Measured gas exchange and hemodynamic data are shown in Table 3. In these patients with severe hypoxemia, the Ve was increased, and Vo2 was raised, whereas the Pv02 was normal. Cardiac output and the Cl were extremely high, while the PVR and the SVR were extremely low. Finally, the P50 was increased (29.5 ±1.5 mm Hg), which was in agreement with other studies. The Va/Q distribution of ventilated and perfused units (Fig 1) was little altered. The hypoxemia was mainly due to the large amount of perfusion flowing through unventilated units for patients 1, 2, 4, and 6 and through unventilated and underventilated areas for patients 3 and 5 (Table 4). The Pa02 predicted from the distribution was always higher than measured values, and the difference between these two values was statistically significant (predicted Pa02 — measured Pa02= +9.27 ±5.9 mm Hg; p<0.01).
These data support the idea that ventilation/perfusion relationships can be affected by an impaired pulmonary circulation. Although these results were derived from a study of only six patients, they were highly concordant. Apart from the patent cirrhosis of the liver, the only criterion of selection of the patients was the severity of the hypoxemia without any history of pulmonary or cardiac disease. The data on pulmonary function are close to normal limits but indicate a tendency towards obstruction of the airways. Nevertheless, the magnitude of the reduction in FEV1? the FEV,/FVC ratio, and FEF25-75%, related partially to the alveolar hypocapnia, is highly unlikely to cause such a severe hypoxemia (Table 2). At the time of the study, none of the patients had either jaundice or evidence of peripheral edema or ascites, although five out of the six had portal hypertension. The results did not appear to be influenced by the impaired portal circulation nor the different origins of the cirrhosis of the liver.
The accuracy of the blood gas analyzer (Corning 175) was routinely checked by comparing measured and real values obtained by tonometer from human blood (measured value = 0.99; tonometric value 4-2.1 mm Hg; n= 112; r = 0.94). In the least-squares fitting algorithm used, a nonzero residual sum of squares may stem from two independent factors: (1) experimental error; or (2) inaccuracy in the model. The low values of the remaining sum of squares (mean value = 4 ± 2.4) indicated a good fit of the experimental data to the model.
Table 3—Gas Exchange and Hemodynamic Data
|Ve, L/min (BTPS)||14.7||10.5||8.1||13.2||14.4||15.4||12.7±2.6|
|Pv02, mm Hg||41||35||41||41.6||40.5||38||39.5 ±2.3|
|Hemoglobin, g/dl||15.1||14.4||18.3||14.6||15.3||15.2||15.5± 1.3|
|PM, mm Hg||29.9||32.2||28||28.6||28.7||27.9||29.2 ± 1.48|
|Vo2, ml/min/sq m||190||240||217||166||210||281||217 ±37|
|Ideal P(A-a)Oa, mm Hg||63||61||41||61||53.5||59||56.4 ±7.5|
|Heart rate, beats per min||95||63||75||84||90||100||85± 13|
|Cardiac output, L/min||11.4||7.7||9.9||12.7||14.1||10.2||11.0 ± 2.1|
|Cl, L/min/sq m||5.56||5.2||5.56||6.55||7.3||7.6||6.3 ±0.92|
|Ppa, mm Hg||6||3||9||10||7||8||7±2|
|Ppcw, mm Hg||2||1||6||8||5||0||4±3|
|PAO, mm Hg||101||74||79||95||84||79||85± 10|
|PVR, mm Hg/L/min||0.35||0.26||0.30||0.16||0.14||0.78||0.33±0.21|
|SVR, mm Hg/L/min||9.04||9.60||7.68||7.32||5.81||7.75||7.87 ± 1.22|
Table 4—Inert Gas Data
|Data*||Case||Mean ± SD|
|Distribution of perfusion|
|True shunt, percent||30.2||26||11.2||15||15.5||20.8||19.8±6.6|
|Q to Va/Q = 0.1, percent||30.2||26||23.1||15||25.5||20.8||23.4±4.7|
|Mean Va/Q||1.25||1.24||0.41||0.78||0.54||0.99||0.87 ±0.32|
|Log SD||0.47||0.45||1.31||0.68||1.6||0.42||0.82 ±0.46|
|Distribution of ventilation|
|Vd/Ve, percent||24.7||23.5||24.8||19.4||25.3||43.8||26.9 ±7.8|
|Mean Va/Q||1.56||1.71||0.95||1.24||1.07||1.18||1.29 ±0.27|
|Log SD||0.47||0.79||0.65||0.66||0.37||0.41||0.56 ±0.15|
|Predicted Pa02, mm Hg||62||57.5||60||81||67.6||63||65.2±7.7|
|(p-m) (mm Hg)||5||6.5||3||18||6.1||17||9.27±5.93t|
Figure 1. Patterns of Va/Q distribution found in the six patients.td/spantd
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