Arterial Partial Pressure Of Carbon Dioxide Research Articles

Fuzzy-based framework for diagnosis of acid–base disorders

The main objective of this research is to develop a fuzzy-based framework for diagnosis of different acid–base disorders. There are several acid–base disorders that cause many clinical complications and their proper diagnosis is the only way for their efficient treatment. The common disorders are metabolic acidosis, metabolic alkalosis, non-anion gap acidosis, anion-gap acidosis, acute respiratory alkalosis and chronic respiratory alkalosis. The proposed fuzzy-based framework was used to diagnose all of these disorders using four parameters directly measured in blood: hydrogen-ion concentration (pH), arterial blood carbon dioxide partial pressure (paCO2), sodium ions concentration (Na+) and chloride ions concentration (Cl−) along with 12 features extracted from the directly measured parameters. The validation results showed that the developed framework has an accuracy of 94%, an average sensitivity of 88% and a specificity of 93%. These results imply that the developed fuzzy-based framework is accurate and reliable one and can be used to help clinicians specially the non-expert ones to provide correct and rapid diagnosis of acid–base disorders.

Transcutaneous Carbon Dioxide Monitoring Accurately Predicts Arterial Carbon Dioxide Partial Pressure in Patients Undergoing Prolonged Laparoscopic Surgery

Transcutaneous Carbon Dioxide Monitoring Accurately Predicts Arterial Carbon Dioxide Partial Pressure in Patients Undergoing Prolonged Laparoscopic Surgery

Lactobacillus rhamnosus HN001 Attenuates Allergy Development in a Pig Model

BackgroundProbiotics have been studied as immunomodulatory agents of allergy. Several human probiotic trials tracking the development of eczema and other forms of allergy have yielded inconsistent results. A recent infant study demonstrated that pre and postnatal Lactobacillus rhamnosus HN001 (HN001) supplementation decreased the prevalence of eczema and IgE associated eczema. However, the influence of HN001 on the incidence of wheeze, asthma, and/or other allergic manifestations has yet to be reported.ObjectiveThis study was conducted to determine the effects of the probiotic HN001 on the development of allergic lung disease in a pig model.MethodsAllergy was induced by a series of subcutaneous and intratracheal sensitizations with Ascaris suum allergen (ASA) during a six week time frame in post-weanling pigs supplemented daily with HN001, or without supplementation. One week following final sensitization intradermal skin tests and respiratory challenges were conducted.ResultsIn response to intradermal and respiratory challenges, ASA-sensitized pigs fed HN001 had less severe skin flare reactions, smaller increases in pleural pressure, and trends towards lower changes in arterial oxygen and carbon dioxide partial pressure levels compared to control pigs. The frequency of ASA-specific IFN-γ-secreting peripheral blood mononuclear cells, as well as the amount of IL-10 produced by ASA-specific cells, was of greater magnitude in probiotic-fed pigs compared to control animals. These observations suggest that differences in clinical responses to the allergen challenges may be related to probiotic-induced modulation of Th1 (IFN-γ) and regulatory (IL-10) cytokine expression.ConclusionsProbiotic supplementation decreased the severity of allergic skin and lung responses in allergen-sensitized pigs with a corresponding increase in IFN-γ expression. A similar correlation between certain allergic responses and increased IFN-γ expression has been reported in human clinical studies of allergy; this pig model of allergy may be indicative of potential probiotic modulation of allergic lung disease in humans.

The ability of hydroxysafflor yellow a to attenuate lipopolysaccharide‐induced pulmonary inflammatory injury in mice

Hydroxysafflor yellow A (HSYA) is a component of the flower of Carthamus tinctorius L. The present study investigated whether HSYA could attenuate acute lung injury (ALI) induced by lipopolysaccharide (LPS) administration. Male Kunming mice were pretreated with HSYA 0.5 h prior to intraperitoneal application of LPS. Arterial blood gas, lung water content index, lung tissue myeloperoxidase (MPO) activity, mRNA expression of inflammatory cytokines, NF-κBp65, p38 mitogen-activated protein kinase (MAPK) and pathological changes in lung morphology were assessed. After LPS administration, all animals displayed increased arterial carbon dioxide partial pressure (PaCO₂), and decreased arterial oxygen partial pressure (PaO₂), arterial oxygen saturation (SO₂), HCO₃⁻ concentration and pH, which were ameliorated by pretreating the animals with HSYA. HSYA administration significantly attenuated inflammatory cell infiltration and alleviated pulmonary edema induced by LPS. Moreover, HSYA decreased NF-κB p65 nuclear translocation, inhibited proinflammatory cytokine TNF-α, IL-1β and IL-6 mRNA expression and promoted antiinflammatory cytokine IL-10 gene expression following LPS injection. Pulmonary p38 MAPK phosphorylation was upregulated 4 h after LPS treatment, which could be suppressed by pretreatment with HSYA. These findings demonstrated the protective effect of HSYA against LPS-induced acute lung injury, which is suggested to be associated with the inhibition of p38 MAPK, NF-κB p65 activation and alteration of inflammatory cytokine expression.

1367 Cerebral Haemodynamics and Carbon Dioxide Reactivity at Children During Severe Nosocomial Pneumonia

Background: Most patients with severe nosocomial pneumonia (SNP) develop potentially irreversible cerebral dysfunctions. We hypothesized that cerebral haemodynamics and carbon dioxide reactivity would be impaired in children with severe nosocomial pneumonia and pathological electroencephalogram patterns. Methods: After approval of the institutional ethics committee, 18 mechanically ventilated patients with severe nosocomial pneumonia and pathological electroencephalogram patterns underwent measurements of cerebral blood flow and jugular venous oxygen saturation before and after reduction of the arterial carbon dioxide partial pressure by 0.84 ± 0.72 kPa by perventilation. The cerebral capillary closing pressure was determined from transcranial Doppler measurements of the arterial blood flow of the middle cerebral artery and the arterial pressure curve. A t test for matched pairs was used for statistical analysis (P < 0.05). Results: During stable mean arterial pressure and cardiac index, reduction of the arterial carbon dioxide partial pressure led to a significant increase of the capillary closing pressure from 24,2 ± 10,2 mmHg to 37,1 ± 13,2 mmHg (P < 0.001), with a consecutive decrease of blood flow velocity in the middle cerebral artery of 23.3 ± 2.2%/kPa (P < 0.001), of cerebral blood flow from 60,2 ± 29,1 ml/100 g/min to 38,1 ± 16,2 ml/100 g/min (P < 0.001) and of jugular venous oxygen saturation from 74,2 ± 8,2% to 64,1 ± 10,0% (P < 0.01). Conclusion: In contrast to other experimental and clinical data, we observed no pathological.

PP-326. Cerebral haemodynamics and carbon dioxide reactivity during neonatal acute pneumonia

After approval of the institutional ethics committee, 21 mechanically ventilated patients with acute pneumonia and pathological electroencephalogram patterns underwent measurements of cerebral blood flow and jugular venous oxygen saturation before and after reduction of the arterial carbon dioxide partial pressure. The cerebral capillary closing pressure was determined from transcranial Doppler measurements of the arterial blood flow of the middle cerebral artery and the arterial pressure curve. A t test for matched pairs was used for statistical analysis (P<0.05).

Cerebral Hemodynamic Effects of Acute Hyperoxia and Hyperventilation after Severe Traumatic Brain Injury

The purpose of this study was to examine the effects of hyperventilation or hyperoxia on cerebral hemodynamic parameters over time in patients with severe traumatic brain injury (TBI). We prospectively studied 186 patients with severe TBI. CO₂ and O₂ reactivity tests were conducted twice a day on days 1-5 and once daily on days 6-10 after injury. During hyperventilation there was a significant decrease in intracranial pressure (ICP), mean arterial pressure (MAP), jugular venous oxygen saturation (Sjvo₂), brain tissue Po₂ (Pbto₂), and flow velocity (FV). During hyperoxia there was an increase in Sjvo₂ and Pbto₂, and a small but consistent decrease in ICP, end-tidal carbon dioxide (etco₂), partial arterial carbon dioxide pressure (Paco₂), and FV. Brain tissue oxygen reactivity during the first 12 h after injury averaged 19.7 ± 3.0%, and slowly decreased over the next 7 days. The autoregulatory index (ARI; normal = 5.3 ± 1.3) averaged 2.2 ± 1.5 on day 1 post-injury, and gradually improved over the 10 days of monitoring. The ARI significantly improved during hyperoxia, by an average of 0.4 ± 1.8 on the left, and by 0.5 ± 1.8 on the right. However, the change in ARI with hyperoxia was much smaller than that observed with hyperventilation. Hyperventilation increased ARI by an average of 1.3 ± 1.9 on the left, and 1.5 ± 2.0 on the right. Pressure autoregulation, as assessed by dynamic testing, was impaired in these head-injured patients. Acute hyperoxia significantly improved pressure autoregulation, although the effect was smaller than that induced by hyperventilation. The very small change in Paco₂ induced by hyperoxia does not appear to explain this finding. Rather, the vasoconstriction induced by acute hyperoxia may allow the cerebral vessels to respond better to transient hypotension. Further studies are needed to define the clinical significance of these observations.

Transcutaneous Carbon Dioxide Monitoring Accurately Predicts Arterial Carbon Dioxide Partial Pressure in Patients Undergoing Prolonged Laparoscopic Surgery

There may be large differences between measurements of end-tidal carbon dioxide partial pressure (Petco(2)) and arterial carbon dioxide partial pressure (Paco(2)) during laparoscopic surgeries. Transcutaneous carbon dioxide (Ptcco(2)) monitoring can be used to noninvasively and continuously estimate Paco(2). In the present study we evaluated the accuracy of Ptcco(2) monitoring in predicting the Paco(2) during laparoscopic surgeries with prolonged pneumoperitoneum. Sixteen patients who underwent laparoscopic radical gastrectomy or radical proctectomy under general anesthesia were included in the study. Their Paco(2), Petco(2), and Ptcco(2) values were measured at 3 time points before and after pneumoperitoneum. Agreement among measures was assessed by the Bland-Altman method. Forty-eight sample sets were obtained. The average Paco(2)- Ptcco(2) difference was -0.9 + or - 6.4 mm Hg (mean + or - 2 SD). The average Paco(2) - Petco(2) difference was 7.5 + or - 7.0 mm Hg (mean + or - 2 SD). Paco(2) - Ptcco(2) was less than or equal to + or -5 mm Hg for 88% of the samples. Paco(2) - Petco(2) was less than or equal to + or -5 mm Hg for 17% of the samples (P < 0.05). While undergoing long-term pneumoperitoneum laparoscopic surgery, Ptcco(2) monitoring is more accurate than is PETCO(2) monitoring in predicting the patients' Paco(2).

Determinants of cerebral oximetry in patients undergoing off-pump coronary artery bypass grafting: an observational study

The present study investigated whether positioning of the heart during off-pump coronary artery bypass grafting leads to changes in regional cerebral oxygen saturation measured by near infrared spectroscopy. In 35 consecutive patients undergoing elective off-pump coronary artery bypass grafting, cerebral oxygen saturation was measured by near infrared spectroscopy. A 20% decrease from baseline values was considered to be cerebral hypoperfusion. Mean arterial pressure, cardiac index, arterial carbon dioxide partial pressure, central venous pressure, haemoglobin concentration, and body temperature were determined simultaneously. Each value was recorded at the following time points: at baseline; after positioning the heart for distal anastomoses of the left anterior descending artery, the circumflex, and the right coronary artery; after repositioning the heart; and after chest closure. Significant changes in each parameter from baseline were detected using repeated-measures analysis of variance. Determinants of cerebral oxygen saturation during surgery were analysed by means of generalized estimation equations. Cerebral oxygen saturation remained constant during grafting of the left anterior descending artery and decreased significantly during grafting of the circumflex (P = 0.001) and the right coronary artery (P < 0.001). Cerebral hypoperfusion was found in seven (20%) patients. Changes in haemoglobin concentration (P = 0.014), arterial CO2 partial pressure (P = 0.001), cardiac output (P < 0.001), and central venous pressure (P = 0.014) determined alterations in cerebral oxygen saturation. Positioning of the heart during off-pump coronary artery bypass grafting leads to a decrease in regional cerebral oxygen saturation. This decrease is associated with changes in cardiac output, haemoglobin concentration, arterial CO2 partial pressure, and central venous pressure.

Paco2 becomes greater than Pvco2 during apnoea testing for brain death diagnosis

The apnoea test is performed to complete the diagnosis of brain death. The most efficient respiratory stimulus is the arterial carbon dioxide partial pressure (Paco2), hence it is used in this test [1, 2]. The patient is disconnected from the ventilator while receiving 100% oxygen via a catheter inserted into the endotracheal tube placed to the level of the carina. The goal of apnoeic oxygenation is to document the absence of breathing once Paco2 arises sufficiently to stimulate the respiratory centre. However, there is no agreement as to what should be the final Paco2 for maximal stimulation. In addition, complications may occur during the performance of the test [3]. As a result of the chance observation of the inversion of Pvco2–Paco2 gradient in a patient with brain death during the apnoea test, we performed simultaneous arterial and central venous gases during the apnoea test in 20 consecutive patients being tested for brain death. We obtained Local Research Ethics approval and relatives’ assent for this. The patients were on two different intensive care units of two university hospitals in Barcelona, between October 2005 and May 2007. They were disconnected from mechanical ventilation while receiving 100% oxygen via a catheter inserted into the tracheal tube to the level of the carina. Simultaneous arterial and central venous blood samples for Paco2 and Pvco2 measurements were obtained before and after the apnoea test. Before the test, mean (SD) Pvco2 (4.67 (0.28)) was greater than Paco2 (4.0 (0.25)) but after the onset of apnoea, this relationship was reversed with Paco2 (7.86 (0.24)) becoming greater than Pvco2 (6.66 (0.24)). This reversal of the venous-arterial CO2 gradient was observed in all the patients and in both hospitals. This finding has been previously reported in arterial and mixed venous samples by Rigg and Cruickshank [4], who investigated CO2 kinetics in two patients undergoing apnoea testing for brain death. They postulated that the reversal of the normal Paco2 and co2 (mixed venous) relationship during apnoea to be a consequence of the Haldane effect: the CO2 dissociation curves are different in reduced and oxygenated haemoglobin. As apnoea testing was performed without oxygenation, it was concluded that reduced haemoglobin was able to carry more CO2 than carbamino compounds explaining how the rise in Paco2 was greater than that in mixed venous co2. However, our patients underwent apnoeic oxygenation and we also observed that the Paco2 became greater than Pvco2, so that reversal of the arterial and venous Pco2 relationship is independent of the absence of oxygen. In two of our patients, blood gas analyses were performed before final disconnection from the ventilator once brain death was diagnosed, and in both cases Paco2 was greater than Pvco2. Fig. 5 shows the changes in one of these patients, with a normal gradient of beginning of the test and inversion from the second minute. Unlike Rigg and Cruikshank [4] we could not take mixed venous samples and our venous samples were from the central venous catheter. The repeated observation of this phenomenon in 20 patients of two hospitals over 18 months suggests that it was not a laboratory mistake. Alterations in Pvco2 (squares; grey line) and Paco2 (circles; black line) over time in a single patient. NB PCO2 given in mmHg. One possible explanation is that the lung parenchyma continues producing CO2 and consuming O2 via the bronchial arteries that empty the bronchial veins into the left auricle. As the patient is apnoeic and not eliminating CO2, an inverse CO2 gradient occurs. Fig. 5 suggests a change in the way in which CO2 is transported, as the Paco2 at 1 min is lower than the Pvco2 at 2 min. There may be an alteration in CO2 transportation from its dissolved form (corresponding to 7% of the total CO2 transported), to transportation linked to the bicarbonate ion or carbamino compounds. Finally, the goal of the apnoea test is to achieve a sufficiently high Paco2 to stimulate respiratory centres in the medulla oblongata. However, in view of a reversed Pvco2 and Paco2 gradient we may have to consider modifying our practice, assessing Pvco2 rather than Paco2 [5].

Predicting dead space ventilation in critically ill patients using clinically available data*

To develop and validate an equation to predict dead space to tidal volume ratio (Vd/Vt) from clinically available data in critically ill mechanically ventilated patients. Prospective, observational study using a convenience sample of patients whose arterial blood gas and respiratory gas exchange had been measured with indirect calorimetry. Medical and surgical critical care units of a university medical center. Adult, mechanically ventilated patients at rest with Fio2 < or =0.60 and no air leaks who had recent arterial blood gas recordings and end-tidal carbon dioxide concentration monitoring. Observational only. Indirect calorimetry was used to determine carbon dioxide production and expired minute ventilation in 135 patients. Tidal volume and respiratory rate were recorded from the ventilator. End tidal carbon dioxide concentration, body temperature, arterial carbon dioxide partial pressure (Paco2), and other clinical data were recorded. Vd/Vt was calculated using the Enghoff modification of the Bohr equation (Paco2 - PECO2/Paco2). Regression analysis was then used to construct a predictive equation for Vd/Vt using the clinical data: Vd/Vt = 0.32 + 0.0106 (Paco2 - ETCO2) + 0.003 (RR) + 0.0015 (age) (R = 0.67). A second group of 50 patients was measured using the same protocol and their data were used to validate the equations developed from the original 135 patients. The equation was found to be unbiased and precise. Vd/Vt is predictable from clinically available data. Whether this predicted quantity is valuable clinically must still be determined.

Accuracy of Postoperative End-tidal Pco2Measurements with Mainstream and Sidestream Capnography in Non-obese Patients and in Obese Patients with and without Obstructive Sleep Apnea

Obtaining accurate end-tidal carbon dioxide pressure measurements via nasal cannula poses difficulties in postanesthesia patients who are mouth breathers, including those who are obese and those with obstructive sleep apnea (OSA); a nasal cannula with an oral guide may improve measurement accuracy in these patients. The authors evaluated the accuracy of a mainstream capnometer with an oral guide nasal cannula and a sidestream capnometer with a nasal cannula that did or did not incorporate an oral guide in spontaneously breathing non-obese patients and obese patients with and without OSA during recovery from general anesthesia. The study enrolled 20 non-obese patients (body mass index less than 30 kg/m) without OSA, 20 obese patients (body mass index greater than 35 kg/m) without OSA, and 20 obese patients with OSA. End-tidal carbon dioxide pressure was measured by using three capnometer/cannula combinations (oxygen at 4 l/min): (1) a mainstream capnometer with oral guide nasal cannula, (2) a sidestream capnometer with a nasal cannula that included an oral guide, and (3) a sidestream capnometer with a standard nasal cannula. Arterial carbon dioxide partial pressure was determined simultaneously. The major outcome was the arterial-to-end-tidal partial pressure difference with each combination. In non-obese patients, arterial-to-end-tidal pressure difference was 3.0 +/- 2.6 (mean +/- SD) mmHg with the mainstream capnometer, 4.9 +/- 2.3 mmHg with the sidestream capnometer and oral guide cannula, and 7.1 +/- 3.5 mmHg with the sidestream capnometer and a standard cannula (P < 0.05). In obese non-OSA patients, it was 3.9 +/- 2.6 mmHg, 6.4 +/- 3.1 mmHg, and 8.1 +/- 5.0 mmHg, respectively (P < 0.05). In obese OSA patients, it was 4.0 +/- 3.1 mmHg, 6.3 +/- 3.2 mmHg, and 8.3 +/- 4.6 mmHg, respectively (P < 0.05). Mainstream capnometry performed best, and an oral guide improved the performance of sidestream capnometry. Accuracy in non-obese and obese patients, with and without OSA, was similar.

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 Arterial Carbon Dioxide Partial Pressure and Sevoflurane on Capillary Venous Cerebral Blood Flow and Oxygen Saturation During Craniotomy

Intraoperative routine monitoring of cerebral blood flow and oxygenation remains a technological challenge. Using the physiological principle of carbon dioxide reactivity of cerebral vasculature, we investigated a recently developed neuromonitoring device (oxygen-to-see, O2C device) for simultaneous measurements of regional cerebral blood flow (rvCBF), blood flow velocity (rvVelo), oxygen saturation (srvO2), and hemoglobin amount (rvHb) at the capillary venous level in patients subjected to craniotomy. Twenty-six neurosurgical patients were randomly assigned to anesthesia with 1.4% or 2.0% sevoflurane end-tidal concentration. After craniotomy, a fiberoptic probe was applied on a macroscopically healthy surface of cerebral tissue next to the site of surgery. Simultaneous measurements in 2 and 8 mm cerebral depth were performed in each patient during lower (35 mm Hg) and higher (45 mm Hg) levels (random order) of arterial carbon dioxide partial pressure (PaCO2). The principle of these measurements relies on the combination of laser-Doppler flowmetry (rvCBF, rvVelo) and photo-spectrometry (srvO2, rvHb). Linear models were fitted to test changes of end points (rvCBF, rvVelo, srvO2, rvHb) in response to lower and higher levels of PaCO2, 1.4% and 2.0% sevoflurane end-tidal concentration, and 2 and 8 mm cerebral depth. RvCBF and rvVelo were elevated by PaCO2 independent of sevoflurane concentration in 2 and 8 mm depth of cerebral tissue (P < 0.001). Higher PaCO2 induced an increase in mean srvO2 from 50% to 68% (P < 0.001). RvVelo (P < 0.001) and srvO2 (P = 0.007) were higher in 8 compared with 2 mm cerebral depth. RvHb was not influenced by alterations in PaCO2 but positively correlated to sevoflurane concentration (P = 0.005). Increases in rvCBF and rvVelo by PaCO2 suggest preserved hypercapnic vasodilation under anesthesia with sevoflurane 1.4% and 2.0% end-tidal concentration. A consecutive increase in srvO2 implies that cerebral arteriovenous difference in oxygen was decreased by elevated PaCO2. Unchanged levels of rvHb signify that there was no blood loss during measurements. Data suggest that the device allows detection of local changes in blood flow and oxygen saturation in response to different PaCO2 levels in predominant venous cerebral microvessels.

Hypercapnic Coma Due to Spontaneous Pneumothorax: Case Report and Review of the Literature

Background: Hypercapnic coma is a rare differential diagnosis in the unconscious patient. One underlying mechanism may be hypoventilation due to spontaneous pneumothorax. Although hypercapnia is not a typical finding in spontaneous pneumothorax in patients with otherwise healthy lungs, under certain circumstances, hypercapnia may readily develop. Objectives: We report a rare case of profound hypercapnic coma due to spontaneous pneumothorax after contralateral pneumonectomy. In addition, we review other causes of hypercapnic coma and its outcome and discuss the relationship between arterial carbon dioxide partial pressure and level of consciousness. Case Report: An 85-year-old man without evidence of trauma or intoxication presented unconscious to our Emergency Department. The physical examination and X-ray study revealed a left-sided spontaneous pneumothorax. A right-sided pneumonectomy 25 years earlier had promoted the development of profound hypercapnic coma. After insertion of a thoracic drain, the coma rapidly resolved without any neurological deficit. Conclusions: Although severe hypercapnia is usually due to decompensation of chronic lung disease, pneumothorax potentially may cause hypercapnic coma. Review of the literature suggests that there is no close correlation between arterial pCO 2 (partial pressure of CO 2) levels and the degree of impairment of consciousness; however, levels exceeding 80 mm Hg are likely associated with significantly impaired consciousness. Hypercapnic coma usually resolves without neurological deficit as arterial pCO 2 tensions decline.

The cardiopulmonary effects of anesthetic induction with isoflurane, ketamine–diazepam or propofol–diazepam in the hypovolemic dog

ObjectiveTo evaluate and compare the cardiopulmonary effects of induction of anesthesia with isoflurane (Iso), ketamine–diazepam (KD), or propofol–diazepam (PD) in hypovolemic dogs. Study designProspective randomized cross–over trial. AnimalsSix healthy intact, mixed breed, female dogs weighing 20.7 ± 4.2 kg and aged 22 ± 2 months. MethodsDogs had 30 mL kg−1 of blood removed at a rate of 1.5 mL kg−1 minute−1 under isoflurane anesthesia. Following a 30–minute recovery period, anesthesia was reinduced. Dogs were assigned to one of three treatments: isoflurane via facemask using 0.5% incremental increases in the delivered concentration every 30 seconds, 1.25 mg kg−1 ketamine and 0.0625 mg kg−1 diazepam intravenously (IV) with doses repeated every 30 seconds as required, and 2 mg kg−1 propofol and 0.2 mg kg−1 diazepam IV followed by 1 mg kg−1 propofol increments IV every 30 seconds as required. Following endotracheal intubation all dogs received 1.7% end–tidal isoflurane in oxygen. Cardiopulmonary variables were recorded at baseline (before induction) and at 5 or 10 minute intervals following endotracheal intubation. ResultsInduction time was longer in Iso (4.98 ± 0.47 minutes) compared to KD (3.10 ± 0.47 minutes) or PD (3.22 ± 0.45 minutes). To produce anesthesia, KD received 4.9 ± 2.3 mg kg−1 ketamine and 0.24 ± 0.1 mg kg−1 diazepam, while PD received 2.2 ± 0.4 mg kg−1 propofol and 0.2 mg kg−1 diazepam. End–tidal isoflurane concentration immediately following intubation was 1.7 ± 0.4% in Iso. Arterial blood pressure and heart rate were significantly higher in KD and PD compared to Iso and in KD compared to PD. Arterial carbon dioxide partial pressure was significantly higher in PD compared to KD and Iso immediately after induction. Conclusions and clinical relevanceIn hypovolemic dogs, KD or PD, as used in this study to induce anesthesia, resulted in less hemodynamic depression compared to isoflurane.

Effects of stomach inflation on haemodynamic and pulmonary function during cardiopulmonary resuscitation in pigs

Aim Stomach inflation during cardiopulmonary resuscitation (CPR) is frequent, but the effect on haemodynamic and pulmonary function is unclear. The purpose of this study was to evaluate the effect of clinically realistic stomach inflation on haemodynamic and pulmonary function during CPR in a porcine model. Methods After baseline measurements ventricular fibrillation was induced in 21 pigs, and the stomach was inflated with 0 L ( n = 7), 5 L ( n = 7) or 10 L air ( n = 7) before initiating CPR. Results During CPR, 0, 5, and 10 L stomach inflation resulted in higher mean pulmonary artery pressure [median (min–max)] [35 (28–40), 47 (25–50), and 51 (49–75) mmHg; P < 0.05], but comparable coronary perfusion pressure [10 (2–20), 8 (4–35) and 5 (2–13) mmHg; P = 0.54]. Increasing (0, 5, and 10 L) stomach inflation decreased static pulmonary compliance [52 (38–98), 19 (8–32), and 12 (7–15) mL/cmH 2O; P < 0.05], and increased peak airway pressure [33 (27–36), 53 (45–104), and 103 (96–110) cmH 2O; P < 0.05). Arterial oxygen partial pressure was higher with 0 L when compared with 5 and 10 L stomach inflation [378 (88–440), 58 (47–113), and 54 (43–126) mmHg; P < 0.05). Arterial carbon dioxide partial pressure was lower with 0 L when compared with 5 and 10 L stomach inflation [30 (24–36), 41(34–51), and 56 (45–68) mmHg; P < 0.05]. Return of spontaneous circulation was comparable between groups (5/7 in 0 L, 4/7 in 5 L, and 3/7 in 10 L stomach inflation; P = 0.56). Conclusions Increasing levels of stomach inflation had adverse effects on haemodynamic and pulmonary function, indicating an acute abdominal compartment syndrome in this CPR model.

Intraocular pressure and its correlation with blood gas parameters in crested caracaras (Caracara plancus) anesthetized with isoflurane and sevoflurane

The intraocular pressure (IOP) and its correlations with arterial carbon dioxide partial pressure (PaCO2) and arterial pH were studied in five crested caracaras (Caracara plancus) anesthetized with isoflurane (ISO) and sevoflurane (SEV). Baseline IOP values were measured in both eyes (M0). Brachial artery was previously catheterized to obtain blood gas and cardiorespiratory analysis. Anesthesia was induced with 5% ISO and maintained with 2.5% for 40 minutes. IOP measurements and blood samples were evaluated in different moments until the end of the procedure. After recovering, a second anesthesia was induced with 6% SEV and maintained with 3.5%. Parameters were evaluated at the same time points of the previous procedure. IOP reduced significantly (P= 0.012) from M0 at all time points and no significative changes were observed between ISO and SEV anesthesias. Correlation between IOP and PaCO2 and between PIO and blood pH were found only for SEV. IOP and blood pH decreased in parallel with IOP, whereas values of PaCO2 increased in caracaras anesthetized with isoflurane and sevoflurane.

Cutaneous Vascular Responses to Hypercapnia During Whole-Body Heating

Hypercapnia may be encountered in lung disease as well as during situations involving rebreathing of previously expired air (e.g., occupational diving). Inhibitory effects of elevated arterial carbon dioxide partial pressure on the central nervous system may result in impaired thermoregulation. This study tested the hypothesis that in heat-stressed subjects, cutaneous vascular responsiveness [expressed as cutaneous vascular conductance (CVC)] would be reduced during hypercapnic exposure. Four men and three women (mean - SD; age: 35 +/- 7 yr) rested supine while wearing a tube-lined suit perfused with 34 degrees C water (normothermia). Following normothermic data collection, 50 degrees C water was perfused through the suit to increase internal temperature approximately 1 degrees C (whole-body heating). In both thermal conditions, a normoxic-hypercapnic (5% CO2, 21% O2, balance N2) gas mixture was inspired while forearm skin blood flux (laser-Doppler flowmetry) was measured continuously and was used for calculation of CVC (skin blood flux/mean arterial pressure). End-tidal CO2 increased similarly throughout hypercapnic exposure during both normothermic and whole-body heating conditions (7.9 +/- 2.4 and 8.3 +/- 1.9 mmHg, respectively). However, CVC was not different between normocapnia and hypercapnia under either thermal condition (normothermia: 0.42 +/- 0.24 vs. 0.39 +/- 0.21 flux units/mmHg for normocapnia and hypercapnia, respectively; heat stress: 1.89 +/- 0.67 vs. 1.92 +/- 0.63 flux units/ mmHg for normocapnia and hypercapnia, respectively). Based on these findings, mild hypercapnia is unlikely to impair heat dissipation by reducing cutaneous vasodilation.