Abstract
Positive pressure ventilation was used for the treatment of pulmonary edema almost 100 years ago [1–2]. During World War II, however, attempts to supply adequate alveolar oxygen tension by raising face-mask pressure in pilots flying at high altitudes were followed in many cases by syncope and loss of consciousness. This phenomenon was considered to be a result of the decrease of venous return (VR) and cardiac output (CO) secondary to the increase of alveolar pressure and to its transmission to the pleural space [3]. This deleterious effect of positive pressure ventilation on cardiac output caused its use to be abandoned in patients with pulmonary edema and heart failure from the late 1940’s through the late 1960’s, when Ashbaugh et al. [4] proposed the use of mechanical ventilation (MV) with positive end-expiratory pressure (PEEP) in the treatment of adult respiratory distress syndrome (ARDS). The widespread use of MV with PEEP that followed this report was associated from the early 1970’s to the possibility of bedside monitoring of cardiovascular function with a Swan- Ganz catheter. This allowed a better understanding of the complex cardiopulmonary interactions. In patients with circulatory failure, the intensivist must be able to understand the consequences of MV on cardiovascular function and to manage correctly, or even to anticipate, their effects on the already compromised tissue oxygenation.
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Armaganidis, A., Kotanidou, A., Roussos, C. (1995). Mechanical Ventilation in Circulatory Failure. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine. Yearbook of Intensive Care and Emergency Medicine, vol 1995. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79154-3_15
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