Causes and hemodynamic findings in chronic severe pulmonary regurgitation
John J. Rommel MD
Division of Cardiology, University of North Carolina, Chapel Hill, North Carolina
J.J. Rommel and P.K. Yadav contributed equally to the manuscript.
Search for more papers by this authorPradeep K. Yadav MD
Division of Cardiology, University of North Carolina, Chapel Hill, North Carolina
J.J. Rommel and P.K. Yadav contributed equally to the manuscript.
Search for more papers by this authorCorresponding Author
George A. Stouffer MD
Division of Cardiology, University of North Carolina, Chapel Hill, North Carolina
Correspondence to: George A. Stouffer M.D. Division of Cardiology University of North Carolina Chapel Hill, NC 27599-7075. E-mail: [email protected]Search for more papers by this authorJohn J. Rommel MD
Division of Cardiology, University of North Carolina, Chapel Hill, North Carolina
J.J. Rommel and P.K. Yadav contributed equally to the manuscript.
Search for more papers by this authorPradeep K. Yadav MD
Division of Cardiology, University of North Carolina, Chapel Hill, North Carolina
J.J. Rommel and P.K. Yadav contributed equally to the manuscript.
Search for more papers by this authorCorresponding Author
George A. Stouffer MD
Division of Cardiology, University of North Carolina, Chapel Hill, North Carolina
Correspondence to: George A. Stouffer M.D. Division of Cardiology University of North Carolina Chapel Hill, NC 27599-7075. E-mail: [email protected]Search for more papers by this authorConflict of interest: The authors have no financial conflicts of interest to disclose.
Abstract
Severe pulmonary regurgitation (PR) most commonly occurs as a sequelae of treatment of pulmonic stenosis or Tetralogy of Fallot with fewer cases of primary pulmonic valvular regurgitation. The amount of PR is influenced by valvular integrity, right ventricular (RV) size, and RV diastolic pressures. In chronic severe PR, the RV remodels to accommodate the regurgitant flow and RV stroke volume increases to maintain effective forward blood flow. Hemodynamic changes include a widened pulmonary artery (PA) pulse pressure and low PA diastolic pressures. As the amount of regurgitation increases, RV end diastolic pressure becomes elevated and systemic cardiac output is reduced, especially with exercise. “Ventricularization” of the PA pressure tracing, in which the contour of the PA pressure is similar to the contour of the RV pressure, is a specific but not sensitive finding in severe PR. © 2015 Wiley Periodicals, Inc.
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