The haemodynamic effects of rocuronium and vecuronium are different under balanced anaesthesia

BACKGROUND: Rocuronium has been reported to have minimal haemodynamic effects. However, this conclusion has been drawn primarily from investigations conducted under narcotic-based anaesthesia. This study was designed to evaluate the cardiovascular effects of rocuronium under isoflurane/N2O/fentanyl anaesthesia and to compare rocuronium's haemodynamic effects to those of vecuronium and pancuronium. METHODS: Anaesthesia was induced with fentanyl 2 micrograms/kg, thiopentone 4 mg/kg, and suxamethonium 0.5 mg/kg in 75 ASA I or II patients. After tracheal intubation, anaesthesia was maintained with isoflurane 0.5% and N2O 50% in oxygen. Five min after intubation (baseline), patients randomly received either vecuronium 100 micrograms/kg, rocuronium 600 micrograms/kg, rocuronium 900 micrograms/kg, rocuronium 1200 micrograms/kg, or pancuronium 140 micrograms/kg. One min after administration of muscle relaxant, mean arterial pressure (MAP) and heart rate (HR) were recorded and were subsequently measured at 1-min intervals for the next 4 min. RESULTS: HR decreased significantly (P < 0.05) at all times compared to baseline in patients receiving vecuronium. HR significantly (P < 0.05) increased in those receiving rocuronium 1200 micrograms/kg or pancuronium. Patients who received vecuronium had a significant (P < 0.05) decrease in MAP at all times compared to baseline. Comparing results between groups, patients who received rocuronium or pancuronium had significantly (P < 0.05) higher MAP compared to those administered vecuronium. CONCLUSION: The haemodynamic effects of rocuronium and vecuronium are different under balanced anaesthesia. Rocuronium may attenuate the fall in MAP that often occurs under balanced anaesthesia without surgical stimulation.     

Prophylactic nefopam administration for post-anesthetic shivering

PURPOSE: Shivering is a frequent postanaesthetic complication. Its definite reason is unknown. Patients with cardiovascular or pulmonary diseases are endangered by postanaesthetic shivering. The aim of this study was to assess the efficacy of nefopam in prophylaxis of shivering. Additionally we investigated the influence of nefopam on haemodynamic parameters and on the time until extubation. METHODS: 30 patients (ASA I-II) were randomly allocated in a double-blind fashion to one of two groups to receive directly after the end of isoflurane application either nefopam (0.15 mg/kg) or placebo (0.9% saline). The period of anaesthesia had to be longer than 60 minutes. All patients received a premedication with lorazepam (0.02 mg/kg) 30-45 minutes prior to surgery. Induction of anaesthesia was standardised: fentanyl (3 micrograms/kg), thiopentone (5 mg/kg), atracurium (0.4 mg/kg). Intraoperatively a mixture of isoflurane, nitrous oxide (60%) and oxygen was used to maintain anaesthesia. The following parameters were evaluated: Age, sex, duration of operation and anaesthesia and the time between the end of application of volatiles and extubation. Heart rate (HR), mean arterial blood pressure (MAP), rectal temperature and O2-saturation were measured at predefined data points. Postoperatively the consumption of analgesic was documented. The severity of shivering was classified in five grades. RESULTS: In the control-group nine patients shivered (60%), whereas in the nefopam group only one patient (6.6%) shivered (p < 0.05). In comparison to the placebo group we observed in the nefopam group a significantly decreased HR 30 and 60 minutes postoperatively (p < or = 0.007 and p < or = 0.002). We did not observe prolonged awakening in the nefopam-treated patients. MAP and O2-saturation showed similar reactions in both groups. CONCLUSION: The data indicate that prophylactic administration of nefopam can suppress postanaesthetic shivering. Prolonged awakening was not observed.     

Epidural midazolam attenuates renal sympathetic nerve activity in rabbits

The effects of epidural midazolam on heart rate (HR), mean arterial pressure (MAP) and the renal sympathetic nerve activity (RSNA) were examined. Under alpha-choloralose anesthesia, 31 male Japanese-white rabbits received epidural catheterization and surgical procedures for measurement of the renal sympathetic nerve activity. Epidural low (0.05%) and high (0.5%) concentrations of midazolam did not affect HR, but significantly decreased MAP and RSNA-spikes (the spike count of RSNA). Intravenous flumazenil significantly increased MAP and RSNA-spikes. These findings suggest that the decrease in RSNA-spikes induced by epidural midazolam is derived from the benzodiazepine receptor. Intramuscular midazolam (0.5%) did not affect HR, but decreased MAP and RSNA-spikes significantly. In the spinal cord dissected rabbits, epidural midazolam (0.5%) did not affect HR and MAP, but significantly attenuated RSNA-spikes. In conclusion, epidural midazolam attenuated RSNA through the benzodiazepine receptors of both the spinal and supraspinal nervous system.     

Prevention and treatment of hypotension during spinal anesthesia

Spinal and epidural anaesthesias alter self-regulation of arterial pressure as they lead to a sympathetic blockade. The extent and the speed of appearance of this blockade conditions the magnitude of the decrease of arterial pressure. So, epidural or spinal anaesthesias may only be performed on hemodynamically stable patients for a non hemorrhagic surgery. The routine fluid preloading is illogical and poorly efficient. Correcting a deep arterial hypotension demands first of all the use of vasoconstricting agents the choice of which depends on the site of the anaesthesia and on the cardiovascular condition of the patient. The occurrence of bradycardia more often indicates a hypovolaemic state.     

Pyramidal control of heart rate and arterial pressure in cats

The pyramidal control of the heart rate (HR) and the arterial pressure (AP) was investigated in the cat. Experiments were conducted in order to determine relative contribution of vagal and sympathetic components to this control. In eighteen anesthetized and curarized cats, electrical stimulations were applied to the pyramidal tract (PT), followed by pharmacological blockade of the sympathetic cardiac control or by bivagotomy. HR and mean arterial pressure (MAP) were recorded in response to pyramidal stimulations before and after bulbar transections sparing only the PT, beta 1-blockade by atenolol administration and/or bilateral vagotomy. Results showed that the stimulation of the PT elicits significant cardiac accelerations and MAP increases in all animals. Furthermore, bulbar transections allowed to conclude that pyramidal influences acted at bulbar level and not on spinal cardiovascular neurons. After beta 1-blockade by atenolol, HR increases were reduced by about 70% and those of MAP by about 30%; after bilateral vagotomy, cardioaccelerations were reduced by about 30% but no significant reductions of MAP were observed; finally, beta 1-blockade combined with vagal section suppressed cardioaccelerations and significantly reduced the MAP increases. These results suggest the existence of a direct cortical control, via the pyramidal tract, to cardiovascular centers of the medulla, probably mediated by pyramidal collaterals. This control appears to be organized following a reciprocal autonomic pattern where the suppression of the vagal inhibition is associated with a concomitant sympathetic excitation. The present work also provides data in favour of a central command coupling somatic programs and cardiac adjustments during motor acts.     

Caudal clonidine and bupivacaine for combined epidural and general anaesthesia in children

BACKGROUND: Clonidine produces analgesia by actions on alpha 2-adrenoceptors and enhances both sensory and motor blockade from epidural injection of local anaesthetics. Low-dose clonidine has been used so far for caudal injection in children. Our aim was to study the perioperative effects of high-dose caudal clonidine when added to low concentration of bupivacaine for combined epidural and general anaesthesia in children. METHODS: After induction of general anaesthesia caudal block was performed either with 1 ml.kg-1 bupivacaine 0.175% with the addition of clonidine 5 micrograms.kg-1 (n = 20), or with 1 ml.kg-1 bupivacaine 0.175% (n = 20). The intraoperative anaesthetic requirements, the perioperative haemodynamic effects, respiratory rate, sedation score, postoperative pain scores and side effects were assessed by a blinded observer. A patient-controlled analgesia system was used for postoperative pain relief. The quality of postoperative pain relief was assessed using Smiley's pain analogue scale. RESULTS: Intraoperative haemodynamic responses did not differ between the groups. However, during emergence from general anaesthesia children in the clonidine group had significantly lower heart rates and blood pressure compared to children in the control group. In addition, heart rates and blood pressures were also lower in the clonidine group in the early postoperative period (P < 0.05). Postoperative analgesia was significantly better in the clonidine group as evidenced by the total number of requests (3 vs 12, P < 0.05) and the total amount of tramadol (20.5 mg vs 72.8 mg, P < 0.05) administered. The duration of the caudal analgesia was significantly longer in the clonidine group (20.9 +/- 7.4 h vs 14.4 +/- 10.9 h, P < 0.05). CONCLUSION: Our results suggest that caudal clonidine 5 micrograms.kg-1 enhances and prolongs caudal blockade with bupivacaine (1.175% in children. It also blocks sympathoadrenergic responses during emergence from anaesthesia. Sedation and cardiovascular effects are observed up to 3 h into the postoperative period.     

Anesthesia in endovascular treatment of aortic aneurysm. Results and perioperative risks

Surgical treatment of aortic aneurysms carries significant cardiovascular risks. Transvascular insertion of endoluminal prostheses is a new, minimally invasive treatment for aortic aneurysms. The pathophysiology of this novel procedure, risks and benefits of different anaesthetic techniques, and typical complications need to be defined. METHODS: With their informed, written consent, 19 male patients aged 48-83 years of ASA physical status III and IV with infrarenal (n = 18) or thoracic (n = 1) aortic aneurysms underwent 23 stenting procedures under general endotracheal (n = 9), epidural (n = 8), or local anaesthesia with sedation (n = 6). Intra-anaesthetic haemodynamics, indicators of postoperative (p.o.) oxygenation and systemic inflammatory response, and perioperative complications were analysed retrospectively and compared between anaesthetic regimens. RESULTS: Groups were well matched with regard to morphometry and preoperative risk profiles (Table I). The use of pulmonary artery pressure monitoring, incidence of intraoperative hypotensive episodes, and p.o. intensive care was more frequent with general anaesthesia. Groups did not differ in total duration of anaesthesia care, incidence and duration of intraoperative hypertensive, brady-, or tachycardic periods, incidence of arterial oxygen desaturation, use of vasopressors, colloid volume replacements, or antihypertensives (Table 2). Postoperatively, all groups showed a similar, significant systemic inflammatory response, i.e., rapidly spiking temperature (p.o. evening: mean peak 38.5 +/- 1.0 degrees C). leucocytosis, and rise of acute-phase proteins without bacteraernia (Table 3). During this period, despite supplemental oxygen, pulse oximetry revealed temporary arterial desaturation in 13 of 18 patients (70%) (Table 3). In 3 patients, hyperpyrexia was associated with intermittent tachyarrhythmias (n = 3) and angina pectoris (n = 1). There was no conversion to open aortic surgery, perioperative myocardial infarction, or death. CONCLUSIONS: Regional and local anaesthesia with sedation are feasible alternatives to general endotracheal anaesthesia for minimally invasive treatment of aortic aneurysms by endovascular stenting. However, invasive monitoring and close postoperative monitoring are strongly recommended with either method. Specific perioperative risks in patients with limited cardiovascular or pulmonary reserve are introduced by the abacterial systemic inflammatory response to aortic stent implantation. Hyperpyrexia increases myocardial and whole-body oxygen consumption, and can precipitate tachyarrhythmias. Hyperfibrino-genaemia may increase the risk of postoperative arterial and venous thromboses. Close monitoring of vital parameters and prophylactic measures, including oxygen supplementation, low-dose anticoagulation, antipyretics, and fluid replacement are warranted until this syndrome resolves.     

Anesthesia-resuscitation in surgery for pheochromocytoma

The perioperative mortality related to cardiovascular complications has been almost completely eliminated in phaeochromocytoma surgery. The anaesthetic management has mainly evolved through refinements in haemodynamic control during the operation. Neither preoperative preparation nor general anaesthesia can totally prevent haemodynamic disturbances during surgical manipulation of the tumour or after removal of the tumour. General anaesthesia, with high doses of opioids, remains the most usual technique. Intraoperative monitoring should include an arterial catheter and a pulmonary arterial catheter. Although a number of antihypertensive drugs have been tested, the preventive use of nicardipine i.v. may provide a simple and effective haemodynamic control. Esmolol, an ultrashort acting agent, ensures a dose-related cardiac beta 1-blockade. It is used for the treatment of arrhythmia and cardiac adrenergic stimulation, which causes tachycardia and increases cardiac output. Volume loading is recognised as the treatment of choice for hypotension following tumour removal. During the postoperative period, the great hazard is hypoglycaemia, and plasma glucose levels should be monitored over the immediate postoperative hours.     

Kaposi''s sarcoma-associated herpesvirus and human herpesvirus 8 (KSHV/HHV8)-associated lymphoma of the bowel. Report of two cases in HIV-positive men with secondary effusion lymphomas

BACKGROUND: We evaluated the ability of the standards issued by the Danish Society of Anaesthesiologists to reflect a blood loss. METHODS: In 9 pigs bled (0-24 ml kg-1 and retransfused (to 28 ml kg-1) during halothane anaesthesia central cardiovascular, thoracic electrical impedance (TI), oxygen, acid-base and temperature variables were recorded. RESULTS: With the recommendation for minor surgery (mean arterial pressure (MAP) and heart rate (HR)), the correlation to the blood loss was 0.74 (P < 0.001) and with that for major surgery (MAP, HR, central venous pressure (CVP) and rectal temperature (Tempr)) it was 0.79 (P < 0.001). With the recommendation for extensive surgery (MAP, HR, CVP, pulmonary artery catheter variables and the central-peripheral temperature difference (delta Tempr-t)), the correlation was 0.84 (P < 0.001). Non-invasive monitoring (MAP, HR, delta Tempr-t, TI and near-infrared spectroscopy of the brain (SinvosO2)) was only slightly better than basal monitoring (r = 0.76, P < 0.001). However, adding arterial base excess (BE), TI, and peripheral temperature (Tempt) to the recommendation for major surgery resulted in a correlation of 0.87 (P < 0.001), while adding BE and TI to the recommendation for extensive surgery raised correlation to only 0.88 (P < 0.001). CONCLUSION: When the recommendations were followed the correlation to the blood loss ranged from 0.74-0.84. However, with the recording of MAP, HR, CVP, delta Tempr-t, BE and TI a correlation of 0.87 was achieved, indicating that a pulmonary artery catheter may not be in need for patients undergoing surgical procedures with expected haemorrhage.     

Interaction of frequency-adaptive pacemakers and anesthetic management. Discussion of current literature and two case reports

We describe unexpected episodes of paced tachycardia in two patients with rate-responsive pacemakers during anaesthesia. Five months after a heart transplant and implantation of a pacemaker a 43-year-old patient suffered cardiac tamponade as a result of chronic pericarditis. The second case involved embolic occlusion of the femoral artery in a 33-year-old female patient previously operated on for tricuspid valve replacement and implantation of a pacemaker. In both cases induction of anaesthesia was performed with fentanyl, etomidate and vecuronium. Following intubation and mechanical ventilation, the heart rates (HR) of the two patients increased to 140 and 130 min-1 respectively. This was interpreted as a sign of inadequate anaesthesia, and therefore additional doses of fentanyl and etomidate were given, with no effect on the tachycardia. After exclusion of other possible reasons for this complication such as hypokalaemia, hypercapnia, hypoxaemia or allergic reactions, unexpected functioning of the rate-responsive pacemakers due to thoracic impedance changes was assumed. Minute ventilation was reduced, lowering paced HR in 3-5 min. CONCLUSIONS: These case reports suggest that anaesthetic management affects the action of rate-responsive pacemakers, causing haemodynamic complications, and inadequate interventions by the anaesthesiologist. Thus, it is necessary for anaesthesiologists to make a preoperative evaluation of the underlying medical disease and the type of pacemaker in order to adjust anaesthetic management accordingly and to understand the haemodynamic responses that may occur during the perioperative period. Preoperative programming to exclude the rate-responsive function is advised.     

Alteration of renal blood flow during epidural anesthesia in normal subjects

The cardiovascular consequences of epidural anesthesia secondary to sympathetic blockade are well documented; however, their repercussions on renal hemodynamics in humans have not been reported. We investigated the effect of epidural anesthesia on renal blood flow (RBF) in 13 healthy volunteers 18-45 yr of age. RBF was measured using paraaminohippurate clearance before and after bilateral T6 epidural sensory block (to ensure adequate sympathetic renal nerve blockade). Epidural anesthesia was established using 22 +/- 3 mL of 2% plain lidocaine (without epinephrine) via L1-L2 epidural catheter; urine output was measured using a three-way Foley catheter. Mean arterial pressure remained > or = 70 mm Hg in all subjects without any pharmacologic intervention. Mean RBF before epidural anesthesia was 16.1 +/- 6.8 mL.kg-1.min-1 and 14.3 +/- 2.9 mL.kg-1.min-1 after bilateral T6 epidural blockade. We conclude that the institution of epidural anesthesia in healthy subjects does not result in a significant change in RBF (P > 0.25).     

Thoracic epidural anaesthesia for coronary artery bypass graft surgery. Effects on postoperative complications

We have performed a retrospective analysis of the peri-operative course of 218 consecutive patients who underwent routine coronary artery bypass graft surgery in this institution. All patients received a standardised general anaesthetic using target-controlled infusions of alfentanil and propofol. One hundred patients also received thoracic epidural anaesthesia with bupivacaine and clonidine, started before surgery and continued for 5 days after surgery. The remaining 118 patients received target-controlled infusion of alfentanil for analgesia for the first 24 h after surgery, followed by intravenous patient-controlled morphine analgesia for a further 48 h. Using computerised patient medical records, we analysed the frequency of respiratory, neurological, renal, gastrointestinal, haematological and cardiovascular complications in these two groups. New arrhythmias requiring treatment occurred in 18% of the thoracic epidural anaesthesia group of patients compared with 32% of the general anaesthesia group (p = 0.02). There was also a trend towards a reduced incidence of respiratory complications in the thoracic epidural anaesthesia group. The time to tracheal extubation was decreased in the epidural group, with the tracheas of 21% of the patients being extubated immediately after surgery compared with 2% in the general anaesthesia group (p < 0.001). There were no serious neurological problems resulting from the use of thoracic epidural analgesia.     

ST segment changes in the ECG. Anesthesia induction with propofol, etomidate or midazolam in patients with coronary heart disease

Induction of anaesthesia with propofol and fentanyl can lead to marked reductions in mean arterial pressure (MAP) and heart rate (HR). Thus, the application of propofol in patients with severely reduced coronary artery perfusion is controversial. METHODS. The study group consisted of 60 patients undergoing coronary artery bypass grafting (CABG). Anaesthesia was induced over 30 s with propofol (P 1.5 mg/kg), etomidate (E 0.3 mg/kg), or midazolam (M 0.15 mg/kg) following a bolus dose of fentanyl (5 micrograms/kg). Vecuronium was used as a muscle relaxant. During induction we continuously measured MAP and HR and recorded the occurrence of myocardial ischaemia using an automatic ST-segment analyser (Marquette 7010). ST-segment deviations of more than 1 mm in leads II and V5 were interpreted as significant signs of myocardial ischaemia. RESULTS. All groups showed reductions in MAP and HR on induction that were marked in the P group. Intubation caused elevation of MAP and HR to pre-induction levels (HR: all groups) or slightly above (MAP: E, M). Four patients in the P group and 3 in each other group showed significant ST-segment deviation prior to induction. In the P group these deviations disappeared in 2 patients after injection while they remained unchanged in the M group. In the E group injection had no effect on the ischaemic ECG changes but produced another case of significant ST-segment deviation. Laryngoscopy and intubation produced no further significant ST-segment deviation in either group. DISCUSSION. Induction is a critical phase of anaesthesia, especially in patients with limited coronary reserve. Induction agents should alleviate the stress response while causing minimal haemodynamic changes. Despite marked reductions in MAP in the P group, the number of patients with ischaemic ECG changes was cut by half. Their number was unchanged or even raised in the other groups. After application of P, with an alleged reduction of coronary perfusion, a compensational reduction in myocardial oxygen consumption may occur.     

Decrease in costs for management of lower airway disease in the pediatric intensive care unit

PURPOSE: Hypertensive patients exhibit exaggerated cardiovascular responses to tracheal extubation. This study was undertaken to examine the inhibitory effects of calcium channel blockers, nicardipine and diltiazem, on haemodynamic changes after tracheal extubation. METHODS: Sixty hypertensive patients (ASA physical status II) undergoing elective orthopaedic (upper and lower extremity) surgery received, in a randomized, double-blind manner, 30 micrograms.kg-1 nicardipine, 0.2 mg.kg-1 diltiazem or saline (as a control) (n = 20 of each) i.v. before tracheal extubation. Changes in heart rate (HR), mean arterial pressure (MAP) and rate-pressure product (RPP) were measured before and after tracheal extubation. RESULTS: The HR, MAP and RPP increased after tracheal extubation in the control group (P < 0.05). The increases in these haemodynamic variables were attenuated with nicardipine or diltiazem. The inhibitory effects of diltiazem on these cardiovascular responses to tracheal extubation were greater than those of nicardipine (HR; 86 +/- 7 vs 101 +/- 10, RPP; 11,437 +/- 1,575 vs 14,675 +/- 2,874, mean +/- SD, P < 0.05). CONCLUSION: Compared with nicardipine, administration of diltiazem produced greater attenuating the circulatory responses to tracheal extubation in hypertensive patients.     

Cardiovascular effects of an intubating dose of rocuronium 0.6 mg kg-1 in anaesthetized patients, paralysed with vecuronium

We have studied, in adult patients, ASA I-II, the cardiovascular effects of an intubating dose of rocuronium 0.6 mg kg-1. After induction, patients were paralysed with vecuronium and the trachea intubated. Heart rate (HR) and non-invasive mean arterial pressure (MAP) were measured every 1 min. After stabilization of HR and MAP, defined as < 3% change over three measurements, rocuronium (n = 20) or saline (n = 10) was injected at random. Mean HR increased initially from 66.6 to 72.1 beat min-1, 4 min after rocuronium, and then decreased gradually to 69.6 beat min-1, that is a net increase of 3.3 beat min-1 over 10 min (P < 0.001), whereas after saline there was a gradual decrease from 65.8 to 60.9 beat min-1 (P < 0.001) over 10 min. From the third minute, HR was significantly higher in the rocuronium group. Mean MAP decreased in both groups within 10 min to a similar extent after rocuronium and saline, that is from 74.9 to 72.1 mm Hg and from 74.7 to 72.2 mm Hg, respectively (both P < 0.001). There were no differences in MAP at any time between the rocuronium and saline groups. We conclude that an intubating dose of rocuronium, in the absence of haemodynamic effects related to paralysis itself, resulted in a limited increase in HR without change in MAP, probably because of its weak vagolytic activity.     

Perioperative ischaemia in aortic surgery: combined epidural/general anaesthesia and epidural analgesia vs general anaesthesia and i.v. analgesia

PURPOSE: The goal of this randomized study was to determine whether combined general and epidural anaesthesia with postoperative epidural analgesia, compared with general anaesthesia and postoperative intravenous analgesia, reduced the incidence of perioperative myocardial ischaemia in patients undergoing elective aortic surgery. METHOD: Patients were randomly assigned to one of two groups. One group (EPI, n = 48) received combined general and epidural anaesthesia and postoperative epidural analgesia for 48 hrs. The other group (GA, n = 51) received general anaesthesia followed by postoperative intravenous analgesia. Anaesthetic goals were to maintain haemodynamic stability (+/- 20% of preoperative values), and a stroke volume > 1 ml.kg-1. A Holter monitor was attached to each patient the day before surgery. Leads 11, V2, and V5 were monitored. Myocardial ischaemia was defined as ST segment depression > 1 mm measured at 80 millisec beyond the J point or an elevation of 2 mm 60 millisec beyond the J point which lasted > 60 sec. An event that lasted > 60 sec but returned to the baseline for > 60 sec and then recurred, was counted as two separate events. The Holter tapes were reviewed by a cardiologist blind to the patient's group. RESULTS: There were no demographic differences between the two groups. Myocardial ischaemia was common; it occurred in 55% of patients. In hospital, preoperative ischaemia was uncommon (GA = 3, EPI = 8). Intraoperative ischaemia was common (GA = 18, EPI = 25). Mesenteric traction produced the largest number of ischaemic (GA = 11, EPI = 11) events. Postoperative ischaemia was most common on the day of surgery. Termination of epidural analgesia produced a burst of ischaemia (60 events in 9 patients). CONCLUSION: Combined general and epidural anaesthesia and postoperative epidural analgesia do not reduce the incidence of myocardial ischaemia or morbidity compared with general anaesthesia and postoperative intravenous analgesia.     

The co-existence of insulin-mediated decreased mean arterial pressure and increased sympathetic nerve activity is not mediated by the baroreceptor reflex and differentially by hypoglycemia

In this study we measured simultaneously and sequentially the lumbar sympathetic nerve activity (LSNA) or renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), and heart rate (HR) in response to insulin with co-existing hypoglycemia or with glucose replacement in normal rats. Sinoaortic denervation (SAD) was used to evaluate the influence of the baroreflex. LSNA, RSNA, MAP and HR were determined using an acquisition processor and computer software. Bolus insulin infusion where the blood glucose was allowed to decrease resulted in an immediate decrease in MAP. The HR decreased for approximately 15 min and subsequently increased. The LSNA increased immediately after insulin infusion peaking at 25 minutes and then recovered toward baseline. Insulin infusion with glucose replacement resulted in a decrease in MAP and HR. The LSNA progressively increased and was maintained throughout the experimental period. Insulin infusion with hypoglycemia increased RSNA and when hypoglycemia was prevented the RSNA decreased. SAD attenuated the decrease in MAP and LSNA response to insulin. Thus, insulin acts to decrease MAP while simultaneously increasing HR, LSNA and RSNA when hypoglycemia is allowed to occur. However, insulin acts to decrease HR and RSNA when euglycemia is maintained. The insulin-induced increase in LSNA is modulated by the baroreflex mechanism. We conclude that insulin has independent direct and indirect effects on LSNA, RSNA, MAP and HR that are modulated by glycemia and the baroreflex.     

The haemodynamic effect of thoracoscopic cardiac sympathectomy

A patient with angina pectoris who had been successfully treated by thoracoscopic cardiac sympathectomy was scheduled to have scalp debridement under general anaesthesia for a scald burn. There were haemodynamic changes during and after the operation including anaesthetic induction, endotracheal intubation, maintenance, and early recovery period. The sympathetic denervated heart showed little chronotropic response to anaesthetic and surgical stimulation. On the contrary, the parasympathetic response was predominant. An episode of severe bradycardia occurred during endotracheal suctioning prior to extubation. The haemodynamic response to cardiac sympathetic denervation corresponded to the efferent effect of beta-receptor blockade     

Effect of thoracic epidural anaesthesia on ventilation-perfusion distribution and intrathoracic blood volume before and after induction of general anaesthesia

BACKGROUND: Gas exchange is impaired during general anaesthesia due to development of shunt and ventilation-perfusion mismatching. Thoracic epidural anaesthesia (TEA) may affect the mechanics of the respiratory system, intrathoracic blood volume and possibly ventilation-perfusion (VA/Q) distribution during general anaesthesia. METHODS: VA/Q relationships were analyzed in 24 patients undergoing major abdominal surgery. Intrapulmonary shunt (Qs/QT), perfusion of "low" VA/Q areas, ventilation of "high" VA/Q regions, dead space ventilation and mean distribution of ventilation and perfusion were calculated from the retention/excretion data of six inert gases. Intrathoracic blood volume (ITBV) and pulmonary blood volume (PBV) were determined with a double indicator technique. Recordings were made before and after administration of 8.5 +/- 1.5 ml bupivacaine 0.5% (n = 12) or 8.3 +/- 1.8 ml placebo (n = 12) into a thoracic epidural catheter and after induction of general anaesthesia. RESULTS: Before TEA, Qs/QT was normal in the bupivacaine group (2 +/- 2%) and the placebo group (2 +/- 3%). TEA covering the dermatomal segments T 12 to T 4 had no effect on VA/Q relationships, ITBV and PBV. After induction of general anaesthesia Qs/QT increased to 8 +/- 4% (bupivacaine group, P < 0.05 and to 7 +/- 2% (placebo group, P < 0.05). ITBV and PBV decreased significantly to the same extent in the bupivacaine group and the placebo group. CONCLUSIONS: TEA has no effect on VA/Q distribution, gas exchange and intrathoracic blood volume in the awake state and does not influence development of Qs/QT and VA/Q inequality after induction of general anaesthesia.     

Effect of spinal sympathetic blockade upon postural changes of blood flow in human peripheral tissues

The effect of head-up tilt upon subcutaneous and skeletal muscle blood flow in the crus was studied before and during epidural blockade in 10 subjects. Relative changes in blood flow were estimated by the local 133Xe washout technique. In subcutaneous tissue head-up tilt induced a decrease in blood flow of about 40% and there was no difference in the vascular response to head-up tilt before and during epidural blockade. In skeletal muscle tissue essentially the same was found as head-up tilt decreased blood flow by about 26% the response being uninfluenced by epidural blockade. In 3 patients local nervous blockade was induced by Lidocaine in 133Xe labelled subcutaneous tissue on one side. During epidural blockade and tilt blood flow increased by 12% whereas blood flow decreased by 30% on the control side. Thus epidural blockade had no influence on the vasoconstrictor response in subcutaneous tissue and skeletal muscle to head-up tilt whereas local blockade was able to prevent the response. Local mechanisms including the local veno-arteriolar reflex appear to play an important role for the observed maintenance of arterial blood pressure in the tilted position during central sympathetic blockade.