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Hypoxaemia

Distribution by Scientific Domains

Medical Sciences	76%
Life Sciences	23%

Distribution within Medical Sciences

Anesthesia & Pain Management	39%
Pediatrics	25%
9 Other Subdomains	36%

Kinds of Hypoxaemia

arterial hypoxaemia

Selected Abstracts

Attenuated endothelin-1 mRNA expression with endothelin-1 receptor blockade during hypoxaemia and reoxygenation in newborn piglets

ACTA PAEDIATRICA, Issue 6 2000
S Medbø
We investigated the cause of decreased plasma endothelin-1 (ET-1) during hypoxaemia and reoxygenation in newborn piglets subjected to simultaneous blocking of the ET-1 receptors. Changes in plasma ET-1 and prepro-ET-1 mRNA expression in the main pulmonary artery and the left lower lobe in the lung were studied in 1-2-d-old piglets. Ten minutes prior to hypoxaemia, the hypoxaemia group (n = 10) was given saline, two groups (both n = 9) were given 1 and 5 mg/kg i.v. SB 217242 (an ET-1 receptor antagonist). Two groups served as normoxic controls, with and without SB 217242 5 mg/kg i.v. Hypoxaemia was induced by ventilating with 8% O2 until base excess was 20mmol/l or mean arterial blood pressure was < 20mmHg. Reoxygenation was performed for 2h with room air. During hypoxaemia, plasma ET-1 decreased in the hypoxaemia group, remained unchanged in the 1-mg group and increased in the 5-mg group. At the end of reoxygenation, plasma ET-1 was above baseline in the 1-mg and 5-mg groups. In the pulmonary artery, the hypoxaemia group showed 2- to 5-fold higher prepro-ET-1 mRNA expression compared to all the other groups (p < 0.05). There were trends for higher prepro-ET-1 mRNA expression in pulmonary tissue in the hypoxaemia group compared to the two receptor-blocking groups (p < 0.07). Conclusions: We conclude that hypoxaemia and reoxygenation increase prepro-ET-1 mRNA expression in the pulmonary artery in newborn piglets. These observations suggest that the half-life of ET-1 is decreased during hypoxaemia and reoxygenation in newborn piglets. [source]

Acute Hypervolaemia Improves Arterial Oxygen Pressure in Athletes with Exercise-Induced Hypoxaemia

EXPERIMENTAL PHYSIOLOGY, Issue 4 2003
Gerald S. Zavorsky
The aim of this study was to determine the effect of acute plasma volume expansion on arterial blood-gas status during 6.5 min strenuous cycling exercise comparing six athletes with and six athletes without exercise-induced arterial hypoxaemia (EIAH). We hypothesized that plasma volume expansion could improve arterial oxygen pressure in a homogeneous sample of athletes - those with EIAH. In this paper we have extended the analysis and results of our recently published surprising findings that lengthening cardiopulmonary transit time did not improve arterial blood-gas status in a heterogeneous sample of endurance cyclists. One 500 ml bag of 10% Pentastarch (infusion condition) or 60 ml 0.9% saline (placebo) was infused prior to exercise in a randomized, double-blind fashion on two different days. Power output, cardiac output, oxygen consumption and arterial blood gases were measured during strenuous exercise. Cardiac output and oxygen consumption were not affected by acute hypervolaemia. There were group × condition interaction effects for arterial oxygen pressure and alveolar-arterial oxygen pressure difference, suggesting that those with hypoxaemia experienced improved arterial oxygen pressure (+4 mmHg) and lower alveolar-arterial oxygen pressure difference (-2 mmHg) with infusion. In conclusion, acute hypervolaemia improves blood-gas status in athletes with EIAH. The impairment of gas exchange occurs within the first minute of exercise, and is not impaired further throughout the remaining duration of exercise. This suggests that arterial oxygen pressure is only minimally mediated by cardiac output. [source]

Body Position and Cardiac Dynamic and Chronotropic Responses to Steady-State Isocapnic Hypoxaemia in Humans

EXPERIMENTAL PHYSIOLOGY, Issue 2 2000
S. Deborah Lucy
Neural mediation of the human cardiac response to isocapnic (IC) steady-state hypoxaemia was investigated using coarse-graining spectral analysis of heart rate variability (HRV). Six young adults were exposed in random order to a hypoxia or control protocol, in supine and sitting postures, while end-tidal PCO2 (PET,CO2) was clamped at resting eucapnic levels. An initial 11 min period of euoxia (PET,O2 100 mmHg; 13.3 kPa) was followed by a 22 min exposure to hypoxia (PET,O2 55 mmHg; 7.3 kPa), or continued euoxia (control). Harmonic and fractal powers of HRV were determined for the terminal 400 heart beats in each time period. Ventilation was stimulated (P < 0.05) and cardiac dynamics altered only by exposure to hypoxia. The cardiac interpulse interval was shortened (P < 0.001) similarly during hypoxia in both body positions. Vagally mediated high-frequency harmonic power (Ph) of HRV was decreased by hypoxia only in the supine position, while the fractal dimension, also linked to cardiac vagal control, was decreased in the sitting position (P < 0.05). However, low-frequency harmonic power (Pl) and the HRV indicator of sympathetic activity (Pl/Ph) were not altered by hypoxia in either position. These results suggest that, in humans, tachycardia induced by moderate IC hypoxaemia (arterial O2 saturation Sa,O2, 85%) was mediated by vagal withdrawal, irrespective of body position and resting autonomic balance, while associated changes in HRV were positionally dependent. [source]

Effect of Maternal Nutrient Restriction in Early Gestation on Responses of the Hypothalamic-Pituitary-Adrenal Axis to Acute Isocapnic Hypoxaemia in Late Gestation Fetal Sheep

EXPERIMENTAL PHYSIOLOGY, Issue 1 2000
Paul Hawkins
Epidemiological and experimental evidence suggests that maternal undernutrition during pregnancy may alter development of fetal organ systems. We have demonstrated previously that fetal hypothalamic-pituitary-adrenal (HPA) axis responses to exogenous corticotropin-releasing hormone (CRH) + arginine vasopressin (AVP), or adrenocorticotrophin hormone (ACTH), are reduced in fetuses of mildly undernourished ewes. To examine these effects further we tested HPA axis responses to acute isocapnic hypoxaemia in fetal sheep at 114-129 days gestation (dGA), following 15% reduction in maternal nutritional intake between 0 and 70 dGA. Fetuses from control (C) and nutrient-restricted (R) ewes were chronically catheterised and plasma ACTH and cortisol responses were determined at 114-115, 120-123 and 126-129 dGA during hypoxaemia (1 h) induced by lowering the maternal inspired O2 fraction (FI,O2). Basal plasma cortisol concentrations and HPA axis responses at 114-115 and 120-123 dGA did not differ between C and R fetuses. At 126-129 dGA, both plasma ACTH (P < 0.01) and cortisol (P < 0.05) responses were smaller in R fetuses compared to C fetuses. Fetal blood gas status, fetal body weight, body proportions and organ weights did not differ between the groups. We conclude that mild maternal undernutrition alters development of the fetal HPA axis producing a reduction in pituitary and adrenal responsiveness to endogenous stimuli. [source]

A controlled rapid-sequence induction technique for infants may reduce unsafe actions and stress

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2009
C. EICH
Background: Classic rapid-sequence induction of anaesthesia (RSI-classic) in infants and small children presents a time-critical procedure, regularly associated with hypoxia. This results in high stress levels for the provider and may trigger unsafe actions. Hence, a controlled induction technique (RSI-controlled) that involves gentle mask ventilation until full non-depolarizing muscular blockade has become increasingly popular. Clinical observation suggests that RSI-controlled may reduce the adverse effects noted above. We aimed to evaluate both techniques with respect to unsafe actions and stress. Methods: In this controlled, randomized simulator-based study, 30 male trainees and specialists in anaesthesiology performed a simulated anaesthesia induction in a 4-week-old infant with pyloric stenosis. Two different RSI techniques, classic and controlled, were applied to 15 candidates each. We recorded the incidence of hypoxaemia, forced mask ventilation, and intubation difficulties. In addition, we measured individual stress levels by ergospirometry, salivary cortisol, and ,-amylase, as well as a post-trial questionnaire. Results: Hypoxaemia always occurred in RSI-classic but not in RSI-controlled, repeatedly resulting in unsafe actions. Subjective stress perception and some objective stress levels were lower in the volunteers performing RSI-controlled. Conclusions: Our data suggest that RSI-controlled, as compared with RSI-classic, leads to fewer unsafe actions and may reduce individual stress levels. [source]

Chronic lung disease: oxygen dogma revisited

ACTA PAEDIATRICA, Issue 2 2001
O D Saugstad
Since the discovery of retrolental fibroplasia, and the role of oxygen in its development, oxygen has been considered a double-edged sword in neonatal medicine, the utmost care being exercised in order not to give too much oxygen (1). However, the important observation that hypoxaemia might induce pulmonary vasoconstriction (2) and airway constriction (3) in infants at risk for bronchopulmonary dysplasia has resulted in only a minor upward adjustment of oxygen supplementation in many neonatal units. Since oxygen toxicity has long been linked not only to retinopathy of prematurity but also to bronchopulmonary dysplasia (4), it is relevant to ask whether an increased FiO2 might have any detrimental effects on babies. [source]

Attenuated endothelin-1 mRNA expression with endothelin-1 receptor blockade during hypoxaemia and reoxygenation in newborn piglets

Circulatory effects of apnoea in elite breath-hold divers

ACTA PHYSIOLOGICA, Issue 1 2009
F. Joulia
Abstract Aim:, Voluntary apnoea induces several physiological adaptations, including bradycardia, arterial hypertension and redistribution of regional blood flows. Elite breath-hold divers (BHDs) are able to maintain very long apnoea, inducing severe hypoxaemia without brain injury or black-out. It has thus been hypothesized that they develop protection mechanisms against hypoxia, as well as a decrease in overall oxygen uptake. Methods:, To test this hypothesis, the apnoea response was studied in BHDs and non-divers (NDs) during static and dynamic apnoeas (SA, DA). Heart rate, arterial oxygen saturation (SaO2), and popliteal artery blood flow were recorded to investigate the oxygen-conserving effect of apnoea response, and the internal carotid artery blood flow was used to examine the mechanisms of cerebral protection. Results:, The bradycardia and peripheral vasoconstriction were accentuated in BHDs compared with NDs (P < 0.01), in association with a smaller SaO2 decrease (,2.7% vs. ,4.9% during SA, P < 0.01 and ,6% vs. ,11.3% during DA, P < 0.01). Greater increase in carotid artery blood flow was also measured during apnoea in BHDs than in controls. Conclusion:, These results confirm that elite divers present a potentiation of the well-known apnoea response in both SA and DA conditions. This response is associated with higher brain perfusion which may partly explain the high levels of world apnoea records. [source]

Abnormalities in cardiac and respiratory function observed during seizures in childhood

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 1 2005
Mary E O'Regan MRCP MRCPCH
The aim of this study was to observe any changes in cardiac and respiratory function that occur during seizures. Thirty-seven children (20 males, 17 females; median age 7y 6mo, range 1y 6mo to 15y 6mo) were studied. We recorded electroencephalograms, respiratory rate, heart rate, electrocardiograms, blood pressure, oxygen saturation, heart rate variability (time domain analysis), and cardiac vagal tone. A respiratory pause was defined as an interruption in respiration lasting more than 3s but less than 15s. Apnoea was defined as absence of respiration for more than 15s. Tachypnoea was defined as a 10% increase in respiratory rate from the pre-ictal baseline. Bradypnoea was defined as a 10% decrease in respiratory rate from the pre-ictal baseline. Significant hypoxia was defined as a saturation of less than 85%. A significant change in heart rate was taken as a 10% increase or decrease below the baseline rate. Data were obtained from 101 seizures: 40 focal seizures, 21 generalized seizures, and 40 absences. Focal seizures were frequently associated with significant respiratory abnormalities, tachypnoea in 56%, apnoea in 30%, frequent respiratory pauses in 70%, and significant hypoxaemia in 40%. The changes seen in respiratory rate were statistically significant. Changes in cardiac parameters, an increase or decrease in heart rate, were observed in only 26% of focal seizures and 48% of generalized seizures. We conclude that seizure activity can disrupt normal physiological regulation and control of respiratory and cardiac activity. [source]

Nitric oxide synthase inhibition in Thoroughbred horses augments O2 extraction at rest and submaximal exercise, but not during short-term maximal exercise

EQUINE VETERINARY JOURNAL, Issue S36 2006
M. MANOHAR
Summary Reason for performing study: Work is required to establish the role of endogenous nitric oxide (NO) in metabolism of resting and exercising horses. Objectives: To examine the effects of NO synthase inhibition on O2 extraction and anaerobic metabolism at rest, and during submaximal and maximal exertion. Methods: Placebo and NO synthase inhibition (with N,-nitro-L-arginine methyl ester [l -NAME] administered at 20 mg/kg bwt i.v.) studies were performed in random order, 7 days apart on 7 healthy, exercise-trained Thoroughbred horses at rest and during incremental exercise leading to 120 sec of maximal exertion at 14 m/sec on a 3.5% uphill grade. Results: At rest, NO synthase inhibition significantly augmented the arterial to mixed-venous blood O2 content gradient and O2 extraction as mixed-venous blood O2 tension and saturation decreased significantly. While NO synthase inhibition did not affect arterial blood-gas tensions in exercising horses, the exercise-induced increment in haemoglobin concentration and arterial O2 content was attenuated. In the l -NAME study, during submaximal exercise, mixed-venous blood O2 tension and haemoglobin-O2 saturation decreased to a greater extent causing O2 extraction to increase significantly. During maximal exertion, arterial hypoxaemia, desaturation of haemoglobin and hypercapnia of a similar magnitude developed in both treatments. Also, the changes in mixed-venous blood O2 tension and haemoglobin-O2 saturation, arterial to mixed-venous blood O2 content gradient, O2 extraction and markers of anaerobic metabolism (lactate and ammonia production, and metabolic acidosis) were not different from those in the placebo study. Conclusion: Endogenous NO production augments O2 extraction at rest and during submaximal exertion, but not the during short-term maximal exercise. Also, NO synthase inhibition does not affect anaerobic metabolism at rest or during exertion. Potential relevance: It is unlikely that endogenous NO release modifies aerobic or anaerobic metabolism in horses performing short-term maximal exertion. [source]

Increased myocardial matrix metalloproteinases in hypoxic newborn pigs during resuscitation: effects of oxygen and carbon dioxide

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2004
W. B. Borke
Abstract Background, Perinatal asphyxia is associated with cardiac dysfunction, and it is important to prevent further tissue injury during resuscitation. There is increasing evidence that myocardial matrix metalloproteinases (MMPs) are involved in myocardial hypoxaemia,reoxygenation injury. Objective, To assess MMPs and antioxidant capacity in newborn pigs after global ischaemia and subsequent resuscitation with ambient air or 100% O2 at different PaCO2 -levels. Methods, Newborn pigs (12,36 h of age) were resuscitated for 30 min by ventilation with 21% or 100% O2 at different PaCO2 levels after a hypoxic insult, and thereafter observed for 150 min. In myocardial tissue extracts, MMPs were analyzed by gelatin zymography and broad matrix-degrading capacity (total MMP). Total endogenous antioxidant capacity in myocardial tissue extracts was measured by the oxygen radical absorbance capacity (ORAC) assay. Results, Matrix metalloproteinase-2 more than doubled from baseline values (P < 0·001), and was higher in piglets resuscitated with 100% O2 than with ambient air (P = 0·012). The ORAC value was considerably decreased (P < 0·001). In piglets with elevated PaCO2, total MMP-activity in the right ventricle was more increased than in the left ventricle (P = 0·008). In the left ventricle, total MMPactivity was higher in the piglets with low PaCO2 than in the piglets with elevated PaCO2 (P = 0·013). Conclusion, In hypoxaemia-reoxygenation injury the MMP-2 level was highly increased and was most elevated in the piglets resuscitated with 100% O2. Antioxidant capacity was considerably decreased. Assessed by total MMP-activity, elevated PaCO2 during resuscitation might protect the left ventricle, and probably increase right ventricle injury of the myocardium. [source]

Acute Hypervolaemia Improves Arterial Oxygen Pressure in Athletes with Exercise-Induced Hypoxaemia

Body Position and Cardiac Dynamic and Chronotropic Responses to Steady-State Isocapnic Hypoxaemia in Humans

Effect of Maternal Nutrient Restriction in Early Gestation on Responses of the Hypothalamic-Pituitary-Adrenal Axis to Acute Isocapnic Hypoxaemia in Late Gestation Fetal Sheep

The role of nurses in preventing adverse events related to respiratory dysfunction: literature review

JOURNAL OF ADVANCED NURSING, Issue 6 2005
Julie Considine BN MN RN RM FRCNA
Aims., This paper reports a literature review examining the relationship between specific clinical indicators of respiratory dysfunction and adverse events, and exploring the role of nurses in preventing adverse events related to respiratory dysfunction. Background., Adverse events in hospital are associated with poor patient outcomes such as increased mortality and permanent disability. Many of these adverse events are preventable and are preceded by a period during which the patient exhibits clearly abnormal physiological signs. The role of nurses in preserving physiological safety by early recognition and correction of physiological abnormality is a key factor in preventing adverse events. Methods., A search of the Medline and CINAHL databases was conducted using the following terms: predictors of poor outcome, adverse events, mortality, cardiac arrest, emergency, oxygen, supplemental oxygen, oxygen therapy, oxygen saturation, oxygen delivery, assessment, patient assessment, physical assessment, dyspnoea, hypoxia, hypoxaemia, respiratory assessment, respiratory dysfunction, shortness of breath and pulse oximetry. The papers reviewed were research papers that demonstrated a relationship between adverse events and various clinical indicators of respiratory dysfunction. Results., Respiratory dysfunction is a known clinical antecedent of adverse events such as cardiac arrest, need for medical emergency team activation and unplanned intensive care unit admission. The presence of respiratory dysfunction prior to an adverse event is associated with increased mortality. The specific clinical indicators involved are alterations in respiratory rate, and the presence of dyspnoea, hypoxaemia and acidosis. Conclusions., The way in which nurses assess, document and use clinical indicators of respiratory dysfunction is influential in identifying patients at risk of an adverse event and preventing adverse events related to respiratory dysfunction. If such adverse events are to be prevented, nurses must not only be able to recognise and interpret signs of respiratory dysfunction, but must also take responsibility for initiating and evaluating interventions aimed at correcting respiratory dysfunction. [source]

Life-threatening systemic toxicity and airway compromise from a common European adder bite to the tongue

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2009
L. C. G. HOEGBERG
A 24-year-old man was bit on the tongue by a European common adder. Within 15 min following envenomation, he experienced tongue swelling, hypotension and impaired consciousness. Antihistamine, corticosteroid and crystalloids were administered. Within 105 min of envenomation, increasing oral, pharyngeal and facial oedema compromised the airway, leading to respiratory failure, concomitant with circulatory failure related to hypoxaemia and systemic toxic effects. Acute tracheotomy secured the airway, and two doses of antivenom successfully treated the systemic, toxic effects. The reaction was severe due to rapid and suspected high-dose uptake of venom, underlining the need for early advanced symptomatic treatment with airway control and early and eventually repeated dosing of antivenom. [source]

A controlled rapid-sequence induction technique for infants may reduce unsafe actions and stress

Differential Effects of Placental Restriction on IGF-II, ACTH Receptor and Steroidogenic Enzyme mRNA Levels in the Foetal Sheep Adrenal

JOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2000
Ross
We have investigated the effects of restriction of placental growth on foetal adrenal growth and adrenal expression of mRNAs for Insulin-like Growth Factor II (IGF-II), the IGF binding protein IGFBP-2, Steroidogenic Factor 1 (SF-1) and adrenocorticotrophic hormone (ACTH) receptor (ACTH-R) and the steroidogenic cytochrome P-450 enzymes: cholesterol side chain cleavage (CYP11A1), 17, -hydroxylase (CYP17) and 21-hydroxylase (CYP21A1); and 3, -hydroxysteroid dehydrogenase/,5,4 isomerase (3,HSD). Endometrial caruncles were removed from non-pregnant ewes before mating (placental restriction group; PR). The total adrenal: foetal weight ratio was higher in PR (n=6 foetuses) than in control foetuses (n=6 foetuses). There was no difference in plasma ACTH concentrations between the PR and control foetuses between 130 and 140 days gestation. Adrenal IGF-II mRNA levels were lower (P<0.05) in the PR group, however, adrenal IGFBP-2 mRNA levels were not different between the PR and control groups. Adrenal ACTH-R mRNA levels were also lower whilst CYP11A1 mRNA levels were increased (P<0.005) in the PR group. We conclude that foetal adrenal growth and steroidogenesis are stimulated as a consequence of foetal growth restriction and that factors other than ACTH are important in foetal adrenal activation during chronic, sustained hypoxaemia. [source]

Outcome of intensive care of homozygous alpha-thalassaemia without prior intra-uterine therapy

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 7-8 2007
Shing YR Lee
Aim: To review the outcome of homozygous alpha-thalassaemia without prior intra-uterine therapy treated in neonatal intensive care unit and identify the factors associated with survival. Methods: The hospital records of all patients with homozygous alpha-thalassaemia treated in our neonatal intensive care unit in the last 15 years were reviewed. A literature search beginning in the year 1980 was done to identify homozygous alpha-thalassaemia actively treated in neonatal intensive care units. Those receiving prior intra-uterine therapy were excluded. The following information was collected: the severity of hydrops, sizes of liver and spleen, haemoglobin level, Apgar score at 5 min, ventilator settings, timing and forms of red blood cell transfusion and presence of persistent hypoxaemia. The survivors and the non-survivors were compared. Results: In our centre, in the last 15 years there were six infants born with homozygous alpha-thalassaemia who did not receive intra-uterine therapy; one survived and five succumbed despite aggressive respiratory therapy. In our literature search there were more reports of survivors (10) than non-survivors (six) for these infants, suggesting a reporting bias towards selection of rare cases of survival. Apgar score of four or above occurred in seven of the eight survivors with data available in the reports, whereas this occurred in four of the 11 non-survivors (P = 0.035, Fisher Exact test). Five of the 11 survivors had abnormal neurological outcome including developmental delay and spastic quadriplegia. Conclusion: Without prior intra-uterine therapy, homozygous alpha-thalassaemia has grave outlook in terms of mortality and morbidity despite aggressive respiratory therapy. [source]

Involvement of thromboxane A2 (TXA2) in the early stages of oleic acid-induced lung injury and the preventive effect of ozagrel, a TXA2 synthase inhibitor, in guinea-pigs

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2004
Yoichi Ishitsuka
ABSTRACT An intravenous injection of oleic acid into animals can produce a lung injury with hypoxaemia and pulmonary vascular hyper-permeability. Although oleic acid lung injury is used as a model of acute respiratory distress syndrome (ARDS), the precise mechanisms of the lung injury are still unclear. We have investigated whether thromboxane A2 (TXA2) participated in the lung injury and have evaluated the efficacy of ozagrel, a TXA2 synthase inhibitor, on the lung injury in guinea-pigs. Oleic acid injection increased the plasma level of TXB2, a stable metabolite of TXA2, and the time-course of plasma TXB2 was similar to that of the decreased partial oxygen pressure of arterial blood (Pao2) induced with oleic acid. Ozagrel administered intravenously 30 min before oleic acid injection prevented the decrease in Pao2 and pulmonary vascular hyper-permeability. It also prevented increases in lactate dehydrogenase activity, a measure of lung cell injury, TXB2 and its weight ratio to 6-keto prostaglandin F1 , in bronchoalveolar lavage fluid. Although ozagrel administered simultaneously with oleic acid ameliorated the decrease in Pao2, post treatment showed little effect. We suggest that TXA2 participated in the oleic acid lung injury, as an "early phase" mediator, and rapidly-acting TXA2 synthase inhibitors were effective in the prevention of acute lung injury. [source]

Grave acidosis after severe anaphylactic bronchospasm: friend or foe?

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2007
M. Pytte
In a 20-year-old woman with known asthma, anaphylactic bronchospasm induced a grave combined respiratory and metabolic acidosis (pHa 6.66) with marked hypoxaemia (SaO2 45%). The beneficial effects of the rightward shift of the oxyhaemoglobin dissociation curve on tissue O2 unloading at such pH was more than offset by the negative effect on SaO2 at the reduced PaO2 (7.0 kPa) found in this patient. This case illustrates the detrimental effect of grave acidosis on arterial blood oxygen content at subnormal PaO2 values, the beneficial effect of a supranormal PaO2 on the SaO2 in such patients, and the rapid remission rate of life-threatening acidosis and blood lactate after adequate ventilation and tissue oxygenation were secured. The initial treatment of the patient and clinically relevant considerations are discussed. [source]

Pulmonary gas exchange abnormalities in liver transplant candidates

LIVER TRANSPLANTATION, Issue 9 2002
Rosmawati Mohamed
Abnormal diffusing capacity is the commonest pulmonary dysfunction in liver transplant candidates, but severe hypoxemia secondary to hepatopulmonary syndrome and significant pulmonary hypertension are pulmonary vascular manifestations of cirrhosis that may affect the perioperative course. We prospectively assessed the extent of pulmonary dysfunction in patients referred for liver transplantation. A total of 57 consecutive patients with chronic liver disease were evaluated. All patients had a chest radiograph, standing arterial blood gas on room air, pulmonary function testing, and Doppler echocardiogram. Those patients with arterial hypoxaemia (PaO2 < 10 kPa) also underwent 99mTc-macroaggregated albumin lung scan, and nine patients had agitated normal saline injection during echocardiography to define further the existence of pulmonary vascular dilatation. Reduced diffusing capacity for carbon monoxide less than 75% of the predicted value was found in 29 of 57 (51%) patients. Although elevated alveolar-arterial oxygen tension difference was detected in 35% (20/57) of the patients, only four (7%) patients had hypoxemia. We were unable to find evidence of intrapulmonary vascular dilatation either on the lung scan or saline-enhanced echocardiography in any of these patients. Reduction in diffusing capacity for carbon monoxide was noted in 75% (18/24) of patients who were transplanted for primary biliary cirrhosis and was accompanied by widened alveolar-arterial oxygen tension in 10 out of 18 (56%) of patients. This study shows that in liver transplant candidates, diffusion impairment and widened alveolar-arterial oxygen tension difference were frequently detected, especially in patients with primary biliary cirrhosis. [source]

Splanchnic vasoconstriction by angiotensin II is arterial pressure dependent

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2002
M. Broomé
Background: Our hypothesis was that splanchnic vasoconstriction by exogenous angiotensin II (Ang II) is significantly potentiated by local mechanisms increasing vasomotor tone and that splanchnic tissue oxygenation during administration of Ang II is perfusion pressure dependent. The aim was to study local splanchnic circulatory effects and tissue oxygenation during intravenous infusion of Ang II at different levels of regional arterial driving pressure in a whole-body large animal model. Methods: Ang II was infused in incremental doses (0,200 ,g,·,h,1) in anaesthetised instrumented pigs (n=8). Mean superior mesenteric arterial pressure (PSMA) was adjusted by a local variable perivascular occluder. Perivascular ultrasound and laser-Doppler flowmetry were used for measurements of mesenteric venous blood flow and superficial intestinal blood flow, respectively. Intestinal oxygenation was evaluated by oxygen tissue tension (PtiO2) and lactate fluxes. Results: Ang II produced prominent and dose-dependent increases in mesenteric vascular resistance (RSMA) when the intestine was exposed to systemic arterial pressure, but Ang II increased RSMA only minimally when PSMA was artificially kept constant at a lower level (50 mmHg) by the occluder. Although Ang II decreased PtiO2 at a PSMA of 50 mmHg, splanchnic lactate production was not observed. Conclusion: We demonstrate that splanchnic vasoconstriction by exogenous Ang II is dependent on arterial driving pressure, suggesting significant potentiation through autoregulatory increases in vasomotor tone. Intestinal hypoxaemia does not seem to occur during short-term infusion of Ang II in doses that significantly increases systemic arterial pressure. [source]

A pediatric patient with a mediastinal mass and pulmonary embolus

PEDIATRIC ANESTHESIA, Issue 4 2006
LAURA L. BURGOYNE BM BS
Summary When anesthetizing a patient with an anterior mediastinal mass, sudden hypoxaemia and cardiovascular collapse may result from compression of a large airway or vascular structure in the mediastinum. We report the case of a pediatric cancer patient with an anterior mediastinal mass, who developed sudden and fatal hypoxaemia and cardiovascular collapse in the hours following sedation. A massive pulmonary thromboembolism was diagnosed at autopsy. We suggest that pulmonary embolism should be considered in the differential diagnosis when a patient with a mediastinal mass develops perioperative hypoxaemia, cardiovascular collapse, or both. [source]

Pentobarbital vs chloral hydrate for sedation of children undergoing MRI: efficacy and recovery characteristics

PEDIATRIC ANESTHESIA, Issue 7 2004
Shobha Malviya MD
Summary Background :,Chloral hydrate (CH) sedation for magnetic resonance imaging (MRI) is associated with significant failure rates, adverse events and delayed recovery. Pentobarbital (PB), reportedly produces successful sedation in 98% of children undergoing diagnostic imaging. This study compared the efficacy, adverse events and recovery characteristics of CH vs PB in children undergoing MRI. Methods :,With Institutional Review Board approval and written consent, children were randomly assigned to receive intravenous (i.v.) PB (maximum 5 mg·kg,1 in incremental doses) or oral CH (75 mg·kg,1) prior to MRI. Sedation was augmented with 0.05 mg·kg,1 doses of i.v. midazolam (maximum 0.1 mg·kg,1) as necessary. Adverse effects, including hypoxaemia, failed sedation, paradoxical reactions and behavioural changes, the return of baseline activity, and parental satisfaction were documented. The quality of MRI scans was evaluated by a radiologist blinded to the sedation technique. Results :,PB facilitated an earlier onset of sedation (P = 0.001), higher sedation scores (P = 0.01), and less need for supplemental midazolam compared with CH. Severe hypoxaemia occurred in two children (6%) in the PB group. Fourteen per cent of the PB group experienced a paradoxical reaction, 9% sedation failure and 11% major motion artefact, compared with 0% (P = 0.05), 3 and 2% (P = NS), respectively, in the CH group. CH and PB were both associated with a high incidence of motor imbalance, and agitation. However, children who received PB had a slower return to baseline activity (P = 0.04). Conclusions :,Although PB facilitated a quicker sedation onset and reduced the requirement for supplemental sedation, it produced a higher incidence of paradoxical reaction and prolonged recovery with a similar failure rate compared with CH. [source]

Directly measured cabin pressure conditions during Boeing 747,400 commercial aircraft flights

RESPIROLOGY, Issue 4 2007
Paul T. KELLY
Background and objectives: In the low pressure environment of commercial aircraft, hypoxaemia may be common and accentuated in patients with lung or heart disease. Regulations specify a cabin pressure not lower than 750 hPa but it is not known whether this standard is met. This knowledge is important in determining the hazards of commercial flight for patients and the validity of current flight simulation tests. Methods: Using a wrist-watch recording altimeter, cabin pressure was recorded at 60 s intervals on 45 flights in Boeing 747,400 aircraft with three airlines. A log was kept of aircraft altitude using the in-flight display. Change in cabin pressure during flight, relationship between aircraft altitude and cabin pressure and proportion of flight time with cabin pressure approaching the minimum specified by regulation were determined. Results: Flight duration averaged 10 h. Average cabin pressure during flight was 846 hPa. There was a linear fall in cabin pressure as the aircraft cruising altitude increased. At 10 300 m (34 000 ft) cabin pressure was 843 hPa and changed 8 hPa for every 300 m (1000 ft) change in aircraft altitude (r2 = 0.993; P < 0.001). Lowest cabin pressure was 792 hPa at 12 200 m (40 000 ft) but during only 2% of flight time was cabin pressure less than 800 hPa. Conclusions Cabin pressure is determined only by the engineering of the aircraft and its altitude and in the present study was always higher than required by regulation. Current fitness-to-fly evaluations simulate cabin conditions that passengers will not experience on these aircraft. There may be increased risks to patients should new or older aircraft operate nearer to the present minimum standard. [source]

Role of arterial blood gas abnormalities in oedema formation in COPD

RESPIROLOGY, Issue 4 2004
Fisun KARADAG
Objective: Renal and hormonal abnormalities, manifesting as oedema or hyponatraemia, are often seen in patients with COPD. The aim of this study was to investigate the effect of airflow obstruction and arterial blood gas abnormalities on oedema formation in COPD patients. Methodology: A total of 58 COPD patients hospitalized for treatment of COPD exacerbation were admitted to the study. Of these, 38 patients had peripheral oedema (group 1) and 20 patients had no oedema (group 2). Results: The mean age was 68 ± 9 years in group 1 and 68 ± 8 years in group 2. On the first day of admission, serum urea was 29.18 ± 12.25 mg/dL and creatinine was 1.62 ± 0.46 mg/dL in group 1, while urea was 15.50 ± 4.59 mg/dL and creatinine was 1.07 ± 0.10 mg/dL in group 2. Hyponatraemia occurred in five patients (13%) in group 1 and one patient (5%) in group 2. There was no difference in severity of airflow obstruction in the two groups; FEV1 was 44 ± 15% of predicted and FEV1/FVC was 53 ± 14 in group 1, while FEV1 was 45 ± 16% of predicted and FEV1/FVC was 54 ± 20 in group 2. There were statistically significant differences in pH (7.32 vs. 7.39; P= 0.013) and in PaCO2 (62 ± 10 mmHg vs. 42 ± 6; P= 0.048) for group 1 compared with group 2. PaO2 (62 ± 17 mmHg vs. 82 ± 27) and Sao2 (87 ± 9%vs. 90 ± 13) were found to be lower in group 1 compared with group 2 but the difference did not reach statistical significance. Conclusion: Alterations in pH and PaCO2 (respiratory acidosis and hypercapnia) appear to have more prominent roles than hypoxaemia in oedema formation in COPD patients. [source]

Hepatopulmonary syndrome associated with autoimmune liver cirrhosis

RESPIROLOGY, Issue 2 2001
Nobukazu Takada
A 46-year-old woman presented for evaluation of liver dysfunction and dyspnoea. Laboratory examination showed high levels of ,-globulin, immunoglobulin (Ig)G, and antinuclear antibodies. Laparoscopy demonstrated hepatic cirrhosis. Despite normal spirometry, hypoxaemia (which was worse in standing position) and a low diffusing capacity were present. The shunt ratio calculated using arterial blood gas was 6.4%, but was 40% when measured using 99mTc-macroaggregated albumin scanning. The discrepancy between the ratios indicated that hypoxaemia was caused by intrapulmonary vascular dilatation. The patient was diagnosed with hepatopulmonary syndrome associated with autoimmune liver cirrhosis. [source]

Cardiovascular and cerebrovascular responses to acute hypoxia following exposure to intermittent hypoxia in healthy humans

THE JOURNAL OF PHYSIOLOGY, Issue 13 2009
Glen E. Foster
Intermittent hypoxia (IH) is thought to be responsible for many of the long-term cardiovascular consequences associated with obstructive sleep apnoea (OSA). Experimental human models of IH can aid in investigating the pathophysiology of these cardiovascular complications. The purpose of this study was to determine the effects of IH on the cardiovascular and cerebrovascular response to acute hypoxia and hypercapnia in an experimental human model that simulates the hypoxaemia experienced by OSA patients. We exposed 10 healthy, male subjects to IH for 4 consecutive days. The IH profile involved 2 min of hypoxia (nadir = 45.0 mmHg) alternating with 2 min of normoxia (peak = 88.0 mmHg) for 6 h. The cerebral blood flow response and the pressor responses to hypoxia and hypercapnia were assessed after 2 days of sham exposure, after each day of IH, and 4 days following the discontinuation of IH. Nitric oxide derivatives were measured at baseline and following the last exposure to IH. After 4 days of IH, mean arterial pressure increased by 4 mmHg (P < 0.01), nitric oxide derivatives were reduced by 55% (P < 0.05), the pressor response to acute hypoxia increased (P < 0.01), and the cerebral vascular resistance response to hypoxia increased (P < 0.01). IH alters blood pressure and cerebrovascular regulation, which is likely to contribute to the pathogenesis of cardiovascular and cerebrovascular disease in patients with OSA. [source]

Effects of hypoxia on diaphragmatic fatigue in highly trained athletes

THE JOURNAL OF PHYSIOLOGY, Issue 1 2007
Ioannis Vogiatzis
Previous work suggests that exercise-induced arterial hypoxaemia (EIAH), causing only moderate arterial oxygen desaturation (: 92 ± 1%), does not exaggerate diaphragmatic fatigue exhibited by highly trained endurance athletes. Since changes in arterial O2 tension have a significant effect on the rate of development of locomotor muscle fatigue during strenuous exercise, the present study investigated whether hypoxia superimposed on EIAH exacerbates the exercise-induced diaphragmatic fatigue in these athletes. Eight trained cyclists (: 67.0 ± 2.6 ml kg,1 min,1; mean ±s.e.m.) completed in balanced order four 5 min exercise tests leading to different levels of end-exercise (64 ± 2, 83 ± 1, 91 ± 1 and 96 ± 1%) via variations in inspired O2 fraction (: 0.13, 0.17, 0.21 and 0.26, respectively). Measurements were made at corresponding intensities (65 ± 3, 80 ± 3, 85 ± 3 and 90 ± 3% of normoxic maximal work rate, respectively) in order to produce the same tidal volume, breathing frequency and respiratory muscle load at each . The mean pressure time product of the diaphragm did not differ across the four exercise tests and ranged between 312 ± 28 and 382 ± 22 cmH2O s min,1. Ten minutes into recovery, twitch transdiaphragmatic pressure (Pdi,tw) determined by bilateral phrenic nerve stimulation, was significantly (P= 0.0001) reduced after all tests. After both hypoxic tests (: 0.13, 0.17) the degree of fall in Pdi,tw (by 26.9 ± 2.7 and 27.4 ± 2.6%, respectively) was significantly greater (P < 0.05) than after the normoxic test (by 20.1 ± 3.4%). The greater amount of diaphragmatic fatigue in hypoxia at lower leg work rates (presumably requiring smaller leg blood flow compared with normoxia at higher leg work rates), suggests that when ventilatory muscle load is similar between normoxia and hypoxia, hypoxia exaggerates diaphragmatic fatigue in spite of potentially greater respiratory muscle blood flow availability. [source]