Near-infrared spectroscopy in adults: effects of extracranial ischaemia and intracranial hypoxia on estimation of cerebral oxygenation

We have studied the effects of extracranial ischaemia and intracranialhypoxia on measurement of cerebral oxygenation using near-infrared,reflectance-mode, cerebral oximetry (Invos 3100 cerebral oximeter)in healthy adult subjects. Under stable systemic conditions,scalp ischaemia induced by a pneumatic tourniquet caused anapparent reduction in mean regional cerebral oxygenation (rSo₂)from mean 72 (SD 6)% to 59 (7)% (n = 8, P < 0.001). rSo₂returned to control values within 1 min of release of the tourniquet.Local scalp ischaemia induced by rapid frontalis muscle exercisecaused a significant reduction (4.5 (2)%) in rSo₂ (n = 12, P< 0.001). The effect of systemic hypoxia on rSo₂ was examinedduring controlled scalp ischaemia. A decrease in mean SpO₂ from98 (2)% to 66 (6)% was associated with a decrease in mean rSo₂from 57 (4)% to 41 (6)%. There was a significant correlationbetween the percentage reduction in rSo₂ and Sp_o2 during hypoxia(r = 0.81, P < 0.001). We conclude that the lnvos cerebraloximeter was capable of detecting tissue hypoxia deep to thescalp under carefully controlled conditions but that it alsowas affected significantly by changes in extracranial bloodflow and oxygenation which may affect its reliability in clinicalpractice. Further work is necessary to define those situationsin which cerebral oximetric monitoring is useful and valid.     

Observational study of perioperative PtcCO2 and SpO2 in non-ventilated patients receiving epidural infusion or patient-controlled analgesia using a single earlobe monitor (TOSCA)

Background: TOSCA, a non-invasive monitor with a single earlobe probe incorporatinga Stow–Severinghaus electrode and optical sensor (LindeMedical Sensors AG, Basel, Switzerland), has previously beenused with ventilated patients and in sleep laboratories. Werecorded transcutaneous carbon dioxide pressures (Ptc_CO2) andoxygen saturations (Sp_O2) in non-ventilated patients to investigateopioid-induced respiratory depression. Methods: This observational cohort study included 28 ASA I and II patients,monitored between 10 p.m. and 6 a.m., before and after electivemajor laparotomy. After operation, patients were kept on oxygen,4 litre min^–1, and received either bupivacaine (0.1%)containing fentanyl (2 µg ml^–1) via epidural catheter(epidural analgesia group, EPI; n = 14) or morphine via patient-controlledanalgesia infusion pump (PCA-morphine group, PCA; n = 14). Results: The preoperative median (lower/upper quartile) Ptc_CO2 was similarin both groups at around 5.5 kPa, but significantly higher afteroperation in PCA with 6.9 kPa (5.6/7.3) (P = 0.02), accompaniedby a longer hypercarbia time >6 kPa of 6.6 h (0.1/8.0) (P= 0.04), and lower respiratory rates of 13.9 breaths min^–1(13.3/15.4) (P = 0.04). In EPI, the corresponding results were5.8 kPa (5.5/6.0), 1.2 h (0.1/4.3), and 16.2 breaths min^–1(14.8/16.7). The perioperative median Sp_O2 in both groups wascomparable within the normal range, although generally higherwhen on supplemental oxygen (P = 0.26). The Sp_O2 time <94%was similar in both groups (P = 0.33) as were pain scores (P= 0.25). Conclusions: Ptc_CO2 recording in patients on PCA-morphine and supplementaloxygen revealed hypercapnia in the presence of normal respiratoryrates and Sp_O2 values. This is recommended as an easy and sensitivemonitor of respiratory depression and may have a role in thesafe administration of opioid-analgesia.     

POSTOPERATIVE ANALGESIA AFTER PAEDIATRIC ORCHIDOPEXY: EVALUATION OF A BUPIVACAINE-MORPHINE MIXTURE

The value of combining morphine with bupi-vacaine for caudalanalgesia was investigated. Thirty children, undergoing orchidopexy,received a caudal block of 0.125% bupivacaine with or withoutmorphine 0.05 mg kg^–1. Analgesia, side-effects, ventilatoryfrequency and oxygen saturation (Sa_o2) were recorded after operation.None of the 15 patients receiving the bupivacaine-morphine mixturerequired postoperative opioids, whereas eight of 15 patientsreceiving bupivacaine alone needed additional opioid analgesia.The incidence of side effects after surgery was similar forthe two groups and there was no detectable difference in ventilatoryfrequency or Sa_o2. The pilot study to this paper was presented to the AnaestheticResearch Society and subsequently published in British Journalof Anaesthesia 1989; 62: 221P.     

Tracheal tube pressure change during magnetic stimulation of the phrenic nerves as an indicator of diaphragm strength on the intensive care unit

Diaphragm strength can be assessed from twitch gastric (TwPgas),twitch oesophageal (TwPoes), and twitch transdiaphragmatic pressure(TwPdi) in response to phrenic nerve stimulation. This requiresthe passage of balloon catheters, which may be difficult. Changesin pressure measured at the mouth during phrenic nerve stimulationavoid the need for balloon catheters. We hypothesized that pressuresmeasured at the tracheal tube during phrenic stimulation, couldalso reflect oesophageal pressure change as a result of isolateddiaphragmatic contraction and, therefore, reflect diaphragmstrength. We aimed to establish the relationship between twitchtracheal tube pressure (TwPet), TwPoes, and TwPdi in patientsin the supine and sitting positions. The phrenic nerves werestimulated magnetically bilaterally, in 14 ICU patients whilesupine and on another occasion while sitting up at 45°.In the sitting position mean TwPoes was 9.1 cm H₂O and TwPet11.3 cm H₂O (mean (SD) difference –2.2 (SD 1.5)). In thesupine position mean TwPoes was 8.1 cm H₂O and TwPet 9.9 cmH₂O (mean difference –1.8 (2.2)). The difference betweenTwPoes and TwPet was less at low twitch amplitude; less than±1 cm H₂O below a mean twitch height of 8 cm H₂O supineand 10 cm H₂O sitting. Sitting TwPet was related to TwPoes r²=0.93and TwPdi r²=0.65 (P<0.01). Supine TwPet was related to TwPoesr²=0.84 and TwPdi r²=0.83 (P<0.01). The mean within occasioncoefficient of variation while sitting was TwPet=13.3%, TwPoes=13.9%,TwPdi=11.2%, and supine TwPet=11.6%, TwPoes=14.6%, TwPdi=11.8%.We conclude that TwPet reflects TwPoes during diaphragmaticstimulation and is worthy of further study to establish itsplace as a guide to the presence of respiratory muscle strengthand fatigue. Br J Anaesth 2001; 87: 876–84     

ANALYSIS OF POSSIBLE FACTORS INFLUENCING Pao2 AND (PAo2--Pao2) IN PATIENTS AWAITING OPERATION

Data on arterial oxygen tension (Pa_o²) and alveolar—arterialPo₂ difference (PA_o²—Pa_o²) have been obtained from 337patients awaiting elective surgery. Statistical analysis ofthese data has assessed both the individual and the combinedinfluence of various factors on Pa_o² and (PA_o²—Pa_o²).The factors of importance in relation to Pa_o² include age, smokinghabits, body build and PA_o². In relation to (PA_o²—Pa_o²)the significant factors include age, Pa_CO2, weight and smokinghabits.     

NITROUS OXIDE SEDATION CAUSES POST-HYPERVENTILATION APNOEA

We have studied, in six normal subjects, the effect of nitrousoxide sedation on the ventilatory pattern and oxygen saturationusing pulse oximetry (Sp_O2) after hyperventilation to an endtidalcarbon dioxide partial pressure (P_CO2) of 3 kPa. This valueof P_CO2 was shown to be less than the apnoeic threshold of allthese subjects when their ventilation vs P_CO2 response curveswere plotted. All subjects became apnoeic when told to relaxfollowing hyperventilation while breathing 75% nitrous oxidefor 90 s. Apnoea was defined as cessation of breathing for 20s or more. The mean duration of apnoea was 78 s (range 29–130s). All subjects demonstrated arterial desaturation (mean Sp_O275%, range 44–87%). In contrast, following hyperventilationwith air, no apnoea was seen in any subject, although therewas some evidence of desaturation (mean Sp_O2 92.5%, range 88–98%).It was concluded that subjects who are sedated with nitrousoxide behave similarly to those who are anaesthetized ratherthan to those who were fully conscious, in that they becomeapnoeic below the apnoeic threshold point. The reduction inSp_O2 after hyperventilation was explained almost entirely byapnoea and may explain abnormalities of respiratory controland hypoxaemia in patients recovering from general anaesthesiaor sedation accompanied by hypocapnia. This mechanism may beof importance in obstetric patients after breathing Entonox,when apnoea and hypoxaemia may reduce oxygen delivery to thefetus. This work was presented to the Anaesthetic Research Societyat the Nottingham Meeting in July 1990. ^*Present address: Doncaster Royal Infirmary, Doncaster.     

EFFECTS OF SUBARACHNOID SPINAL NERVE BLOCK AND ARTERIAL PCO2 ON COLON BLOOD FLOW IN THE DOG

Changes in colon blood flow in greyhounds were measured in responseto acute changes in arterial PCO₂, before and after spinal nerveblock. Colon blood flow increased significantly after spinalnerve block, irrespective of PCO₂. The findings may be of clinicalimportance in man. ^*University Department of Anaesthesia, The General Hospital,Gwendolen Road, Leicester. Department of Surgery, Royal Infirmary, Glasgow. Victoria Infirmary, Glasgow.     

CARBOXYHAEMOGLOBINAEMIA AND PULSE OXIMETRY

We compared measurements obtained with a pulse oximeter (Sp_O2)against values obtained from a CO-oximeter in a patient withcarbon monoxide poisoning. Sp_O2was equal to the sum of the oxyhaemoglobin(HbO) and carboxy haemoglobin (HbCO) values over the range ofHbCO from 30 to 1%. This confirms the experimental findingsthat pulse oximeters measure HbCO as HbO. The patient was treatedwith oxygen (Fl_O2 = 50%) and recovered without any sequelae.Under these circumstances, the half-life of HbCO was approximately2 h.     

Influence of carbamazepine on the dose-response relationship of vecuronium

We have determined the cumulative dose-response relationshipfor vecuronium from the evoked compound electromyogram of thehypothenar muscles in eight patients who were receiving carbamazepine.The ED₅₀, ED₉₀ and ED₉₅ were 29, 52 and 64 µg kg^–1,respectively, and were significantly different (P < 0.05)from those of a control group (ED₅₀, ED₉₀ and ED₉₅ 21, 36 and44 µg kg^–1, respectively). (Br. J. Anaesth. 1994;72: 125–126) Presented at the 10th World Congress of Anaesthesiologists,The Hague, The Netherlands, June 1992.     

ON-LINE Po2 AND PN2o ANALYSIS WITH AN IN VIVO CATHETER ELECTRODE

A technique was developed for the in vivo determination of Po₂and PN₂o with a catheter electrode using double-pulse polarography.The method was evaluated in dog studies comparing readings fromthe electrode with those from a mass spectrometer employingan in vivo probe. The oxygen readings obtained from the catheterelectrode were also compared with values obtained by conventionalblood-gas analysis. Good agreement was observed between theelectrode and the mass spectrometer for both Po₂ and PN₂o. Similaragreement was found between the electrode readings and blood-gasanalysis for Po₂. In the presence of halothane, the electrodeover-read for both Po₂ and PN₂O; a remedy is suggested. Thein vivo electrode provides an effective, less expensive, alternativeto the mass spectrometer for the on-line measurement of Po₂,and PN₂o in vivo. ^*Also Physical Chemistry Laboratory, University of Oxford.     

Regional response of cerebral blood volume to graded hypoxic hypoxia in rat brain

Background. The response of cerebral blood flow to hypoxic hypoxiais usually effected by dilation of cerebral arterioles. However,the resulting changes in cerebral blood volume (CBV) have receivedlittle attention. We have determined, using susceptibility contrastmagnetic resonance imaging (MRI), changes in regional CBV inducedby graded hypoxic hypoxia. Methods. Six anaesthetized rats were subjected to incrementalreduction in the fraction of inspired oxygen: 0.35, 0.25, 0.15,and 0.12. At each episode, CBV was determined in five regionsof each hemisphere after injection of a contrast agent: superficialand deep neocortex, striatum, corpus callosum and cerebellum.A control group (n=6 rats) was studied with the same protocolwithout contrast agent, to determine blood oxygenation leveldependent (BOLD) contribution to the MRI changes. Results. Each brain region exhibited a significant graded increasein CBV during the two hypoxic episodes: 10–27% of controlvalues at 70% Sa_O2, and 26–38% at 55% Sa_O2. There wasno difference between regions in their response to hypoxia.The mean CBV of all regions increased from 3.6 (SD 0.6) to 4.1(0.6) ml (100 g)^–1 and to 4.7 (0.7) ml (100 g)^–1during the two hypoxic episodes, respectively (SchefféF-test; P<0.01). Over this range, CBV was inversely proportionalto Sa_O2 (r²=0.80). In the absence of the contrast agent, changesdue to the BOLD effect were negligible. Conclusions. These findings imply that hypoxic hypoxia significantlyraises CBV in different brain areas, in proportion to the severityof the insult. These results support the notion that the vasodilatoryeffect of hypoxia is deleterious in patients with reduced intracranialcompliance. Br J Anaesth 2002; 89: 287–93     

Impact of peripheral elimination on the concentration-effect relationship of remifentanil in anaesthetized dogs

Background. This study elucidates the impact of sampling sitewhen estimating pharmacokinetic-pharmacodynamic (PK-PD) parametersof drugs such as remifentanil that undergo tissue extractionin the biophase. The interrelationship between the concentrationsof remifentanil predicted for the effect compartment and thosemeasured in arterial, venous, and cerebrospinal fluid were investigatedunder steady-state conditions. Methods. Following induction of anaesthesia with pentobarbital,an arterial cannula (femoral) and two venous catheters (jugularand femoral) were inserted. Electrodes were placed for EEG recordingof theta wave activity. Each dog received two consecutive 5-mininfusions for the PK-PD study and a bolus followed by a 60-mininfusion was started for the steady-state study. Cerebrospinalfluid, arterial and venous blood samples were drawn simultaneouslyafter 30, 40, and 50 min. At the end of the infusion, arterialblood samples were collected for pharmacokinetic analysis. Results. Remifentanil PK-PD parameters based on theta wave activitywere as follows: apparent volume of distribution at steady-state(V_ss) (231±37 ml kg^–1), total body clearance (Cl)(63±16 ml min^–1 kg^–1), terminal eliminationhalf-life (t_1/2ß) (7.71 min), effect compartment concentrationat 50% of maximal observed effect (EC₅₀) (21±13 ng ml^–1),and equilibration rate constant between plasma and effect compartment(k_e0) (0.48±0.24 min). The mean steady-state cerebrospinalfluid concentration of 236 ng ml^–1 represented 52 and74% of that in arterial and venous blood, respectively. Conclusions. Our study re-emphasizes the importance of a samplingsite when performing PK-PD modelling for drugs undergoing eliminationfrom the effect compartment. For a drug undergoing tissue eliminationsuch as remifentanil, venous rather than arterial concentrationswill reflect more exactly the effect compartment concentrations,under steady-state conditions. Declaration of interest. Remifentanil was provided by AbbottLaboratories.     

Transoesophageal echocardiography for the detection and quantification of pleural fluid in cardiac surgical patients

Background: Transoesophageal echocardiography (TOE) can image pleural fluid.Left pleural collections may be easier to detect than right,as the thoracic aorta serves as an acoustic window. Attemptsto quantify pleural fluid using TOE are restricted to a casereport in which volume was predicted by multiplying maximalcross-sectional area (CSA_max) by axial length (AL). A computedtomography (CT) derived formula for quantifying pleural effusionsis maximal effusion depth squared (d²) multiplied by maximaleffusion length. Methods: Eight patients were studied before chest closure following coronarybypass surgery. Fifty millilitre saline aliquots were instilledinto the pleural space until detected by TOE. Saline was theninstilled up to the next 200 ml increment and further 200 mlaliquots added until it spilled from the pleural space. CSA_max,d and AL were measured for each stage and used to calculatepleural fluid volume. Results: Median detection volume (range) was 125 ml (50–200) onthe left and 225 ml (150–300) on the right (P = 0.016).Volume calculated by CSA_max x AL correlated strongly with actualvolume (r² = 0.93 left and 0.92 right) as did volume calculatedby d² x AL (r² = 0.86 left and 0.89 right). Mean differencebetween volume calculated by CSA_max x AL and actual volume was– 51 ml on the left and 45 ml on the right vs –253 ml on the left and – 212 ml on the right for volumecalculated by d² x AL. Conclusions: TOE detects small volumes of pleural fluid on both sides ofthe chest. CSA_max x AL provides a reasonably accurate measureof pleural fluid volume.     

Effects of short-term simultaneous infusion of dobutamine and terlipressin in patients with septic shock: the DOBUPRESS study

Background: Terlipressin bolus infusion may reduce cardiac output and globaloxygen supply. The present study was designed to determine whetherdobutamine may counterbalance the terlipressin-induced depressionin mixed-venous oxygen saturation (Sv_O2) in patients with catecholamine-dependentseptic shock. Methods: Prospective, randomized, controlled study performed in a universityhospital intensive care unit. Septic shock patients requiringa continuous infusion of norepinephrine (0.9 µg kg^–1min^–1) to maintain mean arterial pressure (MAP) at 70(SD 5) mm Hg were randomly allocated to be treated either with(i) sole norepinephrine infusion (control, n=20), (ii) a singledose of terlipressin 1 mg (n=19), or (iii) a single dose ofterlipressin 1 mg followed by dobutamine infusion titrated toreverse the anticipated reduction in Sv_O2 (n=20). Systemic,pulmonary, and regional haemodynamic variables were obtainedat baseline and after 2 and 4 h. Laboratory surrogate markersof organ (dys)function were tested at baseline and after 12and 24 h. Results: Terlipressin (with and without dobutamine) infusion preservedMAP at 70 (5) mm Hg, while allowing to reduce norepinephrinerequirements to 0.17 (0.2) and 0.2 (0.2) µg kg^–1min^–1, respectively [vs1.4 (0.3) µg kg^–1 min^–1in controls at 4 h; each P<0.001]. The terlipressin-linkeddecrease in Sv_O2 was reversed by dobutamine at a mean dose of20 (8) µg kg^–1 min^–1 [Sv_O2 at 4 h: 59 (11)%vs 69 (12)%, P=0.028]. Conclusions: In human catecholamine-dependent septic shock, terlipressin(with and without concomitant dobutamine infusion) increasesMAP and markedly reduces norepinephrine requirements. Althoughno adverse events were noticed in the present study, potentialbenefits of increasing Sv_O2 after terlipressin bolus infusionneed to be weighted against the risk of cardiovascular complicationsresulting from high-dose dobutamine.     

RELATIONSHIP BETWEEN ALVEOLAR DEADSPACE AND ARTERIAL OXYGENATION IN CHILDREN WITH CONGENITAL CARDIAC DISEASE

Fifty-eight children were studied during nitrous oxide in oxygenand fentanyl anaesthesia before undergoing closed or open cardiacsurgery. Fl_O2 was 0.5. Alveolar deadspace was measured usingthe carbon dioxide single breath test (SBT-CO₂) obtained froma computerized online system for monitoring expired CO₂ andairway flow, based on the Servo ventilator, Arterial blood wassampled simultaneously for measurement of Pa_Co2 and Pa_O2. Therewas a marked reciprocal relationship between Pa_O2 and the alveolardeadspace fraction. In children with a normal pulmonary circulationand good oxy-genation, alveolar deadspace fraction was approx.0.05. Shunts which reduced Pa_O2 to 10 kPa produced a deadspacefraction of 0.15. When Pa_O2 was 3–4 kPa, alveolar deadspacefraction was approx. 0.4. In well-oxygenated children, alveolardeadspace fraction was only slightly greater than predictedby a model of the effects of pure right-to-left shunting. Inseverely cyanotic children, the discrepancy between predictedand observed VD^a/v/VT^a/v was greater. The mean arterial-end-tidalCO₂ difference was zero in children in whom Pa_O2 was greaterthan 10 kPa, despite a measurable alveolar deadspace. In severelyhypoxic children, the difference was 1–2 kPa. In a retrospectiveanalysis of published data from anaesthetized adults withoutintracardiac shunting, no relationship was found between alveolardeadspace and Pa_O2. Previously presented in abstract form (Br. J. Anaesth. (1987),59, 928P).     

VENTILATION AND GAS EXCHANGE DURING ANAESTHESIA AND SURGERY IN SPONTANEOUSLY BREATHING INFANTS AND CHILDREN

Minute ventilation (VE) (mlmin^–1), respiratory frequency(f), mixed expired carbon dioxide fraction (FCO₂ and end-tidalcarbon dioxide concentration E'CO₂) (%) were measured, and alveolarventilation (VA), deadspace (VD), deadspace/tidal volume ratio(VD/VT) and carbon dioxide output (VCO₂) calculated in 58 anaesthetized,spontaneously breathing infants and children weighing 2.8–20.5kg.Although minute volumes varied, tidal volume correlated wellwith weight (r = 0.83), with a mean tidal volume (± ISD)of 5.2±1.2mlkg^–1. It was concluded that, by theuse of mean VT + ISD (approximated to 6 ml kg^–1) the freshgas flow in mlmin^–1 should be set at 2.5x6xkgxf(15xkgxf)to avoid rebreathing in various T-piece systems in anaesthetized,intubated and spontaneously breathing infants up to a body weightof 20 kg. End-tidal carbon dioxide concentration was lower inyounger patients who were premedicated with atropine alone thanin the older ones who received opioid premedication also. Respiratoryfrequency, VD/VT and total VD per minute were higher in theyounger age group, which explained the finding of a high VEin relation to VCO₂ for these patients. This inefficiency ofventilation emphasizes the need to minimize apparatus deadspacein breathing systems used for small infants. ^*Department of Anaesthesia, University Hospital, S-22185 Lund,Sweden. Department of Anaesthesia, St George's Hospital, Blackshaw Road,London SW17.     

Beta2 adrenergic antagonist inhibits cerebral cortical oxygen delivery after severe haemodilution in rats

Background. Haemodilution has been associated with neurologicalmorbidity in surgical patients. This study tests the hypothesisthat inhibition of cerebral vasodilatation by systemic ß₂adrenergic blockade would impair cerebral oxygen delivery leadingto tissue hypoxia in severely haemodiluted rats. Methods. Under general anaesthesia, cerebral tissue probes wereplaced to measure temperature, regional cerebral blood flow(rCBF) and tissue oxygen tension (P_BrO₂) in the parietal cerebralcortex or hippocampus. Baseline measurements were establishedbefore and after systemic administration of either a ß₂antagonist (10 mg kg^–1 i.v., ICI 118, 551) or saline vehicle.Acute haemodilution was then performed by simultaneously exchanging50% of the estimated blood volume (30 ml kg^–1) with pentastarch.Arterial blood gases (ABGs), haemoglobin concentration (co-oximetry),mean arterial blood pressure (MAP) and heart rate (HR) werealso measured. Data were analysed using a two-way ANOVA andpost hoc Tukey's test [mean (SD)]. Results. Haemodilution reduced the haemoglobin concentrationcomparably in all groups [71 (9) g litre^–1]. There wereno differences in ABGs, co-oximetry, HR and MAP measurementsbetween control and ß₂ blocked rats, either beforeor 60 min after drug or vehicle administration. In rats treatedwith the ß₂ antagonist there was a significant reductionin parietal cerebral cortical temperature, regional blood flowand tissue oxygen tension, relative to control rats, 60 minafter haemodilution (P<0.05 for each). These differenceswere not observed when probes were placed in the hippocampus. Conclusion. Systemic ß₂ adrenergic blockade inhibitedthe compensatory increase in parietal cerebral cortical oxygendelivery after haemodilution thereby reducing cerebral corticaltissue oxygen tension.     

Cerebral hypoperfusion in immediate postoperative period following coronary artery bypass grafting, heart valve, and abdominal aortic surgery

Perioperative levels of jugular bulb oxyhaemoglobin saturation(Sj_O2) and lactate concentration (Lj), and postoperative durationof Sj_O2<50% were compared between patients undergoing coronaryartery bypass grafting (CABG) (n=86), heart valve (n=14) andabdominal aortic (n=16) surgery. Radial artery and jugular bulbblood samples were aspirated after induction of anaesthesia,during re-warming on cardiopulmonary bypass (CPB) (36°C),on arrival in the intensive care unit (ICU) and, subsequently,at 1, 2 and 6 h after ICU admission. Most patients having heartsurgery were hypocapnic at 36°C on CPB. Following CABG andheart valve surgery, many patients were hypocapnic whereas afterabdominal aortic surgery, most were hypercapnic. During CPBand postoperatively, Sj_O2 and Lj were significantly correlatedto Pa_CO2 and the arterial concentration of lactate (La) respectively(P<0.05). After correction for arterial carbon dioxide tension(Pa_CO2) and La, there were no significant changes in Sj_O2 orLj on CPB. Postoperatively, having corrected for Pa_CO2, therewere significant effects on Sj_O2 over all groups as a resultof time from surgery (P<0.001) and its interaction with operationtype (P<0.001). Following correction for La, there were nopostoperative effects on Lj. No significant differences (P=0.2)in duration of Sj_O2<50% existed between patients undergoingCABG (1054 (82) min), abdominal aortic (893 (113) min) and heartvalve (1073 (91) min) surgery. The lack of significant reciprocaleffects on Lj combined with the frequency of hypocapnia andstrong influence of Pa_CO2on Sj_O2, suggest that Sj_O2<50% duringCPB and after cardiac surgery represents hypoperfusion as aconsequence of hypocapnia rather than cerebral ischaemia. Br J Anaesth 2001; 87: 229–36     

OXYGEN DESATURATION FOLLOWING SEDATION FOR REGIONAL ANALGESIA

Moderate to severe arterial oxygen desaturation (Sa_O2 75–88%)occurred in three of four patients who were given sedation duringregional conduction block without the administration of oxygen.No desaturation occurred in six patients given oxygen 2 litremin^–1 via a nasal catheter during similar procedures.It is concluded that patients undergoing regional conductionblock with concurrent sedation should receive additional oxygenroutinely unless a pulse oximeter is available for monitoring. ^*Address for Correspondence: Department of Anaesthesia, PlymouthGeneral Hospital, Freedom Fields, Plymouth PL4 8QQ.     

Effects of sustained post-traumatic shock and initial fluid resuscitation on extravascular lung water content and pulmonary vascular pressures in a porcine model of shock

Background. The temporal evolution of lung injury followingpost-traumatic shock is poorly understood. In the present studywe have tested the hypothesis that manifestations of pulmonaryvascular dysfunction may be demonstrable within the first hourafter the onset of shock. Methods. Twenty-nine anaesthetized pigs (mean weight 27.4 kg;(SD) 3.2) were randomly allocated to three groups: control (C,n=9), shock resuscitated with either NaCl 0.9% (S, n=10), or4% gelatine (G, n=10). Shock was maintained for 1 h followedby fluid resuscitation with either normal saline or 4% gelatinesolution. Cardiac output (CO), mean arterial pressure (MAP),mixed venous saturation (Sv_O2), blood lactate concentration,mean pulmonary artery pressure (MPAP), MPAP/MAP, pulmonary vascularresistance (PVR), extravascular lung water index (EVLWi), Pa_O2/FI_O2,venous admixture (Q^·_S/Q^·_T), and dynamic lung compliance(C_dyn) were measured at baseline, beginning of shock phase,end of shock phase, and post-resuscitation. Results. At the end of volume resuscitation CO was restoredto control values in both shock groups. MAP remained significantlybelow control values (95% CI: C=70–95, S=28–52,G=45–69 mm Hg) in both shock groups. MPAP/MAP was significantlygreater in both shock groups at the end of the shock phase (95%CI; C=0.15–0.24, S=0.28–0.38, G=0.32–0.42)and at the post-resuscitation phase (95% CI: C=0.12–0.30,S=0.43–0.61, G=0.32–0.49) indicating the presenceof relative pulmonary hypertension. This was associated witha significant increase in PVR in Group S (F=3.9; P<0.05).There were no significant changes in Pa_O2/FI_O2, Q^·_S/Q^·_T,EVLWi, or C_dyn. In a small cohort of animals a measurable increasein EVLWi (>30%) and reduction in C_dyn (>10%) were observed. Conclusions. Pulmonary vascular injury manifesting as relativepulmonary hypertension and increased PVR may occur within thefirst hour after the onset of shock. These changes may not beaccompanied by overt changes in oxygenation, compliance, orEVLWi. Br J Anaesth 2003; 91: 224–32