Anneka Hutton, MD
Pulmonary Critical Care Fellow
University of Alabama at Birmingham (UAB)
Birmingham, Alabama
Disclosure information not submitted.
Ashley Innis, MD
Internal Medicine Resident
University of Miami, United States
Disclosure information not submitted.
Daniel Gutman, MD
Associate Program Director
Florida Atlantic University, United States
Disclosure information not submitted.
Domenico Calcaterra, MD
Attending Physician, Cardiothoracic Surgery
Bethesda Hospital East, United States
Disclosure information not submitted.
Title: Acute Aortic Regurgitation: The Importance of Aortic Pressure Half Time
Case Report Body:
Introduction: Acute aortic regurgitation (AAR) is a medical emergency with staggering mortality. As the commonest causes of AAR are infective endocarditis (IE) and aortic dissection, consideration of AAR is paramount in patients with shock and risk factors for IE.
Description: A 26-year-old female presented to the ED with 4 days of dyspnea and fever. Her history was significant for IV drug abuse and recent MRSA IE for which she completed a 6-week course of antibiotics. She was febrile, tachycardic and tachypneic. Blood pressure was 118/35 mmHg, pulse pressure of 83 mmHg. She had bilateral rales and a 4/6 diastolic murmur over the sternal border. Labs showed a leukocytosis of 29.2, troponin of 0.291 & BNP of 525. EKG was unremarkable. CXR showed enlarged cardiac silhouette, increased vascularity, and bilateral patchy opacities. She received broad spectrum antibiotics. Stat echo revealed tricuspid and aortic valve (AV) vegetative masses. Aortic pressure half time was 152 ms, consistent with severe aortic regurgitation (AR). Emergent AV debridement and bioprosthetic repair were performed. Despite intra-aortic balloon pump, she did not tolerate weaning from cardiopulmonary bypass and expired.
Discussion: AAR results in sudden hemodynamic changes that overwhelm the LV with a precipitous drop in cardiac output. Diagnosis is made with regurgitant flow on echo. Echo findings used to stratify AAR severity include equalization of LV and aortic diastolic pressures and a low “pressure half-time” (PHT). PHT is the time required for 50% reduction in the peak pressure gradient. PHT depends on the compliance of the receiving chamber. If compliance is low, the chamber pressure rises and decreases rapidly, leading to a steeper slope and a lower PHT. In AAR, low left ventricle compliance leads to a lower PHT. Importantly, PHT can be used as a measure of severity of AR: > 500 ms represents mild, 200-500 ms is moderate, and less than 200 represents severe AR. Severe AR necessitates surgical repair. Early surgery is associated with reductions in mortality. In extremis, stabilization with afterload reduction and inotropic support may be used as a temporizing measure. Given the need for emergent surgical intervention and extreme mortality, we urge clinician awareness of PHT and numeric values associated with severe AR.