Acid-base management--is it relevant for the study design of hypothermic neuroprotection?
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Acid-Base Equilibrium↗
Biomedical subjects
P Krafft
Publications and source records attributed to P Krafft.
Waste gas exposure to sevoflurane and nitrous oxide during anaesthesia using the oesophageal-tracheal Combitube small adult.
Exposure to sevoflurane (SEV) and nitrous oxide during ventilation using a Combitube (37Fr) small adult (SA) was compared with waste gas exposure using conventional endotracheal tubes. Trace concentrations of SEV and nitrous oxide were assessed using a direct reading spectrometer during 40 gynaecological laparoscopic procedures under general anaesthesia. Measurements were made at the patients' mouth and in the anaesthetists' breathing zone. Mean (SD) concentrations of SEV and nitrous oxide measured at the patients' mouth were comparable in the Combitube SA (SEV 0.6 (0.2) p.p.m.; nitrous oxide 9.7 (8.5) p.p.m.) and endotracheal tube group (SEV 1.2 (0.8) p.p.m.; nitrous oxide 17.2 (10.6) p.p.m.). These values caused comparable contamination of the anaesthetists' breathing zone (SEV 0.6 (0.2) p.p.m. and nitrous oxide 4.3 (3.7) p.p.m. for the Combitube SA group, compared with SEV 0.5 (0.2) p.p.m. and nitrous oxide 4.1 (1.8) p.p.m. for the endotracheal tube group). We conclude that the use of the Combitube SA during positive pressure ventilation is not necessarily associated with increased waste gas exposure, especially when air conditioning and scavenging devices are available.
Adult↗
The esophageal tracheal combitube as a non-invasive alternative to endotracheal intubation. A review.
The esophageal tracheal combitube (ETC) is a supraglottic airway device that functions as an effective alternative to ventilation via mask and tracheal intubation and is therefore a valuable tool in difficult and emergency airway management. The Com-bitube has proven to be a valuable tool for securing the airways and providing adequate ventilation. Its advantages are that it is easy to insert quickly, it may be inserted blindly or with the aid of a laryngoscope, and it provides adequate ventilation and oxygenation in both esophageal and tracheal position. The combitube allows application of high ventilatory pressures and it minimises the risk of aspiration. Several guidelines including European Resuscitation Council, Ame-rican Heart Association, American Society of Anesthesiologists have included the combitube as a primary rescue device in cannot ventilate cannot intubate situations. It has been used in elective patients as well as in emergency situations in- and out-of-hospital. The combitube can be inserted with minimal movement of the cervical spine and is therefore indicated whenever cervical spine movement is anatomically restricted (e.g. rheumatoid arthritis) or should be functionally restricted (e.g. trauma). Since the combitube isolates the lungs from the esophagus it is especially useful in patients at risk for aspiration (e.g., caesarean section, morbid obesity). The combitube is available in two sizes: 37 F SA (Small Adult) and 41 F. Unfortunately, a pediatric size is not commercially available. Training in the use of the combitube under controlled conditions is prerequisite to being expert in an emergency situation. The combitube is another non-surgical airway in the armamentarium of the anaesthesiologist or emergency provider in case of foreseen or unforeseen difficult airways in patients who can neither be intubated or mask ventilated.
Equipment Design↗
[The difficult airway].
Management of the difficult airway has gained increasing interest, because hypoxia is one of the leading causes of death and of severe neurological sequelae related to anesthesia or resuscitation. The difficult airway algorithm of the American Society of Anesthesiologists as well as the guidelines of the European Resuscitation Council provide recommendations for the prevention of difficulties in tracheal intubation and/or mask ventilation. Especially preoperative patient evaluation is of major importance. Patients history, oral and maxillofacial anatomy, pharyngeal and laryngeal structures as well as cervical spine mobility have to be assessed and awake fiberoptic intubation has to be performed in all cooperative patients with indices pointing towards difficult airways. If problems in intubating the trachea are encountered after induction of anesthesia and mask ventilation is adequate, one must call for help and decide rapidly whether to awaken the patient or to proceed with alternative intubation techniques (e.g. different laryngoscope blades, flexible fiberoptic scope or other fiberoptic techniques, lighted wand, retrograde intubation or surgical airway). In the potentially life-threatening "cannot intubate--cannot ventilate" situation either transtracheal jet ventilation, laryngeal mask airway, the esophageal-tracheal Combitube or a surgical airway have to be performed or have to be inserted immediately. These alternative methods have to be appropriately taught and--as far as possible--to be trained under routine conditions in order to master emergency situations.
Algorithms↗
Intermittent capnography during high-frequency jet ventilation for prolonged rigid bronchoscopy.
BACKGROUND: Gas exchange during high-frequency jet ventilation (HFJV) for prolonged rigid bronchoscopy (RBS) is usually monitored by arterial blood gas analysis. Capnography of expired gases during brief HFJV discontinuation may be a reliable and noninvasive supplemental method. Capnography can be performed either for single breaths or with respiratory rate (RR) reduced to 10 x min(-1). The aim of this study was to demonstrate that capnography during short periods of HFJV discontinuation represents a reliable measure of PaCO2 during prolonged RBS. METHODS: We prospectively investigated 100 consecutive patients (75 male and 25 female) undergoing HFJV for RBS. HFJV was delivered through the rigid bronchoscope at the following settings: working pressure 1.2 bar, rate 100 x min(-1), FIO2 0.99, t(i)/t(tot)0.6. The light guiding channel ending at the distal tip of the rigid bronchoscope was used for gas sampling. Capnograms were assessed at 5 min intervals and compared to PaCO2 from arterial blood samples drawn simultaneously. The accuracy of single breath CO2 sampling was compared with sampling at RR=10 x min(-1). RESULTS: Mean duration of RBS was 30+/-21 min. A significant correlation between capnography (PetCO2) and arterial blood gas analysis (PaCO2) was observed, being r=0.90 for the RR= 10 x min(-1) method and r=0.91 for the single breath method. Mean difference between PaCO2 and PetCO2 was 0.37+/-0.2 kPa throughout the entire study period. No significant differences between single breath sampling or sampling at RR=10 x min(-1) were observed. CONCLUSION: Capnography performed during short periods of HFJV discontinuation reliably and noninvasively reflects PaCO2 during prolonged endoscopic procedures. Capnography during HFJV for RBS may reduce the frequency of arterial blood gas sampling, the duration of unmonitored intervals and costs.
Adult↗
The oesophageal-tracheal Combitube Small Adult.
Airway management during gynaecological laparoscopy is complicated by intraperitoneal carbon dioxide inflation, Trendelenburg tilt, increasing airway pressures and pulmonary aspiration risk. We investigated whether the oesophageal-tracheal Combitube 37 Fr SA is a suitable airway during laparoscopy. One hundred patients were randomly allocated to receive either the Combitube SA (n = 49) or tracheal intubation (n = 51). Oesophageal placement of the Combitube was successful at the first attempt [16 (3) s]. Peak airway pressures were 25 (5) cmH2O. An airtight seal was obtained using air volumes of 55 (13) ml (oropharyngeal balloon) and 10 (1) ml (oesophageal cuff). Significant correlations were observed between patient's height and weight and the balloon volumes necessary to produce a seal. Similar findings were recorded for the control group, with tracheal intubation being difficult in three patients. The Combitube SA provided a patent airway during laparoscopy. Non-traumatic insertion was possible and an airtight seal was provided at airway pressures of up to 30 cmH2O.
Adult↗
Relationship between local cerebral blood flow and metabolism during mild and moderate hypothermia in rats.
BACKGROUND: Hypothermia may interfere with the relationship between cerebral blood flow (CBF) and metabolism. Because this conclusion was based on the analysis of global values, the question remains whether hypothermic CBF/metabolism uncoupling exists on a local cerebral level. This study investigated the effects of hypothermic anesthesia on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU). METHODS: Thirty-six rats were anesthetized with isoflurane (1 minimum alveolar concentration) and artificially ventilated to maintain normal arterial carbon dioxide partial pressure (pH-stat). Pericranial temperature was maintained as normothermic (37.5 degrees C, n = 12) or was reduced to 35 degrees C (n = 12) or 32 degrees C (n = 12). Pericranial temperature was maintained constant for 60 min until LCBF or LCGU were measured by autoradiography. Twelve conscious rats served as normothermic controls. RESULTS: Compared with conscious animals, mean CBF remained unchanged during normothermic anesthesia. Mean CBF significantly increased during mild hypothermia but was unchanged during moderate hypothermia. During normothermic anesthesia, mean CGU was 45% lower than in conscious controls (P < 0.05). No further CGU reduction was found during mild hypothermia, whereas CGU further decreased during moderate hypothermia (48%; P < 0.05). Local analysis showed a linear LCBF/LCGU relationship in conscious (r = 0.94) and anesthetized (r = 0.94) normothermic animals, as well as in both hypothermic groups (35 degrees C: r = 0.92; 32 degrees C: r = 0.95; P < 0.05). The LCBF-to-LCGU ratio increased from 1.4 (conscious controls) to 2.4 (normothermic isoflurane) and 3.6 ml/micromol (mild and moderate hypothermia, P < 0.05). CONCLUSIONS: Decrease of mean CGU at unchanged or increased mean CBF during hypothermic anesthesia may not indicate uncoupling. Local analysis shows a maintained linear relationship that is reset to a higher CBF/CGU ratio.
Acid-Base Equilibrium↗
Right atrial pressure predicts hemodynamic response to apneic positive airway pressure.
OBJECTIVE: To evaluate if the preexistant filling state, assessed by right atrial pressure (RAP), pulmonary artery occlusion pressure (PAOP), and right ventricular end-diastolic volume index (EDVI), would define the subsequent hemodynamic effects of increases in airway pressure (Paw). DESIGN: Prospective open clinical study. SETTING: Postoperative intensive care unit, university hospital. PATIENTS: Twenty-two consecutive ventilator-dependent patients with mild to severe acute lung injury with Murray scores (scoring infiltrates on chest radiograph, oxygenation index, lung compliance, and the level of positive end-expiratory pressure) ranging from 0.5 to 3.0 without history of preexisting cardiopulmonary disease. INTERVENTIONS: Paw varied during apnea from 0 to 10, 20, and 30 cm H2O using inspiratory hold maneuvers of 15 secs. MEASUREMENTS AND MAIN RESULTS: Cardiac index and right ventricular ejection fraction were measured by the thermodilution technique. We made measurements in triplicate using manual injection of iced saline. Right ventricular volumes were calculated. Increasing Paw induced variable changes in cardiac index among subjects (+6% to -43% change from baseline 0 cm H2O Paw values), which correlated with percentage changes in both stroke index (r2 = .89) and right ventricular EDVI (r2 = .75), whereas heart rate and right ventricular ejection fraction did not change. The change in cardiac index from 0 to 30 cm H2O Paw correlated with baseline values for RAP, PAOP, and right ventricular EDVI (r2 = .68, .43, and .34, respectively, p < 0.01). Increases in RAP correlated with lung compliance if baseline RAP was >10 mm Hg but did not if it was < or =10 mm Hg. Similarly, patients with baseline RAP < or =10 mm Hg had a greater decrease in cardiac index than patients with a RAP >10 mm Hg (for 30 cm H2O Paw: -30% +/- 9% vs. -8% +/- 7%, p < .01). CONCLUSIONS: Apneic positive Paw decreased cardiac output mainly by reducing venous return. From the investigated filling variables, RAP was most sensitive in predicting the hemodynamic response, followed by PAOP and right ventricular EDVI. Patients with RAP < or =10 mm Hg, if subjected to aggressive positive pressure ventilation, are at risk of hemodynamic deterioration and organ hypoperfusion.
Adult↗
Effects of positive end-expiratory pressure on hemodynamics and indocyanine green kinetics in patients after orthotopic liver transplantation.
OBJECTIVE: To determine the impact of positive end-expiratory pressure (PEEP) ventilation on hemodynamics and a clinical test for assessment of dynamic liver performance in patients undergoing orthotopic liver transplantation (OLT). DESIGN: Prospective, descriptive patient study. SETTING: University hospital intensive care unit. PATIENTS: A total of 25 patients after OLT. INTERVENTIONS: All patients were intubated and mechanically ventilated with biphasic positive airway pressure. The effects of three different randomly chosen levels of PEEP (0 cm H2O, 5 cm H2O, and 10 cm H2O) were studied in the immediate postoperative period. MEASUREMENTS AND MAIN RESULTS: Systemic hemodynamics, arterial and venous blood gas analyses, and plasma disappearance rate of indocyanine green (ICG(PDR)), using the transpulmonary indicator dilution technique, were obtained simultaneously. For data evaluation, patients were grouped retrospectively according to their hemodynamic response to PEEP (Group A and Group B). In Group A (n = 13), PEEP did not alter cardiac index. In Group B (n = 11), PEEP levels of 5 cm H2O and 10 cm H2O significantly reduced cardiac index and oxygen delivery. ICG(PDR) remained statistically unchanged in both groups. CONCLUSIONS: Short-term pressure-controlled ventilation with PEEP levels of up to 10 cm H2O does not exert detrimental effects on systemic hemodynamics in OLT patients and does not interfere with ICG(PDR). However, it remains to be determined whether these findings could be confirmed under the application of higher PEEP levels over a longer period of time and whether they could be of clinical relevance for the use of indocyanine green as a dynamic liver function test.
Coloring Agents↗
Interaction of acetylcholine and endothelin-1 in the modulation of pulmonary arterial pressure.
OBJECTIVE: The study was designed to investigate the effects of acetylcholine (ACh) on pulmonary circulation with special regard to mediators that could be involved in the mediation of ACh-induced effects. ACh has been reported to induce either vasodilation or vasoconstriction in the pulmonary circulation of different species. DESIGN: Prospective experimental study in rabbits. SETTING: Experimental laboratory in a university teaching hospital. SUBJECTS: Sixty-six adult rabbits of either sex. INTERVENTIONS: The experiments were performed on 66 isolated and ventilated rabbit lungs that were perfused with a cell- and plasma-free buffer solution. ACh was injected in various concentrations after pulmonary artery preconstriction and in untreated lungs. MEASUREMENTS AND MAIN RESULTS: Pulmonary arterial pressure (PAP) and lung weight gain were monitored continuously. Perfusate samples were taken intermittently to determine endothelin-1 (ET-1), thromboxane A2 (TXA2), and prostacyclin (PGI2) concentrations. ACh in final dosages from 10(-5) to 10(-2) M (n = 6 each) was injected into the pulmonary artery of lungs treated with U46619 to induce pulmonary arterial hypertension or was injected into untreated lungs. To analyze the potential mechanisms of action, ACh (10(-5) M) was administered in additional experiments after pretreatment with either ETA receptor antagonist BQ123 (10(-6) M; n = 6) or the cyclooxygenase inhibitor diclofenac (10 microg/mL; n = 6). In preconstricted pulmonary vessels, ACh (10(-3) and 10(-2) M) initially induced a PAP rise for 10 mins followed by a sustained decrease. In untreated lungs, ACh induced an immediate dose-dependent increase in PAP, requiring as long as 30 mins to return to predrug levels. Simultaneously, significantly elevated TXA2 and PGI2 levels were observed. Furthermore, ET-1 was detected in the perfusate, which was free from ET-1 before ACh administration. Pretreatment with BQ123 reduced substantially the ACh (10(-5) M)-induced PAP increase and the release of TXA2 and PGI2. At 5 mins, the PAP maximum was reduced from 18.5 +/- 3.2 mm Hg to 9.9 +/- 0.65 mm Hg by BQ123 pretreatment (p < .01). An inhibition of PAP increase was also observed after diclofenac pretreatment (11.6 +/- 0.4 mm Hg at 5 mins; p < .05). Inhibitory effects at 5 mins were significantly more pronounced in the BQ123 group compared with the diclofenac group. CONCLUSIONS: The effects of ACh on the pulmonary circulation of isolated rabbit lungs depend on ACh concentration and the basal tone of the arterial vasculature. In lungs with a normal pulmonary vascular resistance, ACh administration causes vasoconstriction via the release of ET-1 and TXA2, whereas vasodilation is induced in preconstricted pulmonary vessels.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Mild and moderate hypothermia (alpha-stat) do not impair the coupling between local cerebral blood flow and metabolism in rats.
BACKGROUND AND PURPOSE: The effects of hypothermia on global cerebral blood flow (CBF) and glucose utilization (CGU) have been extensively studied, but less information exists on a local cerebral level. We investigated the effects of normothermic and hypothermic anesthesia on local CBF (LCBF) and local CGU (LCGU). METHODS: Thirty-six rats were anesthetized with isoflurane (1 MAC) and artificially ventilated to maintain normal PaCO(2) (alpha-stat). Pericranial temperature was maintained normothermic (37.5 degrees C, n=12) or was reduced to 35 degrees C (n=12) or 32 degrees C (n=12). Pericranial temperature was maintained constant for 60 min until LCBF and LCGU were measured with autoradiography. Twelve conscious rats served as normothermic control animals. RESULTS: Normothermic anesthesia significantly increased mean CBF compared with conscious control animals (29%, P<0.05). Mean CBF was reduced to control values with mild hypothermia and to 30% below control animals with moderate hypothermia (P<0.05). Normothermic anesthesia reduced mean CGU by 44%. No additional effects were observed during mild hypothermia. Moderate hypothermia resulted in a further reduction in mean CGU (41%, P<0.05). Local analysis showed linear relationships between LCBF and LCGU in normothermic conscious (r=0.93), anesthetized (r=0.92), and both hypothermic groups (35 degrees C r=0. 96, 32 degrees C r=0.96, P<0.05). The LCBF-to-LCGU ratio increased from 1.5 to 2.5 mL/micromol during anesthesia (P<0.05), remained at 2.4 mL/micromol during mild hypothermia, and decreased during moderate hypothermia (2.1 mL/micromol, P<0.05). CONCLUSIONS: Anesthesia and hypothermia induce divergent changes in mean CBF and CGU. However, local analysis demonstrates a well-maintained linear relationship between LCBF and LCGU during normothermic and hypothermic anesthesia.
Acid-Base Equilibrium↗
Improved outcome of ARDS patients: are we really performing better?
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Humans↗
Remifentanil, propofol or both for conscious sedation during eye surgery under regional anaesthesia.
We performed a prospective, randomized study comparing the efficacy and safety of remifentanil, propofol or both for conscious sedation during eye surgery under retrobulbar blockade. Forty-five unpremedicated patients were assigned to receive remifentanil (group R) (n = 15, mean dosage: 0.05 +/- 0.03 microgram kg-1 min-1), propofol (group P) (n = 15, 1.5 +/- 0.5 mg kg-1 h-1) or a combination (group RP) (n = 15, R: 0.03 +/- 0.01 microgram kg-1 min-1; P: 0.7 +/- 0.2 mg kg-1 h-1). Haemodynamic responses were comparable among all groups. Minimum values for respiratory rate were lower in R patients (R: 7 vs. P and RP: 10 breaths min-1). Perioperative blood gas analysis showed differences in maximum carbon dioxide tensions (R: 51.5 vs. P: 48.3 vs. RP: 45.5 mmHg) and decrease in minimum pH values (R: -0.06 vs. P: -0.0 vs. RP: -0.01). All group P patients reported mild to intense pain during retrobulbar block, while 53% of the group R patients were free from pain. In group RP, 60% of patients experienced no pain and the remaining 40% reported mild pain only. Remifentanil, applied as the sole agent, provided superior pain relief and patient comfort when compared with propofol, but produced greater respiratory depression and postoperative nausea. The combination of remifentanil and propofol provided haemodynamic stability, adequate spontaneous respiration and pain relief, with a low risk of untoward side effects.
Adult↗
Characterization and distribution of endothelin receptors in the pulmonary circulation: investigation of isolated, perfused, and ventilated rabbit lungs.
The aim of the study was to investigate the distribution of 2 subtypes of endothelin-receptors, mediating the effects of endothelin-1 (ET-1) in the pulmonary circulation. Until now, it is still unclear, whether ET(A) receptors or ET(B) receptors or even both are localized in pulmonary vessels. The experiments were performed on 72 isolated and ventilated rabbit lungs that were perfused with a cell- and plasma-free buffer solution. The arterial pressure and the lung weight gain were continuously registered. Intermittently perfusate samples were taken for determination of thromboxane A2 (TXA2) and prostacyclin (PGI2). The injection of ET-1 (10(-8) M, n = 6) resulted in a biphasic increase in pulmonary arterial pressure (PAP) that was accompanied by the generation of TXA2 and PGI2. Pretreatment with the ET(A)-receptor antagonist LU135252 (10(-6) M, n = 6) suppressed the pressure response after ET-1 application (P < 0.01 at 120 min) and reduced the generation of TXA2 (P < 0.05 at 120 min) and PGI2 (P < 0.05 at 120 min). Pretreatment with the cyclooxygenase inhibitor diclofenac (10 microg/mL; n = 6) also reduced the PAP increase after ET-1 injection. In contrast to this, the pulmonary vascular pressure reaction after ET-1 application was elevated, when ET(B)-receptor antagonist BQ788 (10(-6) M; n = 6) was given. Furthermore, the PGI2 to TXA2 ratio was shifted from 2.3 to 0.9, reflecting a predominance of vasoconstrictive TXA2. The simultaneous application of LU135252 and BQ788 significantly reduced the PAP increase after ET-1 application, but no beneficial effects were observed compared with the application of LU135252 solely. The injection of the ET(B)-receptor agonist sarafotoxin S6c (S6c; 10(-8) M, n = 6) also induced an increase in PAP that was not attenuated by pretreatment with the ET(B)-receptor antagonist BQ788 (10(-6) M, n = 6). LU135252 (n = 6) as well as the application of LU135252 in combination with BQ788 (n = 6) failed to suppress the pressure response after S6c, whereas the cyclooxygenase inhibitor diclofenac (10 microg/mL, n = 6) alone and in combination with LU135252 and BQ788 (n = 6) was able to prevent the PAP increase after S6c injection (P < 0.001). The results demonstrate that the ET-1-induced increase in pulmonary vascular resistance is mainly mediated via ET(A) receptors, whereas ET(B) receptors seem to mediate vasodilation, which was shown by an imbalance of TXA2 and PGI2 generation. On the other hand, the ET(B)-receptor agonist S6c induced vasoconstriction, which was only attenuated by the cyclooxygenase inhibitor diclofenac. From the current results we conclude that, apart from vasoconstrictor ET(A) receptors, at least 2 ET(B)-receptor subtypes are expressed in the pulmonary circulation, one mediating vasoconstriction, which was not blocked by BQ788, and one mediating vasodilation, which was influenced by BQ788.
Animals↗
ET-1-induced pulmonary vasoconstriction shifts from ET(A)- to ET(B)-receptor-mediated reaction after preconstriction.
Endothelin-1 (ET-1) has been reported to induce pulmonary vasoconstriction via either ET(A) or ET(B) receptors, and vasorelaxation after ET-1 injection has been observed. Our study investigated the effects of ET-1 in isolated rabbit lungs, which were studied at basal tone (part I) and after preconstriction (U-46619; part II). Pulmonary arterial pressure (PAP) and lung weight gain were monitored continuously. In part I, ET-1 (10(-8) M; n = 6; control) was injected after pretreatment with the ET(A)-receptor antagonist BQ-123 (10(-6) M; n = 6) or the ET(B)-receptor antagonist BQ-788 (10(-6) M; n = 6). The same protocol was carried out in part II after elevation of pulmonary vascular tone. ET-1 induced an immediate PAP increase (DeltaPAP 4.3 +/- 0.4 mmHg at 10 min) that was attenuated by pretreatment with BQ-123 (P < 0.05 at 10 min and P < 0.01 thereafter) and that was more pronounced after BQ-788 (P < 0.01 at 10 min and P < 0.001 thereafter). In part II, ET-1 induced an immediate rise in PAP with a maximum after 5 min (DeltaPAP 6.3 +/- 1.4 mmHg), leveling off at DeltaPAP 3.2 +/- 0.2 mmHg after 15 min. Pretreatment with BQ-123 failed to attenuate the increase. BQ-788 significantly reduced the peak pressure at 5 min (0.75 +/- 0.4 mmHg; P < 0.001) as well as the plateau pressure thereafter (P < 0.01). We conclude that ET-1 administration causes pulmonary vasoconstriction independent of basal vascular tone, and, at normal vascular tone, the vasoconstriction seems to be mediated via ET(A) receptors. BQ-788 treatment resulted in even more pronounced vasoconstriction. After pulmonary preconstriction, ET(A) antagonism exerted no effects on PAP, whereas ET(B) antagonism blocked the PAP increase. Therefore, ET-1-induced pulmonary vasoconstriction is shifted from an ET(A)-related to an ET(B)-mediated mechanism after pulmonary vascular preconstriction.
Animals↗
Airway management during cardiopulmonary resuscitation--a comparative study of bag-valve-mask, laryngeal mask airway and Combitube in a bench model.
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Cardiopulmonary Resuscitation↗
Complications with the Combitube.
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Cardiopulmonary Resuscitation↗
A complication of percutaneous tracheostomy while using the Combitube for airway control.
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Bronchoscopy↗