The Effect of Induced Hypotension with Sodium Nitroprusside on Alveolar-srterial Oxygen Tension Difference and Pulmonary Shunting / 대한마취과학회지

The effect of induced hypotension with sodium nitroprusside(SNP) on alveolar-arterial oxygen tension difference and pulmonary shunting in 10 surgical patients with normal pulmonary function was studied under general anesthesia. Heart rate, mean arterial pressure, central venous pressure, blood gases and hemoglobin were measured before, during and after SNP infusion. Using the above data, alveolar-arterial oxygen tension difference and pulmonary shunting were calculated. The results were as follows. 1) Mean arterial pressure decreased significantly from 98+/-9.1mmHg before SNP infusion to 61+/-3.0 mmHg during SNP infusion(p0.05). 4) Alveolar-arterial oxygen tension difference increased from 188+/-29.0mmHg to 196+/-25.0mmHg, but was not statistically significant(p>0.05). 5) Pulmonary shunting increased from 9.0+/-1.83% to 9.2+/-1.50%, but was not statistically significant.(p>0.05). The above findings suggest that pulmonary shunting in patients with normal lung function will not affected during induced hypotension with SNP.

The Effects of Arterial Oxygen Tension following Indueed. Hypotension with Sodium Nitroprusside / 대한마취과학회지

The effect of sodium nitroprusside(SNP) on arterial oxygen tension in 20 neurosurgical patients with normal lung function was studied under general anesthesia. Blood gas, heart rate, mean arterial pressure and central venous pressure were measured before, during and after SNP infusion. The results were as follows:1) Arterial oxygen tension significantly decreased from 177+/-40.6 mmHg before SNP to 138+/-50.1 mmHg during SNP(p<0.005), and increased again to 168+/-44.4 mmHg after SNP. 2) Mixed venous oxygen tension decreased 47+/-8.2 mmHg to 40+/-7.3 mmHg(p<0.005), and increased again to 44+/-10.3 mmHg. 3) Heart rate significantly increased from 92+/-24.6 beats/min to 118+/-27.4 beats/min(p<0.005), and decreased again to 94+/-18.6 beats/min. The above findings have shown a marked reduction in PaO2 when SNP was administered during general anesthesia. After SNP, PaO2, returned to the previous values. It is suggested that the reduction in PaO2, is the result of an increased scatter of ventilation/perfusion relationships in the lung and inhibition of hypoxic pulmonary vasoconstriction by SNP. These results provide evidence that SNP induced hypotension may cause significant impairment in pulmonary gas exchange in patients with normal lung function.