsartan |
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What are the advantages of ARBs over ACE inhibitors?
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They have a more complete blockade of angiotensin action. Furthermore, the ARBs do not affect the levels of bradykinin.
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When would ARBs be considered?
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When the patient cannot tolerate ACE inhibitors.
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What are the indications for the ARBs?
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Hypertension and as a substitute for ACE inhibitors in heart failure (in paitents with severe cough or angioedema).
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By what route and how often are the ARBs administered?
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They are all orally active and can be given once daily.
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What is the main difference between Losartan and the newer ARBs?
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Losartan undergoes extensive first-pass metabolism.
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What happens to the ARBs in the plasma?
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They are highly (90%) plasma protein bound.
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What are the adverse effects of the ARBs?
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They have the same side effect profile as ACE inhibitors but do not cause cough or angioedema.
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Are the ARBs contraindicated in pregnancy just as the ACE inhibitors?
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Yes
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What does your intuition tell you about administrating beta blockers in a patient with heart failure?
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That it would worsen the heart failure because the beta blockers have negative inotropism adding to the already failing heart.
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So why do we then still use the beta blockers in heart failure?
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Because several clinical studies have shown that the beta blockers improve the systolic function and reverse the cardiac remodeling.
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Which are the two beta blockers which are approved in the treatment of HF?
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Carvedilol and long-acting metoprolol.
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Which receptors are blocked by Carvedilol?
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Carvedilol blocks beta1 beta2 and alpha1 receptors.
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Which receptors are blocked with metoprolol?
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Only beta1 receptors.
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Which HF patients are indicated for beta blockers?
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All HF patients with the exception of those in acute HF or asymptomatic patients.
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How should treatment with beta blockers in patients with HF be initiated?
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Treatment with the beta blockers should be initiated slowly (to avoid exacerbation of HF) and the doses should be titrated to effective dose.
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Why are diuretics indicated in HF?
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Because they decrease the workload of the heart by decreasing preload and afterload by reducing the volume of fluid in the body.
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What determines the type of diuretic used?
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Thiazide diuretics are used if the creatinine clearance is not below 50ml per min. Loop diuretics are used when acute lowering of plasma volume is needed or in those patients with renal failure.
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What can happen in large doses of loop diuretics use?
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Volume depletion.
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Why are direct vasodilators indicated in the treatment of HF?
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Because they decrease peripheral vascular resistance and thus decrease afterload and so decrease the workkload of the heart.
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Which are the direct vasodilators used in heart failure?
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Nitrates are commonly used venous dilators.
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In what patients are vasodilators indicated?
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In patients who are intolerant to ACE inhibitors or beta blockers.
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Which is the most commonly used combination of vasodilators for HF?
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Isosorbide nitrate and hydralazine.
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What vasodilators should be avoided in patients with HF?
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Calcium channel blockers.
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How do the inotropic agents work?
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By increasing intracellular calcium concentrations in the myocardial cells, thus enhancing contraction.
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Which are the inotropic agents?
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Amrinone, Milrinone, Digoxin, Digitoxin and Dobutamine.
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Which are the cardiac glycosides?
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Digoxin or digitoxin.
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What are they also known as?
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Digitalis
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Why are they called digitalis?
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Because they come from the digitalis (foxglove) plant.
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What is a shortcoming of the digitalis drugs?
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They show an extremely narrow therapeutic index, meaning that their toxic dose is very close to the effective therapeutic dose.
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Which is the most widely used glycoside?
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Digoxin
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By what mechanism does cacium leave the intracellular fluid after muscle contraction?
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It is either pumped into the sarcoplasmic reticulum or exchanged for sodium with the extracellular fluid.
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What happens to intracellular calcium if inntracellular sodium is raised?
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The concentration gradient for sodium to move into the cell is diminished and thus the driving force for moving calcium out of the cell is also defective. Thus more calcium remains intracellularly for the next contraction, which will then be more forceful.
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And how then, do the cardiac glycosides increase the levels of intracellular sodium?
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They inhibit the sodium/potassium ATPase.
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What are the effects then, of the cardiac glycosides on the ejection fraction?
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They increase contractility of the cardiomyocytes and thus increase the ejection fraction.
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In which patients is digitalis not indicated?
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In patients with diastolic or right sided heart failure.
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What is the major indication for digoxin?
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Left ventricular heart failure with atrial fibrillation.
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When is dobutamine indicated?
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In acute heart failure in a hospital setting.
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How is dobutamine administered?
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Intravenously.
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What is the half life of digoxin?
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36 hours.
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How is digoxin metabolized and excreted?
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Digoxin is mainly excreted unchanged in the kidney.
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What is the difference between digoxin and digitoxin?
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Digitoxin has a much longer half life and is extensively metabolized before it is excreted.
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What is one of the most commonly encountered adverse drug reactions?
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Digitalis toxicity.
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What are the side effects of digitalis?
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Arrhythmias (slowing of atrioventricular conduction associated with atrial arrhythmias)
Anorexia, nausea and vomiting are encountered side effects. Headache, fatigue, confusion, blurred vision and alteration in color perception and halos or dark objects in the visual field. |
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What are the means of treating digitalis toxicity?
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Discontinuation is usually enough. Giving potassium supplements. In worst case administer digoxin immune Fab antibodies which neutralizes digoxin.
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What is the predisposing factors for digitalis toxicity?
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Hypokalemia is the main factor. Other electrolyte disturbances such as hypercalcemia or hypomagnesemia also predispose to digitalis toxicity.
Drugs such as quinidine, verapamil, amiodarone and others may predispose to digitalis toxicity, both by displacing digitalis from plasma protein and by competing for renal clearance. These effects may lead to increased levels of digitalis in the blood and this as we know can cause serious arrhythmias. |
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What are pathological conditions also predisposing to digitalis toxicity?
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Hypothyroidism, hypoxia, renal failure, and myocarditis.
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What is the mechanism of action of Amrinone and Milrinone?
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They are inhibitors of phosphodiesterase, which leads to an increased level of cAMP in the myocytes, followed by an increased Ca++ level annd increased cardiac contractility.
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What is long term treatment with amrinone and milrinone associated with?
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Increased mortality.
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What are the indications for use of amrinone and milrinone?
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Short term treatment of refractory HF.
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What is the hormone which is elevated in patients with advanced heart disease?
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Aldosterone
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Which is the direct antagonist of aldosterone?
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Spironolactone
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When is spironolactone indicated in heart failure?
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Only in the most advanced cases of heart failure.
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What are the adverse effects of spironolactone?
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Gastric disturbances, hyperkalemia, CNS disturbances such as lethargy and confusion, and endocrine abnormalities such as gynecomastia, decreased libido and menstrual irregularities.
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