Endocarditis, Pericarditis, Myocarditis

Three infections, three cardiac layers, three different presentations — and the wrong call can be fatal. Knowing which layer is inflamed changes everything about your nursing assessment.

Infective endocarditis targets the endocardium and valves, causing vegetations (bacteria-laden clots) that can embolize to the brain, kidneys, or lungs. Hallmarks: new or changing murmur, Janeway lesions (painless palms/soles), Osler nodes (painful fingertips), splinter hemorrhages, and persistent low-grade fever. Blood cultures (at least 2–3 sets drawn from different sites before antibiotics) are the key diagnostic step. IV antibiotic therapy typically lasts 4–6 weeks. Pericarditis inflames the pericardial sac. The signature finding is sharp, pleuritic chest pain that worsens when lying flat and improves when the client sits up and leans forward. A pericardial friction rub on auscultation is pathognomonic. Watch for pericardial effusion progressing to cardiac tamponade — Beck's triad: hypotension, muffled heart sounds, JVD. Myocarditis inflames the myocardium itself, often post-viral. It mimics heart failure: fatigue, dyspnea, tachycardia, and subtle chest discomfort. There's no classic murmur or friction rub — the danger is sudden dysrhythmias and dilated cardiomyopathy. Activity restriction is critical during the acute phase.

Key Distinctions

Don't confuse pericarditis chest pain (positional, relieved leaning forward) with MI pain (unrelieved by position). Students mix up Janeway lesions (painless, endocarditis) with Osler nodes (painful, endocarditis) — remember "Jane is painless." Myocarditis lacks the dramatic murmur of endocarditis and the friction rub of pericarditis; its subtlety is exactly what makes it dangerous.

Clinical Pearl

Pericarditis sits up, endocarditis shows its hands, myocarditis hides. Position, peripheral signs, and absence of findings guide your differential assessment.