In patients with depressed myocardial contractility, how is left ventricular afterload MOST likely to be affected by positive pressure ventilation?

  • □ (A) Increased
  • □ (B) Decreased
  • □ (C) Unchanged

Right and left ventricular ejection is affected by alveolar pressure, pleural pressure, and lung volume during the respiratory cycle. During positive pressure ventilation (PPV), the right ventricular afterload increases during the inspiration. This is due to an increase in lung volume and an increase in pulmonary vascular resistance (PVR). The right ventricle is surrounded by pleural pressure, which also increases during inspiration. However, there is a greater increase in alveolar pressure relative to pleural pressure during PPV, which increases the pressure gradient against which the right ventricle has to pump, thus increasing right ventricular afterload.

The situation for the left ventricle is different. Though the left ventricle is also surrounded by pleural pressure, it ejects into the systemic circulation, which is not affected by lung volume and alveolar pressure. The left ventricle has to generate less muscular force in the setting of positive pleural pressure, reflecting a decrease in afterload at a constant arterial pressure. Clinicians should recognize that afterload is not only represented by systemic vascular resistance. An increase in blood viscosity, aortic stenosis, and dynamic obstruction of the left ventricle, as well as a decrease in pleural pressure, leads to an increase in left ventricular afterload.

The impact of changes in left ventricular afterload is significantly dependent on the state of the myocardial contractility. Patients with normal myocardial contractility are much less sensitive to the changes in afterload, while patients with depressed myocardial contractility are very sensitive to changes in the afterload. It is generally accepted that, in patients with depressed myocardial contractility, positive pressure decreases afterload.