Pulmonary Vascular Resistance in Emphysema: Methods

Pulmonary Vascular Resistance in Emphysema: MethodsExplorations of the causes of pulmonary hypertension in patients with chronic airways obstruction reported previously from this laboratory emphasized the role of disturbed respiratory gas exchange as the major factor responsible for increased pulmonary vascular resistance in this population. The early demonstration of reversibility of this vasoconstrictive process following correction of hypercapneic respiratory failure became the basis of management in such patients. It was also apparent, however, that select individuals displayed mild but significant elevations in pulmonary vascular resistance (PVR) at levels of blood oxygenation and hydrogen ion concentration that had a negligible impact on pulmonary hemodynamics in most subjects. The present study was initiated to identify the cause of increased resistance in such patients.
We speculated that this group consists of subjects with the clinical and radiographic features ascribed to type A chronic obstructive pulmonary disease (COPD-A). Such patients have less severe disturbances in Va/Q. relationships than do those in whom type В COPD dominates the clinical picture. Va/ Q. relations are preserved because areas of the lung with the poorest ventilation are also those with the least perfusion as a consequence of disruption of the pulmonary vasculature during enzymatic digestion of the lungs other http://antimicrobialmed.com. This “defense” of blood oxygenation is achieved, however, at the cost of increased resistance to pulmonary blood flow. Respiratory failure with reversible pulmonary hypertension may supervene as the result of acute respiratory infection and/or respiratory muscle failure, but an irreversible and progressive component of increased pulmonary vascular resistance probably results from ongoing anatomic restriction of the bed.
To test this hypothesis, we examined the relation between lung function and resting pulmonary hemodynamics in 12 patients with COPD-A. These observations were compared with analogous findings in 33 patients with chronic, diffuse interstitial lung disease (ILD) reported previously by one of us. The comparison suggests that increases in pulmonary vascular resistance in type A disease, under circumstances where disturbed respiratory gas exchange does not play a significant role, stems from disruption of the microcirculation in a fashion similar to that encountered in patients with ILD of mild to moderate severity.
Patients were recruited from a population referred for pulmonary evaluation who had been diagnosed as having chronic airways obstruction on clinical grounds. From this pool, we selected potential study subjects with emphysema according to the criteria of Nash et al. They described patients with type A COPD as those who display little cough, occasional and scanty sputum, fixed dyspnea, thin body habitus, large translucent lungs with low diaphragms and small cardiothoracic ratio, absence of right ventricular enlargement, and a normal hematocrit. We sought to include patients who ranged from the asymptomatic with minimal functional disturbances to those with marked compromise of pulmonary function. We excluded those with reversible airflow obstruction, respiratory infection, obesity, respiratory muscle weakness, or those with technically unacceptable pulmonary function tests. Specifically, we excluded any patient who demonstrated any of the following characteristics: evidence of airflow obstruction that improved with short-term bronchodilator administration; clinical or radiographic evidence of pulmonary infection; weight greater than 130 percent of ideal body weight; maximal static respiratory pressures greater than 2 SD below normal values with maximal inspiratory pressures corrected for the degree of hyperinflation; and inspiratory vital capacity performed during the diffusing capacity measurement less than 90 percent of the previously determined forced vital capacity (FVC).

This entry was posted in Emphysema and tagged airflow obstruction, emphysema, pulmonary function, pulmonary vascular resistance, resistance pulmonary blood.