Chapter 24 Heart Failure 1. What are the signs of congestive heart failure (CHF)?

For left heart failure are pulmonary edema, crackles, cough and shortness of breath. Right heart failure is the peripheral edema and jugular vein distension. 2. How do drugs for CHF affect preload and afterload? According to Starling Law the more these fibers are stretched the more forcefully they will contract. Drugs that increase preload and contractility will increase the cardiac output (positive inotropic). Drugs that decrease the contractility are called negative inotropic. Because the most common cause of increased afterload is an increase in peripheral resistance due to HTN (in heart failure) drugs used for HF lower blood pressure to create less afterload resulting in less workload for the heart 3. What is now the recommended drug class for heart failure, and how does this class work to decrease symptoms? ACE Inhibitors affect the rennin-angiotensin system, lower blood pressure and reduce the afterload of the heart. They lower peripheral resistance and inhibit aldosterone secretion which reduces blood volume; decrease in blood pressure diminishes afterload thus increasing cardiac output. These drugs also have an effect on vein dilation which decreases pulmonary congestion and reduces peripheral edema. 4. What is responsible for the cough that is seen in about 10% of clients using this drug class? Due to accumulation of bradikinin due to the inhibition of ACE 5. Why should patients using this drug class be monitored for signs of infection and have regular CBCs? Can cause neutropenia or agranulocytosis and assess for signs of infection. Also monitor hyperkalemia and hyponatremia. 6. How do angiotensin receptor blockers (A2RBs) manage CHF? They are similar to ACE inhibitors, they block angiotensin receptors. 7. How are they similar/different than ACE inhibitors? They show equivalent efficacy like ACE inhibitors, but because research has not yet demonstrated a clear advantage of ARBs over other medications, their use in the treatment of HF is usually reserved for clients unable to tolerate the side effects of ACE inhibitors. 8. How do cardiac glycosides work to mange CHF? They cause the heart to beat more forcefully and more slowly improving cardiac output 9. What is it necessary to know heart rate before administering digoxin? Because digoxin can cause dysrhytmias (report a HR lesser than 60 and above 100) the antidote for digoxin toxicity is digoxin immune Fab (Digibind) 10. Why is it necessary to know potassium level before administering digoxin? Because hypokalemia predisposes the client to serious digoxin toxicity 11. What is meant by digitalization? Refer to a procedure in which the dose of cardiac glycoside is gradually increased until tissue becomes saturated with the drug and the symptoms for HF diminish. 12. Why is it necessary to check drug levels with digoxin? Because of drug toxicity 13. What are signs of digoxin toxicity? Includes nausea, vomiting, anorexia, and visual disturbances (seeing halos, a yellow-green tinge, or blurring) 14. How is digoxin toxicity treated? Administer digoxin immune Fab (Digibind) This drug binds and subsequently removes digoxin from the body and prevents effects of overdose. 15. How can we tell if drugs for CHF are effective? When we see an improvement in patient cardiac function

16. What dietary education should a client receiving cardiac glycosides receive? Consume foods high in potassium such bananas, apricots, kidney beans, sweet potatoes and peanut butter. 17. What information/symptoms should a client taking cardiac glycosides report to the health care provider (HCP)? Signs of toxicity (mentioned in q#13), the dysrhytmias, and weight gain of 2 pound or more per day. 18. Should a client receiving ACE inhibitors receive the same dietary instruction as a person receiving digoxin? No because in patients taking ACE inhibitors patients should restrict potassium and Sodium intake to prevent hyperkalemia and hyponatremia. 19. How will diuretics benefit clients with heart failure? They increase urine flow thereby reducing blood volume & cardiac workload, effective in reducing peripheral edema & pulmonary congestion. 20. What dietary information should a client receiving MOST diuretics receive? Keep Sodium intake no more than 4000 mg daily. Diuretics cause hypokalemia be sure to eat food that contains potassium. 21. How does metoprolol manage CHF? Metoprolol is a selective B1 adrenergic blocker, reduces the sympathetic stimulation of the heart, thus decreasing heart workload. This drug has been found to slow the progression of HF and to significantly the long term consequences of the disease. 22. What do you need to know before administering metoprolol? BP and pulse, if the pulse is less than 50-60 beats/minute, notify the physician 23. How does isosorbide (Isordil) work to manage CHF? They act directly to relax blood vessels and lower blood pressure (VEINS) 24. How do phosphodiesterase inhibitors, like milrinone, affect CHF and what is their clinical usefulness? They block the enzyme phosphodiesterase in cardiac and smooth muscle. Blocking phosphodiesterase has the effect on increasing the amount of calcium available for myocardial contraction. This inhibition results in 2 main actions that benefit clients with HF: A positive inotropic action and vasodilation. Cardiac output is increased because of the increase in contractility and the decrease in the lefty ventricular afterload. 25. Why is safety a concern for all clients using CHF therapies, especially elderly? 26. What should nurses regularly monitor in clients being treated for CHF? Diseases that could be cause of HF, BP, HR, Chest pain, Difficulty breathing, weight gain, edema, etc. 27. Can calcium channel blockers be useful in CHF? No because these drug will decrease calcium and decrease contractility. Chapter 25 Angina/MI 1. What education should be given to all clients who have angina or a history of MI? CPR, methods to lower BP & reduce atherosclerosis using positive lifestyle changes: smoking cessation, decreasing dietary fat intake, increasing intake of fruits & veggies, & participating in regular exercise program. Men have a greater risk for MIs and angina occurs more frequently in women & African Americans. 2. How do nitrates affect a response in angina? Nitrates form nitric acid, a potent vasodilator, which reduces the preload on the heart & decreases the cardiac workload & myocardial oxygen demandessentially calming down the heart. 3. How do beta blockers (atenolol) affect a response in angina? These block the beta-1 receptors on the heart decreasing the O2 demand & contractile strength. 4. How do calcium channel blockers (CCBs) affect a response in angina? They inhibit calcium influx into the myocardial cells, relaxing the coronary & peripheral vessels, and slowing the electrical conduction in the heart.

5. What is the most common side effect from nitrate therapy and how is it treated? Headache; it is treated using vasoconstrictors such as Tylenol. 6. In what form(s) can nitrates be administered in an acute anginal attack? Sublingual, buccal (oral), translingual, and IV. 7. What is the protocol for administering NTG during acute chest pain? Short-acting nitrates, such as nitroglycerin, are taken sublingually to quickly terminate an acute attack of angina. Vital signs should be monitored before and after administration. 8. What is the purpose for cycling a nitroglycerine patch off for 6-12 hours? To delay the development of tolerance. When is usually the best time to leave the patch off? During the night. 9. What is the process for placing nitrate patches? Rotate the sites & wash thoroughly after patch removal. 10. How should clients store nitroglycerine tablets? In their original container, away from light, heat, & moisture. 11. What remedies/therapies should clients using nitrates avoid? Concurrent use with Viagra could cause life-threatening hypotension & CV collapse. Use with alcohol & anti-hypertensives may cause additive hypotension. 12. Why are diabetics and asthmatics a concern when beta blockers are used for therapy? Diabetics- Use of beta blockers can mask the s/s of hypoglycemia. Asthmatics- can precipitate bronchospasms in clients with the initial doses. 13. What needs to be assessed before giving beta blockers or CCBs? The clients: apical heart rate, respiratory rate, and blood pressure. 14. What happens if clients suddenly stop using beta blockers or CCBs? The adrenergic receptors they act upon can be over stimulated causing excitation & can exacerbate angina and cause tachycardia or MI in clients with CV disease. 15. Why should grapefruit juice not be given with CCBs? The grapefruit juice can decrease the activity of the enzymes that break down the drug, thus more drug is in the system and toxicity can result. 16. Clients using nitrates may develop reflex tachycardia when the blood pressure drops. What drug class might be given to treat this side effect? A beta-adrenergic blocker 17. What is the significance of weight gain, edema, and SOB in a client being treated for angina? These are signs can be indicative of heart failure and can help the HCP in reassessment of the client. 18. What concern should you have for a client taking any combination of the following: diltiazem, atenolol, digoxin? Concurrent use of CCBs (diltiazem) with atenolol may result in excessive cardiac suppression. When atenolol & digoxin used concurrently may slow AV conduction, leading to heart block. 19. What is the action of reteplase (Retevase) and how is it valuable in an acute MI? This drug acts by cleaving plasminogen to form plasmin which then degrades the fibrin matrix of thrombi. When administered during via IV bolus it works within 20 minutes & can reduce myocardial ischemia that would result from the thrombi. 20. What is the window of opportunity for using this drug? The window of opportunity is 20 minutes to 12 hours after the onset of MI symptoms; if given after this time the drugs are mostly ineffective.