Journal of clinical anesthesia · 1992
The effect of respiratory alkalosis on oxygen consumption in anesthetized patients.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Slater R M, Symreng T, Ping S T, Starr J, Tatman D
Аннотация
STUDY OBJECTIVE: To investigate whether hyperventilation significantly altered oxygen consumption in anesthetized and paralyzed patients undergoing surgery.
DESIGN: Open crossover trial with 1 hour of hyperventilation preceded and followed by 1 hour of normoventilation.
SETTING: University medical center.
PATIENTS: Eight patients (five men and three women) undergoing lengthy orthopedic surgery with general anesthesia and muscle paralysis.
INTERVENTIONS: After baseline normoventilation for 1 hour (Period 1), the anesthetized patients were hyperventilated to an arterial carbon dioxide tension (PaCO2) of 20 to 25 mmHg for 1 hour (Period 2). Patients then experienced another hour of normoventilation (Period 3).
MEASUREMENTS AND MAIN RESULTS: Hemodynamic variables, electrocardiography, temperature, end-tidal partial pressure of CO2 (PETCO2), oxygen consumption (VO2), carbon dioxide production, and minute ventilation were continuously followed throughout the study, and arterial blood gases were drawn at the beginning and end of each study period. During the period of hyperventilation, pH was significantly higher and P.ETCO2 and PaCO2 significantly lower compared with the periods of normoventilation. VO2 was significantly increased during hyperventilation compared with the periods of normoventilation. Hemodynamic variables and temperature were similar in the three study periods.
CONCLUSIONS: In anesthetized paralyzed patients, there is an increase in whole-body VO2 with hypocapnic alkalosis.
DESIGN: Open crossover trial with 1 hour of hyperventilation preceded and followed by 1 hour of normoventilation.
SETTING: University medical center.
PATIENTS: Eight patients (five men and three women) undergoing lengthy orthopedic surgery with general anesthesia and muscle paralysis.
INTERVENTIONS: After baseline normoventilation for 1 hour (Period 1), the anesthetized patients were hyperventilated to an arterial carbon dioxide tension (PaCO2) of 20 to 25 mmHg for 1 hour (Period 2). Patients then experienced another hour of normoventilation (Period 3).
MEASUREMENTS AND MAIN RESULTS: Hemodynamic variables, electrocardiography, temperature, end-tidal partial pressure of CO2 (PETCO2), oxygen consumption (VO2), carbon dioxide production, and minute ventilation were continuously followed throughout the study, and arterial blood gases were drawn at the beginning and end of each study period. During the period of hyperventilation, pH was significantly higher and P.ETCO2 and PaCO2 significantly lower compared with the periods of normoventilation. VO2 was significantly increased during hyperventilation compared with the periods of normoventilation. Hemodynamic variables and temperature were similar in the three study periods.
CONCLUSIONS: In anesthetized paralyzed patients, there is an increase in whole-body VO2 with hypocapnic alkalosis.