Abstract
“Modern” larger mammals developed over the last 65 million years, after the demise of the dinosaurs. All mammals, including hominids, breathe by negative pressure.
Between 1928 and the 1950’s negative-pressure ventilation using so-called “iron lungs” saved countless poliomyelitis epidemic patients, but during the 1950s, when these devices were in short supply, they were largely replaced by smaller, practical, positive pressure ventilation devices and techniques. These had been used previously for thirty years by anaesthetists in operating theatres to enable general anaesthesia for surgery.
However, positive pressure ventilation for longer term respiratory support was quickly recognised to have disadvantages, including the need for intubation and sedation, reduction of cardiac output from reduced systemic venous return, ventilator acquired pneumonia, and ventilator-induced lung injury. Subsequently, lower tidal volumes and plateau inspiratory pressures were introduced to reduce mortality. There is an extensive publication history of these disadvantages over the last 60 years.
Additionally, the limitations of positive pressure ventilation have been further starkly revealed in COVID-19 pneumonia, a condition where the incidences of pneumothorax and pneumomediastinum have been especially prominent and where mechanical ventilation has been shown to stimulate the expression of angiotensin-converting enzyme-2 (ACE2; the receptor for the SARS-Cov-2 virus in the lung). Mechanical ventilation of patients with COVID-19 pneumonia has been shown to facilitate viral propagation in the lung, further accelerating the pulmonary pathology that had necessitated mechanical ventilation in the first place.
The deleterious effects of COVID-19 on the cardiovascular system have been stressed in much of the recent COVID-19 literature worldwide. Acute myocardial injury and chronic damage to the cardiovascular system have been reported. A potential consequence of using positive pressure ventilation is that by forcing air into lungs, which share the space within the chest, it inevitably increases the pressure on the heart and the major veins leading to it. High levels of positive end-expiratory pressure increase intrathoracic pressure, reducing venous return to the heart and decreasing the cardiac index.
The question, therefore, is whether we should continue to pursue development of positive pressure ventilation methods alone, or, whether respiratory medicine needs to re-investigate and develop negative pressure ventilation, the physiological way that the mammalian cardiorespiratory system evolved to function optimally.