What is Myocardial Infarction ? What are Signs, Symptoms and Management of Myocardial Infarction ?
Myocardial Infarction is commonly known as Heart attack, due to blockage of coronary artery and insufficient blood supply to a part of the heart causing death and necrosis of cardiac cells. The coronary artery blockage usually occurs by atherosclerotic plague (which is an unstable cllection of lipids and macrophages)in the wall of a coronary artery. This leads to ischemia and oxygen storage, if untreated, can cause death of heart muscle tissue (Myocardium).
Myocardial Infarction (MI) or Acute Myocardial Infarction
Myocardial infarction is commonly known as Heart attack, is due to blockage of coronary artery and insufficient blood supply to a part of the heart causing death and necrosis of cardiac cells. The coronary artery blockage usually occurs by atherosclerotic plague (which is an unstable collection of lipids and macrophages) in the wall of a coronary artery. This leads to ischemia & oxygen shortage, if untreated, can cause death (necrosis) of heart muscle tissue (myocardium).Signs and symptoms of Myocardial infarction :
Acute myocardial infarction is characterised by:
• Pain or discomfort is similar to that in angina but is much more severe and last longer, usually more than 20 minutes.
• Sudden chest pain typically felt behind the sternum or across the chest and usually described as constricting or crushing in character.
• Sometimes there is no pain but a feeling of discomfort or an unpleasant sense of pressure or weight.
• It may be described as 'only indigestion' indigestion felt in the chest
• Pain is rarely sharp, stabbing or knife-like
• Pain often radiate to one or both arms, more commonly the left arm, the throat, jaw or neck or pass into the shoulders, to the upper abdomen or the back of chest.
• There may be accompanying diaphoresis (sweating),
• Nausea,
• Extreme weakness
• Feeling of impending death (angor animi).
• Some patients have sudden onset of breathlessness while a few number may have no symptoms at all (silent infarction).
• In uncomplicated cases, patient may appear anxious and transient elevation of blood pressure due to sympathetic over activity, an apical 4th heart sound may be audible, otherwise examination of the heart may be un-remarkable with no abnormal other systems.Diagnosis of Myocardial infarction :
Prolonged severe chest pain of myocardial infarction and its lack of relief by rest and sublingual glycerine trinitrite usually differentiate it from that of angina pectoris.
Evidence of muscle necrosis such as:
• Fever
• Leucocytosis
• Increased ESR
• BP usually falls & may never recover its former level.
• There may be evidence of circulatory failure, with cold sweaty extremities
• Pericardial rub may be heard, usually on the 2nd & 3rd day.
ECG changes in MI :
(i) In sub-endocardial infarction: ST segment depression (horizontal or down sloping) occurs and usually persist like angina pectoris where it is transient or short lived.
(ii) In transmural infarction: Early change is high take off of ST segment with broadening of T waves.
(iii) As the infarct evolves the ST segment assumes a convexity upwards. Significant Q waves begin to appear in leads overlying the affected area of myocardium.ST segment gradually returns to base line & T waves are inverted. The R wave amplitude diminishes & in some cases there is complete loss of R waves with appearance QS complex.
(iv) In a completed infarct the changes are:
(a) Pathological Q waves
(b) ST segment becomes isoelectric
(c) T inversion is present
Persistent elevation of ST segment suggests either re-infarction of the same area or formation of a ventricular aneurism.
The area of infarct can be deduced from the leads showing the relevant changes e.g.
Leads II, III, avF – Inferior wall
LeadsV1 to V4 – Antero septal region
Leads I, avL, V4, V5, V6 – Lateral wall
Leads 1, avL, V1 to V6 – Extensive Anterior WallRisk factors of Myocardial infarction :
The risk factors of myocardial infarction are as follows:
• Atherosclerosis
• Smoking cigarettes
• Elevated blood cholesterol and unhealthy LDL (Low density lipoprotein) HDL (High density lipoprotein) ratio i.e. high LDL & low HDL.
• High BP
• Diabetes mellitus
• Advanced age (usually above 60 years)
• Family history of coronary artery disease
• Eating too much fat in the diet
• Male gender
• Chronic kidney diseaseManagement of Acute Myocardial infarction :
Patient should be admitted to ICCU (Intensive coronary care unit) and monitored for:
• Cardiac arrhythmia
• Jugular venous pressure
• Blood Pressure
• Repeated cardio-pulmonary examination to evaluate the response of treatment.
• Oxygen is given by nasal catheter or by mask.
• Injection Morphine can be given by intra venous route.3 mg i/v slowly every 10-15 minutes for relief of pain and anxiety.
• I/V nitro glycerine drip (5 ugm/ minute initially) is another useful drug for relieving pain.
• Diazepam 5-10 mg may be required for sedation.
• After stabilisation of general condition, patient should be properly investigated and evaluated.
Investigations:
• Electrocardiogram in 12 leads
• Blood haemoglobin
• Total and differential leucocytes count (TLC & DLC)
• Bleeding time & clotting time
• Prothrombin time
• Blood urea, uric acid, and serum cretinin
• Liver enzymes like LPK-MB, SGOT, LDH and electrolytes.
Thrombolytic Therapy :
To restore coronary blood flow successfully it is essential to institute thrombolytic drugs within the first few hours following myocardial infarction. It has been observed that thrombolytic drugs started within 6 hours following an acute occlusion can be effective in myocardial salvage; the earlier it is given, the better are the results. They are-(i) Streptokinase (SK) (ii) Urokinase & (iii) Tissue plasminogen activator (TPA)
Streptokinase : can be given I/V or intra-coronary approximate re perfusion rates of 50% & 75% respectively.
TPA : I/V TPA perfusion rates similar to intra coronary streptokinase. Whatever drug is used reocclusion may occur in about 1/5th (20%) of patients.
Following successful thrombolysis, selected patients are taken up for coronary angiography with a view to consider a myocardial revascularisation by PTCA (Percutaneous Tranluminal Coronary Angioplasty) or CABGS (Coronary Artery Bypass Graft Surgery).
In an uncomplicated infarction, gradual and progressive ambulation (sitting in chair, walking in the room, etc.) can be started after 3 or 4 days & patient considered for discharge after about 2 weeks.
Early low level (sub maximal) exercise is recommended, about 3 weeks after an uncomplicated infarction in order to identify patients who are at high risk for sudden death or reinfarction. Patients who develop angina or significant ST depression are at risk and should undergo further evaluation to plan revascularisation procedure.
Post discharge management aims at gradual increase in exercise level.
A beta blocker with or without calcium channel blocking drug and anti-platelet drug (Aspirin) are usually given.
Periodic check-up to monitor progress is done.
Average patient can return to light work in about 4 to 6 weeks after myocardial infarction.Complications of Myocardial infarction :
Complications of MI are divided into early late complications:
Early complications :
• Cardiac arrhythmia
• Cardiac failure
• Cardiogenic shock
• Deep vein thrombosis
• Pulmonary embolism
• Left ventricular thrombosis & arterial embolism
• Pericarditis
• Papillary muscle dysfunction
• Ventricular muscle rupture
• Ventricular septal rupture
• Cardiac tamponade
• Emotional changes
Late complications :
• Late arrhythmias
• Shoulder hand syndrome (Dresaler's syndrome)
• Ventricular aneurysm
• Post infarction angina