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PubMed2004

Baseline hypoxemia as a prognostic marker for pulmonary complications and outcome in patients with acute pancreatitis.

The purpose of the present study was to investigate the prognostic role of severe hypoxemia on admission as an independent risk factor of pulmonary complications and mortality in patients with acute pancreatitis. Pulmonary complications were studied in 166 previously healthy patients with acute pancreatitis. Forty-eight patients (28.9%) developed one or more pulmonary complications, including pleural effusion, atelectasis, pulmonary consolidations, and acute respiratory distress syndrome (ARDS). Pulmonary consolidations (odds ratio = 7.25) and, especially, ARDS (odds ratio = 22.9) were significantly associated with severe baseline hypoxemia (PaO2, <60 mm Hg). Mortality was mainly related to severity of disease (odds ratio = 46.45), while hypoxemia was also found to be an independent risk factor of poor outcome (odds ratio = 9.56). It seems that, in patients with acute pancreatitis, severe hypoxemia on admission may be an early predictive marker of pulmonary complications, especially ARDS, and, independently of severity score, it may also be a marker of poor outcome.

Acute Disease↗

PubMed1994

The effect of hypercapnia and hypoxemia on the cardiovascular responses to isoproterenol.

BACKGROUND: The reason for the increased risk of death with fenoterol and isoproterenol in asthma is unknown but may relate to their cardiovascular effects. Deaths from asthma usually occur outside hospital where hypoxemia, with or without hypercapnia, may exist. Both of these states can influence the cardiovascular system. We investigated whether different gas mixtures modified the cardiovascular effects of isoproterenol. METHOD: Nine healthy men were randomly assigned to receive each of three gas mixtures to achieve (1) normoxia-normocapnia, (2) hypercapnia (end-tidal PaCO2, 50 mm Hg), (3) hypoxemia-hypercapnia (arterial oxygen saturation, 90%; PaCO2, 50 mm Hg). Isoproterenol was administered with each of the gas mixtures. Cardiovascular measurements of heart rate, blood pressure, cardiac index, ejection fraction, fractional shortening, electromechanical systole, and the QTc interval were made before administration of the gases, as well as before and 5 minutes after isoproterenol administration. RESULTS: The changes after hypercapnia were not significantly different from those after normoxia-normocapnia. Hypoxemia-hypercapnia increased heart rate, systolic and diastolic blood pressure, QTc interval, cardiac index, ejection fraction, and fractional shortening. Isoproterenol increased heart rate, systolic blood pressure, QTc interval, cardiac index, ejection fraction, and fractional shortening while the subjects breathed the normoxia-normocapnia gas mixture. It caused similar changes with the other gas mixtures. The changes were additive. CONCLUSION: Isoproterenol and hypoxemia-hypercapnia will increase myocardial oxygen demand and could prove to be detrimental in severe asthma.

Adult↗

PubMed1992

Protection from hypoxemia-induced renal dysfunction by the thiophosphate WR-2721.

The acute renal effects of hypoxemia-reoxygenation and the putative protective action of WR-2721 [S-, 2-(3-aminopropyl-amino)-, etylphosphosphorothioic acid], a drug with specific properties such as PTH-secretion inhibiting, calcium lowering and free radical scavenging activities, were investigated in anesthetized-ventilated rabbits. Glomerular filtration rate (GFR) and renal blood flow (RBF) were assessed by the clearance of inulin and para-aminohippuric acid, respectively. Each animal acted as its own control. Normoxemic control rabbits showed no changes in renal hemodynamics and function during 150 minutes. The administration of WR-2721 (75 mg/kg body wt i.v.) to normoxemic animals induced a significant decrease in MBP, RBF and diuresis, without affecting GFR. It significantly reduced plasma levels of PTH, decreased calcemia and increased urinary calcium excretion. In untreated hypoxemic-reoxygenated rabbits, 45 minutes of severe hypoxemia (PO2 around 35 mm Hg) induced a significant fall in MBP, GFR, RBF and diuresis, which persisted during the 60-minute reoxygenation period. The administration of WR-2721 before hypoxemia or reoxygenation prevented the hypoxemia-induced decrease in GFR and diuresis. Filtration fraction increased significantly. The renal functional improvement observed in hypoxemic rabbits administered WR-2721 could be mediated by its effect on calcium metabolism and/or its oxygen free radical scavenging properties.

Amifostine↗

PubMed2002

Evolution of hypoxemia in patients with severe cirrhosis.

BACKGROUND AND AIM: Hypoxemia is common in patients with cirrhosis but the natural history of this syndrome is unknown. The aim of this study was to follow a series of patients with cirrhosis and to compare patients with and without hypoxemia to determine their risk of complications and survival rate. METHODS: Fifty-eight consecutive Child-Pugh C patients with cirrhosis were included and followed up for 1-18 months. Blood gas measurements and plasma endothelin levels were measured in all patients. Blood gas measurements were repeated in 34 patients. RESULTS: Hypoxemia was present in 35 patients (60%) (alveolar-arterial oxygen (AaO2) gradient > 20 mmHg) but none had pulmonary symptoms. There was no significant difference in liver tests and plasma endothelin levels between hypoxemic and non-hypoxemic patients. The occurrence of variceal bleeding and survival rate was not significantly different between the two groups. The AaO2 gradient worsened in nine patients and normalized in six of the hypoxemic patients. The AaO2 gradient increased to more than 20 mmHg in seven non-hypoxemic patients. There was no relationship between AaO2 gradient changes and Child-Pugh score grade changes. CONCLUSION: Asymptomatic hypoxemia is common in patients with severe cirrhosis but it is not a predictive factor of short-term complications or mortality. These results should be considered when deciding on liver transplantation.

Blood Gas Analysis↗

PubMed2001

Sudden infant death syndrome Part 2: the response of the reticuloendothelial system to hypoxemia and infection.

The incidence of ascites in chicks raised in a high-altitude chamber doubled from 6500 feet to 8000 feet. A similar condition developed in calves transported to pasture at high altitude. Chicks raised in a high-altitude chamber (compared to controls) produced more plasma cells in the germinal centres of the spleen about four days after an antigen challenge. Children usually suffering from a mild respiratory infection at sea level often developed pulmonary edema (HAPE) on transfer to high altitude. Sudden infant death syndrome (SIDS) victims produced more plasma cells in the germinal centers of the spleen. In one survey of SIDS, about half of the infants suffered an upper respiratory tract infection in the two weeks prior to death and the lungs were filled with fluid at autopsy. Elevated levels of hypoxanthine indicated hypoxemia before death, and a presumed response to hypoxemia in SIDS was the presence of extramedullary hematopoiesis in the liver. The effect of prolonged hypoxemia and infection are additive in increasing vascular permeability and the accumulation of edema fluid. The preferential uptake of zinc by edema fluid proteins at the expense of inflammatory cells increases the motility and metabolism of zinc-deprived activated macrophages. Activated macrophages release cytokines which in turn stimulate the release of pro-inflammatory peptides which increase vascular permeability and mortality. These inflammatory peptides are under proteolytic control. The neutral endopeptidase (NEP) is a cell-surface zinc metalloproteinase which modulates toxic shock.Zinc also modulates the inflammatory response of the activated macrophage. Interleukin-12 (IL-12), predominantly a product of macrophages, is involved in regulating both hematopoiesis and the adaptive immune response. IL-12 promotes interferon gamma (IFNgamma) production by T cells. IFNgamma acts on macrophages to release large amounts of nitric oxide (NO). An elevated immune response leads to NO overload, dilation of the cardiovascular system and toxic shock. A mechanism resulting in cardiovascular failure and a shock-like sequence is described in some cases of SIDS.Bradycardia, recorded on cardiorespiratory monitors in six SIDS infants, was considered a late event. Cytokines regulate all aspects of the immune response. Extramedullary hematopoiesis in the liver was one anatomical marker of hypoxemia in SIDS. This survey traces the function of the activated macrophage with the cytokines regulating extramedullary hematopoiesis and the precocious immune response in SIDS.

Altitude↗

PubMed2003

A new rat model of diffuse brain injury associated with acute subdural hematoma: assessment of varying hematoma volume, insult severity, and the presence of hypoxemia.

The aim of this study was to develop a new rat model of diffuse brain injury (DBI) associated with acute subdural hemorrhage (SDH). In order to make this model more clinically relevant, we determined whether the varying hematoma volume, severity of DBI, or the presence of hypoxemia could influence the physiological consequence. SDH was made by an autologous blood injection, while DBI was induced using the impact acceleration model (mild, 450 g/1 m, severe, 450 g/2 m). Physiological parameters measured included intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral blood flow (CBF), and brain tissue water content. In the first series, 23 rats were randomized into the five following groups: Group 1, sham; Group 2, 400 (microL SDH; Group 3, SDH400 + mild DBI; Group 4, SDH400 + severe DBI; and Group 5, SDH300 + severe DBI. Results suggested that SDH300 + severe DBI (Group 5) may be the most suitable model, in which the MABP and CBF temporarily decreased during the SDH induction, but thereafter recovered to the baseline. Conversely, ICP was persistently elevated throughout the experiment. The water content was also significantly higher in both hemispheres compared to that of sham. In the second series, the animal was exposed to a hypoxemic insult (10 or 30 min) in addition to SDH300 + severe DBI (Group 6). The prolonged hypoxemia caused both a severe CBF reduction without recovery and a bilateral brain swelling, whereas the brief hypoxemia showed a gradual CBF recovery from the transient reduction and an increased water content only in the SDH side. These results suggest that these models may be potentially useful to study the combination of DBI and SDH with or without hypoxemia.

Animals↗

PubMed2004

Acute subdural hematoma associated with diffuse brain injury and hypoxemia in the rat: effect of surgical evacuation of the hematoma.

The aim of this study was to assess the effect of rapid or delayed surgical evacuation on the physiological consequence and brain edema formation in a rat model of acute subdural hematoma (SDH) coupled with either diffuse brain injury (DBI) or hypoxemia. The SDH was made by an autologous blood injection, while DBI was induced using the impact acceleration model (mild, 450 g/1 m; severe, 450 g/2 m). Physiological parameters measured included intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral blood flow (CBF), and brain tissue water content. At 1 h (rapid evacuation) or 4 h (delayed evacuation) after the SDH induction, surgical evacuation following a craniotomy was performed using saline irrigation and forceps. The study consisted of three different series, including 400 microL of SDH alone (Series 1), SDH400 + mild DBI (Series 2), and SDH300 + severe DBI + 20 min hypoxemia (Series 3). The hypoxemia was added in Group 3 to produce a steadily increasing ICP. In Series 1 and 2, all rats were randomized into the three following groups: non-, rapid, and delayed evacuation; Series 3 had two groups: non- and rapid evacuation. In Series 1, the surgical evacuation showed no beneficial effects on the brain edema formation assessed at 5 h post-injury. In Series 2, the rapid, but not delayed, evacuation significantly reduced both the increased ICP level and brain water content. The additional insult of hypoxemia (Series 3) resulted in a progressive ICP elevation, persistently depressed CBF, and severe brain swelling. Under this situation, the rapid evacuation exacerbated brain edema. These results have clinical implications for the management of severe traumatic SDH, especially its operative indication and timing.

Animals↗

PubMed2001

Low-dose inhaled carbon monoxide reduces pulmonary vascular resistance during acute hypoxemia in adult sheep.

Carbon monoxide (CO) is produced by the action of the heme oxygenase (HO) complex through the oxidation of heme. CO, like nitric oxide (NO), is a molecular gas that among other actions stimulates guanylyl cyclase and increases cGMP levels in smooth muscle cells, regulating the vascular tone. Acute hypoxia generates pulmonary hypertension and increases the expression of inducible HO isoform (HO-1) in the vascular endothelium. Inhaled NO causes a potent pulmonary vasodilation. We hypothesized that inhaled CO might produce similar actions as NO on pulmonary vascular resistance (PVR). To test our contention, we studied the effects of inhaled CO (40 ppm) in the augmented PVR observed during hypoxemia. Five chronically instrumented German Merino sheep were submitted to a protocol consisting of 20 min of normoxemia (N), 20 min of isocapnic hypoxemia (H20), 20 min of isocapnic hypoxemia plus CO 40 ppm (H40), and 20 min of recovery (R). In the control protocol, we did not administer inhaled CO. Arterial gases and pH, percentage of carboxyhemoglobin (COHb), systemic and pulmonary arterial pressure, systemic and pulmonary vascular resistance, and cardiac output were measured during each period. During H20 period, there was a significant increase in cardiac output and PVR in sheep submitted to both protocols. The sheep treated with inhaled CO (H40 + CO) showed a modest but significant decrease (16%) in the elevated PVR. Our data indicate that inhaled CO decreases pulmonary vascular resistance associated with acute hypoxemia in adult sheep.

Administration, Inhalation↗

PubMed1986

Indomethacin and ketanserin block ethchlorvynol-induced hypoxemia in dogs.

Intravenous injection of ethchlorvynol (ECV) leads to hypoxemia and a permeability pulmonary edema. Whether the hypoxemia is directly attributable to the pulmonary edema or caused by release of mediators has not been explored. Three groups of dogs were studied: (1) ECV, (2) indomethacin--ECV, and (3) ketanserin--ECV. In group 1, 25 to 30 mg/kg of ECV caused a significant fall in PaO2 at 4 min (92 +/- 12.6 to 77 +/- 21 mm Hg, p less than 0.05), which persisted throughout the experiment. The P(A-a)O2 gradient widened significantly at 3 min (22 +/- 11 to 31 +/- 16.8 mm Hg, p less than 0.05) and remained abnormal for the remainder of the experiment. There was no significant fall in PaO2 in groups 2 and 3. Lung tissue water to dry weight ratio increased significantly in all groups at 60 min. Lung tissue water to dry weight ratios were normal at 10 min after ECV injection in additional groups. It was concluded that ECV causes hypoxemia, which is mediated by cyclooxygenase products and 5 hydroxytryptamine. This hypoxemia can be prevented by the administration of drugs that block these products.

Animals↗

PubMed1981

Hypoxemia following pulmonary embolism: a dog model of altering regional perfusion.

We studied the role played by a shift in perfusion to hypoxic lung areas after pulmonary embolism in pst embolic hypoxemia. A tracheal divider was used to separate hypoxic (N2 ventilated) from oxygenated (100 per cent O2 ventilated) lung in anaesthetized dogs. Relative perfusion was assessed from total 133Xenon (133Xe) exhaled from each lung area after intravenous infusions. When one lung area was ventilated with N2 and the other with O2 at a normal PaCO2 to allow hypoxic pulmonary vasoconstriction (HPV), there was a significant (P less than 0.001) shift away from the hypoxic side. Starch or blood clots were then infused to produce pulmonary emboli. Starch emboli were distributed predominantly to the oxygenated lung. After blood clot embolization in normocapnic dogs, pulmonary artery pressure increased 15 torr, perfusion to the hypoxic lung increased from 14 +/- 2 to 23 +/- 1 per cent, and PaCO2 fell from 278 to 186 torr. When the degree of HPV was reduced in another group of dogs by hypocapnea, a similar increase in pulmonary artery pressure (14 torr) created by blood clot embolism did not shift perfusion or create hypoxemia. In all dogs the perfusion shift to hypoxic lung was sufficient to account for all the post embolic hypoxemia. In this dog model, post embolic hypoxemia is explained by preferential distribution of emboli to oxygenated lung followed by perfusion shift to hypoxic lung as the effect of HPV is overcome by pulmonary hypertension.

Animals↗

PubMed1990

Frequent hypoxemia and apnea after sedation with midazolam and fentanyl.

More than 80 deaths have occurred after the use of midazolam (Versed), often in combination with opioids, to sedate patients undergoing various medical and surgical procedures. We investigated the respiratory effects of midazolam (0.05 mg.kg-1) and fentanyl (2.0 micrograms.kg-1) in volunteers. The incidence of hypoxemia (oxyhemoglobin saturation less than 90%) and apnea (no spontaneous respiratory effort for 15 s) and the ventilatory response to carbon dioxide were evaluated. Midazolam alone produced no significant respiratory effects. Fentanyl alone produced hypoxemia in half of the subjects and significant depression of the ventilatory response to CO2, but did not produce apnea. Midazolam and fentanyl in combination significantly increased the incidence of hypoxemia (11 of 12 subjects) and apnea (6 of 12 subjects), but did not depress the ventilatory response to CO2 more than did fentanyl alone. Adverse reactions linked to midazolam and reported to the Department of Health and Human Services highlight apnea- and hypoxia-related problems as among the most frequent adverse reactions. Seventy-eight per cent of the deaths associated with midazolam were respiratory in nature, and in 57% an opioid had also been administered. All but three of the deaths associated with the use of midazolam occurred in patients unattended by anesthesia personnel. We conclude that combining midazolam with fentanyl or other opioids produces a potent drug interaction that places patients at a high risk for hypoxemia and apnea. Adequate precautions, including monitoring of patient oxygenation with pulse oximetry, the administration of supplemental oxygen, and the availability of persons skilled in airway management are recommended when benzodiazepines are administered in combination with opioids.

Adolescent↗

PubMed1984

Mechanisms producing hypoxemia during hemodialysis.

Arterial hypoxemia occurs frequently during hemodialysis. Proposed mechanisms for this phenomenon have included hypoventilation and embolism of granulocyte aggregates. We studied 18 patients with endstage renal failure who required chronic hemodialysis, and measured arterial blood gases, pulmonary gas exchange, and dialyzer gas exchange. During use of acetate as a dialysate buffer, PaO2 decreased to 80 +/- 6.8 torr, whereas during use of the bicarbonate buffer oxygen tension remained at 92 +/- 4.9 torr or greater. Hypoventilation and microembolism were not sufficient to explain the degree of hypoxemia during acetate dialysis. Hypoxemia occurred only after the 1st exposure to acetate; neither an instantaneous change to bicarbonate nor stopping dialysis restored oxygen tension to normal. We conclude that a pharmacologic action of acetate adversely affects lung function, aggravating the decreased alveolar oxygen tension (PAO2) due to hypoventilation. Hypoxemia was not present when bicarbonate was used. Acetate buffer should not be used for dialysis in patients with unstable cardiovascular or respiratory systems.

Acetates↗

PubMed2001

Right ventricular response to high-dose almitrine infusion in patients with severe hypoxemia related to acute respiratory distress syndrome.

OBJECTIVE: To evaluate the effects of high-dose almitrine infusion on gas exchange and right ventricular function in patients with severe hypoxemia related to acute respiratory distress syndrome (ARDS). DESIGN: Prospective study. SETTING: Medicosurgical intensive care department (ten beds). PATIENTS: Nine patients with ARDS and severe hypoxemia (PaO2/FIO2 ratio, <150 torr [20 kPa]). INTERVENTION: High-dose almitrine infusion (16 microg/kg/min for 30 mins). MEASUREMENTS AND MAIN RESULTS: Gas exchange and hemodynamic parameters were recorded before and after almitrine infusion. Right ventricular function was evaluated by using a fast response thermistor pulmonary artery catheter that allowed measurement of right ventricular ejection fraction and calculation of right ventricular end-diastolic and end-systolic volumes. Almitrine did not significantly alter arterial oxygenation and intrapulmonary shunt. Almitrine increased mean pulmonary arterial pressure (MPAP) from 31 +/- 4 to 33 +/- 4 mm Hg (p < .05), pulmonary vascular resistance index from 353 +/- 63 to 397 +/- 100 dyne x sec/ cm5 x m2 (p < .05), and right ventricular end-systolic volume index from 71 +/- 22 to 77 +/- 21 mL/m2 (p < .05); almitrine decreased right ventricular ejection fraction from 36% +/- 7% to 34% +/- 8% (p < .05). Stroke volume index and cardiac index did not change. The almitrine-induced changes in right ventricular ejection fraction were closely correlated with the baseline MPAP (r2 = .71, p < .01). CONCLUSION: In patients with severe hypoxemia related to ARDS, high-dose almitrine infusion did not improve arterial oxygenation and impaired the loading conditions of the right ventricle. The decrease in right ventricular ejection fraction induced by almitrine was correlated with the baseline MPAP. Thus, high-dose almitrine infusion may be harmful in ARDS patients with severe hypoxemia and pulmonary hypertension.

Adult↗

PubMed1997

Cerebral blood flow during hypoxemia and hemodilution in rabbits: different roles for nitric oxide?

Hypoxemia and anemia are associated with increased CBF, but the mechanisms that link the changes in PaO2 or arterial O2 content (CaO2) with CBF are unclear. These experiments were intended to examine the contribution of nitric oxide. CaO2 in pentobarbital-anesthetized rabbits was reduced to approximately 6.5 mL O2/dL by hypoxemia (PaO2 approximately 24 to 26 mm Hg) or hemodilution with hetastarch (hematocrit approximately 14% to 15%). Animals with normal CaO2 (approximately 17.5 to 18 mL O2/dL) served as controls. In part I, each animal was given 3, 10, and 30 mg/kg N omega-nitro-L-arginine methyl ester (L-NAME) intravenously (total 43 mg/kg) to inhibit production of nitric oxide. Forebrain CBF was measured with radioactive microspheres approximately 15 to 20 minutes after each dose. Baseline CBF was greater in hypoxemic rabbits (111 +/- 31 mL x 100 g-1 x min-1, mean +/- SD) than in hemodiluted (70 +/- 22 mL x 100 g-1 min-1) or control animals (39 +/- 12 mL x 100 g-1 min-1). L-NAME (which reduced brain tissue nitric oxide synthase activity by approximately 65%) reduced CBF in hypoxemic animals to 80 +/- 23 mL x 100 g-1 x min-1 (P < 0.0001), but had no significant effect on CBF in either anemic or control animals. In four additional rabbits, further hemodilution to a CaO2 of approximately 3.5 mL O2/dL increased baseline CBF to 126 +/- 21 mL x 100 g-1 min-1, but again there was no effect of L-NAME. In part II, animals were anesthetized as above, and a close cranial window was prepared. The cyclic GMP (cGMP) content of the artificial CSF superfusate was measured under baseline conditions, and then after the reduction of CaO2 to approximately 6.5 mL O2/dL by either hypoxemia or hemodilution. Concentrations of cGMP did not change during either control conditions or after hemodilution. However, cGMP increased significantly with the induction of hypoxemia. The cGMP increase in hypoxemic animals could be blocked with L-NAME. These results suggest that nitric oxide plays some role in hypoxemic vasodilation, but not during hemodilution.

Animals↗

PubMed1998

Reversal of hypoxemia by inhaled nitric oxide in children with severe hepatopulmonary syndrome, type 1, during and after liver transplantation.

BACKGROUND: The hepatopulmonary syndrome with profound hypoxemia is a rare but severe complication for children with liver cirrhosis. It can be reversed by liver transplantation (LT), which is now regarded as a good indication. However, previous reports have described cases of transient or fatal deteriorations of intrapulmonary shunting after pediatric liver transplantation with dramatically worsening hypoxemia. METHODS AND RESULTS: A similar case during and after LT in a 4-year-old girl with severe hepatopulmonary syndrome is described with prompt reversal of hypoxemia by inhaled nitric oxide, which was discontinued definitely until day 14 after LT. CONCLUSIONS: During or after LT, worsening hypoxemia may be improved by using inhaled nitric oxide in pediatric patients undergoing liver transplantation for liver cirrhosis and hepatopulmonary syndrome. The mechanisms are unclear, but may involve mismatching lung ventilation-perfusion. However, additional clinical reports are necessary before accepting these results.

Administration, Inhalation↗

PubMed2002

Acute hypoxemia in humans enhances the neutrophil inflammatory response.

The neutrophil (PMN) is regarded as a key component in the hyperinflammatory response known as the systemic inflammatory response syndrome. Acute respiratory distress syndrome (ARDS) and subsequent multiple organ failure (MOF) are related to the severity of this hyperinflammation. ICU patients who are at highest risk of developing MOF may have acute hypoxic events that complicate their hospital course. This study was undertaken to evaluate the effects of acute hypoxia and subsequent hypoxemia on circulating PMNs in human volunteers. Healthy subjects were exposed to a changing O2/N2 mixture until their O2 saturation (SaO2) reached a level of 68% saturation. These subjects were then exposed to room air and then returned to their baseline SaO2. PMNs were isolated from pre- and post-hypoxemic arterial blood samples and were then either stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or PMA alone, or they were primed with L-alpha-phosphatidylcholine, beta-acetyl-gamma-O-alkyl (PAF) followed by fMLP activation. Reactive oxygen species generation as measured by superoxide anion production was enhanced in primed PMNs after hypoxemia. Protease degranulation as measured by elastase release was enhanced in both quiescent PMNs and primed PMNs after fMLP activation following the hypoxemic event. Adhesion molecule upregulation as measured by CD11b/CD18, however, was not significantly changed after hypoxemia. Apoptosis of quiescent PMNs was delayed after the hypoxemic event. TNFalpha, IL-1, IL-6, and IL-8 cytokine levels were unchanged following hypoxemia. These results indicate that relevant acute hypoxemic events observed in the clinical setting enhance several PMN cytotoxic functions and suggest that a transient hypoxemic insult may promote hyperinflammation.

Acute Disease↗

PubMed2001

Cerebral hypoxemia-ischemia and reoxygenation with 21% or 100% oxygen in newborn piglets: effects on extracellular levels of excitatory amino acids and microcirculation.

OBJECTIVE: To determine whether reoxygenation with 21% oxygen is preferable to 100% oxygen in normalizing extracellular levels of excitatory amino acids in the brains of hypoxic-ischemic newborn piglets and to compare this model of combined hypoxemia-ischemia to a previously used model of global hypoxemia. DESIGN: Prospective, randomized animal study. SETTING: Surgical research laboratory. SUBJECTS: Twenty-four anesthetized piglets, 1-3 days old. INTERVENTIONS: Hypoxemia-ischemia was achieved by normoventilation with 8% oxygen and temporary occlusion of the common carotid arteries. After 20 mins, reoxygenation-reperfusion was started with 21% oxygen (HI 21% group, n = 12) or 100% oxygen (HI 100% group, n = 12) for 30 mins followed by 21% oxygen. All piglets were observed for 2 hrs. MEASUREMENTS AND MAIN RESULTS: We measured extracellular concentrations of amino acids in striatum and hypoxanthine in cerebral cortex (microdialysis), microcirculation in cerebral cortex (laser Doppler), plasma hypoxanthine, and mean arterial pressure. During the 2-hr reoxygenation-reperfusion period, levels of amino acids were significantly higher in the HI 21% group compared with the HI 100% group (glutamate, p = 0.02; aspartate, p = 0.03). Mean arterial pressure was significantly lower in the HI 21% group (p = 0.04). Microcirculation decreased to <10% of baseline during hypoxemia-ischemia and normalized during reoxygenation-reperfusion in the HI 100% group, but it remained at a significantly lower level in the HI 21% group (p = 0.03). CONCLUSIONS: Significantly higher levels of excitatory amino acids in striatum, significantly lower mean arterial pressure, and a significantly greater degree of hypoperfusion in cerebral cortex were found after reoxygenation with 21% oxygen compared with 100% oxygen in normocapnic, hypoxemic-ischemic newborn piglets. This suggests a less favorable outcome in the group receiving room air.

Journal Article↗

PubMed2006

Refractory hypoxemia in right ventricular infarction: a case report.

Right ventricular infarction has many clinical features. Although hypoxemia is a common presenting symptom with multiple causes in the setting of myocardial infarction, the authors present a case resulting from an acute right-to-left shunt secondary to a previously dormant patent foramen ovale. A 74-year-old male presented to the hospital after feeling unwell for the previous 2 days. Initial evaluation revealed marked hypoxemia without respiratory distress. Electrocardiographic findings and cardiac seromarkers revealed a completed inferior myocardial infarction. The patient's hypoxemia was refractory to 100% oxygen, indicating a right-to-left shunt. A transesophageal echocardiogram confirmed clinical suspicions for a right-to-left shunt through a patent foramen ovale. Despite sporadic reports in the literature, this still is a poorly recognized clinical condition. The authors review a case report that will enable the general intemist to consider a right-to-left shunt in the setting of hypoxemia in myocardial infarction.

Aged↗