This chapter addresses section F10(i) of the CICM 2017 syllabus document, “Describe the physiological consequences of intermittent positive pressure ventilation and positive end-expiratory pressure”. Though the original intention was to fashion a brief summary of these effects (because how much material could there possibly be), after marinading in the literature the "summary" bloated out to truly absurd proportions, and had to be split into three sections. However, this does not negate the need for a summary. Thus, this chapter is offered as a shorter quicker option for those who do not necessarily need every last reference. 

For something we intensivists do so routinely, it is surprising that the effects of mechanical ventilation have only attracted three past paper questions:

• Question 2 from the first paper of 2016
• Question 3 from the second paper of 2014
• Question 5(p.2) from the first paper of 2009

 These questions are essentially identical, in the sense that all of them ask about the physiological effects of positive pressure ventilation. Question 2 from the first paper of 2016 asked specifically for the effects of 10cm of PEEP, whereas Question 3 from the second paper of 2014 and Question 5(p.2) from the first paper of 2009 asked about PEEP in general.

In summary:

Respiratory effects of positive pressure ventilation:

• PEEP increases functional residual capacity (FRC)
• By increasing FRC, PEEP:
  • Increases alveolar recruitment, which gives rise to:
    • Improved V/Q matching
    • Increased total gas exchange surface
  • Increases lung compliance
  • Decreases the work of breathing (done against compliance)
• Positive pressure may also redistribute lung water out of the lung interstitium
• Excessive positive pressure leads to
  • Overdistension and lung injury
  • Worsening V/Q matching
  • "Biotrauma", i.e. cytokine leak and extrapulmonary organ dysfunction

Cardiovascular effects of positive pressure ventilation:

• Effects on the right ventricle and the pulmonary circulation:
  • Increased intrathoracic pressure is transmitted to central veins and the right atrium, decreasing right ventricular preload
  • Increased intrathoracic pressure is transmitted to pulmonary arteries
  • Transmitted alveolar pressure increases pulmonary vascular resistance
  • Increased pulmonary vascular resistance increases right ventricular afterload
  • Thus, increased afterload and decreased preload has the net effect of decreasing the right ventricular stroke volume. 
• Effects on the left ventricle and the systemic circulation:
  • Decreased preload by virtue of lower pulmonary venous pressure
  • Decreased afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit
  • Thus, decreased LV stroke volume
• Effects on overall cardiovascular function:
  • Decreased cardiac output
  • Decreased myocardial oxygen consumption

Other organ system effects of positive pressure ventilation:

• Raised intracranial pressure, if the PEEP is very high
• Water retention due to increased ADH release and aldosterone secretion
• Sodium retention due to decreased ANP release and aldosterone secretion
• Decreased renal perfusion and GFR (due to decreased cardiac output and increased renal venous pressure)
• Decreased hepatic perfusion and thus decreased metabolic clearance of drugs
• Decreased splanchnic perfusion, resulting id decreased intestinal motility and poor gastric emptying
• Decreased gastric perfusion, increasing the risk of stress ulceration
• Neutrophil retention in the pulmonary capillaries
• Impaired lymphatic drainage from the lungs