Alexander Loeckinger

Sevoflurane, but not Propofol, Significantly Prolongs the Q-T Interval

Prolongation of the Q-T interval may be associated with polymorphic ventricular tachycardia known as torsade de pointes, syncope and sudden death. Existing data show that isoflurane prolongs the Q-T interval, whereas halothane shortens it. The aim of this study was to determine whether sevoflurane or propofol affects the Q-T interval. Thirty female patients undergoing gynecologic surgery were randomly assigned to two groups, one receiving inhaled induction with sevoflurane and the other receiving total IV anesthesia with propofol. Before and 20 min after the induction, a six-lead electrocardiogram was recorded, and blood pressure was measured. The Q-T interval and heart rate adjusted Q-T interval (Q-Tc interval) were significantly prolonged during the administration of anesthesia with sevoflurane, while the Q-T interval was significantly shortened, and the Q-Tc interval was statistically unaffected during propofol anesthesia administration. We conclude that, in otherwise healthy female patients, sevoflurane prolongs the Q-Tc. Implications In this study, we evaluated the effect of sevoflurane induction and anesthesia versus propofol induction and anesthesia on the Q-T interval. Sevoflurane significantly prolonged the Q-T interval and the heart rate adjusted Q-T interval, whereas propofol shortened the Q-T interval but not the heart rate adjusted Q-T interval.

Continuous Positive Airway Pressure at 10 cm H2O During Cardiopulmonary Bypass Improves Postoperative Gas Exchange

Postbypass pulmonary dysfunction including atelectasis and increased shunting is a common problem in the intensive care unit. Negative net fluid balance and continuous positive airway pressure (CPAP) have been used to reduce the adverse effects of cardiopulmonary bypass (CPB) on the lung. To determi

Recombinant angiotensin-converting enzyme 2 improves pulmonary blood flow and oxygenation in lipopolysaccharide-induced lung injury in piglets.

Objective: To study angiotensin-converting enzyme 2 in a piglet model with acute respiratory distress syndrome and to evaluate the therapeutic potential of this substance in a preclinical setting, as this model allows the assessment of the same parameters required for monitoring the disease in human intensive care medicine. The acute respiratory distress syndrome is the most severe form of acute lung injury with a high mortality rate. As yet, there is no specific therapy for improving the clinical outcome. Recently, angiotensin-converting enzyme 2, which inactivates angiotensin II, has been shown to ameliorate acute lung injury in mice. Design: Prospective, randomized, double-blinded animal study. Setting: Animal research laboratory. Subjects: Fifteen anesthetized and mechanically ventilated piglets. Interventions: Acute respiratory distress syndrome was induced by lipopolysaccharide infusion. Thereafter, six animals were assigned randomly into angiotensin-converting enzyme 2 group, whereas another six animals served as control. Three animals received angiotensin-converting enzyme 2 without lipopolysaccharide pretreatment. Measurements and Main Results: Systemic and pulmonary hemodynamics, blood gas exchange parameters, tumor necrosis factor-&agr;, and angiotensin II levels were examined before acute respiratory distress syndrome induction and at various time points after administering angiotensin-converting enzyme 2 or saline. In addition, ventilation-perfusion distribution of the lung tissue was assessed by the multiple inert gas elimination technique. Animals treated with angiotensin-converting enzyme 2 maintained significantly higher Pao2 than the control group, and pulmonary hypertension was less pronounced. Furthermore, angiotensin II and tumor necrosis factor-&agr; levels, both of which were substantially increased, returned to basal values. Multiple inert gas elimination technique revealed a more homogeneous pulmonary blood flow after treatment with angiotensin-converting enzyme 2. In intergroup comparisons, there were no differences in pulmonary blood flow to lung units with subnormal ventilation/perfusion ratios. Conclusions: Angiotensin-converting enzyme 2 attenuates arterial hypoxemia, pulmonary hypertension, and redistribution of pulmonary blood flow in a piglet model of acute respiratory distress syndrome, and may be a promising substance for clinical use.

Inert gas exchange during pneumoperitoneum at incremental values of positive end-expiratory pressure

UNLABELLED Laparoscopy is a surgical technique for a growing variety of abdominal operations. In patients undergoing this procedure, arterial blood oxygenation and hemodynamics are frequently depressed. This study evaluated the effect of different levels of positive end-expiratory pressure (PEEP) during intraperitoneal CO(2) insufflation on the lungs ventilation-perfusion distribution in a porcine model. We studied 13 anesthetized pigs with an intraperitoneal pressure of 15 cm H(2)O applied at either incremental values of PEEP (5-20 cm H(2)O, increments of 5 cm H(2)O) or a constant PEEP of 5 cm H(2)O. The effects of CO(2) pneumoperitoneum on inert gas exchange and hemodynamics were examined with the multiple inert gas elimination technique. During pneumoperitoneum, gas exchange was most augmented by 15 and 20 cm H(2)O of PEEP. Although the differences in hemodynamics between the individual settings were insignificant, 10 cm H(2)O of PEEP provided the smallest impairment of hemodynamics. We conclude that PEEP of 15 H(2)O during pneumoperitoneum resulted in a modest hemodynamic depression but significant gas exchange augmentation in our experiment. IMPLICATIONS Anesthetized pigs, with a pneumoperitoneum of 15 cm H(2)O, were treated either with incremental values of positive end-expiratory pressure (5-20 cm H(2)O, increments of 5 cm H(2)O) or with a constant positive end-expiratory pressure of 5 cm H(2)O. Fifteen and 20 cm H(2)O resulted in significantly improved pulmonary gas exchange compared with 5 cm H(2)O.

Decompression-Triggered Positive-Pressure Ventilation During Cardiopulmonary Resuscitation Improves Pulmonary Gas Exchange and Oxygen Uptake

Background—Intermittent positive-pressure ventilation (IPPV) is the “gold standard” of ventilation during cardiopulmonary resuscitation (CPR), but continuous positive airway pressure (CPAP) is increasingly discussed as an alternative. This study investigated hemodynamics and pulmonary gas exchange applying CPAP enhanced with pressure support ventilation (CPAPPSV) during CPR. Methods and Results—Twenty-four pigs were subjected to ventricular fibrillation and CPR with CPAPPSV, CPAP, or IPPV. Measurements were taken before (hemodynamics, blood gases, inert gas measurements) and 10 (hemodynamics, blood gases) and 20 (hemodynamics, blood gases, inert gas measurements) minutes after induction of ventricular fibrillation. Although no significant intergroup differences in hemodynamics were found, arterial partial pressure of oxygen (Pao2) was significantly higher during CPAPPSV compared with CPAP or IPPV (98±10, 61±27, and 71±30 mm Hg, respectively, P <0.05). CPAPPSV resulted in an alveolar-arterial partial pressure of oxygen difference of 56±17 mm Hg, whereas during CPAP, 83±21 mm Hg was detected, and during IPPV, 98±29 mm Hg was detected (P <0.05). Pulmonary blood flow to lung units with a normal &OV0312;a/&OV0422; ratio in percent of cardiac output was 76±17% during CPAPPSV, 61±21% during CPAP (P <0.01), and 54±13% during IPPV (P <0.01). Oxygen uptake (&OV0312;o2) was significantly higher during CPAPPSV than with the other ventilation modes (P <0.05) and comparable to the baseline value in intragroup comparison. Return of spontaneous circulation was recorded in 8 of 8 animals in the CPAPPSV group, in 6 of 8 in the CPAP group, and in 3 of 8 in the IPPV group. Conclusions—CPAPPSV provides a straightforward and effective alternative to IPPV or CPAP during CPR that provides significantly higher Pao2 and &OV0312;o2.

Administration of oxygen before tracheal extubation worsens gas exchange after general anesthesia in a pig model

Administration of 100% oxygen before tracheal extubation is common clinical practice. We determined the effect of this technique on postoperative gas exchange in a porcine model using the multiple inert gas elimination technique. After general anesthesia with mechanical ventilation for a period of 30 min (inspiratory fraction of oxygen of 0.3), anesthesia was discontinued, and the pigs were randomized to an inspiratory fraction of oxygen of 0.3 or 1.0 until they could be safely extubated. Thirty minutes after extubation while breathing air, blood flow to poorly ventilated units had significantly increased in pigs that had been administered 100% oxygen as compared with those receiving 30% oxygen (17% ± 15% versus 7% ± 5%;P = 0.009). We conclude that exposure to 100% oxygen before extubation may cause an undesirable alteration in gas exchange.

Tezosentan Decreases Pulmonary Artery Pressure and Improves Survival Rate in an Animal Model of Meconium Aspiration

Acute pulmonary arterial hypertension in acute lung injury aggravates the clinical course and complicates treatment. Increased release and turnover of endogenous endothelin-1 is known to be a major determinant in the pathophysiology of pulmonary arterial hypertension of various etiologies. We tested whether intravenous tezosentan, a dual endothelin receptor antagonist, reduced pulmonary artery pressure in a pig model of acute lung injury induced by meconium aspiration. Acute pulmonary arterial hypertension was induced in 12 anesthetized and instrumented pigs by instillation of human pooled meconium in a 20% solution. Hemodynamic and gas exchange parameters were recorded every 30 min. Six animals received tezosentan 5 mg/kg after 0 and 90 min; six animals served as controls. Tezosentan led to a decrease of mean pulmonary artery pressure (PAP) from 33.4 ± 4.0 mm Hg to 24.7 ± 2.1 mm Hg and pulmonary vascular resistance (PVR) from 7.8 ± 1.4 mm Hg · L–1 · min · m2 to 5.2 ± 0.7 mm Hg · L–1 · min · m2. All animals treated with tezosentan survived, whereas in the control group four out of six animals died. Tezosentan improved survival and decreased pulmonary artery pressure in a porcine model of acute pulmonary arterial hypertension after meconium aspiration. Tezosentan has the potential for effective pharmacological treatment of pulmonary arterial hypertension following acute lung injury.

Isoflurane and sevoflurane anesthesia in pigs with a preexistent gas exchange defect

Background Decreased arterial partial pressure of oxygen (Pao2) during volatile anesthesia is well-known. Halothane has been examined with the multiple inert gas elimination technique and has been shown to alter the distribution of pulmonary blood flow and thus Pao2. The effects of isoflurane and sevoflurane on pulmonary gas exchange remain unknown. The authors hypothesized that sevoflurane with a relatively high minimum alveolar concentration (MAC) would result in significantly more gas exchange disturbances in comparison with isoflurane or control. Methods This study was performed in a porcine model with an air pneumoperitoneum that generates a reproducible gas exchange defect. After a baseline measurement of pulmonary gas exchange (multiple inert gas elimination technique) during propofol anesthesia, 21 pigs were randomly assigned to three groups of seven animals each. One group received isoflurane anesthesia, one group received sevoflurane anesthesia, and one group was continued on propofol anesthesia (control). After 30 min of volatile anesthesia at 1 MAC or propofol anesthesia, a second measurement (multiple inert gas elimination technique) was performed. Results At the second measurement, inert gas shunt was 15 ± 3% (mean ± SD) during sevoflurane anesthesia versus 9 ± 1% during propofol anesthesia (P = 0.02). Blood flow to normal ventilation/perfusion (&OV0312;A/&OV0422;) lung areas was 83 ± 5% during sevoflurane anesthesia versus 89 ± 1% during propofol anesthesia (P = 0.04). This resulted in a Pao2 of 88 ± 11 mmHg during sevoflurane anesthesia versus 102 ± 15 mmHg during propofol anesthesia (P = 0.04). Inert gas and blood gas variables during isoflurane anesthesia did not differ significantly from those obtained during propofol anesthesia. Conclusions In pigs with an already existent gas exchange defect, sevoflurane anesthesia but not isoflurane anesthesia causes significantly more gas exchange disturbances than propofol anesthesia does.

Pulmonary gas exchange in coronary artery surgery patients during sevoflurane and isoflurane anesthesia.

As the surgical population ages, the number of patients presenting with coronary artery disease and age-related loss of pulmonary recoil will increase. Although their influence on gas exchange in this population remains unknown, sevoflurane and isoflurane are used for an increasing variety of surgical procedures. We examined pulmonary gas exchange (multiple inert gas elimination technique) in 30 patients presenting for coronary artery bypass grafting. After a baseline measurement taken during midazolam anesthesia, patients were continued on sevoflurane (n = 10), isoflurane (n = 10), or midazolam (n = 10) for 20 min, then a second measurement was taken. During sevoflurane and isoflurane anesthesia, blood flow to lung areas with a low ventilation/perfusion ratio (&OV0312;a/&OV0422;) was significantly increased in comparison with control. During sevoflurane anesthesia, blood flow to lung areas with a normal &OV0312;a/&OV0422; ratio (76 ± 12 versus control: 89 ± 5, mean ± sd) and Pao2 (138 ± 31 versus control: 156 ± 35 mm Hg, mean ± sd) were depressed, whereas an increase in &OV0312;a/&OV0422;-dispersion (log sdQ) was observed during isoflurane anesthesia. We conclude that both sevoflurane and isoflurane alter the distribution of perfusion in the lung, but only sevoflurane significantly depresses Pao2.

Pulmonary function after emergence on 100% oxygen in patients with chronic obstructive pulmonary disease: a randomized, controlled trial.

Background: During emergence from anesthesia, breathing 100% oxygen is frequently used to provide a safety margin toward hypoxemia in case an airway problem occurs. Oxygen breathing has been shown to cause pulmonary gas exchange disorders in healthy individuals. This study investigates how oxygen breathing during emergence affects lung function specifically whether oxygen breathing causes added hypoxemia in patients with chronic obstructive pulmonary disease. Methods: This trial has been conducted in a parallel-arm, case-controlled, open-label manner. Fifty-three patients with chronic obstructive pulmonary disease were randomly allocated (computer-generated lists) to breathe either 100 or 30% oxygen balanced with nitrogen during emergence from anesthesia. Arterial blood gas measurements were taken before induction and at 5, 15, and 60 min after extubation. Results: All participants tolerated the study well. Patients treated with 100% oxygen had a higher alveolar–arterial oxygen pressure gradient (primary outcome) compared with patients treated with 30% oxygen (25 vs. 20 mmHg) and compared with their baseline at the 60-min measurement (25 vs. 17 mmHg). At the 60-min measurement, arterial partial pressure of oxygen was lower in the 100% group (62 vs. 67 mmHg). Arterial partial pressure of carbon dioxide and pH were not different between groups or measurements. Conclusions: In this experiment, the authors examined oxygen breathing during emergence—a widely practiced maneuver known to generate pulmonary blood flow heterogeneity. In the observed cohort of patients already presenting with pulmonary blood flow disturbances, emergence on oxygen resulted in deterioration of oxygen-related blood gas parameters. In the perioperative care of patients with chronic obstructive pulmonary disease, oxygen breathing during emergence from anesthesia may need reconsideration.