The wide swings of intrathoracic pressure during respiratory cycles and hyperinflation modify the extramural pressure surrounding the heart and blood vessels and have serious circulatory consequences. In the presence of bronchial obstruction, intrapleural pressure may fall to -30 cmH 2O during inspiration and to -50 cmH2O during forced inspiration. This profoundly negative pressure is directly transmitted to the right atrium and there is an enormous increase in venous return from the inferior vena cava. Consequently, right ventricular preload increases.
Hyperinflation may compress and stretch the capillary network, contributing to an increase in pulmonary arterial resistances. Intra-alveolar pressure is the extramural pressure for capillaries. It is positive in distended alveoli ventilated by partially occluded bronchi (auto-PEEP), profoundly negative in completely occluded areas, and approaches zero to -3 cmH2O in normally ventilated alveoli. Globally, this results in a mean pressure value approaching zero, which is greater than intrapleural pressure. These phenomena result in an increase in afterload for the right ventricle which is surrounded by deep negative pressures, i.e. intrathoracic pressures. Hence the right ventricular ejection fraction falls, leading to increased end-diastolic volume. The right ventricle dilates and squeezes the left ventricle, since both are contained in a common inextensible pericardium. This effect, which is known as diastolic ventricular interference, occurs in parallel. Preload of the left ventricle is lower, owing to a reduced pulmonary blood flow following decreased right ventricular output, and produces ventricular interference in series. A decrease in the left ventricular compliance further impairs its filling. This is because of changes in the left ventricular configuration induced by compression of the right ventricle. The negative intrathoracic pressure augments the transmural aortic pressure, causing an increased left ventricular afterload. Thus left ventricular stroke volume decreases during inspiration, leading to the fall in systolic blood pressure known as pulsus paradoxu s. This physiological inspiratory fall in systolic blood pressure can reach 10 mmHg. This phenomenon is markedly enhanced during an asthma attack, and pulsus paradoxus has been measured up to 50 mmHg. An inverse correlation between pulsus paradoxus and FEV1 has been documented. However, this is not always reliable. Pulsus paradoxus may be weak in patients experiencing a very severe asthma attack when they are exhausted and unable to generate the required marked negative intrapleural pressures. It is probably a better reflection of pleural pressure swings than of spirometric indices of airflow obstruction.
The enormous increase in lung volumes with the concomitant development of PEEP may have a compressive effect on the heart. Moreover, venous return may be limited by the flattened diaphragm muscle, which compresses the inferior vena cava at the entrance to the thorax. Pulmonary circulation is also impaired by overdistended alveoli and associated high pressures. All these factors further reduce right and left ventricular preload and may impair cardiac output.
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