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Physiological effects

Up Dysynchrony e-lectures Figure 5a & 5b Modes of ventilation Non-invasive ventilation Physiological effects Specific ventilators

Respiratory system

  • decreased lung compliance
  • more uneven distribution of ventilation
  • increase in dead space and in ratio of dead space to tidal volume

Patients with normal lungs

  • fall in FRC and increased alveolar to arterial oxygen gradient
  • due to extensive dependent atelectasis

Patients with abnormal lungs

  • in patients who have been hypoventilating near residual volume, mechanical ventilation will increase FRC and tidal volume

Cardiovascular system

Positive pressure ventilation results in:

  • rise in pleural pressure
  • rise in intra-abdominal pressure
  • increased lung volumes

All these produce cardiovascular changes. 

The extent of these changes relative to any given level of airway pressure will depend on the lung and chest wall compliance and airway resistance

In any individual patient the overall effects will depend on the patient's underlying pathophysiology.








LV preload is usually (but not invariably) reduced by a variety of mechanisms

Venous return

  • in a volume resuscitated patient
    • venous return does not fall
      • intrathoracic pressure is positive rather than negative but
      • intra-abdominal pressure also rises
      • pressure gradient between abdomen and thorax is maintained
  • in a patient with an open abdomen
    • venous return should fall
      • intra-abdominal pressure does not rise
      • pressure gradient not maintained




  • in a volume depleted patient
    • collapse of intra-abdominal veins and SVC occurs
    • result of positive pressure intrathoracic pressure
    • in abdomen collapse appears to occur behind the liver as a result of positive pleural pressure transmitted through the diaphragm and liver
    • in superior vena cava
    • results in a fall in venous return, RV stroke volume and hence LV preload





  • changes in LVEDV do not necessarily parallel changes in RVEDV
    • RV and LV confined by pericardium
    • as a result increase in RVEDV decreases LV compliance and vice versa
    • in a patient with pulmonary hypertension a reduction in venous return as a result of positive pressure ventilation will reduce the size of a dilated RV and hence increase LV compliance and LV preload

Pulmonary vascular resistance

  • decreased RV stroke volume and hence LV preload because of compression of pulmonary vessels by positive alveolar pressure

LV compliance

  • at high lung volumes lungs compress the heart reducing LV compliance and hence LV end-diastolic volume


  • afterload = wall tension (T) during contraction

    where Ptm= transmural pressure, R=radius and H=wall thickness
  • transmural pressure=intraventricular pressure-pleural pressure
  • pleural pressure increased by positive pressure
  • therefore transmural pressure and afterload must be decreased by positive pressure ventilation

Myocardial oxygen consumption

  • myocardial oxygen consumption was previously thought to be determined by stroke work. However it is now known that it is determined by the sum of stroke work and elastance-defined potential work. The latter is the potential energy in the ventricle at end-systole. Figure below illustrates this relationship. Myocardial oxygen consumption is proportional to the shaded area. As mechanical ventilation generally decreases preload and afterload it shifts the pressure-volume loop to the left and down decreasing elastance-defined potential work and thus myocardial oxygen consumption.

  • in patients with coronary artery disease reducing myocardial oxygen consumption may improve the balance between oxygen demand and supply resulting in an improvement in LV function. Thus in these patients mechanical ventilation may increase LV contractility.

Cardiac output

  • overall effect depends on whether ventricle is normal or abnormal
  • in a patient with normal LV contractility increased intrathoracic pressure decreases LVEDV more than LVESV resulting in a fall in stroke volume (figure below)

Fig. 1

  • in a patient with decreased LV contractility, ­ intrathoracic pressure decreases LVEDV less than LVESV resulting in a rise in stroke volume (figure below). Note the decreased slope of the end systolic pressure volume relationship due to decreased contractility


  • renal blood flow falls if cardiac output falls
  • Decreased sodium secretion due to fall in cardiac output and decreased secretion of atrial natriuretic factor
  • Increased water retention due to increased secretion of ADH, particularly in children.


  • increased intrathoracic pressure decreases venous drainage from head and may increase ICP. If, however, mechanical ventilation results in a decrease in PaCO2 ICP may actually fall
  • NB adverse effects of mechanical ventilation are far outweighed by benefits in brain injured patients

Further reading

Jardin F, Vieillard-Baron A. Right ventricular function and positive pressure ventilation in clinical practice: from hemodynamic subsets to respirator settings. Intensive Care Med 2003; 29:1426-1434

Pinsky MR. The hemodynamic consequences of mechanical ventilation: an evolving story. Intensive Care Med 1997; 23:493-503

Pinsky MR. Recent advances in the clinical application of heart-lung interactions. Curr Opin Crit Care 2002; 8:26-31

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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