Pulmonary Vascular Resistance in Emphysema: Terminology

Pulmonary Vascular Resistance in Emphysema: TerminologyOther sources of increased vascular resistance merit consideration. The range of arterial 02 tension and pHa observed in our subjects (Table 1) is generally accepted as reflecting levels of alveolar 02 tension that are not capable of evoking pulmonary vasoconstriction. Wright and colleagues examined patients with clinical and functional abnormalities similar to those in the present series. Inspiration of 100 percent oxygen had no effect on pulmonary arterial pressures, blood flow, or calculated ohmic resistance at rest, suggesting that hypoxic vasoconstriction did not play an appreciable role in their subjects and supporting the notion that abnormalities in respiratory gas exchange encountered in the present series were not hemodynamically significant.
Wright et al also suggested that pulmonary hypertension during exercise in these individuals might stem from an increase in intrathoracic pressure if the time constant of the obstructed lung were longer than the time constant of the chest wall as postulated by Harris et al. This conclusion is not easily evaluated because ventilation and pleural pressures were not included in their report. In our series, resting ventilation remained constant during the study period, and we attempted to minimize the effect of pleural pressure swings by averaging hemodynamic measurements over three respiratory cycles more canadian neighbor pharmacy. Furthermore, we excluded patients whose intensity of dyspnea precluded use of a mouthpiece to measure minute ventilation.
There are still other possible sources of increased vascular resistance to be considered. The study of Schrijen et al suggested that PVR may rise with increased lung distention. They demonstrated a correlation between increased PVR and increased FRC during mild exercise in patients with COPD. As in other studies, however, there was no correlation between resting FRC and PVR. Fletcher and colleagues suggested that PVR may rise with nocturnal desaturation in patients with COPD. Their study included a “mix” of patients with COPD as opposed to our selected group of patients with COPD-A. Despite the lack of correlation between exercise-induced hypertension and acute desaturation in patients with emphysema, we cannot rule out a contribution of sustained nocturnal desaturation to elevated resting pulmonary vascular tone in our patients.
The nomenclature of diseases characterized by chronic airflow obstruction has a strong, if subconscious, influence on the clinician’s approach to patient treatment. The current tendency to lump a variety of conditions under the rubric COPD blurs important distinctions in a fashion that may be disadvantageous to the patient. Patients with type A and type В COPD are easily discernible in their “pure” forms and display different physiologic disturbances, varying clinical courses, and disparate responses to therapies. Experience indicates that even in the majority of patients with a “mixed” clinical picture, one of the types usually dominates and determines the natural history of the disease. Identification of this functionally dominant component aids in defining therapeutic goals and prognosis.

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