He had been through this before. The patient, a 57-year-old man with diastolic heart failure, COPD, hypertension, and diabetes mellitus, had come through the doors of this emergency department many times. He had a favorite seat in triage. He knew what questions the nurse would ask him once he was in a room, and that the doctor would repeat those same questions. Then the tests and labs, then moved upstairs for a couple of days before going home, hopefully feeling better. He knew all of this. Today, though, everything he thought he knew was wrong.
He was hypoxic (SpO2 70%) and short of breath on presentation to the emergency department. Exam was remarkable for generalized edema, diffuse crackles, and JVD elevation. He was presumed to have an exacerbation of his diastolic heart failure, and was admitted for treatment. His symptoms were not improving despite aggressive diuresis. A transthoracic echocardiogram was performed.
The echocardiogram showed normal left ventricular size and performance (ejection fraction of 65%) without any wall motion abnormality. The right atrium and ventricle, however, were markedly enlarged, and there was decreased right ventricular systolic contractility. The right-sided dilation was causing significant tricuspid insufficiency. The estimated pulmonary artery systolic pressure was 27 mm Hg above the right atrial pressure. A notable finding was a D-shaped septum, implying a relative increase in right ventricular end-diastolic pressure. These findings were concerning for increased pulmonary arteriolar vascular resistance versus worsening volume overload. The patient underwent a right heart catheterization to assess this.
The right heart catheterization showed that the pulmonary artery pressure was 72/31 (mean 46) mm Hg with an occlusion pressure of 18 mm Hg. This indicates essentially high-normal left-sided pressures and severe pulmonary hypertension. Much to everybody's surprise, the patient, rather than suffering from left ventricular diastolic failure (heart failure with preserved ejection fraction) that would require elevated left ventricular end diastolic pressures, was actually underfilling his left ventricle. The patient had severe pulmonary hypertension with right-sided heart failure (cor pumonale). Multiple possible etiologies for the patient's pulmonary hypertension, included COPD, chronic cocaine use causing pulmonary fibrosis/ILD, and chronic hypoxia from untreated obstructive sleep apnea. He had a prescription for CPAP, but had refused to wear it. The right ventricle was hypertrophied and dilated, indicating that this was chronic rather than acute.
Find a complete discussion of this case, additional studies, and two videos on May 5 in the EMN iPad app and on May 12 in the Spontaneous Circulation blog on www.EM-News.com, where the EMN app can also be downloaded for free.
Click and Connect!Access the links in EMN by reading this issue on our website or in our iPad app atwww.EM-News.com. Comments about this article?Write to us email@example.com.© 2014 by Lippincott Williams & Wilkins