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Fibrinolytic therapy (see below) should be given as soon as possible because it results in coronary vessel recanalization and a significant reduction in mortality. During an acute myocardial infarction, lethal arrhythmias may occur. Patients should therefore be admitted to the coronary care unit (CCU) as soon as possible. Here, the ECG should be monitored continuously for the first 48 hours to allow the detection of arrhythmias such as ‘R on T’ ventricular ectopic beats, which may precipitate ventricular fibrillation. Ventricular fibrillation must be recognized promptly and resuscitation started immediately. Therefore, patients should not be kept in casualty departments waiting for ECGs and chest X-rays but should be admitted immediately to the CCU. If this is not possible then the accident and emergency department must have the staff and facilities to provide the treatment required in the first few hours.

A 12-lead ECG showing an acute anterolateral myocardial infarction.

A 12-lead ECG showing an acute anterolateral myocardial infarction.

AN INTRAVENOUS CANNULA is always inserted so that emergency intravenous medication can be administered, e.g. iv. magnesium.
THE PAIN OF MYOCARDIAL INFARCTION should be treated promptly with powerful analgesics such as morphine (10-20 mg i.v. or s.c.) or diamorphine (5-10 mg i.v. or s.c.) combined with antiemetics such as cyclizine (50 mg i.v.) or metoclopramide (10 mg i.v.). OXYGEN is usually given routinely because during an acute myocardial infarction the arterial Po, is reduced. Oxygen at 60% is administered by face mask or nasal cannulae for several hours following myocardial infarction.
FIBRI OLYTle THERAPY should be considered as soon as the diagnosis is suspected regardless of age if there is no contraindication. These agents can achieve early reperfusion in 50-70% of patients (compared with a spontaneous reperfusion rate of less than 30%) and have been shown to reduce the extent of ventricular damage, and the early and I-year mortality rates associated with myocardial infarction. A reduction in expected mortality of up to 30% is possible if these agents are given within he first 3-6 hours following infarction, but some benefit may be achieved even up to 24 hours. Although many physicians administer these drugs on the history alone, provided there are no contraindications it is desirable that typical electrocardiographic evidence of early infarction should also be available prior to their administration. Oral aspirin therapy (150 mg daily) should accompany the fibrinolytic therapy and be continued for at least 4 weeks after infarction.
Three fibrinolytic agents are currently licensed for use in acute myocardial infarction. Streptokinase is most commonly used. The recommended doses of these drugs are shown. Recombinant tissue plasminogen activator (rt-PA) achieves higher reperfusion rates than the other two agents, and when it is administered early and in association with full heparinization leads to a definite (14%) reduction of 30 day mortality. It is, however, associated with a slight increase in stroke and is more expensive than non-selective fibrinolytics. Although the single-injection administration of anistreplase confers some advantage over the other two agents (both of which are given as an intravenous infusion of at least 1 hour), this is also considerably more expensive than streptokinase. Both streptokinase and anistreplase increase the patient’s antistreptokinase antibody level, which falls to baseline levels after 3-6 months. These antibodies reduce  the effectiveness of a repeat dose and theoretically increase the risk of an anaphylactic reaction. Repeat usage of these drugs within 3 months is therefore not recommended. If repeat administration is deemed necessary, it should be preceded by intravenous methylprednisolone. The use of rt- PA, or even urokinase (neither of which provokes antibody formation), is preferable in these circumstances. Because of the small risk of bleeding following fibrinolytic therapy, all patients should have their blood group assessed in case of the need for transfusion. Because of the risk of reperfusion arrhythmias, patients should be monitored during and after fibrinolytic therapy. The ventricular arrhythmias that develop are usually short-lived and do not require treatment, but, rarely, ventricular fibrillation can occur.
An alternative approach is immediate coronary angioplasty, which is particularly useful when there are contraindications to thrombolysis. The results are perhaps better than thrombolytic therapy, but angioplasty is only available in large centres.

Fibrinolytic therapy for acute myocardial infarction.

Fibrinolytic therapy for acute myocardial
infarction.

ANTICOAGULATION is given to myocardial infarction patients to prevent thromboembolic complications from prolonged  immobilization. Usually subcutaneous heparin (5000 U, 8-hourly) is sufficient for this purpose. Patients who receive rt-PA must receive immediate and full doses of heparin (10000 U bolus, plus 1000 U hourly). ACE INHIBITORS. Patients who suffer from transient or chronic heart failure or who have a depressed ejection fraction on echocardiography following an acute myocardial infarction should receive an ACE inhibitor. This therapy reduces mortality and slows the progression of left ventricular function after infarction.
PERSISTENT PAIN can be treated with nitrates. If there is no hypotension, sublingual glyceryl trinitrate should be given. Alternatively, especially if the haemodynamic situation is not stable, continuous intravenous infusion of either isosorbide dinitrate or glyceryl trinitrate should be considered.
ANXIOUS PATIENTS should be reassured and mild sedation, in addition to analgesia, may be necessary. A quiet atmosphere should reduce anxiety. BED REST is advised for the first 24-48 hours, after which the patient is progressively mobilized. Smoking is not allowed. Home versus hospital care of myocardial infarction victims CCUs were developed to facilitate the detection and treatment of arrhythmias occurring in the immediate postinfarction period. However, it has been suggested that the coronary care ward is a frightening environment that may itself increase the incidence of these arrhythmias. There have been several studies comparing home care and coronary ward care of patients with myocardial infarction. The conclusions have been controversial, but home care can be considered if:
• The patient has suffered a myocardial infarction 24 hours or more previously
• There are no complications such as shock or arrhythrma
• The patient is aged 70 years or older
• The patient has concurrent terminal disease
However, most patients suffering from myocardial infarction should be cared for in the CCU of a hospital, where sudden and perhaps fatal complications can be promptly recognized and effectively treated.

Mobile coronary care units

Because a large proportion of deaths from myocardial infarction are due to arrhythmias that occur in the first few minutes of the infarction, it is logical to train ambulance personnel in methods of advanced cardiac life support and to provide them with the equipment to perform these techniques (intravenous infusion, endotracheal intubation and ventilation and ECG monitoring and defibrillation). Ambulances manned and equipped in this way are called mobile CCUs, coronary rescue vehicles or cardiac resuscitation vehicles. This kind of ambulance is sent to those patients who have severe chest pain or who have collapsed unconscious. Together with the training in basic life support of a significant proportion (at least one-third) of the general public, mobile CCUs have reduced the incidence of sudden unexpected cardiac death, whether due to myocardial infarction or to arrhythmias unrelated to acute myocardial infarction. This service is now becoming generally available throughout the UK as part of the statutory ambulance service.

COMPLICATIONS

In the acute phase, i.e. the first 2-3 days following a myocardial infarction, cardiac arrhythmias, cardiac failure and pericarditis are the most common complications. Later, recurrent infarction, angina, thromboembolism, mitral valve regurgitation, and ventricular septal or free wall rupture may occur. Late complications include the postmyocardial infarction syndrome (Dressler’s syndrome), shoulder-hand syndrome, ventricular aneurysm and recurrent cardiac arrhythmias.

Cardiac arrhythmias

These are described in detail. VENTRICULAR EXTRASYSTOLES. These commonly occur after myocardial infarction. Their occurrence may precede the development of ventricular fibrillation. If they are frequent (more than 5 min “), multiform (different shapes) or R-on- T (falling on the upstroke or peak of the preceding T wave), they may be treated with lignocaine 50-100 mg i.v. over 5 min followed by 1-4 mg min-1 by continuous infusion, which is slowly reduced and discontinued over 24 hours. Such treatment has not been shown to reduce the likelihood of subsequent ventricular tachycardia or fibrillation.
VENTRICULAR TACHYCARDIA. This may degenerate into ventricular fibrillation or may itself produce serious haemodynamic consequences. It is treated with intravenous lignocaine. If haemodynamic deterioration occurs, the tachycardia is immediately treated with synchronized cardioversion (initially 200 J).
VENTRICULAR FIBRILLATION. This may occur in the first few hours or days following a myocardial infarction in the absence of severe cardiac failure or cardiogenic shock. This is known as primary ventricular fibrillation. It is treated with prompt defibrillation (200-400 J). Intravenous lignocaine is usually prescribed in an attempt to prevent recurrences of ventricular fibrillation. The prognosis is usually very good because the electrical derangement is only transient.
When ventricular fibrillation occurs in the setting of heart failure, shock or aneurysm, it is called secondary ventricular fibrillation. It is treated in a similar way to primary ventricular fibrillation, but the prognosis is very poor unless the underlying haemodynamic or mechanical cause can be corrected.
ATRIAL FIBRILLATION. This occurs in about 10% of patients with myocardial infarction. It is due to atrial irritation caused by heart failure, pericarditis and atrial ischaemia or infarction. It may be managed with intravenous digoxin or intravenous amiodarone and by treatment of the underlying pathology. It is not usually a longstanding problem.
SINUS BRADYCARDIA. This is especially associated with acute inferior wall myocardial infarction. Symptoms emerge only when the bradycardia is severe. When symptomatic, treatment consists of elevating the foot of the bed and giving intravenous atropine 600 }Lgif necessary. When sinus bradycardia occurs, an escape rhythm such as idioventricular rhythm (wide QRS complexes with a regular rhythm at 50-100 b.p.m.) or idiojunctional rhythm (narrow QRS complexes) may occur. Usually no specific treatment is required.
It has been suggested that sinus bradycardia following myocardial infarction may predispose to the emergence of ventricular fibrillation. Severe sinus bradycardia associated with symptoms or the emergence of unstable rhythms may need treatment with temporary pacing.
SINUS TACHYCARDIA. This is produced by heart failure, fever and anxiety. Usually no specific treatment is needed.
CONDUCTION DISTURBANCES. These are common following myocardial infarction. AV nodal delay (firstdegree AV block) or higher degrees of block may occur during acute myocardial infarction, especially of the inferior wall. First-degree block does not need treatment, but progressive or complete block may need treatment with atropine or an artificial temporary pacemaker. Such blocks may last for only a few minutes but frequently persist for days or several weeks; they are rarely permanent.
Acute anterior wall myocardial infarction may produce damage to the distal conduction system (the His bundle or the bundle branches). The development of complete heart block usually implies a large myocardial infarction  and a poor prognosis. The ventricular escape rhythm is slow and unreliable and a temporary pacemaker is necessary. This form of block is often permanent.
The development of complete AV block can be expected in 20-30% of cases where progressive bundle branch block (right bundle branch block and then right bundle branch block with a QRS axis shift) has already occurred .
Cardiac failure and cardiogenic shock Heart failure after acute myocardial infarction is graded according to a clinical classification. Mild left heart failure (a few basal crackles that persist after coughing, an extra heart sound and upper lobe blood division on the chest X-ray) occur in about 40% of patients with acute myocardial infarction. Treatment for a few days with a mild diuretic such as a thiazide is usually all that is needed for symptomatic relief but an ACE inhibitor should be given.
A large myocardial infarction may lead to severe heart failure and pulmonary oedema. In such cases more prolonged and powerful diuretics and vasodilator treatment is necessary.
In very severe cases a pulmonary artery balloon catheter is used to measure the pulmonary artery and ‘left atrial’ pressures and the cardiac output. Treatment is with loop diuretics, vasodilators and, occasionally, digoxin.
Severe heart failure may also follow ventricular septal rupture or mitral valve papillary muscle rupture. Both of these conditions present with worsening heart failure, a systolic thrill and a loud pan-systolic murmur, widely heard over the precordium. Often, echo cardiography and right heart catheterization with a balloon catheter is needed to differentiate between these two conditions. Both are associated with a poor prognosis, but vigorous treatment including early surgical correction may be successful.

Progression from different types of fascicular

Progression from different types of fascicular

A 12-lead ECG demonstrating a prolonged PR

A 12-lead ECG demonstrating a prolonged PR

Killip (clinical) classification of heart failure in patients with acute myocardial infarction.

Killip (clinical) classification of heart failure in
patients with acute myocardial infarction.

Ventricular asynergy and papillary muscle dysfunction (not rupture) may produce mild mitral regurgitation in association with heart failure. This causes a transient, soft, pan-systolic murmur in up to half of those with acute myocardial infarction. In these cases no specific treatment is necessary for the mitral regurgitation. Cardiac rupture results in almost immediate cardiac tamponade and is usually fatal within a few minutes. Electromechanical dissociation, i.e. no pulse or cardiac output but a persistently normal rhythm on the ECG, is the classical presentation. Treatment is rarely successful. Cardiogenic shock is an extreme form of cardiac failure or circulatory collapse. Its features and management are described. The mortality from this condition is about 90%. The majority of those rescued have a complication that can be treated surgically (e.g. left ventricular aneurysm, torrential mitral regurgitation or ventricular septal perforation).

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