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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous gasping is frequently observed during cardiac arrest, especially when mechanical ventilation is withheld during precordial compression. We related spontaneous gasping to pulmonary gas exchange and cardiac resuscitability in a rodent model of cardiac arrest. Ventricular fibrillation was electrically induced in 15 Sprague-Dawley rats. After 4 min untreated ventricular fibrillation, precordial compression was initiated. Coronary perfusion pressure was maintained between 25 and 30 mm Hg. Oxygen was supplied at the tracheal tube port coincident with start of precordial compression in 10 animals. Five additional control animals were identically treated except they were mechanically ventilated coincident with start of precordial compression. After 6 min precordial compression, defibrillation was attempted and five of 10 nonventilated animals, and all control animals, were resuscitated by direct current countershock. In the successfully resuscitated, nonventilated animals, the frequency of spontaneous gasping during precordial compression progressively increased to an average of 19 gasps/min but it was < 6 gasps/min in nonresuscitated animals. More frequent gasping was associated with correspondingly greater arterial PO2 (110 versus 51 mm Hg, p < 0.01) and lesser PCO2 (55 versus 91 mm Hg, p < 0.01). In control animals, no spontaneous gasping was observed during precordial compression. Arterial PO2 and PCO2 of mechanically ventilated animals was more like that of spontaneously gasping rats. According, the frequency of spontaneous gasping in absence of mechanical ventilation is predictive of cardiac resuscitation success and associated with improved arterial oxygenation and CO2 removal.
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PMID:Spontaneous gasping during cardiopulmonary resuscitation without mechanical ventilation. 808 62

Coronary perfusion pressure and its relation with the expired carbon dioxide concentration (end-tidal CO2) was examined in a rodent model of sustained ventricular fibrillation and subsequent cardiopulmonary resuscitation. Equipressor dosages of the pure alpha 1-agonist methoxamine, the mixed alpha/beta-agonists epinephrine and norepinephrine were randomly compared with 0.9% NaCl. Thirty two Sprague-Dawley rats were anesthetized and catheters were advanced into the aorta, right ventricle, right atrium and inferior vena cava. After 4 min of untreated ventricular fibrillation external chest compression was initiated and defibrillation was attempted after 8 min. Drugs were infused for 3 min during cardiopulmonary resuscitation into the inferior vena cava. A 60-min survival period followed methoxamine administration in 7 of 8 (P < 0.019 vs. NaCl), after epinephrine in 4 of 8, after norepinephrine in 5 of 8, and after NaCl in only 2 of 8 animals. Resuscitation success was determined by coronary perfusion and mean aortic pressures generated during cardiopulmonary resuscitation but not by arterial or venous blood gases. Adrenergic agents increased coronary perfusion and mean aortic pressures but decreased end-tidal CO2 which failed to correlate with these pressures. Accordingly, alpha-adrenergic agents mitigated the accuracy of end-tidal CO2 as a non-invasive hemodynamic monitor and predictor of survival after rodent cardiopulmonary resuscitation.
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PMID:Determinants of survival after rodent cardiac arrest: implications for therapy with adrenergic agents. 809 98

In cases of life-threatening status asthmaticus which are refractory to drug therapy, the administration of inhalation anesthetics can be life-saving as they help alleviate bronchial spasm. We had an 11-year-old female patient suffering from status asthmaticus who was moribund from severe CO2 narcosis and was not responding to any of the conventional therapies. She finally fell into ventricular fibrillation. After cardiopulmonary resuscitation, we administered 2.0% isoflurane in oxygen. Within half an hour, her high inspiratory pressure was dramatically decreased, and then the isoflurane concentration was maintained at 1.0%. After 14 hours of isoflurane anesthesia, PaCO2 decreased to the normal level and the isoflurane treatment was discontinued. The endotracheal tube was removed 4 hours later. She had an uneventful recovery and was discharged from the hospital 11 days later. With its low metabolic rate and therefore low organ toxicity, as well as its low arrhythmogenicity with remarkable bronchodilating activity, we feel isoflurane may well be superior to other inhalation anesthetics in the treatment of status asthmaticus.
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PMID:[A critical patient relieved from status asthmaticus with isoflurane inhalation therapy]. 843 81

A study was undertaken to determine the pattern of end-tidal carbon dioxide (ETCO2) changes during asphyxia-induced cardiac arrest in a pediatric canine model. Eleven intubated, anesthetized, paralyzed dogs (mean age, 4.1 mo; mean weight, 5.5 kg) were used. Asphyxia was induced by clamping the endotracheal tube (ETT) and discontinuing ventilation. Cardiac arrest ensued a few minutes later, after which closed-chest cardiopulmonary resuscitation (CPR) and ventilation were initiated. The ETCO2 level was recorded at baseline and every minute during CPR. Mean baseline ETCO2 was 31.9 mm Hg. The initial ETCO2 immediately after unclamping the ETT (mean, 35 mm Hg) was higher than subsequent values (mean, 12.4 mm Hg; P < .001). There was a sudden increase in ETCO2 to a mean of 27.0 mm Hg at or just before return of spontaneous circulation (ROSC) in all 11 cases (P < .01). During CPR, ETCO2 levels were initially high, decreased to low levels, and increased again at ROSC. This pattern, not previously described, is different from that observed in animal and adult cardiac arrest caused by ventricular fibrillation, during which ETCO2 decreases to almost zero after the onset of arrest, begins to increase after the onset of effective CPR, and increases to normal levels at ROSC. In this model of asphyxial arrest, continued cardiac output prior to arrest allows continued delivery Of CO2 to the lungs, resulting in higher alveolar CO2; this, in turn, is reflected as increased ETCO2 once ventilation is resumed during CPR. Further study is needed to determine whether the pattern Of ETCO2 changes can be used prospectively to define the etiology of cardiac arrest.
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PMID:End-tidal carbon dioxide changes during cardiopulmonary resuscitation after experimental asphyxial cardiac arrest. 876 52

The effects of manual and a new mechanical chest compression device (Heartsaver 2000) during prolonged CPR with respect to haemodynamics and outcome were tested in a prospective, randomized, controlled experimental trial during ventricular fibrillation in 12 dogs of 9-13 kg body weight after 1 min of cardiac arrest. During the first 10 min of CPR the dogs were resuscitated according to the Basic Life Support (BLS) algorithm, followed by 20 min of Advanced Life Support (ALS) algorithm. After 30 min of CPR both manual and mechanical CPR groups were resuscitated following a standardized ALS protocol. During CPR, coronary perfusion pressure and end tidal CO2 were greater with mechanical CPR. All animals were successfully resuscitated and neurological deficit scores were not different. The CPR trauma score was less in the mechanical group. Mechanical external chest compression provided better haemodynamics than the manual technique, though outcome did not differ. Both optimally performed manual and mechanical techniques produce flow sufficient to maintain organ viability for 30 min of CPR after a 1 min arrest interval.
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PMID:A comparison of prolonged manual and mechanical external chest compression after cardiac arrest in dogs. 892 87

At present, there are only a limited number of objective measures available to clinicians resuscitating patients from cardiac arrest. The electrocardiogram and end-tidal CO2 are easily applied, but the data they produce are of only limited utility in evaluating the efficacy of chest compression and in choosing the sequence of therapies. In particular, we are in need of an objective test that can tell us when the myocardium will defibrillate into a perfusing rhythm. The ventricular fibrillation waveform holds information that we have not yet begun to utilize. Parameters derived from power spectrum analysis, such as ventricular fibrillation median frequency, appear promising. Combination of both old and new parameters may allow us to more accurately evaluate the efficacy of therapy.
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PMID:Objective measurements for guiding initiation, sequencing, and discontinuation of life-support intervention. 915 46

There is currently no practical method for determining cardiopulmonary resuscitation (CPR) efficacy in the field. We investigated the relationship between the volume of carbon dioxide (CO2) excreted in the airway (CO2EX) when tidal volume and respiratory rate are controlled, and cardiac output (CO), an indicator of CPR efficacy, to determine the potential of CO2EX as a practical noninvasive field monitor of CPR efficacy. Thirteen mongrel dogs were anesthetized, instrumented and ventilated 13 times/min at a fixed tidal volume with an infrared airway CO2 sensor. CO2EX = (PCO2/bar. press) x (tidal vol) x (breaths/min), and expressed in ml/min per kg. Sequences of control, CPR with 3-4 different compression forces, and recovery measurements were recorded 10-15 times/animal. CO2EX and CO fell simultaneously with ventricular fibrillation. CPR immediately increased CO2EX and CO. Both changed consistently and in the same direction as compression force. Return of spontaneous circulation immediately increased CO2EX and CO above controls, with a gradual return to control levels. CO2EX was always below 8 ml-CO2/min/kg during CPR and above this during spontaneous circulation. With alveolar ventilation controlled, CO2 movement is regulated by CO, CO distribution and CO2 stores shifts. Normally, CO accounts for 15% of CO2EX variability. In this study CO accounted for > or = 65% of CO2EX variability during CPR, indicating CO2EX changes were primarily due to CO changes. When ventilation is controlled, CO2EX during CPR reliably tracks changes in CO. Therefore, CO2EX may provide a practical noninvasive method of determining CPR efficacy as the CPR is being performed.
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PMID:The relationship between airway carbon dioxide excretion and cardiac output during cardiopulmonary resuscitation. 917 88

Currently, there are no practical means of prospectively determining cardiopulmonary resuscitation (CPR) adequacy in the field. Airway CO2 excretion can be noninvasively and stably measured under changing environmental conditions. We investigated the relationships between the volume of airway CO2 excreted (CO2EX) during CPR to regional blood flow (RBF) and survival. A total of 21 dogs were randomly divided into four CO2EX groups (< 5, 5-6, > 6-7 and > 7 ml CO2/min per kg), anesthetized, instrumented and ventilated with an in-line infrared airway CO2 sensor. Anesthesia was reduced and baseline measurements made. Ventricular fibrillation (VF) was initiated and resuscitation withheld for 3 min, followed by 17 min of CPR. Compression force alone was adjusted to maintain predetermined CO2EX. Animals were resuscitated, monitored for 2 h and observed for an additional 22 h. RBF was determined at baseline, 16 min post-VF and 60 min post-resuscitation. Mean CO2EX during CPR was significantly higher in survivors than nonsurvivors. The probability of survival increased as CO2EX increased. The highest CO2EX group had the highest rate of survival (86%), but did not always have significantly higher cardiac output (CO), myocardial or cerebral blood flows (MBF, CBF) than the lowest CO2EX group with a 0% survival rate. These data suggest survival is tracked better by CO2EX than by CO, MBF or CBF. Therefore, CO2EX appears to provide a practical reliable noninvasive method of determining CPR efficacy in the field.
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PMID:The relationship of carbon dioxide excretion during cardiopulmonary resuscitation to regional blood flow and survival. 931 97

The haemodynamic effects of variations in the relative duration of the compression and active decompression (4 cm/2 cm) during active compression-decompression cardiopulmonary resuscitation (ACD-CPR), 30/70, 50/50 and 70/30, were tested in a randomized cross-over design during ventricular fibrillation in seven anaesthetized pigs (17-23 kg) using an automatic hydraulic chest compression-decompression device. Duty cycles of 50/50 and 70/30 gave significantly higher values than 30/70 for mean carotid blood flow (32 and 36 vs. 21 ml min-1, transit time flow probe, cerebral blood flow (30 and 34 vs. 19, radionuclide microspheres), mean aortic pressure (35 and 41 vs. 29 mmHg) and mean right atrial pressure (24 and 33 vs. 16 mmHg). A higher mean aortic, mean right atrial and mean left ventricular pressure for 70/30 were the only significant differences between 50/50 and 70/30. There were no differences in myocardial blood flow (radionuclide microspheres) or coronary perfusion pressure (CPP, aortic-right atrial pressure) between the three different duty cycles. CPP was positive in both the early and late compression period and during the whole decompression period. The expired CO2 was significantly higher with 70/30 than 30/70 during the compression phase of ACD-CPR. Beyond that no significant differences in the expired CO2 levels were observed. In conclusion a reduction of the compression period to 30% during ACD-CPR reduced the cerebral circulation, the mean aortic and right atrial pressures with no effect on the myocardial blood flow of varying the compression-decompression cycle.
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PMID:Effect of different compression--decompression cycles on haemodynamics during ACD-CPR in pigs. 957 28

It is still controversial whether sodium bicarbonate is effective for the correction of acidemia during cardiopulmonary resuscitation (CPR). To resolve this issue, we must clarify the influence of acidosis accompanied by cardiac arrest on the cardiac and cerebral resuscitability. The influence of acidosis on cardiac resuscitability The factors which determine the cardiac resuscitability during asystole or ventricular fibrillation are the presser response to administered catecholamines and the threshold of defibrillation. However, there is still no evidence that acidosis inhibits these factors during CPR. Recent reports suggested that CO2 itself impaired cardiac resuscitability rather than acidosis. On the other hand, our study using isolated perfused rat hearts proposed that the effect of acidosis is not still eliminated. The influence of acidosis on the cerebral resuscitability There are two contrary opinions. One is that acidosis deteriorates the cerebral damage after resuscitation. The other is that acidosis is rather protective against the cerebral damage. In the studies which support the latter opinion, the evaluation of the effect of reperfusion is lacking. Accordingly, any factors which develop during the reperfusion phase may be enhanced by acidosis. These findings indicate that the influence of acidosis accompanied by cardiac arrest is complicated and that it includes many unresolved questions. Until we clarify these questions, we can not conclude that the correction of acidemia is necessary during CPR.
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PMID:[Cardiopulmonary cerebral resuscitation and acidosis]. 972 Mar 25


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