Medical Inspection – Health Blog

Airflow obstruction was severe in all but patient 8, and all but one subject (patient 2) showed marked air trapping (Table 1). Hyperinflation was noticed only in patient 5. The Deo was reduced in four subjects (patients 2, 3, 5, and 6) (Table 1). Table 2 provides the metabolic, hemodynamic, and gas exchange data at rest and during exercise, before and after nifedipine. Nifedipine was well tolerated by all the patients and did not produce any symptomatic adverse side effect.

Rest Before Nifedipine

Oxygen uptake, heart rate, and Qt were normal. Mean pulmonary artery pressure (Ppa) was slightly increased (19 ±1 mm Hg; range, 14 to 25 mm Hg) but right ventricular stroke work index (RVSWI, 8.2 ±0.5 g-m/m²) was within normal limits. Capillary wedge pressure was normal (4 ± 1 mm Hg). Gas exchange was mildly impaired with some degree of arterial hypoxemia (range, 67 to 83 mm Hg) and mild increases in both the P(A-a)o₂ (Table 2) and the percentage of venous admixture (Qs/Qt, 10 ± 1 per­cent). None of the patients had C0₂ retention, but all had Vd/Vt values higher than 40 percent. The inert gas data showed only small amounts of shunt and/or blood flow to lung units with Va/Q ratios lower than 0.1 (less than 1 percent of Qt, each) (Table 2). Seven of the eight patients showed a broad unimodal blood flow distribution without shunt (Fig 1); patient 7 showed a bimodal blood flow distribution. Only patient 5 had a noticeable amount of shunt (2.6 percent of Qt). Four patients (patients 1, 3, 5, and 7) had bimodal ventilation distributions with a substantial percentage of Ve distributed to high Va/Q areas (10 to 100) (Table 2 and Fig 1). The dispersion of the blood flow and ventilation distributions (Logsn Q and Logs_D V, re­spectively) (normal range, 0.3 to 0.6) and the overall amount of Va/Q mismatching estimated from raw retention and excretion values (DISP R-E*) were moderate to severely increased with respect to nor­mal. generic cialis 20mg

Table 1—General Data and Lung Function Results

Rest After Nifedipine (vs Rest Before Nifedipine)

Neither Ppa nor Pw (4 ± 1 to 3 ± 1 mm Hg) changed but Qt increased (Table 2). Consequently, TPVR fell.

Besides, for a given flow Ppa was always lower after nifedipine (Fig 2). The RVSWI did not change (8.2 ± 0.5 to 9.1 ± 1.2 g*m/m²). As previously reported, Ve increased slightly (9.4 to 10.4 L.min) but signif­icantly (p<0.05) after nifedipine. As a result, PaC0₂ fell and arterial pH rose. The Vd/Vt did not change (Table 2). Oxygen exchange worsened: Pa0₂ showed a trend to be lower (76 to 71 mm Hg, p = 0.06), P(A-a)o₂ was larger (28 to 36 mm Hg, p<0.05), and Qs/Qt was higher (10 ± 1 to 15 ±2 percent, p<0.05). Because of the above-mentioned increase in Qt 0₂ delivery improved (992 ±85 to 1,228 ±97 ml-min p<0.005). Ventilation-perfusion mismatching in­creased after nifedipine (higher DISP R-E*, p<0.001) (Table 2). Specifically, the blood flow distribution shifted toward a lower Va/Q ratio (Q decreased, p<0.01) and became wider (Log_SI) Q increased, p<0.005) (Table 2). A separate low Va/Q mode of blood flow appeared in five subjects (patients 1, 2, 4, 6, and 8) (Fig 1). These changes are in keeping with previous results and strongly suggest release of HPV. Despite the increase observed in the dispersion of the ventilation, distribution (Log_SI) V) was not modified by nifedipine. However, this increase in Ve probably explains the significantly higher V observed at rest after giving the drug (Table 2).
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Table 2—Metabolic, Hemodynamic, and Gas Exchange Data

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