Hypoxemic Group Research Articles

Clinical and microbiological characteristics of community-acquired pneumonia in human immunodeficiency virus-infected patients: a retrospective analysis of 79 HIV/AIDS patients

HIV infections are prevalent; however, the clinical characteristics of these patients are atypical. In the present study, we analysed 79 patients who were newly diagnosed with HIV/acquired immunodeficiency syndrome (AIDS) at Ruijin Hospital between January 1998 and August 2011 to improve awareness of the physicians' diagnoses and to elucidate the risk factors for community-acquired pneumonia (CAP) and the progression to severe pneumonia or respiratory failure in AIDS patients. The patients were divided into a CAP group (A) and a non-CAP group (B). Furthermore, group A was divided into a severe pneumonia group (A1 ) and a non-severe pneumonia group (A2 ). The serum albumin (25.60 ± 5.31 vs 34.00 ± 6.90; P < 0.05) and CD4 cell count (28.5 ± 30.5 vs 229.50 ± 229.45; P < 0.05) of group A were much lower than those of group B. The serum albumin and CD4 cell count negatively correlated with the incidence of CAP. The CD4 cell count (24.15 ± 25.1 vs 47.85 ± 132.5; P < 0.05) and partial pressure of oxygen (7.86 ± 1.43 vs 9.41 ± 2.15; P < 0.05) of group A1 were significantly lower than those of group A2 . Low serum albumin levels and high blood urea nitrogen levels were the risk factors of hypoxaemia in group A. Early screening and diagnosis of AIDS, as well as nutritional support, would prevent AIDS patients from developing CAP or progressing to severe pneumonia or respiratory failure.

Adverse Influence of Mixed Acidemia on the Biocompatibility of Continuous Veno‐Venous Hemofiltration With Respect to the Lungs

Experimental data indicate that hypercapnic adidosis has anti-inflammatory effects. These anti-inflammatory effects may even be a beneficial property in case of low tidal volume ventilation with consecutive hypercapnic acidosis. It is unclear whether these anti-inflammatory effects predominate in critically ill patients who suffer from multiple pro- and anti-inflammatory insults like extracorporeal organ support (pro-inflammatory), metabolic acidosis (pro- and anti-inflammatory), as well as hypoxia (pro-inflammatory). Eighteen pigs were randomized into three groups, mechanically ventilated and connected to a continuous veno-venous hemofiltration (CVVH) as pro-inflammatory insult. A reference group with normal acid-base state obtained normoventilation; a normoxemic acidemia group obtained normoxemic, mixed acidemia due to infusion of lactic and hyperchloremic acid and low tidal volume ventilation, and in a hypoxemic acidemia group the mixed acidemia was paralleled by hypoxemia. Lung histology including pulmonary leukocyte invasion, blood gases, blood cell counts, and hemodynamics were examined. The histological examination of the lungs of acidemic pigs showed a suppressed invasion of leukocytes and thinner alveolar walls compared with normoventilated and with hypoxemic pigs. Enhanced congestion and alveolar red blood cells (RBCs) combined with an increase of the pulmonary artery pressure were observed in acidemic pigs in comparison with the reference group. Normoxemic acidemia reduced the pro-inflammatory reaction to the CVVH and mechanical ventilation in the ventilated lung areas in the form of pulmonary leukocyte invasion. However, this did not result in reduced scores for lung injury. Instead, an increased score for criteria which represent lung injury (congestion and alveolar RBCs) was observed in acidemic pigs.

Acute effects of transcutaneous electrical diaphragmatic stimulation on respiratory pattern in COPD patients: cross-sectional and comparative clinical trial

BackgroundTranscutaneous electrical diaphragmatic stimulation (TEDS) has been used to improve respiratory muscle strength in patients with respiratory muscle weakness. However, this physical therapy resource has not been studied in chronic obstructive pulmonary disease (COPD). ObjectiveTo evaluate the respiratory pattern during one session of TEDS in COPD patients. MethodFifteen COPD patients participated in one TEDS session for plethysmographic analysis and assessment of peripheral oxygen saturation (SpO2) and heart rate (HR). After the session, patients were divided into two groups: Responder (R; n=9) and Non-Responder (NR; n=6) to TEDS. Statistic analysis was performed using the Shapiro-Wilk normality test and two-way ANOVA. For the parameters that showed interaction, the Student t test was used (P<0.05). ResultsR group consisted mainly of men, with lower SpO2 and higher HR than NR group. When time (before and during) and groups (R and NR) were compared (interaction), there were differences in the parameters minute ventilation (Vent), inspiratory tidal volume (ViVol), expiratory tidal volume (VeVol), and respiratory rate (Br/M). In the intergroup comparison, differences were observed in the parameters Vent, ViVol, and VeVol. A significant effect was also observed for time in change in end-expiratory lung volume level (qDEEL), phase relation during inspiration (PhRIB); phase relation during expiration (PhREB); phase relation of entire breath (PhRTB), and phase angle (PhAng). During TEDS, there was an increase in SpO2 and a reduction in HR in both groups. ConclusionsThe most hypoxemic group with greater HR responded to TEDS and there was interaction between group and time of analysis for the pulmonary volumes. The time factor had an influence on the two groups with an increase in thoracoabdominal asynchrony.

Iron Deficiency Anemia Detection from Hematology Parameters in Adult Congenital Heart Disease Patients

Iron deficiency anemia is the most common single cause of anemia worldwide. The purpose of our study was to estimate the prevalence of anemia in adult congenital heart disease (ACHD) patients, compare different hematology parameters between hypoxemic and nonhypoxemic ACHD patients, and determine which parameters detect iron deficiency anemia in hypoxemic ACHD patients. ACHD patients were studied and blood samples collected for determination of hemoglobin, derived red cell indices, serum iron, apoferritin, total iron-binding capacity, transferrin saturation index, C-reactive protein (CRP), and N-terminal proB-type natriuretic peptide (NT-proBNP) levels. Two hundred seventy-eight ACHD patients, mean age 31.6 ± 14.3 years old, were studied. One hundred sixty-seven (60%) patients were male. Two hundred forty-five patients were nonhypoxemic and 33 patients were hypoxemic. Hypoxemic ACHD patients had significant higher hemoglobin concentration (g/dL) (17.5 ± 3.5 vs. 14.6 ± 1.7, P <.001), red cell distribution width (RDW) (%) (17.0 ± 3.3 vs. 14.1 ± 7.6, P <.034), apoferritin (ng/mL) (19.8 [4.1-147.2] vs. 38.0 [6.7-191.2], P =.019), CRP (mg/dL) (0.50 [0.0-3.8] vs. 0.12 [0.0-1.4], P <.001), and NT-proBNP (pg/mL) (409.3 [33.3-9830.8] vs. 5.2 [0.0-1068.4], P <.001) levels than nonhypoxemic ACHD patients. Serum iron, total iron-binding capacity, and transferrin saturation index were not statistically significant between hypoxemic and nonhypoxemic ACHD patients. In the hypoxemic group, 15 (45%) patients had apoferritin levels <20 ng/mL and eight (24%) patients developed microcytosis and hypochromia. A RDW above the normal range (>14.5%) in hypoxemic ACHD patients allowed the detection of an apoferritin level <20 ng/mL with a sensitivity of 93%. RDW seems to be a useful and economic tool to detect low serum apoferritin levels in hypoxemic ACHD patients.

Hypoxemic Versus Normoxemic Reperfusion in a Large Animal Model of Severe Ischemia-Reperfusion Injury

Prior studies have suggested a significant benefit of using deliberate hypoxemia to reperfuse ischemic tissue beds, primarily by reducing free radical injury. We sought to examine the effects of a hypoxemic reperfusion strategy in a large animal model of severe truncal ischemia. Adult swine were subjected to 30 min of supraceliac aortic occlusion and randomized to two groups: normoxemia group (n = 9), with resuscitation at a pO2 >100 mmHg or hypoxemia group (n = 10), with initial resuscitation at a pO2 of 30-50. The two groups were compared using physiologic parameters, fluid and pressor requirements, inflammatory and oxidative markers, and histologic analysis of end-organ injury. All animals developed significant hemodynamic instability immediately upon reperfusion. Average mean arterial pressure at baseline rose significantly after 30 min of cross-clamp (76.8 versus 166.3 mmHg, P < 0.001). Upon reperfusion, all animals required epinephrine and fluids to maintain mean arterial pressure (MAP) greater than 60 mmHg. After stabilization, the two groups were similar in terms of central and pulmonary hemodynamics. The hypoxemic group required more mean total epinephrine (18.35 mg versus 5.28 mg, P < 0.01) with no significant difference in total fluid volume (hypoxemic 9111 ml versus 8420 mL, P = 0.730). The hypoxemic group demonstrated a more severe metabolic acidosis at all time intervals after reperfusion (pH 7.02 versus 7.16 and lactate 17 versus 13, both P < 0.01). There was no difference in malondialdehyde concentration between the two groups, but the hypoxemic group had a higher antioxidant reductive capacity at all intervals after 30 min of reperfusion (0.23 versus 0.27 uM, P = 0.03). While there was significant end-organ damage on pathologic examination of all liver and kidney specimens (mean severity of injury 1.59 and 1.76, respectively, on a scale of 1-3), there was no significant difference between the two groups. A hypoxemic reperfusion strategy in this large animal model failed to demonstrate any significant clinical benefit. Although there was chemical evidence of improved antioxidant capacity with hypoxemia, it was associated with more instability, metabolic and physiologic derangements, and no evidence of end-organ protection.

Is it possible to predict which patients with mild pneumonias will develop hypoxemia?

Usually, mortality due to mild community-acquired pneumonias (CAP) (Pneumonia severity index (PSI) classes I-III) is low (<3%), but the appearance of hypoxemia significantly increases mortality. Our aim was to determine the clinical parameters associated with risk factors of developing hypoxemia in subjects with mild CAP (PSI I-III) and the clinical outcomes of the hypoxemic group. We analyzed clinical characteristics and the outcomes of patients with mild CAP and hypoxemia (PaO2/FiO2<300), in a prospective, multicenter cohort study of 1195 patients. Mild pneumonias (PSI I-III) were found in 645 cases (53.9%), of which 217 (33.6%) presented hypoxemia according to a PaO2/FiO2<300. Patients with PaO2/FiO2<300 required more ICU admissions, mechanical ventilation, and developed septic shock than other PSI I-III patients. The clinical parameters associated with hypoxemia were: COPD, bilateral chest X-ray involvement, and hypoalbuminemia. We conclude that patients with COPD, those with bilateral chest X-ray involvement, or hypoalbuminemia were significantly more likely to have hypoxemia in mild CAP. Hypoxemic patients with low-risk pneumonia have worse clinical outcomes, including more ICU admission, need for mechanical ventilation and presence of septic shock than non-hypoxemic low-risk patients.

Transtracheal jet ventilation in a porcine model

Hypoxemia is a frequent event during difficult airway management. We propose to use transtracheal jet ventilation (TTJV) early during the management of complex difficult airway scenarios. The objective of this porcine study is to highlight the benefit of oxygenation via prophylactic TTJV. Eighteen pigs (Sus scrofa) were divided into two equal groups. In Group A, pigs were anesthetized and no lung ventilation was conducted following administration of succinylcholine and prior to tracheal intubation. Group B, after induction of anesthesia, received transtracheal ventilation using 100% oxygen. In both groups intubation was performed after waiting 90 seconds. All intubations were achieved in less than 30 seconds. Post-intubation arterial blood gases demonstrated significant hypoxemia in Group A (PaO2 22.6 + 5.8 mm Hg), while in Group B oxygenation substantially improved (PaO2 470.3 + 17.0 mm Hg). The arterial CO2 retention was associated with mild respiratory acidosis (pH 7.26 ± 0.05) in Group A only. These findings prove that prophylactic TTJV can improve oxygenation and allow extra time for definitive management of difficult airway.

Changes in Aortic Distension Waveforms in Acute Hypoxemia and Acidosis: Fetal Lamb Study

The objective was to investigate the relationship between fetal aortic distension waveforms and fetal hypoxemia and/or acidosis. Aortic distension waveforms were recorded using an echo-tracking system in nine late-gestation catheterized fetal lambs. Under hypoxic conditions induced by inhalation of gas mixture, fetal blood pressure and aortic distension waveforms were recorded. Four parameters, namely peak systolic and end diastolic diameter, amplitude (ΔD) and ratio of ΔD to end diastolic diameter (%ΔD), were obtained, and correlations between these parameters and partial arterial oxygen tension (PaO 2) and pH of fetal blood gas were analyzed. These four parameters were compared between the control, hypoxemic and asphyxic groups. The ΔD and %ΔD were significantly correlated with PaO 2 and pH using linear regression analysis. Both the ΔD and %ΔD decreased significantly, in a stepwise fashion, in the hypoxemic and asphyxiated groups compared with controls using repeated measured analysis of variance. It was concluded that fetal aortic distension waveforms proved to be a useful tool to detect the deterioration in the fetal circulation secondary to intrauterine hypoxemia/asphyxia. (E-mail: satohs@oitakenbyo.jp)

Influence of Radix Astragali on nitric oxide and endothelin-1 in pulmonary tissue in hypoxemic pulmonary hypertension in rats

To study the influence of Radix Astragali (RA) on pulmonary tissue endothelin-1 (ET-1) and nitric oxide (NO) in hypoxic pulmonary hypertension rats. Twenty one healthy male Wistar rats weighing 210-310 g were divided into three group at random with 7 in each. The rats in control group were raised in ordinary room condition; those in hypoxic group were raised in ordinary pressure hypoxic box [concentration of O(2) was (10.0 +/- 0.5)%] for 8 hours a day, for 30 days; those in RA group were raised in the same condition as hypoxic group and treated with an intraperitoneal injection of RA 8 g/kg per day. The rats in the control group and hypoxic group were given the same volume of intraperitoneal injection of normal saline. Mean pulmonary arterial pressure (mPAP), mean carotid artery pressure (mCAP) were measured via right cardiac catheterization, concentration of NO in pulmonary tissue was measured by radioimmunoassay. (1) The mPAP (mm Hg) (21.9 +/- 1.6) and ET-1 (pg/ml) (309.1 +/- 58.1) in hypoxemic group were significantly higher than those in RA group (16.2 +/- 0.8, 287.7 +/- 57.5) and control group (15.3 +/- 0.8, 241.1 +/- 52.5) (P < 0.01, < 0.05), but the difference between RA group and control group was not significant. (2) NO (micromol/L) in pulmonary tissue in hypoxemic group (6.5 +/- 0.3) was lower than that in RA group and control group (9.2 +/- 0.9), NO in RA group was higher than that in hypoxic group but lower than that in control group (P < 0.05). (3) There was no significant difference in mCAP among the three groups (P > 0.05). (4) Under electron microscope, the endothelial cells of arterioles of the lung tissue of control group were flat and had normal morphology. However, in the lung tissue of hypoxic group, there were proliferation, hypertrophy and swelling of endothelial cells of pulmonary medium and small arteries and plenty of mitochondria and endoplasmic reticula in cytoplasm. Chronic hypoxia can result in reconstruction and endothelial lesion in pulmonary arterioles of rats, elevation of mPAP and ET-1 in pulmonary tissue, and decrease of NO. Injection of Radix Astraglai can reverse the reconstruction of pulmonary vessels partially, regulate the concentration of ET-1 and NO in pulmonary tissue, which may have certain therapeutic effects on pulmonary arteriolar changes induced by hypoxia.

Polymorphisms of interferon-inducible genes OAS-1 and MxA associated with SARS in the Vietnamese population

We hypothesized that host antiviral genes induced by type I interferons might affect the natural course of severe acute respiratory syndrome (SARS). We analyzed single nucleotide polymorphisms (SNPs) of 2′,5′-oligoadenylate synthetase 1 (OAS-1), myxovirus resistance-A (MxA), and double-stranded RNA-dependent protein kinase in 44 Vietnamese SARS patients with 103 controls. The G-allele of non-synonymous A/G SNP in exon 3 of OAS-1 gene showed association with SARS ( p = 0.0090). The G-allele in exon 3 of OAS-1 and the one in exon 6 were in strong linkage disequilibrium and both of them were associated with SARS infection. The GG genotype and G-allele of G/T SNP at position −88 in the MxA gene promoter were found more frequently in hypoxemic group than in non-hypoxemic group of SARS ( p = 0.0195). Our findings suggest that polymorphisms of two IFN-inducible genes OAS-1 and MxA might affect susceptibility to the disease and progression of SARS at each level.

ACE1 polymorphism and progression of SARS

We have hypothesized that genetic predisposition influences the progression of SARS. Angiotensin converting enzyme (ACE1) insertion/deletion (I/D) polymorphism was previously reported to show association with the adult respiratory distress syndrome, which is also thought to play a key role in damaging the lung tissues in SARS cases. This time, the polymorphism was genotyped in 44 Vietnamese SARS cases, with 103 healthy controls who had had a contact with the SARS patients and 50 controls without any contact history. SARS cases were divided into either non-hypoxemic or hypoxemic groups. Despite the small sample size, the frequency of the D allele was significantly higher in the hypoxemic group than in the non-hypoxemic group (p=0.013), whereas there was no significant difference between the SARS cases and controls, irrespective of a contact history. ACE1 might be one of the candidate genes that influence the progression of pneumonia in SARS.

Phospholipid composition of human myocardium in children with normoxemic and hypoxemic congenital heart diseases

Samples of myocardial tissue were obtained during cardiac surgery from children operated for different types of normoxemic and hypoxemic congenital heart diseases. The phospholipid composition was analyzed by thin layer chromatography. The concentration of total phospholipids (PL), phosphatidylcholine and phosphatidylethanolamine (PE) was found lower in atrial tissue of both normoxemic and hypoxemic groups in comparison with the ventricles. When comparing the difference between hypoxemic and normoxemic defects, hypoxemia was found to increase the concentration of total PL, PE and phosphatidylserine in ventricles and total PL and PE in the atria. The increased level of particular phospholipid species may represent adaptive mechanisms to hypoxemia in children with congenital heart diseases.

Cardiovascular response to acute hypoxemia in adult rats hypoxemic neonatally.

To determine the effects of chronic hypoxemia neonatally on the cardiovascular response to acute hypoxemia in adulthood. Experiments were conducted on adult rats (82+/-2 days) which had been made chronically hypoxemic (hypobaric hypoxia equivalent to FiO(2)=0.14) during the first ten days of life but raised in room air (Neonatally Hypoxemia) as well as on adult rats never previously hypoxemic (Control). The animals were instrumented with catheters in the right common carotid artery and superior vena cava for measurements of mean systemic arterial pressure (MAP), central venous pressure, heart rate (HR), arterial blood gases, and arterial as well as mixed venous O(2) saturation. Oxygen consumption (VO(2)) was measured allowing calculation of cardiac index (CI), stroke volume index (SVI) and systemic vascular resistance index (SVRI). The rats were made acutely hypoxemic by exposure to FiO(2)=0.10 for 20 min. HR increased and MAP decreased to similar extents in both groups during acute hypoxemia. However, SVI and CI increased significantly (P<0.05) during acute hypoxemia in the Neonatally Hypoxemic group (24+/-6%, 41+/-8%) but respectively decreased and did not change in the Control animals (-13+/-6%, 2+/-6%). SVRI fell significantly more during hypoxemia in the Neonatally Hypoxemic animals than in the Control group (36+/-4% vs. 14+/-5%). Hypoxemia experienced in early life has long-term effects on the cardiovascular response to acute hypoxemia at maturity. This may have important implications for individuals hypoxemic in early life due to congenital cyanotic heart defects or pulmonary disease secondary to prematurity.

Total body catecholamine kinetics before and after birth in spontaneously hypoxemic fetal lambs.

To study the effect of fetal hypoxemia on perinatal norepinephrine and epinephrine total body kinetics, 13 near-term fetal lambs were instrumented with vascular catheters under general anesthesia. One week later, norepinephrine and epinephrine kinetics were measured in normoxemic (n = 7) or spontaneously hypoxemic fetuses (n = 6) with isotope dilution methodology. Hypoxemic fetuses had lower body (P < 0.02) and placental (P = 0.01) weights and a threefold elevation in plasma norepinephrine (P < 0.005) and epinephrine (P < 0.025) associated with correspondingly higher total body norepinephrine (P < 0.005) and epinephrine (P < 0.05) spillovers. After birth, total body norepinephrine and epinephrine spillover increased 45% and 3.2-fold, respectively, in normoxemic animals (both P < 0.001). However, in the hypoxemic group, norepinephrine total body spillover was unchanged between fetal and 1-h lambs and then fell in 4-h lambs (P < 0.005). In addition, total body epinephrine release rose postnatally (P < 0.05) but less than in the normoxemic group (P < 0.02). No differences in norepinephrine or epinephrine total body clearance occurred between normoxemic and hypoxemic groups in either fetal or newborn lambs. These findings indicate that in hypoxemic and growth-restricted fetuses 1) elevated circulating norepinephrine and epinephrine levels are related to increased sympathoadrenal activity and 2) birth is associated with an initial maintenance and subsequent decline in global sympathetic activity but a blunting of adrenal medullary activation.

Reengineering Respiratory Support Following Extubation: Avoidance of Critical Care Unit Costs

We prospectively investigated alternative clinical practice strategies for critically ill trauma patients following extubation to evaluate the cost-effectiveness of these maneuvers. The primary change was elimination of the routine use of postextubation supplemental oxygen, with concurrent utilization of noninvasive positive pressure ventilatory support (NPPV) to manage occurrences of postextubation hypoxemia. Prospective, consecutive accrual of patients undergoing extubation. Trauma ICU in a university hospital. All patients received mechanical ventilation using pressure support ventilation (PSV) with continuous positive airway pressure (CPAP) as the primary mode. The patients were extubated to room air following a 20-min preextubation trial of 5 cm H(2)O CPAP at FIO(2) of 0.21, and demonstrating a spontaneous respiratory rate </= 38 breaths/min, pH >/= 7.30, PaCO(2) </= 50 mm Hg, and PaO(2) >/= 50 mm Hg. The subgroup of patients who became hypoxemic (pulse oximetric saturation < 88%) within 24 h of extubation were treated with NPPV for up to 48 h duration. Patients who failed NPPV were reintubated. Four hundred fifty-one (84%) patients were successfully extubated to room air. Seventy-two patients (13%) became hypoxemic within 24 h, and NPPV was administered. Fifty-two patients (72% of those who were hypoxemic) responded to NPPV, while 20 patients failed to respond to therapy, were reintubated, and received mechanical ventilation for a mean of 4 days. Thirteen additional patients (2%) were reintubated for reasons other than hypoxemia. The overall reintubation rate for the group (n = 536) was 6.2%; for the postextubation hypoxemic group who failed NPPV, the reintubation rate was 3.7%. The elimination of routine supplemental oxygen via nasal cannula following extubation resulted in a potential direct cost avoidance of $50,006.88 for 451 patient days. Moreover, the 52 patients who were spared reintubation and mechanical ventilation provided an additional potential cost avoidance of $19,740.24 in unused ventilator days per patient. Eliminating the routine use of supplemental oxygen and employing NPPV as a method to prevent reintubation can facilitate a more aggressive, cost-effective strategy for the management of the trauma ICU patient who has been extubated.

Differences in spontaneous breathing pattern and mechanics in patients with severe COPD recovering from acute exacerbation.

The aims of this study were to assess spontaneous breathing patterns in patients with chronic obstructive pulmonary disease (COPD) recovering from acute exacerbation and to assess the relationship between different breathing patterns and clinical and functional parameters of respiratory impairment. Thirty-four COPD patients underwent assessment of lung function tests, arterial blood gases, haemodynamics, breathing pattern (respiratory frequency (fR), tidal volume (VT), inspiratory and expiratory time (tI and tE), duty cycle (tI/ttot), VT/tI) and mechanics (oesophageal pressure (Poes), work of breathing (WOB), pressure-time product and index, and dynamic intrinsic positive end-expiratory pressure (PEEPi,dyn)). According to the presence (group 1) or absence (group 2) of Poes swings during the expiratory phase (premature inspiration), 20 (59%) patients were included in group 1 and 14 (41%) in group 2. Premature inspirations were observed 4.5+/-6.4 times x min(-1) (range 1-31), i.e. 20+/-21% (3.7-100%) of total fR calculated from VT tracings. In group 1 the coefficient of variation in VT, tE, tI/ttot, PEEPi,dyn, Poes and WOB of the eight consecutive breaths immediately preceding the premature inspiration was greater than that of eight consecutive breaths in group 2. There were no significant differences in the assessed parameters between the two groups in the overall population, whereas patients with chronic hypoxaemia in group 1 showed a more severe impairment in clinical conditions, mechanics and lung function than hypoxaemic patients in group 2. In spontaneously breathing patients with chronic obstructive pulmonary disease recovering from an acute exacerbation, detectable activity of inspiratory muscles during expiration was found in more than half of the cases. This phenomenon was not associated with any significant differences in anthropometric, demographic, physiological or clinical characteristics.

Cerebral excitatory amino acids and Na+, K+‐ATPase activity during resuscitation of severely hypoxic newborn piglets

We tested the hypothesis that early brain recovery in hypoxic newborn piglets is improved by resuscitating with an O2 supply close to the minimum level required by the newborn piglet brain. Severely hypoxic 2‐5‐d‐old anaesthetized piglets were randomly divided into three resuscitation groups: hypoxaemic (n= 8), 21% O2 (n= 8), and 100% O2 groups (n= 8). The hypoxaemic group was mechanically ventilated with 12‐18% O2 adjusted to achieve a cerebral venous O2 saturation of 17‐23% (baseline; 45 ± 1%, mean ± SEM). During the 2h resuscitation period, extracellular aspartate and glutamate concentrations in the cerebral striatum were higher during hypoxaemic resuscitation (p= 0:044 and p= 0:055, respectively) than during resuscitation with 21% O2 or 100% O2, suggesting an unfavourable accumulation of potent excitotoxins during hypoxaemic resuscitation. The cell membrane Na+, K+‐ATPase activity of cerebral cortical tissue after 2h resuscitation was similar in the three groups (p= 0:30). In conclusion, hypoxaemic resuscitation did not normalize early cerebral metabolic recovery as efficiently as resuscitation with 21% O2 or 100% O2. Resuscitation with 21% O2 was as efficient as resuscitation with 100% O2 in this newborn piglet hypoxia model.

Early cerebral metabolic and electrophysiological recovery during controlled hypoxemic resuscitation in piglets.

We tested the hypothesis that controlled hypoxemic resuscitation improves early cerebral metabolic and electrophysiological recovery in hypoxic newborn piglets. Severely hypoxic anesthetized piglets were randomly divided into three resuscitation groups: hypoxemic, 21% O2, and 100% O2 groups (8 in each group). The hypoxemic group was mechanically ventilated with 12-18% O2 adjusted to achieve a cerebral venous O2 saturation of 17-23% (baseline; 45 +/- 1%). Base excess (BE) reached -22 +/- 1 mM at the end of hypoxia. During a 2-h resuscitation period, no significant differences in time to recovery of electroencephalography (EEG), quality of EEG at recovery, or extracellular hypoxanthine concentrations in the cerebral cortex and striatum were found among the groups. BE and plasma hypoxanthine, however, normalized significantly more slowly during controlled hypoxemic resuscitation than during resuscitation with 21 or 100% O2. We conclude that early brain recovery during controlled hypoxemic resuscitation was as efficient as, but not superior to, recovery during resuscitation with 21 or 100% O2. The systemic metabolic recovery from hypoxia, however, was delayed during controlled hypoxemic resuscitation.

Cerebral excitatory amino acids and Na+,K+-ATPase activity during resuscitation of severely hypoxic newborn piglets.

We tested the hypothesis that early brain recovery in hypoxic newborn piglets is improved by resuscitating with an O2 supply close to the minimum level required by the newborn piglet brain. Severely hypoxic 2-5-d-old anaesthetized piglets were randomly divided into three resuscitation groups: hypoxaemic (n = 8), 21% O2 (n = 8), and 100% O2 groups (n = 8). The hypoxaemic group was mechanically ventilated with 12-18% O2 adjusted to achieve a cerebral venous O2 saturation of 17-23% (baseline; 45 +/- 1%, mean +/- SEM). During the 2h resuscitation period, extracellular aspartate and glutamate concentrations in the cerebral striatum were higher during hypoxaemic resuscitation (p = 0.044 and p = 0.055, respectively) than during resuscitation with 21% O2 or 100% O2, suggesting an unfavourable accumulation of potent excitotoxins during hypoxaemic resuscitation. The cell membrane Na+,K+-ATPase activity of cerebral cortical tissue after 2 h resuscitation was similar in the three groups (p = 0.30). In conclusion, hypoxaemic resuscitation did not normalize early cerebral metabolic recovery as efficiently as resuscitation with 21% O2 or 100% O2. Resuscitation with 21% O2 was as efficient as resuscitation with 100% O2 in this newborn piglet hypoxia model.

Clinical significance of hypoxemia without congestive heart failure in patients presenting with acute myocardial infarction.

This study investigated the clinical significance of hypoxemia without apparent clinical congestive heart failure in patients with acute myocardial infarction (AMI). Sixty-two patients with AMI of the Killip group I and Forrester subset I state were stratified into a hypoxemia group and a normoxemia group. The increase in the neutrophil count and the severity of the coronary artery disease as graded by Gensini's score were significantly higher in the hypoxemic group. The cardiac index was lower in hypoxemic than normoxemic patients. Myocardial scintigraphy revealed no acute difference in defect scores (DS) or left ventricular ejection fraction (LVEF) between the two groups, but DS was significantly higher (p < 0.01) and LVEF was lower (p < 0.01) in the hypoxemic group 2 years after infarction. Patients with hypoxemia have a more severe angiographic coronary pathology than normoxemic patients, and latent cardiac hypofunction occurs.