Ventilatory and cardiac responses to pulmonary embolism: consequences for gas exchange and blood pressure.
Acute thromboembolic pulmonary embolism (PE) is a life threatening condition that can lead to pulmonary hypertension and right ventricular dysfunction or failure. There is typically an increase in ventilation rate and cardiac output as a response to PE prior to cardiac failure, which is at least in part due to systemic hypoxemia. Here we assess the response of the lungs to changes in these parameters using anatomically-based computational models of pulmonary perfusion, ventilation and gas exchange. We show that increases in ventilation and cardiac output improve overall gas exchange in PE. However, this comes at the cost of an increased pulmonary blood pressure, which may contribute to pulmonary hypertension as a result of PE.
Auckland Bioengineering Institute,The University of Auckland, Private Bag 92019, Auckland, New Zealand. alys.clark@auckland.ac.nz
Alys R
AR
Clark
Mohit
M
Bajaj
Margaret L
ML
Wilsher
David G
DG
Milne
Merryn H
MH
Tawhai
D000328:Adult; D000792:Angiography; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000378:metabolism; D002302:Cardiac Output; D003198:Computer Simulation; D004452:Echocardiography; D006801:Humans; D006973:Hypertension / Q000473:pathology; D000860:Hypoxia / Q000473:pathology; D008168:Lung / Q000473:pathology; D008953:Models, Anatomic; D010477:Perfusion; D011655:Pulmonary Embolism / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange; D013610:Tachycardia / Q000473:pathology; D014057:Tomography, X-Ray Computed; D018497:Ventricular Dysfunction, Right / Q000473:pathology
D002245:Carbon Dioxide