♦ Skeletal muscle changes leading to reduced muscle bulk (including respiratory muscles) and exaggerated ergoreflex. The increased stiffness of the lungs increases the work of breathing
♦ Increased arterial chemoceptor sensitivity
♦ These first two aspects contribute to an abnormal ventilatory response; there is an objective increase in ventilation for a given amount of carbon dioxide production. The degree of increase correlates with the severity of exercise limitation
♦ Increased anatomical dead space (oropharynx, trachea and bronchi) ventilation due to raised respiratory rates.
♦ Increased physiological dead space ventilation due to reduction of apical perfusion
♦ Airflow obstruction and wheezing in a setting of acute pulmonary oedema is well recognized clinically.13'50 Some patients with left ventricular dysfunction exhibit an increase in bronchial responsiveness following Methacoline51'52 but this finding has not been universal and the significance of these reports remain unclear53-56
♦ Diffusion abnormalities at the gas/air interface
♦ Anxiety and depression aggravating ventilatory abnormalities and perception of breathlessness
♦ Splinting of the diaphragm in the presence of significant ascites.
Was this article helpful?