Outcome after prehospital defibrillation remains dire. The aim of the present study was to elucidate the pathophysiology of cardiac arrest and to suggest ways to improve outcome. Ventricular fibrillation (VF) was induced in air-ventilated pigs, after which ventilation was withdrawn. After 6.5 min of VF, ventilation with 100% oxygen was initiated. In six pigs (group I), defibrillation was the only treatment carried out. In another six pigs (group II), mechanical chest compression-decompression CPR (mCPR) was carried out for 3.5 min followed by a 40-s hands-off period before defibrillation. If unsuccessful, mCPR was resumed for a further 30 s before a second or a third, 40-s delayed, shock was given. In a final six pigs (group III) mCPR was applied for 3.5 min after which up to three shocks (if needed) were given during on-going mCPR. Return of spontaneous circulation (ROSC) occurred in none of the pigs in group I (0%), in 1 of six pigs in group II (17%) and in five of six pigs in group III (83%). During the first 3 min of VF arterial blood was transported to the venous circulation, with the consequence that the left ventricle emptied and the right ventricle became greatly distended. It took 2 min of mCPR to establish an adequate coronary perfusion pressure, which was lost when the mCPR was interrupted. During 30 s of mCPR coronary perfusion pressure was negative, but a carotid flow of about 25% of basal value was obtained. In this pig model, VF caused venous congestion, an empty left heart, and a greatly distended right heart within 3 min. Adequate heart massage before and during defibrillation greatly improved the likelihood of return of spontaneous circulation (ROSC).
"The theoretical background for requiring CPR first in case of prolonged VF is that it can restrict the end organ ischemia, lead the cardiac metabolic state to a proper condition for defibrillation and reduce the amount of a reperfusion injury [5,6,7,8]. In spite of such theoretical background and several reports with data, there are a number of studies with an opposing view also. "
[Show abstract][Hide abstract] ABSTRACT: Defibrillation is no longer universally recommended as initial intervention for the reversal of ventricular fibrillation (VF) after a prolonged and untreated cardiac arrest. We sought to examine this issue in an animal model where a prolonged untreated VF was induced. The aim of this study was to investigate the potential mechanism of the detrimental effect of defibrillation prior to cardiopulmonary resuscitation (CPR) in prolonged cardiac arrest model. VF was electrically induced in 32 domestic male swine weighing 40±3 kg and remained untreated for 15 minutes. The animals were then randomly allocated to either the initial defibrillation group or the chest compression group. Mean aortic pressure, right atrial pressure and coronary perfusion pressure (CPP) were continuously measured during the performance. The dimensions of the left ventricle (LV) were assessed by echocardiographic methods. The CPP induced by CPR after defibrillation was significantly lower in the initial defibrillation group than in the chest compression group; 1 minute after defibrillation (9±3 mmHg vs. 14.8±7 mmHg (P<0.05)), and after 5 minutes 16±5 mmHg vs. 21.7±1 mmHg (P<0.05). The LV volumes were reduced from 18±2 mmHg to 14±1 mmHg after defibrillation (P<0.05). In brief, this study showed that the conducting defibrillation prior to chest compression may cause a contracture of the LV, resulting in lowering CPP, thus dropping the efficiency of chest compression in a prolonged cardiac arrest model.
"A CPP of only 5 mmHg, as seen in the manual group, probably explains the lower ROSC rate. Another possible explanation for the higher ROSC rate in the LUCAS CPR group was that they were defibrillated during ongoing compressions . However, in the present study the delay between compressions and defibrillation was only 2 seconds, which is too short for a significant drop in CPP. "
[Show abstract][Hide abstract] ABSTRACT: Optimal manual closed chest compressions are difficult to give. A mechanical compression/decompression device, named LUCAS, is programmed to give compression according to the latest international guidelines (2005) for cardiopulmonary resuscitation (CPR). The aim of the present study was to compare manual CPR with LUCAS-CPR.
30 kg pigs were anesthetized and intubated. After a base-line period and five minutes of ventricular fibrillation, manual CPR (n = 8) or LUCAS-CPR (n = 8) was started and run for 20 minutes. Professional paramedics gave manual chest compression's alternating in 2-minute periods. Ventilation, one breath for each 10 compressions, was given to all animals. Defibrillation and, if needed, adrenaline were given to obtain a return of spontaneous circulation (ROSC).
The mean coronary perfusion pressure was significantly (p < 0.01) higher in the mechanical group, around 20 mmHg, compared to around 5 mmHg in the manual group. In the manual group 54 rib fractures occurred compared to 33 in the LUCAS group (p < 0.01). In the manual group one severe liver injury and one pressure pneumothorax were also seen. All 8 pigs in the mechanical group achieved ROSC, as compared with 3 pigs in the manual group.
LUCAS-CPR gave significantly higher coronary perfusion pressure and significantly fewer rib fractures than manual CPR in this porcine model.
[Show abstract][Hide abstract] ABSTRACT: Lund University Cardiopulmonary Assist System (LUCAS) is a new gas-driven CPR device providing automatic chest compression and active decompression. This is a report of the first 100 consecutive cases treated with LUCAS due to out-of-hospital cardiac arrest (58% asystole, 42% ventricular fibrillation (VF)). Safety aspects were also investigated and it was found that LUCAS can be used safely regarding noise levels and oxygen concentrations within the ambulance. A crash test (10G) showed no displacement of the device from the manikin. Of the 71 patients with witnessed cardiac arrest, 39% received bystander CPR. In those 28 patients where LUCAS-CPR was initiated more than 15 min after the ambulance alarm and in the 29 unwitnessed cases, none survived for 30 days. Of the 43 witnessed cases treated with LUCAS within 15 min, 24 had VF and 15 (63%) of these cases achieved a stable return of spontaneous circulation (ROSC) and 6 (25%) of them survived with a good neurological recovery after 30 days; 5 (26%) of the 19 patients with asystole achieved ROSC and 1 (5%) survived for over 30 days. One patient where ROSC could not be achieved was transported with on-going LUCAS-CPR to the catheter laboratory and after PCI for an occluded LAD a stable ROSC occurred, but the patient never regained consciousness and died 15 days later. To conclude, establishment of an adequate cerebral circulation as quickly as possible after cardiac arrest is mandatory for a good outcome. In this report patients with a witnessed cardiac arrest receiving LUCAS-CPR within 15 min from the ambulance call had a 30-day survival of 25% in VF and 5% in asystole, but if the interval was more than 15 min, there were no 30-day survivors.
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