End-tidal Carbon Dioxide Tension Research Articles

Implications of Exercise-Induced Pulmonary Arterial Hypertension

To characterize the hemodynamic and ventilatory responses to exercise in a group of patients with unexplained dyspnea, increased risk for pulmonary arterial hypertension (PAH), and an elevated mean pulmonary artery pressure (mPAP; >30 mm Hg) on exercise. A total of 37 symptomatic patients at risk of PAH and 20 healthy controls underwent a cardiopulmonary exercise test and were assessed for quality of life (QOL). Patients had a pulmonary artery catheter in situ during the exercise test. Seventeen subjects had exercise-induced PAH (EIPAH), which we defined as mPAP ≤ 25 mm Hg at rest, and mPAP > 30 mm Hg and pulmonary artery wedge pressure <20 mm Hg on exercise. These subjects had reduced peak exercise cardiac output (72% ± 19% predicted). Further, compared with matched controls, subjects with EIPAH had reduced peak oxygen consumption (1.2 ± 0.4 vs 1.7 ± 0.5 L · min, P < 0.05), an elevated ventilatory equivalent for carbon dioxide (41.0 ± 7.3 vs 31.0 ± 2.9, P < 0.05) and reduced end-tidal carbon dioxide tension (32.6 ± 3.6 vs 39.4 ± 2.7 mm Hg, P < 0.05) at the anaerobic threshold. These exercise abnormalities were associated with impaired QOL (P < 0.05). Elevated pulmonary artery pressure on exercise can be associated with hemodynamic and ventilatory abnormalities typical of PAH, along with impaired exercise capacity and reduced QOL.

End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhage

End-tidal carbon dioxide tension (Pet(CO(2))) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on Pet(CO(2)) being an accurate surrogate for arterial carbon dioxide tension (Pa(CO(2))), the latter being the physiologically relevant variable. This study tested the hypothesis that Pet(CO(2)) provides an accurate assessment of Pa(CO(2)) during the aforementioned conditions. Comparisons between these measures were made: 1) after two levels of heat stress (N = 11); 2) during combined heat stress and simulated hemorrhage [via lower-body negative pressure (LBNP), N = 8]; and 3) during an end-tidal clamping protocol to attenuate heat stress-induced reductions in Pet(CO(2)) (N = 7). Pet(CO(2)) and Pa(CO(2)) decreased during heat stress (P < 0.001); however, there was no group difference between Pa(CO(2)) and Pet(CO(2)) (P = 0.36) nor was there a significant interaction between thermal condition and measurement technique (P = 0.06). To verify that this nonsignificant trend for the interaction was not due to a type II error, Pet(CO(2)) and Pa(CO(2)) at three distinct thermal conditions were also compared using paired t-tests, revealing no difference between Pa(CO(2)) and Pet(CO(2)) while normothermic (P = 0.14) and following a 1.0 ± 0.2°C (P = 0.21) and 1.4 ± 0.2°C (P = 0.28) increase in internal temperature. During LBNP while heat stressed, measures of Pet(CO(2)) and Pa(CO(2)) were similar (P = 0.61). Likewise, during the end-tidal carbon dioxide clamping protocol, the increases in Pet(CO(2)) (7.5 ± 2.8 mmHg) and Pa(CO(2)) (6.6 ± 3.4 mmHg) were similar (P = 0.31). These data indicate that mean Pet(CO(2)) reflects mean Pa(CO(2)) during the evaluated conditions.

Hemodynamic Perturbations During Robot-Assisted Laparoscopic Radical Prostatectomy in 45° Trendelenburg Position

Robot-assisted laparoscopic radical prostatectomy has gained widespread use. However, circulatory effects in patients subjected to an extreme Trendelenburg position (45°) are not well characterized. We studied 16 patients (ASA physical status I-II) with a mean age of 59 years scheduled for robot-assisted laparoscopic radical prostatectomy (45° head-down tilt, with an intraabdominal pressure of 11-12 mm Hg). Hemodynamics, echocardiography, gas exchange, and ventilation-perfusion distribution were investigated before and during pneumoperitoneum, in the Trendelenburg position and, in 8 of the patients, also after the conclusion of surgery. In the 45° Trendelenburg position, central venous pressure increased almost 3-fold compared with the initial value, with an associated 2-fold increase in mean pulmonary artery pressure and pulmonary capillary wedge pressure (P<0.01). Mean arterial blood pressure increased by 35%. Heart rate, stroke volume, cardiac output, and mixed venous oxygen saturation were unaffected during surgery, as were echocardiographic heart dimensions. After induction of anesthesia, isovolumic relaxation time was prolonged, with no further change during the study. Deceleration time was normal and stable. In the horizontal position after pneumoperitoneum exsufflation, filling pressures and mean arterial blood pressure returned to baseline levels. Pneumoperitoneum reduced lung compliance by 40% (P<0.01). Addition of the Trendelenburg position caused a further decrease (P<0.05). Arterial blood acid-base balance was normal. End-tidal carbon dioxide tension increased whereas arterial carbon dioxide was unaffected with unchanged ventilation settings. Pneumoperitoneum increased PaO2 (P<0.05). Ventilation-perfusion distribution, shunt, and dead space were unaltered during the study. Pneumoperitoneum and 45° Trendelenburg position caused 2- to 3-fold increases in filling pressures, without effects on cardiac performance. Filling pressures were normalized immediately after surgery. Lung compliance was halved. Gas exchange was unaffected. No perioperative cardiovascular complications occurred.

Effect of exchange of tracheal tube for laryngeal mask airway(LMA) on intratracheal extubation stress response under deep anesthesia level after surgery in elderly patients with hypertension

To investigate the effect of exchange of tracheal tube for a laryngeal mask airway (LMA) on intratracheal extubation stress response under deep anesthesia level after surgery in elderly patients with hypertension. From October 2008 to June 2009, 40 hypertension patients aged from 65 to 78 years scheduled for upper abdominal surgery were randomly divided into 2 groups, one was extubated intratracheal tube when being awake (group TT, n = 20) and the other was extubated and exchanged for LMA under deep anesthesia (group LM, n = 20). The American Society of Anesthesiologists (ASA) of the patients were I o rII. The data of mean arterial pressure (MAP), heart rate(HR), pulse oxygen saturation (SPO(2)), end-tidal carbon dioxide tension (P(ET)CO(2)) and rate pressure product(RPP) were recorded before induction of anesthesia (T(0)), suction (T(1)) and at 0 (T(2)), 5(T(3)), and 10 (T(4)) and 15 min (T(5)) after extubation tracheal tube or LMA in two groups. The indices mentioned above also were recorded before and after extubation in group LM. Blood samples were taken at T(0), skin incision, T(2), T(3), for determination of serum concentrations of blood glucose and cortisol. The airway adverse events in the recovery period were recorded. Compared with group LM, MAP, HR and RPP were significantly higher at T(1), T(2), T(3) than T(0) in group TT (P < 0.05). There was no significant difference in the indices mentioned above during extubated intratracheal tube and exchanged for LMA under deep anesthesia in group LM (P > 0.05). The incidence rate of glossoptosis in group TT was significantly higher than those in group LM (P < 0.01), while complications, such as cough, bucking, breath holding during the recovery stage in group TT were more than those in group LM (P < 0.05). Compared with the baseline value, blood glucose and cortisol concentration level were significantly increased in group TT than in group LM (P < 0.01). Exchange of tracheal tube for LMA under deep anesthesia during recovery stage can decrease the stress response during the recovery stage and attenuate the harmful response of respiratory tract. It is suitable for the elderly patients with hypertension.

Clinical significance of end-tidal carbon dioxide tension monitoring during mechanical ventilation

End-tidal carbon dioxide tension or concentration monitoring is characterized with noninvasive,convenient and fast reaction,which Can be continuously monitored and dynamically displayed On electrocardiogram monitor.The technique has been extensively applied in the operation room,intensive care unit and emergency room. Key words: Respirator; Respiratory failure; End-tidal carbon dioxide monitoring

End-tidal Carbon Dioxide Tension Accurately Assesses Arterial Carbon Dioxide Concentration During Moderate Heat Stress

PURPOSE: Whole-body heat stress reduces cerebral perfusion and cerebral vascular conductance. Reductions in arterial carbon dioxide concentration (PaCO2), as reflected by changes in end-tidal carbon dioxide tension (PETCO2), accompanying heat stress have been implicated in contributing to these cerebral vascular changes. While PETCO2 provides an accurate index of PaCO2 in a variety of normothermic settings, its accuracy as an index of PaCO2 during heat stress conditions remains unknown. The aim of this study was to test the hypothesis that PETCO2 is an accurate index of PaCO2, during heat stress with and without an orthostatic stress. METHODS: Internal temperature (telemetry pill), PaCO2 (radial artery catheter), and PETCO2 (capnograph) were assessed in 8 healthy individuals during four separate conditions performed sequentially; 1) normothermia (NT), 2) NT + ∼30 mmHg lower body negative pressure (NT + LBNP), 3) passive heat stress (HS), and 4) passive heat stress + ∼30 mmHg lower body negative pressure (HS + LBNP). RESULTS: Internal temperature was significantly elevated during HS from 37.0 0.3 to 38.1 ± 0.4 °C and was further elevated during HS + LBNP to 38.3 ± 0.4 (both P < 0.05 relative to NT). Two-way repeated measures analysis of variance revealed a significant main effect of condition (P < 0.01); however, there was not a significant main effect of measurement device (i.e. PETCO2 vs. PaCO2; P > 0.05) nor was there a significant interaction (see Table). CONCLUSION: These results indicate that PETCO2 provides an accurate index of PaCO2 during normothermic and moderate heat stress conditions with and without orthostatic stress. Supported by NIH Grants HL61388 & HL84072Values are mean ± SD *Significant differance relative to NT and NT + LBNP.

Effectiveness Of End-tidal Carbon Dioxide Clamping In The Heat Stressed Human

During moderate to pronounced passive heat stress end-tidal carbon dioxide tension (PETCO2) is reduced by approximately 3 - 8 mmHg, which in part contributes to the decreases in cerebral blood flow and cerebrovascular conductance that occur in this thermal condition. Clamping devices have been used to manipulate PETCO2 in normothermic humans, however, their effectiveness in clamping arterial carbon dioxide tension (PaCO2) while heat stressed is unknown. PURPOSE: The aim of this study was to test the hypothesis that in the heat stressed human PETCO2 accurately tracks PaCO2 when PETCO2 is clamped at normothermic levels. METHODS: Internal temperature (telemetry pill), PaCO2 (radial artery catheter), and PETCO2 (capnograph) were assessed in 7 healthy individuals during three conditions performed sequentially; 1) normothermia (NT), 2) passive heat stress (HS), and 3) passive heat stress when PETCO2 was clamped at normothermic levels (HS+Clamp). Clamping was achieved using a computer controlled sequential gas delivery breathing circuit (RespiractTM). RESULTS: Heat stress increased internal temperature from 37.0 ± 0.3 to 38.4 ± 0.4 °C (P < 0.001). While normothermic values of PaCO2 (40.4 ± 3.4 mmHg) and PETCO2 (38.8 ± 3.5 mmHg; P = 0.12) were similar, HS resulted in significantly greater reductions in PaCO2 (D 10.1 ± 3.0 mmHg) relative to PETCO2 (D 7.8 ± 3.5 mmHg; P = 0.04). HS+Clamp caused comparable increases in PaCO2 (D 6.6 ± 3.4 mmHg) and PETCO2 (D 7.5 ± 2.8 mmHg: P = 0.30), however, because the decrease in PaCO2 due to HS was greater than PETCO2, absolute PaCO2 during HS+Clamp remained significantly lower (PaCO2: 36.8 ± 4.9 mmHg; PETCO2: 38.5 ± 5.2 mmHg; P < 0.01). CONCLUSION: These results indicate that despite a difference in absolute PETCO2 and PaCO2 during heat stress+clamp conditions, clamping caused similar increases between PETCO2 and PaCO2. Supported by NIH Grants HL61388 & HL84072

A Nasal Catheter for the Measurement of End-Tidal Carbon Dioxide in Spontaneously Breathing Patients

Several devices have been proposed to monitor end-tidal carbon dioxide tension (Petco(2)) in spontaneously breathing patients; however, many have been reported to be inaccurate. We designed this study to investigate the accuracy of a balloon-tipped nasal catheter in measuring Petco(2) in nontracheally intubated, spontaneously breathing patients. The catheter was assembled using a 14-F rubber Foley catheter, a tracheal tube pilot balloon, and the plastic sheath from an 18-gauge needle. The catheter was connected to the sampling tube of a gas analyzer. Petco(2) and Paco(2) were determined simultaneously in 20 otherwise healthy postsurgical patients while receiving oxygen. The mean Petco(2) - Paco(2) difference was -4.4 +/- 1.6 (SD) mm Hg with a correlation coefficient r = +0.87 (P < 0.001). Our results suggest that a balloon-tipped nasal catheter can provide a simple, easy, and reliable method for Petco(2) measurement in nontracheally intubated, spontaneously breathing patients.

Clinical significance of arterial and end-tidal carbon dioxide tension difference (a-ETDCO2) in pulmonary gas exchange

Clinical significance of arterial and end-tidal carbon dioxide tension difference (a-ETDCO2) in pulmonary gas exchange

Surfactant Protein D, a Marker of Lung Innate Immunity, Is Positively Associated With Insulin Sensitivity

OBJECTIVEImpaired lung function and innate immunity have both attracted growing interest as a potentially novel risk factor for glucose intolerance, insulin resistance, and type 2 diabetes. We aimed to evaluate whether surfactant protein D (SP-D), a lung-derived innate immune protein, was behind these associations.RESEARCH DESIGN AND METHODSSerum SP-D was evaluated in four different cohorts. The cross-sectional associations between SP-D and metabolic and inflammatory parameters were evaluated in two cohorts, the cross-sectional relationship with lung function in one cohort, and the longitudinal effects of weight loss on fasting and circadian rhythm of serum SP-D and cortisol concentrations in one prospective cohort.RESULTSIn the cross-sectional studies, serum SP-D concentration was significantly decreased in subjects with obesity and type 2 diabetes (P = 0.005) and was negatively associated with fasting and postload serum glucose. SP-D was also associated with A1C, serum lipids, insulin sensitivity, inflammatory parameters, and plasma insulinase activity. Smoking subjects with normal glucose tolerance, but not smoking patients with type 2 diabetes, showed significantly higher serum SP-D concentration than nonsmokers. Serum SP-D concentration correlated positively with end-tidal carbon dioxide tension (r = 0.54, P = 0.034). In the longitudinal study, fasting serum SP-D concentration decreased significantly after weight loss (P = 0.02). Moreover, the main components of cortisol and SP-D rhythms became synchronous after weight loss.CONCLUSIONSThese findings suggest that lung innate immunity, as inferred from circulating SP-D concentrations, is at the cross-roads of inflammation, obesity, and insulin resistance.

Effects of Retroperitoneal or Transperitoneal Laparoscopic Surgery on Hemodynamic and Respiratory Function in Old Patients

Purpose: To compare the effects of retroperitoneal laparoscopic surgery (RPL) and transperitoneal laparoscopic surgery (TPL) on the hemodynamic and ventilatory functions in old patients. Methods: Thirty-two senior patients underwent either RPL or TPL. Swan-Ganz and radial artery catheters were placed to monitor hemodynamic functions. Artery blood samples were obtained to analyze ventilatory functions. Results: For hemodynamic changes in both TPL and RPL, central venous pressure, mean pulmonary arterial pressure and pulmonary capillary wedge pressure significantly increased 10 min after CO₂ insufflation and decreased to preanesthesia levels roughly 30 min after insufflation relief. For ventilatory functions, in both TPL and RPL, peak airway pressure, partial pressure of arterial carbon dioxide (PaCO₂), end-tidal carbon dioxide tension (PetCO₂), carbon dioxide output (VCO₂), and the difference between PaCO₂ and PetCO₂ (Pa-PetCO₂) all increased significantly 10 min after CO₂ insufflation and returned to the preanesthesia level 20 min after CO₂ desufflation. However, increments of PaCO₂, VCO₂ and Pa-PetCO₂ were significantly higher in RPL than in TPL, and did not return to the preanesthesia level until 30 min after CO₂ desufflation. Conclusion: For senior patients, TPL and RPL have similar effects on hemodynamic functions. However, RPL tends to cause much more change in the respiratory measurements.

Impaired Vascular Regulation in Patients with Obstructive Sleep Apnea

Impaired endothelium-dependent vasodilation has been documented in patients with sleep apnea. This impairment may result in blood flow dysregulation during apnea-induced fluctuations in arterial blood gases. To test the hypothesis that hypoxic and hypercapnic vasodilation in the forearm and cerebral circulation are impaired in patients with sleep apnea. We exposed 20 patients with moderate to severe sleep apnea and 20 control subjects, to isocapnic hypoxia and hyperoxic hypercapnia. A subset of 14 patients was restudied after treatment with continuous positive airway pressure. Cerebral flow velocity (transcranial Doppler), forearm blood flow (venous occlusion plethysmography), arterial pressure (automated sphygmomanometry), oxygen saturation (pulse oximetry), ventilation (pneumotachograph), and end-tidal oxygen and carbon dioxide tensions (expired gas analysis) were measured during three levels of hypoxia and two levels of hypercapnia. Cerebral vasodilator responses to hypoxia (-0.65 +/- 0.44 vs. -1.02 +/- 0.72 [mean +/- SD] units/% saturation; P = 0.03) and hypercapnia (2.01 +/- 0.88 vs. 2.57 +/- 0.89 units/mm Hg; P = 0.03) were smaller in patients versus control subjects. Hypoxic vasodilation in the forearm was also attenuated (-0.05 +/- 0.09 vs. -0.10 +/- 0.09 unit/% saturation; P = 0.04). Hypercapnia did not elicit forearm vasodilation in either group. Twelve weeks of continuous positive airway pressure treatment enhanced hypoxic vasodilation in the cerebral circulation (-0.83 +/- 0.32 vs. -0.46 +/- 0.29 units/% saturation; P = 0.01) and forearm (-0.19 +/- 0.15 vs. -0.02 +/- 0.08 units/% saturation; P = 0.003), and hypercapnic vasodilation in the brain showed a trend toward improvement (2.24 +/- 0.78 vs. 1.76 +/- 0.64 units/mm Hg; P = 0.06). Vasodilator responses to chemical stimuli in the cerebral circulation and the forearm are impaired in many patients with obstructive sleep apnea. Some of these impairments can be improved with continuous positive airway pressure.

Bedside end-tidal CO2 tension as a screening tool to exclude pulmonary embolism

End tidal carbon dioxide tension (P(ET,CO(2))) is a surrogate for dead space ventilation which may be useful in the evaluation of pulmonary embolism (PE). We aimed to define the optimal P(ET,CO(2)) level to exclude PE in patients evaluated for possible thromboembolism. 298 patients were enrolled over 6 months at a single academic centre. P(ET,CO(2)) was measured within 24 h of contrast-enhanced helical computed tomography, lower extremity duplex or ventilation/perfusion scan. Performance characteristics were measured by comparing test results with clinical diagnosis of PE. PE was diagnosed in 39 (13%) patients. Mean P( ET,CO(2)) in healthy volunteers did not differ from P( ET,CO(2)) in patients without PE (36.3+/-2.8 versus 35.5+/-6.8 mmHg). P(ET,CO(2 )) in patients with PE was 30.5+/-5.5 mmHg (p<0.001 versus patients without PE). A P(ET,CO(2)) of >or=36 mmHg had optimal sensitivity and specificity (87.2 and 53.0%, respectively) with a negative predictive value of 96.6% (95% CI 92.3-98.5). This increased to 97.6% (95% CI 93.2-99.) when combined with Wells score <4. A P(ET,CO(2)) of >or=36 mmHg may reliably exclude PE. Accuracy is augmented by combination with Wells score. P( ET,CO(2)) should be prospectively compared to D-dimer in accuracy and simplicity to exclude PE.

The effects of reduced end‐tidal carbon dioxide tension on cerebral blood flow during heat stress

Passive heat stress reduces arterial carbon dioxide partial pressure (P(aCO2)) as reflected by 3 to 5 Torr reductions in end-tidal carbon dioxide tension (P(ETCO2)). Heat stress also reduces cerebrovascular conductance (CBVC) by up to 30%. While is a strong regulator of CBVC, it is unlikely that the relatively small change in during heating is solely responsible for the reductions in CBVC. This study tested the hypothesis that P(aCO2), referenced by P(ETCO2), is not the sole mechanism for reductions in CBVC during heat stress. Mean arterial blood pressure (MAP), P(ETCO2), middle cerebral artery blood velocity (MCA V(mean)), and calculated CBVC (MCA V(mean)/MAP) were assessed in seven healthy individuals, during three separate conditions performed sequentially: (1) normothemia, (2) control passive heat stress and (3) passive heat stress with P(ETCO2) clamped at the normothermic level (using a computer-controlled sequential gas delivery breathing circuit). MAP was similar in the three thermal conditions (P = 0.55). Control heat stress increased internal temperature approximately 1.3 degrees C, which resulted in decreases in P(ETCO2), MCA V(mean) and calculated CBVC (P < 0.001 for all variables). During heat stress + clamp conditions internal temperature remained similar to that during the control heat stress condition (P = 0.31). Heat stress + clamp successfully restored to the normothermic level (P = 0.99) and increased MCA V(mean) (P = 0.002) and CBVC (P = 0.008) relative to control heat stress. Despite restoration of P(ETCO2), MCA V(mean) (P = 0.005) and CBVC (P = 0.03) remained reduced relative to normothermia. These results indicate that heat stress-induced reductions in , as referenced by P(ETCO2), contribute to the decrease in MCA V(mean) and CBVC; however, other factors (e.g. perhaps elevated sympathetic nerve activity) are also involved in mediating this response.

Transient influence of end-tidal carbon dioxide tension on the postural restraint in cerebral perfusion

In the upright position, cerebral blood flow is reduced, maybe because arterial carbon dioxide partial pressure (Pa(CO(2))) decreases. We evaluated the time-dependent influence of a reduction in Pa(CO(2)), as indicated by the end-tidal Pco(2) tension (Pet(CO(2))), on cerebral perfusion during head-up tilt. Mean arterial pressure, cardiac output, middle cerebral artery mean flow velocity (MCA V(mean)), and dynamic cerebral autoregulation at supine rest and 70 degrees head-up tilt were determined during free breathing and with Pet(CO(2)) clamped to the supine level. The postural changes in central hemodynamic variables were equivalent, and the cerebrovascular autoregulatory capacity was not significantly affected by tilt or by clamping Pet(CO(2)). In the first minute of tilt, the decline in MCA V(mean) (10 +/- 4 vs. 3 +/- 4 cm/s; mean +/- SE; P < 0.05) and Pet(CO(2)) (6.8 +/- 4.3 vs. 1.7 +/- 1.6 Torr; P < 0.05) was larger during spontaneous breathing than during isocapnic tilt. However, after 2 min in the head-up position, the reduction in MCA V(mean) was similar (7 +/- 5 vs. 6 +/- 3 cm/s), although the spontaneous decline in Pet(CO(2)) was maintained (P < 0.05 vs. isocapnic tilt). These results suggest that the potential contribution of Pa(CO(2)) to the postural reduction in MCA V(mean) is transient, leaving the mechanisms for the sustained restrain in MCA V(mean) to be identified.

The Effects Of Reduced End-tidal Carbon Dioxide Tension On Cerebrovascular Conductance During Heat Stress

The Effects Of Reduced End-tidal Carbon Dioxide Tension On Cerebrovascular Conductance During Heat Stress

Investigating medetomidine‐buprenorphine as preanaesthetic medication in cats

The objective of this study was to investigate medetomidine-buprenorphine preanaesthetic medication in cats. Forty American Society of Anesthesiologists (ASA) I female cats were enrolled in this prospective, blinded, clinical study. Cats were randomised into one of four groups: group M30 were injected intramuscularly with 30 microg/kg medetomidine, groups M10+B, M30+B and M50+B received 10, 30 and 50 microg/kg of medetomidine, respectively, each in combination with 20 microg/kg buprenorphine. After 30 minutes, a sedation score was allocated. Anaesthesia was induced using intravenous propofol and maintained using isoflurane in oxygen, while cats underwent ovariohysterectomy. Heart rate, respiratory rate, end-tidal carbon dioxide tension and oxygen saturation of haemoglobin were recorded. Atipamezole was administered intramuscularly at volatile agent discontinuation. Time taken to lift their head, sit in sternal and stand were recorded along with quality of recovery. M30+B cats required significantly less isoflurane compared with M30 cats. Heart rate and oxygen saturation of haemoglobin were significantly lower in M50+B cats than in M30 cats. All M+B groups experienced significantly better recoveries compared with the medetomidine only M30 control group. The addition of buprenorphine to medetomidine preanaesthetic medication in cats reduces volatile agent vaporiser setting and improves the quality of recovery from anaesthesia.

Autonomic and cerebrovascular abnormalities in mild COPD are worsened by chronic smoking

Patients with chronic obstructive pulmonary disease (COPD) may develop hypercapnia and hypoxia, two main determinants of cerebral blood flow. The current authors tested whether cerebrovascular regulation was altered in mild COPD, modified by manoeuvres acutely improving autonomic cardiovascular modulation or influenced by smoking habit. In 15 eucapnic normoxic mild COPD patients (eight smokers) and 28 age-matched controls (14 smokers), midcerebral artery blood flow velocity (MCFV), end-tidal carbon dioxide tension (P(ET,CO2)), arterial oxygen saturation (S(a,O2)), ECG and blood pressure at rest were monitored during progressive hypercapnic hyperoxia, isocapnic hypoxia, slow breathing and oxygen administration. MCFV, arterial baroreflex and dynamic MCFV-blood pressure relationships were compared by phase analysis. COPD and control smokers showed higher MCFV (when corrected for P(ET,CO2)), lower cerebrovascular resistance index and lower sensitivity to hypercapnia than nonsmokers, with equal sensitivity to S(a,O2) and similar phase analysis. Arterial baroreflex was depressed in all COPD patients. Slow breathing and oxygen administration improved baroreflex sensitivity and reduced MCFV in all COPD patients. Patients with mild chronic obstructive pulmonary disease show autonomic dysfunction. Chronic smoking induces cerebral vasodilation and impairs cerebrovascular control. All abnormalities can be partly corrected by improving the cardio- and cerebrovascular autonomic modulation, suggesting that functional autonomic abnormalities are already present at an early stage of disease.

The utility of cardiac sonography and capnography in predicting outcome in cardiac arrest

Emergency physicians and intensivists are increasingly utilizing capnography and bedside echocardiography during medical resuscitations. These techniques have shown promise in predicting outcomes in cardiac arrest, and no cases of return of spontaneous circulation in the setting of sonographic cardiac standstill and low end-tidal carbon dioxide have been reported. This case report illustrates an example of such an occurrence. Our aims are to report a case of return of spontaneous circulation in a patient with sonographic cardiac standstill, electrocardiographic pulseless electrical activity, and low end-tidal carbon dioxide tensions and to place the case in the context of previous literature on this topic. Case report and brief review of the literature. In 254 cases reported, no patient has survived in the setting of sonographic cardiac standstill and low end-tidal carbon dioxide tension, making the reported case unique. This case should serve to illustrate the utility and limitations of combined cardiac sonography and end-tidal carbon dioxide measurement in determining prognosis during cardiac arrest.

Voluntary Respiratory Control and Cerebral Blood Flow Velocity upon Ice-Water Immersion

In non-habituated subjects, cold-shock response to cold-water immersion causes rapid reduction in cerebral blood flow velocity (approximately 50%) due to hyperventilation, increasing risk of syncope, aspiration, and drowning. Adaptation to the response is possible, but requires several cold immersions. This study examines whether thorough instruction enables non-habituated persons to attenuate the ventilatory component of cold-shock response. There were nine volunteers (four women) who were lowered into a 0 degrees C immersion tank for 60 s. Middle cerebral artery mean velocity (CBFV) was measured together with ventilatory parameters and heart rate before, during, and after immersion. Within seconds after immersion in ice-water, heart rate increased significantly from 95 +/- 8 to 126 +/- 7 bpm (mean +/- SEM). Immersion was associated with an elevation in respiratory rate (from 12 +/- 3 to 21 +/- 5 breaths, min(-1)) and tidal volume (1022 +/- 142 to 1992 +/- 253 ml). Though end-tidal carbon dioxide tension decreased from 4.9 +/- 0.13 to 3.9 +/- 0.21 kPa, CBFV was insignificantly reduced by 7 +/- 4% during immersion with a brief nadir of 21 +/- 4%. Even without prior cold-water experience, subjects were able to suppress reflex hyperventilation following ice-water immersion, maintaining the cerebral blood flow velocity at a level not associated with impaired consciousness. This study implies that those susceptible to accidental cold-water immersion could benefit from education in cold-shock response and the possibility of reducing the ventilatory response voluntarily.