Symposium Lectures

SUDDEN CARDIAC DEATH IN THE COMMUNITY Out-of-hospital cardiac arrest: whom do we save and what is the outcome? Of the 137,000 deaths from coronary disease per annum, approximately 50% die before reaching hospital. In a significant proportion of the deaths, this is the first presentation of coronary artery disease. Relatively little is known about the exact cause of these deaths or how to predict those patients at highest risk of sudden death. In a recent review of the 320 people suffering an out-of-hospital cardiac arrest (OHCA) in the Edinburgh area, only 80 reached hospital alive and of these, only 40 were discharged from hospital. This represents a 12% survival rate! Possible areas for improvement include early recognition of cardiac arrest, by-stander cardiopulmonary resuscitation (CPR), reduced response time of the emergency services, early defibrillation (where appropriate) and early transfer to hospital. To treat appropriately patients suffering an OHCA, predictors of outcome would help. In another study, several factors were associated with an improved outcome. Cardiopulmonary resuscitation by a trained operator significantly improved outcome when compared to CPR by an untrained person or family member: from 30 to 60%. Outcome was further improved when CPR was performed by trained ambulance personnel to above 70%, possibly due to the early use of defibrillation. The clinical state of the patient also predicted outcome: self-ventilation was a good prognostic factor as was an initial presenting cardiac rhythm of ventricular tachycardia (VT) or ventricular fibrillation (VF) rather than electromechanical dissociation (EMD) or asystole. In addition, neurological status on admission as assessed by the Glasgow Coma Scale (GCS) correlated with survival. The majority of survivors admitted to hospital die before discharge from sequelae of ischaemic brain injury rather than cardiac failure. Indeed, cardiac status is a poor indicator of outcome in these patients. In a follow-on study of OHCA patients, cognitive dysfunction was assessed at least six months after discharge. Over 95% were discharged to their own home while the others were discharged to further-care institutions. Thirty-five patients were compared with a control group made up of patients who suffered a myocardial infarction with no cardiac arrest. In the controls, cognitive function was within normal limits; in 40% of patients with an OHCA significant memory impairment was observed. This was chronic, persisting at three year follow-up and it appears to be due to generalised brain atrophy (associated with a general reduction in brain mass) rather than due to damage to specific areas of the brain in OHCA patients. Currently, no other specific tests will predict survival. However, two plasma markers of neuronal damage have been proposed as possible candidates; neuron specific enolase (NSE), which despite its name is also found in red blood cells, and plasma S-100, which are both elevated following significant brain injury. In 143 OHCA patients studied prospectively at 24–48 hours and 72–96 hours, plasma concentration of these markers were correlated to outcome. Neuron specific enolase was shown not to be specific as marked overlap was noted between survivors and nonsurvivors. However, detection of plasma S-100 over a certain concentration predicted a mortality of 100%. Plasma S-100 concentrations also relate to significant memory deficit in the survivors. However, this plasma concentration was three times higher than previously quoted and clearly more research in this area is needed. In the future, the development of plasma markers alongside clinical details may allow more appropriate triage and treatment for those suffering an OHCA as well as counselling relatives about the likely outcome.