M. Ramez Salem

Head and neck position for direct laryngoscopy.

The sniffing position (SP) has traditionally been considered the optimal head position for direct laryngoscopy (DL). Its superiority over other head positions, however, has been questioned during the last decade. We reviewed the scarce literature on the subject to examine the evidence either in favor or against the routine use of the SP. A standard definition for the position should be used (e.g., 35° neck flexion and 15° head extension) to avoid confusion about what constitutes a proper SP and to compare the results from different studies. Although several theories were proposed to explain the superiority of the SP, the three axes alignment theory is still considered a valid anatomical explanation. Although head elevation is needed to achieve the desired neck flexion, the elevation height may vary from one patient to another depending on head and neck anatomy and size of the chest. In infants and small children, for example, no head elevation is needed because the size and shape of the head allow axes approximation in the head-flat position. Horizontal alignment of the external auditory meatus with the sternum, in both obese and non-obese patients, indicates, and can be used as a marker for, proper positioning. Analysis of the available literature supports the use of the SP for DL. To achieve a proper SP in obese patients, the “ramped” (or the back-up) position should be used. The SP does not guarantee adequate exposure in all patients, because many other anatomical factors control the final degree of visualization. However, it should be the starting head position for DL because it provides the best chance at adequate exposure. Attention to details during positioning and avoidance of minor technical errors are essential to achieve the proper position. DL should be a dynamic procedure and position adjustment should be instituted in case poor visualization is encountered in the SP.

Direct effects of propofol on myocardial contractility in in situ canine hearts.

The pronounced decrease in arterial blood pressure evident during anesthetic induction with propofol has raised the possibility that propofol has a direct negative inotropic effect. Previous attempts to evaluate this mechanism in vivo have been inconclusive because of confounding variables associated with intravenous administration of propofol. Accordingly, in the current study, steady-state changes in myocardial contractility and related hemodynamic parameters were assessed during intracoronary infusions of propofol in seven open-chest dogs anesthetized with fentanyl and midazolam. The left anterior descending coronary artery (LAD) was cannulated and perfused at controlled pressure (100 mmHg) with normal arterial blood. In LAD-perfused myocardium, contractility was evaluated from measurements of percent segmental shortening (%SS) obtained with ultrasonic crystals. Coronary blood flow in LAD was measured electromagnetically and used to calculate myocardial oxygen consumption (MVO2; Fick principle) and coronary propofol concentration. Propofol was infused into the LAD at 150, 300, 600, and 1,200 micrograms/min (P-150, P-300, P-600, P-1,200). These infusion rates yielded calculated blood concentrations of 7 +/- 1, 15 +/- 1, 26 +/- 2, and 50 +/- 5 micrograms.ml-1, respectively. The calculated blood concentrations at P-150 were in the clinical range, whereas those at P-300, P-600, and P-1,200 were supratherapeutic. P-150 had no effect on %SS, whereas higher infusion rates caused decreases in %SS. Changes in MVO2 by propofol generally paralleled changes in %SS. At P-150 and P-300, coronary blood flow was proportional to MVO2, whereas at P-600 and P-1,200, coronary blood flow was in excess of the prevailing MVO2, resulting in increased coronary venous oxygen tension.(ABSTRACT TRUNCATED AT 250 WORDS)

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

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 ≥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 ≥90%, although a decrease in ETco2 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.

Regional hemodynamics and oxygen supply during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension.

Studies were performed in ten pentobarbital-anesthetized, open chest dogs to evaluate regional circulatory effects of isovolemic hemodilution alone, and in combination with adenosine-induced controlled hypotension. Regional blood flow measured with 15-μm radioactive microspheres was used to calculate regional oxygen supply. Hemodilution with 5% dextran (40,000 molecular weight) reduced arterial hematocrit and oxygen contentby approximately one-half and caused heterogeneous changes in regional blood flows; flow decreased in the spleen, was unchanged in the renal cortex, liver, skeletal muscle and skin, and increased in the duodenum, pancreas, brain and myocardium; however, only inthe brain and myocardium were increases in flow sufficient to preserve oxygen supply. Intravenous infusion of adenosine reduced aortic pressure by 50% and reduced flow in most tissues (renal cortex, pancreas, liver, spleen, skin, and brain), with the result that oxygen deficits were produced or accentuated in these organs. The magnitude of flow reductions in the renal cortex (−73%) and cerebral cortex (−37%) were noteworthy. In themyocardium, direct coronary vasodilation by adenosine caused parallel increases in blood flow and oxygen supply to levels exceeding prevailing metabolic requirements. It is concluded that 1) during isovolemic hemodilution alone, oxygen supply to the brain and myocardium is maintained at the expense of oxygen supply to less critical organs and, 2) during combined isovolemic hemodilution and adenosine−induced hypotension, oxygen is oversupplied to the myocardium but undersupplied to the brain and kidney. These latter effects suggest the need for extensive clinical monitoring of patients in whom combined isovolemic hemodilution and adenosine−induced hypotension is utilized.

Neutrophils pretreated with volatile anesthetics lose ability to cause cardiac dysfunction.

Background Volatile anesthetics can precondition the myocardium against functional depression and infarction following ischemia–reperfusion. Neutrophil activation, adherence, and release of superoxide play major roles in reperfusion injury. The authors tested the hypothesis that pretreatment of neutrophils with a volatile anesthetic, i.e., simulated preconditioning, can blunt their ability to cause cardiac dysfunction. Methods Studies were performed in 60 buffer-perfused and paced isolated rat hearts. Left ventricular developed pressure served as an index of myocardial contractility. Polymorphonuclear neutrophils and/or drugs were added to coronary perfusate for 10 min, followed by 30 min of recovery. Platelet-activating factor was used to stimulate neutrophils. Pretreatment of neutrophils consisted of incubation with 1.0 minimum alveolar concentration (MAC) isoflurane or sevoflurane for 15 min, followed by washout. Additional studies were performed with 0.25 MAC isoflurane. Effects of superoxide dismutase were compared to those of volatile anesthetics. Superoxide production was measured by spectrophotometry. Neutrophil adherence to coronary vascular endothelium was estimated from the difference between neutrophils administered and recovered in coronary venous effluent. Results Activated neutrophils caused marked, persistent reduction (> 50%) in left ventricular developed pressure. Isoflurane and sevoflurane at 1.0 MAC and superoxide dismutase abolished this effect. Isoflurane and sevoflurane reduced superoxide production of activated neutrophils by 29% and 33%, respectively, and completely prevented the platelet-activating factor–induced increases in neutrophil adherence. Isoflurane at 0.25 MAC blunted, but did not abolish, the neutrophil-induced decreases in left ventricular developed pressure. Conclusion Neutrophils pretreated with 1.0 MAC isoflurane or sevoflurane lost their ability to cause cardiac dysfunction, while those pretreated with a concentration of isoflurane as low as 0.25 MAC were partially inhibited. This action of the volatile anesthetics was associated with reductions in superoxide production and neutrophil adherence to the coronary vascular endothelium. Our findings suggest that inhibitory actions on neutrophil activation and neutrophil-endothelium interaction may contribute to the preconditioning effects of volatile anesthetics observed in vivo during myocardial ischemia-reperfusion.

Preoperative Pregnancy Testing in Ambulatory Surgery: Incidence and Impact of Positive Results

Background The incidence of unrecognized early pregnancy and its influence on the surgical and anesthetic course in patients presenting for elective ambulatory surgery have not been previously determined. The current study was designed to determine the incidence of unrecognized pregnancy in women presenting for ambulatory surgery. In addition, it examined how discovery of the pregnancy altered the anesthetic or surgical course.

Hemodynamic responses to endotracheal extubation after coronary artery bypass grafting

After coronary artery bypass grafting (CABG) surgery, patients may remain at risk for myocardial ischemia and infarction and ventricular dysrhythmias. The hemodynamic responses to endotracheal extubation and the efficacy of intravenous lidocaine pretreatment were studied after CABG surgery and overnight mechanical ventilation. Twenty-five patients were divided into two groups: group 1 (n = 13) patients who had tracheal extubation after pretreatment with a placebo; group 2 patients who received lidocaine (1 mg/kg IV) before tracheal extubation. Hemodynamic data, electrocardiographic tracings, and arterial blood gases were obtained before tracheal extubation, during suctioning, and 1, 5, and 20 min after tracheal extubation. Group 1 patients displayed significant increases in heart rate, arterial blood pressure, rate-pressure product, right atrial pressure, and cardiac index during suctioning and within 1 min of tracheal extubation, returning to preextubation level by 5 min. There were no significant changes in pulmonary and systemic resistance indices. Hemodynamic changes in group 2 patients were similar to those in group 1. Both in the absence and presence of lidocaine, tracheal extubation caused hemodynamic responses that were small in magnitude and brief in duration. These responses were not associated with electrocardiographic or enzymatic evidence of myocardial ischemia or infarction, or with ventricular dysrhythmias. Compared with the well-documented hemodynamic responses to tracheal intubation, we found that extubation of the trachea after CABG surgery was associated with less pronounced responses. This may be related to avoidance of laryngoscopy and possibly accommodation to the endo-tracheal tube. These modest hemodynamic responses of extubation of the trachea after CABG surgery were not modified by intravenous lidocaine.

The Bainbridge and the "reverse" Bainbridge reflexes: history, physiology, and clinical relevance.

Francis A. Bainbridge demonstrated in 1915 that an infusion of saline or blood into the jugular vein of the anesthetized dog produced tachycardia. His findings after transection of the cardiac autonomic nerve supply and injection of the cholinergic blocking drug atropine demonstrated that the tachycardia was reflex in origin, with the vagus nerves constituting the afferent limb and a withdrawal of vagal tone the primary efferent limb. Subsequent investigators demonstrated that the increase in venous return was detected by stretch receptors in the right and left atria. In the 1980s, it was shown convincingly that the Bainbridge reflex was present in primates, including humans, but that the reflex was much less prominent than in the dog. This difference may be due to a more dominant arterial baroreceptor reflex in humans. A “reverse” Bainbridge reflex has been proposed to explain the decreases in heart rate observed under conditions in which venous return is reduced, such as during spinal and epidural anesthesia, controlled hypotension, and severe hemorrhage. The Bainbridge reflex is invoked throughout the anesthesia literature to describe the effect of changes in venous return on heart rate in patients in the surgical and critical care settings, but a critical analysis of the experimental and clinical evidence is lacking. Our main objectives in this review are to summarize the history of the Bainbridge reflex, to describe its anatomy and physiology, and to discuss the evidence for and against it having an influence on heart rate changes observed clinically. The interaction of the Bainbridge reflex with the arterial baroreceptor and Bezold–Jarisch reflexes is discussed.

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.

Effectiveness of the self-inflating bulb for verification of proper placement of the esophageal tracheal combitube®

The esophageal tracheal Combitube Registered Trademark (ETC; Sheridan Catheter Corporation, Argyle, NY) is a twin-lumen tube used to establish emergency ventilation. After blind placement, ventilation is performed via the proximal lumen if it is in the esophagus or via the distal lumen if it is in the trachea. This investigation was designed to test the reliability of the self-inflating bulb (SIB) in identifying the location of the ETC and facilitating its proper positioning in anesthetized patients. In Group 1 (n = 26), the ETC was introduced blindly. In Group 2 (n = 20), the tube was placed in the trachea (eight patients) or once in the trachea and once in the esophagus, randomly (12 patients) under direct vision rigid laryngoscopy by the anesthesiologist performing the intubation. In both groups, the efficacy of the SIB in identifying the location of the ETC was tested by a second blinded anesthesiologist. In Group 1, blind insertion of the ETC resulted in esophageal placement in all patients, and in each case was correctly identified. The second anesthesiologist reported no reinflation when the compressed SIB was connected to the distal lumen. When the compressed SIB was connected to the proximal lumen, instantaneous reinflation was observed in 23 patients, delayed reinflation (2-4 s) in two and no reinflation (> 4 s) in one patient. Instantaneous reinflation occurred in these three patients after repositioning of the ETC. In Group 2, the second anesthesiologist correctly identified the location of the ETC in all cases. The results confirm previous findings that blind introduction of the ETC leads to esophageal placement and yields adequate ventilation. Furthermore, the SIB can easily and quickly identify the location of the ETC and facilitates its positioning using a simple algorithm. This may be of importance if the ETC is used in patients whose lungs cannot be ventilated by mask and whose trachea cannot be intubated. (Anesth Analg 1995;80:122-6)