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Valvular Hemodynamics
Morton J. Kern, MDProfessor of Medicine
Chief of CardiologyAssociate Chief CardiologyUniversity California Irvine
Orange, California
Hemodynamic Problems for the Cath Lab
• Valvular heart disease:• Aortic stenosis/insufficiency• Mitral stenosis/insufficiency
• Intraventricular gradients• Pericardial effusion/tamponade• Constrictive/restrictive physiology• Coronary Hemodynamics• Intracardiac Shunts
Tri/MV valves open
Pa/Ao valves are closed
Pa/Ao valves open
Tri/MV valves close
Pa/Ao valves close
Tri/MV valves opensystole
=Valve action
BAMC Case #3117: Patient: 61 yo maleDx: 3V CAD filter: 50 Hz/ sample 250 Hz
Pre ContrastNormal LV and Aortic Pressure Fluid-filled system micromanometer transducers Fluid filled, FA sheath
Mechanism of AS: LV-Ao Gradient
Consequences of LV-Ao Gradient:
1. late peaking Systolic murmur
2. Single A23. Slow pulse upstroke
LV
Fusmann and Feldman T, Cath and CV Int 53:553;2001
Hemodynamics of ASPeak to peak pressure gradients differ between ECHO and CATH
Peak instantaneous P-P
Unshifted=larger Grad
Parham and Kern, Cath and CV Int 53:553;2001
Retrograde hemodynamic Assessment of Prosthetic Valves with a Pressure Wire
Base 10 Dob+Pace 80 20 Dob + Pace 95
Dobutamine challenge for LG AS
P-P = 50mmHgCO = 4.2l/m
AVA = 0.6cm2
Grayburn, P. A. Circulation 2006;113:604-606
What should you do with Symptomatic AS patient, low gradient, low flow? The Dobutamine Challenge
AVA = 0.7cm2
AVA = 1.0cm2
AVA = 1.5cm2
Fixed area
Hemodynamics of Aortic Insufficiency• Greatest Diastolic Gradient early • Volume filling LV is rapid• LVEDP will be high unless
compensated