The management of arrhythmias following an acute myocardial infarction

Arrhythmias are extremely common early after AMI. An arrhythmiasis defined by exclusion, either because the sequence of myocardial depolarisation is other than normal or because certain arbitrary limits are exceeded. It follows that the term arrhythmia encompasses a complex heterogeneous group. Although arrhythmias are defined in electrical terms they are only important because of their immediate, delayed or potential haemodynamic consequences. These occur because of changes in heart rate, loss of atrial transport function, increased myocardial oxygen consumption, decreased myocardial blood flow or loos of synchronicity of ventricular contraction. The sensible and effective management of arrhythmias following acute myocardial infarction requires an appraisal of the haemodynamic consequences, if any, which follow the initiation of the arrhythmia. The indications for treating an arrhythmia must be the immediate, delayed or potential haemodynamic loss rather than the mere preseence of a rhythm which falls outside the limits of normal. This distinction is perhaps most clearly seen in the case of atrio-ventricular conduction disturbances.     

Overview of contemporary reperfusion strategies in acute ST-elevation myocardial infarction

The rupture of an atherosclerotic plaque in an epicardial coronary artery with subsequent occlusive coronary thrombosis has been established as the decisive event in the pathogenesis of an acute coronary syndrome, which encompasses the clinical entities of unstable angina, non-ST- and ST-elevation myocardial infarction. This article focuses on contemporary treatment strategies for patients with acute ST-elevation myocardial infarction and reviews the role of pharmacologic thrombolysis and mechanical reperfusion by percutaneous transluminal approaches. Statements of the latest guidelines for the treatment of ST-elevation myocardial infarction are included, as well as some recently distributed information not covered by the guideline publications. Finally, some future perspectives for the treatment of acute ST-elevation myocardial infarction are outlined.     

Overview of contemporary reperfusion strategies in acute ST-elevation myocardial infarction

The rupture of an atherosclerotic plaque in an epicardial coronary artery with subsequent occlusive coronary thrombosis has been established as the decisive event in the pathogenesis of an acute coronary syndrome, which encompasses the clinical entities of unstable angina, non-ST- and ST-elevation myocardial infarction. This article focuses on contemporary treatment strategies for patients with acute ST-elevation myocardial infarction and reviews the role of pharmacologic thrombolysis and mechanical reperfusion by percutaneous transluminal approaches. Statements of the latest guidelines for the treatment of ST-elevation myocardial infarction are included, as well as some recently distributed information not covered by the guideline publications. Finally, some future perspectives for the treatment of acute ST-elevation myocardial infarction are outlined.     

The acute myocardial infarction

Cardiovascular death is the number one cause of death in the United States, with a rate that is more than double that for cancer. Over half of these cardiovascular deaths are due to acute myocardial infarction. Management of the patient with acute myocardial infarction during and after hospitalization is discussed with an emphasis on primary and secondary prevention, patient autonomy and decision making. There is also a review of the directions that treatment of acute myocardial infarction will take in the future.     

Peripartum acute myocardial infarction: management perspective

Acute myocardial infarction in pregnancy and puerperium is an uncommon event with substantial morbidity and mortality rates. Atherosclerosis may be the cause, but often the coronary arteries are healthy at angiography. In such cases, the suggested mechanism is a decreased coronary perfusion related to coronary spasm or in situ thrombosis. Most pregnant women who died after myocardial infarction did so at the time of initial infarction, and maternal mortality was greatest if the infarction was late in pregnancy. Increasing cardiovascular stresses of late pregnancy, especially when intensified by parturition, seriously compromise women with ischemic heart disease. Therefore, there should be efforts to limit myocardial oxygen demand throughout pregnancy, and particularly during parturition. It is important for diagnosis to have increased awareness of its possible occurrence. Although principles of management can be generalized, it is necessary to provide individualized care for these high-risk patients by a multidisciplinary team of cardiologists, anesthesiologists, and obstetricians.     

Clinical management of the patient with an acute myocardial infarction.

The clinical care of patients with myocardial infarction has evolved to embrace not only palliative measures but also strategies to decrease pre-hospital delay and direct interventional measures to promote myocardial salvage. Thrombolysis has emerged as a therapy that significantly improves mortality and morbidity, particularly if administered early in the infarction process. Major thrombolytic agents and their administration schedules, adverse reactions, and adjunctive therapies are reviewed.     

Advances in the early diagnosis and management of acute myocardial infarction.

The effective early diagnosis of acute myocardial infarction still rests primarily on the clinical history and the electrocardiogram. ST segment elevation is specific though sometimes short lived and less than ideally sensitive; but with bundle branch block it defines a population that benefits importantly from thrombolysis. Novel electrode configurations can further enhance diagnosis but have not become popular. Biochemical markers are rarely of help in the first four hours and cardiac scanning is impractical for routine care. Computerised diagnostic systems show promise in prototype but are not widely available. Early management involves reestablishing coronary flow by thrombolytic and antithrombotic agents and reducing myocardial oxygen requirement by analgesics and beta blockers. Nitrates and magnesium have limited roles. Immediate access to defibrillation and advanced life support is mandatory. Diagnosis and management can only begin after help has been sought. Public alertness to the symptoms of myocardial infarction and a coordinated response by health care personnel are fundamental to successful care.     

Drug-induced myocardial ischemia and acute myocardial infarction.

Myocardial infarction generally occurs in the presence of known risk factors and identifiable coronary artery disease. Atypical presentations due to therapeutic and illicit drug use are documented, however, and lead to the consideration of alternative pathophysiologic rationales for myocardial infarction. This article discusses central nervous system stimulants and other drugs that have the potential for myocardial damage and their nursing implications.     

Thrombolysis after acute myocardial infarction.

Appropriate use of a thrombolytic agent may save 20 to 30 lives per 1000 treatments. Thrombolysis should be considered in all patients presenting with cardiac chest pain lasting more than 30 minutes for up to 12 hours after symptom onset. ECG criteria include ST elevation of at least 1 mm in limb leads and/or at least 2 mm in two or more adjacent chest leads or left bundle branch block. There is no upper age limit. All patients should also receive oral aspirin and subcutaneous (intravenous with rt-PA) heparin. Other adjuvant treatments have been reviewed previously in this journal. Streptokinase is the drug of choice except where there is persistent hypotension, previous streptokinase or APSAC at any time, known allergy to streptokinase, or a recent proven streptococcal infection. In these circumstances the patient should receive rt-PA. Additional indications for rt-PA, based on subset analysis by the GUSTO investigators, include patients with ALL of the following: age less than 75 years, presentation within four hours of symptom onset, and ECG evidence of anterior acute myocardial infarction. Treatment should be initiated as soon as possible. The greatest benefit is observed in patients treated early, pain to treat intervals of less than one hour make possible mortality reductions of nearly 50%. "When" matters more than "where": fast tracking to the CCU is one option but A&E initiated thrombolysis is feasible and timely. Prehospital thrombolysis is appropriate in certain geographical situations. The development of practical guidelines for thrombolysis represents the most comprehensive example of evidence based medicine. Streptokinase was first shown to influence outcome in acute myocardial infarction nearly 40 years ago. More recently alternative regimes have been evaluated in several prospective randomised controlled trials yielding pooled data on nearly 60,000 patients. However, systematic review of cumulative data reveals a statistically significant mortality gain for intravenous streptokinase over placebo which could have been identified as early as 1971-at least 15 years before it became generally used in clinical practice.