Search

Aims: Acute heart failure (AHF) poses a major threat to hospitalized patients for its high mortality rate and serious complications. The aim of this study is to determine whether hypocapnia [defined as the partial pressure of arterial carbon dioxide (PaCO 2 ) below 35 mmHg] on admission could be associated with in-hospital all-cause mortality in AHF., Methods and Results: A total of 676 patients treated in the coronary care unit for AHF were retrospectively analysed, and the study endpoint was in-hospital all-cause mortality. The 1:1 propensity score matching (PSM) analysis, Kaplan-Meier curve, and Cox regression model were used to explore the association between hypocapnia and in-hospital all-cause mortality in AHF. Receiver operating characteristic (ROC) curve and Delong's test were used to assess the performance of hypocapnia in predicting in-hospital all-cause mortality in AHF. The study cohort included 464 (68.6%) males and 212 (31.4%) females, and the median age was 66 years (interquartile range 56-74 years). Ninety-eight (14.5%) patients died during hospitalization and presented more hypocapnia than survivors (76.5% vs. 45.5%, P < 0.001). A 1:1 PSM was performed between hypocapnic and non-hypocapnic patients, with 264 individuals in each of the two groups after matching. Compared with non-hypocapnic patients, in-hospital mortality was significantly higher in hypocapnic patients both before (22.2% vs. 6.8%, P < 0.001) and after (20.8% vs. 8.7%, P < 0.001) PSM. Kaplan-Meier curve showed a significantly higher probability of in-hospital death in patients with hypocapnia before and after PSM (both P < 0.001 for the log-rank test). Multivariate Cox regression analysis showed that hypocapnia was an independent predictor of AHF mortality both before [hazard ratio (HR) 2.22; 95% confidence interval (CI) 1.23-3.98; P = 0.008] and after (HR 2.19; 95% CI 1.18-4.07; P = 0.013) PSM. Delong's test showed that the area under the ROC curve was improved after adding hypocapnia into the model (0.872, 95% CI 0.839-0.901 vs. 0.855, 95% CI 0.820-0.886, P = 0.028). PaCO 2 was correlated with the estimated glomerular filtration rate (r = 0.20, P = 0.001), left ventricular ejection fraction (r = 0.13, P < 0.001), B-type natriuretic peptide (r = -0.28, P < 0.001), and lactate (r = -0.15, P < 0.001). Kaplan-Meier curve of PaCO 2 tertiles and multivariate Cox regression analysis showed that the lowest PaCO 2 tertile was associated with increased risk of in-hospital mortality in AHF (all P < 0.05)., Conclusions: Hypocapnia is an independent predictor of in-hospital mortality for AHF., (© 2023 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Background: An association between spontaneous hyperventilation, delayed cerebral ischemia, and poor clinical outcomes has been reported in subarachnoid hemorrhage. We evaluated the relationship between early pCO 2 changes, ischemic lesions and outcomes in patients with intracerebral hemorrhage (ICH)., Methods: Consecutive patients with spontaneous ICH were enrolled in an observational cohort study conducted between 2006 and 2019. Patient characteristics and discharge outcome were prospectively recorded. Arterial blood gas (ABG) measurements and mechanical ventilation settings in the first 72 h of admission were retrospectively collected. MRI images were adjudicated for diffusion-restricted lesions consistent with ischemia and distant from the hematoma. We examined the associations between pCO 2 changes, ischemic lesions, and discharge outcomes by univariate and adjusted analyses., Results: ABG data were available for 220 patients. Hyperventilation occurred in 52 (28%) cases and was not associated with clinical severity. Lower initial pCO 2 was associated with greater risk of in-hospital death (OR 0.94 per mmHg, 95%CI [0.89, 0.996], p = 0.042) after adjustment for ICH Score, pneumonia and mechanical ventilation requirements. MRI data were available for 33 patients. Lower pCO 2 was associated with a higher risk of ischemic lesions, except in patients with low initial systolic blood pressure (p < 0.05 for main and blood pressure interaction effects), after adjustment for other predictors., Conclusions: In ICH patients with spontaneous ventilation, lower pCO 2 was independently associated with greater risk of in-hospital death. In patients with elevated initial blood pressure, who undergo blood pressure reduction per guideline recommendations, lower pCO 2 was associated with increased risk to develop ischemic lesions., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Introduction: Cerebral edema (CE) is the most severe complication of diabetic ketoacidosis (DKA) in children. There is no accurate knowledge of CE pathogenesis and its onset has been related to intravenous rehydration therapy during the initial treatment., Objectives: To estimate the prevalence of CE among DKA patients treated at Hospital General de Niños Pedro de Elizalde with intravenous rehydration and analyze potential risk factors for the development of CE., Materials and Methods: Cross-sectional prevalence study and exploratory analysis to compare clinical and laboratory characteristics between patients with and without CE. Patients aged 1-18 years hospitalized with the diagnosis of DKA between January 1st, 2005 and December 31st, 2014 were included., Results: A total of 693 DKA events from 561 medical records were analyzed. Ten patients had evidence of CE (1.44 %; 95 % confidence interval: 0.8-2.6). Patients with CE had higher serum urea levels (p &#60; 0.001), lower carbon dioxide pressure (p &#60; 0.001), and lower serum sodium levels (p &#60; 0.001) than those without CE., Conclusion: The prevalence of CE among DKA patients was 1.44 %, smaller than that reported in our country (1.8 %). The risk factors at admission associated with CE development were high serum urea levels, hyponatremia, and hypocapnia., Competing Interests: None, (Sociedad Argentina de Pediatría.)

Background: Hypocapnia induces cerebral vasoconstriction leading to a decrease in cerebral blood flow, which might precipitate cerebral ischemia. Hypocapnia can be intentional to treat intracranial hypertension or unintentional due to a spontaneous hyperventilation (SHV). SHV is frequent after subarachnoid hemorrhage. However, it is understudied in patients with severe traumatic brain injury (TBI). The objective of this study was to describe the incidence and consequences on outcome of SHV after severe TBI., Methods: We conducted a retrospective, observational study including all intubated TBI patients admitted in the trauma center and still comatose 24 h after the withdrawal of sedation. SHV was defined by the presence of at least one arterial blood gas (ABG) with both PaCO 2  < 35 mmHg and pH > 7.45. Patient characteristics and outcome were extracted from a prospective registry of all intubated TBI admitted in the intensive care unit. ABG results were retrieved from patient files. A multivariable logistic regression model was developed to determine factors independently associated with unfavorable outcome (defined as a Glasgow Outcome Scale between 1 and 3) at 6-month follow-up., Results: During 7 years, 110 patients fully respecting inclusion criteria were included. The overall incidence of SHV was 69.1% (95% CI [59.9-77]). Patients with SHV were more severely injured (median head AIS score (5 [4-5] vs. 4 [4-5]; p = 0.016)) and exhibited an elevated morbidity during their stay. The proportion of patients with an unfavorable functional neurologic outcome was significantly higher in patients with SHV: 40 (52.6%) versus 6 (17.6%), p = 0.0006. After adjusting for confounders, SHV remains an independent factor associated with unfavorable outcome at the 6-month follow-up (OR 4.1; 95% CI [1.2-14.4])., Conclusions: SHV is common in patients with a persistent coma after a severe TBI (overall rate: 69%) and was independently associated with unfavorable outcome at 6-month follow-up.

Objectives: To determine the frequency of hyperoxia and hypocapnia during pediatric extracorporeal membrane oxygenation and their relationships to complications, mortality, and functional status among survivors., Design: Secondary analysis of data collected prospectively by the Collaborative Pediatric Critical Care Research Network., Setting: Eight Collaborative Pediatric Critical Care Research Network-affiliated hospitals., Patients: Age less than 19 years and treated with extracorporeal membrane oxygenation., Interventions: Hyperoxia was defined as highest PaO2 greater than 200 Torr (27 kPa) and hypocapnia as lowest PaCO2 less than 30 Torr (3.9 kPa) during the first 48 hours of extracorporeal membrane oxygenation. Functional status at hospital discharge was evaluated among survivors using the Functional Status Scale., Measurements and Main Results: Of 484 patients, 420 (86.7%) had venoarterial extracorporeal membrane oxygenation and 64 (13.2%) venovenous; 69 (14.2%) had extracorporeal membrane oxygenation initiated during cardiopulmonary resuscitation. Hyperoxia occurred in 331 (68.4%) and hypocapnia in 98 (20.2%). Hyperoxic patients had higher mortality than patients without hyperoxia (167 [50.5%] vs 48 [31.4%]; p < 0.001), but no difference in functional status among survivors. Hypocapnic patients were more likely to have a neurologic event (49 [50.0%] vs 143 (37.0%]; p = 0.021) or hepatic dysfunction (49 [50.0%] vs 121 [31.3%]; p < 0.001) than patients without hypocapnia, but no difference in mortality or functional status among survivors. On multivariable analysis, factors independently associated with increased mortality included highest PaO2 and highest blood lactate concentration in the first 48 hours of extracorporeal membrane oxygenation, congenital diaphragmatic hernia, and being a preterm neonate. Factors independently associated with lower mortality included meconium aspiration syndrome., Conclusions: Hyperoxia is common during pediatric extracorporeal membrane oxygenation and associated with mortality. Hypocapnia appears to occur less often and although associated with complications, an association with mortality was not observed.

Objective: The aim of this study was to investigate whether patients with chronic neck pain have changes in their transcutaneous partial pressure of arterial carbon dioxide (PtcCO2) and whether other physical and psychologic parameters are associated., Design: In this cross-sectional study, 45 patients with chronic idiopathic neck pain and 45 healthy sex-, age-, height-, and weight-matched controls were voluntarily recruited. The participants' neck muscle strength, endurance of the deep neck flexors, neck range of movement, forward head posture, psychologic states (anxiety, depression, kinesiophobia, and catastrophizing), disability, and pain were assessed. PtcCO2 was assessed using transcutaneous blood gas monitoring., Results: The patients with chronic neck pain presented significantly reduced PtcCO2 (P < 0.01). In the patients, PtcCO2 was significantly correlated with strength of the neck muscles, endurance of the deep neck flexors, kinesiophobia, catastrophizing, and pain intensity (P < 0.05). Pain intensity, endurance of the deep neck flexors, and kinesiophobia remained as significant predictors into the regression model of PtcCO2., Conclusions: Patients with chronic neck pain present with reduced PtcCO2, which can reach the limits of hypocapnia. This disturbance seems to be associated with physical and psychologic manifestations of neck pain. These findings can have a great impact on various clinical aspects, notably, patient assessment, rehabilitation, and drug prescription.

Background: The impact of hypocapnia on outcome in aneurysmal subarachnoid hemorrhage (SAH) is unclear, although hypocapnia is associated with poor outcome in other brain injuries. We sought to determine the incidence and impact of hypocapnia in mechanically ventilated patients with aneurysmal SAH., Methods: We assembled a retrospective cohort of 102 consecutive mechanically ventilated patients with aneurysmal SAH admitted to an academic neurosurgical intensive care unit (ICU). Ventilation records, arterial blood gas data, and clinical outcomes were reviewed. The primary outcome was 3-month Glasgow Outcome Scale, with secondary outcomes of ICU and hospital mortality and symptomatic vasospasm., Results: Hypocapnia was common (92% of patients had 1 or more PaCO2 measurements <35 mm Hg), with 68% of these measurements occurring while breathing spontaneously with minimal ventilator support. Median duration of hypocapnia was 4 days (interquartile range, 2 to 12). Forty-eight percent of all PaCO2 measurements on a given day were below 30 mm Hg. Unfavorable outcome (Glasgow Outcome Scale <4) occurred in 52 of 89 patients (58.4%). ICU and hospital mortality was 26.5% and 32.4%, respectively, and 34% developed symptomatic vasospasm. Duration of hypocapnia was associated with unfavorable outcome (adjusted odds ratio 1.33 for each additional day of hypocapnia) and symptomatic vasospasm (adjusted odds ratio 1.25 for each additional day of hypocapnia), but not ICU or hospital mortality. These associations appeared robust in sensitivity analyses to address potential misclassification and ascertainment bias., Conclusions: Hypocapnia is common in ventilated patients with aneurysmal SAH, and a significant proportion of this developed spontaneously despite minimal ventilator support. The duration of hypocapnia is independently associated with poor functional outcomes and symptomatic vasospasm. Further study is warranted to confirm a causal link between hypocapnia and poor outcomes, and to confirm whether tight control of PaCO2 might improve outcomes in aneurysmal SAH.

Objective: To determine the incidence of hypo- and hyper-capnia in a European cohort of ventilated newborn infants., Design and Setting: Two-point cross-sectional prospective study in 173 European neonatal intensive care units., Patients and Methods: Patient characteristics, ventilator settings and measurements, and blood gas analyses were collected for endotracheally ventilated newborn infants on two separate dates., Results: A total of 1569 blood gas analyses were performed in 508 included patients with a mean±SD Pco2 of 48±12 mm Hg or 6.4±1.6 kPa (range 17-104 mm Hg or 2.3-13.9 kPa). Hypocapnia (Pco2<30 mm Hg or 4 kPa) and hypercapnia (Pco2>52 mm Hg or 7 kPa) was present in, respectively, 69 (4%) and 492 (31%) of the blood gases. Hypocapnia was most common in the first 3 days of life (7.3%) and hypercapnia after the first week of life (42.6%). Pco2 was significantly higher in preterm infants (49 mm Hg or 6.5 kPa) than term infants (43 mm Hg or 5.7 kPa) and significantly lower during pressure-limited ventilation (47 mm Hg or 6.3±1.6 kPa) compared with volume-targeted ventilation (51 mm Hg or 6.8±1.7 kPa) and high-frequency ventilation (50 mm Hg or 6.7±1.7 kPa)., Conclusions: This study shows that hypocapnia is a relatively uncommon finding during neonatal ventilation. The higher incidence of hypercapnia may suggest that permissive hypercapnia has found its way into daily clinical practice.

Background: Partial pressure of arterial CO2 (Paco(2)) is a regulator of cerebral blood flow after brain injury. Recent guidelines for the management of cardiac arrest recommend maintaining Paco(2) at 40 to 45 mm Hg after successful resuscitation; however, there is a paucity of data on the prevalence of Paco(2) derangements during the post-cardiac arrest period and its association with outcome., Methods and Results: We analyzed a prospectively compiled and maintained cardiac arrest registry at a single academic medical center. Inclusion criteria are as follows: age ≥18, nontrauma arrest, and comatose after return of spontaneous circulation. We analyzed arterial blood gas data during 0 to 24 hours after the return of spontaneous circulation and determined whether patients had exposure to hypocapnia and hypercapnia (defined as Paco(2) ≤30 mm Hg and Paco(2) ≥50 mm Hg, respectively, based on previous literature). The primary outcome was poor neurological function at hospital discharge, defined as Cerebral Performance Category ≥3. We used multivariable logistic regression, with multiple sensitivity analyses, adjusted for factors known to predict poor outcome, to determine whether post-return of spontaneous circulation hypocapnia and hypercapnia were independent predictors of poor neurological function. Of 193 patients, 52 (27%) had hypocapnia only, 63 (33%) had hypercapnia only, 18 (9%) had both hypocapnia and hypercapnia exposure, and 60 (31%) had no exposure; 74% of patients had poor neurological outcome. Hypocapnia and hypercapnia were independently associated with poor neurological function, odds ratio 2.43 (95% confidence interval, 1.04-5.65) and 2.20 (95% confidence interval, 1.03-4.71), respectively., Conclusions: Hypocapnia and hypercapnia were common after cardiac arrest and were independently associated with poor neurological outcome. These data suggest that Paco(2) derangements could be potentially harmful for patients after resuscitation from cardiac arrest.

Objectives: Pilot studies have described the occurrence of sleep apnea in patients with precapillary pulmonary hypertension (PH). However, there are no data on the prevalence of sleep-related breathing disorders in larger patient cohorts with PH., Methods: 169 patients with a diagnosis of PH confirmed by right heart catheterisation and clinically stable in NYHA classes II or III were prospectively investigated by polygraphy (n = 105 females, mean age: 61.3 years, mean body mass index: 27.2 kg/m(2)). Recruitment was independent of sleep-related symptoms and the use of vasodilator drugs or nasal oxygen., Results: 45 patients (i.e. 26.6%) had an apnea-hypopnea-index (AHI) >10/h. Of these, 27 patients (i.e. 16%) had obstructive sleep apnea (OSA) and 18 patients (i.e. 10.6%) had central sleep apnea (CSA). The mean AHI was 20/hour. As a polygraphy had been performed with nasal oxygen in half of the patients without evidence for sleep apnea, the frequency of CSA was probably underestimated. Patients with OSA were characterized by male gender and higher body mass index whereas, those with CSA were older and hypocapnic., Conclusions: At least every fourth patient with PH suffers from mild-to-moderate sleep apnea. Considering the anthropometric characteristics of the patients studied, the prevalence of both OSA and CSA seem to be higher in PH than in the general population., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Purpose: Arterial hyperoxia after resuscitation has been associated with increased mortality in adults. The aim of this study was to test the hypothesis that post-resuscitation hyperoxia and hypocapnia are associated with increased mortality after resuscitation in pediatric patients., Methods: We performed a prospective observational multicenter hospital-based study including 223 children aged between 1 month and 18 years who achieved return of spontaneous circulation after in-hospital cardiac arrest and for whom arterial blood gas analysis data were available., Results: After return of spontaneous circulation, 8.5% of patients had hyperoxia (defined as PaO(2)>300 mm Hg) and 26.5% hypoxia (defined as PaO(2)<60 mm Hg). No statistical differences in mortality were observed when patients with hyperoxia (52.6%), hypoxia (42.4%), or normoxia (40.7%) (p=0.61). Hypocapnia (defined as PaCO(2)<30 mm Hg) was observed in 13.5% of patients and hypercapnia (defined as PaCO(2)>50 mm Hg) in 27.6%. Patients with hypercapnia or hypocapnia had significantly higher mortality (59.0% and 50.0%, respectively) than patients with normocapnia (33.1%) (p=0.002). At 24h after return of spontaneous circulation, neither PaO(2) nor PaCO(2) values were associated with mortality. Multiple logistic regression analysis showed that hypercapnia (OR, 3.27; 95% CI, 1.62-6.61; p=0.001) and hypocapnia (OR, 2.71; 95% CI, 1.04-7.05; p=0.04) after return of spontaneous circulation were significant mortality factors., Conclusions: In children resuscitated from cardiac arrest, hyperoxemia after return of spontaneous circulation or 24h later was not associated with mortality. On the other hand, hypercapnia and hypocapnia were associated with higher mortality than normocapnia., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Heart failure (HF) and sleep apnoea (SA) association has been recognized but whether it results from confounding factors (hypertension, ischaemia, obesity) remains unclear.We aimed to determine the prevalence of SA in HF and to identify potential risk factors for SA in HF population., Methods: We prospectively evaluated 103 patients with stable HF on optimized therapy. In-laboratory polysomnography was performed. Type and severity of SA were defined according international criteria. Demographic, anthropometric and clinical characteristics were collected. Continuous data are expressed as median and interquartile range., Results: SA was found in 72.8%, moderate to severe in a significant proportion (apnoea-hypopnoea index > or = 15- 44.7% of all patients) and predominantly obstructive (60.0% of patients with SA). Most patients were non-sleepy (Epworth < 10- 66%). SA patients were predominantly men (85.3 vs 60.7%, p-0.015), had larger neck (38.0 (35.0-42.0) vs 35.0 (33.2-38.0) cm, p-0.003), severe systolic dysfunction, (63.9 vs 33.3%, p-0.018), left ventricle (LV) hypertrophy (16.2 vs 0.0%, p-0.03), LV and left atria (LA) dilatation (49.0 (44.0-52.0) vs 42.0 (38.0-48.0) mm, p < 0.001; 60.0 (54.0-65.0) vs 56.0 (52.0-59.0) mm, p-0.01). However, only LA diameter was an independent predictor of SA. Higher body-mass index (BMI) was associated with moderate to severe SA. Patients with obstructive SA had larger neck and a trend for higher BMI, snoring and sleepiness. Hypocapnia was not associated with central SA., Conclusions: In our HF population, SA was prevalent, frequently asymptomatic and without characteristic risk factors. Unlike previously reported, obstructive SA was the predominant type. These results suggest that SA is underdiagnosed in HF and there is a possible correlation between them, independent of confounding factors. Recent advances in HF therapy might influence prevalence and type of SA in this population.

To investigate the incidence of iatrogenic dyscarbia in survivors of out-of-hospital cardiac arrest treated with induced mild hypothermia.We performed a retrospective cohort study of the ventilatory management based on blood gas analyses of patients resuscitated from prehospital cardiac arrest. In the pilot phase, we assessed the ventilatory management in the patients treated in one university hospital during a 4-year study period. Subsequently, a more recent (1-year) retrospective cohort of resuscitated patients from all five Finnish university hospitals concerning the first 48h after hospital admission was analyzed. Core temperatures and temperature corrected (or non-corrected) blood gas analysis results with focus on carbon dioxide tension were analyzed. In addition, a survey was performed to investigate the ventilatory strategies in all Finnish hospitals providing mild hypothermia for cardiac arrest victims.The pilot cohort suggested a high incidence of hypo- or hyper-carbia during hypothermia treatment. In the multicenter patient population of 122 patients contributing a total of 1627 measurements, the PaCO(2) distribution was as follows: less than 4 kPa in 148 samples out of 1627 (9%), 4-4.6 kPa in 404 (25%), 4.7-6 kPa in 887 (55%) and more than 6 kPa in 188 samples (12%). There was a significant difference in the incidence of hypercarbia between the hospitals (p<0.05).We conclude that normocarbia was achieved/maintained only in approximately 55% of the samples. The incidence of hypo- or hyper-carbia (dyscarbia) was high (45%). This may predispose for serious derangements in the cerebral perfusion of the resuscitated patient. These results call for vigilance in adjustment of the ventilatory management to meet the needs of the patients treated with mild hypothermia.

Background: The arterial partial pressure of carbon dioxide (PaCO2) represents the balance between CO2 production and consumption. Abnormal increase or decrease in PaCO2 can affect the body's internal environment and function. Permissive hypercapnia has aroused more attention as a novel ventilatory therapy. The aim of this study was to elucidate the effects of hypercapnia and hypocapnia on the functions of such neonatal organs as the lung and brain., Data Sources: The PubMed database was searched with the keywords "hypocapnia", "hypercapnia" and "newborn"., Results: Hypocapnia is a risk factor for potential damage to the central nervous system, such as periventricular leukomalacia, intraventricular hemorrhage, cerebral palsy, cognition developmental disorder, and auditory deficit. Hyperventilation can lessen pulmonary artery hypertension to certain extent, but hypocapnia can aggravate ischemia/reperfusion-induced acute lung injury. Severe hypercapnia can induce intracranial hemorrhage, even consciousness alterations, cataphora, and hyperspasmia. Permissive hypercapnia can improve lung injury caused by diseases of the respiratory system, lessen mechanical ventilation-associated lung injury, reduce the incidence of bronchopulmonary dysplasia and protect against ventilation-induced brain injury. In addition, permissive hypercapnia plays a role in expanding cerebral vessels and increasing cerebral blood flow., Conclusions: Severe hypercapnia and hypocapnia can cause neonatal brain injury and lung injury. Permissive hypercapnia can increase the survival of neonates with brain injury or respiratory system disease, and lessen the brain injury and lung injury caused by mechanical ventilation. However, the mechanism of permissive hypercapnia needs further exploration to confirm its safety and therapeutic utility.

Objective: To examine the incidence of severe hypocarbia (PaCO2 <30 mm Hg) in patients with severe pediatric traumatic brain injury before and after publication of the 2003 pediatric guidelines (PG)., Design: Retrospective cohort analysis., Setting: Harborview Medical Center, Seattle, Washington (January 1, 1995, to December 31, 2005)., Patients: Children <15 yrs of age with severe pediatric traumatic brain injury., Interventions: None., Measurements and Main Results: The pre-PG group (before August 1, 2003) included 375 patients and the post-PG group included 89 patients. Post PG guidelines, there was a trend toward earlier (45 vs. 32 mins; p = .05) and more frequent (7.1 vs. 8.4 samples; p = .06) PaCO2 sampling within 48 hrs of admission. Children 0-2 yrs had a longer time (75.0 mins) between admission and first PaCO2 sample than older children (44.3 mins; p < .01). The youngest children also had the highest incidence of severe hypocarbia on the first PaCO2 sample (31% vs. 19%; p = .02). Incidence of severe hypocarbia was high and did not decline (60% vs. 52%; p = .2) after the PG guidelines. However, over the 11 yrs, the odds of severe hypocarbia decreased (adjusted odds ratio 0.9; 95% confidence interval 0.84-0.96). During both periods, the incidence of severe hypocarbia was highest during the first 2 hrs after hospital admission. Intracranial pressure monitors were used more frequently post-PG. In 62 of 82 (77%) patients with severe hypocarbia in whom an intracranial pressure monitor was in place, the preceding intracranial pressure was <20 mm Hg. Severe hypocarbia independently predicted inpatient mortality (adjusted odds ratio 2.8; 95% confidence interval 1.3-5.9)., Conclusions: Although PaCO2 sampling was more frequent during the post-PG period and severe hypocarbia decreased during successive study years, the incidence of severe hypocarbia remained high during the first 48 hrs after hospital admission during the post-PG period. Time to PaCO2 sampling was longer in young children and associated with more severe hypocarbia. The presence of severe hypocarbia predicted mortality.

Background: The San Diego Paramedic Rapid Sequence Intubation (RSI) Trial documented an increase in mortality after paramedic RSI, with hyperventilation identified as a contributing factor in a small subgroup analysis. Here we explore factors affecting outcome in the entire cohort of patients undergoing paramedic RSI to confirm previous findings. This also represents a synthesis of findings from previous analyses, Methods: Adult trauma patients with severe head injury (Glasgow Coma Scale score, 3-8) who could not be intubated without RSI were prospectively enrolled in the trial. This analysis excluded patients without traumatic brain injury (head/neck abbreviated injury score <2 or failure to meet Major Trauma Outcome Study criteria) or death in the field or within 30 minutes of arrival. Each remaining trial patient was matched to two nonintubated historical controls from the county trauma registry based on: age, sex, mechanism, abbreviated injury scores for each body system, and Injury Severity Score. Logistic regression, cohort analysis, mean least squares regression, and discordant group analysis were used to explore the impact of various factors on outcome., Results: Of the 426 trial patients, 352 met inclusion criteria for this analysis and were hand-matched to 704 controls. Trial patients and controls were identical with regard to all matching variables. Mortality was increased in RSI patients versus matched controls (31.8 versus 23.7%; odds ration, 1.5; 95% confidence interval, 1.1-2.0; p < 0.01). Hyperventilation was associated with an increase in mortality, whereas transport by aeromedical crews after paramedic RSI was associated with improved outcomes. The reported incidence of aspiration pneumonia was higher for the RSI patients., Conclusion: Paramedic RSI was associated with an increase in mortality compared with matched historical controls. The association between hyperventilation and mortality was confirmed. In addition, patients transported by helicopter after paramedic RSI had improved outcomes. Paramedic RSI did not seem to prevent aspiration pneumonia.

Background: Central sleep apnea (CSA) and Cheyne-Stokes respiration have been reported in association with stroke, but their pathophysiologic correlates have not been well described., Objective: To test the hypotheses that (1) CSA in patients with stroke is associated with nocturnal hypocapnia and (2) in those stroke patients with CSA and with left ventricular (LV) systolic dysfunction, periodic breathing (PB) will have a Cheyne-Stokes respiration pattern in which cycle duration is greater than in those without LV systolic dysfunction., Methods: We prospectively performed polysomnography and echocardiography in 93 patients with stroke. CSA was defined as central apneas and hypopneas occurring at a rate of 10 or more per hour of sleep. In patients with CSA, we compared PB cycle duration between those with normal and impaired LV systolic function (LV ejection fraction [LVEF] > 40% and < or = 40%, respectively)., Results: CSA was found in 19% of subjects who had lower nocturnal transcutaneous PCO2 (39.3 +/- 0.9 vs. 42.8 +/- 0.8 mmHg, p = 0.015) and a higher prevalence of LVEF of 40% or less (22 vs. 5%, p = 0.043) than stroke patients without CSA. There was no significant difference in stroke location or type between the two groups. In patients with CSA, those with LVEF of 40% or less had a longer PB cycle than those with an LVEF of more than 40% (66.6 +/- 5.6 vs. 46.6 +/- 2.9 seconds, p = 0.006), but had no symptoms of heart failure., Conclusion: In patients with stroke, CSA is associated with hypocapnia and occult LV systolic dysfunction but is not related to the location or type of stroke. The presence of LV systolic dysfunction is associated with a Cheyne-Stokes pattern of hyperpnea.

Introduction: Inadvertent hyperventilation has been documented during aeromedical transports but has not been studied following paramedic rapid sequence intubation (RSI). The San Diego Paramedic RSI Trial was designed to study the impact of paramedic RSI on outcome in patients with severe head injury. This analysis explores ventilation patterns in a cohort of trial patients undergoing end-tidal CO2 (ETCO2) monitoring., Methods: Adult patients with severe head injury (Glasgow Coma Score: 3-8) unable to be intubated without RSI were prospectively enrolled in the trial. Midazolam and succinylcholine were used for RSI; rocuronium was administered following tube confirmation. Standardized ventilation protocols were used by most paramedics; however, one agency instituted ETCO2 monitoring during the second trial year, with paramedics instructed to target ETCO2 values of 30 to 35 mmHg. The incidence and duration of inadvertent hyperventilation (ETCO2: <30 mmHg) and severe hyperventilation (ETCO2: <25 mmHg) were explored for patients undergoing ETCO2 monitoring. The initial, final, minimum, and maximum values for ETCO2 and the maximum and minimum ventilatory rate values were also calculated using descriptive statistics (95% confidence interval). The pattern of ETCO2 values over time and distribution of recorded ventilatory rate values were explored graphically., Results: A total of 76 trial patients had adequate ETCO2 data for this analysis. The mean values for initial, final, maximum, and minimum ETCO2 were 40.8 (range: 37.5-44.2), 28.4 (range: 25.4-31.4), 45.1 (range: 41.4-48.8), and 23.5 mmHg (range: 21.4-25.5), respectively. The mean maximum and minimum ventilatory rate values were 36.0/minute (range: 33.5-38.5) and 12.8/minute (range: 11.9-13.7), respectively. ETCO2 values less than 30 and 25 mmHg were documented in 79% and 59% of patients, respectively, with mean durations of 485 (range: 378-592) and 390 seconds (range: 285-494)., Conclusion: Inadvertent hyperventilation is common following paramedic RSI, despite ETCO2 monitoring and target parameters.

We experienced a family in whom sleep apnea syndrome (SAS) was recognized in six members and habitual snoring in seven members among 26 subjects of four generations. In all members with snoring, the disorder was noticed before the age of 20. Hypercapnic response study showed normal findings, and ultrafast magnetic resonance image of the upper airway revealed that the obstruction of the upper airway occurred at the velopharyngeal portion during apneic episodes in all SAS-afflicted subjects. In this family, the similar craniofacial structural abnormalities were thought to cause the aggregated occurrences of the disorders at young ages, and obesity was regarded as a contributor for the aggravated symptoms.

Recent reports have suggested that increases in venoarterial difference in PCO2 (VAPCO2) and arteriovenous difference in pH (AVpH) represent valuable markers of tissue hypoxia in shock states associated with low cardiac output. We compared the values of VAPCO2 and AVpH with that of blood lactate in their relationship to changes in O2 uptake (VO2) and O2 delivery (DO2) during an acute reduction in blood flow induced by cardiac tamponade. In 13 anesthetized and mechanically ventilated dogs, a catheter was inserted into the pericardium to inject saline and to measure the intrapericardial pressure. VO2 was derived from expired gas analysis. DO2 was calculated by the product of the thermodilution cardiac index and the arterial O2 content. The critical DO2 (DO2crit) was found at 9.9 +/- 1.8 ml/kg.min. VAPCO2 and AVpH, which were 7.1 +/- 4.6 mm Hg and 0.028 +/- 0.025 U, respectively, at baseline, progressively increased to reach 17.5 +/- 6.6 mm Hg and 0.114 +/- 0.054 U, respectively, at DO2crit (both p < 0.01). Below DO2crit they increased more dramatically. These changes were related to both arterial hypocapnia and mixed venous hypercapnia. CO2 excretion decreased from 5.8 +/- 2.0 ml/kg-min at baseline to 3.9 +/- 0.9 ml/kg.min at DO2crit (p < 0.01). End-tidal CO2 tension significantly fell below DO2crit. Lactate levels increased from 2.1 +/- 0.5 to 3.5 +/- 0.5 mmol/L at DO2crit (P < 0.01) and to 6.9 +/- 2.1 mmol/L (p < 0.01) at the end of the study. There was no statistically significant difference between the DO2crit calculated for VAPCO2, AVpH, lactate, or VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Although hyperventilation with hypocapnia is frequently used in the management of neurosurgical patients in whom sensory-evoked potentials may be monitored, the effects of hypocapnia on evoked potentials have not been described with precision. In the present experiment, the effects of randomized arterial carbon dioxide tensions of 20, 25, 30, and 35 mm Hg on spinal, subcortical, and cortical somatosensory-evoked potentials (SEPs) were measured in dogs anesthetized with 1.40% isoflurane. Other variables known to affect the SEP (temperature, blood pressure, and arterial oxygen tension) were stable throughout the experiment. Hypocapnia caused reductions in the latencies of the early peaks of the spinal and subcortical SEPs. These differences were small, consisting of a 2% shortening of latency at 20 mm Hg carbon dioxide tension when compared with 35 mm Hg. No changes were detected in the later subcortical and cortical latencies. SEP amplitudes were also unchanged. These results in a controlled animal study corroborate the direction and magnitude of changes due to hypocapnia observed by other investigators in surgical patients. The magnitude of the changes indicates that SEP monitoring sensitivity is not compromised by clinically useful levels of induced hypocapnia during isoflurane anesthesia. Because hypocapnia may produce small SEP changes, baseline recordings should be acquired prior to initiation of hyperventilation. It is not warranted, however, to impute a severe deterioration of the SEP to hypocapnia alone, and causes must be sought elsewhere in a patient's status and management.