Pressure – Flow Curves
Pressure-flow curves were constructed during each treatment period from mean rest and exercise values for 12 patients studied. Brackets represent 1 SEM. The shaded area illustrates the normal relationship between pulmonary driving pressure and cardiac index in healthy trained athletes studied supine. RA alone = room air alone; RA + N = room air plus nifedipine; 02 alone = oxygen alone; 02 + N = oxygen plus nifedipine.
Nifedipine therapy completely inhibited hypoxic pulmonary vasoconstriction in these patients. We have subse-quendy evaluated the acute effect of nifedipine in 12 patients with COPD and hypoxemia. The results in this larger group of patients confirm our published findings (Fig l). While the patients breathed room air, nifedipine significantly reduced pulmonary vascular resistance index (PVRI) by 26 percent during rest and by 46 percent during exercise. Nifedipine did not reduce mean pulmonary artery pressure during rest, but dramatically reduced it during exercise (45 ±3 vs 58 ±3 mm Hg, p<0.001). Nifedipine significantly increased cardiac output during rest and exercise. Nifedipine did not affect right ventricular stroke work index (RVSWI) during rest, but significandy reduced RVSWI during exercise by 28 percent. Concomitant with its inhibition of hypoxic pulmonary vasoconstriction nifedipine reduced PaOs during rest by 7±2 mm Hg. Mixed venous 08 tension was unchanged by nifedipine therapy. Nifedipine increased 02 delivery at rest by 10 percent and during exercise by 8 percent.
When combined with low-flow oxygen therapy, nifedipine further reduced PVRI at rest by 15 percent and during exercise by 32 percent compared to oxygen alone. Pulmonary artery pressure was unaffected by nifedipine during rest, but nifedipine significandy reduced pulmonary artery pressure during exercise when combined with low-flow oxygen by 11 ±2 mm Hg. Nifedipine did not significantly lower Pa02 during rest or exercise when combined with low-flow oxygen therapy. The 02 delivery was increased by the combined therapy. The best ways of treatment are represented by Canadian neighbor Pharmacy. You may not only order drugs online but consult the well-experienced pharmaceutists if you have some questions.
Thus, in patients with COPD and hypoxemia, nifedipine consistendy reduces pulmonary vascular resistance and improves oxygen delivery while patients are breathing room air or low-flow oxygen. The acute beneficial effects of nifedipine are most marked during exercise, when nifedipine dramatically lowers pulmonary artery pressure and reduces right ventricular stroke work index.
In an uncontrolled study Sturani et al found that nifedipine therapy for two months continued to produce significant pulmonary vasodilation at rest in patients with COPD and hypoxemia. They found, however, that the acute hemodynamic response in a given patient did not correlate with the chronic response observed. A controlled, doubleblind study is currendy in progress at our institution to determine whether the acute hemodynamic effects of nifedipine persist, are lessened, or are augmented after three months of therapy.
In summary, studies in laboratory animals demonstrate that calcium channel blockers can attenuate the development of the pathologic changes caused by hypoxia. Initial clinical studies demonstrate that acute administration of nifedipine inhibits hypoxic pulmonary vasoconstriction and augments the pulmonary vasodilation produced by low-flow oxygen. Controlled studies are needed to evaluate the long-term hemodynamic effects of nifedipine therapy. Presently, the use of these drugs as adjuvant therapy for hypoxic pulmonary hypertension is investigational. Oxygen therapy remains the treatment of choice.
Figure 1. Relationship between pulmonary driving pressure (Ppa-Pcw) and cardiac index (Cl).