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August 10, 1984

The Cardiovascular Effects of Mechanical Ventilation and Positive End-Expiratory Pressure

Author Affiliations

From the Chest Service, Department of Medicine, San Francisco General Hospital, and the University of California, San Francisco.

JAMA. 1984;252(6):807-811. doi:10.1001/jama.1984.03350060051030

IN PATIENTS with diffuse lung disease due to the adult respiratory distress syndrome (ARDS), mechanical ventilation (MV), and positive endexpiratory pressure (PEEP) commonly are used to improve the Pao2. This is done despite the fact that MV and PEEP may depress cardiac output and thereby reduce systemic oxygen transport.1 In this article, the complex and often controversial cardiovascular effects of MV and PEEP are reviewed by focusing on the determinants of cardiac output. Guidelines to minimize the cardiovascular effects of MV and PEEP in patients with ARDS are also provided.

Determinants of Cardiac Output  Cardiac output is the product of the ventricular stroke volume and heart rate. Heart rate is influenced by sympathetic and parasympathetic nervous system activity that is mediated in part by the baroreceptor reflex involving receptors in the carotid sinus and aortic arch. Stroke volume is determined by three factors: (1) preload, the length of cardiac muscle