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In a postmortem study of the hearts of two young women who died suddenly and unexpectedly, we found a remarkably similar and distinctive ganglionitis, predominantly in the region of the sinus node. Both women had ventricular fibrillation at the time of collapse. Vesicular neuritis and older neural degeneration were present in other regions of the heart. Except for focal fibromuscular dysplasia of the sinus node artery and atrioventricular node artery of one heart, there was no other significant anatomic abnormality in either heart. The functional significance of this cardiac ganglionitis is unclear, but its location in and around the conduction system makes it a possible cause of the fatal electrical instability. Recognition that ganglionitis of the heart may be associated with sudden death should stimulate a number of additionally useful studies.
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PMID:Cardiac ganglionitis associated with sudden unexpected death. 49 5

Clinical and pathologic changes in 87 patients who could not be resuscitated from an episode of sudden cardiovascular collapse are described and compared with observations from patients in the same community who were successfully resuscitated from ventricular fibrillation. Findings in patients who died suddenly generally did not differ when the patients were groups by electrocardiographic rhythm on arrival of the mobile coronary aid unit. The pathologic changes of acute thrombosis and recent myocardial infarction did not occur with sufficient frequency in the entire group to be considered causally related to the sudden collapse, occurring in 10 and 5 percent of cases, respectively. Although most patients had evidence of obstructive coronary disease and old myocardial infarction, 8 percent had no significant vascular disease, acute thrombosis, myocarditis or valve disease that might be implicated as a factor in sudden death. There was no relation between age and severity of obstructive coronary disease or frequency of old myocardial infarction in patients who died suddenly. Complete atherosclerotic occlusion in one or more coronary vessels occurred in 51 of 87 (59 percent) and old myocardial infarction in 48 of 87 (55 percent). Although the mean age of this autopsy population was similar to that of all patients in the community who have had ventricular fibrillation on arrival of the aid unit, the nonsurvivors had a greater incidence of myocardial infarction and symptomatic heart disease (73 of 87) than did survivors. Comparison of this autopsy group with persons from the community who were resuscitated from ventricular fibrillation and subsequently had coronary angiograms indicates that the severity of coronary stenosis does not distinguish between survivors and nonsurvivors of an episode of ventricular fibrillation and suggests that other factors influence the outcome of an episode of ventricular fibrillation.
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PMID:Pathology of the heart in sudden cardiac death. 87 Nov 13

The first phase of accidental drowning begins with asphyxia, due to either laryngospasm (10-15 percent of cases) or water aspiration. The second phase is characterized by water and electrolyte changes in the blood. The physiopathological modifications caused by drowning in fresh water differ from those of drowning in sea water. The hypotonic fresh water quickly diffuses in the bloodstream. The consequences are, in many cases, hypervolemia with pulmonary edema, hemolysis, hyperkalemia with risk of ventricular fibrillation, diminution of hemoglobin, and a relative decrease in plasma concentration of Na, Cl, Ca, and albumin. Further, inactivation and washing out of the anti-atelectasis factor from the alveoli by fresh water facilitate the formation of atelectasis. In cases of accidental drowing in sea water the osmotic gradient is in inverse: the electrolytes of aspirated salt water diffuse in the circulation, whereas the blood serum and the plasma albumin pass into the alveoli. Acute pulmonary edema often follows these pathological changes. Hypovolemia with circulatory collapse, hemoconcentration with rise in hemoglobin, hematocrit, sodium, potassium and albumin, and, finally, an elevated risk of thromboembolism due to increased blood viscosity, represent further complications. On the other hand, ventricular fibrillation is rare, hemolysis is absent and atelectasis usually does not occur.
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PMID:[Physiopathology of accidental drowning]. 112 62

In 56 patients, frequency analysis of the electrocardiogram of ventricular fibrillation exhibited power spectra with a distinct dominant frequency. The greatest success for resuscitation from ventricular fibrillation is recorded when ventricular fibrillation develops after the patient comes under coronary care. Of the 41 patients in whom the onset and first 8 s of ventricular fibrillation were artefact-free the mean dominant frequency of primary ventricular fibrillation (no cardiogenic shock or cardiac failure) in 21 patients was 6.2 +/- 0.2 Hz, significantly higher than the mean dominant frequency of the first 8 s of secondary ventricular fibrillation (cardiogenic shock or heart failure) (4.0 +/- 0.2 Hz, 20 patients, p = 0.0001). In these patients the peak-to-trough amplitude (ECG) of the first 8 s of ventricular fibrillation was similar in both primary and secondary ventricular fibrillation as was the mean duration of ventricular fibrillation prior to the first DC shock. There was a significantly lower success rate for resuscitation from secondary ventricular fibrillation (6 of 20 patients) compared with resuscitation from primary ventricular fibrillation (18 of 21 patients, chi 2 17.8, p = 0.001). Of the remaining 15 patients who were collapsed between 3 and 20 min before the arrival of the mobile coronary care unit, the dominant frequency of the first 8 s of ventricular fibrillation fell with increased duration of collapse (from 5.5 Hz at 3 min to a mean of 2.1 Hz at 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Frequency analysis of ventricular fibrillation and resuscitation success. 843 54

Early external defibrillation is the single most effective intervention in patients with out-of-hospital cardiac arrest. Literature data indicate that instructing emergency medical technicians (EMTs) to use defibrillators is beneficial, provided the local emergency medical system is well organized. We tried to estimate the potential benefit of early defibrillation in some centres in Belgium by retrospectively analyzing the data from the Belgian Cardio-Pulmonary-Cerebral Resuscitation Registry collected between 1983 and 1987 in Belgian centres with a Mobile Intensive Care Unit (MICU). The data show that 2310 out of 3371 patients (69%) were first attended by the EMTs; on subsequent arrival of the MICU-teams, 584 of these 2310 patients i.e. 17% of the whole study population, presented with ventricular fibrillation. Analysis of estimated time factors in these 2310 patients revealed that the median time interval between collapse and start of resuscitation by EMTs was 8 min; the median time interval between collapse and start of MICU-resuscitation attempts was 16 min. The duration of EMT-resuscitation before MICU-arrival was probably more than 5 min and 10 min in 58% and 23% of the cases respectively. It is concluded that EMTs can be expected to reach a substantial number of ventricular fibrillation victims within a few minutes after the collapse and many minutes before arrival of the MICU. Therefore, training of EMTs in the use of semi-automatic defibrillators seems worthwhile in MICU-served regions in Belgium.
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PMID:Should semi-automatic defibrillators be used by emergency medical technicians in Belgium? The Belgian Cerebral Resuscitation Study Group. 131 84

A 63-year-old female was admitted to the hospital because of collapse. She had no history of cardiovascular disease. Prior to admission she used co-trimoxazole, paracetamol, calcium tablets and 50 mg terodiline (Mictrol) daily because of bladder instability. Electrocardiography showed QT prolongation and polymorphous ventricular tachycardia with torsades de pointes. During admission she developed ventricular fibrillation, needing defibrillation. After withdrawal of terodiline and treatment with isoprenaline the symptoms and all ECG abnormalities disappeared. In this case terodiline was suspected of having been the causative agent. Terodiline shows structural resemblance to the anti-arrhythmic agent prenylamine, a known cause of torsades de pointes. Recently terodiline has been temporarily withdrawn from the worldwide market in order to investigate the causal relationship between this drug and cardiac arrhythmia and conduction disturbances.
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PMID:[Polymorph ventricular tachycardia with torsades de pointes caused by administration of terodiline (Mictrol)]. 137 Jul 30

The efficacy of lidocaine to prevent ventricular fibrillation during the prehospital phase of suspected acute myocardial infarction was assessed 3 hours after administration in a randomized controlled trial. A total of 204 patients examined within 6 hours after onset of symptoms were included, and acute myocardial infarction was later confirmed in 63% of these. Lidocaine, administered as a 100 mg intravenous bolus dose followed by a 300 mg intramuscular injection, failed to prevent ventricular fibrillation, which was observed in 2 (2.1%) of 96 patients in the lidocaine group and in 3 (3.0%) of 101 patients in the placebo group (p = 0.95; odds ratio 0.7, 95% confidence interval 0.4 to 1.3). In addition, sudden cardiac collapse with unknown heart rhythm was observed in three patients who received lidocaine (3.1%) compared with none in the placebo group (p = 0.23; odds ratio 7.6, 95% confidence interval 2.8 to 22.1). The results of this small study suggest that lidocaine, even when given in a high dose, is ineffective in preventing ventricular fibrillation when administered before hospitalization for suspected acute myocardial infarction. Prophylactic use of lidocaine in this situation may therefore not be warranted or advisable.
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PMID:Lidocaine to prevent ventricular fibrillation in the prehospital phase of suspected acute myocardial infarction: the North-Norwegian Lidocaine Intervention Trial. 146 2

The literature on isolated right ventricular infarction is reviewed and local experience is reported. Chronic lung disease is an important risk factor. Chest pain and breathlessness are common. Syncope and sudden collapse can also occur. Rhythm disorders include sinus bradycardia, atrial fibrillation and ventricular tachycardia or fibrillation. Atrioventricular block is rare. Hypotension and a right-sided fourth heart sound are common. Cautious use of slow-release nitroglycerin is not hazardous in the absence of hypotension. High doses of steroids and anticoagulants can be helpful. The prognosis is usually good, although sudden collapse can occur due to ventricular fibrillation, rupture of the right ventricular free wall or massive pulmonary embolism.
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PMID:Isolated right ventricular infarction. 151 57

The first link in the "chain of survival" concept is the activation of the emergency medical system (EMS) by a bystander after recognition of cardiac arrest (CA) or its immediate prodrome. Our ongoing study is aimed at evaluating the current effectiveness of bystander EMS activation for all cases of CA in the city and area of Mainz. Methods. Starting February 1991, we began to prospectively examine collapse-intervention intervals in all cases of CA treated by our physician-manned ambulance. Precision voice recorders carried by the ambulance crews are activated and linked to the EMS dispatcher to time the arrival of the ambulance vehicle. Time intervals starting from the time of collapse are then reconstructed from the dispatcher's time and the tapes. The emergency phone number dialled initially by the bystander and the time of collapse in witnessed cardiac arrests are identified. RESULTS. Sixty-six CAs were witnessed and included in this study. In 20% of those cases, the number dialled initially by the bystander was 19222 (EMS dispatcher), in 38% 110 (police), and in 42% other numbers (family practitioners or their on-call service, fire department). The time interval, as median (25th percentile; 75th percentile), between collapse and receipt call by the emergency dispatchers was 4 min (2; 8) for all patients (n = 66), and 6.5 min (3; 12) whenever numbers other than emergency phone numbers were dialled. All following time intervals (start of BLS or ACLS procedures) showed differences (P less than 0.05) between the 110 or 19222 group [BLS: 8.5 min (4.8; 13.1) or 10 min (7.35; 12.1); ACLS: 11.3 min (9.1; 13.45) or 12.9 min (10.6; 21.5)] vs the group, in which other phone numbers were initially dialled [BLS: 15.25 min (9.25; 19.4); ACLS: 20.11 min (12.6; 28.3)]. The first ECG rhythm showed VF in 56% and 54% in case 110 and 19222 were dialled, but only in 32% in the other group. CONCLUSION. Even one single weak link in the "chain of survival" can lower overall survival rates. An indispensable, but apparently underrated component of an effective EMS includes an informed citizenry able to call swiftly for help. Lack of an unequivocal emergency number, well known and accepted by the citizens, produces confusion and delays. In our systems, the correct medical emergency phone number (19222) was dialled in 20% of the cases only, thus demonstrating clearly the lack of public awareness of this 5-digit number. In a higher percentage, the three-digit police number (110) was dialled. In cases where numbers other than emergency numbers were dialled (42%), the longest time intervals between collapse and receipt of call by the dispatchers occurred, associated with the longest time intervals until initiation of CPR and the lowest percentage of patients found in ventricular fibrillation. We conclude that establishment of a simple three-digit EMS phone number, preferentially Europe-wide, in combination with an intensification of public awareness, could be a vital step not only to reduce time intervals between collapse and CPR in our EMS system but also to improve survival.
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PMID:[The emergency telephone number--the essential weak link in an emergency system. Prospective studies involving cardiac arrests observed by bystanders]. 163 20

Nine patients (eight males) are reported with one or more episodes of circulatory collapse in the absence of overt heart disease or other known causes of arrhythmias; sudden arrhythmic death occurred in one of these patients. Age at first episode ranged from 16 to 41 (mean, 28) years. In seven patients, ventricular fibrillation was documented at the time of resuscitation. One patient had ventricular flutter. In the remaining patient, documentation of the arrhythmia during the collapse was not available. Four patients had frequent early ventricular premature beats, and in three of these patients, they were accompanied by episodes of rapid nonsustained polymorphic ventricular tachycardia. Failure to suppress this ectopic activity by drug therapy seems to be of prognostic significance. Of the three patients showing persistence of frequent early ventricular premature beats, one died suddenly, and two had recurrences of symptomatic arrhythmic episodes. The value of noninvasive and invasive tests in the management of these patients is not clear, with the exception of exercise testing in patients with exercise-related arrhythmias and long-term electrocardiographic monitoring in patients with frequent spontaneous ventricular ectopic activity. Follow-up varied from 21 to 192 (mean, 84) months. One patient died suddenly 21 months after his first collapse. Selection of antiarrhythmic drug therapy was largely empirical. In view of the relative rarity of sudden arrhythmic death in the absence of heart disease and the many uncertainties about its mechanism(s) and management, a worldwide registry of these patients is suggested.
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PMID:Sudden arrhythmic death without overt heart disease. 172 10


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