Effects of clonidine premedication upon hemodynamic changes associated with laryngoscopy and tracheal intubation

The authors studied 30 patients undergoing general anesthesia in order to evaluate whether oral clonidine premedication could attenuate the hemodynamic changes associated with laryngoscopy and tracheal intubation. Patients were randomly assigned to one of two groups; clonidine group (n = 15) who received oral clonidine of approximately 5 micrograms.kg-1, or control group (n = 15) who received no clonidine. The magnitude of increases in mean blood pressure from baseline values following laryngoscopy and tracheal intubation in the clonidine group was significantly smaller as compared with that in the control group (20 +/- 12 vs. 31 +/- 14 mmHg, mean +/- SD, P less than 0.05). There was also a significant difference between the two groups in the incidence of systolic blood pressure increases above 180 mmHg following laryngoscopy and tracheal intubation (0% vs. 26%, P less than 0.05). However, no significant difference was noted between the two groups in the heart rate responses to laryngoscopy and tracheal intubation. It is concluded that oral clonidine of 5 micrograms.kg-1 as a preanesthetic medication could attenuate the pressor responses associated with laryngoscopy and tracheal intubation.     

Intravenous administration of isosorbide dinitrate attenuates the pressor response to laryngoscopy and tracheal intubation

In order to evaluate the effect of isosorbide dinitrate (ISDN), administered as a bolus intravenous injection, on the circulatory response to tracheal intubation, mean arterial pressure (MAP), and heart rate (HR) in response to laryngoscopy for 30 s followed by tracheal intubation were compared in patients not receiving ISDN (control) and receiving 40 micrograms/kg or 80 micrograms/kg of ISDN 45 s before starting laryngoscopy. Each group consisted of 10 patients undergoing elective surgery. Forty-five seconds after starting laryngoscopy, MAP was significantly (P less than 0.01) lower in patients receiving 80 micrograms/kg ISDN than in those receiving no or 40 micrograms/kg ISDN. HR increased to a similar extent in the three groups. These results indicate that a bolus injection of ISDN (80 micrograms/kg) is a simple, practical and highly effective means of attenuating the hypertensive response to direct laryngoscopy and tracheal intubation.     

Effects of nicardipine on the circulatory responses to tracheal intubation in normotensive and hypertensive patients

This study was undertaken to examine the effects of nicardipine on circulatory responses to laryngoscopy and tracheal intubation in normotensive (n = 39) and hypertensive (n = 36) patients. Laryngoscopy and tracheal intubation were performed after induction of anaesthesia with thiamylal, followed by administration of intravenous saline or nicardipine 20 or 30 micrograms.kg-1 and suxamethonium. Blood pressure and heart rate were recorded, and rate-pressure product was calculated. Nicardipine 20 and 30 micrograms.kg-1 prevented the increase in mean arterial pressure after intubation in normotensive and hypertensive patients (p less than 0.01 compared with saline). The changes in heart rate after intubation were significantly greater in normotensive patients than in hypertensive patients when 20 or 30 micrograms.kg-1 of nicardipine was given (p less than 0.05 and p less than 0.01 respectively). Rate-pressure product increased significantly (p less than 0.01) after intubation in normotensive patients whether nicardipine was administered or not, but the increase was suppressed completely by nicardipine 20 or 30 micrograms.kg-1 in hypertensive patients. We conclude that nicardipine is effective in preventing the circulatory responses to laryngoscopy and tracheal intubation in hypertensive patients.     

Propofol is superior to thiopental for intubation without muscle relaxants

PURPOSE: To compare intubating conditions and cardiovascular changes following induction of anesthesia and tracheal intubation in patients receiving either lidocaine-remifentanil-propofol or lidocaine-remifentanil-thiopental prior to induction. METHODS: In a randomized, double-blind study 76 healthy adult patients were assigned to one of two groups: lidocaine 1.5 mg.kg(-1), remifentanil 2 mug.kg(-1) and propofol 2 mg.kg(-1) (Group P) or lidocaine 1.5 mg.kg(-1), remifentanil 2 mug.kg(-1) and thiopental 5 mg.kg(-1) (Group T). Ninety seconds after the administration of the hypnotic agent, laryngoscopy and tracheal intubation were attempted. Intubating conditions were assessed as excellent, good or poor on the basis of ease of ventilation, jaw relaxation, position of the vocal cords, and patient's response to intubation and slow inflation of the tracheal cuff. The mean arterial pressure (MAP) and heart rate (HR) were measured 45 sec after hypnotic agent administration, immediately after tracheal intubation, two and five minutes after intubation. RESULTS: Excellent intubating conditions were obtained in 84% of Group P patients and 50% of Group T patients (P < 0.05). The percentage decrease from baseline MAP was significantly higher in Group P than in Group T postinduction (27.4% +/- 11.6 vs 21.8% +/- 10.0) and immediately postintubation (19.0% +/- 16.7 vs 11.2% +/- 14.9). The percentage change from baseline HR was significantly higher in Group P than in Group T postinduction (13.8% +/- 9.7 vs 0.5% +/- 12.4), immediately postintubation (8.7% +/- 13.7 vs 2.1% +/- 13.1), and two minutes postintubation (7.04% +/- 14.3 vs 3.5% +/- 14.3). CONCLUSION: Lidocaine-remifentanil-propofol is superior to lidocaine-remifentanil-thiopental for tracheal intubation without muscle relaxants. However, it induces more hypotension and bradycardia.     

Comparison of nicardipine, diltiazem and verapamil for controlling the cardiovascular responses to tracheal intubation

We have compared the efficacy of three calcium channel blockers, nicardipine, diltiazem and verapamil, in attenuating the cardiovascular responses to laryngoscopy and intubation in 60 normotensive patients (ASA I) undergoing rapid sequence induction of anaesthesia with thiopentone and fentanyl. We also examined whether or not these blockers inhibited catecholamine release induced by intubation. The patients were allocated to one of four groups (n = 15 for each): saline (control), nicardipine 30 micrograms kg-1, diltiazem 0.2 mg kg-1 or verapamil 0.1 mg kg-1. Verapamil and the three other drugs were administered 45 s and 60 s before the start of direct laryngoscopy, respectively, in a double-dummy design. Anaesthesia was induced with thiopentone 4 mg kg-1 i.v. and fentanyl 2 micrograms kg-1 i.v. Tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. During anaesthesia, ventilation was assisted or controlled with 1% isoflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 s was attempted 2 min after administration of thiopentone and vecuronium. Patients receiving saline exhibited significant increases in systolic and diastolic arterial pressures (AP), heart rate (HR) and plasma concentrations of catecholamines associated with tracheal intubation. The increase in AP was attenuated in patients treated with any calcium channel blocker. The greatest effect was elicited by verapamil, which attenuated the increase in HR, although nicardipine seemed to enhance tachycardia. All three drugs failed to suppress the increase in plasma catecholamine concentrations in response to tracheal intubation. These findings suggest that bolus injection of verapamil 0.1 mg kg-1 was a more effective method of controlling hypertension and tachycardia associated with intubation than diltiazem 0.2 mg kg-1 or nicardipine 30 micrograms kg-1, and that these prophylactic effects were not caused by inhibition of the catecholamine response.      

RETRACTED ARTICLE: Effects of calcium channel blockers on circulatory response to tracheal intubation in hypertensive patients: nicardipine versus diltiazem

We studied the circulatory responses to laryngoscopy and tracheal intubation in 37 hypertensive patients who received nicardipine 30 μg · kg^?1 iv (Group N, n = 12), diltiazem 0.3 mg · kg^?1 (Group D, n = 12) or saline placebo (Group C, n = 13) 60 sec before the initiation of laryngoscopy. Anaesthesia was induced with thiopentone 5 mg · kg^?1 iv, and succinylcholine 2 mg · kg^?1 iv was used to facilitate tracheal intubation after precurarization with vecuronium 0.02 mg · kg^?1 iv. In patients in Group C heart rate (HR) increased from 79 ± 14 (baseline) to 110 ± 12 (P < 0.05) associated with tracheal intubation; mean arterial pressure (MAP) increased from 116 ± 8 to 140 ± 77 (P < 0.05) and rate-pressure product (RPP) increased from 13385 ± 2393 to 21251 ± 3883 (P < 0.05). The changes from baseline values in HR and RPP after tracheal intubation in Group D were less than those in Groups C and N (P < 0.05). The increase in MAP following tracheal intubation in Groups N and D was lower than that in Group C (P < 0.05). We conclude that, compared with nicardipine, administration of diltiazem iv is associated with less circulatory response to tracheal intubation in hypertensive patients.     

Ephedrine, dopamine, or doubtamine to treat hypotension with propofol during epidural anesthesia

PURPOSE: To compare the efficacy of ephedrine, dopamine and dobutamine for circulatory support during thoracic epidural anesthesia after anesthetic induction with propofol. METHODS: Forty patients undergoing lobectomy or mastectomy were divided into four groups of 10: a control group received no vasopressor; an ephedrine group received 5 mg ephedrine when the mean arterial pressure (MAP), measured every 2.5 min, decreased by 10% from baseline; dopamine and dobutamine groups received 5 microg x kg(-1) x min(-1) dopamine or 3 microg x kg(-1) x min(-1) dobutamine from five minutes after epidural injection of local anesthetic to the end of tracheal intubation. Anesthesia was induced with 2 mg x kg(-1) propofol. The MAP and heart rate (HR) were measured at baseline, 20 min after epidural injection, three minutes after propofol, and one minute after tracheal intubation. RESULTS: In the control group, MAP and HR decreased from 86+/-9 mmHg, 74+/-8 bpm to 62+/-9 mm Hg; P<0.0001, 60+/-8 bpm; P = 0.0003 after propofol. After tracheal intubation, MAP was restored to (81+/-13 mmHg, 70+/-13 bpm). In the ephedrine, dopamine, and dobutamine groups, MAP and HR remained unchanged during epidural anesthesia and propofol induction. However, after tracheal intubation, MAP and HR increased in the ephedrine (104+/-11 mm Hg; P = 0.004, 87+/-11 bpm; P<0.0001) and dobutamine (117+/-13 mm Hg; P = 0.0005, 100+/-11 bpm; P<0.0001) groups, but not in the dopamine group compared with baseline. CONCLUSION: Dopamine is preferable to ephedrine and dobutamine in providing hemodynamic stability during propofol induction and tracheal intubation following epidural anesthesia.     

Sevoflurane requirements for tracheal intubation with and without fentanyl

We studied 80 healthy ASA 1 patients (aged 20-52 yr) to determine if fentanyl affects sevoflurane requirements for achieving 50% probability of no movement in response to laryngoscopy and tracheal intubation (MAC- TI). Patients were allocated randomly to one of four fentanyl dose groups (0, 1, 2 and 4 micrograms kg-1). Patients in each group received sevoflurane at a pre-selected end-tidal concentration according to an 'up-down' technique. After steady state sevoflurane concentration had been maintained for at least 10 min, fentanyl was administered i.v. Tracheal intubation was performed 4 min after administration of fentanyl, and patients were assessed as moving or not moving. Heart rate (HR) and mean arterial pressure (MAP) were recorded before induction of anaesthesia, just before administration of fentanyl, just before laryngoscopy for intubation, and after intubation. The MAC-TI of sevoflurane was 3.55% (95% confidence intervals 3.32-3.78%), and this was reduced markedly to 2.07%, 1.45% and 1.37% by addition of fentanyl 1, 2 and 4 micrograms kg-1, with no significant difference in the reduction between 2 and 4 micrograms kg-1, showing a ceiling effect. Fentanyl attenuated haemodynamic responses (HR and MAP) to tracheal intubation in a dose-dependent manner, even with decreasing concomitant sevoflurane concentration. Fentanyl 4 micrograms kg-1 suppressed the changes in HR and MAP more effectively than fentanyl 1 or 2 micrograms kg-1 at sevoflurane concentrations close to MAC-TI.      

Esmolol for control of increases in heart rate and blood pressure during tracheal intubation after thiopentone and succinylcholine

Esmolol, an ultra-short-acting cardioselective beta-adrenergic blocker, was investigated in a double-blind prospective protocol for its ability to control haemodynamic responses associated with tracheal intubation after thiopentone and succinylcholine. Thirty ASA physical status I patients received a 12-minute infusion of esmolol (500 micrograms X kg-1 X min-1 for four minutes, then 300 micrograms X kg-1 X min-1 for 8 minutes) or saline. Five minutes after the start of the drug/placebo infusion, anaesthesia was induced with 4 mg X kg-1 thiopentone followed by succinylcholine for tracheal intubation. Prior to induction esmolol produced significant decreases in heart rate (HR) (9.3 +/- 1.8 per cent) and rate-pressure product (RPP) (13.1 +/- 1.8 per cent), systolic blood pressure (SAP) (4.3 +/- 1.5 per cent) and mean arterial blood pressure (MAP) (1.7 +/- 2.0 per cent). Increases in HR, SAP and RPP after intubation were approximately 50 per cent less in patients given esmolol compared to patients given placebo. There were highly significant differences in HR (p less than 0.0001), and RPP (p less than 0.0005) and significant differences in SAP (p less than 0.05) when the maximal esmolol post-intubation response was compared to the maximal placebo response. Infusion of esmolol in the dose utilized in this study significantly attenuated but did not completely eliminate cardiovascular responses to intubation.     

Second dose thiopentone attenuates the haemodynamic response to laryngoscopy and intubation

The study was undertaken to evaluate the effectiveness of large (divided) thiopentone dosage on the peripheral haemodynamic response to laryngoscopy and intubation. Seventy-six (76) patient aged 18 to 67 years were sequentially assigned to either the second dose thiopentone group (n = 36) or the control group (n = 40). The first group had 4 mg.kg-1 thiopentone for induction of anaesthesia, then 1.5 mg.kg-1 suxamethonium chloride for muscle relaxation and a second dose of thiropentone (4 mg.kg-1) just before laryngoscopy and intubation. The control group had thiopentone 4 mg.kg-1 for induction of anaesthesia, suxamethonium 1.5 mg.kg-1 for muscle relaxation and then laryngoscopy and intubation. The heart rate (HR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), and rate pressure product (RPP) were measured before induction of anaesthesia and after laryngoscopy and intubation. The difference in the values represented the haemodynamic response to laryngoscopy and intubation. The second dose thiopentone technique compared with the control group, significantly attenuated the post-intubation rise in HR (19.7 vs. 30.9), SAP (18.0 vs. 37.5) and RPP (4795.4 vs. 8440.0). The post intubation rise in DAP (33.9 vs. 42.5) and MAP (31.9 vs. 42.0) didn't show significant difference between the two groups.     

Intracranial pressure during induction of anaesthesia and tracheal intubation with etomidate-induced EEG burst suppression

This study was designed to determine if induction of anaesthesia with etomidate titrated to an early EEG burst suppression pattern would produce minimal changes in cerebral perfusion pressure, and prevent increases in intracranial pressure (ICP) associated with tracheal intubation. Eight patients, 18-71 yr, with intracranial space-occupying lesions, were studied. In each patient ICP was monitored via a lateral ventriculostomy catheter placed preoperatively. In the operating room, an ECG, a radial arterial line, and a two-channel computerized EEG were placed. Control (awake) measurements of MAP (mmHg), ICP (mmHg), CPP (mmHg), heart rate (HR-bpm), EEG power (picowatts-pW), and spectral edge frequency (SEF, Hz) were obtained. Anaesthesia was induced with etomidate, 0.2 mg.kg-1 iv, followed immediately by an etomidate infusion, 20 mg.min-1, iv, and vecuronium 0.2 mg.kg-1 iv. When early burst suppression was achieved, the etomidate infusion was stopped and tracheal intubation performed. The etomidate dose (bolus plus infusion) required to reach burst suppression was 1.28 +/- 0.11 mg.kg-1. Compared with awake control values (mean +/- SE), the period from induction to burst suppression was associated with a 50% decrease in ICP (22 +/- 1 vs 11 +/- 1 mmHg, P less than 0.01), but there were no changes in MAP, CPP, or HR. The decrease in ICP was maintained during the first 30 sec and the following 60 sec after intubation as MAP and HR remained unchanged. Our results suggest that when etomidate was administered to early burst suppression pattern on EEG, minimal changes in CPP occurred during induction of anaesthesia and a marked reduction in ICP was maintained following tracheal intubation.     

艾司洛尔对患者麻醉诱导气管插管时脑电双频谱指数的影响

Objective To evaluate the effect of esmolol on bispectral index (BIS) in patients undergoing orotracheal intubation during induction of anesthesia and to investigate the mechanism of inhibiting the cardiovascular responses to tracheal intubation.Methode Forty patients in physical status of ASA Ⅰ or Ⅱ and aged 20-60 years were randomly divided into 2 groups ( n = 20 each): esmolol group (group E) and control group (group C). Anesthesia was induced with midazolam 0.1 mg/kg, fentanyl 5 μg/kg and vecuronium 0.1 mg/kg. In group E, esmolol 1 mg/kg was given intravenously before anesthesia induction and followed by an infusion of esmolol 250 μg· kg- 1·min-1, while a comparable volume of saline was given for group C. Mean arterial pressure (MAP), heart rate (HR) and BIS were recorded before esmolol administration, before induction of anesthesia, before orotracheal intubation, and at 1, 2 and 5 min after intubation, respectively.Results There were no significant differences in HR, MAP and BIS between the two groups before tracheal intubation. HR and MAP significantly increased after tracheal intubation in both groups, but BIS only in group C significantly increased after intubation.HR, MAP and BIS were significantly lower after intubation in group E than in group C ( P＜ 0.05).Conclusion Esmolol can decrease BIS during tracheal intubation and its antinociceptive property is related to the mechanism of inhibiting cardiovascular responses to tracheal intubation.     

Haemodynamic effects of induction of general anaesthesia with propofol during epidural anaesthesia

PURPOSE: To clarify whether propofol administration during thoracic or lumbar epidural anaesthesia intensifies the haemodynamic depression associated with epidural anaesthesia. METHODS: Patients (n = 45) undergoing procedures of similar magnitude were randomly divided into three study groups: a control group (n = 15) receiving general anaesthesia alone and two study groups undergoing thoracic (n = 15) and lumbar epidural anaesthesia (n = 15) before induction of general anaesthesia. All patients received 2 mg.kg-1 propofol at a rate of 200 mg.min-1, followed by a continuous infusion of 4 mg.kg-1.hr-1. Mean arterial blood pressure (MAP) and heart rate (HR) were measured at baseline, three minutes after induction, and one minute after tracheal intubation in all three groups and at 20 min after epidural anaesthesia was established in the thoracic and lumbar groups. RESULTS: Following epidural anaesthesia, MAP decreased from 94 +/- 14 (SD) at baseline to 75 +/- 11 mmHg (P < 0.0001) in the thoracic group and from 92 +/- 12 to 83 +/- 15 mmHg in the lumbar group. After propofol administration, MAP decreased further in the thoracic group to 63 +/- 9 mmHg (P = 0.0077) and to 67 +/- 10 mmHg (P = 0.0076) in the lumbar group. The MAP following propofol induction in the thoracic group (P < 0.0001) and in the lumbar group (P = 0.0001) was lower than MAP in the control group (81 +/- 9 mmHg). HR decreased only in response to thoracic epidural anaesthesia (P = 0.0066). CONCLUSION: The hypotensive effects of propofol are additive to those of epidural anaesthesia, resulting in a profound decrease in mean arterial pressure.     

Intravenous Magnesium Sulfate Administration Reduces Propofol Infusion Requirements during Maintenance of Propofol-N2O Anesthesia: Part I: Comparing Propofol Requirements According to Hemodynamic Responses: Part II: Comparing Bispectral Index in Control and Magnesium Groups

Background: The authors investigated whether an intravenous administration of magnesium sulfate reduces propofol infusion requirements during maintenance of propofol-N2O anesthesia.

Methods: Part I study: 54 patients undergoing total abdominal hysterectomy were randomly divided into two groups (n = 27 per group). The patients in the control group received 0.9% sodium chloride solution, whereas the patients in the magnesium group received magnesium (50 mg/kg as a bolus, then 8 mg [middle dot] kg-1 [middle dot] h-1). To maintain mean arterial blood pressure (MAP) and heart rate (HR) at baseline value, the propofol infusion rate was changed when the MAP or the HR changed. The amount of propofol infused excluding the bolus dosage was divided by patient's body weight and total infusion time. Part II study: Another 20 patients were randomly divided into two groups (n = 10 per group). When the MAP and HR had been maintained at baseline value and the propofol infusion rate had been maintained at 80 [mu]g [middle dot] kg-1 [middle dot] min-1 (magnesium group) and 160 [mu]g [middle dot] kg-1 [middle dot] min-1 (control group), bispectral index (BIS) values were measured.

Results: Part I: The mean propofol infusion rate in the magnesium group (81.81 +/- 13.09 [mu]g [middle dot] kg-1 [middle dot] min-1) was significantly less than in the control group (167.57 +/- 47.27). Part II: BIS values in the control group (40.70 +/- 3.89) were significantly less than those in the magnesium group (57.80 +/- 7.32).     

Anesthesia and hypertension: the effect of clonidine on perioperative hemodynamics and isoflurane requirements

Thirty patients (ASA physical status II-III) with a history of arterial hypertension, whose blood pressure (BP) control varied from normotension to moderate hypertension (diastolic BP less than 110 mmHg), scheduled for elective surgery under general anesthesia, were randomly assigned to two groups. Group 1 was premedicated 90-120 min prior to induction with diazepam 0.15 mg X kg-1 po; group 2, in addition, received clonidine 5 micrograms X kg-1 po. Anesthetic depth was assessed by on-line aperiodic analysis of the electroencephalogram. Following lidocaine 1 mg X kg-1 and fentanyl 2 micrograms X kg-1 (group 1 only), anesthesia was induced with thiopental 3-4 mg X kg-1 and vecuronium 0.1 mg X kg-1 was used to facilitate endotracheal intubation. Anesthesia was maintained with isoflurane in N2O/O2 and supplemented by fentanyl. In group 2, clonidine produced a rapid preoperative control of systolic and diastolic BP from 166 +/- 32/95 +/- 14 to 136 +/- 80 +/- 11 (P less than 0.01), was more effective in blunting the reflex tachycardia associated with laryngoscopy and endotracheal intubation than lidocaine-fentanyl pretreatment. It significantly reduced the intraoperative lability (coefficient of variation) of systolic (P less than 0.01) and diastolic BP and heart rate (HR) (P less than 0.05), and resulted in significantly slower HR during recovery (P less than 0.01). Anesthetic requirements for isoflurane were reduced 40% (P less than 0.01) in group 2; narcotic supplementation was also significantly reduced (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Drug interactions with sufentanil. Hemodynamic effects of premedication and muscle relaxants.

Induction of anesthesia with synthetic opioids is occasionally accompanied by undesirable hemodynamic changes such as tachycardia and hypertension, or bradycardia and hypotension. We hypothesized that drug interactions cause many of these adverse responses. Therefore, we conducted a randomized double-blind study to investigate the interactive effect of premedication and muscle relaxants on the hemodynamic response to induction with intravenous (iv) sufentanil 10 micrograms.kg-1. Eighty patients with left ventricular ejection fraction greater than or equal to 0.40, undergoing elective coronary artery surgery, were premedicated with either morphine 0.1 mg.kg-1 and scopolamine 6 micrograms.kg-1 intramuscularly, or lorazepam 60 micrograms.kg-1 orally, and paralyzed with either pancuronium 0.1 mg.kg-1 or vecuronium 0.1 mg.kg-1 iv. The four treatment groups were SP (morphine-scopolamine + pancuronium), LP (lorazepam + pancuronium), SV (morphine-scopolamine + vecuronium), and LV (lorazepam + vecuronium). Hemodynamics were recorded at three time periods: 1) control, 2) induction, and 3) intubation. Premedication-relaxant interactions significantly affected hemodynamics. In group SP, mean heart rate (HR) increased significantly on induction (56 +/- 11 to 69 +/- 13 beats.min-1), while mean arterial pressure (MAP) and cardiac index (CI) were unchanged. HR, MAP, and CI were significantly higher after induction in group SP compared to the other three groups. In group LP, mean HR increased less than in group SP (56 +/- 8 to 62 +/- 14 beats.min-1), whereas MAP and CI declined significantly. In group SV, HR and CI were unchanged, but MAP declined significantly. In group LV, HR was stable, whereas both MAP and CI declined significantly. The incidence of pharmacologic interventions during the study period also differed significantly among groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of i.v. verapamil effects on cardiovascular responses in normotensive patients during laryngoscopy

Laryngoscopy and intubation are known to increase systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and heart rate (HR). In this study, we demonstrated that the injection of intravenous verapamil (0.1 mg/kg) prior to laryngoscopy can blunt the cardiovascular responses to laryngoscopy and intubation and result in stable hemodynamic profile in normotensive patients.     

Intravenous anesthesia with propofol in intracranial surgery]

OBJECTIVES: To analyze the repercussions of intravenous anesthesia with propofol as the single hypnotic drug on intracranial pressure (ICP) and cerebral perfusion pressure (CPP), and also to study the time until recovery from anesthesia and to tracheal extubation as well as intraoperative hemodynamic changes in patients undergoing surgery to remove a supratentorial brain tumor. PATIENTS AND METHODS: Twenty-three ASA I/II patients scheduled for exeresis of a supratentorial brain tumor were studied. A fiberoptic sensor placed in direct contact with the dura mater was used to measure ICP. Anesthetic induction was achieved with propofol (2 mg/kg). Propofol (12 and 9 mg/kg/h for 10 min and 6 mg/kg/h throughout the rest of the operation) was used for maintenance. Mean arterial pressure (MAP), heart rate (HR), ICP and CPP were recorded at baseline and 1, 2, 3 and 4 min after induction, during laryngoscopy and tracheal intubation; 1, 3, 5, 10, 15 and 20 min after tracheal intubation (L + 1, L + 3, L + 5, L + 10, L + 15, L + 20), upon placement of a craniostat; upon skin incision; upon withdrawal of propofol perfusion; and during extubation. The following variables were recorded after awakening: time until eye opening after receiving a verbal command, time until extubation and time until orientation. Analysis of variance for repeated measures (ANOVA) was performed on the results. RESULTS: MAP decreased significantly from baseline at the following times: during the post-induction period, upon placement of the craniostat, upon skin incision and when the propofol infusion was switched off. HR increased significantly during laryngoscopy and at the following moments: intubation, post intubation (L + 1, L + 3, L + 5), craniostat placement, and extubation. ICP was lower throughout the surgical period except during laryngoscopy, when this variable increased significantly. CPP decreased significantly after induction and returned to baseline after intubation. CPP was significantly higher after surgery. Recovery times after weaning from propofol infusion until eye opening in response to an order and until orientation were 13 +/- 3 and 22 +/- 4 min, respectively. The mean interval between withdrawal of propofol until extubation was 18 min. CONCLUSIONS: Intravenous anesthesia with propofol in intracranial surgery (supratentorial tumors) affords hemodynamic stability and lowers ICP except during laryngoscopy. Early recovery from anesthesia allows for neurological assessment and vigilance during the immediate postoperative period.     

The effect of an intermediate dose of labetalol on heart rate and blood pressure responses to laryngoscopy and intubation.

STUDY OBJECTIVE: To evaluate the efficacy of an intermediate dose of labetalol (0.4 mg/kg) for attenuation of heart rate (HR) and blood pressure (BP) responses to laryngoscopy and intubation. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Inpatient gynecology service at a university medical center. PATIENTS: Two groups of 18 patients each undergoing elective surgery under general anesthesia. INTERVENTIONS: Patients received either 0.4 mg/kg of labetalol or an equal volume of normal saline 5 minutes prior to laryngoscopy and intubation. MEASUREMENTS AND MAIN RESULTS: HR and BP were measured upon arrival in the operating room (OR) (baseline) and at 1 minute intervals thereafter for 4 minutes prior to intubation and through 10 minutes following intubation. The labetalol group had a significantly lower HR from induction through 1 minute following intubation. Intragroup differences in HR were greatest immediately following laryngoscopy and intubation (33% increase above baseline for the placebo group vs 1% for the labetalol group, p less than 0.05). At the same time, a significant increase in mean arterial pressure (MAP) from baseline was noted in both groups (29% for the placebo group vs 23% for the labetalol group), but the difference between the groups was not significant. CONCLUSIONS: An intermediate dose of labetalol blunted the HR response to laryngoscopy and intubation during rapid-sequence induction in healthy patients but had a minimal effect on BP.     

Effects of nilvadipine on the cardiovascular responses to tracheal intubation.

STUDY OBJECTIVE: To evaluate the efficacy of nilvadipine given orally in attenuating the hypertensive response to laryngoscopy and intubation. DESIGN: Controlled, randomized, double-blind study. SETTING: Induction of anesthesia for elective surgery at a university hospital. PATIENTS: Thirty normotensive patients (ASA physical status I) undergoing elective surgery were divided into three groups of ten patients each. INTERVENTIONS: Either 2 mg of nilvadipine, 4 mg of nilvadipine, or a placebo (control) was administered orally 90 minutes before induction of anesthesia. Anesthesia was induced with thiopental sodium 5 mg/kg intravenously, and tracheal intubation was facilitated with vecuronium 0.2 mg/kg. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide (N2O) in oxygen. Laryngoscopy lasting 30 seconds was attempted 2 minutes after administration of thiopental sodium and vecuronium. MEASUREMENTS AND MAIN RESULTS: Patients receiving the placebo showed a significant increase in mean arterial pressure (MAP) and heart rate associated with tracheal intubation. The increase in MAP following tracheal intubation was significantly lower in nilvadipine-treated patients than in the control group (p less than 0.05). However, neither dose of nilvadipine attenuated the tachycardic response to intubation. CONCLUSIONS: Oral administration of nilvadipine before induction of anesthesia is a simple and practical method for attenuating pressor response to laryngoscopy and tracheal intubation after standard elective induction under additional 1% enflurane-N2O anesthesia.