RESUMO
Studies of great number of patients with chronic nonspecific pulmonary disease suggest that high levels of pulmonary hypertension are only observed in cases of pulmonary-arterial thromboembolism and primary pulmonary hypertension. In other pulmonary diseases, the significance of pulmonary hypertension seems to be overestimated, as blood pressure in the pulmonary circulation network has values, indicative of the absence of gross morphologic changes of the vascular bed of the lungs. The available indirect methods for the diagnosis of pulmonary hypertension in chronic nonspecific pulmonary disease patients with rather small blood pressure in the pulmonary circulation network are shown to be of little value. Large functional reserves of the right cardiac ventricle which make it possible to cope with a sudden pressure overstrain (to say nothing of the slowly augmenting one) are pointed out. It follows therefore that either as yet unknown factors contribute to the pathogenesis of chronic pulmonary heart decompensation, or there is virtually no decompensation, while the demonstrated clinical symptoms of systemic circulatory congestion are of extracardiac origin. Various aspects of the assessment of the role of pulmonary hypertension and clinical symptoms of decompensated pulmonary heart will be discussed in the next communication.
Assuntos
Pressão Sanguínea , Cardiomegalia/etiologia , Hipertensão Pulmonar/fisiopatologia , Artéria Pulmonar/fisiopatologia , Doença Cardiopulmonar/etiologia , Doença Crônica , Ventrículos do Coração/fisiopatologia , Humanos , Hipertensão Pulmonar/complicaçõesRESUMO
Combined findings in 89 patient over 20 with an interatrial septum defect (IASD) have shown that the frequency of pulmonary hypertension increases with age. Electrocardiographic criteria of pulmonary hypertension do not allow a reliable diagnosis with pressures below 50 mm Hg. Tone I amplitude, Q - Tone I duration, the extent of splitting and correlation of Tone II components cannot be used as PCG criteria of pulmonary hypertension either. The Q - "systolic murmur peak" interval decreases as pulmonary arterial pressure goes up. Systolic murmur amplitude is not relevant for the diagnosis of either the IASD, or pulmonary hypertension. Diastolic murmurs associated with secondary IASD are a more frequent finding, but show no distinctive features.