Severe Hypocapnia Research Articles

Clinical practice and effect of carbon dioxide on outcomes in mechanically ventilated acute brain-injured patients: a secondary analysis of the ENIO study

PurposeThe use of arterial partial pressure of carbon dioxide (PaCO2) as a target intervention to manage elevated intracranial pressure (ICP) and its effect on clinical outcomes remain unclear. We aimed to describe targets for PaCO2 in acute brain injured (ABI) patients and assess the occurrence of abnormal PaCO2 values during the first week in the intensive care unit (ICU). The secondary aim was to assess the association of PaCO2 with in-hospital mortality.MethodsWe carried out a secondary analysis of a multicenter prospective observational study involving adult invasively ventilated patients with traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracranial hemorrhage (ICH), or ischemic stroke (IS). PaCO2 was collected on day 1, 3, and 7 from ICU admission. Normocapnia was defined as PaCO2 > 35 and to 45 mmHg; mild hypocapnia as 32–35 mmHg; severe hypocapnia as 26–31 mmHg, forced hypocapnia as < 26 mmHg, and hypercapnia as > 45 mmHg.Results1476 patients (65.9% male, mean age 52 ±\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\\pm$$\\end{document} 18 years) were included. On ICU admission, 804 (54.5%) patients were normocapnic (incidence 1.37 episodes per person/day during ICU stay), and 125 (8.5%) and 334 (22.6%) were mild or severe hypocapnic (0.52 and 0.25 episodes/day). Forced hypocapnia and hypercapnia were used in 40 (2.7%) and 173 (11.7%) patients. PaCO2 had a U-shape relationship with in-hospital mortality with only severe hypocapnia and hypercapnia being associated with increased probability of in-hospital mortality (omnibus p value = 0.0009). Important differences were observed across different subgroups of ABI patients.ConclusionsNormocapnia and mild hypocapnia are common in ABI patients and do not affect patients' outcome. Extreme derangements of PaCO2 values were significantly associated with increased in-hospital mortality.

Changes in lung mechanics and ventilation-perfusion match: comparison of pulmonary air- and thromboembolism in rats

BackgroundPulmonary air embolism (AE) and thromboembolism lead to severe ventilation-perfusion defects. The spatial distribution of pulmonary perfusion dysfunctions differs substantially in the two pulmonary embolism pathologies, and the effects on respiratory mechanics, gas exchange, and ventilation-perfusion match have not been compared within a study. Therefore, we compared changes in indices reflecting airway and respiratory tissue mechanics, gas exchange, and capnography when pulmonary embolism was induced by venous injection of air as a model of gas embolism or by clamping the main pulmonary artery to mimic severe thromboembolism.MethodsAnesthetized and mechanically ventilated rats (n = 9) were measured under baseline conditions after inducing pulmonary AE by injecting 0.1 mL air into the femoral vein and after occluding the left pulmonary artery (LPAO). Changes in mechanical parameters were assessed by forced oscillations to measure airway resistance, lung tissue damping, and elastance. The arterial partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) were determined by blood gas analyses. Gas exchange indices were also assessed by measuring end-tidal CO2 concentration (ETCO2), shape factors, and dead space parameters by volumetric capnography.ResultsIn the presence of a uniform decrease in ETCO2 in the two embolism models, marked elevations in the bronchial tone and compromised lung tissue mechanics were noted after LPAO, whereas AE did not affect lung mechanics. Conversely, only AE deteriorated PaO2, and PaCO2, while LPAO did not affect these outcomes. Neither AE nor LPAO caused changes in the anatomical or physiological dead space, while both embolism models resulted in elevated alveolar dead space indices incorporating intrapulmonary shunting.ConclusionsOur findings indicate that severe focal hypocapnia following LPAO triggers bronchoconstriction redirecting airflow to well-perfused lung areas, thereby maintaining normal oxygenation, and the CO2 elimination ability of the lungs. However, hypocapnia in diffuse pulmonary perfusion after AE may not reach the threshold level to induce lung mechanical changes; thus, the compensatory mechanisms to match ventilation to perfusion are activated less effectively.

Distribution of Oxygen Tension on Microvessels and in Tissue of Rat Brain Cortex at Severe Arterial Hypocapnia

Arterial hypocapnia (AH), induced by voluntary or forced hyperventilation of the lungs, is accompanied by a decrease in cerebral blood flow (due to an increase in the arteriole tone) and an increase in the affinity of hemoglobin for oxygen. As a result, an insufficient oxygen supply to cortical tissue take place and zones with a critically low oxygen tension (pO2) are formed in brain tissue. The distribution of pO2 to cerebral cortex during AH has not been studied enough. The aim of the work was to evaluate the effectiveness of oxygen supply to brain tissue at the level of arterial and venous microvessels at AH. To do this, the following tasks were set: 1) to study the distribution of the pO2 on the arterial and venous microvessels of the rat cerebral cortex; 2) to analyze tissue pO2 profiles near the walls of these microvessels. On anesthetized Wistar rats under conditions of forced hyperventilation (PaCO2 = 17.1 ± 0.7 mm Hg), the distribution of oxygen tension on the wall of pial and radial arterioles with a lumen diameter of 7–70 μm and on the wall of pial and ascending venules with a lumen diameter of 7–300 µm was studied. In tissue, near the wall of cortical arterioles and venules with a lumen diameter of 10–20 μm, tissue pO2 profiles were measured. Measurements of pO2 during spontaneous breathing of the animal with air served as a control. All pO2 measurements were made using platinum polarographic microelectrodes with a tip diameter of 3–5 μm. Visualization of the electrode tip and microvessels was carried out using a LUMAM-K1 microscope with epiobjectives of the contact type. This work presents for the first-time direct measurements of pO2 on the walls of arterioles and venules of the rat cerebral cortex and in tissues at different distances from the walls of these microvessels at AH. It has been shown that AH results in significant decrease in the oxygen supply to cerebral cortex, that is manifested by a significant drop of the pO2’s on venous microvessels and in tissue in the immediate vicinity of the studied microvessels. It has been shown, that the role of arterioles as a direct source of oxygen to brain tissue, is significantly reduced during arterial hypocapnia. Forced hyperventilation results in significant deterioration of oxygen supply to cerebral cortex, despite elevated pO2 values in the systemic arterial blood and in blood of systemic cerebral veins (sagittal sinus).

Estimated Cerebral Perfusion Pressure and Intracranial Pressure in Septic Patients.

Sepsis-associated brain dysfunction (SABD) is frequent and is associated with poor outcome. Changes in brain hemodynamics remain poorly described in this setting. The aim of this study was to investigate the alterations of cerebral perfusion pressure and intracranial pressure in a cohort of septic patients. We conducted a retrospective analysis of prospectively collected data in septic adults admitted to our intensive care unit (ICU). We included patients in whom transcranial Doppler recording performed within 48h from diagnosis of sepsis was available. Exclusion criteria were intracranial disease, known vascular stenosis, cardiac arrhythmias, pacemaker, mechanical cardiac support, severe hypotension, and severe hypocapnia or hypercapnia. SABD was clinically diagnosed by the attending physician, anytime during the ICU stay. Estimated cerebral perfusion pressure (eCPP) and estimated intracranial pressure (eICP) were calculated from the blood flow velocity of the middle cerebral artery and invasive arterial pressure using a previously validated formula. Normal eCPP was defined as eCPP ≥ 60mmHg, low eCPP was defined as eCPP < 60mmHg; normal eICP was defined as eICP ≤ 20mmHg, and high eICP was defined as eICP > 20mmHg. A total of 132 patients were included in the final analysis (71% male, median [interquartile range (IQR)] age was 64 [52-71] years, median [IQR] Acute Physiology and Chronic Health Evaluation II score on admission was 21 [15-28]). Sixty-nine (49%) patients developed SABD during the ICU stay, and 38 (29%) were dead at hospital discharge. Transcranial Doppler recording lasted 9 (IQR 7-12) min. Median (IQR) eCPP was 63 (58-71) mmHg in the cohort; 44 of 132 (33%) patients had low eCPP. Median (IQR) eICP was 8 (4-13) mmHg; five (4%) patients had high eICP. SABD occurrence and in-hospital mortality did not differ between patients with normal eCPP and patients with low eCPP or between patients with normal eICP and patients with high eICP. Eighty-six (65%) patients had normal eCPP and normal eICP, 41 (31%) patients had low eCPP and normal eICP, three (2%) patients had low eCPP and high eICP, and two (2%) patients had normal eCPP and high eICP; however, SABD occurrence and in-hospital mortality were not significantly different among these subgroups. Brain hemodynamics, in particular CPP, were altered in one third of critically ill septic patients at a steady state of monitoring performed early during the course of sepsis. However, these alterations were equally common in patients who developed or did not develop SABD during the ICU stay and in patients with favorable or unfavorable outcome.

Distribution of Oxygen Tension on Microvessels and in Tissue of Rat Brain Cortex at Severe Arterial Hypocapnia

Distribution of Oxygen Tension on Microvessels and in Tissue of Rat Brain Cortex at Severe Arterial Hypocapnia

Physiological responses during a single rebirthing (Breath work) session

Objective: The present report aimed to look at the physiological responses during a typical single Rebirthing session. Material and Methods: Ten healthy young women participated in the study. Their mean age, weight, and height were 37±2.7 years, 54.1±6.4 kg, and 161.2±4.9 cm, respectively. The Rebirthing sessions took place at the Israeli Rebirthing Center in Tel-Aviv. The treatments were carried out by a qualified Rebirthing therapist that has experienced thousands of rebirthing sessions during the last 15 years. Sessions were performed in a dark, quiet room and executed in a one-to-one set-up with the same trained therapist. After around 40-50 minutes, the session approached its end. Metabolic, cardiovascular, pulmonary, and gas-exchange variables were measured breath-by-breath using a commercial portable metabolic system. All data were transmitted wirelessly to an adjacent room in the clinic and continuously monitored by the study's chief researcher. Results: The primary study findings demonstrated that a typical Rebirthing session involving long (45-50 minutes) voluntary hyperventilation generated VO2, RER, HR, and O2 pulse matching well with the physiological demands of the procedure (breath work). At the same time, the ventilatory-related responses exhibited, as expected, exaggerated outcomes, illustrated by the high session's peak and average values of the depth (tidal volume), breathing frequency, and minute ventilation. Gas-exchange attributes showed extremely shallow end-tidal CO2 levels, high end-tidal O2, high respiratory exchange ratio, and very high levels of O2 and CO2 ventilatory equivalents. No significant grievances regarding participants' physical and mental/emotional feelings were reported in the present study. Conclusions: The present study could not solve the apparent divergence between the observed (acute) physiological responses (mainly severe Hypocapnia) and the subjective participants' pleasant emotional state, and in many cases, spiritually uplifting, at the end of each treatment session.

Post-Resuscitation Partial Pressure of Arterial Carbon Dioxide and Outcome in Patients with Out-of-Hospital Cardiac Arrest: A Multicenter Retrospective Cohort Study.

We aimed to estimate the association between PaCO2 level in the patient after out-of-hospital cardiac arrest (OHCA) resuscitation with patient outcome based on a multicenter prospective cohort registry in Japan between June 2014 and December 2015. Based on the PaCO2 within 24 h after return of spontaneous circulation (ROSC), patients were divided into six groups as follows: severe hypocapnia (<25 mmHg), mild hypocapnia (25–35 mmHg,), normocapnia (35–45 mmHg), mild hypercapnia (45–55 mmHg), severe hypercapnia (>55 mmHg), or exposure to both hypocapnia and hypercapnia. Multivariate logistic regression analysis was conducted to calculate the adjusted odds ratios (aORs) and 95% confidence interval (CI) for the 1-month poor neurological outcome (Cerebral Performance Category ≥ 3). Among the 13,491 OHCA patients, 607 were included. Severe hypocapnia, mild hypocapnia, severe hypercapnia, and exposure to both hypocapnia and hypercapnia were associated with a higher rate of 1-month poor neurological outcome compared with mild hypercapnia (aORs 6.68 [95% CI 2.16–20.67], 2.56 [1.30–5.04], 2.62 [1.06–6.47], and 5.63 [2.21–14.34], respectively). There was no significant difference between the outcome of patients with normocapnia and mild hypercapnia. In conclusion, maintaining normocapnia and mild hypercapnia during the 24 h after ROSC was associated with better neurological outcomes than other PaCO2 abnormalities in this study.

Silent Hypoxia in COVID-19: A Case Series

Background: The coronavirus disease 2019 (COVID-19) pandemic is an ongoing global crisis challenging the worldwide healthcare systems. Many patients present with a mismatch of profound hypoxemia and few signs of respiratory distress (i.e., silent hypoxemia). This particular clinical presentation is often cited, but data are limited. Main Body: We describe dyspnea sensation as assessed by using the BORG scale in pulmonary patients admitted to the emergency room during a 4-week period and transferred to the respiratory department of Siloah Hospital, Hannover, Germany. From October 1 to November 1, 2020, 82 patients with hypoxemia defined as oxygen demand to achieve an oxygen saturation (SpO₂) ≥92% were included. In 45/82 (55%) patients, SARS-CoV-2 was detected by PCR on admission. Among non-COVID patients, exacerbation of COPD was the main diagnosis (15/37, 41%). All subjects rated their perceived dyspnea using the modified Borg CR10 scale. Patients in the non-COVID group suffered from more dyspnea on the modified Borg CR10 scale (median 1, IQR: 0–2 vs. median 5, IQR: 3–6, p < 0.001). In multivariate analysis, “silent hypoxemia” as defined by the dyspnea Borg CR10 scale ≥5 was independently associated with COVID-19 and presence of severe hypocapnia with an odds ratio of 0.221 (95% confidence interval 0.054, 0.907, p 0.036). Conclusion: Among pulmonary patients with acute hypoxemia defined as oxygen demand, patients suffering from COVID-19 experience less dyspnea compared to non-COVID patients. “Silent” hypoxemia was more common in COVID-19 patients.

Abstract 13737: Enhanced Prehospital End-Tidal CO2 Monitor Data Analysis for Intubated Severe Traumatic Brain Injury: Striking Findings From the EPIC Study

Background: Studies show that EMS patients are often inadvertently hyperventilated (HV), resulting in hypocapnia. In TBI, HV markedly increases mortality. We evaluated continuous prehospital ETCO2 data in intubated TBI patients. Methods: Analysis of monitor data files (Philips MRx™) from a sample of intubated TBI cases in the EPIC Study (NIH-R01NS071049). Results: Among hundreds of cases, graphical display of continuous ETCO2 from 3 subjects dramatically exemplified commonly-occurring inadvertent HV. Fig 1 shows unrecognized HV lasting nearly 15 min. Fig 2 reveals nearly 14 min of increasing ventilatory rate and progressively worsening hypocapnia. Fig 3 shows nearly 4 min of HV that ends abruptly with clear, sudden recognition and slowing of ventilatory rate that leads to restoration of normal ETCO2 in only a few breaths. The corresponding EMS patient care records (PCR) failed to document the presence, severity, and duration of HV. Conclusions: In a study emphasizing prevention of HV, subsequent evaluation of continuous ETCO2 data revealed many cases of unintentionally rapid manual ventilation and severe hypocapnia, often occurring for long periods. These findings, even in the face of explicit guideline-based training, demonstrate a clear need for routine access to continuous monitor data among intubated patients for quality improvement and in clinical studies. Review of PCRs does not reliably identify mismanagement of ventilation. Furthermore, these findings make it likely that real-time audiovisual feedback technology would improve ventilatory management by alerting providers to unidentified HV that results from the frequent distractions occurring during EMS care.

Hypocapnia Alone Fails to Provoke Important Electrocardiogram Changes in Coronary Artery Diseased Patients.

BackgroundThere is still an urgent clinical need to develop non-invasive diagnostic tests for early ischemic heart disease because, once angina occurs, it is too late. Hypocapnia has long been known to cause coronary artery vasoconstriction. Some new cardiology tests are accompanied by the claim that they must have potential diagnostic value if hypocapnia enhances their cardiac effects in healthy subjects. But no previous study has tested whether hypocapnia produces bigger cardiac effects in patients with angina than in healthy subjects.MethodsSevere hypocapnia (a PetCO2 level of 20 mmHg) lasting >15 min was mechanically induced by facemask, while conscious and unmedicated, in 18 healthy subjects and in 10 patients with angina and angiographically confirmed coronary artery disease, awaiting by-pass surgery. Each participant was their own control in normocapnia (where CO2 was added to the inspirate) and the order of normocapnia and hypocapnia was randomized. Twelve lead electrocardiograms (ECG) were recorded and automated measurements were made on all ECG waveforms averaged over >120 beats. 2D echocardiography was also performed on healthy subjects.ResultsIn the 18 healthy subjects, we confirm that severe hypocapnia (a mean PetCO2 of 20 ± 0 mmHg, P < 0.0001) consistently increased the mean T wave amplitude in leads V1–V3, but by only 31% (P < 0.01), 15% (P < 0.001) and 11% (P < 0.05), respectively. Hypocapnia produced no other significant effects (p > 0.05) on their electro- or echocardiogram. All 10 angina patients tolerated the mechanical hyperventilation well, with minimal discomfort. Hypocpania caused a similar increase in V1 (by 39%, P < 0.05 vs. baseline, but P > 0.05 vs. healthy controls) and did not induce angina. Its effects were no greater in patients who did not take β-blockers, or did not take organic nitrates, or had the worst Canadian Cardiovascular Society scores.ConclusionNon-invasive mechanical hyperventilation while awake and unmedicated is safe and acceptable, even to patients with angina. Using it to produce severe and prolonged hypocapnia alone does produce significant ECG changes in angina patients. But its potential diagnostic value for identifying patients with coronary stenosis requires further evaluation.

PaCO2 at Early Stage is Associated with Adverse Cardiovascular Events in Acute Carbon Monoxide Poisoning

Purpose: The objective was to determine the association between PaCO2 and adverse cardiovascular events (ACVEs) in carbon monoxide (CO)-poisoned patients. Methods: This retrospective study included 194 self-breathing patients after CO poisoning with an indication for hyperbaric oxygen therapy and available arterial blood gas analysis at presentation and 6 hours later. The baseline characteristics and clinical course during hospitalization were collected and compared. The mean PaCO2 during the first 6 hours after presentation was calculated. Results: The incidence rates of moderate (30 mmHg&lt; PaCO2 &lt;35 mmHg) or severe (PaCO2 ≤30 mmHg) hypocapnia at presentation after acute CO poisoning were 40.7% and 26.8%, respectively. The mean PaCO2 during the first 6 hours was 33 (31-36.7) mmHg. The incidence of ACVEs during hospitalization was 50.5%. A significant linear trend in the incidence of ACVEs was observed across the total ranges of PaCO2 variables. In multivariate regression analysis, mean PaCO2 was independently associated with ACVEs (OR 0.798 (95% CI 0.641-0.997)). Conclusion: Mean PaCO2 during the first 6 hours was associated with increased ACVEs. Given the high incidence of ACVEs and PaCO2 derangement and the observed association between PaCO2 and ACVEs, this study suggests that 1) PaCO2 should be monitored at the acute stage to predict and/or prevent ACVEs; and 2) further study is needed to validate this result and investigate early manipulation of PaCO2 as treatment.

PaCO2 at Early Stage is Associated with Adverse Cardiovascular Events in Acute Carbon Monoxide Poisoning

Purpose: The objective was to determine the association between PaCO2 and adverse cardiovascular events (ACVEs) in carbon monoxide (CO)-poisoned patients. Methods: This retrospective study included 194 self-breathing patients after CO poisoning with an indication for hyperbaric oxygen therapy and available arterial blood gas analysis at presentation and 6 hours later. The baseline characteristics and clinical course during hospitalization were collected and compared. The mean PaCO2 during the first 6 hours after presentation was calculated. Results: The incidence rates of moderate (30 mmHg&lt; PaCO2 &lt;35 mmHg) or severe (PaCO2 ≤30 mmHg) hypocapnia at presentation after acute CO poisoning were 40.7% and 26.8%, respectively. The mean PaCO2 during the first 6 hours was 33 (31-36.7) mmHg. The incidence of ACVEs during hospitalization was 50.5%. A significant linear trend in the incidence of ACVEs was observed across the total ranges of PaCO2 variables. In multivariate regression analysis, mean PaCO2 was independently associated with ACVEs (OR 0.798 (95% CI 0.641-0.997)). Conclusion: Mean PaCO2 during the first 6 hours was associated with increased ACVEs. Given the high incidence of ACVEs and PaCO2 derangement and the observed association between PaCO2 and ACVEs, this study suggests that 1) PaCO2 should be monitored at the acute stage to predict and/or prevent ACVEs; and 2) further study is needed to validate this result and investigate early manipulation of PaCO2 as treatment.

Effects of moderate and severe hypocapnia on intracerebral perfusion and brain tissue oxygenation in piglets.

Hypocapnia is a common alteration during anesthesia in neonates. To investigate the effects of hypocapnia and hypocapnia combined with hypotension (HCT) on cerebral perfusion and tissue oxygenation in anesthetized piglets. Thirty anesthetized piglets were randomly allocated to groups: moderate hypocapnia (mHC), severe hypocapnia (sHC), and HCT. Cerebral monitoring comprised a tissue oxygen partial pressure and a laser Doppler probe inserted into the brain tissue as well as a near-infrared spectroscopy (NIRS) sensor placed on the skin, measuring regional oxygen saturation. Hypocapnia was induced by hyperventilation (target PaCO2 mHC: 3.7-4; sHC: 3.1-3.3kPa) and hypotension by blood withdrawal and nitroprusside infusion (mean blood pressure: 35-38mmHg). Data were analyzed at baseline, during (Tr20, Tr40, Tr60) and after (Post20, Post40, Post60) treatment. Compared to baseline, tissue oxygen partial pressure decreased significantly and equally during all treatments (mean [SD] at baseline: mHC 35.7 [32.45]; sHC: 28.1 [20.24]; HCT 25.4 [10.3] and at Tr60: mHC: 29.9 [27.36]; sHC: 22.2 [18.37]; HCT: 18.4 [9.5] mmHg). Decreased laser Doppler flow was detected with all treatments at Tr20 (mHC: 0.9 [0.18]; sHC: 0.88 [0.15]; HCT: 0.97 [0.13] proportion from baseline). Independently of group, regional oxygen saturation varied only after reverting and not during treatment. Blood lactate, pH, HCO3- , and PaO2 increased during treatment with no differences between groups. This animal model revealed reduced cerebral blood flow and brain tissue oxygenation during hypocapnia without detectable changes in regional oxygen saturation as measured by NIRS. Changes occurred as early as during moderate hypocapnia.

Association between hypocapnia and ventilation during the first days of life and brain injury in asphyxiated newborns treated with hypothermia

Purpose: Therapeutic hypothermia is the standard treatment for asphyxiated newborns. Since hypocapnia is common in these newborns, the aim of this study was to assess the association among hypocapnia, ventilation, and brain injury.Methods: We conducted a retrospective cohort study of all asphyxiated newborns treated with hypothermia from 2008 to 2014. Partial pressure of carbon dioxide (pCO2), ventilatory status, and modes of ventilation were recorded during the first 4 days of life. Brain injury was evaluated using brain magnetic resonance imaging. Differences between intubated and nonintubated newborns and between the newborns who developed brain injury or not were assessed.Results: One hundred ninety-eight asphyxiated newborns were treated with hypothermia. During the first 2 days of life, intubated newborns had consistently lower pCO2 levels (respectively, 29.01 ± 8.55, p < .001 on day 1 of life and 33.65 ± 7.12, p = .004 on day 2 of life). Fifty-nine percent of the intubated newborns developed brain injury versus only 43% of the nonintubated newborns (p = .046). The lowest pCO2 levels averaged over the first 4 days of life were significantly decreased in newborns developing brain injury (p = .02) and significantly associated with brain injury severity (p = .01). After adjusting for potential cofounders, the lowest pCO2 averaged over days 1–4 of life remained significantly associated with an increased risk of brain injury (odds ratio [95%CI]: 1.07 [1.00–1.14]; p = .04).Conclusions: Intubated and ventilated asphyxiated newborns experienced more severe hypocapnia, and had higher incidences of brain injury. Hypocapnia during the first 4 days of life was associated with an increased risk of developing (more severe) brain injury.

Severe diabetic ketoacidosis complicated by hypocapnic seizure.

In clinical practice, seizures independent of hypoglycemia are observed in patients with type 1 diabetes mellitus (T1DM) more frequently than expected by chance, suggesting a link. However, seizures during management of diabetic ketoacidosis (DKA) have generally been considered a bad prognostic factor, and usually associated with well-known biochemical or neurological complications. We present the case of a 17-year-old girl with known T1DM managed for severe DKA complicated by hypocapnic seizure. We review the literature on this rare occurrence as well as outline other possible differentials to consider when faced with the alarming combination of DKA and seizure.Learning points:Seizures during DKA treatment require immediate management as well as evaluation to determine their underlying cause.Their etiology is varied, but a lowered seizure threshold, electrolyte disturbances and serious neurological complications of DKA such as cerebral edema must all be considered.Sudden severe hypocapnia may represent a rare contributor to seizure during the treatment of DKA.

AltitudeOmics: Resetting of Cerebrovascular CO2 Reactivity Following Acclimatization to High Altitude.

Previous studies reported enhanced cerebrovascular CO2 reactivity upon ascent to high altitude using linear models. However, there is evidence that this response may be sigmoidal in nature. Moreover, it was speculated that these changes at high altitude are mediated by alterations in acid-base buffering. Accordingly, we reanalyzed previously published data to assess middle cerebral blood flow velocity (MCAv) responses to modified rebreathing at sea level (SL), upon ascent (ALT1) and following 16 days of acclimatization (ALT16) to 5260 m in 21 lowlanders. Using sigmoid curve fitting of the MCAv responses to CO2, we found the amplitude (95 vs. 129%, SL vs. ALT1, 95% confidence intervals (CI) [77, 112], [111, 145], respectively, P = 0.024) and the slope of the sigmoid response (4.5 vs. 7.5%/mmHg, SL vs. ALT1, 95% CIs [3.1, 5.9], [6.0, 9.0], respectively, P = 0.026) to be enhanced at ALT1, which persisted with acclimatization at ALT16 (amplitude: 177, 95% CI [139, 215], P < 0.001; slope: 10.3%/mmHg, 95% CI [8.2, 12.5], P = 0.003) compared to SL. Meanwhile, the sigmoidal response midpoint was unchanged at ALT1 (SL: 36.5 mmHg; ALT1: 35.4 mmHg, 95% CIs [34.0, 39.0], [33.1, 37.7], respectively, P = 0.982), while it was reduced by ~7 mmHg at ALT16 (28.6 mmHg, 95% CI [26.4, 30.8], P = 0.001 vs. SL), indicating leftward shift of the cerebrovascular CO2 response to a lower arterial partial pressure of CO2 (PaCO2) following acclimatization to altitude. Sigmoid fitting revealed a leftward shift in the midpoint of the cerebrovascular response curve which could not be observed with linear fitting. These findings demonstrate that there is resetting of the cerebrovascular CO2 reactivity operating point to a lower PaCO2 following acclimatization to high altitude. This cerebrovascular resetting is likely the result of an altered acid-base buffer status resulting from prolonged exposure to the severe hypocapnia associated with ventilatory acclimatization to high altitude.

A case of dilated cardiomyopathy who experienced repetitive ventricular fibrillation associated with severe hypocapnia

A case of dilated cardiomyopathy who experienced repetitive ventricular fibrillation associated with severe hypocapnia

Pulmonary and circulatory parameter guided anesthesia in patients with ischemic stroke undergoing endovascular recanalization

Background and purposeEndovascular recanalization in ischemic stroke is often performed under general anesthesia. Some studies have shown a detrimental effect of general anesthesia. The reasons are unknown.MethodsThis was an observational...

Brain cell swelling during hypocapnia increases with hyperglycemia or ketosis

Severe hypocapnia reduces cerebral blood flow (CBF) and is known to be a risk factor for diabetic ketoacidosis (DKA)-related cerebral edema and cerebral injury in children. Reductions in CBF resulting from hypocapnia alone, however, would not be expected to cause substantial cerebral injury. We hypothesized that either hyperglycemia or ketosis might alter the effects of hypocapnia on CBF and/or cerebral edema associated with CBF reduction. We induced hypocapnia (pCO₂ 20 ± 3 mmHg) via mechanical ventilation in three groups of juvenile rats: 25 controls, 22 hyperglycemic rats (serum glucose 451 ± 78 mg/dL), and 15 ketotic rats (β-hydroxy butyrate 3.0 ± 1.0 mmol/L). We used magnetic resonance imaging to measure CBF and apparent diffusion coefficient (ADC) values in these groups and in 17 ventilated rats with normal pCO₂ (40 ± 3 mmHg). In a subset (n = 35), after 2 h of hypocapnia, pCO₂ levels were normalized (40 ± 3 mmHg) and ADC and CBF measurements were repeated. Declines in CBF with hypocapnia occurred in all groups. Normalization of pCO₂ after hypocapnia resulted in hyperemia in the striatum. These effects were not substantially altered by hyperglycemia or ketosis. Declines in ADC (suggesting brain cell swelling) during hypocapnia, however, were greater during both hyperglycemia and ketosis. We conclude that brain cell swelling associated with hypocapnia is increased by both hyperglycemia and ketosis, suggesting that these metabolic conditions may make the brain more vulnerable to injury during hypocapnia.

Characterization of the relationship between inspiratory neural discharges and the micturition reflex in decerebrate and urethane‐anesthetized adult in vivo rat

Previous studies have characterized respiratory neural outputs during the micturition reflex (MR). However, these studies primarily were conducted in cats, and it is not known if the relationship seen in the cat model is maintained in rodent models. To begin to address this issue, we recorded bladder pressure and phrenic (Phr), hypoglossal (XII) and pudendal motor nerve activity in decerebrate or urethane‐anesthetized vagi‐intact adult rats during passive bladder filling and active bladder contraction. Spontaneous MRs were elicited by slow infusion of saline into the bladder. The data show increased Phr post‐inspiratory activity and a transient increase followed by a transient decrease in burst frequency (due to changes in TE). Small XII neural discharges were observed during expiration while the bladder actively contracted. In contrast to cat data, no changes in Phr or XII amplitude were observed. Finally, while severe hypercapnia and hypocapnia affected respiratory patterns, they did not affect the MR. We conclude that, while there are some similarities to the cat model, a different relationship between respiration and micturition occurs in rat. Supported by HL63175