Intraoperative partial pressure of arterial carbon dioxide levels and adverse outcomes in patients undergoing lung transplantation.

OBJECTIVE: Patients undergoing lung transplantation (LTx) often experience abnormal hypercapnia or hypocapnia. This study aimed to investigate the association between intraoperative PaCO2 and postoperative adverse outcomes in patients undergoing LTx. METHODS: We retrospectively reviewed the medical records of 151 patients undergoing LTx. Patients' demographics, perioperative clinical factors, and pre- and intraoperative PaCO2 data after reperfusion were collected and analyzed. Based on the PaCO2 levels, patients were classified into three groups: hypocapnia (≤35 mmHg), normocapnia (35.1-55 mmHg), and hypercapnia (>55 mmHg). Univariate and multivariable logistic regressions were used to identify independent risk factors for postoperative composite adverse events and in-hospital mortality. RESULTS: Intraoperative hypercapnia occurred in 69 (45.7%) patients, and hypocapnia in 17 (11.2%). Patients with intraoperative PaCO2 of 35.1-45 mmHg showed a lower incidence of composite adverse events (53.3%) and mortality (6.2%) (P < 0.001). There was no significant difference in composite adverse events and mortality among preoperative PaCO2 groups (P > 0.05). Compared with intraoperative PaCO2 at 35.1-45 mmHg, the risk of composite adverse events in hypercapnia group increased: the adjusted OR was 3.07 (95% confidence interval [CI]: 1.36-6.94; P = 0.007). The risk of death was significantly higher in hypocapnia group than normocapnia group, the adjusted OR was 7.69 (95% CI: 1.68-35.24; P = 0.009). Over ascending ranges of PaCO2, PaCO2 at 55.1-65 mmHg had the strongest association with composite adverse events, the adjusted OR was 6.40 (95% CI: 1.18-34.65; P = 0.031). CONCLUSION: These results demonstrate that intraoperative hypercapnia independently predicts postoperative adverse outcomes in patients undergoing LTx. Intraoperative hypocapnia shows predictive value for postoperative in-hospital mortality in LTx.

Beyond Anesthesia Toxicity: Anesthetic Considerations to Lessen the Risk of Neonatal Neurological Injury.

Infants who undergo surgical procedures in the first few months of life are at a higher risk of death or subsequent neurodevelopmental abnormalities. Although the pathogenesis of these outcomes is multifactorial, an understanding of the nature and pathogenesis of brain injury in these infants may assist the anesthesiologist in consideration of their day-to-day practice to minimize such risks. This review will summarize the main types of brain injury in preterm and term infants and their key pathways. In addition, the review will address key potential pathogenic pathways that may be modifiable including intraoperative hypotension, hypocapnia, hyperoxia or hypoxia, hypoglycemia, and hyperthermia. Each of these conditions may increase the risk of perioperative neurological injury, but their long-term ramifications are unclear.

Respiratory and hemodynamic contributions to emotion-related pre-syncopal vasovagal symptoms.

Vasovagal reactions are conventionally understood as resulting from systemic changes in cardiovascular activity; however, there exists a complementary perspective focused on specific changes in cerebral vasoconstriction associated with hyperventilation-induced hypocapnia. The present study investigated the role of cardiovascular and respiratory activity in self-reported pre-syncopal vasovagal reactions to a surgery video in a sample of 49 healthy women. Participants who indicated more previous real-life episodes of dizziness reported experiencing significantly more symptoms in the laboratory consistent with a vasovagal response. They also showed lower total peripheral resistance and higher pre-ejection period in general, suggesting lower sympathetic nervous system activity. Significant decreases in end-tidal carbon dioxide (PETCO2) occurred during the surgery video among susceptible participants, without significant increases in respiration rate. Further, participants who experienced reductions from the neutral video in PETCO2, systolic blood pressure, or both, reported vasovagal symptoms during the surgery video. The results suggest that patterns of respiration associated with decreases in PETCO2 may contribute to vasovagal symptoms reported in non-clinical groups as well as those with blood-injection-injury phobia and are associated with susceptibility to dizziness.

Hypocapnia measured by end-tidal carbon dioxide tension during anesthesia is associated with increased 30-day mortality rate.

STUDY OBJECTIVE: To evaluate the relationship between intraoperative end-tidal carbon dioxide (etco2) values and clinical outcomes with special attention on 30-day postoperative mortality and secondarily on hospital length of stay (LOS). DESIGN: Retrospective, observational study. SETTING: Surgical theaters of the University Hospital Center of Charleroi. PATIENTS: Five thousand three hundred seventeen patients ASA I-IV undergoing various surgical procedures (except pediatric and cardiac surgery) under general anesthesia. INTERVENTIONS: No intervention on the patients. MEASUREMENTS: The mean etco2 level measured during anesthesia was secondarily extracted from an electronic information management system. Patients were divided into 2 separate groups based on etco2 values less than or greater than or equal to 35 mm Hg. The primary end point was the in- and outhospital mortality in the 30-day period after surgery. The second was the LOS more than 6 days. MAIN RESULTS: Hypocapnia occurred in 66% of the patients. Mortality rate at 30-day was 84 of 3554 (2.4%) in the low etco2 group vs 15 of 1763 (0.9%) in the other (odds ratio, 2.99 [1.69-5.28]; P<.001). In multivariate analysis, age and ASA scores had significant independent associations with mortality rate. Adjusting for these factors had an effect on the relative odds ratio of etco2 on mortality of 1.99 ([1.11-3.56]; P<.001). Patients with low etco2 experienced higher LOS (14.1±9.4 vs 13.1±8.9 days; P<.001). Thirty five percent of the patients in the low etco2 group were still hospitalized more than 6 days compared with 30% in the other (P<.001). CONCLUSION: Low etco2 level during anesthesia is associated with an increase in postoperative mortality rate and LOS. These results emphasize the importance of preventing hypocapnia during anesthesia to improve surgical outcomes.

Episodes of hypo- and hypercapnia in a cohort of mechanically ventilated VLBW infants: the role of adequate staffing.

In preterm neonates, the use of invasive ventilation may be mandatory because of respiratory distress syndrome (RDS). In this short communication, we demonstrate that invasive ventilation in this susceptible cohort may be associated with episodes of both hypo- and hypercapnia, and that inadequate ventilatory support is associated with the occurrence rate of bronchopulmonary dysplasia (BPD; p < 0.05). Also, inadequate mechanical ventilation is aggravated by a shortage of medical staff.

Association Between Arterial Carbon Dioxide Tension and Outcome in Patients Admitted to the Intensive Care Unit After Coronary Artery Bypass Surgery.

OBJECTIVES: The aim of this study was to determine the association between PaCO2 and patient outcome in patients admitted to the intensive care unit (ICU) after coronary artery bypass grafting (CABG). DESIGN: A retrospective cohort study. SETTING: Single-institutional, university hospital. PARTICIPANTS: All patients admitted to the ICU after CABG between January 2009 and December 2012. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Based on PaCO2 status during the first 24 hours after CABG, 1,011 patients were classified into 4 groups: normocapnia, hypocapnia, hypercapnia, and dual hyper/hypocapnia. The 30-day mortality rate was 0.7% (n = 4) for normocapnia, 1.5% (n = 4) for hypocapnia, 2.2% (n = 3) for hypercapnia, and 7.5% (n = 4) for the dual-exposure group. The extubation times were 13.3±21.7 hours, 15.8±21.37 hours, 21.79±39.70 hours, and 42.29±75.35 hours, respectively. After adjusting for confounding variables, the dual hypocapnia and hypercapnia exposure group was associated with increased 30-day mortality (odds ratio [OR] = 8.08; 95% confidence interval [CI], 1.82-35.86; p = 0.006) and delayed extubation (OR = 2.40; 95% CI, 1.24-4.64; p = 0.010). CONCLUSIONS: Exposure to both hypocapnia and hypercapnia within 24 hours after CABG was associated independently with increased risk of 30-day mortality and delayed extubation. Exposure to either hypocapnia or hypercapnia alone was not associated with patient outcome.

Impact of hypocapnia and cerebral perfusion on orthostatic tolerance.

We examined two novel hypotheses: (1) that orthostatic tolerance (OT) would be prolonged when hyperventilatory-induced hypocapnia (and hence cerebral hypoperfusion) was prevented; and (2) that pharmacological reductions in cerebral blood flow (CBF) at baseline would lower the 'CBF reserve', and ultimately reduce OT. In study 1 (n = 24; aged 25 ± 4 years) participants underwent progressive lower-body negative pressure (LBNP) until pre-syncope; end-tidal carbon dioxide (P ET , CO 2) was clamped at baseline levels (isocapnic trial) or uncontrolled. In study 2 (n = 10; aged 25 ± 4 years), CBF was pharmacologically reduced by administration of indomethacin (INDO; 1.2 mg kg(-1)) or unaltered (placebo) followed by LBNP to pre-syncope. Beat-by-beat measurements of middle cerebral artery blood flow velocity (MCAv; transcranial Doppler), heart rate (ECG), blood pressure (BP; Finometer) and end-tidal gases were obtained continuously. In a subset of subjects' arterial-to-jugular venous differences were obtained to examine the independent impact of hypocapnia or cerebral hypoperfusion (following INDO) on cerebral oxygen delivery and extraction. In study 1, during the isocapnic trial, P ET , CO 2 was successfully clamped at baseline levels at pre-syncope (38.3 ± 2.7 vs. 38.5 ± 2.5 mmHg respectively; P = 0.50). In the uncontrolled trial, P ET , CO 2 at pre-syncope was reduced by 10.9 ± 3.9 mmHg (P ≤ 0.001). Compared to the isocapnic trial, the decline in mean MCAv was 15 ± 4 cm s(-1) (35%; P ≤ 0.001) greater in the uncontrolled trial, yet the time to pre-syncope was comparable between trials (544 ± 130 vs. 572 ± 180 s; P = 0.30). In study 2, compared to placebo, INDO reduced resting MCAv by 19 ± 4 cm s(-1) (31%; P ≤ 0.001), but time to pre-syncope remained similar between trials (placebo: 1123 ± 138 s vs. INDO: 1175 ± 212 s; P = 0.53). The brain extracted more oxygen in face of hypocapnia (34% to 53%) or cerebral hypoperfusion (34% to 57%) to compensate for reductions in delivery. In summary, cerebral hypoperfusion either at rest or induced by hypocapnia at pre-syncope does not impact OT, probably due to a compensatory increase in oxygen extraction.

Brain changes to hypocapnia using rapidly interleaved phosphorus-proton magnetic resonance spectroscopy at 4 T.

Substantial controversy persists in the literature concerning the physiologic consequences hypocapnia, or low partial pressure of carbon dioxide (PaCO(2)). Invasive animal studies have demonstrated large pH increases (>0.25 U), phosphocreatine (PCr) decreases (>30%), and adenosine triphosphate (ATP) decreases (>10%) after hyperventilation (HV) (20 mm Hg PaCO(2)). However, using magnetic resonance spectroscopy, HV studies in awake humans have demonstrated only small pH changes ( approximately 0.05 U) and no changes in PCr or ATP. It remains important to ascertain whether this failure to detect PCr changes in human studies reflects a true absence of changes, or a limitation in data fidelity. The present study used a rapidly interleaved phosphorus-proton spectroscopy acquisition from large samples at high magnetic field (4 T), to measure pH, PCr, inorganic phosphate, beta-ATP, and lactate changes with high temporal and signal sensitivity. Five of six subjects had usable data. During 20 mins HV, PaCO(2) reached a minimum at 16 mins (17 mm Hg); however, the maximum pH change (+0.047) peaked earlier (14 mins). Maximal lactate increases were measured at 15 mins. By 10 mins, maximum changes were observed for PCr (-3.4%) and inorganic phosphate (+6.4%). No changes in beta-ATP were observed. The peak in pH, despite continued decreases in PaCO(2), suggests active buffering during HV. These data, and the small magnitude of early PCr and inorganic phosphate changes, do not support substantial energy compromise during HV. Other mitigating factors, such as anesthesia-induced deregulation of the cerebrovasculature, might have contributed to the exaggerated metabolic changes observed in previous animal investigations.

Hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption.

Acid-base disturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patients. We examined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolated and continuously perfused rat lung model. We found that alveolar fluid reabsorption after 1 hour was impaired by low levels of CO2 partial pressure (PCO2; 10 and 20 mm Hg) independent of pH levels (7.7 or 7.4). In addition, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this process. The hypocapnia-mediated decrease of alveolar fluid reabsorption was associated with decreased Na,K-ATPase activity and protein abundance at the basolateral membranes of distal airspaces. The effect of low PCO2 on alveolar fluid reabsorption was reversible because clearance normalized after correcting the PCO2 back to normal levels. These data suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Conceivably, correction of hypocapnic alkalosis in critically ill patients may contribute to the normalization of lung ability to clear edema.

Effect of controlled hyperventilation on the pressor response to laryngoscopy and tracheal intubation.

Pressor response to laryngoscopy and tracheal intubation includes rises in blood pressure and heart rate. This response may be harmful in the presence of cerebral or myocardial diseases. Although different preventive measures have been developed the choice of the agent or method has not been defined clearly. Hypocapnia is commonly used in anesthesia practice for different indications. It depresses the cardiovascular system and lowers the cardiac output. This study investigated the effect of controlled hyperventilation on the pressor response to laryngoscopy and tracheal intubation in three groups of healthy adult patients with different levels of end tidal CO2. The blood pressure and heart rate were recorded during induction of general anesthesia before and after laryngoscopy and tracheal intubation. The pressor responses to laryngoscopy and tracheal intubation in hypocapnic and normocapnic groups were comparable. Moderate degrees of controlled hyperventilation caused relatively more fluctuation in blood pressure during induction of anesthesia. It can be concluded that controlled hyperventilation has no beneficial effect upon the pressor response to laryngoscopy and tracheal intubation.

Hypocarbia in the ventilated preterm infant and its effect on intraventricular haemorrhage and bronchopulmonary dysplasia.

OBJECTIVE: To examine the relationship between PaCO2 levels in ventilated very preterm infants and (i) the incidence of severe intraventricular haemorrhage (IVH) and periventricular leukomalacia (PVL); and (ii) bronchopulmonary dysplasia (BPD). METHODS: A retrospective cohort analysis of preterm infants comparing PaCO2 levels with the incidence of severe IVH/PVL and BPD was carried out on patients born at less than 29 weeks gestation from 1992 to 1994 and admitted to the tertiary neonatal intensive care unit at the King Edward Memorial Hospital (314 infants). During the first 96 h, PaCO2 levels were examined including lowest and highest PaCO2 levels, mean PaCO2 levels and duration of hypocarbia both pre- and post-surfactant administration. RESULTS: Of the 314 infants, there were 40 early neonatal deaths (less than 48 h) who were not included in the analysis. Of the 274 surviving infants, 72 (26%) infants had severe IVH. Infants whose PaCO2 fell below 30 mmHg at any stage in the first 48 h of life had an increased risk of severe IVH or PVL (odds ratio 2.38; 95% CI 1.27-4.49; P = 0.007). Of the 265 survivors to 36 weeks corrected gestational age, 134 (51%) had BPD. Infants with at least three PaCO2 values less than 30 mmHg in the first 24 h of life had an increased risk of BPD (odds ratio 2.21; 95% CI 1.05-4.57; P = 0.036). CONCLUSIONS: The risk of severe IVH/PVL was significantly increased by hypocarbia. There was also an association between hypocarbia and BPD, particularly when hypocarbia was prolonged. These findings suggest that avoidance of hypocarbia may reduce the incidence of severe IVH/PVL and BPD in preterm infants.

Cerebral vasoconstriction in vasovagal syncope: any link with symptoms? A transcranial Doppler study.

BACKGROUND: Cerebral vasoconstriction has been described previously in vasovagal syncope (VVS). This phenomenon appears paradoxical in view of the well-known decrease of systemic vascular resistances taking places during VVS. We aimed to assess (1) whether cerebral vasoconstriction in VVS is an independent paradoxical phenomenon and (2) whether cerebral vasoconstriction has any link with symptoms and/or VVS onsets. METHODS AND RESULTS: Seven young patients with recurrent VVS participated in the study. Each patient underwent monitoring of heart rate, blood pressure, cerebral blood flow velocity (by means of transcranial Doppler), end-tidal PCO(2), peripheral oximetry, respiratory rate, and tidal volumes both at rest and during head-up tilt. All the subjects experienced tilt-induced VVS. A significant increase of respiratory tidal volumes was observed in each subject >/=160 seconds before VVS. This deep breathing induced a PCO(2) decrease and, consequently, also a decrease in cerebral blood flow velocity and increase in cerebrovascular resistance (expressed by the increase of the pulsatility index). Within 40 seconds, 5 subjects started complaining of discomfort, in the absence of any significant blood pressure drop. CONCLUSIONS: Cerebral vasoconstriction is not a paradoxical phenomenon when it occurs before tilt-induced VVS but rather is only the physiological consequence of the hyperventilation-induced hypocapnia that occurs in habitual fainters. The large lag between the onset of syncope and cerebral vasoconstriction excludes the hypothesis that VVS is dependent on abnormal behavior of cerebral hemodynamics.

Hypocapnia and hypercapnia in respiratory management of newborn infants.

Recent experimental and clinical data demonstrate that both hypocapnia and hypercapnia during the neonatal period may result in beneficial or adverse consequences. Multiple retrospective studies report a strong association between PaCO2 levels less than 25 to 30 mm Hg and an increased incidence of cystic PVL and CP in preterm infants. Prolonged exposure to PaCO2 values less than 25 to 30 mm Hg is also associated with hearing loss in term and near-term infants. A low tidal volume strategy combined with permissive hypercapnia is potentially a strategy that could prevent lung injury. Clearly, more randomized, controlled trials are needed before this latter strategy or that of permissive hypercapnia can be recommended routinely for preterm, near-term, or term gestation infants with respiratory disorders.

Reliable noninvasive parameters for early detection of cardiopulmonary compromise induced by carbon dioxide thoracoretroperitoneum in minimally invasive thoracolumboendoscopic spine surgery.

BACKGROUND: Using a novel endoscopic retroperitoneal approach for thoracolumbar anterior spine fusion, we examined the cardiopulmonary effects of the inevitably associated carbon dioxide (CO2) thoracoretroperitoneum and evaluated noninvasive parameters, which may provide early and adequate recognition of cardiopulmonary dysfunction. METHODS: Under balanced anesthesia and paralysis, six pigs subjected to endoscopic CO2 thoracoretroperitoneal spine fusion underwent extensive pulmonary and hemodynamic online monitoring throughout the operative procedure. Open thoracophrenolumbotomy in six pigs served as a control procedure. RESULTS: In contrast to unchanged cardiopulmonary parameters during open thoracolumbar spine surgery, CO2 thoracoretroperitoneum caused significant hypercapnia, hypoxia, and acidemia with concomitant tachycardia, pulmonary hypertension, and systemic hypotension. Ventilatory adjustment, CO2 evacuation, or both promptly reversed the cardiopulmonary effects. Noninvasively assessed end-tidal CO2, peak respiratory pressure, and heart rate were early clues for detecting the tension pneumothorax-like cardiopulmonary dysfunction, as indicated by a significant correlation with the invasively assessed pulmonary hemodynamic parameters and arterial blood gases. CONCLUSIONS: During endoscopic thoracolumbar spine fusion, CO2 thoracoretroperitoneum induces cardiopulmonary dysfunction, which, however, can be detected reliably by changes in end-tidal CO2, peak respiratory pressure, and heart rate, and which can be corrected immediately by appropriate ventilatory adjustments. Therefore, endoscopic CO2 thoracoretroperitoneal spine fusion might not necessarily require extraordinarily extensive and invasive monitoring of systemic and pulmonary hemodynamics, but ventilatory adjustment and intrathoracic pressure evacuation should be readily available to reexpand the lung, and to facilitate rapid normalization of hemodynamic conditions.

Effect of hypocapnea on CBF and extracellular intermediates of secondary brain injury.

We examined the metabolic response of the brain underlying subdural hematomas or surrounding contusions to hyperventilation and looked for evidence of ischemia. Twelve consecutive patients with severe traumatic brain injury (TBI) (GCS < 8) who required surgery for evacuation of subdural hematoma or hemorrhagic contusion were studied. At surgery, a microdialysis catheter was placed into the cortex in a gyrus adjacent to the contusion or underlying the subdural hematoma. A thermal diffusion flow probe was placed on the cortex directly above the dialysis catheter. On days 1 and 3 post injury, two trials of hyperventilation were performed which dropped the patients' pCO2 10 mm Hg for 30 minutes. Monitoring of CBF and collection of dialysis fluid continued throughout each hyperventilation trial. Data was analyzed for a three hour window surrounding each hyperventilation. Brief periods of hyperventilation did not cause a significant elevation of the extracellular lactate/pyruvate ratio or glutamate level in areas of the brain likely to be the most vulnerable to secondary injury. In spite of hyperventilation leading to a significant decline in local CBF in 20% of the trials, there was no evidence of ischemia or excitatory amino acid release associated with hyperventilation.

[Percutaneous closure of an right-left interatrial shunt acquired after pneumonectomy]. / La fermeture percutanée du shunt droit-gauche interauriculaire acquis après pneumonectomie.

Right to left shunt through a patent foramen ovale after pneumonectomy is a rare complication. Its clinical presentation is a severe dyspnea with posture dependency. The diagnosis is easily confirmed by contrast echocardiography. The purpose of this article is to expose the interest of interventional catheterization and transcatheter closure. This method appears to be a viable alternative to surgery for those patients with precarious respiratory function.

Adaptation to oral breathing after anterior nasal packing.

We report the changes in blood gas tensions in a group of 17 patients during a five-day period of anterior nasal packing after endonasal surgery. Significant hypocapnia was observed in the early postoperative period, which was followed by significant hypoxemia within the first 48 h after surgery, and also shortly after removal of the nasal pack. Analyses of the changes in blood gas tensions suggested disturbances in the ventilation-perfusion ratio. Most subjects required a period of 48 h to adapt to oral breathing.