and non-invasive ventilation. TTE revealed biventricular dilatation with severe global systolic dysfunction, and raised pulmonary pressures. A small residual pericardial effusion remained. CT coronary angiogram revealed calcium score of zero. He was discharged on bisoprolol, ramipril, and ivabradine. Progress TTE 6 weeks post-pericardiocentesis revealed resolution of systolic function. Discussion: Three possible mechanisms include pre/ afterload mismatch [1], unmasking of pre-existing LV dysfunction [3], and myocardial stunning from compression of epicardial vessels [4]. Literature reviews [2, 5] note that PDS occurred after drainage of 450-2100ml, onset within seconds to weeks, a third of cases were fatal, and two thirds of systolic dysfunction normalised. Intercostal catheters are routinely clamped to prevent re-expansion pulmonary oedema, however no such guidelines exist for pericardiocentesis. Here we suggest limiting immediate drainage to 200ml in order to reduce the likelihood of PDS. Conclusion: Further research on limiting the rate and volume of drainage may clarify how to prevent PDS.

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