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Cardiovascular effects of mechanical ventilation
  1. Lara Shekerdemian,
  2. Desmond Bohn
  1. Department of Critical Care, Hospital For Sick Children, 555 University Avenue, Toronto M5G 1X8, Canada
  1. Dr L Shekerdemian, Paediatric Intensive Care Unit, Great Ormond Street Hospital, London WC1N 3JH, UK. email:101732.2171{at}compuserve.com

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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 effects 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 effects 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.1 Over a century later Kussmaul described pulsus paradoxus (the inspiratory absence of the radial pulse) in patients with tuberculous pericarditis.2

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.

The influence of ventilation on cardiac function

Spontaneous and mechanical ventilation induce changes in intrapleural or intrathoracic pressure and lung volume, which can independently affect the key determinants of cardiovascular performance: atrial filling or preload; the impedance to ventricular emptying or afterload; heart rate and myocardial contractility. Changes in intrathoracic pressure are transmitted to the intrathoracic structures: namely the heart and pericardium, and the great arteries and veins. Spontaneous inspiration produces a negative pleural pressure, and the reduction in intrathoracic pressure is transmitted to the right atrium. In contrast, intermittent positive pressure ventilation (IPPV) produces inspiratory increases in intrathoracic pressure and therefore …

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