HALOTHANE METABOLISM IN CHILDREN

Halothane (1% v/v inspired) was administered for 60 min to sixchildren of mean age 74 months (range 14–119 months).Uptake of halothane was measured from the difference in theconcentration in inspired and expired gas and varied from 176to 310 mg kg^–1, depending on minute ventilation. Afteradministration of halothane ceased, its elimination in expiredgas was measured in four patients until the conclusion of anaesthesia;32–37% of the absorbed halothane was expired 90 min afterhalothane administration ceased. Urinary excretion of trifluoro-aceticacid, fluoride and bromide was measured for up to 1 week. Ofthe absorbed halothane, 11.4% (range 6.3–18.2%) was excretedin urine as trifluoroacetic acid and 0.37% (range 0.10–0.64%)as inorganic fluoride. The urinary half-life of trifluoraceticacid was 41.8 h (range 10.4–59.1 h). The quantitativeand qualitative metabolism of halothane via the reductive andoxidative pathways in children are comparable to values foundin adults. No differences in the metabolism of halothane bychildren were found which would explain the different incidenceof halothane-associated hepatitis compared with adults.     

PHARMACOKINETICS OF ALFENTANIL DURING AND AFTER A FIXED RATE INFUSION

Twenty-nine patients (age range 14–81 yr) undergoing orthopaedicsurgery received alfentanil 100 µg kg^–1 given astwo i.v. boluses followed by a fixed rate infusion of 1 µgkg^–1 min^–1 for 44–445 min. Additional 1-mgbolus doses of alfentanil were administered as required. Plasmasamples were assayed for alfentanil using radio-immunoassay.Pharmacokinetic parameters were estimated by a model-independentapproach and by curve-fitting. Regression analysis showed nostatistical relationship between T, CI or Vd and the durationof the infusion, total dose or body weight. We found no significantcorrelation between age and T of alfentanil for patients youngerthan 40 yr. For patients older than 40 yr, T increased linearlywith age. There was no significant decrease in Cl with age,although the lower values for CI (100–200 ml min^–1)were generally found in subjects older than 60 yr. The presentstudy demonstrated that a 100-µg kg^–1 loading doseand a 1-µg kg^–1 min^–1 infusion may be appropriatefor analgesia in general surgical procedures.     

DISPOSITION OF INFUSIONS OF ATRACURIUM AND ITS METABOLITE, LAUDANOSINE, IN PATIENTS IN RENAL AND RESPIRATORY FAILURE IN AN ITU

A study of plasma atracurium and laudanosine concentrationswas undertaken in 14 critically ill patients who received abolus dose of atracurium 0.6 mg kg^–1 followed by an infusionof 0.6mg kg^–1 h^–1 for a period of 11–47 h.Seven of the patients had normal renal function and seven werein acute renal failure. In both groups plasma concentrationsof atracurium reached a plateau of approximately 1300 ng ml^–1within30 min of the bolus dose. The drug disappeared from the plasmawithin 120 min after discontinuation of the infusion. Therewas no difference between the two groups with respect to thepharmacokinetic parameters derived for atracurium. In the patientswith normal renal function, plasma laudanosine concentrationreached a plateau of apprpximately 1200ng ml^–1 within10h. In patients with renal failure there was a greater variationin the plasma laudanosine concentration: the highest value recordedwas 4300 ng ml^–1. Patients with renal failure had a significantlylonger mean elimination half-life for laudanosine (1418 minv. 375min; P < 0.05) and Vd (4.52 litre kg^–1 v. 240litre kg^–1; P < 0.01) than the patients with normalrenal function. ^*Present address: Southport General Hospital, Scarisbrick NewRoad, Southport, Merseyside PR8 6LF.     

CLINICAL COMPARISON OF THE BAIN AND MAGILL ANAESTHETIC SYSTEMS DURING SPONTANEOUS RESPIRATION

The Bain and Magill anaesthetic breathing systems were comparedfor spontaneous breathing during nitrous oxide in oxygen andhalothane anaesthesia. A mean fresh gas flow (Vf) of 150mlkg^–1min^–1(SD±30,range 106–250) was required with the Bain system to preventrebreathing sufficient to cause respiratory stimulation; meanfresh gas flow/expired minute volume (JVF/Vfe) was 1.49 (SD±0.32,range 0.86–2.17). Equivalent figures for the Magill attachmentwere a mean VFof 82mlkg^–1min^–1(SD±19,range43–125),while mean VF/Vfc was 0.76)(SD±0.19)range0.38–1.23,P<0.001).Theresultsattest the efficiency of the Magill attachment in termsof gas economics, and indicate the very high flows requiredto avoid respiratory stimulation in some subjects when the Bainsystem is used.     

ISOLATED HUMAN BLOOD PLATELETS DISCRIMINATE BETWEEN ANAESTHETIC AND NON-ANAESTHETIC GASES AT HIGH PRESSURES

We have compared the effects of the anaesthetic gases nitrogenand argon on adenosine diphosphate (ADP)-induced human bloodplatelet aggregation with the effects of the non-anaestheticgas helium. All three gases showed dose-dependent inhibitionof platelet aggregation. For nitrogen and argon there was alinear relationship between gas pressure and inhibition of aggregationover the range 15–68 atmospheres absolute (atm abs), whereashelium had a threshold for inhibition of approximately 34 atmabs. The inhibition by all gases was reversible after slow decompression.At pressures greater than 55 atm abs, nitrogen produced lessinhibition than helium, indicating anaesthetic-pressure antagonism.Whereas pressure alone and the anaesthetic gases inhibited aggregation,the platelet shape change elicited by ADP was resistant to bothnitrogen and helium, indicating that ADP binding and the earlyevents in platelet activation were relatively unaffected bythese conditions. Preliminary accounts of some of these data have been presentedat the 3rd International Conference on Molecular and CellularMechanisms of Anaesthesia, Calgary, Alberta, 1984 and at theUndersea Medical Society Annual Meeting, Long Beach, California,1985 [18].     

Effects of haemoglobin-based oxygen carrier hemoglobin glutamer-200 (bovine) on intestinal perfusion and oxygenation in a canine hypovolaemia model

The objective of this investigation was to study the effectsof the first marketed haemoglobin-based oxygen carrier, Hemoglobinglutamer-200 (bovine) (Hb-200) (Oxyglobin^®) on splanchnicperfusion and oxygenation in a canine model of acute hypovolaemia.Twelve anaesthetized dogs [mean weight 30.8 (S.D. 1.4) kg] wereinstrumented for recordings of heart rate (HR), mean arterialpressure (MAP), central venous pressure (CVP), cardiac outputand cranial mesenteric arterial (CMA) and venous blood flows(CMV). Total and plasma haemoglobin (Hb), oxygen content andsaturation, lactate concentration, pH and blood gases were analysedin arterial, mixed venous and mesenteric venous blood samples.Measurements were made before (baseline) and after 1 hof haemorrhage, after which animals were resuscitated with eithershed blood (controls) or Hb-200 until HR, MAP and CVP returnedto prehaemorrhage levels. Recordings were repeated immediatelyand 3 h after termination of fluid resuscitation, afterwhich organ specimens were obtained for microscopic examination.Haemorrhage (average 32 ml kg^–1) reduced MAPto 50 mm Hg, increased HR and systemic vascular resistance(SVR), and was accompanied in both the systemic and the splanchniccirculation by significant decreases in blood flow, Hb contentand oxygen delivery (DO₂), and lactic acidosis. In controls,all variables recovered to baseline after isovolaemic resuscitationwith shed blood. In dogs resuscitated with a small volume ofHb-200 (10 ml kg^–1), HR, MAP, CVP and CMA andCMV blood flows returned to baseline. However, cardiac output,total Hb, oxygen content and systemic and mesenteric DO₂ remaineddepressed while SVR increased further. Mesenteric and systemicacid–base status recovered in both groups, and there wasno difference in microscopic tissue damage between groups. Thus,Hb-200 reconstituted splanchnic perfusion and oxidative metabolismin spite of pronounced systemic vasoconstriction and insufficientrestoration of CO and DO₂; it may improve diffusive oxygen transportin the microvasculature by virtue of haemodilution and its highefficiency in the uptake and release of oxygen. Br J Anaesth 2001; 86: 683–92     

Inhalation anaesthetics increase heart rate by decreasing cardiac vagal activity in dogs

Inhalation anaesthetics decrease heart rate in isolated heartsbut mostly increase heart rate in the intact organism, althoughmost inhibit sympathetic drive. Differences in the degree ofincrease in heart rate between agents may be related to differencesin their vagolytic action. To test this hypothesis, we studied theeffects of halothane (H), isoflurane (I), enflurane (E), sevoflurane (S)and desflurane (D) [1–3 MAC (minimum alveolar concentration)]on heart rate and heart rate variability (HRV) as a measureof cardiac vagal activity in seven dogs. HRV was analysed inthe time domain as the standard deviation of the RR interval(SDNN) and in the frequency domain as power in the high-frequency(HF, 0.15–0.5 Hz) and low-frequency (LF, 0.04–0.15 Hz)ranges. Heart rate increased with anaesthetic concentrationand there were corresponding decreases in SDNN, HF power and LFpower. Heart rate increased most with D (+40 beats min^–1),least with H (+8 beats min^–1) and to an intermediate extentwith S, I and E. SDNN and HF power, as measures of vagal activity, changedin the opposite direction and decreased in the same order asheart rate increased. However, SDNN and HF power correlatedsignificantly with heart rate [r=–0.81 (0.04) and –0.81 (0.03)respectively] and were independent of the anaesthetic and its concentration(P<0.05). Consistent with our hypothesis, these results suggestthat differences between agents in the degree of increase inheart rate are explained by differences in their vagolytic action. Br J Anaesth 2001; 87: 748–54     

Effects of helium on high frequency jet ventilation in model of airway stenosis

Background. The addition of helium to the inspired gas may facilitateventilation in the presence of clinically evident upper airwayobstruction. However, there are no data on the effects of usinga helium–oxygen mixture during high frequency jet ventilation(HFJV) in upper airway obstruction. Methods. HFJV at a frequency of 150 min^–1 (driving pressure2 bar, inspiratory time 30%) was applied to a trachea–lungmodel to simulate ventilation through varying degrees of fixedlaryngotracheal stenosis (2.5–8.5 mm). HFJV was deliveredfrom above, through and below the level of stenosis to simulatesupraglottic, transglottic and infraglottic administration.Measurements of distal tracheal pressures were repeated foreach route at steady state for each stenosis diameter usingboth 100% oxygen and helium–oxygen (50% oxygen, 50% helium).The output of the ventilator was measured during operation onoxygen and helium–oxygen. Results. Peak, mean and end-expiratory pressures were greaterduring simulated supraglottic HFJV than during transglotticand infraglottic HFJV, and pressures increased markedly as thediameter of the stenosis decreased for all routes of ventilation(P<0.001). Generated pressures during HFJV using helium–oxygenand 100% oxygen were very similar overall, although reductionsin pressures were observed during ventilation with helium–oxygenvia the transglottic and transtracheal routes at stenosis diameters<4 mm (P<0.05). However, HFJV with the helium–oxygenmixture increased the delivered gas volumes by     

Effects of carbon dioxide vs helium pneumoperitoneum on hepatic blood flow

Background: Elevated intraabdominal pressure due to gas insufflation for laparoscopic surgery may result in regional blood flow changes. Impairments of hepatic, splanchnic, and renal blood flow during peritoneal insufflation have been reported. Therefore we set out to investigate the effects of peritoneal insufflation with helium (He) and carbon dioxide (CO₂) on hepatic blood flow in a porcine model. Methods: Twelve pigs were anesthetized and mechanically ventilated with a fixed tidal volume after the stabilization period. Peritoneal cavity was insufflated with CO₂ (n= 6) or He (n= 6) to a maximum intraabdominal pressure of 15 mmHg. Hemodynamic parameters, gas exchange, and oxygen content were studied at baseline, 90 mm and 150 min after pneumoperitoneum, and 30 min after desufflation. Determination of hepatic blood flow with indocyanine green was made at all measured points by a one-compartment method using hepatic vein catheterization. Results: A similar decrease in cardiac output was observed during insufflation with both gases. Hepatic vein oxygen content decreased with respect to the baseline during He pneumoperitoneum (p < 0.05), but it did not change during CO₂ insufflation. Hepatic blood flow was significantly reduced in both the He and CO₂ pneumoperitoneums at 90 min following insufflation (63% and 24% decrease with respect to the baseline; p < 0.001 and p < 0.05, respectively) being this decrease marker in the He group (p= 0.02). Conclusions: These findings suggest that helium intraperitoneal insufflation results in a greater impairment on hepatic blood flow than CO₂ insufflation. Received: 27 March 1996/Accepted: 19 January 1997     

Estimation of Volume Doubling Time and Cell Loss in an Experimental Rat Glioma Model in Vivo

Summary  We estimated the volume doubling time (Vd) of the ethylnitrosourea-induced rat glioma by serial magnetic resonance imaging, and the results were compared with potential doubling time (Tp) determined immunohistochemically.  Vd ranged from 3.3 to 29.2 days (11.03±7.74) and Tp ranged from 2.3 to 13.3 days (6.81±3.33). Each tumour showed a wide range of bromodeoxyuridine (BUdR) labelling indices (LI), however, Vd and Tp correlated well with BUdR-LI. Vd was estimated as 17.6×BUdR-LI^−0.63 (R=−0.76, P<0.001, n=13) and Tp was estimated as 22.6×BUdR-LI^−1.02 (R=−0.92, P<0.0001, n=12).  In addition, we compared the apoptotic indices (AI), determined by terminal deoxynucleotidyltransferase(Tdt)-mediated biotinylated dUTP-biotin nick-end labelling (TUNEL) techniques, with BUdR-LI and mitoses indices (MI). The results were: AI=0.23+0.25Ln(BUdR-LI) (R=0.971, n=8, P<0.0001) and AI=1.05+0.29Ln(MI) (R=0.937, n=8, P<0.001). Cell loss factors (CLF) also correlated well with BUdR-LI and MI. However, CLF calculated from Tp and Vd were lower than the values previously presumed, probably because of shorter Vd than true doubling time for tumour cell population. These results suggest that even malignant tumours retain a mechanism of adjusting their growth at least partly.     

Treatment of cardiogenic shock with levosimendan in combination with beta-adrenergic antagonists

Levosimendan, a calcium sensitizer, was used in combinationwith ß-adrenergic antagonists in a man aged 56 yrwith cardiogenic shock, complicating acute myocardial infarction,who developed severe tachycardia after dobutamine administration.The patient's trachea was intubated, his lungs were ventilated,and he was started on dopamine 5 µg kg^–1 min^–1and dobutamine 5 µg kg^–1 min^–1, titrated toa mean arterial pressure 65 mm Hg. He progressively became tachycardiac(>120 beats min^–1) with a cardiac index (CI) of 1.4litre min^–1 m^–2 despite adequate preload. Levosimendan6 µg kg^–1 was administered intravenously over 10min followed by a continuous infusion of 0.2 µg kg^–1min^–1 for 24 h. Within 30 min, the patient's CI increasedto 2.2 litre min^–1 m^–2, but the heart rate (HR)also increased from 142 to 155 beats min^–1. Esmolol 1mg kg^–1 i.v. was administered with a consequent transientdecrease in HR to 110 beats min^–1 without adverse haemodynamiceffects; however, HR increased again shortly afterwards. Carvedilol3.125 mg orally twice a day was then administered, and the dosewas increased to 6.25 mg orally twice daily on the followingday. Subsequently, HR decreased over time and both catecholamineswere discontinued 14 h after starting levosimendan infusion.The trachea was extubated within 20 h and the patient was dischargedto the ward on day 4 after admission. In conclusion, levosimendanin combination with a ß-adrenergic antagonist mayhave beneficial effects in patients with cardiogenic shock whoexhibit tachycardia in response to inotropic agents.     

The predictive value of the base deficit for the cardiac index in post-arrest patients in the intensive care unit

We undertook a retrospective clinical study to determine therelationship of the calculated base deficit and cardiac indexin post cardiac arrest patients admitted to the intensive careunit. Twenty consecutive admissions to an 8-bed general adult intensivecare unit over a 2-yr period mean age 62.9 yr (range 24–86)included 17 males and 3 females with a diagnosis of post-cardio-respiratoryarrest were studied. All patients were receiving mechanicalventilation and had an arterial line and a pulmonary arterycatheter inserted on admission. Serial arterial blood gases and cardiac output measurementstaken were reviewed for the first 24 h of admission from thecase notes. The number of measurements recorded ranged fromfour to nine arterial gas samples over the 24 h. The cardiacoutput was measured using thermodilution with 10 ml of coldsaline. All the data were collected from measurements takenwithin 20 min of each other. Linear regression analysis demonstratedno consistent relationship between the calculated base deficitand cardiac index (r = 0.02, P = 0.82) when data were pooledfor the study group. In four of the study group however, thereappeared to be a good relationship (r = –0.78, r = –0.76,r = –0.82, r = 0.79: P<0.05) but this was not reflectiveof the overall trend (Table 23). Three patients showed a strongnegative correlation that is as the cardiac index decreasedthe base deficit increased and one the opposite trend. Our data suggest that the calculated base deficit is a poorpredictor of the cardiac index in post cardiac arrest patients.We recommend that the base deficit should be applied with cautionin the clinical assessment of cardiac output.     

CARDIOVASCULAR EFFECTS OF I.V. INDUCTION IN CHILDREN: COMPARISON BETWEEN PROPOFOL AND THIOPENTONE

We have compared the haemodynamic responses to i.v. propofol2.5 mg kg^-1 with those to thio-pentone 5.0 mg kg^-1 in 41 healthyChinese children at induction of anaesthesia. They were allocatedto four groups according to their age and induction agent received:group 1 <2yr, propofol, n = 9; group II < 2 yr, thiopentone,n = 9; group III 2–12 yr. propofol, n = 12; group IV 2–12yr, thiopentone, n = 11. Anaesthesia was maintained by spontaneousventilation with 70% nitrous oxide and 0.5% halothane in oxygen.Arterial pressure and heart rate were monitored by automaticoscillo -tonometer. Stroke volume was measured by two-dimensionalechocardiography and pulse Dopper. Measurements were made beforeinduction and at 1-min intervals for 5 min after induction.The reduction in mean arterial pressure was significantly greaterafter propofol (28–31%) than after thiopentone (14–21%)(P = 0.001). The reduction in cardiac index (10–15%) afterinduction was not significantly different between the two agents(P = 0.122). Baroref/ex mediated increases in heart rate andsystemic vascular resistance were less after propofol than afterthiopentone. The baroreceptor reflex was more attenuated inchildren aged less than 2 yr than in older children. (Br. J.Anaesth. 1993; 70: 647–653) ^*Present address: Department of Anaesthesia, Addenbrookes Hospital,Hills Road, Cambridge     

COMPARISON OF THE MAGILL AND LACK ANAESTHETIC BREATHING SYSTEMS IN ANAESTHETIZED PATIENTS

The Magill and Lack anaesthetic breathing systems were comparedby measuring inspired and expired carbon dioxide concentrationsand expired minute volumes in lightly anaesthetized, unstimulatedsubjects. There were no significant differences between thetwo breathing systems at fresh gas flow rates of approximately50 and 70 ml kg^–1 min^–1. Inspired carbon dioxideconcentrations increased in one of six subjects at the higherfresh gas flow rate using the Magill system and in two usingthe Lack system. Inspired carbon dioxide concentration did notincrease in only one of six subjects at the lower fresh gasflow rate with both systems. Expired carbon dioxide concentrationsand expired minute volume increased in the majority of subjectsat both fresh gas flow rates using each system. We concludethat a fresh gas flow rate greater than 70 ml kg^–1 min^–1(which approximated to alveolar minute volume in our subjects)should be supplied to the Magill and Lack breathing systems. ^*Present address: Burton General Hospital, New Street, Burtonupon Trent, Staffordshire DE14 3QH.     

SELECTIVE DEPRESSION BY ALFENTANIL OF GROUP III AND IV SOMATOSYMPATHETIC REFLEXES IN THE DOG

The effect of alfentanil on sympathetic reflexes evoked by supramaximalelectrical stimulation of the radial nerve has been observedin five dogs anaesthetized with -chloralose, paralysed withsuxamethonium and artificially ventilated. In five dogs duringthe infusion of alfentanil at a rate of 20 µg kg^–1min^–1 the late long latency sympathetic response evokedby unmyelinated fibres (group IV, C) was abolished at a meandose of 68.8 (SE 2.85) µg kg^–1. The infusion ratewas then increased to 200 µg kg^–1 min^–1 andthe early, short latency response evoked by small myelinatedfibres (group III, A) was eliminated at mean total dose of 809(SE 72) µg kg^–1. When the infusion was stopped thegroup III reflex returned within 1–5 min and recoveryto approximately 50% of control for both reflexes occurred within15–60 min in different preparations. Mean arterial pressureand mean heart rate decreased from 140 (6) mm Hg and 132 (11)beat min^–1 to 100 (7) mm Hg and 70 (6) beat min^–1,respectively, by the time the group IV response was eliminated;that is, after a mean infusion time of 3.4 min. Thereafter,there was no further cardiovascular depression. Within 3 minof the administration of naloxone 2 mg i.v., the sympatheticreflexes, arterial pressure and heart rate returned to withincontrol values.     

Erythropoietin therapy and preoperative autologous blood donation in children undergoing open heart surgery

We assessed the feasibility and efficacy of subcutaneous erythropoietinalpha (EPO) therapy and preoperative autologous blood donation(ABD) in children undergoing open heart surgery. Thirty-ninechildren were treated consecutively with EPO (100 U kg^–1s.c. three times a week in the 3 weeks preceding the operationand i.v. on the day of surgery) and two ABDs were made (Group 1).As controls to compare transfusion requirements, 39 consecutiveage-matched patients who had undergone open heart surgery duringthe two preceding years were selected (Group 2). In a meantime of 20 (SD 5) days, 96% of scheduled ABDs were performedand only three mild vasovagal reactions were observed. The meanvolume of autologous red blood cells (RBC) collected was 6 (1) ml kg^–1and the mean volume of autologous RBC produced as a result ofEPO therapy before surgery was 7 (3) ml kg^–1,corresponding to a 28 (11)% increase in circulating RBC volume.The mean volume of autologous RBC collected was not differentfrom that produced [6 (1) vs 7 (3) ml kg^–1,P=0.4]. Allogenic blood was administered to three out of 39children in Group 1 (7.7%) and to 24 out of 39 (61.5%) in Group2. Treatment with subcutaneous EPO increases the amount of autologousblood that can be collected and minimizes allogenic blood exposurein children undergoing open heart surgery. Br J Anaesth 2001; 87: 429–34     

Cardioprotection by sevoflurane against reperfusion injury after cardioplegic arrest in the rat is independent of three types of cardioplegia

Background. Sevoflurane protects the heart against reperfusioninjury even after cardioplegic arrest. This protection may dependon the cardioplegic solution. Therefore, we investigated theeffect of sevoflurane on myocardial reperfusion injury aftercardioplegic arrest with University of Wisconsin solution (UW),Bretschneider’s cardioplegia (HTK), and St Thomas’Hospital solution (STH). Methods. We used an isolated rat heart model where heart rate,ventricular volume, and perfusion pressure were constant. Thehearts underwent 30 min of normothermic ischaemia followed by60 min of reperfusion. Seven groups were studied (n=9 each).Three groups received 7°C cold cardioplegic solutions (UW,HTK, STH) during the first 2 min of ischaemia at a flow of 2ml min^–1. In three groups (UW+Sevo, HTK+Sevo, STH+Sevo),sevoflurane was additionally added to the perfusion medium (membraneoxygenator) at 3.8% (1.5 MAC) during the first 15 min of reperfusionafter cardioplegic arrest. Nine hearts served as untreated controlgroup (control). We measured left ventricular developed pressure(LVDP) and infarct size. Results. LVDP was similar in all groups during baseline (130(SEM 2) mm Hg). HTK and STH improved recovery of LVDP duringreperfusion from 5 (1) (control) to 67 (7) (HTK) and 52 (8)mm Hg (STH, both P<0.05), while UW had no effect on myocardialfunction (7 (2) mm Hg). In the sevoflurane-treated groups, LVDPat the end of the experiments was not significantly differentfrom the respective group without anaesthetic treatment (UW+Sevo11 (2); HTK+Sevo 83 (8); STH+Sevo 64 (8) mm Hg; P=ns). Infarctsize was reduced in the HTK and STH groups (HTK 20 (4); STH17 (3)%; P<0.05) compared with controls (39 (5)%; P<0.05),but not in the UW group (52 (4)%). Compared with cardioplegiaalone, sevoflurane treatment during reperfusion reduced infarctsize (UW+Sevo 31 (4); HTK+Sevo 8 (1); STH+Sevo 4 (1)%; P<0.05). Conclusion. We conclude, that the protection against reperfusioninjury offered by sevoflurane is independent of the three cardioplegicsolutions used. Br J Anaesth 2002; 88: 828–35     

Adenosine-induced cardiac arrest and EEG changes in patients with thoracic aorta endovascular repair

Background. We studied haemodynamic and metabolic variables,and cerebral function after cardiac arrest induced by high doseof adenosine in patients undergoing thoracic aorta endovascularrepair. Methods. Arterial blood pressure, blood gas values and EEG wererecorded continuously in 15 patients undergoing anaesthesia(isoflurane) for endovascular thoracic aorta repair. Cardiacarrest was induced by different doses of adenosine (Adrekar®,Sanofi-Synthelabo, Berlin, Germany; 0.4–1.8 mg kg^–1body weight). Serum concentrations of neurone-specific enolase(NSE) were determined before and after stent graft implantation.Neurological function was assessed before and after surgery. Results. After adenosine, the heart beat stopped immediatelyfor 18–58 s in close relation to the adenosine dose. EEGpower was significantly reduced to –57%, but reached normalvalues within 5 min after cardiac arrest. In particular, thefast alpha- and beta-EEG-frequencies sensitively reflected patients'EEG activity during the procedure. No intraoperative increasesin NSE concentrations, and no neurological dysfunctions aftersurgery, were observed. Conclusion. After adenosine-induced cardiac arrest, changesin haemodynamic variables and EEG power spectra reversed completelywithin 1 and 5 min, respectively, without persistent brain dysfunctionafter stent graft implantation.     

Cardioventilatory coupling in heart rate variability: the value of standard analytical techniques

In a group of spontaneously breathing anaesthetized subjects,we examined the ability of simple spectral and non-linear methodsto detect the presence of cardioventilatory coupling in heartrate time series. Using the proportional Shannon entropy (H_RI–1)of the RI_–1 interval (interval between inspiration andthe preceding ECG R wave) as a measure of coupling, we foundno correlation between H_RI–1 and either the fractal dimensionor approximate entropy of the heart rate time series. We alsoobserved no difference in the distribution of heart rate variability(HRV) spectral power in three frequency ranges (high, 0.15–0.45 Hz;low, 0.08–0.15 Hz; very low, 0.02–0.08 Hz)between uncoupled epochs and coupling patterns I, III and IV.Because of its association with low breathing frequencies, patternII coupling epochs showed exaggerated low-frequency power asthe high-frequency ‘respiratory’ peak fell intothe low-frequency range. We conclude that coupling pattern islargely independent of autonomic tone and that these standardmethods of HRV analysis are limited in their ability to detectthe presence of cardioventilatory coupling in heart rate timeseries. Br J Anaesth 2001; 87: 819–26     

Sinus bradycardia associated with traumatic haemothorax

A 39-year-old male suffered a closed chest deceleration injury.He presented with clinical and radiological signs consistentwith trauma to the thoracic aorta, but also developed sinusbradycardia which was relieved by drainage of a haemothorax.The possible mechanisms of the changes in heart rate are discussedand direct compression of the vagus nerve is proposed to explainthis previously unreported finding. (Br. J. Anaesth. 1994; 72:358–360)