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.     

Are sildenafil and theophylline effective in the prevention of high-altitude pulmonary edema?

High-altitude pulmonary edema reflects a potentially life-threatening condition affecting susceptible persons in the second night after ascent to altitudes above 2500 m. Currently, nifedipine is the only pharmacological intervention approved for both, prevention and treatment of high-altitude pulmonary edema. We evaluated the application of the phosphodiesterase-V inhibitor sildenafil combined with the non-selective phosphodiesterase-inhibitor theophylline as preventive agents. In theory, the proposed regimen can impede the two main pathophysiological features of high-altitude pulmonary edema: the deleteriously high pulmonary artery pressure (sildenafil's task) on the one hand, and the activation of an inflammatory cascade (theophylline's task) on the other hand. We suggest that these orally applicable phosphodiesterase inhibitors might be useful in the prevention of high-altitude pulmonary edema.     

Airway Management during Spaceflight: A Comparison of Four Airway Devices in Simulated Microgravity

Background: The authors compared airway management in normogravity and simulated microgravity with and without restraints for laryngoscope-guided tracheal intubation, the cuffed oropharyngeal airway, the standard laryngeal mask airway, and the intubating laryngeal mask airway.

Methods: Four trained anesthesiologist-divers participated in the study. Simulated microgravity during spaceflight was obtained using a submerged, full-scale model of the International Space Station Life Support Module and neutrally buoyant equipment and personnel. Customized, full-torso manikins were used for performing airway management. Each anesthesiologist-diver attempted airway management on 10 occasions with each device in three experimental conditions: (1) with the manikin at the poolside (poolside); (2) with the submerged manikin floating free (free-floating); and (3) with the submerged manikin fixed to the floor using a restraint (restrained). Airway management failure was defined as failed insertion after three attempts or inadequate device placement after insertion.

Results: For the laryngoscope-guided tracheal intubation, airway management failure occurred more frequently in the free-floating (85%) condition than the restrained (8%) and poolside (0%) conditions (both, P < 0.001). Airway management failure was similar among conditions for the cuffed oropharyngeal airway (poolside, 10%; free-floating, 15%; restrained, 15%), laryngeal mask airway (poolside, 0%; free-floating, 3%; restrained, 0%), and intubating laryngeal mask airway (poolside, 5%; free-floating, 5%; restrained, 10%). Airway management failure for the laryngoscope-guided tracheal intubation was usually caused by failed insertion (> 90%), and for the cuffed oropharyngeal airway, laryngeal mask airway, and intubating laryngeal mask airway, it was always a result of inadequate placement.     

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. IMPLICATIONS: Blood flow to lung units with a low V(A)/Q ratio was significantly larger in pigs that had been exposed to 100% oxygen before extubation as compared with those exposed to 30% oxygen before extubation.     

Augmented spontaneous breathing and pulmonary gas exchange during pneumoperitoneum

BACKGROUND AND OBJECTIVE: Ventilation of the lungs with positive end-expiratory pressure during pneumoperitoneum has been shown to improve the arterial partial pressure of oxygen. The implications of spontaneous breathing on pulmonary gas exchange remain unknown in this setting. We therefore sought to examine the influence of pressure-support ventilation with spontaneous breathing on gas exchange during simulated laparoscopy. METHODS: Ten pigs were subjected to pneumoperitoneum at a pressure of 15 cmH2O. Animals received, in a random order, pressure-support and pressure-controlled ventilation for 60 min per mode. Inert gas and haemodynamic measurements were performed before changing to a subsequent mode. RESULTS: Pressure-support ventilation was more efficient than pressure-controlled ventilation regarding perfusion of normal V(A)/Q lung areas (78 +/- 4% vs. 72 +/- 5%) (P < 0.05), alveolar-arterial partial pressure of oxygen difference (9.73 +/- 1.3 vs. 11.2 +/- 1.2 kPa) and arterial partial pressure of oxygen (14.93 +/- 1.6 vs. 13.7 +/- 2.0 kPa) (P < 0.05). CONCLUSIONS: Pressure-support ventilation resulted in significantly better gas exchange than pressure-controlled ventilation in this model of simulated laparoscopy.     

Pulmonary gas exchange after cardiopulmonary resuscitation with either vasopressin or epinephrine

OBJECTIVE: It is well established that epinephrine administered during cardiopulmonary resuscitation results in pulmonary gas exchange disturbances. It is uncertain how vasopressin affects gas exchange after cardiopulmonary resuscitation. DESIGN: Prospective, randomized experimental study. SETTING: Animal research laboratory. SUBJECTS: Twenty domestic pigs. INTERVENTIONS: Animals were subjected to ventricular fibrillation and cardiopulmonary resuscitation by using either vasopressin or epinephrine. Hemodynamic and pulmonary gas exchange (multiple inert gas elimination technique) variables were recorded before cardiopulmonary resuscitation and 10, 30, 60, and 120 mins after return of spontaneous circulation when either epinephrine (control) or vasopressin was used. MEASUREMENTS AND MAIN RESULTS: At 10 mins after return of spontaneous circulation, blood flow to low V /Q lung units was increased in animals treated with epinephrine (17.8 +/- 6 vs. 2.6 +/- 3%, mean +/- sd, p<.01). Resulting carbon dioxide elimination was impaired in animals treated with epinephrine but not in animals treated with vasopressin (PaCO2, 55 +/- 2 vs. 46 +/- 4 torr, p<.05). Thirty minutes after return of spontaneous circulation, blood flow to lung units with a normal VA /Q ratio was reduced in animals treated with epinephrine (79 +/- 1 vs. 84 +/- 12%, p<.05), resulting in a depressed PaO2 (147 +/- 4 vs. 127 +/- 10 torr, p<.05). CONCLUSION: Vasopressin compared with epinephrine for cardiopulmonary resuscitation resulted in better gas exchange variables in the early postresuscitation phase.     

Continuous positive airway pressure at 10 cm H(2)O 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 determine whether CPAP at 10 cm H(2)O during CPB results in improved postoperative gas exchange in comparison with deflated lungs during CPB, we examined 14 patients scheduled for elective cardiac surgery. Seven patients received CPAP at 10 cm H(2)O during CPB, and in the other seven patients, the lungs were open to the atmosphere (control). Measurements were taken before and after CPB, after thoracic closure, and 4 h after CPB in the intensive care unit. CPAP at 10 cm H(2)O resulted in significantly more perfusion of lung areas with a normal ventilation/perfusion distribution (V(A)/Q) and significantly less shunt and low V(A)/Q perfusion 4 h after CPB in comparison with the control group. Consequently, arterial oxygen partial pressure was significantly higher and alveolar-arterial oxygen partial pressure difference was significantly smaller. We conclude that CPAP at 10 cm H(2)O during CPB is a simple maneuver that improves postoperative gas exchange. IMPLICATIONS: Inflation of the lungs at a pressure of 10 cm H(2)O as compared with leaving the lungs deflated during cardiopulmonary bypass was examined. Lung inflation during bypass resulted in significantly improved postoperative gas exchange.     

Sevoflurane progressively prolongs the QT interval in unpremedicated female adults

Thirty-six unpremedicated women due for gynaecological surgery were examined for time-dependent prolongation of the QT interval in the electrocardiogram (ECG) before and after induction of anaesthesia using either sevoflurane or propofol. The conventional inhalational technique to induce anaesthesia with sevoflurane. ECG recordings were taken before, 2, 5 and 10 min after drug administration. Sevoflurane significantly lengthened (P < 0.001) the heart rate corrected QT interval within 10 min from 434 +/- 5 ms to 459 +/- 6 ms (mean +/- SEM). Already after 2 min of sevoflurane application a trend towards prolongation was visible. The critical value of 440 ms in the rate-corrected QT interval was exceeded in four patients in the sevoflurane group (n = 18) but in only in one patient in the propofol group (n = 18). Rate-corrected QT interval prolongation caused by sevoflurane needs to be recognized early in order to prevent the critical ventricular tachycardia torsade de pointes.     

Pressure support ventilation with the ProSeal laryngeal mask airway. A comparison of sevoflurane, isoflurane and propofol

BACKGROUND AND OBJECTIVE: There are no data about the influence of anaesthetics on cardiovascular variables during pressure support ventilation of the lungs through the laryngeal mask airway. We compared propofol, sevoflurane and isoflurane for maintenance of anaesthesia with the ProSeal laryngeal mask airway during pressure support ventilation. METHODS: Sixty healthy adults undergoing peripheral musculo-skeletal surgery were randomized for maintenance with sevoflurane end-tidal 2%, isoflurane end-tidal 1.1% or propofol 6 mg kg(-1) h(-1) in oxygen 33% and air. Pressure support ventilation comprised positive end-expiratory pressure set at 5 cmH2O, and pressure support set 5 cmH2O above positive end-expiratory pressure. Pressure support was initiated when inspiration produced a 2 cmH2O reduction in airway pressure. A blinded observer recorded cardiorespiratory variables (heart rate, mean blood pressure, oxygen saturation, airway occlusion pressure, respiratory rate, expired tidal volume, expired minute volume and end-tidal CO2), adverse events and emergence times. RESULTS: Respiratory rate and minute volume were 10-21% lower, and end-tidal CO2 6-11% higher with the propofol group compared with the sevoflurane or isoflurane groups, but otherwise cardiorespiratory variables were similar among groups. No adverse events occurred in any group. Emergence times were longer with the propofol group compared with the sevoflurane or isoflurane groups (10 vs. 7 vs. 7 min). CONCLUSION: Lung ventilation is less effective and emergence times are longer with propofol than sevoflurane or isoflurane for maintenance of anaesthesia during pressure support ventilation with the ProSeal laryngeal mask airway. However, these differences are small and of doubtful clinical importance.     

Sildenafil modulates hemodynamics and pulmonary gas exchange

The effects of sildenafil (Viagra) on hemodynamics and pulmonary gas exchange remain uncertain. The aim of this study was to investigate what effect sildenafil had on gas exchange. A total of 24 anesthetized pigs were randomly assigned into four groups of six animals each: Group Low received 25 mg of sildenafil, which is equivalent to half the recommended dose for humans; group Normal received 50 mg; group High received 100 mg; and one group served as control. Inert gas and hemodynamic measurements were performed to define dose-dependent effects of sildenafil on cardiac and pulmonary function. Measurements were taken 30, 60, and 90 min after the administration of sildenafil via gastric tube. All doses of sildenafil caused significant increases in intrapulmonary shunt flow (maximum amplitude, 4.4 +/- 0.3 to 11.9 +/- 0.5%; mean +/- SEM), which was reflected by marked decreases in PaO2. Sildenafil elicited some significant increases in cardiac index (CI) (high dose, 142 +/- 10 to 196 +/- 13 ml x kg(-1), mean +/- SEM). Mean arterial pressure was significantly depressed after the high dose of sildenafil. Pulmonary artery pressure was decreased after high-dose sildenafil (maximum amplitude, 16 +/- 1.6 to 14 +/- 1.8, mean +/- SEM). No significant differences between the three treatment groups were found. Sildenafil represents and orally active substance with phosphodiesterase V inhibitory and cardiac output-increasing actions. PaO2 decrease after 50 and 100 mg of sildenafil was observed in the presence of significant rises in pulmonary shunt flow and CI.