Disease relevance of Cardiopulmonary Resuscitation

• INTERVENTIONS: After intravenous epinephrine (administered according to American Heart Association guidelines) and defibrillation efforts had failed, patients in cardiac arrest who were having cardiopulmonary resuscitation received 40 U of vasopressin intravenously and then defibrillation [1].
• Treatment of prolonged ventricular fibrillation. Immediate countershock versus high-dose epinephrine and CPR preceding countershock [2].
• Donor variables analyzed were age, gender, ABO blood group, cause of death, length of stay in the intensive care unit, use of pressors or pitressin, need for cardiopulmonary resuscitation, terminal serum transaminases, and ischemia time [3].
• During insulin-induced hypoglycemia, plasma glucagon immunoreactivity did not increase in the CPR nonresponders but increased significantly in the CPR responders [4].
• Left ventricular pressure and segment length were measured before and after 5 min of CPR in 22 dogs either given epinephrine (0.015 mg/kg body weight at the onset and after 4 min) or pretreated with propranolol (2 mg/kg) and given epinephrine during CPR [5].

Psychiatry related information on Cardiopulmonary Resuscitation

• The dialysis-specific living will asks about choices for life-sustaining treatment (cardiopulmonary resuscitation and dialysis) based on one's health state (current health; permanent coma; terminal illness; mild, moderate, or severe stroke; dementia) [6].
• The order of task sensitivity to disruption by chlorpromazine was TRD = PR = IRA = DMTS = CPR in which sensitivity was defined as a significant alteration in any aspect of task performance [7].
• Thus, the order of task sensitivity to any disruption by atropine is learning = color and position discrimination greater than time perception = short-term memory and attention = motivation (IRA = CPR greater than TRD = DMTS = PR) [8].
• The charts of 191 geriatric psychiatric inpatients with major depressive disorder or bipolar disorder were examined to determine demographic and psychiatric factors associated with the advance directive to have cardiopulmonary resuscitation (CPR) or not to have it in a life-threatening situation [9].
• History of epilepsy in first-degree relatives, maternal diseases in the two years before pregnancy, placental pathologies, low gestational age, being small for dates, neonatal convulsions and the need for cardiopulmonary resuscitation were associated with partial epilepsy, cerebral palsy and mental retardation [10].

High impact information on Cardiopulmonary Resuscitation

• High-dose epinephrine in cardiopulmonary resuscitation [11].
• Neurologic outcome, as measured by the Glasgow coma score, was better with active compression-decompression (8.0 +/- 1.3) than with standard CPR (3.5 +/- 0.3; P < 0.02) [12].
• Logistic regression modeling showed that the presence of organ failure (odds ratio [OR], 8.9; 95% confidence interval [CI], 3.3 to 23.9), the residents' estimates of the probability of surviving CPR (OR, 0.94; 95% CI, 0.88 to 0.99), and nonwhite race (OR, 2.7; 95% CI, 1.1 to 6.3) were associated with the determination of quantitative futility [13].
• OBJECTIVE--Active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) appears to improve ventilation and coronary perfusion when compared with standard CPR [14].
• Sodium bicarbonate in CPR [15].

Chemical compound and disease context of Cardiopulmonary Resuscitation

• Another 12 animals were randomly allocated after 4 minutes of cardiac arrest, followed by 8 minutes of basic life support CPR, to receive, every 5 minutes, either vasopressin (late vasopressin: 0.4 and 0.8 U/kg, respectively; n=6), or epinephrine (late epinephrine: 45 and 200 microg/kg, respectively; n=6) [16].
• During 20 minutes of CPR initiated immediately upon ventricular fibrillation in anesthetized dogs, left ventricular blood flow was similar with epinephrine (45 +/- 9 ml/min/100 g) or phenylephrine (47 +/- 8 ml/min/100 g) infusion [17].
• CONCLUSIONS: During experimental ventricular fibrillation and CPR, epinephrine increased intrapulmonary shunt approximately 300% more than saline or methoxamine and significantly reduced arterial oxygen saturation [18].
• To determine the value of sodium bicarbonate in resuscitation from ventricular fibrillation and the prevention of spontaneous refibrillation, sodium bicarbonate (1 meq/kg) or placebo was administered on a random basis to 16 pentobarbital-anesthetized dogs 18 min after the induction of ventricular fibrillation and cardiopulmonary resuscitation [19].
• A recent uncontrolled clinical trial has suggested that the adenosine antagonist aminophylline might improve the outcome of cardiopulmonary resuscitation from refractory bradyasystolic cardiac arrest [20].

Biological context of Cardiopulmonary Resuscitation

• BACKGROUND: Why pulmonary gas exchange deteriorates after administration of epinephrine during cardiopulmonary resuscitation (CPR) is unclear [18].
• Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine [17].
• Pulmonary ventilation/perfusion defects induced by epinephrine during cardiopulmonary resuscitation [21].
• Epinephrine produced higher cerebral and myocardial perfusion pressures during CPR with simultaneous chest compression-ventilation when the abdomen was unbound rather than bound because abdominal binding increased intracranial and venous pressures [22].
• We found that 3 mM cysteine and 5 mM dithiothreitol (DTT) did not decrease PMN phagocytosis, but abolished CPR inhibition by OPZ [23].

Anatomical context of Cardiopulmonary Resuscitation

• Excess bicarbonate administration during CPR may result in a marked dissociation between arterial and CSF pH as a consequence of rapid CO2 diffusion across the blood-brain barrier [24].
• We suggest that urine CPR less than 20 micrograms/day is an index of insulin dependency, although in a state of extreme decompensation of B-cells such as in ketoacidosis, urine CPR can be decreased low even in NIDDM [25].
• The present study was designed to examine the hypothesis that hypothalamic-pituitary-adrenal axis activity as measured by 24-h cortisol production rate (CPR) and plasma levels of free cortisol is linked to increased body fat in adults, and that increased cortisol levels with aging results from increased CPR [26].
• Simultaneous arterial (aortic), mixed venous (pulmonary artery), and myocardial venous (great cardiac vein) blood gas and lactate concentrations were obtained in 12 dogs before and during cardiac arrest and CPR [27].
• Conversely, CRF positive neurons appeared in large numbers, some being labeled with WGA, in the caudal periventricular region (CPR), and in the dorsomedial to lateral hypothalamic area (DLH), especially in the latter [28].

Associations of Cardiopulmonary Resuscitation with chemical compounds

• Second, the concentration product ratio (CPR), the ratio of the measured calcium oxalate concentration product before to that after incubation of the sample with calcium oxalate monohydrate crystal, was measured in seven uremic and seven normal serum ultrafiltrates [29].
• The degree of supersaturation was correlated with ultrafiltrate oxalate (RSR, r = 0.99, r = 29, P less than 0.001; CPR, r = 0.75, n = 11, P less than 0.001) [29].
• INTERPRETATION: After initially unsuccessful out-of-hospital CPR, thrombolytic therapy combined with heparin is safe and might improve patient outcome [30].
• BACKGROUND: Successful outcomes after cardiopulmonary resuscitation remain disappointingly infrequent, in animal studies, administration of exogenous vasopressin during closed- and open-chest cardiopulmonary resuscitation has recently been shown to be more effective than optimal doses of epinephrine in improving vital organ blood flow [1].
• Despite cardiopulmonary resuscitation and the administration of epinephrine, atropine, isoproterenol, and sodium bicarbonate, recovery of the sinus and junctional tissues was infrequent [31].

Gene context of Cardiopulmonary Resuscitation

• Coagulopathy after successful cardiopulmonary resuscitation following cardiac arrest: implication of the protein C anticoagulant pathway [32].
• Pretreatment with the ETA antagonist FR139317 and the ETB antagonist BQ788 inhibited CPR increases with ET-1 infusion [33].
• Carboxypeptidase R (EC 3.4.17.20) (CPR) and carboxypeptidase N (EC 3.4.17.3) (CPN) cleave carboxy-terminal arginine or lysine residues from biologically active peptides such as kinins or anaphylatoxins in the circulation thereby regulating their activities [34].
• Homeostasis assessment model of insulin resistance (HOMA-IR), homeostasis assessment model of beta-cell function, HbA(1c), C-peptide in 24-h pooled urine (urine CPR), and plasma concentrations of 8-epi-PGF2alpha, tumor necrosis factor-alpha (TNF-alpha), plasminogen activator inhibitor type 1, and adiponectin were measured at various times [35].
• We analyzed whether PAI-1 concentrations might predict cerebral outcome after cardiopulmonary resuscitation [36].

Analytical, diagnostic and therapeutic context of Cardiopulmonary Resuscitation

• Technetium-99m stannous pyrophosphate myocardial scintigraphy after cardiopulmonary resuscitation with cardioversion [37].
• The arterial acidemia observed during CPR was untreated in a control group, corrected to a pH of 7.3 with the use of sodium bicarbonate, or maintained below pH 6.5 with intravenous lactic acid after 14 minutes of CPR [38].
• The ratio of the difference between basal and 30-min CPR values and basal and 30-min OGTT blood glucose values [delta CPR: delta BS(30)'] as well as the delta IRI: delta BS(30') ratio was significantly decreased in cirrhotics (P less than 0.01) [39].
• Although CPR significantly increased with increasing body mass index and percentage body fat, free cortisol levels remained independent of body composition and leptin levels due to increased cortisol clearance rates [26].
• In addition, 24-h plasma free cortisol levels were increased with age in association with increased CPR, independent of body size [26].

References