Pathophysiology Of Constriction
Exaggerated Ventricular ...
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Pathophysiology Of Constriction

Exaggerated Ventricular Interdependence:

 • Limited Cardiac Filling due to Fixed Volume → Septum Shifts L/R to Accommodate RV/LV Filling During Inspiration/Expiration

 • Rapid Early Ventricular Filling and then Abrupt Cessation due to Stiff Pericardium: ↑ E-Wave Velocity + ↓ A-wave (E/A > 1)

 • In addition to Intrathoracic-lntracardiac Pressure Disassociation → Exaggerated Ventricular Interdependence during Resp →

 • Variation in Inflow Across A-V Valves → > 25% ↓ Peak MV Velocity and >40% ↑ Peak TV Velocity During Inspiration (opposite Exp.)

Intrathoracic-lntracardiac Dissociation:

 • Normal - Under normal circumstances, the change in intrathoracic pressure with respiration is transmitted to the intrapericardial (heart chambers) structures and extra- pericardial (pulmonary vasculature) equally → MV Inflow Gradient Remains Constant Through Respiration. With inspiration, the intrathoracic pressure ↑ and with expiration ↓

 • Constriction - With constriction, the ↓ intrathoracic pressure is transmitted to the extra-pericardial pulmonary capillaries but constriction limits the ↓ intrathoracic pressure being transmitted to the heart chambers. ↓ MV Inflow Gradient During Inspiration. With inspiration, the intrathoracic pressure ↓ and with expiration ↑



- Karan Desai MD @karanpdesai via CardioNerds @cardionerds



#constriction #constrictive #pericarditis #pathophysiology #cardiology #dissociation 
Contributed by

Dr. Gerald Diaz
@GeraldMD
Board Certified Internal Medicine Hospitalist, GrepMed Editor in Chief 🇵🇭 🇺🇸 - Sign up for an account to like, bookmark and upload images to contribute to our community platform. Follow us on IG:  https://www.instagram.com/grepmed/ | Twitter: https://twitter.com/grepmeded/
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