Cardiac Tamponade

Overall incidence: 2 pts per 10,000 population

2% incidence due to trauma in penetrating injuries

Post-cardiac surgery: Greater incidence after valve replacement (0.6%), compared to CABG (0.2%)

Early diagnosis and prompt treatment are crucial in mitigating mortality and morbidity.

Effusion can irritate myocardium, causing atrial and ventricular dysrhythmias.

Regional cardiac tamponade is more common after cardiac surgery, where a localized effusion or hematoma compresses a single chamber.

Sudden death from cardiac tamponade typically presents as a PEA arrest.

Sudden deterioration in hemodynamics

Catastrophic cardiac collapse upon anesthetic induction and/or mechanical ventilation

Uncontrolled bleeding

End-organ injury from poor perfusion

Rebound hypertension after release of tamponade

Pericardial effusion is the anatomic diagnosis, whereas tamponade is the pathophysiologic diagnosis resulting in obstructive shock.

Pericardial sac normally contains ∼20 mL of fluid. It is the duration of time that an effusion accumulates that determines the likelihood of an acute tamponade.

The pericardial pressure-volume curve is exponential in that once the effusion exceeds the limit of pericardial stretch, small increments of fluid create a steep rise in pressure.

Transmural pressure = P _in (chamber) − P _out (pericardial), such that when the transmural pressure becomes negative, the chamber collapses.

A compensatory sympathetic response leads to tachycardia and systemic vasoconstriction in order to maintain cardiac output and BP. Loss of endogenous sympathetic tone (e.g., induction of anesthesia) can lead to cardiovascular collapse.

As the stroke volume becomes fixed, cardiac output becomes dependent on heart rate.

Ventricular interdependence occurs when the septum shifts during the respiratory cycle due to the external constraint of the tightening pericardial sac. During inspiration, the septum shifts to the left, decreasing the LV stroke volume. During expiration, the septum shifts to the right, decreasing RV filling. However, the opposite occurs in positive-pressure ventilation.

• Pulsus paradoxus: An exaggerated drop in systolic BP (>10 mm Hg) with spontaneous inspiration.

• Beck’s triad: Hypotension/JVD/muffled heart tones.

• CXR: Cardiomegaly with globular heart.

• ECG: Sinus tachycardia, low voltage, PR depression, diffuse ST elevations, and electrical alternans.

• CVP tracing: The y descent is abolished due to an increase in intrapericardial pressure, preventing diastolic filling of the ventricles.

• PA catheter: Equalization of diastolic pressures across chambers.

• ECHO: RV can collapse in early diastole and RA can collapse in late diastole. LA collapse is rare, but highly specific for tamponade. One may see the heart swinging within effusion. IVC dilation without respiratory variation correlates with elevated right atrial pressure in tamponade. Doppler study may demonstrate substantial variation in transvalvular flow velocities with respiratory cycle.

Be suspicious of localized clot in post–cardiac surgery that may not be evident on transthoracic ECHO.

Post cardiac surgery (valves > vessels)

Thoracic aortic dissection

Traumatic mediastinal injury

Pacemaker lead perforation

Malignant effusion (especially breast and lung)

Mediastinal radiation

ESRD (uremic effusion)

Post MI (Dressler syndrome, ventricular wall rupture)

Infectious (viral, fungal, TB)

Myxoedema

Collagen vascular disease (lupus, rheumatic disease)