Co-administration of ephedrine prevents reductions in cardiac output and systemic oxygen delivery secondary to lung compression maneuvers during one-lung ventilation, without reducing arterial oxygenation

2011 ◽  
Vol 25 (2) ◽  
pp. 163-169 ◽  
Author(s):  
Seiji Ishikawa ◽  
Fumi Makino ◽  
Satomi Kobinata ◽  
Hiroyuki Ito ◽  
Tatsuyuki Kawano ◽  
...  
2019 ◽  
Vol 8 (9) ◽  
pp. 1438
Author(s):  
Tae Soo Hahm ◽  
Heejoon Jeong ◽  
Hyun Joo Ahn

Systemic oxygen delivery (DO2) is a more comprehensive marker of patient status than arterial oxygen saturation (SaO2), and DO2 in the range of 330–500 mL min−1 is reportedly adequate during anaesthesia. We measured DO2 during one-lung ventilation (OLV) for thoracic surgery—where the risk of pulmonary shunt is significant, and hypoxia occurs frequently—and compared sevoflurane and propofol, the two most commonly used anaesthetics in terms of DO2. Sevoflurane impairs hypoxic pulmonary vasoconstriction. Thus, our hypothesis was that propofol-based anaesthesia would show a higher DO2 value than sevoflurane-based anaesthesia. This was a double-blinded randomised controlled trial conducted at a university hospital from 2017 to 2018. The study population consisted of patients scheduled for lobectomy under OLV (N = 120). Sevoflurane or propofol was titrated to a bispectral index of 40–50. Haemodynamic variables were measured during two-lung ventilation (TLV) and OLV at 15 and 45 min (OLV15 and OLV45, respectively) using oesophageal Doppler monitoring. The mean DO2 (mL min−1) was not different between the sevoflurane and propofol anaesthesia groups (TLV: 680 vs. 706; OLV15: 685 vs. 703; OLV45: 759 vs. 782, respectively). SaO2 was not correlated with DO2 (r = 0.09, p = 0.100). Patients with SaO2 < 94% showed adequate DO2 (641 ± 203 mL min−1), and patients with high SaO2 (> 97%) showed inadequate DO2 (14% of measurements < 500 mL min−1). In conclusion, DO2 did not significantly differ between sevoflurane and propofol. SaO2 was not correlated with DO2 and was not informative regarding whether the patients were receiving an adequate oxygen supply. DO2 may provide additional information on patient status, which may be especially important when patients show a low SaO2.


2020 ◽  
Vol 48 (3) ◽  
pp. 289-295
Author(s):  
Man-Li Zheng ◽  
Shao-Ru He ◽  
Yu-Mei Liu ◽  
Lin Chen

AbstractBackgroundThe aim of this study was to assess the normal values of the Smith-Madigan inotropy index (SMII) and oxygen delivery index (DO2I) in low-birth-weight (LBW) and very-low-birth-weight (VLBW) newborns on the first 3 days of life, and to identify how different degrees of maturity influence cardiovascular alterations during the transitional period compared with term neonates.MethodsTwenty-eight VLBW newborns, 46 LBW newborns and 50 normal full-term newborns admitted to our department were studied. Hemodynamics of the left heart were measured in all neonates over the first 3 days using the Ultrasonic Cardiac Output Monitor (USCOM). This was combined with hemoglobin concentration and pulse oximetry to calculate DO2I. Blood pressure was combined with the hemodynamic measures and hemoglobin concentration to calculate SMII.ResultsSMII showed statistically significant differences among the three groups (VLBW 0.48 ± 0.11; LBW 0.54 ± 0.13; term 0.69 ± 0.17 W/m2 P < 0.001), which was in line with the following myocardial parameters: stroke volume index (SVI) and cardiac index (CI) (P < 0.001 and <0.001). For systemic oxygen delivery (DO2) parameters, significant differences were found for DO2I (P < 0.001) while hemoglobin concentration and pulse oximetry demonstrated no significant differences. In the VLBW group, SMII and DO2I showed no significant change over the 3 days.ConclusionNormal inotropy and systemic DO2I values in VLBW neonates over the first 3 days of life were assessed. SMII and DO2I were significantly lower in VLBW neonates during the first 72 h of life. With increasing birth weight, higher myocardial inotropy and DO2 were found. The addition of USCOM examination to standard neonatal echocardiography may provide further important information regarding cardiac function.


1995 ◽  
Vol 82 (4) ◽  
pp. 940-946. ◽  
Author(s):  
P. Slinger ◽  
W. A. C. Scott

Background Because maintaining arterial oxygenation (PaO2) during one-lung ventilation (OLV) can be a clinical problem, it is useful to be aware of factors that influence PaO2 in this situation and are under the control of the anesthesiologist. It is unknown whether, among the commonly used volatile anesthetic agents, one is associated with higher PaO2 levels. Clinical studies suggest that isoflurane provides superior PaO2 during OLV than does halothane. These have not been compared to enflurane. The authors studied PaO2 and hemodynamics during OLV with 1 MAC enflurane versus 1 MAC isoflurane. Methods Twenty-eight adults who had prolonged periods of OLV anesthesia with minimal trauma to the nonventilated lung (thoracoscopic or esophageal surgery) were studied in a cross-over design. Patients were randomized to two groups: Group 1 received 1 MAC enflurane in oxygen from induction until after the first 30 min of OLV, then were switched to 1 MAC isoflurane. In group 2, the order of the anesthetics was reversed. Results Isoflurane was associated with higher PaO2 values during OLV (P &lt; 0.0001). Mean PaO2 (+/- SD) after 30 min OLV isoflurane was 231 (+/- 125) mmHg versus 184 (+/- 106) mmHg after 30 min OLV enflurane. The difference in PaO2 between the two anesthetics was most marked in the patients with the highest PaO2 during OLV: PaO2 isoflurane PaO2 enflurane varies; is directly proportional to PaO2 isoflurane (r = 0.65, P &lt; 0.001). There were no other significant differences between anesthetic gases in the measured hemodynamic or respiratory variables. In the subgroup of patients with pulmonary artery catheters (n = 7), PaO2 correlated with cardiac output during OLV for both anesthetics (r = 0.81, P &lt; 0.001). Conclusions During OLV, the PaO2 values with 1 MAC isoflurane were greater than those with enflurane. The dependence of PaO2 on cardiac output does not support the hypothesis that an increase in cardiac output will cause a decrease in hypoxic pulmonary vasoconstriction and a decrease in PaO2 during OLV.


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