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The influence of inspiratory flow rate (TI), without changing respiratory frequency, tidal volume, and FIO2, was investigated in 11 normal lungs in patients undergoing mechanical ventilation because of central respiratory failure due to stable coma. The patients were anesthetized and paralyzed. They first received a conventional ventilation (TI = 25 percent, pause = 10 percent) and then, were submitted to four different TI values, randomly administered without any end-inspiratory pause (EIP) (TI = 20 percent; TI = 33 percent; TI = 50 percent; TI = 67 percent). In the middle and at the end of the procedure, a return to basal conditions was introduced. At each ventilator setting, the following were obtained: respiratory flow (Pneumotachograph Fleish No. 2), airway pressure, FRC changes (inductive plethysmography), arterial and mixed venous blood gases, hemodynamic data, and VA/Q ratios distribution using multiple inert gases technique. EIP suppression provides a significant increase in VA/Q mismatch (until TI = 50 percent) and in shunt effect (between 3 and 9 percent of cardiac output [QT]). The absence of simultaneous PaO2 change is due to increasing PVO2 linked to a higher QT. The shorter the TI, the higher the PaCO2 connected with a relative alveolar hypoventilation. However, increasing TI without EIP significantly decreases ventilation distribution inequalities. This improvement is concomitant with a rise in FRC (FRC67-FRC20 = 0.340 +/- 0.450, p < 0.05) without any change in other variables or auto-PEEP production. In summary, in subjects with very slight mechanical lung impairment (peak inspiratory pressure = 20.5 +/- 5.3 cm H2O at TI = 20 percent and 15.2 +/- 3.3 cm H2O at TI = 67 percent), this study confirms the deleterious effect of EIP suppression and TI decrease. One can compensate for this effect of EIP absence by increasing TI as soon as it reaches TI = 67 percent, ie, inverse ratio ventilation.

In a series of 23 patients with COPD, Wagner et al showed three distinct patterns of VA/Q distributions and a correlation between Burrows' clinical classification and the observed distribution patterns. Using the inert gas method, we studied 51 patients suffering from severe but stable COPD (FEV1 = 0.84 +/- 0.38 L; PaO2 = 58.5 +/- 10.5 mm Hg; PaCo2 = 48 +/- 6 mmHg; Ppa = 22 +/- 8 mmHg) breathing room air in a steady state. The H pattern (high mode of VA in high VA/Q) was found in 24 cases. There was an L pattern (Q mode in low VA/Q units) in nine cases and an HL (high-low) pattern in 16 cases (two patients were assigned another group). The analysis of the distribution data confirmed that VA/Q heterogeneity was the main factor underlying gas exchange disturbances in COPD. The PaO2 of the H subjects was higher than that of both HL (p less than 0.02) and L subjects. The true shunt value in the L group was significantly lower than in the H and HL groups. However, the relationship between clinical or functional aspects and distribution was not direct. The fraction of patients of H, HL, or (H + HL) types was nearly identical in the three clinical groups. The H pattern was found to be predominant in cases of COPD.

Arterial oxygen desaturation is commonly found in patients with cirrhosis of the liver, but severe hypoxemia is unusual. To investigate the mechanism of the impairment in gas exchange, six severely hypoxemic (mean PaO2, 55.9 +/- 5.9 mm Hg) cirrhotic patients (five confirmed by biopsy), without pulmonary or cardiovascular disease and in the absence of acute hepatic disease, were submitted to right heart catheterization. Inequalities of VA/Q were estimated in the respiratory steady state using the multiple inert gas technique. The mean pulmonary arterial pressure was low (7.2 +/- 2.3 mm Hg) and the cardiac output high (Q = 11.0 +/- 2.06 L/min), indicating a low PVR. The VA/Q mismatching of the ventilated and perfused units ranged from mild to moderate, but a large percentage of Q flowed through unventilated areas. Furthermore, there was a significant difference between predicted and measured PaO2 (9.27 +/- 5.9 mm Hg; p less than 0.01), which was attributed to either an unmeasured postpulmonary shunt (between portal and pulmonary vein) or a diffusion defect. The impairment in gas exchange in these patients is thus due primarily to an intrapulmonary, and possibly extrapulmonary, shunt. This was thought to be due mainly to an impaired regulatory mechanism of the microcirculation by the hepatic dysfunction.