Left Ventricular Dysfunction after Myocardial Infarction
Acute Hypertensive Crisis
The benefits of captopril in hypertension and heart failure result primarily from suppression of the renin-angiotensin-aldosterone system (RAAS). As an angiotensin-converting enzyme (ACE) inhibitor, it inhibits ACE, which converts angiotensin I to angiotensin II. Angiotensin II binds to AT1 receptors on smooth muscles to produce vasoconstriction and an increase in blood pressure. Angiotensin II also stimulates the adrenal cortex to secrete aldosterone. Aldosterone causes the distal tubules and collecting ducts of the kidneys to reabsorb water and sodium in exchange for potassium, which results in an expansion in extracellular volume and an increase in blood pressure. Inhibition of ACE leads to decreased plasma angiotensin II, leading to vasodilation and decreased aldosterone secretion. Small increases in serum potassium, as well as, sodium and fluid loss may occur due to a decrease in aldosterone secretion. Administration of captopril results in a reduction of peripheral arterial resistance in hypertensive patients. ACE also metabolizes bradykinin, a peptide that causes vasodilation. ACE inhibitors impede the breakdown of bradykinin, resulting in vasodilation and a bradykinin-evoked cough.
Captopril should be taken 1 hour before meals. Therapy initiation requires analysis of recent antihypertensive drug treatment, the extent of blood pressure elevation, and salt restriction. If possible, the previous antihypertensive drug regimen should be stopped 1 week before starting captopril. The daily dose of captopril may be increased every 24 hours under continuous medical supervision. For patients with significant renal impairment, the initial daily dosage should be reduced and smaller increments utilized for titration.
Left Ventricular Dysfunction after Myocardial Infarction
Acute Hypertensive Crisis
In general, the patient's BUN, electrolytes, serum creatinine, and blood pressure should be monitored routinely. If captopril is initiated in patients with impaired renal function and/or collagen vascular disease, the complete blood count with differential should be evaluated before starting treatment and at two-week intervals for about 3 months, then periodically after that. All patients treated with captopril should be counseled to report any signs of infection, including sore throat or fever. Patients with heart failure should be followed closely for the first 2 weeks of treatment and whenever the dose of captopril is titrated, especially in patients with preexisting hypotension, hyponatremia, diabetes, azotemia, or those taking potassium supplements due to the potential for excessive hypotension, arrhythmia and conduction defects. According to the latest hypertension guidelines, patients with or without CVD or increased ASVD risk should maintain a blood pressure of less than 130/80 mm Hg while on therapy. On the other hand, according to the diabetes guidelines, adult patients (18 to 65 years) with both diabetes and hypertension have a goal blood pressure of less than 140/90 mm Hg
Correction of hypotension is the primary concern through volume expansion with an intravenous infusion of normal saline. Excessive hypotension has been rarely seen in hypertensive patients but is a possible consequence of captopril use in salt/volume depleted persons. ACE inhibitors have rarely been associated with a syndrome that begins with cholestatic jaundice and progresses to fulminant hepatic necrosis and sometimes death. If a marked elevation of hepatic transaminases or jaundice occurs, captopril should be discontinued. A persistent, dry, hacking, nonproductive cough that occurs within the first few months of treatment can also occur with captopril therapy. ACE inhibitor-induced cough is caused by the inhibition of the degradation of bradykinin and generally resolves within 1 to 4 weeks after discontinuation.
Captopril is a widely prescribed drug in clinical medicine. Healthcare workers (physicians and nurse practitioners) who prescribe this medication for hypertension should be aware of its side effects and the need to monitor electrolytes and renal function. In some patients, captopril may produce a chronic cough, and in such scenarios, the drug should be discontinued and another class of antihypertensive should be used. The pharmacist should keep track of the patient's medications to avoid polypharmacy and drug interactions.
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