Cardiotonic-Inotropic Drugs Nursing Pharmacology Study Guide

Generic and Brand Names

Cardiac glycosides: deslanoside (Cedilanid-D), digitoxin (Crystodigin), digoxin (Lanoxin, Lanoxicaps).

Phosphodiesterase inhibitors: amrinone, inamirone (Inocor), cilostazol (Pletal), milrinone (Primacor), enoximone (Perfan).

Disease Spotlight: Heart Failure

Heart failure is a syndrome of cardiac muscle dysfunction, driven by conditions that overwork the heart. Coronary artery disease (CAD) starves the myocardium of blood and is the most common cause. Cardiomyopathy enlarges the heart and fatigues the muscle. Valvular disease causes reflux and ventricular overload that overstretches the myocardium.

Manifestations follow the side that failed. Left-sided HF is mostly pulmonary, because the left ventricle cannot push blood into the periphery. Pulmonary veins engorge, producing tachypnea, dyspnea, orthopnea, cough, and hemoptysis. Severe cases progress to pulmonary edema, which is life-threatening because it blocks gas exchange. Right-sided HF develops when the right heart must work harder to push blood into pulmonary circulation; pressure rises in that normally low-pressure system, venous return backs up, neck veins distend, central venous pressure climbs, the liver and spleen congest and enlarge, and dependent limbs develop pitting edema.

Cardiac Glycosides

Cardiac glycosides come from foxglove (digitalis). They raise intracellular calcium in cardiac muscle, increasing contractility.

Therapeutic Action

More calcium enters during contraction, increasing the force of contraction (positive inotropic effect). Cardiac output and renal perfusion rise; better renal blood flow decreases renin release, downplaying the renin-angiotensin-aldosterone system (RAAS) so more fluid is excreted in the urine. The drop in blood volume eases the heart's workload. The drug also slows cell relaxation, so it strengthens contraction without raising rate (negative chronotropic effect).

Indications

Primarily for decreasing cardiac workload and relieving HF. Digoxin is specifically indicated for atrial flutter, atrial fibrillation, and paroxysmal atrial tachycardia.

It is widely used for heart defects in children, but the safety margin is small, so the nurse should recalculate and re-validate the dose with another nurse before administration, and monitor serum digoxin and signs of digitalis toxicity carefully. Teach adults the manifestations of toxicity to report, caution them against switching digoxin brands (bioavailability differs and raises toxicity risk), and teach them to take and assess their own heart rate. Safety in pregnancy is not established; digoxin enters breast milk but has not been linked to neonatal adverse effects, though caution still applies. Older adults are more prone to toxicity from conditions that impair metabolism and excretion, so monitor renal and hepatic function and teach relatives to check heart rate and regularity.

Pharmacokinetics

Contraindications and Cautions

Contraindicated with allergy to any digitalis component; ventricular tachycardia or fibrillation (potentially fatal, treat with another drug); heart block or sick sinus syndrome (worsened by slowed AV conduction); idiopathic hypertrophic subaortic stenosis (IHSS), where increased contraction obstructs the aortic outflow tract; acute myocardial infarction (more force damages the muscle further); renal insufficiency (the drug is renally excreted, raising toxicity risk); and pregnancy and lactation.

Adverse Effects

CNS: headache, weakness, drowsiness, vision changes (classically a yellow halo around objects). CV: arrhythmias. GI: GI upset, anorexia. Signs of digitalis toxicity: anorexia, nausea, vomiting, malaise, depression, and irregular rhythms (heart block, arrhythmias, ventricular tachycardia).

Interactions

Digoxin immune Fab (DigiFab) is the antidote; these antibodies bind digoxin so it cannot reach its site of action. It is used when serum digoxin is >10 ng/mL and serum potassium is >5 mEq/L. Verapamil, amiodarone, quinine, erythromycin, tetracycline, and cyclosporine increase digoxin's therapeutic and toxic effects, so the digoxin dose is decreased. Potassium-losing diuretics raise the risk of cardiac arrhythmias. Thyroid hormones, metoclopramide, and penicillamine decrease digoxin's effect, so the dose is increased. Cholestyramine, charcoal, colestipol, antacids, bleomycin, cyclophosphamide, and methotrexate decrease absorption, so digoxin is taken 2-4 hours after these. St. John's wort and psyllium decrease the effect; ginseng, hawthorn, and licorice increase toxicity risk.

Phosphodiesterase Inhibitors

By blocking phosphodiesterase, these drugs raise cyclic adenosine monophosphate (cAMP), which drives calcium into the myocardium and increases contractility. They also prolong sympathetic stimulation, producing three major effects: vasodilation, increased oxygen consumption, and arrhythmias.

They are indicated only for short-term treatment of patients not responding to cardiac glycosides, vasodilators, and diuretics, and reserved for severe situations because they carry a risk of fatal ventricular arrhythmias. Not recommended for children. Safety in pregnancy and lactation is not established. As with glycosides, teach adults to report adverse effects and to monitor their own heart rate, and monitor renal and hepatic function closely in older adults.

Pharmacokinetics

Contraindications and Cautions

Contraindicated with allergy to phosphodiesterase inhibitors and bisulfites; severe aortic or pulmonary valvular disease and acute MI (both worsened by increased contraction and oxygen demand); and fluid volume deficit (worsened by increased renal perfusion and urine output).

Adverse Effects

CV: ventricular arrhythmias, ventricular fibrillation, hypotension, chest pain. GI: nausea, vomiting, GI upset, abdominal pain. Hematologic: thrombocytopenia. Hypersensitivity reactions: vasculitis, pericarditis, pleuritis, ascites. Also burning at the IV injection site.

Interactions

In solution with furosemide, a precipitate forms.

Nursing Considerations

Assessment

Screen for the contraindications above (renal insufficiency, fluid volume deficit, acute MI, hypersensitivity). Do a full baseline physical. Record baseline weight and track recent changes for fluid status. Assess heart rate and blood pressure closely for changes that warrant a dose change, auscultate heart sounds for abnormal sounds and conduction problems, and track urinary pattern and output as a gross marker of renal function. Get a baseline ECG for rate and rhythm. Monitor serum electrolytes and renal function (add CBC and hepatic function for phosphodiesterase inhibitors).

Nursing Diagnoses

• Risk for fluid volume deficit related to increased renal perfusion from the drug
• Decreased cardiac output related to inefficient myocardial contractility (and hypotension with phosphodiesterase inhibitors)
• Ineffective tissue perfusion related to decreased blood flow
• Risk for injury related to easy bruising secondary to thrombocytopenia (phosphodiesterase inhibitors)

Implementation

For cardiac glycosides, check dose and preparation carefully given the narrow safety margin, and do not give with food or antacids (they decrease absorption). Count the apical pulse for one full minute before each dose. Withhold the drug if the pulse is less than 60 beats per minute in adults or 90 beats per minute in infants; recheck the apical pulse after one hour, and if it stays low, document, withhold the dose, and notify the physician. Assess pulse rhythm for arrhythmias, an early sign of toxicity. Weigh the patient daily and check dependent areas for edema and degree of pitting. Monitor serum digoxin level as ordered (assay therapeutic range 0.5-2 ng/mL). For heart failure, current AHA/ACC/HFSA guidance targets a lower level, roughly 0.5-0.9 ng/mL and below 1.0 ng/mL, because levels of 1.2 ng/mL and higher are linked to increased mortality without added benefit. Keep emergency drugs and equipment at the bedside: potassium salts and lidocaine for arrhythmias, phenytoin for seizures, atropine for clinically significant bradycardia, and a cardiac monitor.

For phosphodiesterase inhibitors, protect the drug from light, ensure IV patency, weigh daily and track intake and output, and watch for petechiae and easy bruising signaling thrombocytopenia. Monitor the IV site for burning or irritation.

For both, provide comfort measures (small frequent meals for GI upset, safety measures for drowsiness and weakness, adequate room lighting for visual disturbances), promote rest, and teach the drug name, indication, and adverse effects to watch for.

Evaluation

Monitor response by assessing HF manifestations, arrhythmias, and serum digoxin level. Watch for adverse effects (visual changes, worsening HF, arrhythmias, thrombocytopenia). Confirm the patient can name the drug, its indication, and the adverse effects to watch for, and monitor adherence.

Frequently Asked Questions

What does a positive inotropic drug do? It increases the force of each heart contraction. In heart failure, a stronger squeeze raises cardiac output and renal perfusion, which eases the heart's workload and helps the body clear excess fluid.

Why do you check an apical pulse before giving digoxin? Digoxin slows the heart rate, so a low rate signals possible toxicity. Count the apical pulse for one full minute and withhold the dose if it is below 60 beats per minute in adults or 90 in infants, then recheck and notify the prescriber if it stays low.

What is the antidote for digoxin toxicity? Digoxin immune Fab (DigiFab) binds digoxin so it cannot reach its site of action. It is used in severe toxicity, for example when the serum digoxin level is above 10 ng/mL or serum potassium is above 5 mEq/L.

What digoxin level is considered safe in heart failure? The general assay therapeutic range is 0.5 to 2 ng/mL, but current AHA/ACC/HFSA heart failure guidance aims lower, about 0.5 to 0.9 ng/mL and below 1.0 ng/mL, because higher levels raise mortality without added benefit.

What are the early signs of digitalis toxicity? Anorexia, nausea, and vomiting often come first, along with malaise, visual changes such as a yellow halo around objects, and new irregular rhythms. Report these promptly because arrhythmias can be life-threatening.

Why are phosphodiesterase inhibitors only used short-term? They strengthen contraction but also carry a real risk of fatal ventricular arrhythmias, so they are reserved for severe heart failure that has not responded to glycosides, vasodilators, and diuretics.