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Arterial Blood Gas (arterial + blood_gas)

Distribution by Scientific Domains
Medical Sciences85%

Terms modified by Arterial Blood Gas

  • arterial blood gas analysis
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    Selected Abstracts

    Topiramate-induced metabolic acidosis: report of two cases

    DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 10 2001
    Chun-hung Ko MRCP FHKAM Medical Officer
    Two children who presented with symptomatic metabolic acidosis after being put on topiramate (TPM) are reported. The first patient was an 11-year-old male with refractory complex partial epilepsy who was put on TPM for 13 months. He developed hyperventilation 1 week after increasing the dose to 300mg/day. Arterial blood gas revealed hyperchloraemic metabolic acidosis with partial respiratory compensation: pH 7.36, PCO2 27.2 mmHg, bicarbonate 14.9 mEq/L, base excess -8.9 mmol/L. Hyperventilation and acidosis resolved after administration of sodium bicarbonate and reduction of the dose of TPM. The second patient was a female who developed increasing irritability at age 16 months and 21 months, each time associated with introduction of TPM and resolved promptly upon withdrawal of the drug. Venous blood gas taken during the second episode revealed pH 7.34, PCO2 37.4 mmHg, bicarbonate 20.4 mEq/L, base excess -4.2 mmol/L. The predominant mechanism of TPM-induced hyperventilation involves inhibition of carbonic anhydrase at the proximal renal tubule, resulting in impaired proximal bicarbonate reabsorption. The occurrence of hyperpnoea or mental status change in any patient who is on TPM should prompt an urgent blood gas sampling, with correction of the acid-base disturbances accordingly. [source]

    In vivo electroporation and ubiquitin promoter , a protocol for sustained gene expression in the lung

    THE JOURNAL OF GENE MEDICINE, Issue 7 2006
    Amiq Gazdhar
    Abstract Background Gene therapy applications require safe and efficient methods for gene transfer. Present methods are restricted by low efficiency and short duration of transgene expression. In vivo electroporation, a physical method of gene transfer, has evolved as an efficient method in recent years. We present a protocol involving electroporation combined with a long-acting promoter system for gene transfer to the lung. Methods The study was designed to evaluate electroporation-mediated gene transfer to the lung and to analyze a promoter system that allows prolonged transgene expression. A volume of 250 µl of purified plasmid DNA suspended in water was instilled into the left lung of anesthetized rats, followed by left thoracotomy and electroporation of the exposed left lung. Plasmids pCiKlux and pUblux expressing luciferase under the control of the cytomegalovirus immediate-early promoter/enhancer (CMV-IEPE) or human polyubiquitin c (Ubc) promoter were used. Electroporation conditions were optimized with four pulses (200 V/cm, 20 ms at 1 Hz) using flat plate electrodes. The animals were sacrificed at different time points up to day 40, after gene transfer. Gene expression was detected and quantified by bioluminescent reporter imaging (BLI) and relative light units per milligram of protein (RLU/mg) was measured by luminometer for p.Pyralis luciferase and immunohistochemistry, using an anti-luciferase antibody. Results Gene expression with the CMV-IEPE promoter was highest 24 h after gene transfer (2932 ± 249.4 relative light units (RLU)/mg of total lung protein) and returned to baseline by day 3 (382 ± 318 RLU/mg of total lung protein); at day 5 no expression was detected, whereas gene expression under the Ubc promoter was detected up to day 40 (1989 ± 710 RLU/mg of total lung protein) with a peak at day 20 (2821 ± 2092 RLU/mg of total lung protein). Arterial blood gas (PaO2), histological assessment and cytokine measurements showed no significant toxicity neither at day 1 nor at day 40. Conclusions These results provide evidence that in vivo electroporation is a safe and effective tool for non-viral gene delivery to the lungs. If this method is used in combination with a long-acting promoter system, sustained transgene expression can be achieved. Copyright © 2006 John Wiley & Sons, Ltd. [source]

    The case for venous rather than arterial blood gases in diabetic ketoacidosis

    EMERGENCY MEDICINE AUSTRALASIA, Issue 1 2006
    Anne-Maree Kelly
    Abstract Objectives:, For patients with diabetic ketoacidosis (DKA), arterial blood gas (BG) sampling for measurement of pH and bicarbonate has been considered an essential part of initial evaluation and monitoring of progress. There is growing evidence that venous values can be clinically acceptable alternatives to arterial measurements. This article summarizes the recent evidence regarding the validity of venous BG sampling in DKA. Methods:, Medline search for the years 1995 to present, hand search of reference lists, search of on-line evidence-based medicine sites. Results:, In patients with DKA the weighted average difference between arterial and venous pH was 0.02 pH units (95% limits of agreement ,0.009 to +0.021 pH units) and between arterial and venous bicarbonate was ,1.88 mEq/L. Conclusions:, There is reasonable evidence that venous and arterial pH have sufficient agreement as to be clinically interchangeable in patients with DKA who are haemodynamically stable and without respiratory failure. There is some evidence that venous and arterial bicarbonate also agree closely in DKA but this requires confirmation. [source]

    Clinical, urodynamic and endoscopic characteristics of the Stanford pouch ileal neobladder constructed with absorbable staples

    INTERNATIONAL JOURNAL OF UROLOGY, Issue 12 2000
    M Cemil Uygur
    Abstract Purpose The clinical, urodynamic and endoscopic aspects of the Stanford pouch ileal neobladder formed with absorbable staples were investigated. Methods A Stanford pouch ileal neobladder was formed using absorbable staples after radical cystoprostatectomy in 30 male patients with the diagnosis of muscle invasive carcinoma of the bladder between 1995 and 1998. The mean age of the patients was 62 (range 41,70) years. Patients were followed with arterial blood gas, serum biochemistry, pouch cystography, urodynamic tests and endoscopy. Results Five (16.7%) patients had early postoperative complications and three were related to the neobladder. One year postoperatively, low grade (I, II) vesicoureteral reflux was present in five (16.7%) cases. The mean preoperative and 6 months postoperative serum creatinine levels were 1.07 ± 0.3 mg/dL and 1.2 ± 0.4 mg/dL, respectively, but the difference was not statistically significant (P = 0.1). Six months postoperatively the mean serum chloride level was 109 ± 4.5 (range 100,113) mmol/L and the mean arterial blood pH was 7.37 ± 0.2 (range 7.3,7.4). Two (6.7%) patients required oral alkaline supplementation because of high chloride levels. All the patients except one were continent throughout the day after 1 year. However, nocturnal enuresis was present in 25 (83.3%) cases. The pouch capacity was increased gradually up to 12 months postoperatively and the mean pouch capacity 12 months postoperatively was 460 ± 95.8 mL. Micturition occurred spontaneously in most patients while some needed abdominal straining. None of the patients had a residual urine of more than 60 mL. The mean maximum flow rate 6 months postoperatively was 9.8 (range 5.4,15.0) mL/s. After 6 months the stapled edge was noticed as a nodular line. One year postoperatively only a white scar could be observed at the suture line. Conclusion The Stanford pouch ileal neobladder constructed using absorbable staples was able to provide a good capacity,low pressure reservoir with a low rate of complications. [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]

    Utility of pulse oximetry in the detection of arterial hypoxemia in liver transplant candidates

    LIVER TRANSPLANTATION, Issue 4 2002
    Gary A. Abrams MD Assistant Professor of Medicine
    Hepatopulmonary syndrome, arterial hypoxemia caused by intrapulmonary vasodilatation, occurs in approximately 10% of patients with cirrhosis. The severity of hypoxemia affects liver transplant candidacy and is associated with increased morbidity and mortality posttransplantation. Screening guidelines for detecting the presence of arterial hypoxemia do not exist. The aim of this study is to investigate the accuracy and utility of pulse oximetry in the detection of hypoxemia (PaO2 < 70 mm Hg) in patients with cirrhosis. Two hundred prospective liver transplant candidates were compared with 94 controls. Arterial oxyhemoglobin saturation was obtained by pulse oximetry (SpO2) and compared with simultaneous arterial blood gas (ABG) oxyhemoglobin values (SaO2; bias = the difference). PaO2, carboxyhemoglobin, methemoglobin, and routine clinical and biochemical parameters were investigated to account for the bias. SpO2 overestimated SaO2 in 98% of patients with cirrhosis (mean bias, 3.37%; range, ,1% to 10%). Forty-four percent of patients with cirrhosis and controls had a bias of 4% or greater. No clinical or biochemical parameters of cirrhosis accounted for the overestimation of pulse oximetry. Twenty-five subjects with cirrhosis were hypoxemic, and an SpO2 of 97% or less showed a sensitivity of 96% and a positive likelihood ratio of 3.9 for detecting hypoxemia. An SpO2 of 94% or less detected all subjects with an arterial PaO2 less than 60 mm Hg. Pulse oximetry significantly overestimates arterial oxygenation, and the inaccuracy is not influenced by liver disease. Nevertheless, pulse oximetry can be a useful screening tool to detect arterial hypoxemia in patients with cirrhosis, but a higher threshold for obtaining an ABG must be used. [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]