Changes In End-tidal Carbon Dioxide Research Articles

Nothing beats quality-controlled manual chest compressions: End-tidal carbon dioxide changes between manual cardiopulmonary resuscitation and with active compression–decompression device

Nothing beats quality-controlled manual chest compressions: End-tidal carbon dioxide changes between manual cardiopulmonary resuscitation and with active compression–decompression device

Baroreflex Activation Therapy Lowers Arterial Pressure Without Apparent Stimulation of the Carotid Bodies

Carotid baroreflex activation therapy produces a sustained fall in blood pressure in patients with resistant hypertension. Because the activation electrodes are implanted at the level of the carotid sinus, it is conceivable that the nearby located carotid body chemoreceptors are stimulated as well. Physiological stimulation of the carotid chemoreceptors not only stimulates respiration but also increases sympathetic activity, which may counteract the effects of baroreflex activation. The aim of this exploratory study is to investigate whether there is concomitant carotid chemoreflex activation during baroreflex activation therapy. Fifteen participants with the Rheos system were included in this single-center study. At arrival at the clinic, the device was switched off for 2 hours while patients were at rest. Subsequently, the device was switched on at 6 electric settings of high and low frequencies and amplitudes. Respiration and blood pressure measurements were performed during all device activation settings. Multilevel statistical models were adjusted for age, sex, body mass index, antihypertensive therapeutic index, sleep apnea, coronary artery disease, systolic blood pressure, and heart rate. There was no change in end-tidal carbon dioxide, partial pressure of carbon dioxide, breath duration, and breathing frequency during any of the electric settings with the device. Nevertheless, mean arterial pressure showed a highly significant decrease during electric activation (P<0.001). Carotid baroreflex activation therapy using the Rheos system did not stimulate respiration at several electric device activation energies, which suggests that there is no appreciable coactivation of carotid body chemoreceptors during device therapy.

Impaired cerebrovascular reactivity in multiple sclerosis.

Cerebrovascular reactivity (CVR) is an inherent indicator of the dilatory capacity of cerebral arterioles for a vasomotor stimulus for maintaining a spontaneous and instant increase of cerebral blood flow (CBF) in response to neural activation. The integrity of this mechanism is essential to preserving healthy neurovascular coupling; however, to our knowledge, no studies have investigated whether there are CVR abnormalities in multiple sclerosis (MS). To use hypercapnic perfusion magnetic resonance imaging to assess CVR impairment in patients with MS. A total of 19 healthy volunteers and 19 patients with MS underwent perfusion magnetic resonance imaging based on pseudocontinuous arterial spin labeling to measure CBF at normocapnia (ie, breathing room air) and hypercapnia. The hypercapnia condition is achieved by breathing 5% carbon dioxide gas mixture, which is a potent vasodilator causing an increase of CBF. Cerebrovascular reactivity was calculated as the percent increase of normocapnic to hypercapnic CBF normalized by the change in end-tidal carbon dioxide, which was recorded during both conditions. Group analysis was performed for regional and global CVR comparison between patients and controls. Regression analysis was also performed between CVR values, lesion load, and brain atrophy measures in patients with MS. A significant decrease of mean (SD) global gray matter CVR was found in patients with MS (3.56 [0.81]) compared with healthy controls (5.08 [1.56]; P = .001). Voxel-by-voxel analysis showed diffuse reduction of CVR in multiple regions of patients with MS. There was a significant negative correlation between gray matter CVR and lesion volume (R = 0.6, P = .004) and a significant positive correlation between global gray matter CVR and gray matter atrophy index (R = 0.5, P = .03). Our quantitative imaging findings suggest impairment in functional cerebrovascular pathophysiology, by measuring a diffuse decrease in CVR, which may be the underlying cause of neurodegeneration in MS.

The role of capnography during upper endoscopy in morbidly obese patients: a prospective study

BackgroundPulmonary depression remains a major concern when performing upper endoscopy in the morbidly obese patient. The aim of this prospective study is to determine the effects of sedation and role of capnography during preoperative upper endoscopy in obese patients. MethodsEighty-two consecutive diagnostic upper gastrointestinal endoscopies were performed in morbidly obese patients in an outpatient setting. Data on amount of drug administration and cardiorespiratory change were recorded. ResultsMean body mass index and duration of procedure was 46.4±8.2 kg/m2 and 9.4 ± 2.5 minutes, respectively. The mean dose of propofol was 139.5±45.1 mg. No clinically significant cardiorespiratory complications occurred. Respiratory depression (RD) was seen in 33/82 (40.2%) patients and included a mean absolute change in end-tidal carbon dioxide (EtCO2) of 7.1±8.5 mm Hg from baseline (P = .001). 54/82 (65.9%) patients had subclinical RD with 27/54 (50%) having RD. Abnormal EtCO2 detected all episodes of RD. The sensitivity and negative predictive value in determining RD by a change in EtCO2>10 mm Hg or an absent EtCO2 waveform during any point of the procedure was 81% and 78%, respectively. The relative risk was 2.3. ConclusionCapnography provided a real time assessment of changes in ventilation and can detect early phases of respiratory depression. Utilization of propofol as a means for sedation, with extended advanced monitoring technique, can allow for reduced adverse outcomes in morbidly obese patients undergoing upper endoscopy.

Role of perioperative monitoring in diagnosis of massive intraoperative cardiopulmonary embolism.

Massive thrombotic intraoperative pulmonary emboli (IOPE) is rare but carries a great degree of morbidity and mortality. This is the first study to formally assess the utility of various tools for the diagnosis of these events and the impact of each tool on mortality. Due to both the infrequent occurrence of these events and the high mortality of massive IOPE, it was cost-prohibitive to prospectively randomize patients to study commonly used diagnostic tools. Hence, a descriptive review of all reported cases in the literature was performed. This review yielded 146 cases for past 4 decades. Following a careful review of these cases, the alerting monitor for the occurrence of IOPE was recorded. Furthermore, we recorded the confirming diagnostic tool and the outcome of these patients. We compared 4 monitoring tools: (1) end-tidal carbon dioxide; (2) central catheter pressures; (3) echocardiography; and (4) standard monitoring of vital signs. Pre-event use of transesophageal echocardiography had no survival benefit. End-tidal carbon dioxide changes as an alerting tool were associated with improved survival compared to changes in vital signs (P<0.0001). Signs of right heart strain were associated with greater mortality, but direct thrombus visualization was not. Echocardiography appears to be useful for diagnosis of massive IOPE. Compared with hemodynamic collapse, end-tidal carbon dioxide decline as the presenting sign of massive IOPE may be associated with a better prognosis because it may represent earlier detection of IOPE and allow for more time to intervene.

The role of capnography in endoscopy patients undergoing nurse-administered propofol sedation: a randomized study

Objective. Standard benzodiazepine/opioid cocktail has proven inferior to propofol sedation during complicated endoscopic procedures and in low-tolerance patients. Propofol is a short-acting hypnotic with a potential risk of respiratory depression at levels of moderate to deep sedation. The existing literature on capnography for endoscopy patients sedated with nurse-administered propofol sedation (NAPS) is limited. Can the addition of capnography to standard monitoring during endoscopy with NAPS reduce the number, duration, and level of hypoxia. Materials and methods.This study was a randomized controlled trial with an intervention group (capnography) and a control group (without capnography). Eligible subjects were consecutive patients for endoscopy at Gentofte Hospital compliant with the criteria of NAPS. Results. Five hundred and forty patients, 263 with capnography and 277 without capnography, were included in the analysis. The number and total duration of hypoxia was reduced by 39.3% and 21.1% in the intervention group compared to the control group (p > 0.05). No differences in actions taken against insufficient respiration were found. Changes in end-tidal carbon dioxide (R = 0.177, p-value < 0.001) and respiratory rate (R = 0.092, p-value < 0.001) were correlated to oxygen saturation (SpO2) up to 36 s prior to changes in SpO2. Conclusions.Capnography seems to reduce the number and duration of hypoxia in NAPS patients (p > 0.05). Capnography is able to detect insufficient respiration that may lead to hypoxia prior to changes in pulse oximetry. However, due to a limited clinical benefit and additional costs associated with capnography, we do not find capnography necessary during the use of NAPS.

In Reply

We thank Drs. Youngblood and Sondergaard for their letters regarding our recently published article.1We agree with Dr. Youngblood1 that standard monitoring already provides substantial information about our patients’ hemodynamic status. Today, pulse pressure variation (PPV) and its corresponding noninvasive parameters are easily available and used in clinical practice.2 In recent years, PPV analysis algorithms have been integrated into different standard monitoring systems,3 and PPV can be reliably assessed on a noninvasive basis by plethysmography.4 Thus, standard monitoring evolves, and today PPV can be considered a standard hemodynamic parameter for a larger population of patients who require perioperative invasive blood pressure monitoring with an arterial line. When no arterial line is required, pulse oximetry devices, which provide the respective functional hemodynamic parameters, can be applied to assess and predict fluid responsiveness. Clearly, continuous end-tidal carbon dioxide monitoring may further support clinical decision making—but still this requires validation in large perioperative clinical studies. In addition, one has to keep in mind that the changes in end-tidal carbon dioxide, induced by a passive leg raising, cannot always be assessed during surgery.We read with interest Dr. Sondergaard’s acerbic letter regarding our article; we thank him for the querulous interest he has shown in our work. Neither our results nor our discussion demonstrate that the PPV should replace cardiac output (CO) measurements. Dr. Sondergaard’s reference of our work when making this claim suggests that he is less familiar with our results.We do demonstrate that when estimating CO trends, volume expansion-induced changes in PPV is superior to standard measures of arterial pressure.1,5 PPV is interesting because it identifies patients who will benefit from fluid loading and volume expansion-induced changes in PPV allows for ongoing assessment of fluid-loading efficacy. This provides the clinician with important information which then allows for CO optimization.Does an increased CO, as a result of fluid loading, result in improved postoperative outcomes? Dr. Sondergaard will be disappointed when we affirm that we do not have the answer to this question. He may be even more disappointed when we affirm that the answer to this question can probably not be framed in his favored “YES/NO” format.CO is only one of the components of oxygen delivery, and maximizing CO, through fluid administration, does not equate to optimization of oxygen delivery. Fluid loading always causes hemodilution, and hemoglobin concentration plays a key role in oxygen delivery. It is therefore possible that increasing CO, by administering a large fluid load, may actually decrease oxygen delivery. Oxygen delivery is the true parameter to optimize, but it remains difficult to measure and several parameters should be simultaneously optimized to achieve ideal oxygen delivery. PPV and volume expansion-induced changes in PPV are only two of the tools, which may be used to achieve this goal. Using them in isolation may be appropriate in some clinical settings, but it will always remain suboptimal.Our aim in conducting this study was to explore the predictive performance of PPV under ideal conditions. As a result, we did not record the number of patients who were not selected because of atrial fibrillation.May we offer a more balanced and less jejune set of conclusions than those purportedly “obvious” conclusions drawn by Dr. Sondergaard?NO; CO measurements alone is not sufficient for optimization of oxygen delivery. Fluid loading impacts hemoglobin concentration, and neither volume expansion-induced changes in PPV nor direct CO measurements reliably reflect this.NO; because there is no strong and definitive evidence to suggest that “validated” and calibrated dilution methods with continuous, updated arterial curve–based calculation of CO impact on postoperative outcomes, we do not have to use them (“…no monitoring tool, no matter how accurate, by itself has improved patient outcome.”)6NO; we do not find ourselves compelled to adopt cardiovascular models from giants such as Guyton or Dr. Sondergaard. Eminence is rarely, if ever, a substitute for evidence.YES, key opinion holders in the European intensive care community should be very cautious about promoting any device or system that has not clearly demonstrated its ability to improve postoperative outcomes.Having matured beyond Dr. Sondergaard’s preoccupation with dreams of the conceptualization and intellectualization of endeavors past explored, we have actually evaluated PVV to understand its abilities and limitations. Although PPV informs clinicians on how fluid loading impacts on CO, there is a common misconception that fluid loading is required when PPV is high—this requires correcting.PPV requires engagement, interpretation, and judgment. For this reason, we have developed the grey zone concept, which we offer to Dr. Sondergaard in the hope that he would evaluate it empirically in a clinical study.

End-Tidal Carbon Dioxide as a Measure of Stress Response to Clustered Nursing Interventions in Neurologic Patients

Guidelines recommend rest periods between nursing interventions for patients with a neurologic diagnosis but do not specify a safe number of interventions. To examine the physiological stress response to clustered nursing interventions in neurologic patients receiving mechanical ventilation. Prospective, comparative, descriptive design to examine effects of clustered interventions (≥6 interventions in a single nursing interaction) versus nonclustered interventions on patients' stress. Stress response was defined as a 10% change in end-tidal carbon dioxide from before the interaction to (1) 5 and 10 minutes after the start of the interaction, (2) at the end of the interaction, and (3) 15 minutes after the interaction. The mean percent change in end-tidal carbon dioxide at 5 minutes differed significantly between patients with clustered interventions and patients with nonclustered interventions (6.7% vs -0.2%; P = .001). Patients with clustered interventions were significantly more likely than patients with low clustering to exhibit a stress response at 5 minutes (24.3% vs 0%; P = .01). Neurologic patients receiving mechanical ventilation who experienced 6 or more clustered nursing interventions showed a higher mean change in end-tidal carbon dioxide than did patients who received fewer than 6 clustered interventions. These findings suggest that providing fewer interventions during 1 nursing interaction may minimize induced stress in neurologic patients receiving mechanical ventilation.

End-tidal carbon dioxide and arterial pressure for predicting volume responsiveness by the passive leg raising test: reply to Piagnerelli and Biston

Dear Editor, We thank Drs. Piagnerelli and Biston for their interest in our study ‘‘Endtidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test’’ that was recently published in Intensive Care Medicine [1]. We also thank them for their valuable comments [2]. They point out that our inclusion criteria could represent limitations of the study that were not stated in the manuscript. First, concerning the proportion of patients with cardiac arrhythmias and as recognized by Drs. Piagnerelli and Biston themselves, one advantage of the passive leg raising (PLR) test is that it remains valid in such a situation. As suggested by our colleagues in their letter, we compared the diagnostic ability of the changes in end-tidal carbon dioxide induced by the PLR test to predict fluid responsiveness in patients with and without arrhythmias. In the 11 patients (17 % of the population) with arrhythmias, the area under the receiver operating characteristics curve was 0.92 ± 0.18. In the 54 patients without arrhythmias, it was 0.97 ± 0.02. Thus, this study corroborates previous works, including a meta-analysis, in showing that the PLR test is valid in patients with an irregular cardiac rhythm. Second, concerning norepinephrine administration, we agree that changing its dose might change cardiac preload and preload dependence, as recently demonstrated. This is the reason why the dose of norepinephrine was kept unchanged during the study time. Since norepinephrine was administered in almost all our patients (97 %), we cannot compare the PLR test validity in patients with and without vasoconstrictor administration. Finally, we disagree with Drs. Piagnerelli and Biston when they suppose that our results might have been different in patients with higher tidal volumes. Indeed, though it is true that a low tidal volume invalidates indices of preload responsiveness based on the respiratory variations of hemodynamic signals, there is absolutely no reason why it should change the reliability of the PLR test. Obviously, the hemodynamic effects of PLR, which depend upon the transfer of blood from the leg splanchnic compartment, cannot be influenced by the tidal volume. To conclude, we strongly believe that the results of our study may also apply in patients with cardiac arrhythmias, norepinephrine administration and non-low-tidal volume. As we did in the article [1], we emphasize that it might apply only to patients under mechanical ventilation without spontaneous breathing activity. Also, these results are limited to patients without any right ventricular failure and intra-abdominal hypertension since these two conditions were not investigated in the study.

Changes in End-Tidal Carbon Dioxide and Volumetric Carbon Dioxide as Predictors of Volume Responsiveness in Hemodynamically Unstable Patients

The purpose of this study was to determine whether changes in PETCO2 and exhaled CO2 (VCO2) can predict fluid responsiveness after a preload challenge. A retrospective review of prospectively recorded data. A medical intensive care unit of a university-affiliated tertiary care hospital. Mechanically ventilated patients undergoing a preload challenge. In the authors' intensive care unit, fluid responsiveness is determined by a passive leg raising (PLR) maneuver and/or a 500-mL crystalloid challenge. An increase in the stroke volume index >10% as measured by a NICOM bioreactance cardiac output monitor (Cheetah Medical, Inc, Vancouver, WA) is used to determine fluid responsiveness. PETCO2 and volumetric capnography (VCO2) were monitored via a combined CO2 and flow sensor capnostat (Respironics NM3 Monitor; Philips Healthcare, Eindhoven, Netherlands). Patients were mechanically ventilated with tidal volumes controlled at 8 mL/kg, allowing for consistent minute ventilation. During the study period, 44 challenges (10 PLR and 34 fluid boluses) were performed on 34 patients. There were 24 (54%) positive "fluid" responses. PETCO2 increased by 5.9% ± 7.6% in the responders compared with 1.4% ± 4.4% in the nonresponders (p = 0.02). Similarly, VCO2 increased by 11.0% ± 8.6% in the responders compared with 0.8% ± 5.6% in the nonresponders (p = 0.001). The area under the receiver operating characteristic curve was 0.67 (95% confidence interval, 0.48-0.80) for PETCO2 and 0.79 (95% confidence interval, 0.63-0.89) for VCO2. PETCO2 and VCO2 were predictive of fluid responsiveness only in those patients without underlying lung disease. The stroke volume variation was 15.8 ± 3.7 in the responders compared with 13.6 ± 4.8 in the nonresponders (p = 0.15). Dynamic changes in PETCO2 and VCO2 may be used as adjunctive indicators of fluid responsiveness in patients without underlying lung disease.

End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test

In stable ventilatory and metabolic conditions, changes in end-tidal carbon dioxide (EtCO(2)) might reflect changes in cardiac index (CI). We tested whether EtCO(2) detects changes in CI induced by volume expansion and whether changes in EtCO(2) during passive leg raising (PLR) predict fluid responsiveness. We compared EtCO(2) and arterial pulse pressure for this purpose. We included 65 patients [Simplified Acute Physiology Score (SAPS) II = 57 ± 19, 37 males, under mechanical ventilation without spontaneous breathing, 15 % with chronic obstructive pulmonary disease, baseline CI = 2.9 ± 1.1 L/min/m(2)] in whom a fluid challenge was decided due to circulatory failure and who were monitored by an expiratory-CO(2) sensor and a PiCCO2 device. In all patients, we measured arterial pressure, EtCO(2), and CI before and after a fluid challenge. In 40 patients, PLR was performed before fluid administration. The PLR-induced changes in arterial pressure, EtCO(2), and CI were recorded. Considering the whole population, the fluid-induced changes in EtCO(2) and CI were correlated (r (2) = 0.45, p = 0.0001). Considering the 40 patients in whom PLR was performed, volume expansion increased CI ≥ 15 % in 21 "volume responders." A PLR-induced increase in EtCO(2) ≥ 5 % predicted a fluid-induced increase in CI ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %) and specificity of 100 (82-100) %. The prediction ability of the PLR-induced changes in CI was not different. The area under the receiver-operating characteristic (ROC) curve for the PLR-induced changes in pulse pressure was not significantly different from 0.5. The changes in EtCO(2) induced by a PLR test predicted fluid responsiveness with reliability, while the changes in arterial pulse pressure did not.

Impact of Extracranial–Intracranial Bypass on Cerebrovascular Reactivity and Clinical Outcome in Patients With Symptomatic Moyamoya Vasculopathy

The purpose of this study was to evaluate in symptomatic moyamoya patients the effect of surgical revascularization on impaired cerebrovascular reactivity (CVR) and its relationship to clinical outcome. Brain revascularization was performed using a direct superficial temporal artery to middle cerebral artery bypass or indirect encephalo-dural-arterial synangiosis. CVR was measured pre- and 3 months postoperatively using blood oxygen level-dependent MRI during iso-oxic hypercapnic changes in end-tidal carbon dioxide. Outcomes were assessed by MRI, clinical examination, and modified Rankin Scale scores. Fifty-five hemispheres were revascularized in 39 patients (superficial temporal artery to middle cerebral artery in 47, encephalo-dural-arterial synangiosis in 8). Surgery reversed CVR impairment in 52 hemispheres (94.5%) and in 36 of 39 patients (92.3%; Fisher exact test, P<0.001), and this was predictive of a patent extracranial-intracranial bypass. New, clinically silent perioperative hemorrhages, cortical foci of ischemia, or new white matter T2 hyperintensities were detected after 11 surgeries (20%), but no new lesions arose after 3 postoperative months. One patient had a clinical perioperative stroke (1.8%). In clinical follow-up, 37 of 39 patients (95%) had stable or improved modified Rankin Scale scores and 2 patients (5.1%) worsened. No patients with patent bypasses or CVR improvements exhibited new clinical symptoms, but failure of CVR improvement corresponded to a poorer long-term outcome (Fisher exact test, P<0.001). Cerebral revascularization surgery is a safe and effective treatment for reversing preoperative CVR defects and may prevent recurrence of preoperative symptoms. Moreover, CVR measurements may be useful in long-term follow-up and for predicting bypass patency.

Utility of endtidal carbon dioxide monitoring in detection of hypoxia during sedation for brain magnetic resonance imaging in children with developmental disabilities

We have shown previously that children with developmental disabilities have three times higher incidence of sedation-related hypoxia when compared with normal children. Our objectives were to describe the changes in endtidal carbon dioxide (ETCO(2)) values and the utility of ETCO(2) monitoring in earlier identification of hypoxia during sedation for brain magnetic resonance imaging (MRI) in children with developmental disabilities. We conducted a prospective observational study of a convenience sample of 150 children with developmental disabilities aged 1-10 years who received intravenous sedation for brain MRI. Children were sedated and monitored according to the institution's sedation protocol. We recorded ETCO(2) levels, hypoxia, and adverse events during sedation. Hypoxia was defined as SpO(2) < 93%. A change in ETCO(2) level ≥ 10 mm Hg from presedation baseline, an intra-sedation ≥ 50 mm Hg, and loss of capnographic waveform were considered as significant ETCO(2) abnormalities. Of the children, 80.7% (121/150) were sedated with a combination of pentobarbital and fentanyl. ETCO(2) abnormalities were noted in 42.6% (64/150) of sedation encounters. Hypoxia occurred in 18% (27/150) of subjects. ETCO(2) abnormalities were documented in 19(70%) patients with hypoxia before changes in pulse oximetry were noted. ETCO(2) changes were noted a mean of 4.38 ± 1.89 min prior to occurrence of hypoxia. ETCO(2) abnormalities and hypoxia occur commonly during sedation in children with developmental disabilities. ETCO(2) monitoring is useful in early recognition of impending hypoxia during sedation in children with developmental disabilities.

The influence of changes in end‐tidal carbon dioxide upon the Bispectral Index*

Carbon dioxide is known to affect consciousness in animals and humans. We surmised that changes in end-tidal carbon dioxide during anaesthesia might affect the Bispectral Index. Twenty-four patients due to undergo surgery were anaesthetised with fentanyl and a propofol infusion. The Bispectral Index, pulse rate and blood pressure were recorded while end-tidal carbon dioxide levels were changed. The patients acted as their own controls as they were subjected to high, normal and low levels of end-tidal carbon dioxide (3-12 kPa) according to a randomised sequence. There were no changes in the Bispectral Index or haemodynamic variables resulting from manipulation of the end-tidal carbon dioxide. At the level of hypnosis involved in this study, changes in end-tidal carbon dioxide, within the range tested, do not result in changes in the Bispectral Index.

Effect of Small Bowel Perforation During Laparoscopy on End-Tidal Carbon Dioxide: Observation in a Small Animal Model

There are currently no reports in the literature regarding changes in end-tidal carbon dioxide (ETCO(2)) when the small bowel is deliberately or inadvertently perforated during laparoscopic surgery. The aim of this study was to assess the influence of small bowel perforation during laparoscopy on ETCO(2) in a rat model. Two groups of Wistar rats (n = 8/group) were anesthetized, tracheostomized, and mechanically ventilated at a fixed tidal volume and respiratory rate. After a stabilization phase of 30 min, CO(2) pneumoperitoneum was established to 5 mmHg in one group and 12 mmHg in the other group, and maintained for 30 min. A small bowel perforation was then created and pneumoperitoneum was reestablished for another 30 min. Blood pressure, heart rate, peak ventilatory pressure, and ETCO(2) were recorded throughout the experiment. No significant changes in blood pressure throughout the experiment were noted in either group. The ventilatory pressure increased in both groups after the induction of pneumoperitoneum. In the 5 mmHg group, there was a modest increase in ETCO(2) following the induction of pneumoperitoneum (from 39.4 +/- 1.9 to 41.1 +/- 1.4, P = 0.014), and a further increase following the small bowel perforation (from 41.1 +/- 1.4 to 42 +/- 0.8, P = 0.007). In the 12 mmHg group, there was no change in ETCO(2) after the induction of pneumoperitoneum; however, there was a substantial increase in ETCO(2) following bowel perforation (35.0 +/- 2.0 to 49.8 +/- 7.1, P = 0.002). ETCO(2) increases when the small bowel is perforated during CO(2) pneumoperitoneum. This increase seems more substantial under higher pneumoperitoneal pressures. Small bowel injury may enable the diffusion of CO(2) through the bowel mucosa, causing ETCO(2) elevation. Therefore, an abrupt increase in ETCO(2) observed during laparoscopy may indicate small bowel injury.

Quantified Changes in End-tidal Carbon Dioxide During Procedural Sedation Are Associated with Specific Clinical Signs of Respiratory Depression

Quantified Changes in End-tidal Carbon Dioxide During Procedural Sedation Are Associated with Specific Clinical Signs of Respiratory Depression

Cerebral haemodynamics in patients with chronic renal failure: effects of haemodialysis

We measured middle cerebral artery (MCA) flow velocity (FV), dynamic pressure autoregulation, and carbon dioxide reactivity (CRCO(2)) in patients with chronic renal failure before and after haemodialysis using transcranial Doppler ultrasonography. Twelve patients on long-term haemodialysis were recruited. MCA FV was measured continuously. The transient hyperaemic response test was used to assess cerebral autoregulation, and per cent change in FV per kPa change in end-tidal carbon dioxide was calculated to assess CRCO(2). All measurements were recorded before and after haemodialysis. MCA FV (mean [sd]) decreased from 57 (10) cm s(-1) before to 46 (13) cm s(-1) after haemodialysis (P<0.01). The transient hyperaemic response ratio (THRR) was (mean [sd]) 1.29 (0.13) before haemodialysis and did not change significantly following haemodialysis (1.36 [0.10]). CRCO(2) was 21.7 (8.3)% kPa(-1) before haemodialysis and remained unchanged afterwards (20.9 [3.8]% kPa(-1)). Values in normal subjects for MCA FV, THRR and CRCO(2) are 56 (12) cm s(-1), 1.26 (0.13) and 22 (6)% kPa(-1), respectively. MCA FV decreases significantly after haemodialysis. Dynamic pressure autoregulation and CRCO(2) remain normal in patients with chronic renal failure, and are not altered significantly by haemodialysis.

Spontaneous ventilation with remifentanil in children

Remifentanil is a short-acting drug that allows us to study the specific respiratory effects of potent opioid analgesics. The purpose of this study is to describe the effects of a remifentanil infusion during spontaneous ventilation in children. Pharmacokinetic studies provide useful information on the time course of opioid blood concentrations; however, they cannot be easily translated into infusion administration guidelines for pediatric clinical practice. A total of 32 children, aged 2-7 years, undergoing restorative dentistry, spontaneously breathing under sevoflurane anesthesia were enrolled in the study. After an initial bolus dose of remifentanil, an infusion was administered in ascending logarithmic increments at 10 min intervals. Increments were discontinued when endtidal carbon dioxide exceeded 9 kPa (70 mmHg), desaturation occurred (SpO2 < 94%) or with the onset of apnea (>5 s). The maximum tolerated dose was determined for each subject. Endtidal carbon dioxide, minute ventilation and respiratory rate were continuously recorded. The median tolerated dose of remifentanil was 0.127 microg.kg(-1).min(-1) (range: 0.053-0.3 microg.kg(-1).min(-1)). When comparing the last four incremental increases in each subject, 35% change in respiratory rate occurred in the last 10 min period while changes in endtidal carbon dioxide and minute ventilation were gradual and of less magnitude. There was no correlation between age and respiratory rate. There is a large variation in the dose of remifentanil tolerated by children while breathing spontaneously under anesthesia. A respiratory rate of <10 b.min(-1) appears to be the best predictor of the maximum tolerated dose.

The effect of changes in end-tidal carbon dioxide on vascular reactivity of skin

The effect of changes in end-tidal carbon dioxide on vascular reactivity of skin

Effects of ephedrine, dobutamine and dopexamine on cerebral haemodynamics: transcranial Doppler studies in healthy volunteers

Sympathomimetic drugs are assumed to have no direct effects on cerebral haemodynamics on the basis of animal experiments; there is little evidence of their direct effects in humans. This study aimed to address this issue. The effects of ephedrine, dobutamine, and dopexamine on cerebral autoregulation, cerebral vascular reactivity to carbon dioxide, estimated cerebral perfusion pressure, and zero flow pressure (ZPF) were studied in 10 healthy volunteers using transcranial Doppler ultrasound. The strength of autoregulation was measured using the transient hyperaemic response test. The reactivity to carbon dioxide was measured as the change in middle cerebral artery flow velocity with a step change in end-tidal carbon dioxide. For the estimated cerebral perfusion pressure and the ZFP, established formulae were used which utilized instantaneous values of arterial pressure and middle cerebral artery flow velocity. Measurements were made at baseline and after i.v. infusion of the study drug to an endpoint of 25% increase in mean arterial pressure (MAP) (ephedrine, dobutamine) or cardiac index (dopexamine). There was no significant change in the strength of autoregulation (from (mean (SD)) 1.07 (0.16) to 1.07 (0.18); from 1.07 (0.16) to 1.03 (0.19); from 1.04 (0.12) to 1.04 (0.25)), reactivity to carbon dioxide (from 40% (8) to 36 (10); from 37 (12) to 37 (11); from 45 (12) to 43 (11)) with ephedrine, dobutamine, or dopexamine, respectively. Despite a clinically significant increase in MAP with ephedrine and dobutamine and a clinically significant increase in cardiac index with dopexamine, the estimated cerebral perfusion pressure did not change significantly (from 81 (38) to 60 (16) mm Hg with ephedrine; from 67 (22) to 63 (11) mm Hg with dobutamine; from 87 (27) to 79 (17) mm Hg with dopexamine). The ZFP increased significantly with ephedrine (from 29 (10) to 44 (11) mm Hg) and dobutamine (from 35 (14) to 43 (10) mm Hg) but not dopexamine (from 3 (23) to 11 (22) mm Hg). Sympathomimetic agents do not significantly change cerebrovascular homeostasis as assessed by the transient hyperaemic response test, reactivity to carbon dioxide and estimated cerebral perfusion pressure.