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Acute hyperventilation increases oxygen consumption and decreases peripheral tissue perfusion in critically ill patients.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zhou Yuankai, He Huaiwu, Cui Na, Wang Hao, Zhou Xiang, Long Yun
Аннотация
PURPOSE: This study aimed to evaluate the effects of acute hyperventilation on central venous-to-arterial carbon dioxide tension difference (Pv-aCO2), central venous oxygen saturation (ScvO2), central venous-to-arterial CO2 difference/arterial-central venous O2 difference ratio (CO2GAP-Ratio), and peripheral perfusion index (PI) in hemodynamically stable critically ill patients.
METHODS: Fifty-four mechanically ventilated patients were evaluated. The cardiac index, Pv-aCO2, ScvO2, CO2GAP-Ratio, PI, and arterial and venous blood gas parameters were measured in the first set of measurements. Then, alveolar ventilation was increased by raising the respiratory rate (10 breaths/min). After a 30 min hyperventilation period, the second set of measurements was recorded.
RESULTS: Acute hyperventilation induces an increase in Pv-aCO2 (from 3.87 ± 1.31 to 8.44 ± 1.81 mmHg, P < 0.001) and a decrease in ScvO2(from 71.78 ± 4.82 to 66.47 ± 5.74%, P < 0.001). The CO2GAP-Ratio was significantly increased(from 0.97 ± 0.40 to 1.74 ± 0.46, P < 0.001), and the PI showed a remarkable decrease caused by acute hyperventilation(from 1.82 ± 1.14 to 1.40 ± 0.99，P = 0.04). Hyperventilation-induced ∆_Pv-aCO2 was negatively correlated with ∆PaCO2(r = -0.572, P<0.001). The change in ∆_PaCO2 was correlated with ∆_ScvO2(r = 0.450, P<0.001). However, the left ventricular outflow tract velocity time integral (LVOT-VTI) remained unchanged during hyperventilation.
CONCLUSIONS: Acute hyperventilation induced an increase in oxygen consumption and decreased peripheral tissue perfusion in patients. For critical care patients, it is necessary to pay attention to the influence of hyperventilation on peripheral tissue perfusion indices and oxygen consumption indices.
METHODS: Fifty-four mechanically ventilated patients were evaluated. The cardiac index, Pv-aCO2, ScvO2, CO2GAP-Ratio, PI, and arterial and venous blood gas parameters were measured in the first set of measurements. Then, alveolar ventilation was increased by raising the respiratory rate (10 breaths/min). After a 30 min hyperventilation period, the second set of measurements was recorded.
RESULTS: Acute hyperventilation induces an increase in Pv-aCO2 (from 3.87 ± 1.31 to 8.44 ± 1.81 mmHg, P < 0.001) and a decrease in ScvO2(from 71.78 ± 4.82 to 66.47 ± 5.74%, P < 0.001). The CO2GAP-Ratio was significantly increased(from 0.97 ± 0.40 to 1.74 ± 0.46, P < 0.001), and the PI showed a remarkable decrease caused by acute hyperventilation(from 1.82 ± 1.14 to 1.40 ± 0.99，P = 0.04). Hyperventilation-induced ∆_Pv-aCO2 was negatively correlated with ∆PaCO2(r = -0.572, P<0.001). The change in ∆_PaCO2 was correlated with ∆_ScvO2(r = 0.450, P<0.001). However, the left ventricular outflow tract velocity time integral (LVOT-VTI) remained unchanged during hyperventilation.
CONCLUSIONS: Acute hyperventilation induced an increase in oxygen consumption and decreased peripheral tissue perfusion in patients. For critical care patients, it is necessary to pay attention to the influence of hyperventilation on peripheral tissue perfusion indices and oxygen consumption indices.