D.K., a 72-year-old man, had a myocardial infarction (MI) 5 years ago. He has be
ID: 125501 • Letter: D
Question
D.K., a 72-year-old man, had a myocardial infarction (MI) 5 years ago. He has been diagnosed with classic (stable) angina. D.K. is prescribed acebutolol. His baseline vital signs are blood pressure 108/58; pulse 56 (at times irregular); and respirations 28. His past medication history includes asthma.
What assessments should the nurse make while D.K. is taking acebutolol?
Would another beta blocker, propranolol, be an appropriate medication for D.K.? How are these two beta blocker different. Explain your answer.
How do beta blockers work to manage angina?
Explanation / Answer
What assessments should the nurse make while D.K. is taking acebutolol?
Nursing Implications
Assessment & Drug Effects
• Monitor BP and cardiac status throughout therapy. Observe for and report marked bradycardia or hypotension, especially when patient is also receiving a catecholamine-depleting drug (e.g., reserpine).
• Monitor I&O ratio and pattern and report changes to physician (e.g., dysuria, nocturia, oliguria, weight change).
• Monitor for S&S of CHF, especially peripheral edema, dyspnea, activity intolerance.
• Lab tests: Monitor for drug-induced positive ANA titer during long-term therapy, especially in women and older adults; periodic CBC with long-term therapy.
Patient & Family Education
• Know parameters for withholding drug (e.g., pulse less than 60).
• Note: Common adverse effects include insomnia, drowsiness, and confusion.
• Do not drive or engage in potentially hazardous activities until response to drug is known.
• Do not increase, decrease, omit, or discontinue drug regimen without advice from the physician. Abrupt withdrawal may worsen angina or precipitate MI in patient with heart disease.
• Contact physician promptly at the first signs or symptoms of CHF
• Report muscle and joint pain to physician. Discontinuation of drug therapy usually reverses these adverse effects.
• Monitor for loss of glycemic control if diabetic.
• Note: Drug may mask symptoms of hypoglycemia and potentiate insulin-induced hypoglycemia in diabetics.
• Avoid use of OTC oral cold preparations and topical nasal decongestants unless approved by the physician.
• Do not breast feed while taking this drug without consulting physician.
Would another beta blocker, propranolol, be an appropriate medication for D.K.?
Some beta-adrenergic receptor blocking agents (i.e., beta-blockers) like propranolol are contraindicated in patients with bronchial asthma or with a history of bronchial asthma, or severe chronic obstructive pulmonary disease. In general, beta-adrenergic receptor blocking agents should not be used in patients with bronchospastic diseases. Beta blockade like propranolol may adversely affect pulmonary function by counteracting the bronchodilation produced by catecholamine stimulation of beta-2 receptors. If beta-blocker therapy is necessary in these patients, an agent with beta-1 selectivity (e.g., acebutolol, atenolol, metoprolol, betaxolol) is considered safer, but should be used with caution nonetheless. Cardioselectivity is not absolute and can be lost with larger doses.
How do the beta blockers differ? Explain.
Acebutolol is a cardioselective beta blocker with ISA (intrinsic sympathomimetic activity; see article on pindolol). It is therefore more suitable than non cardioselective beta blockers, if a patient with asthma or chronic obstructive pulmonary disease(COPD) needs treatment with a beta blocker. (For these reasons, it may be a beta-blocker of choice in inclusion in Polypill strategies). In doses lower than 800mg daily its constricting effects on the bronchial system and smooth muscle vessels are only 10% to 30% of those observed under propranolol treatment, but there is experimental evidence that the cardioselective properties diminish at doses of 800mg/day or more.
How do beta blockers work to manage angina?
Beta blockers are first-line therapy in the treatment of chronic stable angina, particularly effort-induced angina.
MECHANISM OF ACTION — The physiologic effects of catecholamines (norepinephrine and epinephrine) are mediated by activation of specific alpha and beta adrenergic receptors. There are at least three distinct types of beta receptors:
• Beta-1, which are found primarily in heart muscle. Activation of these receptors results in increases in heart rate, contractility, and atrioventricular (AV) conduction, and a decrease in AV node refractoriness.
• Beta-2, which are present in heart muscle but are more prominent in bronchial and peripheral vascular smooth muscle. Activation of these receptors results in vasodilatation and bronchodilatation.
• Beta-3, which are found in adipose tissue and the heart. Activation of these receptors may mediate catecholamine-induced thermogenesis and may reduce cardiac contractility.
Beta blockers act by competitively inhibiting catecholamines from binding to these receptors. Some are more selective for the beta-1 receptor.
Upregulation of beta receptors — Beta receptor density is a dynamic process that can change under varying physiologic conditions. In particular, chronic beta blocker therapy leads to an increase in receptor density. This can be clinically important, since sudden withdrawal of the beta blocker results in transient supersensitivity to catecholamines, possibly precipitating angina, myocardial infarction, or death. These complications can occur even in patients without previously apparent coronary disease.
Cardiovascular effects of beta blockers — The beneficial therapeutic effects of beta blockade in patients with stable angina pectoris are mediated by a reduction in myocardial oxygen demand. Myocardial oxygen demand varies directly with heart rate, contractility, and left ventricular wall stress, each of which is diminished by beta blockade. The decrease in wall stress is mediated in part by the antihypertensive action of these drugs.
The decline in heart rate is determined both by the degree to which the heart rate is sympathetically activated (as with exercise or stress) and to the properties of the beta blocker. Those drugs with intrinsic sympathomimetic activity may actually increase the resting heart rate. They are, however, still effective in the treatment of angina because it is the reduction in the exercise heart rate that is of primary importance.
The negative inotropic effects of beta blockers may, at least theoretically, have a favorable impact on myocardial oxygen consumption in the patient with angina. In the past, beta blockers were avoided in patients with left ventricular dysfunction, from concern that negative inotropic effects could precipitate or worsen heart failure. However, extensive clinical experience and the results of major clinical trials have demonstrated that these agents actually prolong survival in patients with heart failure. In such patients, beta blocker therapy should be initiated at low dose, and volume overload should be corrected prior to the initiation of therapy.
Beta blockers may also affect coronary blood flow, although there are competing effects. Beta blockers inhibit adrenergically mediated coronary vasodilation, thereby increasing coronary vascular resistance and decreasing coronary blood flow. However, this potentially deleterious effect is overcome by the reductions in heart rate (which enhances coronary perfusion by prolonging diastole) and myocardial oxygen demand.
Nonselective beta blockers may exacerbate coronary vasospasm in patients with variant angina and should be avoided.
A large number of studies have shown that beta-blockers are useful in the treatment of angina pectoris. Favourable effects of beta blockers are decreased heart rate, contractility and wall tension, the three main causes of myocardial oxygen consumption. Beta-blockers also favorably affect myocardial oxygen supply/demand balance by prolongation of the total duration of diastole. In addition, beta-blockers may promote redistribution of coronary blood flow toward the endocardium and ischemic areas. Beta-blockers are standard therapy for patients with stable angina pectoris, silent myocardial ischemia and unstable angina pectoris. In the treatment of all these forms of myocardial ischemia beta-blockers could be used in conjunction with nitrates and calcium antagonists.
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