THE PATHOPHYSIOLOGY OF RESPIRATORY GAS EXCHANGE

Abstract

Respiratory gas exchange involves the transfer of oxygen from the atmosphere to the metabolizing cell, and the movement of carbon dioxide in the opposite direction. Contributing to this phenomenon are various cardiorespiratory processes including ventilation, gas diffusion, perfusion, and transport and tissue delivery. Three major groups of patients were studied to investigate areas of abnormalities in these processes. Patients with primary pulmonary hypertension (PPM) showed major abnormality in the ventilation-perfusion matching as well as having poor cardiac output, both resulting in low mixed venous oxygen saturation and hypoxaemia at rest. Both exercise and prostacyclin infusion failed to alter the ventilation-perfusion imbalance although the latter caused improvement in arterial oxygenation by improving the mixed venous oxygen as a result of increased cardiac output. Patients with chronic obstructive pulmonary disease (COPD) also showed abnormal gas exchange. It was shown that in this group as well as in the PPH patients, the presence of ventilation-perfusion mismatching and exaggerated phasic variation in pulmonary end-capillary CO2 made estimation of cardiac output using alveolar gas exchange (Fick Principle) imprecise. By contrast to these two groups, recipients of heart-lung transplantation have no afferent innervation to their lungs and hearts. Nonetheless they manifested normal gas exchange at rest. Abnormalities developed on exercise, with suboptimal cardiac response and increase ventilated response. Exercise gas diffusion was also impaired. These studies demostrated the interrelationship of various abnormalities of gas exchange, the knowledge of which are essential for understanding the pathophysiology of disease processes.