Acute Pericarditis

Decide which pericardial syndrome you actually have - Uncomplicated acute pericarditis is an inflammatory chest-pain problem; the anesthetic question is whether there is an effusion with tamponade physiology. Echocardiography answers it: right ventricular diastolic collapse, right atrial systolic collapse, transmitral respirophasic flow variation over 25%, and a dilated IVC collapsing less than 50% on inspiration.

Rate beats volume - A small effusion that accumulated fast — after cardiac surgery, after an electrophysiology procedure, free-wall rupture post-MI, penetrating trauma — tamponades at volumes a chronic malignant effusion would shrug off. Do not be reassured by a size measurement alone.

Tamponade physiology dictates the induction - Filling is pressure-limited, so output lives on preload, heart rate, and sympathetic tone. Positive pressure ventilation further cuts venous return and can precipitate arrest. This is why almost all pericardial decompressions are done under local anesthesia or light sedation — drain first, induce after.

Beck's triad and pulsus paradoxus - Hypotension, jugular venous distension, and muffled heart sounds, with an absent y descent on the JVP tracing. Pulsus paradoxus is a greater than 10 mmHg inspiratory systolic fall, over 80% sensitive for tamponade once an effusion is present. Read it off the arterial line; automatic cuffs cannot measure it, and its absence does not rule tamponade out.

Volume and pressors are a bridge only - Oxygen, volume expansion, and legs elevated buy time. Definitive treatment is pericardiocentesis, a pericardial window, or in penetrating trauma an operative approach — and removing even the first small volume of fluid often transforms the hemodynamics.

The ECG you will actually see - Acute pericarditis gives diffuse concave-up ST elevation with PR depression and PR elevation in aVR, changes that are not confined to a coronary distribution — that is what separates it from STEMI. In tamponade the usual finding is sinus tachycardia; low voltage and electrical alternans are classic but uncommon.

What caused it changes the case - Uremic pericarditis responds to intensified dialysis and carries a higher rate of bloody aspirate; tuberculous, purulent, and malignant effusions carry much higher rates of recurrence and progression to constriction. Malignant tamponade carries an 80% mortality at 12 months versus under 15% for non-malignant causes.

Medications they arrive on - High-dose NSAIDs (ibuprofen, indomethacin, naproxen), or aspirin when post-MI or already on antiplatelet therapy, plus adjunctive colchicine typically continued 3 to 6 months. Corticosteroids are second line and raise the recurrence rate. Factor the NSAID and aspirin effect into bleeding and regional planning.

Pericardiocentesis has its own complications - Coronary or internal mammary vessel injury, right ventricular puncture, liver laceration, pneumothorax, and arrhythmia. Have the arterial line, defibrillator pads, and blood available before it starts.

Recognize recurrence postoperatively - After cardiac surgery or an EP procedure, rising filling pressures with a falling cardiac output and a narrowing pulse pressure should send you to a bedside echo rather than to more volume. Post-cardiotomy tamponade is frequently fatal when the recognition is late.

The pericardium is a double-layered fibroelastic sac — a visceral layer on the epicardium and a richly innervated parietal layer — separated by 15 to 50 mL of serous fluid. Acute pericarditis is inflammation of that sac. Roughly 90% is idiopathic or viral; the rest is uremic, tuberculous, purulent, malignant, autoimmune, post-myocardial infarction (Dressler syndrome), post-cardiotomy, traumatic, or drug-induced. The dense parietal innervation is why over 90% present with sharp, pleuritic, positional retrosternal pain.

Inflammation usually brings an effusion, and what matters hemodynamically is the rate of accumulation, not the volume. A slowly filling sac stretches and tolerates a large effusion; a fast one compresses the chambers at small volumes, limits diastolic filling, and produces cardiac tamponade — obstructive shock and a true emergency. Months to years later, pericardial thickening can instead produce constrictive pericarditis (covered in its own entry).