Title

Cardiac tamponed masking as decompensated RV failure in a PH patient.

Document Type

Conference Proceeding

Publication Date

2017

Publication Title

Am J Respir Crit Care Med

Abstract

A 63 year old male presented with lower extremity swelling and shortness of breath. Physical exam showed elevated JVF, edema and cyanosis of lips. His blood pressure was 102/56, with a heart rate of 87 BPM and oxygen saturations of 92% on 4 liters via NC. Patient was told that he had congestive heart failure and was treated with Lasix good response, but over the last 3 weeks he reported worsening shortness of breath (NYHA IV symptoms). Patient underwent transthoracic echocardiogram during his admission that showed enlarged right atrium and ventricle with severe right ventricular dysfunction and a right ventricular systolic pressure of 99 mm Hg. Their was a small to moderate pericardial effusion. He subsequently underwent a RHC which showed a mean pulmonary artery pressure of 61, PCWP of 18 and a CI of 1.87. The mild PCWP elevation was thought to be the result of impaired diastole resulting from flattening of interventricular septum from severe RV volume and pressure overload. Patient was started on Milrinone, Lasix and remodulin with improvement in hemodynamics. Two weeks later patient presented hypotensive Blood pressure 73/50, pulse 106 requiring inotropic and pressor support with milrinone and levophed. Repeat echo showed lower right ventricular systolic pressure of 61 with slight increase in pericardial effusion causing excessive respiratory variation in the tricuspid valve. Patient was emergently taken to the cath lab with gentle removal of 130ml of fluids with improvement in hemodynamics. A total of 250cc of fluid was removed over the next 3 days before the drained was removed. Patient was weaned off levophed and milirone. Serological and microbiological studies were unrevealing. Discussion In patient with PH, the classic clinical features of tamponade may be masked as decompensated right ventricular failure from pulmonary hypertension. This is because, although pericardial effusion decreases ventricular volume and compliance, the right ventricle may be more resistance to collapse due to the high intra-cavitary pressures. The high pressures cause mean right atrial and right ventricular end-diastolic pressure to significantly exceed mean left atrial pressure which can cause exaggerated respiratory variation in tricuspid transvalvular flow velocity like in our patient. Pericardial drainage is the treatment of choice, but care should be taken for gradual removal due to concern that rapid removal in an already dilated ventricle can cause a decrease in diastolic filing leading to acute ventricular decompensation.

Volume

195

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