Cardiovascular effects of mechanical ventilation.

The heart and lungs work closely to meet the tissues’ oxygen demands. If the balance between oxygen demand and supply becomes disturbed in critical illness, tissue hypoxia and cell death can rapidly result. An essential part of critical care is to maintain cardiopulmonary function with the help of pharmacotherapy, fluid management, and respiratory support. Paradoxically, interventions aimed at improving the function of one system can sometimes have undesirable eVects on the other and, although the pulmonary consequences of cardiac disease are well recognised, the influences of changes in pulmonary physiology on cardiac function are less well appreciated. Cardiopulmonary interactions (the eVects of spontaneous and mechanical ventilation on the circulation) were first documented in 1733, when Stephen Hales showed that the blood pressure of healthy people fell during spontaneous inspiration. Over a century later Kussmaul described pulsus paradoxus (the inspiratory absence of the radial pulse) in patients with tuberculous pericarditis. Cardiopulmonary interactions are present in health, and can be exaggerated or abnormal in the presence of disease. This article will provide an overview of this broad topic. By emphasising the underlying physiological principles and the influence of disease states upon these, we hope that respiratory support will then be tailored to the individual patient.