Myocardial Infarction

Myocardial Infarction
A myocardial infarction (heart attack) is where a coronary artery has become blocked thus preventing the supply of blood to an area of myocardium.  The myocardium becomes rapidly ischaemic and then necrotic.  One or more layers of the myocardium may be affected depending on the severity of the infarct.  Fibrous tissue forms in the necrotic area.  The affects on the patient are dependent on the location and amount of tissue affected.  Death may ensue immediately, within a few hours or the patient may survive. The fibrous / necrotic area is unable to contract or to conduct electrical impulses and therefore will reduce the efficiency of the chamber affected.  There are five main types of myocardial infarction: -

Anterior wall – This is due to an occlusion of the left anterior descending artery and affects the front wall of the left ventricle.  The papillary muscles and intraventricular septum may also be affected (anteroseptal).  This sort of infarction has disastrous consequences on the patient by reducing the cardiac output dramatically.  Cardiogenic shock is a very real state following an anterior infarction.
Lateral wall – This is due to an occlusion of the lateral branch of the circumflex artery.  If the left anterior descending artery is also occluded this will result in an Anterolateral Infarct.
Inferior wall – This is due to an occlusion of the right coronary artery and results in an infarction of the base of the left ventricle.
Posterior wall – This is due to an occlusion of the posterior branch of the right coronary or left circumflex artery.  It affects the back wall of the left ventricle.
Right ventricular infarction – This is due to occlusion of the right coronary artery or sometimes the left circumflex artery.  A right ventricular infarct may occur in conjunction with an inferior or posterior left ventricular infarction.  A right ventricular infarction will affect the pulmonary circulation and oxygenation of the blood due to decreased cardiac output from the right ventricle.
(Back to the top ­)

Symptoms of Myocardial Infarction
Pain – This is severe, usually retrosternal and may radiate into the jaw, shoulders and down the arms.  It is described as a tight band around the chest and lasts for several hours.  It is unrelieved by GTN.

Dyspnoea – This is due to either the pain or pulmonary congestion caused by pulmonary hypertension and pulmonary oedema.  There is also an increase in the myocardial oxygen demand.  If the left ventricle is affected, the cardiac output will be reduced and a shock state may exist.

Extreme pallor – This is due to the decreased cardiac output and redirection of blood away from the skin to the major organs.  The skin will also feel cool and clammy.

Nausea and vomiting – This is due to pain, redirection of blood away from the gastrointestinal system (splanchnic circulation), release of adrenaline and other catecholamines into the blood (fight / flight response) and from side effects of medications used to treat the condition and symptoms.

General fatigue – This is due to reduced cardiac output and generalised muscle ischaemia.  The patient will be prostrated during the attack and this may also be a cause of this.

Tachyrhythmias – This is due to the heart trying to compensate for the low cardiac output by increasing the rate (rate x stroke volume = cardiac output).  The myocardium also becomes very irritable following infarction due to release of metabolites and electrolytes such as potassium and calcium from dying cells.  This results in ventricular arrhythmias such as VT, VF and SVT.

Hypotension – This is due to reduced cardiac output.  Initially the patient may be hypertensive due to the aggravated compensation mechanisms.

Pyrexia – The patient’s temperature rises to around 39°C due to release of metabolites during the inflammatory process initiated by the necrotic tissue and widespread death of cells.  This normally occurs over 24 – 48 hours and returns to normal within 7 days.

Sense of Impending Doom – This is due to the release of adrenaline and other catecholamines as part of the compensation mechanism.  Also the real fear of death exists due to the nature of the disease and the information known by the general public.  It may also be that the patient is normally an anxious / highly-strung individual who worries a lot.

(Back to the top ­)

Diagnosis of Myocardial Infarct
The diagnosis is made on three aspects: -

ECG changes – During an infarct there is normally ST elevation and T wave inversion, there may also be the formation of q waves.  The location of the infarct will be identified by which leads are affected in a 12 lead ECG.  An inferior infarct is identified by reciprocal changes in the leads facing the opposite wall.
Anterior wall –V1 – V4.
Lateral wall – I, aVL, V5 and V6.
Inferior wall – II, III, aVF.
Septum – V2 and V3.
Colquhoun M. C. (1993)



Changes in the cardiac enzymes (CPK, AST and LDH).  Intramuscular injections must be avoided at all times when cardiac enzyme monitoring is performed.  This is because damage to skeletal muscle during insertion of needles etc. causes a release of these enzymes giving falsely high and inaccurate readings.
Clinical picture – Symptoms displayed as described above.
(Back to the top ­)

Treatment of Myocardial Infarction
The management of a myocardial infarction is with regard to alleviation of symptoms, prevention of extension of the infarct and detection / treatment of the complications of a myocardial infarct.

The first priority with these patients is to maintain a clear airway and breathing, monitoring will be established as soon as the patient arrives in the resuscitation room.  (NB This will have already been initiated by the ambulance crew).  It is also likely that intravenous access will have been established unless the patient was brought in by relatives.

A high percentage of prescribed oxygen will be administered via a facemask unless contraindicated by chronic respiratory disease.  This will serve to optimise the patient’s oxygenation.

Chest pain and nausea are relived by diamorphine and an anti-emetic given intravenously.  Diamorphine also acts by offloading the heart and reducing the preload and afterload.  If the patient has pulmonary oedema, diuretics may also be given.  A central line may be sited to monitor the central venous pressure; this will give an indication of the preload in the right side of the heart.  Antiarryhthmics may be given if the patient is displaying arrhythmias.  Any electrolyte imbalance will be treated immediately in order to stabilise the myocardium as much as possible.

Unless contraindicated, the patient may be given antithrombolytic agents such as streptokinase, Tissue Plasminogen Activator (tPA) in order to dissolve the clot in the coronary artery.  When these are given bleeding must be monitored for.

Contraindications for thrombolytic therapy include: -


  History of gastric ulcers.

  Recent surgery (within 2 weeks).

  Previous treatment with streptokinase or tPA.

  Allergic reaction to thrombolytics.

  Recent trauma (within 2 weeks).
A restful environment is essential for these patients in order to reduce the amount of stress and anxiety they feel.  Information that is honest and understood is invaluable, these patients are extremely frightened.  Visitors should be reduced to immediate family or significant others and the lengths of time they visit should be tailored to the patient’s needs.  It may be that someone is more relaxed when a particular person is present than when not.  Each patient’s needs should be assessed individually and acted upon accordingly.

(Back to the top ­)

Complications of Myocardial Infarction
The complications of a myocardial infarction are as follows: -


Arrhythmias – These usually occur within the first 48 hours following an infarct and may be life-threatening.  They are due to myocardial irritability caused by lack of oxygen (ischaemia), release of potassium and calcium from dead cells and disturbances to the conductive mechanism of the heart.  This is particularly true when the area around the sinoatrial or atrioventricular nodes is affected.  Myocardial irritability is identified by the number of ventricular ectopics seen.  There is a danger that an ectopic may fall on the T wave (r on T) and ventricular fibrillation ensues.

Heart failure – Backpressure from the ventricle affected onto the atrium on the same side exists due to the ventricle being unable to expel the blood in it effectively.  This will cause backpressure on either the pulmonary circulation (causing pulmonary oedema) or the systemic circulation (peripheral in organ oedema).  The cautious use of diuretics and vasodilators may minimise this.

Pericarditis – This is thought to be caused by an autoimmune response initiated by the necrotic tissue within the heart causing an inflammatory reaction in the pericardium.  The symptoms of this are similar to the infarct though the pain is longer lasting and a pericardial rub may be heart on auscultation.

Mitral regurgitation – This is due to either papillary muscle infarct or rupture that causes the mitral (left side) valve to become incompetent.  This will worsen any cardiac failure by allowing blood to enter the left atrium during systole.

Myocardial rupture – This is due to the weakened area of necrotic myocardium and is likely to occur within seven days post infarct.  It is more often seen in patients with a transmural infarct (infarct extends through all the layers of the heart) and may cause a cardiac tamponade.  An intraventricular septal rupture can occur within 2 weeks following the infarct and is a very serious complication.  It allows the flow of blood from the left to right sides of the heart and will flood the lungs with pulmonary oedema.  The blood entering the aorta will also be severely diminished causing cardiogenic shock.  The combination of these is likely to kill the patient outright depending on the size of the rupture.  Emergency surgery is the only treatment for this.

Myocardial aneurysm – This is the ballooning out of the infracted myocardial tissue into the chamber affected.  This may seriously reduce the cardiac output and will cause the heart to contract in an abnormal fashion.  The size of this can be identified my echocardiography.  Surgery is the only treatment.

Emboli – These form when clots formed in the necrotic areas break free and enter the bloodstream.  Pulmonary, cerebral or deep vein thrombosis may form.  Also further myocardial infarction may occur if the emboli enter the coronary arteries.  Emboli may or may not kill the patient outright, it will depend on the location and size of the vessel they are blocking.  Anticoagulant drugs such as heparin and aspirin will be given and the patient closely monitored for further emboli or moving of the emboli to other areas.

When the patient is discharged from the coronary care / high dependency unit to a medical ward, their lifestyle is examined and teaching about how to change their lifestyle to one that will minimise the risk of a repeat infarct will begin.  Involvement with a dietician is essential in order for the patient to start to look at their diet and alcohol intake.