The laryngeal mask airway ProSeal™ as a temporary ventilatory device in grossly and morbidly obese patients before laryngoscope-guided tracheal intubation

We determined the efficacy of the laryngeal mask airway ProSeal™ (PLMA) as a temporary ventilatory device in morbidly obese patients before laryngoscope-guided tracheal intubation. Sixty patients (body mass index 35–60 kg/m2) scheduled for elective surgery, who preferred airway management under general anesthesia, were studied. The induction of anesthesia was with midazolam/fentanyl/propofol and maintenance was with sevoflurane 1%–3% in oxygen 100%. The PLMA was inserted and an effective airway established. Rocuronium was given IV for paralysis. Oropharyngeal leak pressure, ease of gastric tube placement, residual gastric volume, fiberoptic position of the airway/drainage tube, and ease of ventilation at a tidal volume of 8 mL/kg was determined. The PLMA was then removed and laryngoscope-guided tracheal intubation attempted. The number of insertion/intubation attempts (maximum two each) and time taken to establish an effective airway with each device were recorded. An effective airway was obtained at the first insertion attempt in 90% of patients (54/60) and at the second attempt in 10% (6/60). The time taken to provide an effective airway was 15 ± 7 s (7–42 s). Oropharyngeal leak pressure was 32 ± 8 cm H2O (12–40 cm H2O). The residual gastric volume was 36 ± 46 mL (0–240 mL). Positive pressure ventilation without air leaks was possible in 95% of patients (57/60). The vocal cords were seen from the airway tube in 75% of patients (45/60), but the esophagus was not seen. The fiberoptic view from the drainage tube revealed mucosa in 93% of patients (56/60) and an open upper esophageal sphincter in 7% (4/60). Tracheal intubation was successful at the first attempt in 90% of patients (54/60), at the second attempt in 7% (4/60), and failed in 3% (2/60). In these latter two patients, the PLMA was reinserted and surgery performed uneventfully with the PLMA. The time taken to tracheally intubate the patient was 13 ± 10 s (8–51 s). There were no episodes of hypoxia (Spo2 <90%) or other adverse events. There were no differences in insertion success rate, or the time to successful insertion between the PLMA and laryngoscope-guided intubation. We conclude that the PLMA is an effective temporary ventilatory device in grossly or morbidly obese patients before laryngoscope-guided tracheal intubation

The physiologic perspective in fluid management in vascular anesthesiology

Vascular surgery patients frequently suffer from atherosclerosis and peripheral arterial occlusive disease generating endothelial dysfunction. Furthermore, ischemia and reperfusion during surgery damage endothelial cells and, especially, the endothelial glycocalix. The damage of the glycocalix promotes an increase in permeability. Not only crystalloids, which freely diffuse between the intravascular and the interstitial compartment, but also colloidal fluids cross from the intravascular space in the interstitial space with the consequence of edema formation. Possible tissue edema may result in an impairment of tissue oxygenation, leading to wound healing disturbances and initiation of inflammatory responses up to tissue apoptosis. Particularly in vascular anesthesia, this possibly means that colloids only should be administered in acute volume resuscitation immediately after unclamping a big vessel for immediate volume restoration. Which colloidal fluid should be administered is still under intense discussion. From a theoretical physiologic point of view, iso-osmolar albumin is the best choice regarding volume effect, antioxidative properties, and protection against destruction of the glycocalix. Nonetheless, albumin experimentally has not lived up to its promise in the clinical setting. Thus, further well-conducted large randomized clinical trials are necessary to ascertain the optimal fluid therapy in vascular surgery patients

Oxygen availability in a HAPE-positive and a HAPE-negative woman before and during a visit to 3480 meters

Background: Testing the hypoxic ventilatory response (HVR) at low-altitude helps to detect those who do not hyperventilate appropriately in hypoxia but might not necessarily predict the HVR and the risk to develop acute mountain sickness (AMS) at high altitude. However, a low HVR seems to be particularly prevalent in individuals susceptible to high-altitude pulmonary edema (HAPE+). In this short communication, we assessed differences in physiological parameters in two comparable women before and 3 hours after exposure to 3,480 meters. One woman had a (clinically diagnosed) history of high-altitude pulmonary edema (HAPE+) while the other did well at previous exposures to high altitude (HAPE-).Methods: Heart rate, blood pressure, ventilation, arterial blood gas variables, arterial haemoglobin saturation, haemoglobin concentration, arterial oxygen content and delta plasma volume were measured or calculated before and after arrival at high altitude.Results: At high altitude, plasma volume decreased in the HAPE- woman which in turn increased haemoglobin concentration. Ventilation was elevated in the HAPE- but not in the HAPE + woman. Arterial oxygen content fell in the HAPE + while it was preserved in the HAPE- woman. This resulted from lower peripheral oxygen saturation (-35%), lower haemoglobin concentration (-12%) and lower arterial partial pressure of oxygen (-59%) in the HAPE+.Conclusion: Considerable haemoglobin desaturation and lack of haemoconcentration were characteristics of the HAPE + woman when exposed to high altitude, while the higher arterial oxygen content in the HAPE- woman was related to both haemoconcentration and hyperventilation (and associated haemoglobin saturation)

A Focused Review on the Maximal Exercise Responses in Hypo- and Normobaric Hypoxia: Divergent Oxygen Uptake and Ventilation Responses

The literature suggests that acute hypobaric (HH) and normobaric (NH) hypoxia exposure elicits different physiological responses. Only limited information is available on whether maximal cardiorespiratory exercise test outcomes, performed on either the treadmill or the cycle ergometer, are affected differently by NH and HH. A focused literature review was performed to identify relevant studies reporting cardiorespiratory responses in well-trained male athletes (individuals with a maximal oxygen uptake, VO2max &gt; 50 mL/min/kg at sea level) to cycling or treadmill running in simulated acute HH or NH. Twenty-one studies were selected. The exercise tests in these studies were performed in HH (n = 90) or NH (n = 151) conditions, on a bicycle ergometer (n = 178) or on a treadmill (n = 63). Altitudes (simulated and terrestrial) varied between 2182 and 5400 m. Analyses (based on weighted group means) revealed that the decline in VO2max per 1000 m gain in altitude was more pronounced in acute NH vs. HH (&minus;7.0 &plusmn; 1.4% vs. &minus;5.6 &plusmn; 0.9%). Maximal minute ventilation (VEmax) increased in acute HH but decreased in NH with increasing simulated altitude (+1.9 &plusmn; 0.9% vs. &minus;1.4 &plusmn; 1.8% per 1000 m gain in altitude). Treadmill running in HH caused larger decreases in arterial oxygen saturation and heart rate than ergometer cycling in acute HH, which was not the case in NH. These results indicate distinct differences between maximal cardiorespiratory responses to cycling and treadmill running in acute NH or HH. Such differences should be considered when interpreting exercise test results and/or monitoring athletic training

Hemorrhagic Shock: Blood Marker Sequencing and Pulmonary Gas Exchange

Background: The early identification of internal hemorrhage in critically ill patients may be difficult. Besides circulatory parameters, hemoglobin and lactate concentration, metabolic acidosis and hyperglycemia serve as laboratory markers for bleeding. In this experiment, we examined pulmonary gas exchange in a porcine model of hemorrhagic shock. Moreover, we sought to investigate if a chronological order of appearance regarding hemoglobin, lactatemia, standard base excess/deficit (SBED) and hyperglycemia exists in early severe hemorrhage. Methods: In this prospective, laboratory study, twelve anesthetized pigs were randomly allocated to exsanguination or a control group. Animals in the exsanguination group (n = 6) endured a 65% blood loss over 20 min. No intravenous fluids were administered. Measurements were taken before, immediately after, and at 60 min after the completed exsanguination. Measurements included pulmonary and systemic hemodynamic variables, hemoglobin concentration, lactate, base excess (SBED), glucose concentration, arterial blood gases, and a multiple inert gas assessment of pulmonary function. Results: At baseline, variables were comparable. Immediately after exsanguination, lactate and blood glucose were increased (p = 0.001). The arterial partial pressure of oxygen was increased at 60 min after exsanguination (p = 0.04) owing to a decrease in intrapulmonary right-to-left shunt and less ventilation-perfusion inequality. SBED was different to the control only at 60 min post bleeding (p &lt; 0.001). Hemoglobin concentration did not change at any time (p = 0.97 and p = 0.14). Conclusions: In experimental shock, markers of blood loss became positive in chronological order: lactate and blood glucose concentrations were raised immediately after blood loss, while changes in SBED lagged behind and became significant one hour later. Pulmonary gas exchange is improved in shock

Hemorrhagic Shock: Blood Marker Sequencing and Pulmonary Gas Exchange

Background: The early identification of internal hemorrhage in critically ill patients may be difficult. Besides circulatory parameters, hemoglobin and lactate concentration, metabolic acidosis and hyperglycemia serve as laboratory markers for bleeding. In this experiment, we examined pulmonary gas exchange in a porcine model of hemorrhagic shock. Moreover, we sought to investigate if a chronological order of appearance regarding hemoglobin, lactatemia, standard base excess/deficit (SBED) and hyperglycemia exists in early severe hemorrhage. Methods: In this prospective, laboratory study, twelve anesthetized pigs were randomly allocated to exsanguination or a control group. Animals in the exsanguination group (n = 6) endured a 65% blood loss over 20 min. No intravenous fluids were administered. Measurements were taken before, immediately after, and at 60 min after the completed exsanguination. Measurements included pulmonary and systemic hemodynamic variables, hemoglobin concentration, lactate, base excess (SBED), glucose concentration, arterial blood gases, and a multiple inert gas assessment of pulmonary function. Results: At baseline, variables were comparable. Immediately after exsanguination, lactate and blood glucose were increased (p = 0.001). The arterial partial pressure of oxygen was increased at 60 min after exsanguination (p = 0.04) owing to a decrease in intrapulmonary right-to-left shunt and less ventilation-perfusion inequality. SBED was different to the control only at 60 min post bleeding (p p = 0.97 and p = 0.14). Conclusions: In experimental shock, markers of blood loss became positive in chronological order: lactate and blood glucose concentrations were raised immediately after blood loss, while changes in SBED lagged behind and became significant one hour later. Pulmonary gas exchange is improved in shock

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 90%), and for the cuffed oropharyngeal airway, laryngeal mask airway, and intubating laryngeal mask airway, it was always a result of inadequate placement. Conclusion: The emphasis placed on the use of restraints for conventional tracheal intubation in microgravity is appropriate. Extratracheal airway devices may be useful when restraints cannot be applied or intubation is difficult

Cutaneous Microvascular Blood Flow and Reactivity in Hypoxia

As is known, hypoxia leads to an increase in microcirculatory blood flow of the skin in healthy volunteers. In this pilot study, we investigated microcirculatory blood flow and reactive hyperemia of the skin in healthy subjects in normobaric hypoxia. Furthermore, we examined differences in microcirculation between hypoxic subjects with and without short-term acclimatization, whether or not skin microvasculature can acclimatize. Fourty-six healthy persons were randomly allocated to either short-term acclimatization using intermittent hypoxia for 1 h over 7 days at an FiO2 0.126 (treatment, n = 23) or sham short-term acclimatization for 1 h over 7 days at an FiO2 0.209 (control, n = 23). Measurements were taken in normoxia and at 360 and 720 min during hypoxia (FiO2 0.126). Microcirculatory cutaneous blood flow was assessed with a laser Doppler flowmeter on the forearm. Reactive hyperemia was induced by an ischemic stimulus. Measurements included furthermore hemodynamics, blood gas analyses and blood lactate. Microcirculatory blood flow increased progressively during hypoxia (12.3 ± 7.1–19.0 ± 8.1 perfusion units; p = 0.0002) in all subjects. The magnitude of the reactive hyperemia was diminished during hypoxia (58.2 ± 14.5–40.3 ± 27.4 perfusion units; p = 0.0003). Short-term acclimatization had no effect on microcirculatory blood flow. When testing for a hyperemic response of the skin's microcirculation we found a diminished signal in hypoxia, indicative for a compromised auto-regulative circulatory capacity. Furthermore, hypoxic short-term acclimatization did not affect cutaneous microcirculatory blood flow. Seemingly, circulation of the skin was unable to acclimatize using a week-long short-term acclimatization protocol. A potential limitation of our study may be the 7 days between acclimatization and the experimental test run. However, there is evidence that the hypoxic ventilatory response, an indicator of acclimatization, is increased for 1 week after short-term acclimatization. Then again, 1 week is what one needs to get from home to a location at significant altitude