An airline cardiac arrest program.

BACKGROUND: As many as 1000 lives are lost annually from cardiac arrest in commercial aircraft. Ventricular fibrillation (VF), the most common mechanism, can be treated effectively only with prompt defibrillation, whereas the current policy of most airlines is to continue cardiopulmonary resuscitation pending aircraft diversion. The objective of this study was to assess the impact of making semiautomatic external defibrillators (AEDs) available for use on airline passengers with cardiac arrest. METHODS AND RESULTS: AEDs were installed on international Qantas aircraft and at major terminals, selected crew were trained in their use, and all crew members were trained in cardiopulmonary resuscitation. Supervision was provided by medical volunteers or (remotely) by airline physicians. During a 64-month period, AEDs were used on 109 occasions: 63 times for monitoring an acutely ill passenger and 46 times for cardiac arrest. Twenty-seven episodes of cardiac arrest occurred in aircraft, often (11 of 27 [41%]) unwitnessed, and they were usually (21 of 27 [78%]) associated with asystole or pulseless idioventricular rhythm. All 19 arrests in terminals were witnessed; VF was present in 17 (89%). Overall, defibrillation was initially successful in 21 of 23 cases (91%). Long-term survival from VF was achieved in 26% (2 of 6 in aircraft and 4 of 17 in terminals). The ability to monitor cardiac rhythm aided decisions on diversion, which was avoided in most passengers with asystole or idioventricular rhythm. CONCLUSIONS: AEDs in aircraft and terminals, with appropriate crew training, are helpful in the management of cardiac emergencies. Survival from VF is practicable and is comparable with the most effective prehospital ambulance emergency services. Costly aircraft diversions can be avoided in clearly futile situations, enhancing the cost-effectiveness of the program.

The revolution and evolution of prehospital cardiac care.

Prehospital cardiac care, first established in Belfast, Northern Ireland, in 1966, may be called revolutionary in that it was a radical break from existing practices. The Belfast program "moved" the coronary care unit into the community by treating the early complications of acute myocardial infarcation. The program staffed a mobile coronary care unit with a physician and nurse and demonstrated that patients with out-of-hospital sudden cardiac arrest could be resuscitated. The idea of prehospital cardiac care spread to other countries after publication of the Belfast experience in the Lancet. The first program in the United States, stationed at St Vincent's Hospital in New York, NY, began in 1968 and was modeled after the Belfast program. The physician-staffed model, however, was not widely imitated in the United States. Rather, beginning in 1969, programs using specially trained personnel, know as paramedics, began in Miami, Fla, Seattle, Wash, Columbus, Ohio, Los Angeles, Calif, Portland, Ore, and Nassau County, New York. Paramedic-staffed programs were designed not only to treat early complications of acute myocardial infarction, but also to attempt resuscitation for primary cardiac arrest. Most of the early paramedic programs were based in fire departments. Other programs used private ambulance or police personnel. Prehospital cardiac care has evolved significantly in the past 3 decades. Some notable developments include the tiered response system, training of the general public in cardiopulmonary resuscitation, low-energy defibrillators, automatic external defibrillators, and 12-lead electrocardiographic telemetry. The basic lesson of prehospital cardiac care is that the timely provision of cardiopulmonary resuscitation and defibrillation saves lives.

Thrombolytic therapy in cardiogenic shock: effect of increased aortic pressure and rapid tPA administration.

OBJECTIVES: To investigate the effect of an increase in aortic pressure combined with rapid tissue plasminogen activator infusion on hemodynamic stability and patency of the infarct-related artery in patients with acute myocardial infarction complicated by profound hypotension or cardiogenic shock. BACKGROUND: Thrombolytic therapy improves mortality in relatively stable patients with acute myocardial infarction but not in patients with cardiogenic shock. Recent canine studies have demonstrated that a moderate increase in low aortic pressure improves thrombolysis. Conceivably, then, decreased thrombolytic efficacy in cardiogenic shock is due, at least in part, to a low aortic pressure impairing delivery of the thrombolytic agent. PATIENTS AND METHODS: For patients presenting within 6 h of an acute myocardial infarction complicated by profound hypotension or cardiogenic shock, an inotropic agent was rapidly administered to increase the systolic aortic pressure to approximately 110 mmHg, and 100 mg of tissue plasminogen activator was administered intravenously over 45 to 60 mins. RESULTS: Eight consecutive patients meeting the study criteria were treated over 18 months. In six of eight patients, the inotropic agent increased systolic blood pressure over 10 mins, from a mean of 64 +/- 12 mmHg to 102 +/- 12 mmHg. In the two patients whose blood pressure did not increase, early angiography in one demonstrated occlusion of the infarct-related artery, and both of the patients died. In the other six patients there was clinical and hemodynamic evidence of early reperfusion, and infarct-related arteries were patent on angiography. These six patients survived at least 30 days, with four having a favourable clinical outcome and two having a functional limitation due to heart failure. CONCLUSIONS: These results are consistent with experimental data indicating that an increase in aortic pressure combined with rapid tissue plasminogen activator infusion may increase thrombolytic efficacy when an acute myocardial infarction is complicated by profound hypotension or cardiogenic shock.

Dynamic left ventricular outflow tract obstruction due to concentric left ventricular hypertrophy: effect of pacing with a short AV interval.

Dual chamber pacing with a short atrioventricular (AV) interval has emerged as a novel therapeutic approach in dynamic left ventricular outflow tract obstruction. A morbidly obese 65-year-old man with previous borderline hypertension and documented normal coronary arteries and concentric left ventricular hypertrophy who underwent uneventful elective hip replacement is reported. Eight hours postoperatively the patient developed junctional tachycardiac and hypotension. Echocardiogram revealed concentric left ventricular hypertrophy with dynamic left ventricular outflow tract obstruction and peak gradient of 262 mmHg. The patient improved with intravenous fluid replacement. The gradient fell to 112 mmHg 14 days later. Twelve days later the patient developed symptomatic sinus pauses and a dual chamber pacemaker was implanted. After testing various AV intervals, the lowest gradient of 138 mmHg was associated with an AV interval of 100 ms. One year later the gradient was 37 mmHg at the same AV interval, with a higher gradient at shorter and longer AV intervals. Dual chamber pacing with a short AV interval has been associated with improvement in hypertrophic obstructive cardiomyopathy. This case suggests the benefit of this therapy may extend to acquired forms of dynamic left ventricular outflow tract obstruction such as concentric left ventricular hypertrophy.

Return to arc welding following defibrillator implantation.

A male arc welder who was fitted with an implantable defibrillator wished to return to his former employment. Device testing and ambient magnetic field measurements were performed at his place of work. During welding, artifacts were seen on the intracardiac electrogram but there was no resulting disturbance of sensing function. Measured field strengths were too low to result in device inactivation. The patient resumed his work without incident. This appears to be the first reported case of a patient with an implantable defibrillator returning to this "electrically hostile" environment following thorough screening.

Deaths from ischaemic heart disease in Belfast.

There were 1323 deaths due to ischaemic heart disease in Belfast from 20 July 1981 to 19 July 1982. Some 496 (37%) of these were in persons aged less than 70 years. By World Health Organisation criteria 247 (19%) of these deaths were classified as definite myocardial infarction and 749 (57%) as possible myocardial infarction. Dyspnoea, collapse, and typical pain were the main symptoms at the onset of the fatal attack. In hospital only 12% of deaths in persons aged less than 70 years and 14% of those aged greater than or equal to 70 years were due to presumed primary rhythm disturbance, whereas outside hospital these proportions were 78% and 59% respectively. The median survival time was 84 minutes and was shortest in men aged less than 70 years (62 minutes). Outside hospital a relative was the most likely aid sought initially (70%) and the median delay time from onset of symptoms to calling for medical aid was eight minutes. Among 128 witnessed deaths in persons aged less than 70 years occurring outside hospital due to presumed primary rhythm disturbance the median survival time was 8 X 25 minutes. Improvements in facilities available for resuscitation including public education could result in the prevention of a proportion of deaths caused by primary rhythm disturbances.

Left atrial rhabdomyosarcoma and the use of digital gated computed tomography in its diagnosis.

A case of left atrial rhabdomyosarcoma presenting in a patient with known mitral stenosis is described. Computed tomography of the left atrium, gated to the electrocardiogram cycle, was used to visualise the site and extension of the tumour.

Amiodarone-induced hypothyroidism. A common complication of prolonged therapy: a report of eight cases.

Amiodarone is a widely used antiarrhythmic drug, which contains 75 mg of iodide per 200 mg of active substance. Eight of our patients receiving long-term amiodarone therapy became hypothyroid. Seven of these patients had no previous history of thyroid dysfunction or goiter. Antithyroid antibodies were absent, and standard perchlorate discharge tests were positive in seven patients when hypothyroidism was diagnosed. In one patient, amiodarone therapy was withdrawn; over the next nine months, the hypothyroidism resolved, and results of the perchlorate discharge test reverted to normal. We conclude that amiodarone-induced hypothyroidism is similar to previously described iodide-induced hypothyroidism. It may develop in the absence of a previous history of thyroid disease, and all patients receiving long-term amiodarone therapy should therefore be regularly monitored for hypothyroidism.

Atrial pacing: intracardiac conduction assessed by his bundle electrograms acquired from the permanent atrial electrode at implantation.

His bundle electrograms were recorded from conventional J-shaped atrial electrodes at implantation in twelve consecutive patients who had sinus node disorder. Five patients with impairment of atrioventricular conduction, received atrioventricular (DVI) pacemakers. His bundle recording by this method is simple and reliable, avoids the discomfort of the conventional technique, and represents a new application for the well established atrial "J" electrode.

Calcium antagonists and beta blockade--a useful combination.

Treatment of angina with a single drug often proves unsatisfactory because of dose-related unwanted effects or occasionally an adverse effect on the angina. A combination of a beta-blocking agent and a calcium antagonist drug might achieve satisfactory control of angina at acceptable doses of each drug. Widespread application of combination therapy would, however, be inappropriate if the beta-blocker component were to have adverse effects among patients with rest pain as a prominent symptom, suggestive of coronary 'spasm'. The reported adverse effects of beta-blocking agents are likely to be related to bradycardia and are not apparent if excessive slowing is avoided by individual dose adjustment or if bradycardia is corrected by pacing. Supposed failure of these agents to control cardiac pain not infrequently results from inadequate dosage. Combination therapy will attenuate the increases in heart rate and contractility resulting from stress while coronary perfusion will be maintained and the associated level of arterial blood pressure reduced. The theoretical benefits have been confirmed in clinical investigations in which the effect of combination therapy has been compared with that of one or both of the constituent drugs given alone. Reports of bradycardia (specific to inclusion of verapamil in the combination), hypotension or cardiac failure developing during combination therapy emphasize the need for careful dose titration of both beta-blocker and calcium antagonist in each patient. The possible additional role of nitrates is undefined, but inclusion of these agents is likely to prove especially valuable where left ventricular function is grossly impaired and in the management of unstable angina.

Beta-sympathetic blockade with chronotropic compensation in the management of heart disease.

This presentation briefly describes the sympathetic and parasympathetic control of the heart, particularly in relation to coronary vascular effects. Autonomic disturbances following myocardial infarction and their significance are discussed. The influence of the autonomic system in chronic coronary heart disease is considered, particularly in relation to the beneficial effects which may be obtained by the combined use of beta-blocking drugs and cardiac pacing. Nine anginal patients with spontaneous or drug-induced bradycardia received temporary pacing and 27 others had pacemakers implanted. Pain was well controlled in the former group. Long term pacing produced worth-while benefit in 67% of the patients followed for periods up to 6 months, the figure falling to 50% among those followed for 24 months. Eight of the 27 relapsed. Thus, correction of bradycardia by pacing often produced a beneficial long term effect. A second group of 14 patients with ventricular arrhythmias was treated with beta-blocking agents combined with pacing. So far, 10 of these 14 have had their arrhythmias controlled either by the initial or by a modified drug regime. The results indicate that among patients with chronic coronary artery disease, beta-blockade to minimize cardiac sympathetic activity, coupled with pacing to prevent loss of chronotrophic control, often represents an effective combination for the management of refractory angina or arrhythmias.

D.C. conversion in patients on amiodarone.

3 patients with atrial fibrillation, of varying origin, have been successfully converted to sinus rhythm by D.C. shock while on the antiarrhythmic drug amiodarone. D.C. shock did not cause rhythm disturbance. D.C. conversion may not be contraindicated in patients taking amiodarone.

Amiodarone-induced ventricular fibrillation.

Amiodarone, 600 mg orally daily, was used in an attempt to control supraventricular tachyarrhythmias in a patient with the sick sinus syndrome. Twenty days from the onset of therapy the Q-T interval lengthened. Episodes of ventricular flutter, ventricular fibrillation and self-terminating ventricular tachyarrhythmia (torsade de pointes) developed on the 28th day of amiodarone therapy. Temporary cardiac pacing prevented further episodes of ventricular fibrillation. Despite the suggestion that this drug may be given in large doses for long periods of time since it has a wide safety margin, we feel that the risk of lethal arrhythmias is such that caution is required in its use.