Tracheal intubating conditions and apnoea time after small-dose succinylcholine are not modified by the choice of induction agent.

BACKGROUND: In a randomized, double-blind clinical trial, we studied the effect of different i.v. induction drugs on tracheal intubation conditions and apnoea time after small-dose (0.6 mg kg(-1)) succinylcholine used to facilitate orotracheal intubation at an urban, university-affiliated community medical centre. METHODS: One hundred and seventy-five ASA I and II adult patients scheduled to undergo surgical procedures requiring general anaesthesia and tracheal intubation were allocated to one of five groups according to i.v. anaesthetic induction drug used. General anaesthesia was induced by i.v. administration of lidocaine 30 mg and propofol 2.5 mg kg(-1) (Group 1), thiopental 5 mg kg(-1) (Group 2), lidocaine 30 mg and thiopental 5 mg kg(-1) (Group 3), etomidate 0.3 mg kg(-1) (Group 4), or lidocaine 30 mg and etomidate 0.3 mg kg(-1) (Group 5). After loss of consciousness, succinylcholine 0.6 mg kg(-1) was given i.v. followed by direct laryngoscopy and tracheal intubation after 60 s. Measurements included intubation conditions recorded during laryngoscopy 60 s after succinylcholine administration, and apnoea time. RESULTS: Overall, clinically acceptable intubation conditions were met in 168 out of the 175 patients studied (96%). They were met in 35/35 patients in Group 1, 33/35 patients in Group 2, 34/35 patients in Group 3, 33/35 patients in Group 4, and 33/35 patients in Group 5. Mean (SD) apnoea time was 4.0 (0.4), 4.2 (0.3), 4.2 (0.6), 4.1 (0.2) and 4.1 (0.2) min respectively in Groups 1-5. There were no differences in the intubation conditions or apnoea times between the groups. CONCLUSIONS: The use of succinylcholine 0.6 mg kg(-1) produced the same favourable intubation conditions and a short apnoea time regardless of the induction drug used.

Preoxygenation with tidal volume and deep breathing techniques: the impact of duration of breathing and fresh gas flow.

UNLABELLED: Various techniques of "preoxygenation" before anesthetic induction have been advocated, including tidal volume breathing (TVB) for 3-5 min, four deep breaths (DB) in 0.5 min, and eight DB in 1 min. However, no study has compared the effectiveness of these techniques, assessed extending deep breathing beyond 1 min, or investigated the influence of fresh gas flow (FGF) in the same subjects using a circle absorber system. In 24 healthy adult volunteers breathing oxygen from a circle absorber system by tight-fitting mask, we compared TVB/5 min and deep breathing at a rate of 4 DB/0.5 min for 2 min at 5, 7, and 10 L/min FGF. Inspired and end-tidal respiratory gases were measured at 0.5-min intervals. During TVB, end-tidal oxygen (ETO2) increased rapidly and plateaued by 2.5 min at 86%, 88%, and 88% with 5, 7 and 10 L/min FGF, respectively. ETO2 values of > or =90% were attained between 3 and 4 min. Four DB/0.5 min increased ETO2 to 75%, 77%, and 80% at 5, 7, and 10 L/min FGF. Eight DB/min resulted in ETO2 values of 82% and 87% at 7 and 10 L/min, respectively. Extending deep breathing to 1.5 and 2 min with 10 L/min FGF increased ETO2 by > or =90%, although a decrease in ETCo(2) was noted. We concluded that TVB/3-5 min was effective in achieving maximal "preoxygenation" whereas 4 DB/0.5 min resulted in submaximal "preoxygenation," and thus should be used only when time is limited. Increasing FGF from 5 to 10 L/min does not enhance "preoxygenation" with either TVB or 4 DB/0.5 min. Deep breathing yields maximal "preoxygenation" when extended to 1.5 or 2 min, and only when high (10 L/min) FGF is used. IMPLICATIONS: Using a circle absorber system, normal breathing of oxygen for 3-5 min achieves optimal oxygenation of the lungs; whereas 4 deep breaths in 30 s does not. However, extending deep breathing to 1.5-2 min and using a high flow of oxygen improves oxygenation of the lungs to the same degree as normal breathing for 3-5 min. This may have important implications for patient safety.

Verification of endotracheal tube position.

The goals of tracheal intubation are to place the tube in the trachea and to position the tube at an appropriate depth inside the trachea. Various clinical signs and technical aids are described to verify tracheal intubation and to diagnose esophageal intubation. Many of these methods fail under certain circumstances. Not all these methods can be applied in every intubation, but it is essential that the clinician involved in tracheal intubation have the necessary airway management skills, perform these tests accurately, and interpret the results correctly. Prioritization of these tests depends on many factors, including familiarity, availability of monitors, and the location of intubation. Viewing the tube passing between the cords during direct laryngoscopy and visualization of the tracheal rings and carinae with a fiberoptic scope after intubation are the only fullproof methods of confirming tracheal intubation. In the nonarrested patient, carbon dioxide monitoring quickly can differentiate tracheal from esophageal intubation. In the arrested patient, however, carbon dioxide monitoring can be unreliable, although it can be useful as a prognostic indicator of the efficacy of resuscitation. Devices such as [figure: see text] the self-inflating bulb and esophageal detector device may be more useful in patients with cardiac arrest, but they also can yield false results. Placing the distal tip of the tube in the middle of the trachea can be accomplished by positioning the upper end of the cuff 2 cm below the cords during direct laryngoscopy or by placing the distal tip of the tube 4 cm above the carinae with the aid of a fiberoptic scope. The position of the tube always should be verified by clinical assessment (e.g., auscultation). If direct visualization cannot be done, referencing the marks on the tube, transillumination techniques, or cuff maneuvers can be helpful. In the emergency and critical care settings, a chest radiograph easily can detect malpositioned tracheal tubes that may not be detected by routine clinical assessment. Other techniques (e.g., use of fiberoptic scopes, cuff maneuvers, transillumination) can decrease the need for frequent chest radiographs. Based on available information, two algorithms are proposed: one for emergency intubation (Fig. 9) and the other for verification of tracheal tube position in elective intubation (Fig. 10). These algorithms are designed [figure: see text] to assist the clinician and should not be substituted for clinical judgment. Under no circumstances should clinical signs be ignored in the presence of conflicting information from monitors and technical aids.

Efficacy of preoxygenation with tidal volume breathing. Comparison of breathing systems.

BACKGROUND: Preoxygenation before tracheal intubation is intended to increase oxygen reserves and delay the onset of hypoxemia during apnea. Various systems are used for preoxygenation. Designed specifically for preoxygenation, the NasOral system uses a small nasal mask for inspiration and a mouthpiece for exhalation. One-way valves in the nasal mask and the mouthpiece ensure unidirectional flow. This investigation compares the efficacy of preoxygenation using the standard circle system with the NasOral system and five different resuscitation bags. METHODS: Twenty consenting, healthy volunteers were studied in the supine position for 5-min periods of tidal volume breathing using the circle absorber system, the NasOral system, and five resuscitation bags in a randomized order. Data were collected during room air breathing and at 30-s intervals during 5 min of oxygen administration. Inspired oxygen, end-tidal oxygen, and end-tidal nitrogen were measured by mass spectrometry. RESULTS: At 2. 5 min of oxygenation, end-tidal oxygen plateaued at 88.1 +/- 4.8 and 89.3 +/- 6.4% (mean +/- SD) for the circle absorber and NasOral systems, respectively. This was associated with inverse decreases in end-tidal nitrogen. At no time did these end-tidal oxygen or nitrogen values differ from each other. Three of the resuscitation bags (one disk type and two duck-bill type with one-way exhalation valves) delivered inspired oxygen more than 90%, and the end-tidal oxygen plateaued between 77 and 89% at 2 min of tidal volume breathing. The other two resuscitation bags (both duck-bill bags without exhalation valves) delivered inspired oxygen less than 40%, and the end-tidal oxygen values ranged between 21.8 +/- 5.0 and 31.9 +/- 8.7%. CONCLUSIONS: The circle absorber and NasOral systems were equally effective in achieving maximal preoxygenation during tidal volume breathing. Resuscitation bags differed markedly in effectiveness during preoxygenation; those with duck-bill valves without one-way exhalation valves were the least effective. Thus, the use of these bags should be avoided for preoxygenation.

Direct coronary vasomotor effects of sevoflurane and desflurane in in situ canine hearts.

BACKGROUND: An extracorporeal system was used to investigate the direct coronary vasomotor effects of sevoflurane and desflurane in vivo. The role of the adenosine triphosphate-sensitive potassium channels (KATP channels) in these effects was evaluated. METHODS: Twenty-one open-chest, anesthetized (fentanyl-midazolam) dogs were studied. The left anterior descending coronary artery was perfused at controlled pressure (80 mmHg) with normal arterial blood or arterial blood equilibrated with either sevoflurane or desflurane. Series 1 (n = 16) was divided into two groups of equal size on the basis of whether sevoflurane (1.2, 2.4, and 4.8%) or desflurane (3.6, 7.2, and 14.4%) was studied. The concentrations for the anesthetics corresponded to 0.5, 1.0, and 2.0 minimum alveolar concentration (MAC), respectively. Coronary blood flow (CBF) was measured with an ultrasonic, transit-time transducer. Local coronary venous samples were obtained and used to evaluate changes in myocardial oxygen extraction (EO2). In series 2 (n = 5), changes in CBF by 1 MAC sevoflurane and desflurane were assessed before and during intracoronary infusion of the KATP channel inhibitor glibenclamide (100 microg/min). RESULTS: Intracoronary sevoflurane and desflurane caused concentration-dependent increases in CBF (and decreases in EO2) that were comparable. Glibenclamide blunted significantly the anesthetic-induced increases in CBF. CONCLUSIONS: Sevoflurane and desflurane have comparable coronary vasodilative effects in in situ canine hearts. The KATP channels play a prominent role in these effects. When compared with data obtained previously in the same model, the coronary vasodilative effects of sevoflurane and desflurane are similar to those of enflurane and halothane but considerably smaller than that of isoflurane.

Nitric oxide does not modulate whole body oxygen consumption in anesthetized dogs.

The effects of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and the NO donor sodium nitroprusside (SNP) on whole body O2 consumption (VO2) were assessed in 16 dogs anesthetized with fentanyl or isoflurane. Cardiac output (CO) and mean arterial pressure (MAP) were measured with standard methods and were used to calculate VO2 and systemic vascular resistance (SVR). Data were obtained in each dog under the following conditions: 1) Control 1, 2) SNP (30 microg. kg-1. min-1 iv) 3) Control 2, 4) L-NAME (10 mg/kg iv), and 5) SNP and adenosine (30 and 600 microg. kg-1. min-1 iv, respectively) after L-NAME. SNP reduced MAP by 29 +/- 3% and SVR by 47 +/- 3%, while it increased CO by 39 +/- 9%. L-NAME had opposite effects; it increased MAP and SVR by 24 +/- 4% and 103 +/- 11%, respectively, and it decreased CO by 37 +/- 3%. Neither agent changed VO2 from the baseline value of 4.3 +/- 0.2 ml. min-1. kg-1, since the changes in CO were offset by changes in the arteriovenous O2 difference. Both SNP and adenosine returned CO to pre-L-NAME values, but VO2 was unaffected. We conclude that 1) basally released endogenous NO had a tonic systemic vasodilator effect, but it had no influence on VO2; 2) SNP did not alter VO2 before or after inhibition of endogenous NO production; 3) the inability of L-NAME to increase VO2 was not because CO, i.e., O2 supply, was reduced below the critical level.

Isoflurane-induced dilation of porcine coronary arterioles is mediated by ATP-sensitive potassium channels.

BACKGROUND: Isoflurane causes increases in coronary blood flow in vivo, which are mediated by the adenosine triphosphate (ATP)-sensitive potassium channels, but the role of the arterioles (resistance vessels) in these responses is controversial. METHODS: Medium porcine coronary arterioles (internal diameter, 172 +/- 51 [SD] microm) were placed in a chamber supplied with Kreb's buffer, pressurized (40 mmHg), and preconstricted with acetylcholine (10(-8)-10(-6) M). Vascular diameter (VD) was assessed using an optical density video-detection system. Isoflurane (in 95% oxygen and 5% carbon dioxide) was added to buffer using a membrane oxygenator supplied by a calibrated vaporizer. In series 1 (n = 14), 2% isoflurane was administered according to an abrupt (ISO-A) and gradual (ISO-G) protocol. In series 2 (n = 13) and 3 (n = 6), ISO-A (1.5%) was assessed before and after glibenclamide (an ATP-sensitive potassium channel antagonist) or 8-phenyltheophylline (a nonselective adenosine receptor antagonist), respectively. In series 4 (n = 5), validation studies were performed using sodium nitroprusside and adenosine diphosphate to verify that the vascular smooth muscle and endothelium of the vessels were functionally intact. In series 5 (n = 6), ISO-A (0.75 and 1.5%) was compared during preconstriction with acetylcholine and the thromboxane analog U46619 (10(-6) M). RESULTS: ISO-G caused essentially concentration-dependent increases in VD. At 2% isoflurane, the increases in VD were greater during ISO-A than ISO-G. Glibenclamide, but not 8-phenyltheophylline, attenuated isoflurane-induced increases in VD. Both sodium nitroprusside and adenosine diphosphate caused dose-dependent increases in VD. Isoflurane caused equivalent concentration-dependent increases in VD during acetylcholine and U46619. CONCLUSIONS: Isoflurane is a concentration-dependent dilator of porcine coronary arterioles preconstricted with acetylcholine or U46619. This effect is blunted by gradual administration, suggesting that the vessels may adapt to the relaxing effects of isoflurane. Isoflurane-induced dilation of coronary arterioles is mediated by the ATP-sensitive potassium channels but not by the adenosine receptors.

Is calcium a coronary vasoconstrictor in vivo?

BACKGROUND: Calcium produces constriction in isolated coronary vessels and in the coronary circulation of isolated hearts, but the importance of this mechanism in vivo remains controversial. METHODS: The left anterior descending coronary arteries of 20 anesthetized dogs whose chests had been opened were perfused at 80 mmHg. Myocardial segmental shortening was measured with ultrasonic crystals and coronary blood flow with a Doppler flow transducer. The coronary arteriovenous oxygen difference was determined and used to calculate myocardial oxygen consumption and the myocardial oxygen extraction ratio. The myocardial oxygen extraction ratio served as an index of effectiveness of metabolic vasodilation. Data were obtained during intracoronary infusions of CaCl2 (5, 10, and 15 mg/min) and compared with those during intracoronary infusions of dobutamine (2.5, 5.0, and 10.0 microg/min). RESULTS: CaCl2 caused dose-dependent increases in segmental shortening, accompanied by proportional increases in myocardial oxygen consumption. Although CaCl2 also increased coronary blood flow, these increases were less than proportional to those in myocardial oxygen consumption, and therefore the myocardial oxygen extraction ratio increased. Dobutamine caused dose-dependent increases in segmental shortening and myocardial oxygen consumption that were similar in magnitude to those caused by CaCl2. In contrast to CaCl2, however, the accompanying increases in coronary blood flow were proportional to the increases in myocardial oxygen consumption, with the result that the myocardial oxygen extraction ratio remained constant. CONCLUSIONS: Calcium has a coronary vasoconstricting effect and a positive inotropic effect in vivo. This vasoconstricting effect impairs coupling of coronary blood flow to the augmented myocardial oxygen demand by metabolic vascular control mechanisms. Dobutamine is an inotropic agent with no apparent direct action on coronary resistance vessels in vivo.

Efficacy of the self-inflating bulb in differentiating esophageal from tracheal intubation in the parturient undergoing cesarean section.

We studied the efficacy of the self-inflating bulb (SIB) in differentiating tracheal from esophageal intubation in 40 parturients undergoing elective cesarean section under general anesthesia. After induction and muscle relaxation, the trachea was intubated under direct vision with cuffed tube. In 20 parturients, the esophagus was also intubated with an identical tube. Before ventilation was initiated, an independent anesthesiologist checked tube positions with the SIB using two techniques. In one technique (T1), the SIB was compressed before connection to the tube; in the other technique (T2), the SIB was first connected to the tube and then compressed. The speed of reinflation was graded as rapid, delayed, and none. Tracheal tube position was reassessed immediately before and after delivery. Before initiation of controlled ventilation, the incidence of false negative results was 47.5% with T1 and 27.5% with T2 but significantly decreased to 17.5% with T1 and 7.5% with T2 when retested before delivery. After delivery, no false negative results occurred. The incidence of false positive results immediately after induction was 30% with T1 and 35% with T2. The mechanism of false negative responses may be attributed to decreased functional residual capacity leading to reduced caliber of intrathoracic airways and terminal airway closure; whereas false positive responses may be related to an incompetent gastroesophageal junction. We conclude that the SIB is unreliable for differentiating tracheal from esophageal intubation in the parturient undergoing cesarean section.

Role of adenosine triphosphate-sensitive potassium channels in coronary vasodilation by halothane, isoflurane, and enflurane.

BACKGROUND: Halothane, isoflurane, and enflurane cause coronary vasodilation and cardiac depression. This study was performed to assess the role of adenosine triphosphate (ATP)-sensitive potassium channels (KATP channels) in these effects. METHODS: Twenty-five thoracotomized dogs were anesthetized with fentanyl and midazolam. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs. One reservoir was supplied with arterial blood free of a volatile anesthetic, and the second reservoir was supplied with arterial blood equilibrated in an oxygenator with a 1 minimum alveolar concentration of either halothane (0.9%, n = 10), isoflurane (1.4%, n = 8), or enflurane (2.2%, n = 7). Coronary blood flow (CBF) was measured using a Doppler flow transducer, and segmental shortening (SS) was measured with ultrasonic crystals. Responses to the volatile anesthetics were assessed under control conditions, during intracoronary infusion of the KATP channel inhibitor glibenclamide (100 micrograms/min), and after cessation of glibenclamide (recovery). The effectiveness of glibenclamide was verified from inhibition of coronary vasodilator responses to the KATP channel opener cromakalim without effect on those to the KATP channel-independent vasodilators, sodium nitroprusside and acetylcholine. RESULTS: Under control conditions, the volatile anesthetics caused pronounced increases in CBF (isoflurane > halothane = enflurane), and decreases in SS (enflurane > halothane = isoflurane). Glibenclamide blunted significantly (and reversibly) the increases in CBF, but it had no effect on the decreases in SS. CONCLUSIONS: The KATP channels play an important role in coronary vasodilation but apparently are not involved in cardiac depression caused by halothane, isoflurane, and enflurane in canine hearts in situ.

Investigations into the mechanisms of coronary vasodilation by contrast media in dogs.

RATIONALE AND OBJECTIVES: The study was performed to clarify the mechanisms underlying contrast-induced coronary vasodilation. METHODS: The left anterior descending coronary artery of 14 open-chest dogs was perfused at constant pressure. Coronary blood flow (CBF) was measured electromagnetically and used to calculate myocardial oxygen consumption (MVO2). Responses were evaluated during intracoronary infusions (2 mL/ minute) of the ionic contrast medium, Hypaque-76, and the nonionic contrast medium, Isovue-370, and compared with those caused by hypertonic saline solutions with comparable osmolarities. Studies also were conducted using Isovist-300, which is a new nonionic and iso-osmolar contrast medium. RESULTS: Hypaque-76 and Isovue-370 caused initial peak increases in CBF (reflecting decreases in coronary vascular resistance), which waned rapidly to achieve more modest steady-state increases within 2 to 3 minutes. Both the peak and steady-state increases in CBF were greater during Hypaque-76 than during Isovue-370. The increases in CBF caused by the contrast medium were greater than those caused by the corresponding saline solution. Neither Hypaque-76 nor Isovue-370 changed MVO2-Isovist-300 had no effect on CBF or MVO2. CONCLUSIONS: The coronary vasodilation by contrast media is the result of a direct vasorelaxing effect rather than secondary to a metabolic mechanism. Hyperosmolarity can account only in part for contrast-induced coronary vasodilation.