Magnitude and implications of spontaneous hemodynamic variability in primary pulmonary hypertension

Abstract

The pulmonary artery (PA) pressure and pulmonary resistance at rest have been noted to vary spontaneously in patients with primary pulmonary hypertension. To evaluate this variation, in 12 patients (8 women, 4 men, aged 43 ± 13 years), hourly measurements were made for 6 consecutive hours of heart rate, systemic and PA pressures, cardiac output, systemic and pulmonary resistance. After these baseline measurements the patients were tested with hydralazine and nifedipine therapy. Spontaneous variability in pulmonary pressures and resistances occurred in each patient, with the amount of variation (coefficient of variation) in PA pressure averaging 8% and in total pulmonary resistance 13% over the 6 hours. The patients with the most variability in mean PA pressure also had the most variability in cardiac output (r = 0.69, p = 0.02). Variability also correlated with the severity of the disease, as the patients with the highest total pulmonary resistances also had the most variation for that factor (r = 0.91, p < 0.01). The amount of variability did not correlate, however, with the acute response to either hydralazine or nifedipine administration. Based on the average coefficients of variation in these 12 patients, estimates were obtained of the percent change needed for an observed change to be attributed to a drug effect with 95% confidence. From these estimates, it was projected that for a single patient, a mean change in pulmonary resistance of 36% or a mean change in PA pressure of 22% would be required in order to attribute the changes to a drug effect. Thus, spontaneous hemodynamic variability is a common phenomenon in patients with primary pulmonary hypertension and may account for substantial changes in PA pressure and pulmonary resistance at rest.