Key messages

• The effects of ventilation on the circulation are due to changes in lung volume and intrathoracic pressure and the effort necessary to generate them.

• Spontaneous ventilatory efforts can occur in a subject on mechanical ventilation and will increase metabolic demands on the heart.

• Pulmonary vascular resistance is affected by lung volume changes.

Small lung volumes, as occur with acute lung injury, increase pulmonary vascular resistance by the process of hypoxic pulmonary vasoconstriction. Overdistension will also increase pulmonary vascular resistance by alveolar vessel compression.

• Ventilatory strategies that restore lung volume toward normal will maintain low pulmonary vascular resistance, whereas those that overdistend the lung will decrease blood flow to the overdistended lung units, increasing dead-space ventilation and pulmonary vascular resistance.

• Changes in intrathoracic pressure alter the pressure gradients for both venous return and left ventricular ejection. These effects can be used to identify patients with normal or reduced cardiac functional reserve.

Increasing intrathoracic pressure will decrease venous return and unload the left ventricle, decreasing intrathoracic blood volume. In normal conditions cardiac output will decrease, whereas in heart failure cardiac output will either remain constant or, if augmented by the afterload reduction effect, increase. Decreasing intrathoracic pressure will have the opposite effect and may precipitate cardiac failure and pulmonary edema in patients with borderline cardiac function, while augmenting cardiac output in normal subjects.

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