Effects of milrinone on jugular bulb oxygen saturation and cerebrovascular carbon dioxide reactivity in patients undergoing coronary artery bypass graft surgery

Background. Jugular bulb oxygen saturation () is a surrogate marker for global cerebral oxygenation. The effectof milrinone on and the cerebrovascular carbon dioxide reactivity (CCO2R) was investigated. Methods. Thirty patients scheduled for coronary artery bypassgraft surgery (CABG) were studied prospectively. After sternotomy,normoventilation (at T₁; =4.7–5.0 kPa) and hyperventilation (at T₂; =3.3–3.7 kPa) were induced and the changes in () and (), and (CCO₂R) were measured. After normoventilationwas re-established (at T₃), milrinone 50 µg kg^–1was given (at T₄), followed by hyperventilation (at T₅), and, and CCO₂R were measured. Results. After milrinone administration at normoventilation(T₃ and T₄), cardiac index and mixed venous oxygen saturationincreased, while mean arterial pressure and systemic vascularresistance index decreased, without a significant change in. Before milrinone administration (T₁ andT₂), hyperventilation decreased and , and showed positive linear correlation with . After milrinone administration (T₄ and T₅), hyperventilation decreased and , and showed positive linear correlation with . There was no significant difference in CCO₂R before and after milrinone administration(13.3 (5.7)% kPa^–1 and 12.3 (3.9)% kPa^–1, respectively). Conclusions. Although milrinone induced significant haemodynamicchanges, and CCO₂R were unchanged duringits administration.     

RELATIONSHIP OF VENTILATORY DEPRESSION TO STEADY-STATE BLOOD PETHIDINE CONCENTRATIONS

An i.v. infusion regimen was developed to permit rapid attainmentof steady-state blood pethidine concentrations (C_p26). In 10adult volunteers (12 studies) the relationship of pethidineC_p26 to the ventilatory effects of the drug were examined. Meanpethidine C_p26 ranged from 170 to 1320 ng ml_–1, with amedian C_p26 of 480 ng ml^–1. Increased end-tidal (PE' _co2)and mixed venous and decreased slope (I/Pco₂) and position(ISO-I) of the carbon dioxide response wereall significant (P<0.001) for C_P26. (1) 480 and (2) >480ng ml^-1. The averaged changes in PE'_co2, ,I/Pco₂, and ISO-I expressed as a per cent of respectivecontrol variables, were shown to be linear functions of C_P26.It is concluded that, under conditions of C_P26, significantventilarory depression occurs at blood pethidine concentrationsless than those required for analgesia. The possible significanceof these findings in volunteers is discussed in terms of thisapplication to the clinical setting of postoperative pain andits management after general anaesthesia.     

THE CONCEPT OF DEADSPACE WITH SPECIAL REFERENCE TO THE SINGLE BREATH TEST FOR CARBON DIOXIDE

We present a review and a theoretical analysis of factors determiningairway deadspace (VD^aw) and alveolar deadspace (VD^alv), thetwo constituents of physiological deadspace (VD^phys). VD^aw isthe volume of gas between the lips and the alveolar/fresh gasinterface, the location of which is determined by inspiratoryflow pattern and airway geometry. VD^alv can be caused by incompletealveolar gas mixing and associated / mismatching within the terminal respiratoryunits, temporal / mismatching within units, spatial / mismatching between units, and venous admixture. Most causes of VD^phys are influencedby inspiratory flow pattern and the time available for gas diffusionand distribution. Analysis can be made from the single breathtest for carbon dioxide (SBT–CO₂) which is the plot offraction of carbon dioxide in expired gas against expired volume.The common causes of VD^alv are associated with a sloping SBT-CO₂phase III. Combination of SBT-CO₂ with PaCO₂ yields VD^phys andVD^alv. A sloping phase III with a negative arterial-end-tidalPco₂ gradient implies compensation by perfusion for early emptying,overventilated alveoli.     

One-lung ventilation induces hyperperfusion and alveolar damage in the ventilated lung: an experimental study

Background: One-lung ventilation (OLV) increases mechanical stress in thelung and affects ventilation and perfusion (V, Q). There areno data on the effects of OLV on postoperative / matching. Thus, thiscontrolled study evaluates the influence of OLV on / distribution in a pigmodel using a gamma camera technique [single-photon emissioncomputed tomography (SPECT)] and relates these findings to lunghistopathology after OLV. Methods: Eleven anaesthetized and ventilated pigs (V_T=10 ml kg^–1,FI_O2=0.40, PEEP=5 cm H₂O) were studied. After lung separation,OLV and thoracotomy were performed in seven pigs (OLV group).During OLV and in a two-lung ventilation (TLV), control group(n=4) ventilation settings remained unchanged. SPECT with ^81mKr(ventilation) and ^99mTc-labelled macro-aggregated albumin (perfusion)was performed before, during, and 90 min after OLV/TLV. Finally,lung tissue samples were harvested and examined for alveolardamage. Results: OLV affected ventilation and haemodynamic variables, but therewere no differences between the OLV group and the control groupbefore and after OLV/TLV. SPECT revealed an increase of perfusionin the dependent lung compared with baseline (49–56%),and a corresponding reduction of perfusion (51–44%) innon-dependent lungs after OLV. No perfusion changes were observedin the control group. This resulted in increased low / regions anda shift of /areas to 0.3–0.5 (10^–0.5–10^–0.3) independent lungs of OLV pigs and was associated with an increaseddiffuse alveolar damage score. Conclusions: OLV in pigs results in a substantial / mismatch, hyperperfusion, and alveolar damagein the dependent lung and may thus contribute to gas exchangeimpairment after thoracic surgery.     

REBREATHING CHARACTERISTICS OF THE BAIN CIRCUIT An Experimental and Theoretical Study

The Bain circuit was studied in a model lung on the assumptionthat, in addition to the ratio of fresh gas flow to total ventilation(FG/E), different time fractions of the respiratory cycle might influencerebreathing. We found that the time fraction for active expiration(FE_t) governed rebreathing for each FG/E value. With FE_t, as an independentvariable, a theoretical formula was derived for rebreathing.Rearranging this formula made it possible to calculate the necessaryincrease in ventilation to keep end-tidal carbon dioxide constantfor each FG/E. Thus, at a fresh gas flow of 70 ml kg^-1 min^-1,I has to be increased 2.6 times. For spontaneously breathing patients inhalation anaestheticsthat do not depress carbon dioxide sensitivity seem to be bettersuited to use in the Bain circuit. The FE_CO2 can then kept constantthrough increased ventilation in spite of the concomitant increasein rebreathing     

VENTILATORY RESPONSES TO CARBON DIOXIDE IN CHILDREN DURING NITROUS OXIDE-HALOTHANE ANAESTHESIA

The ventilatory response to carbon dioxide was studied in 12unpremedicated children, aged 20–68 months, weighing between10 and 20 kg, under nitrous oxide-halothane anaesthesia. Tidalvolume (VT) and end-tidal carbon dioxide tension (PE'_CO2) werecontinuously measured by pneumotachograph and capnograph. Minuteventilation (), respiratory rate (f), mean in-spiratory flow (VT) and effective inspiratorycycle (T1/T^tot) were calculated during anaesthesia at threedifferent inspired halothane concentrations (0.5, 7 and 1.5%).The ventilatory response to carbon dioxide was determined byrelating the increase in ventilation during exposure to 2% carbondioxide to the change in end-tidal carbon dioxide concentration.When the inspired concentration of halothane increased, therewere significant decreases in , VT, , and a significant increase in PE'_CO2 The slope of the carbon dioxide response under lightnitrous oxide-halothane anaesthesia (0.5% halothane) was relativelyflat (18.64 ml min^–1 kg^– mm Hg^-1) when comparedwith the mean values published for anaesthetized adults, childrenor neonates. When the inspired concentration of halothane wasincreased, the slope decreased significantly (39% of initialvalue at 1 % inspired halothane, 26% at 1.5%). The additionof carbon dioxide produced significant increases in , VT and but no change in respiratory rate. No statistical differencewas observed in the slope of carbon dioxide response betweenthe initial and "control" periods which were measured at thesame inspired halothane concentration (0.5%).     

FRESH GAS REQUIREMENTS OF AN ENCLOSED AFFERENT RESERVOIR BREATHING SYSTEM IN ANAESTHETIZED, SPONTANEOUSLY VENTILATING CHILDREN

We have determined the minimum fresh gas flow rate (F) for use with the Ohmeda enclosedafferent reservoir breathing system (EAR) in 10 anaesthetizedchildren breathing spontaneously. First, we determined the F required to prevent rebreathing asdetected by increased total ventilation (E) and end-tidal carbon dioxide partial pressure.Second, we used a mathematical model to calculate the degreeof rebreathing occurring at each F.A F equal to the predictedalveolar ventilation was sufficient to prevent clinically detectablerebreathing in all pateints. From the model, no rebreathingoccurred when F//E was 0.78 or more. We have shown previously thatthe EAR functions efficiently during controlled ventilationwith a F = 0.6x weight^0.5.As this F is slightly greaterthan the predicted alveolar ventilation, we suggest that theEAR may be used with a F =0.6 x weight ^0.5 regardless of the mode of ventilation.     

VENTILATORY EFFECTS AND PLASMA CONCENTRATION OF MORPHINE IN MAN

The relationship between the plasma concentration of morphineand morphine-induced changes in ventilation and the ventilatoryresponse to carbon dioxide was studied in 17 healthy adultsundergoing elective surgery under general anaesthesia. Eachsubject was given morphine sulphate 0.15 mg kg^–1 i.m.;ventilation (E), end-tidal Pco₂(PE'_CO2), mixed venous PV_CO2(P_CO2)and ventilatory response to carbon dioxide (E/P_CO2) were measured before and within 90 min afterinjection. Mixed venous P_CO2 and E/P_CO2were measured by standard rebreathing methods; plasma morphineconcentration was measured by radioimmunoassay. Maximum plasmamorphine ranged from 30 to 120 ng ml^–1, between 4 and60 min after injection. There was a significant increase inmixed venous PE'_CO2 (P<0.001), and PE'_CO2 (P<0.01) aftermorphine while E decreased insignificantly. Morphine displaced the carbon dioxide responsecurve to the right (P<0.01) and E/P_CO2decreased from 12.3 to 10.0 litre min^–1 kPa^–1 (P<0.05).The magnitude of changes in E and E/P_CO2 were not relatedto the peak plasma concentration of morphine or to the meanconcentration immediately before and after the carbon dioxideresponse measurement. Plasma concentrations of morphine, underthe conditions of the present study, are not an objective indicatorof pharmacological activity between one patient and another. Presented in part at the VI World Congress of Anaesthesiology,MexicoCity, Mexico, April 1976     

PULMONARY BLOOD FLOW DURING CLOSED HEART SURGERY: Use of a Modified Formula Ratio to Assess Adequacy of Palliation of Systemic-Pulmonary Artery Shunts

The ability to assess changes in pulmonary blood flow, usinga modified ratio (), was evaluated in 12 infants withcongenital heart disease and complete intracardiac mixing whounderwent modified Blalock-Taussig shunt procedures. At thevarious measuring stages there were no major changes in meanarterial pressure or heart rate. Arterial oxygen tensions andsaturation increased (P < 0.01) and the arterial to end-tidalcarbon dioxide difference (Pa_CO2–PE'_CO2) was significantlyreduced (P < 0.001) after completion of the shunt procedure.There was a significant increase in mean after chest closure (P < 0.001), which was seento correlate well with early clinical outcome. Two patientswho did not demonstrate any increase in over the course of the procedure had failed shunts.The limitations of use of the are discussed. A modified ratio of less than unity after surgery is strongly indicativeof inadequate palliation. Present address: Department of Anaesthesiology, University ofTexas Health Science Center at Dallas, 5323 Harry Hines Blvd,Dallas, Texas 75235, U.S.A.     

Contamination of anaesthetic gases with nitric oxide and its influence on oxygenation

Editor—I read with interest the article by Hess and colleagues¹and its accompanying editorial by Marczin² on the effect ofadministration of compressed air (AIRc) or nitrous oxide onarterial in ventilated patients, in comparison with a control period where synthetic air (AIRs) was used. Theauthors attributed a higher to increased nitric oxide contaminating the former two mixtures. The difference in when receiving AIRc vsAIRs (0.5 kPa) was not clinically significant, as might be expectedgiven that the nitric oxide levels with AIRc were much smallerthan those used therapeutically to improve oxygenation. The increase in with nitrous oxide was much more significant (2.2 kPa or >15%). However, from the evidenceavailable, it     

Low- vs high-dose almitrine combined with nitric oxide to prevent hypoxia during open-chest one-lung ventilation

Background. Almitrine combined with inhaled nitric oxide (NO)can prevent hypoxia during one-lung ventilation (OLV). The optimaldose of almitrine that would provide therapeutic advantage withfew side-effects during open-chest OLV has not been established. Methods. Forty-two patients undergoing thoracotomy were randomlyallocated to three groups: placebo, almitrine 4 µg kg^–1min^–1 and inhaled NO 10 p.p.m. (ALM4+NO), and almitrine16 µg kg^–1 min^–1 and inhaled NO 10 p.p.m.(ALM16+NO). Gas exchange, haemodynamic and respiratory variablesand plasma concentrations of almitrine and lactate were monitored.Measurements were obtained with the patient awake (baseline),after induction of anaesthesia with two-lung ventilation (control2LV), 20 min after treatment (2LV+T), and then at 10, 20 and30 min of OLV (OLV10', OLV20' and OLV30') with 1. Results. In the placebo group, OLV impaired and increased pulmonary shunt [16 (SD 7) kPa and 42 (10)% respectively].These improved with ALM4+NO [26 (10) kPa and 31 (7)%; P<0.001].ALM16+NO further improved to 36 (13) kPa (P<0.0001) but gave no improvement in the shunt. Mean pulmonaryartery pressure was similar in the placebo and ALM4+NO groups[20 (4) vs 23 (5) mm Hg], whereas it was increased in the ALM16+NOgroup to 28 (8) mm Hg (P<0.01). Plasma concentrations ofalmitrine and lactate were unaltered by the treatments. Conclusions. Low-dose almitrine (4 µg kg^–1 min^–1)together with inhaled NO significantly improves oxygenationduring open-chest OLV, without modifying pulmonary haemodynamics.An increased dose of almitrine (16 µg kg^–1 min^–1)with inhaled NO further improves arterial oxygenation, but alsoincreases mean pulmonary artery pressure.     

PATTERN OF RESPIRATION AND RESPONSES TO CARBON DIOXIDE DURING TRICHLOROETHYLENE ANAESTHESIA IN THE CAT

Tidal volume (VT), minute ventilation (E), the duration of inspiration and expiration, andPa_co2, were measured via a tracheostomy in adult cats anaesthetizedwith 0.7%, 1% and 1.5% (inspired) trichloroethylene (TCE). Thetracheal cannula was occluded at intervals at the start of inspirationand the tracheal pressure was measured to assess the force ofcontraction of the respiratory muscles. Anaesthesia with TCE0.7% was associated with an increase in E, a reduction in VT, and a marked increase in respiratoryfrequency and mean inspiratory flow rate, but Pa_co2 values didnot differ significantly from those in conscious animals. Ventilationwas also greater than in conscious animals during anaesthesiawith TCE 1%. TCE 1.5% caused a significantly greater Pa_co2,than in conscious animals. All concentrations of TCE causeda reduction in the ventilatory response to carbon dioxide, measuredby the steady-state method. Cervical vagal section did not abolishthe tachypnoea caused by TCE. ^*Present addresses: Ente Ospedaliera Regionale, Ospedale Maggiore,Piazza Ospedale, 34100 Trieste, Italy. Present addresses: Department of Anaesthetics, Royal Infirmaryof Edinburgh, Edinburgh EH3 9YW.     

A SYSTEM FOR THE CONTINUOUS MEASUREMENT OF OXYGEN UPTAKE AND CARBON DIOXIDE OUTPUT IN ARTIFICIALLY VENTILATED PATIENTS

A continuous, non-invasive system is described for measuringoxygen uptake () and carbon dioxide output () in mechanically ventilated patients. Inspiratory and mixed expiratory gas sampleswere pumped through fine-bore tubing to a remote mass spectrometerfor analysis. The expiratory flow transducer of a Siemens Servo900B ventilator was used for expiratory flow measurement andinspiratory flow was calculated from this using the Haldanetransformation. A desk-top computer calculated , and respiratory quotient. The system has been validated against standard methodsof gas analysis and flow measurement ( mean difference –lOml min^–1: SD9.13; mean difference 8.12ml min^–1:SD4.66). Comparison with Douglas bag measurements in patientshas been made ( mean difference 10.7ml min^–1: SD9.8; mean difference –1.07ml min^–1: SD4.7).     

Pressure support ventilation during fibreoptic intubation under propofol anaesthesia

Goal of the study. To assess the benefit of pressure supportventilation during fibreoptic intubation performed under propofolanaesthesia in patients having an anticipated difficult intubation. Procedures. Thirty-two patients with ENT cancer, and havingat least two criteria for anticipated difficult intubation wereprospectively included. All patients received topical lidocaine2% and propofol by plasma target control infusion (initial targetconcentration 3 µg ml^–1, then adjusted to maintainloss of consciousness without apnoea). They were randomly assignedbetween two groups: spontaneous breathing (SB) or pressure supportventilation (with a support level set at 10 cm H₂O) both usingFI_O2=1. Conditions for fibreoptic intubation, respiratory parameters(pulse oxymetry, ventilatory frequency, tidal volume and after intubation) and haemodynamicparameters were recorded. Results. Patient characteristic data and intubation conditionswere similar between both groups. All patients had a successfulfibreoptic intubation and none needed a rescue procedure becauseof desaturation. In spite of a longer duration of intubation, after intubation was lower and tidal volume during intubation was higher with pressuresupport ventilation than in SB patients [38.1 (4.2) vs 42.3(4.7) mm Hg and 371 (139) vs 165 (98) ml, respectively]. Desaturationepisodes were observed in two SB patients conversely to no episodeduring pressure support ventilation, probably because of thehigher minute ventilation. Conclusion. Pressure support represents a useful method to improveventilation during fibreoptic intubation under propofol anaesthesiain patients with an anticipated difficult intubation. Presented in abstract at the ASA meeting 2003.     

Ephedrine and phenylephrine for the treatment of maternal hypotension in a chronic sheep model of increased placental vascular resistance

Background. We hypothesized that ephedrine and phenylephrineare equal with respect to uterine and placental haemodynamicsand fetal acid–base status after exposure to maternalhypoxaemia and hypotension in a chronic sheep model of increasedplacental vascular resistance (R_UA). Methods. At 114–135 days gestation, chronically instrumentedfetal sheep underwent placental embolization leading to increasedR_UA. Twenty-four hours after embolization, the ewes were anaesthetizedand randomized to receive boluses of ephedrine (n=7) or phenylephrine(n=6) for epidural-induced hypotension after maternal hypoxaemia.Uterine (Q_UtA) and placental (Q_UA) volume blood flows and uterinevascular resistance (R_UtA) and R_UA were recorded. Uterine (PI_UtA)and umbilical artery (PI_UA) pulsatility indices were obtainedby Doppler ultrasonography. Fetal arterial blood samples wereanalysed for acid–base values and lactate concentrations. Results. During hypotension, Q_UtA, fetal pH, BE, and decreased whereas R_UtA, PI_UtA, R_UA,and fetal lactate concentration increased. With ephedrine, Q_UtA,R_UtA, PI_UtA, R_UA, and fetal returned to baseline. Fetal pH, BE, and lactate concentrationdid not change from hypotensive values. With phenylephrine,Q_UtA remained lower (P=0.007) and R_UtA (P=0.007), PI_UtA (P=0.013),and R_UA (P=0.050) higher than at baseline. Fetal returned to baseline and fetal pH and BE did notchange from hypotensive values. However, fetal lactate concentrationincreased further (mean difference 1.49, 95% confidence interval0.72–2.26 mmol litre^–1; P=0.004). Conclusions. In a chronic sheep model of increased placentalvascular resistance, compared with ephedrine administration,phenylephrine administration was associated with impaired uterineand placental haemodynamics and increased fetal lactate concentrations. Presented in part at the Euroanaesthesia 2005 Meeting, Vienna,Austria, May 28–31, 2005.     

VENTILATORY RESPONSES TO REBREATHING AND CARBON DIOXIDE INHALATION DURING ANAESTHESIA IN CHILDREN

In 12 spontaneously breathing intubated children (9.3–25kg), ventilatory responses to rebreathing and to the inhalationof carbon dioxide (CO₂) were investigated during halothane anaesthesiafor minor surgical procedures. A T-piece (Mapleson F system)was used, modified by the insertion of a pneumotachograph anda paediatric airway adaptor of an in-line capnograph in thepatient limb. Exhaled gas was collected for determination ofexpired CO₂ content. Measurements were made when the fresh gasflow (FGF) was at the borderline for rebreathing (FGF^r) andduring 10 min with a mean FGF 44% lower, producing a maximalinspired CO₂ (I_{CO2 max}) (%) of 1.45±0.38% (mean±1 SD). Measurements were repeated 5 min after returning to aflow exceeding FGF^r and then during CO₂ inhalation for 10 minafter the addition of 1.24±0.32 % CO₂ (mean±1SD) to this flow. During both rebreathing and CO₂ inhalationend-tidal CO₂ (E_CO2) was unchanged and did not increase significantly (18%), but duringCO₂ inhalation alveolar ventilation increased (P < 0.05),indicating an adequate and intact response to this level ofCO₂ inhalation. Estimations of I_{CO2 max} could be made from theexpression: l_CO2 max(%) = –0.7 x FGF/ +2.5 and FGF to minute ventilation () ratios lower than 1 were found to produce l_CO2max of 1.8% or higher. Such low FGF are likely to result inrebreathing within the alveolar ventilation and are thus ofclinical importance. We believe that to increase the marginof safety in anaesthetized spontaneously breathing children,FGF of at least 1.5 to 2 times should be used. Present addresses:^*Department of Anaesthesia, University HospitalS–22185 Lund, Sweden Department of Anaesthesia, Manchester Royal Infirmary, OxfordRoad, Manchester M13 9WL.     

Estimation of pulmonary blood flow from sinusoidal gas exchange during anaesthesia: a theoretical study

We simulated the use of simultaneous sinusoidal changes of inspiredO₂ and N₂O (Williams et al., J Appl Physiol, 1994; 76: 2130–9)at fractional concentrations up to 0.3 and 0.7, respectively,to estimate FRC and pulmonary blood flow (PBF) during anaesthesia,using O₂ as an insoluble indicator. Hahn’s approximateequations, which neglect the effect of pulmonary uptake and excretionon expiratory flow, estimate dead space and alveolar volume (V_A)with systematic errors less than 10%, but yield systematic errorsin PBF which are approximately proportional to FI_N2O in magnitude.A correction factor (1 – )^–1 forHahn’s equations for PBF (where is the mean partial pressure of the soluble indicator) reducesthe dependence of PBF estimates on FI_N2O, and the solution ofequations describing the simultaneous mass balance of both indicatorsyields accurate results for a wide range of mean FI_N2O. However,PBF estimates are sensitive to measurement errors and a thirdgas must be present to ensure that the indicator gases behave independently. Br J Anaesth 2000; 85: 371–8     

IMPROVEMENT OF BRAIN ELECTRICAL ACTIVITY DURING TREATMENT OF PORCINE MALIGNANT HYPERTHERMIA WITH DANTROLENE

Three months before this study, susceptibility for malignanthyperthermia (MH) had been tested in 15 pigs. In all pigs, MHwas triggered by administration of 1% halothane. Brain electricalactivity was examined during therapy of MH with and withoutadministration of dantrolene. From the EEG, power densitiesin selected frequencies and the median frequency of the powerspectrum were calculated. Therapy was started when severe respiratorychanges were observed (Pa_co2 > 10 kPa, mixed venous oxygentension ( < 4 kPa. At this time, heart rate exceeded 150 beat min^–1, mean arterialpressure (MAP) was less than 60 mm Hg and median frequency wasless than 2 Hz. EEG was isoelectric (n=6) or showed slow polymorphicdelta-activity. For therapy, administration of all anaestheticswas terminated, 100% oxygen was delivered and ventilation wasincreased four-fold. Acidosis was treated by administrationof sodium bicarbonate 2–4 mmol litre^–1 kg^–1.Animals were allocated randomly to one of two groups: groupI (control, n=7) received no dantrolene; group II (n=8) receiveddantrolene 2.5 mg kg^–1 i.v. All variables were measuredover a period of 60 min after therapy: EEG, HR and MAP wererecorded continuously and blood-gas tensions, arterial po tassiumand glucose concentrations and pH were measured every 150 s.In group I (no dantrolene) minor, transient improvements inEEG activity were noted, but all animals died within 15–25mm after the start of therapy. In dantrolene-treated animals,EEG total power and median frequency increased within 5 min.The improvement in brain electrical activity occurred beforeany significant increases in MAP, Pa_o2 and or decreases in all Pa_co2 or potassium plasma concentration.Our results in dicate that dantrolene given for the treatmentof a fulminant MH crisis helps to improve, not only haemodynamicstate and metabolism, but also recovery of neuronal activity.(Br. J. Anaesth. 1993; 71: 881–884)     

Combined high frequency ventilation and kinetic therapy for the management of severe hypoxia in adult respiratory distress syndrome

Pressure controlled inverse ratio ventilation (PCIRV) is oftenused as the initial therapeutic manoeuvre to improve oxygenationin severe adult respiratory distress syndrome (ARDS). When thisalone fails, however, there is no consensus as to which therapyto resort to. We have used combined high frequency ventilation(CHFV) along with kinetic therapy (KT) to treat three patientswith ARDS and resistant hypoxia. The basis for this treatmentwas our previous clinical observation that the two techniquestogether produced a greater improvement in oxygenation thaneither used alone. In CHFV a Monsoon jet ventilator was used to superimpose highfrequency jet ventilation (rate 300 cycles min^–1, inspiratorytime 0.3, driving pressure 1 bar) on pressure controlled ventilation(rate 10 breaths min^–1, inspiratory pressure 30 mbar).At the same time patients were positioned on a kinetic therapypressure relief low air-loss bed (KCI) and rotated through atotal angle of 90°. Three Pa_O2/F_O2 valuesfor each patient are shown in Table 14 and these correspondto (a) PCIRV alone (b) after 1 h of combined therapy and (c)after 24 h of combined therapy. The combination of CHFV with kinetic therapy produced improvementin oxygenation in all patients. Each of these individual therapiesis believed to act through a different physiological mechanism.¹² It is possible that the two together may, therefore, producegreater improvement than either therapy applied on its own.The number of such cases that present to one institution limitsour small study, but we believe the significant improvementin oxygenation warrants further investigation.     

Do fluid administration and reduction in norepinephrine dose improve global and splanchnic haemodynamics?

We studied global and splanchnic haemodynamics in patients withseptic shock, while reducing norepinephrine doses by progressivefluid loading administration. Ten patients (six female, fourmale, aged 39–86 yr, mean 61 yr) were assessed using atranspulmonary thermo-dye dilution technique to measure cardiacoutput, intrathoracic blood volume and total blood volume. Splanchnicblood flow was measured by the steady state indocyanine greentechnique using a hepatic venous catheter. Gastric mucosal bloodflow was estimated by regional carbon dioxide tension (P_CO2). Hydroxyethylstarch was infused in two stageswhile maintaining mean arterial pressure, allowing a reductionin norepinephrine dose from 0.54 to 0.33 to 0.21 µg kg^–1min^–1. Mean () heart rate significantly decreased, from 104 (13) to 94 (15) beats min^–1. Totalblood volume index (mean ()) increased from 2650 (638) to 3655 (885) ml m^–2, intrathoracic blood volumeindex from 888 (204) to 1050 (248) ml m^–2 and cardiacindex from 3.6 (1.0) to 4.0 (0.9) litres min^–1 m^–2.Splanchnic blood flow did not change significantly–eitherabsolute (from 0.81 to 0.98 litres min^–1 m^–2) orfractional (from 22.3% to 23.9%). Gastric mucosal (P_CO2) increased from 7.5 (2.5) to 9.0 (2.8) kPa. TheP₂ gap, i.e. the difference between regionaland end-tidal P₂, increased from 3.1 (2.5)to 4.0 (2.9) kPa. Marked individual variation in responses suggeststhat norepinephrine dose reduction by fluid loading in patientswith stabilized septic shock does not necessarily increase globalor splanchnic blood flow.