PubMed Health⌕ Search

Biomedical subjects

A H Idris

Publications and source records attributed to A H Idris.

At least 19 recordsLinked to original sources
PubMed1998

Severe ventilatory compromise due to gastric distention during pediatric cardiopulmonary resuscitation.

We describe a child in cardiac arrest with severe ventilatory compromise due to gastric distention. During cardiopulmonary resuscitation (CPR), positive pressure ventilation may lead to gastric insufflation because of decreased pulmonary compliance and decreased lower esophageal sphincter tone. Essentially, gas delivered will follow the path of least resistance, which may be to the stomach. In our patient, gastric distention precluded effective ventilation and gastric decompression relieved ventilatory compromise. The values and pitfalls of clinical evaluation and capnography are presented.

Cardiopulmonary Resuscitation↗
PubMed1998

Influence of tidal volume on the distribution of gas between the lungs and stomach in the nonintubated patient receiving positive-pressure ventilation.

OBJECTIVES: When ventilating a nonintubated patient in cardiac arrest, the European Resuscitation Council has recently recommended a decrease in the tidal volume from 0.8 to 1.2 L to 0.5 L, partly in an effort to decrease peak flow rate, and therefore, to minimize stomach inflation. The purpose of the present study was to examine the validity of the European Resuscitation Council's recommendation in terms of gas distribution between lungs and stomach in a bench model that simulates ventilation of a nonintubated patient with a self-inflatable bag representing tidal volumes of 0.5 and 0.75 L. DESIGN: A bench model of a patient with a nonintubated airway was used consisting of face mask, manikin head, training lung (lung compliance, 50 mL/cm H2O; airway resistance, 5 cm H2O/L/sec), adjustable lower esophageal sphincter pressure (LESP) and simulated stomach. SETTING: University hospital laboratory. SUBJECTS: Thirty healthcare professionals. INTERVENTIONS: Healthcare professionals performed 1-min bag-mask ventilation at each LESP level of 5, 10, and 15 cm H2O at a rate of 12 breaths/min, using an adult and pediatric self-inflating bag, respectively. Volunteers were blinded to the LESP, which was randomly varied. MEASUREMENTS AND MAIN RESULTS: Both types of self-inflating bags induced stomach inflation, with higher stomach and lower lung tidal volumes when the LESP was decreased. Lung tidal volume with the pediatric bag was significantly (p < .05) lower at all LESP levels when compared with the adult bag, and ranged between 240 mL at an LESP of 15 cm H2O and 120 mL at an LESP of 5 cm H2O. Stomach tidal volume with the adult bag ranged between 250 mL at an LESP of 15 cm H2O and increased to 550 mL at an LESP of 5 cm H2O. Stomach tidal volume with the pediatric bag was significantly lower (p < .05) at all LESP levels when compared with the adult bag and ranged between 70 mL at an LESP of 15 cm H2O and 300 mL at an LESP of 5 cm H2O. CONCLUSIONS: Our data support the recommendation of the European Resuscitation Council to decrease tidal volumes to 0.5 L when ventilating a cardiac arrest victim with an unprotected airway. A small tidal volume may be a better trade-off in the basic life support phase, as this may provide reasonable ventilation while avoiding massive stomach inflation.

Adult↗
PubMed1997

Poor correlation of mouth-to-mouth ventilation skills after basic life support training and 6 months later.

The purpose of the present study was to evaluate the cardiopulmonary resuscitation (CPR) skills of medical students after a 2-h basic life support class (n = 129) and 6 months later (n = 113). Mean +/- SD written test score decreased from 6.4 +/- 0.7 to 6.2 +/- 0.8 (P = 0.03). Mean +/- SD breaths delivered before CPR decreased from 2.9 +/- 0.6 to 2.2 +/- 1.2 (P = 0.0001), ventilation rate increased from 12.2 +/- 1.9 to 14.3 +/- 5.0 breaths/min (P = 0.0001), tidal volume increased from 0.75 +/- 0.2 to 0.8 +/- 0.31 (P = 0.11), minute ventilation from 9.1 +/- 2.6 to 10.8 +/- 3.61 (P = 0.0001), and stomach inflation from 13 +/- 22 to 18 +/- 27% of CPR breaths (P = 0.11). Mean +/- SD chest compression/min decreased from 56 +/- 9 to 54 +/- 12 (P = 0.34), depth of chest compression increased from 41 +/- 6 to 46 +/- 7 mm (P = 0.0001), hands held incorrectly on the thorax increased from 22 +/- 27 to 23 +/- 32% (P = 0.59), and leaning on the chest from 4 +/- 12 to 18 +/- 28% of compressions (P < 0.0001). In summary, ventilation skills were unpredictable; there was only a 5% chance that a given student would achieve the same mouth-to-mouth ventilation performance in both the BLS class and 6 months later. Despite the respiratory mechanics of the CPR manikin which prevented stomach inflation much better than an unconscious patient with an unprotected airway, stomach inflation occurred repeatedly. Teachers of basic life support classes need to consider the respiratory mechanics of the CPR manikin being used to assure clinically realistic and appropriate mouth-to-mouth ventilation skills.

Adult↗
PubMed1996

Utstein-style guidelines for uniform reporting of laboratory CPR research. A statement for healthcare professionals from a task force of the American Heart Association, the American College of Emergency Physicians, the American College of Cardiology, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, the Institute of Critical Care Medicine, the Safar Center for Resuscitation Research, and the Society for Academic Emergency Medicine. Writing Group.

Explore the source record for details and available documents.

Animals↗
PubMed1996

Utstein-style guidelines for uniform reporting of laboratory CPR research: a statement for health care professionals from a Task Force of the American Heart Association, the American College of Emergency Physicians, the American College of Cardiology, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, the Institute of Critical Care Medicine, the Safar Center for Resuscitation Research, and the Society for Academic Emergency Medicine.

Explore the source record for details and available documents.

Animals↗
PubMed1996

Reassessing the need for ventilation during CPR.

In the United States debate continues about the necessity of ventilation during CPR because of fear of contracting infectious diseases. Three questions will be considered in this article. First, is ventilation necessary for the treatment of cardiac arrest? Second, is mouth-to-mouth ventilation any better than no ventilation at all? Third, are other techniques of ventilation as effective or more effective than mouth-to-mouth ventilation during basic life support CPR? Although research is still inconclusive with regard to the need for ventilation during CPR, recent findings have clarified the effect of ventilation during low blood flow states and how ventilation influences resuscitation. Ventilation affects oxygenation, carbon dioxide elimination, and pH during times of low rates of blood flow. Ventilation may be unnecessary during the first few minutes of CPR. Under conditions of prolonged, untreated cardiac arrest, ventilation during CPR affects return of spontaneous circulation. Isolated hypoxemia and hypercarbia independently have adverse effects on survival of cardiac arrest. Because ventilation with exhaled gas contains as much as 4% CO2 and less oxygen than air, it may have adverse effects during CPR. Spontaneous gasping may provide sufficient ventilation during CPR. Chest compression alone provides some pulmonary ventilation and gas exchange. Active chest compression-decompression may improve gas exchange better than does standard chest compression. Other forms of manual ventilation may also have a role in CPR.

Animals↗
PubMed1996

Utstein-style guidelines for uniform reporting of laboratory CPR research. A statement for healthcare professionals from a Task Force of the American Heart Association, the American College of Emergency Physicians, the American College of Cardiology, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, the Institute of Critical Care Medicine, the Safar Center for Resuscitation Research, and the Society for Academic Emergency Medicine.

Explore the source record for details and available documents.

Animals↗
PubMed1995

The tumor suppressor gene WT1 inhibits ras-mediated transformation.

Wilms' tumor belongs to a small group of pediatric neoplasms that have served as paradigms of human cancers in which recessive mutations play a primary role in tumorigenesis. WT1 is a candidate tumor suppressor gene that is mutationally inactivated in a proportion of both familial and sporadic Wilms' tumors. Recent studies demonstrated that WT1 can partially suppress growth of a Wilms' tumor cell line in vitro and in vivo. We investigated the ability of WT1 to inhibit the expression of the transformed phenotype in non-Wilms' tumor cells. The expression of WT1 cDNA in ras-transformed NIH3T3 cells yielded large, flat cells that exhibited complete contact-inhibition. These morphologic changes were associated with decreased proliferation, suppression of clonogenicity in soft agar and inhibition of tumor growth in nude mice. Moreover, expression of WT1 in non-transformed NIH3T3 cells resulted in similar morphologic changes and profound resistance to transformation by an activated ras oncogene. These studies suggest that tumor inhibition by WT1 in these cells may be achieved by interference with the ras-mediated signalling pathway.

3T3 Cells↗
PubMed1995

Automatic mechanical device to standardize active compression-decompression CPR.

STUDY OBJECTIVE: To develop an automatic mechanical device capable of performing active compression-decompression (ACD) CPR in laboratory animals. DESIGN: A swine model was used to study standard and ACD CPR. One-minute periods of standard mechanical chest compressions were alternated with mechanical ACD CPR. SETTING: University hospital laboratory. INTERVENTIONS: A commercially available device that provided standard chest compressions only was modified to deliver ACD CPR. RESULTS: The absolute difference in intrapleural pressure and tidal volume almost doubled during ACD CPR compared with that with standard CPR. CONCLUSION: The presence of a greater negative change in intrapleural pressure confirmed that active decompression of the chest had occurred and that the device was capable of performing ACD CPR. The device provides consistent rate, depth, force, and duty cycle.

Animals↗
PubMed1995

Does hypoxia or hypercarbia independently affect resuscitation from cardiac arrest?

STUDY OBJECTIVE: In a previous cardiopulmonary resuscitation (CPR) study in swine, ventilation was associated with improved rate of return of spontaneous circulation (ROSC) compared with nonventilated animals, which had greater hypoxia and hypercarbic acidosis. We used the same model to determine the independent effect of hypoxia and hypercarbic acidosis on ROSC after cardiac arrest. DESIGN: Laboratory model of cardiac arrest. SETTING: University teaching hospital laboratory. PARTICIPANTS: Domestic swine (23 to 61 kg). INTERVENTIONS: Twenty-four swine were randomly assigned to three groups receiving ventilation during CPR with 85% O2/15% N2 (control), 95% O2/5% CO2 (hypercarbia), or 10% O2/90% N2 (hypoxia). All animals had ventricular fibrillation for 6 min without CPR, then CPR with one of the ventilation gases for 10 min, then defibrillation. Animals without ROSC received epinephrine, 85% O2, CPR for another 3 min, and defibrillation. MEASUREMENTS AND RESULTS: During the tenth minute of CPR, the hypercarbic group had more mean (SD) arterial hypercarbia than the control group (PCO2, 47 +/- 6, compared with 34 +/- 6; p < 0.01), and greater mixed venous hypercarbia (PCO2, 72 +/- 14, compared with 59 +/- 8; p < 0.05), while mean arterial and mixed venous PO2 was not significantly different. The hypoxic group had significantly less mean arterial (43 +/- 9 compared with 228 +/- 103 mm Hg) and mixed venous (22 +/- 5 compared with 35 +/- 7 mm Hg) PO2 when compared with the control group (p < 0.01), while mean arterial and mixed venous PCO2 were not significantly different. Thus, the model succeeded in producing isolated hypercarbia without hypoxia in the hypercarbic group and isolated hypoxia without hypercarbia in the hypoxic group. The rate of ROSC was 6/8 (75%) for the control group, 1/8 (13%) for the hypercarbic group, and 1/8 (13%) for the hypoxic group (p < 0.02). CONCLUSIONS: Both hypoxia and hypercarbia independently had an adverse effect on resuscitation from cardiac arrest. In this model with a prolonged interval of untreated cardiac arrest, adequate ventilation was important for resuscitation.

Analysis of Variance↗
PubMed1994

Changes in arterial and mixed venous blood gases during untreated ventricular fibrillation and cardiopulmonary resuscitation.

This investigation was designed to evaluate the changes in arterial and mixed venous acid-base conditions during untreated ventricular fibrillation and after institution of cardiopulmonary resuscitation (CPR). Fifty-two swine (weight: 25-40 kg) were studied after induction of ventricular fibrillation. In a subgroup of 10 animals, 10-min CPR trials were performed. Arterial and mixed venous blood gases were monitored at baseline, after 5 min of untreated ventricular fibrillation (nonintervention interval) and after 10 min of mechanical CPR. Standard CPR was performed at compression rates of 100/min with a 60% duty cycle. Arterial pH, Pco2, and HCO3 were unchanged when baseline values were compared with those obtained after 5 min of untreated ventricular fibrillation, while arterial Po2 decreased from 81 to 69 torr. Mixed venous pH decreased from 7.41 to 7.35, Pco2 increased from 43 to 48 torr, Po2 decreased from 40 to 38 torr and HCO3 decreased from 28 to 26 mEq/l (P < 0.05). Although these changes were statistically significant, many remain in the normal range. Both arterial and mixed venous pH and HCO3 fell further after 9 min of CPR and Pco2 increased (P < 0.05). Alterations in mixed venous pH and Pco2 were more apparent than corresponding changes in arterial blood gas composition. We conclude that untreated cardiac arrest may be accompanied by normal arterial and mixed venous blood gas levels. Tissue acidosis is only revealed after tissue perfusion is restored and is most accurately reflected in the mixed venous blood gas composition. This apparent paradox provides insight into the relationship between tissue perfusion and arterial and mixed venous acid-based composition.

Acid-Base Equilibrium↗
PubMed1994

Ventilation caused by external chest compression is unable to sustain effective gas exchange during CPR: a comparison with mechanical ventilation.

OBJECTIVE: To compare the tidal volume, minute ventilation, and gas exchange caused by mechanical chest compression with and without mechanical ventilatory support during cardiopulmonary resuscitation (CPR) in a laboratory model of cardiac arrest. DESIGN: A laboratory swine model of CPR was used. Eight animals with and eight animals without mechanical ventilation received chest compression (100/min) for 10 min. Coronary perfusion pressure, tidal volume, and minute ventilation were recorded continuously. INTERVENTIONS: Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. RESULTS: During the first minute of chest compression, mean (+/- S.D.) minute ventilation was 11.2 +/- 5.9 l/min in the mechanically ventilated group and 4.5 +/- 2.8 l/min in the group without mechanical ventilation (P = 0.01). Minute ventilation gradually declined to 5.8 +/- 1.4 l/min and 1.7 +/- 1.6 l/min, respectively, during the last minute of chest compression (P < 0.0001). After 10 min of chest compression, mean arterial pH was significantly more acidemic in the group without mechanical ventilation (7.16 +/- 0.13 compared with 7.30 +/- 0.07 units) and PCO2 was higher (62 +/- 19 compared with 35 +/- 9 mmHg). Mixed venous PCO2 was also higher (76 +/- 15 compared with 61 +/- 8 mmHg). CONCLUSION: Standard chest compression alone produced measurable tidal volume and minute ventilation. However, after 10 min of chest compression following 6 min of untreated ventricular fibrillation, it failed to sustain pulmonary gas exchange as indicated by significantly greater arterial and mixed venous hypercarbic acidosis when compared with a group receiving mechanical ventilation.

Acid-Base Equilibrium↗
PubMed1994

Lack of uniform definitions and reporting in laboratory models of cardiac arrest: a review of the literature and a proposal for guidelines.

BACKGROUND: Researchers are interested in improved uniformity of definitions and standards of reporting data for human CPR studies, and international guidelines (Utstein style) have been developed. However, no guidelines exist for animal CPR investigations. OBJECTIVE: To assess published animal CPR studies for adequacy of reporting and uniformity of methods and definitions regarding such important factors as the interval from the onset of ventricular fibrillation to the start of CPR (the nonintervention interval), ventilation, chest compression, coronary perfusion pressure, and return of spontaneous circulation. DESIGN: A blinded review of the methodology described in 42 articles concerned with animal CPR research published during the last ten years. An article had to report cardiac arrest and CPR as part of the protocol and return of spontaneous circulation as one of the outcome variables in order to be included in this study. We excluded abstracts, nonresuscitation models, and human CPR studies. MEASUREMENTS AND MAIN RESULTS: There was wide variation in the experimental methods reported in the studies. The nonintervention interval ranged from 0 to 15 minutes. The majority of studies initiated CPR within three minutes after the onset of ventricular fibrillation. Twenty-two percent of studies reported tidal volume, and 18% reported minute ventilation. Of the 14 studies that used blood pressure or coronary perfusion pressure as a target for titration of chest compression force, 12 used different target blood pressure values. We found 29 different definitions of return of spontaneous circulation. The duration of return of spontaneous circulation ranged from 30 seconds to 60 minutes; however, 52% of studies did not report a duration. CONCLUSION: Important differences exist in animal CPR research methodology among laboratories. Failure to define or report minute ventilation, coronary perfusion pressure, and return of spontaneous circulation made it difficult to compare studies. In order to make valid comparisons of studies, blood flow and ventilation should be measured and controlled when they are not experimental variables. Uniform definitions and guidelines for reporting should be developed for laboratory CPR research.

Animals↗
PubMed1994

End-tidal carbon dioxide during extremely low cardiac output.

STUDY OBJECTIVE: A number of studies have shown that expired CO2 concentration is closely related to cardiac output, but that cardiac output was not controlled as an independent variable. In addition, the partial pressure of end-tidal CO2 (PETCO2) during extremely low cardiac output has not been reported. The objective of the present study was to measure PETCO2 during well-controlled, very low blood flow rates under conditions of constant minute ventilation. DESIGN: Ten anesthetized, intubated, and mechanically ventilated swine (weight, 43 to 102 kg) were placed on two ventricular assist devices in order to control cardiac output. Minute ventilation was measured and kept constant. Ventricular assist device output (measured with an ultrasonic flow probe); PETCO2; and aortic, pulmonary artery, and central venous pressures were recorded continuously. INTERVENTIONS: After electrical induction of ventricular fibrillation, pump output was decreased in steps. MEASUREMENTS AND MAIN RESULTS: Cardiac index ranged from 0 to 5,371 mL/min/m2; 59% of PETCO2 measurements were made at cardiac indexes of less than 1,313 mL/min/m2 (30 mL/min/kg). The relationship of PETCO2 levels to cardiac index was determined with linear regression analysis; P < .05 was statistically significant. PETCO2 correlated significantly with cardiac index (P < .0001). The best-fit line by least-squares analysis produced the equation: PETCO2 = 4.98 + 0.012 [cardiac index] (r2 = .82). CONCLUSION: Under conditions of constant minute ventilation, PETCO2 correlated closely with cardiac index over a large range of blood flow rates, including extremely low rates.

Animals↗