Cardiovascular Medications

Inotropic Support, ACE Inhibitors, and Angiotensin Receptor Blockers

Cardiovascular pharmacotherapy often focuses on optimizing the pump action of the heart and managing vascular tone. Digoxin acts as a cardiac glycoside that increases myocardial contractility by inhibiting the sodium-potassium ATPase pump. At the same time, the medication slows the heart rate primarily by increasing vagal activity. Because of its profound effect on cardiac conduction, safe nursing practice requires assessing the patient's apical pulse for one full minute prior to administration. If an adult patient's apical heart rate falls below 60 beats per minute, the nurse must withhold the dose.

Monitoring circulating drug levels is crucial when administering digoxin because of its narrow therapeutic window. When treating heart failure, clinicians generally target a serum digoxin concentration of approximately 0.5 to 0.9 ng/mL, recognizing that toxicity can occur even within the older reference range of 0.5 to 2.0 ng/mL. Serum electrolyte balance directly influences this risk, as hypokalemia increases the patient's vulnerability to digoxin toxicity. Nurses must remain vigilant for early manifestations of toxicity, which include anorexia, nausea, vomiting, and fatigue. Digoxin toxicity may cause visual changes, such as blurred vision or yellow-green halos, but gastrointestinal and visual symptoms do not occur in a reliable sequence. For severe digoxin toxicity, digoxin immune fab serves as the specific antidote.

Renin-angiotensin-aldosterone system inhibitors are primary agents for regulating systemic vascular resistance and blood pressure. Angiotensin-converting enzyme (ACE) inhibitors are readily identified by the suffix '-pril'. These agents lower blood pressure, but they can cause hyperkalemia by decreasing aldosterone secretion. A frequent adverse effect is a persistent, nonproductive dry cough, which results from bradykinin accumulation. A far more dangerous complication is ACE inhibitor, associated angioedema, a potentially fatal reaction that requires immediate assessment and definitive airway protection when indicated.

When patients develop an intractable cough that prevents them from continuing an ACE inhibitor, clinicians commonly prescribe angiotensin receptor blockers (ARBs), which end in the suffix '-sartan'. While ARBs provide an alternative pathway for managing blood pressure without the bradykinin-mediated cough, both ACE inhibitors and ARBs share a strict contraindication regarding pregnancy. Both drug classes can cause severe fetal injury, particularly when taken during the second and third trimesters.