ContentsPAGE

1a. Introduction 3

1b. Epidemiology 4

1.1 Risk factors

2. Pathophysiology 5

3. Causes 6

4. Classification 7

5. Symptoms 8

6. Diagnosis 9

6.1 Diagnostic criteria

6.2 Physical examination

6.3 Electrocardiogram

6.4 Cardiac markers

6.5 Angiography

6.6 Histopathology

7. First aid 12

7.1 Immediate care

7.2 Automatic external defibrillation (AED)

7.3 Emergency services

7.4 Wilderness first aid

7.5 Air travel

8. Treatment 13

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8.1 First line

8.2 Reperfusion

8.2.1 Thrombolytic therapy

8.2.2 Percutaneous coronary intervention

8.2.3 Coronary artery bypass surgery

8.3 Monitoring for arrhythmias

8.4 Rehabilitation

8.5 Secondary prevention

8.6 New therapies under investigation

9. Complications 16

9.1 Congestive heart failure

9.2 Myocardial rupture

9.3 Life-threatening arrhythmia

9.4 Pericarditis

9.5 Cardiogenic shock

10. Prognosis 17

11. Legal implications 17

12. Conclusion 18

13. References 18

INTRODUCTION

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Myocardial infarction (also known as heart attack) is one of the most common and deadly end results of heart disease,

and is usually the result of some underlying disease such as coronary artery disease (which is a disease of occluded

coronary blood vessels).

The disease limits and eventually stops blood flow to the particular area of the heart muscle/myocardium supplied by

the occluded coronary artery, thus resulting in a reduced amount of oxygen and other essential nutrients needed by the

heart muscle in order for it to be able to function as an effective pump.

The lack of oxygenated blood to the myocardium results in death of cardiac cells and myocardial damage which causes

loss of cardiac contractility therefore decreased cardiac output.

One of the most common symptoms of myocardial infarction is chest pain and the extent of myocardial cell death determines the size of the infarction.

1. EPIDEMIOLOGY

1.1 RISK FACTORS The risk factors are what predisposes the person to getting heart disease in the first place as they make the person more prone to being ill. Some of the risk factors can be modified (meaning they can be reversed/changed) by lifestyle changes (e.g. eating healthy), and physical exercise, thus reducing the chances of infarction. They may include any of the following:

1. Age – the disease occurs most commonly in old age (i.e. > 65 years).

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2. Gender – males are more at risk of coronary artery disease, especially after the age of 65, and females are more at risk between the ages of 20 to 65 years.

3. Family history – this predisposes the person to a higher risk of coronary artery disease.4. Smoking – cigarette smoke is known to have certain substances/gases that cause damage to blood vessel

walls, thereby increasing the risk of myocardial infarction. 5. High blood pressure (Hypertension) – this is a common risk factor in many disorders e.g. Diabetes Mellitus

and also increases the risk of myocardial infarction as it can lead to the development of atherosclerosis, and the risk is associated with both systolic dysfunction (which occurs as a result of loss of contractile function of the damaged myocardium) and diastolic dysfunction (which occurs straight after systolic dysfunction leads to an increased left ventricular end diastolic distensibility which may cause hypertrophy.

6. Obesity – increases the risk of coronary artery disease, stroke and hence myocardial infarction as it increases strain on the heart, raises blood pressure, cholesterol levels, and increases the risk of Diabetes.

7. Diabetes Mellitus – this disorder is more common in obese people who are also more likely to develop hypertension, and it increases the risk of myocardial infarction because it increases the progression rate of arthrosclerosis and adversely affects blood cholesterol levels.

8. Cholesterol (body fats) – high blood cholesterol levels are associated with an increased risk of atherosclerosis in myocardial infarction and it usually the main component of an atherosclerotic plaque.

The above diagram illustrates one of risk factors of MI and its sources. www.urac.org

2. PATHOPHYSIOLOGY of MYOCARDIAL INFARCTION

Myocardial infarction as was mentioned previously is the irreversible damage of the heart muscle, caused by a prolonged oxygen shortage (Hypoxia) as a result of coronary artery occlusion.

MECHANISM of OCCLUSIONThe occlusion usually occurs as a result of the formation of a plaque on the inner wall of the blood vessel, thereby decreasing the diameter of the blood vessel in that area. Eventually the atherosclerotic plaque raptures, leading to the formation of a blood clot/thrombus that may lead to partial or total occlusion of the artery. Prolonged impairment of blood flow to the heart muscle leads to death of myocardial cells and tissue (these cannot be repaired or replaced), after

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some time fibrotic scar formation occurs in the area of the damage. The infracted area can also serve as a source for the formation of life threatening arrhythmias such as ventricular tachycardia/VT and ventricular fibrillation/VF.

The damage to the myocardium also causes a disruption in the electrical activity of the heart and causes conduction of impulses through the heart to be slowed down.

MECHANISM of MYOCARDIAL DAMAGECell death begins in the endocardium because it is most distal to the arterial supply and the longer the duration of the occlusion, the greater the area of damage. From the endocardium, the damage spreads to the myocardium and then to the epicardium, which is the closest layer of heart muscle to the arterial supply. It then spreads laterally to areas of collateral perfusion. The severity depends on:(a) The amount of occlusion in the artery – i.e. the more proximal the occlusion, the larger the area of heart

muscle at risk of being damaged,(b) The length of time of the occlusion – i.e. the longer the period of time of the occlusion, the more irreversible the

damage becomes, and(c) The presence/absence of collateral circulation (circulation in two branches that run parallel to each other/side

by side) – the larger the infarction, the greater the chances of death due to pump failure.

Each coronary artery supplies blood to a region of the heart muscle. If an artery is occluded (blocked) there is no blood supply to that region.

dark red = artery blue = outlines region of heart affected by blockage

Circumflex occlusionback of heart

Left anterior descending (LAD) occlusionfront of heart

Right coronary artery (RCA) occlusion

front of heart

3. CAUSES

(a) Coronary Artery Thrombosis – this is a blood clot that forms inside the artery or any of its branches causing an obstruction to blood flow and it is the most common cause of a myocardial infarction.

Blood clotting does not usually form in normal arteries; however they do form in the presence of an atherosclerotic plaque (fatty deposit) that forms in the lining of the coronary artery. These plaques form over a number of years in one or sometimes more than one branch of a coronary artery until the plaque has shell like feeling on the outside and a softer fatty layer on the inside. After some time the plaque raptures (bursts) exposing the inner layer to blood, which in turn stimulates the clotting mechanism – leading to the formation of blood clots that eventually cause an obstruction in the artery/arteries.

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The above diagrams show Fat formation & Plaque rapturehttp://www.clevelandclinic.org/

(b) Spasm - During coronary artery spasm, the coronary arteries constrict on, causing lack of blood supply to the heart muscle which might lead to ischemia if it persists. It may occur at rest and can also occur in people without significant coronary artery disease. If coronary artery spasm occurs for a long period of time, a heart attack can occur.

Coronary artery Spasm. http://www.clevelandclinic.org/

4. CLASSIFICATION

6.2 ST ELEVATION MYOCARDIAL INFARCTION / STEMI – This type of infarction is caused by a prolonged period of blood supply to the heart muscle and it is an indication that a large area of heart muscle is affected by the infarction, thus causing the noted electrocardiographic (ECG) changes.

6.2 NON-ST ELEVATION MYOCARDIAL INFARCTION / NSTEMI – This type of MI does not normally cause ECG changes. The blockage of an artery in this case is usually partial or temporary, thus meaning that the extent of the damage to the myocardium is not large enough to cause notable ECG changes.

6.2 UNSTABLE ANGINA / UA – Angina is a clinical syndrome caused by myocardial ischemia characterized by chest discomfort/pain. It is referred to as coronary insufficiency or Pre-Infarct angina and follows a progressive pattern. The discomfort / pain experienced by the patient may be of varying intensity, last for a longer period of time, may be brought about by less effort, or occur spontaneously at rest and can also occur in any combination of the above mentioned symptoms. The ECG changes noted in this condition are associated mainly with ST segment and T wave changes.

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6.2 Q WAVE MYOCARDIAL INFARCTION (Previously referred to as Transmural MI) – This type of infarction includes necrosis (tissue death) of the whole affected area of cardiac muscle i.e. from the endocardium right through to the myocardium and epicardium. It usually occurs in the early hours of the morning when there is increased adrenergic/ sympathetic activity as well as increased blood fibrinogen (a glycoprotein & precursor of fibrin which is involved in blood clotting) levels and increased platelet adhesiveness.

6.2 NON-Q WAVE MYOCARDIAL INFARCTION (Previously referred to as Sub-endocardial MI) – In this case, necrosis does not affect all the layers of the heart muscle i.e. it might affect only the myocardium or both the endocardium and myocardium. Non- Q wave MI usually causes ST segment and T wave abnormalities. Early spontaneous reperfusion usually occurs with this type of MI mostly because there is no sustained coronary artery spasm which might contribute to the occlusion.

The amount of damage to the heart muscle depends on the size of the area supplied by the blocked artery and

the time between injury and treatment. http://www.clevelandclinic.org/

This ECG represents ST changes that take place with an infarction. www.ljm.org.ly/

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5. SYMPTOMS

1. Chest pain – this is the most common symptom and is usually characterized by chest tightness.

2. Shortness of breath (dyspnea) – this is due to decreased cardiac output (therefore increased oxygen demand) as a result of compromised left ventricular function (LV failure), thus pulmonary congestion and/ edema.

3. Nausea and vomiting -

4. Palpitations – this is because the heart is trying to compensate for the poor ventricular contraction by increasing the heart rate to try and pump out enough blood.

5. Sweating (diaphoresis) -

6. Syncope (dizziness) – poor LV function lowers cardiac output, and therefore blood supply to the brain will be decreased and dizziness results.

7. Fatigue – this is also due to the great oxygen demand.

The above is an example of a patient presenting with chest pain. www.wv-hsta.org/

6. DIAGNOSIS The diagnosis of MI varies from one patient to the next with regard to their individual symptoms. A straight forward diagnosis can be made for those patients who have notable atherosclerotic risk factors as well as symptoms that suggest lack of blood supply to the heart muscle. MI is considered to be a medical emergency and a person suspected of having an MI undergoes the following procedures and tests: ECG, Blood Tests, and Coronary Angiography.

6.1 DIAGNOSTIC CRITERIA – 2 or more of the following WHO Guidelines may indicate the presence of a definite MI.(a) history of ischemic chest pain lasting for more than 20 minutes;

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(b) changes in serial / sequential ECG tracings; and(c) Instability of cardiac biomarkers such as Troponin 1, Creatine Kinase, and Lactate Dehydrogenase enzymes

specific to the heart.

6.2 PHYSICAL EXAMINATION – Patients do not always present with the same symptoms, therefore on physical examination the presentation will be different for each patient. For example, one patient might be restless with anxiety resulting in an increase in respiratory rate (due to a sense of suffocation) and irregular heart rate; while another might present with pale skin due to anxiety, and varying blood pressure and perspiration can also be experienced. And since long-term infarction results in decreased cardiac contractility, heart failure can also develop.

6.3 ELECTROCARDIOGRAM / ECG – The main aim of the ECG is to determine the presence of ischemia or coronary injury because it is sensitive to detecting ischemia and infarction and there are certain ECG changes that will indicate the presence of disease. These changes can include early ECG changes of T wave inversion and ST depression which may indicate infarction. The hallmark of acute myocardial infarction is the development of abnormal Q waves (their presence is usually indicative of tissue death) which may appear a few hours after the onset of symptoms. The primary diagnostic ECG changes consist of ST elevation with the development of T wave inversion and Q wave abnormalities.

Wall AffectedLeads Showing

ST Segment Elevation

Leads Showing Reciprocal ST Segment Depression Suspected Culprit Artery

Septal V1, V2 None Left Anterior Descending (LAD)

Anterior V3, V4 None Left Anterior Descending (LAD)

Anteroseptal V1, V2, V3, V4 None Left Anterior Descending (LAD)

Anterolateral V3, V4, V5, V6, I, aVL II, III, aVF Left Anterior Descending (LAD), Circumflex (LCX),

or Obtuse Marginal

Extensive anterior (Sometimes called Anteroseptal with Lateral extension)

V1,V2,V3, V4, V5, V6, I, aVL II, III, aVF Left main coronary artery (LCA)

Inferior II, III, aVF I, aVL Right Coronary Artery (RCA) or Circumflex (LCX)

Lateral I, aVL, V5, V6 II, III, aVF Circumflex (LCX) or Obtuse Marginal

Posterior (Usually associated with Inferior or Lateral but can be isolated)

V7, V8, V9 V1,V2,V3, V4Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX))

Right ventricular (Usually associated with Inferior) II, III, aVF, V1, V4R I, aVL Right Coronary Artery (RCA)

Not only does the ECG leads with ST segment elevation help the clinician determine the area of damaged myocardium, but also helps in by making it easier to identify the occluded artery. The following table shows the ECG changes that take place as well as the affected area of the heart wall. www.wikipedia.com/

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6.4 CARDIAC MARKERS / ENZYMES – These are proteins from cardiac tissue released into the blood stream when damage to the heart muscle occurs. These enzymes are contained in the cardiac cells within membranes associated with specialized cellular function such as contraction and they include- Creatine Phosphokinase (CK-MB), Myoglobin, and Troponin. Once they are outside the cell, they are cleared from the interstitial by cardiac lymphatics. And once they exceed the capacity of the cardiac lymphatics to clear them, they become detectable in circulation.

(a) Creatine Kinase-MB – is a biomarker that is highly sensitive and specific for to the heart. When infarction occurs, MB2 which is the tissue form of creatine kinase is initially released in small amounts so that CK-MB remains within normal limits. Even so, the ratio between MB and MB2 will differ which helps in making a diagnosis.

(b) Myoglobin – is a protein found in both skeletal and cardiac muscle and also happens to bind to oxygen. It is a sensitive indicator of muscle injury and its rise can help determine the infarct size and although it is not specific for cardiac muscle, it helps in the diagnosis of MI.

(c) Troponin T & I – These are regulatory muscle proteins released by damaged myocardial cells and are more specific for MI than MB-CK. They increase plasma levels a few hours after an infarction occurs.

(d) Lactate Dehydrogenase – This is another protein which becomes elevated with the occurance of a myocardial injury. It increases a few days after the onset of symptoms and lasts up to 10 days. It is less commonly used nowadays.

6.5 ANGIORAPHY – This is a percutaneous procedure that involves the making of an incision in the groin area for the insertion of a cardiac catheter into the femoral artery which helps to gain access to the heart and its coronary arteries. Once the catheter is inside the occluded vessel, dye or contrast medium is injected into the artery and X-Ray pictures of the coronaries are taken. This helps to see the extent of the occlusion and which branches are affected, thereby making it easier for the Cardiac Surgeon to decide whether that vessel should be opened up by insertion of a balloon or stent to keep it open (Coronary Angioplasty).

This is an angiograph picture showing the area of occlusion. www.ljm.org.ly/

6.6 HISTOPATHOLOGY – This is the study of the structural/ anatomical changes that take place during the occurrence of an infarction. The histological characteristics of an infarction are usually examined in specimens obtained from

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infarct-related coronary artery lesions in patients with initial infarction who undergo directional coronary atherectomy (removal of an atheroma by the use of a single-blade balloon) following intracoronary thrombolysis within 6 hours after the onset of chest pain. Removed tissues were fixed in buffered formaldehyde and embedded in paraffin, and the thick paraffin sections are then stained with hematoxylin-eosin and examined by light microscopy which revealed the presence of thrombus and/ intramural hemorrhage in the samples. High incidences of cholesterol cleft, foam cell, calcium deposit and intimal proliferation are also observed which further suggest that thrombus and/ intramural hemorrhage are important factors that contribute in the onset of a myocardial infarction.

 This is a section of the subepicardial myocardium from an autopsy case of a 71 year old Asian male. The features are those of acute myocardial infarction showing neutrophilic infiltrate along with areas of necrosis, diffuse interstitial edema and pale myocytes with fading nuclei and decreased striations. www.histopathology-india.net/Heart5.htm

7. FIRST AID Since myocardial infarction is regarded as a common medical emergency, the emergency medical principles that apply in First Aid courses also apply with a myocardial infarction.

6.2 IMMEDIATE CARE – In the case of severe chest pain/ infarction, it is advisable to call for immediate help to prevent / minimize further damage to the heart. The patient should sit in a position that will allow them to be able to breathe normally without too much effort/ trouble (e.g. half sitting with knees bent). In case of unconsciousness, it is important to have an external defibrillator at hand (if possible). Aspirin dissolved or given sublingually (for quicker absorption by the body) also helps prevent further clot formation in the arteries. Glyceril Trinitrate/TNT can also be give as it helps dilate (relax) blood vessels and therefore allows for more blood flow, thus reducing the chest pain.The person who is with the patient before the Medics arrive is responsible for getting the patient’s particulars as well as any other information that might help accelerate the treatment of the patient such as the severity/ nature of the pain, patient activities at the time of onset.

6.2 AUTOMATIC EXTERNAL DEFIBRILLATION/ AED – Installation of external defibrillators in public places may help reduce the number of deaths due to sudden heart attacks as they are able to monitor and analyze cardiac rhythm and determine whether the patient can be shocked.

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6.2 EMERGENCY SERVICES – They differ in their way of treating patients of suspected MI. Even so, all emergency services make it easier for patients to gain medical treatment. The treatment may include – Aspirin; TNT (given sublingually); Thombolytic therapy; Oxygen; and Morphine. A 12 Lead ECG can help in recognizing patients with ST elevation MI, therefore providing a basis for medical staff at a hospital to perform emergency coronary angioplasty and open the occluded vessel.

6.2 WILDERNESS FIRST AID – Under these circumstances, it is important to remove the person who’s suspected of having a heart attack to an area that provides easy access to medical care. This saves time and the trouble of having to carry the person in the event of them losing consciousness.

6.2 AIR TRAVELL – It is wise to have First Aid kits with different medication in this type of public transport as you never know when they might be needed. Having staff that is well equipped in terms of dealing with these kinds of emergencies and in the event of an MI, the pilot can land in the nearest Airport and notify them of the emergency in order to get faster access to medical treatment. It is also important for the person who knows they suffer from heart disease to carry their medication as this might prove helpful in the case of them having chest pain or even a heart attack.

8. TREATMENT Myocardial Infarction is a serious medical emergency that requires immediate and effective medical therapy in order to prevent extended myocardial damage. Any delay in treatment might lead to severe and extensive damage of the heart muscle.

8.1 FIRST LINE – This is given in order to give the patient more time to get to a medical facility and to get proper treatment. It also helps to reduce the pain and may include: Morphine for pain; Oxygen incase the patient struggles to breathe; TNT to relax blood vessels and allow more blood flow to the heart muscle; and Aspirin to prevent further clotting of blood and damage to the heart, hence reducing mortality.

8.2 REPERFUSION – This is an important part of the treatment of myocardial infarction and includes 3 types – Thrombolytic therapy; Angioplasty; and Bypass surgery. Reperfusion is important mainly in patients with STEMI or those showing recent bundle branch blocks on a 12 Lead ECG.

8.2.1 Thrombolytic Therapy – This treatment is indicated mainly in ST elevation MI and is usually more effective within the first 2 hours of the onset of symptoms. Thrombolytics prevent further formation of thrombi/ clots and allow for blood flow to occur. They may include the following drugs: Streptokinase; Urokinase; Alteplase; Reneplase which are easy to use. Heparin which is an anticoagulant may also be given to thin the blood.

8.2.2 Percutaneous Coronary Intervention/ PCI – This is the second option following thrombolytic therapy that is used to open occluded coronaries. As in coronary angiography, Angioplasty includes the insertion of a catheter (with a balloon) into the femoral artery to gain access to the heart and its coronary arteries. During this procedure, dye is also injected in order to locate the occluded vessel and X-Ray photos are also taken and the balloon or stent or both are deployed into the area of the vessel with the occlusion to try and open it up.

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Anticoagulants especially Heparin and Clopidogrel are given for the duration of the procedure to prevent blood from clotting. TNT is also sometimes given to minimize allow blood to flow through the vessel.

A stent is a latticed, metal scaffold that is placed within the coronary artery during a PCI to keep the vessel open.

www.lifespan.org/.../10/000469.html

8.2.3 Coronary Artery Bypass Surgery/ CABG – This technique is used in patients that have a high risk of left main coronary artery thrombosis during a coronary intervention and those who are more prone to Cardiogenic shock and is usually done a few weeks after the occurance of an acute myocardial infarction. It involves implantation of an artery/ vein (usually taken from the internal mammary artery or the saphenous vein) into the aorta to bypass the occlusion. This procedure is more successful in patients that have a less number of occluded vessels.

heart.health.ivillage.com/.../bypasssurgery2.cfm

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8.3 MONITORING for ARRHYTHMIAS – This is done to prevent the occurance of life threatening arrhythmias and treatment such as anti-arrhythmic agents is given to prevent development of arrhythmias especially after an acute infarction. After the procedure, monitoring of the patient’s condition/ improvement is continued in the hospital ward or Cardiac ICU.

8.4 REHABILITATION - The aim of cardiac rehabilitation is to optimize/ produce effective cardiac function and improve quality of life of the patient. Light exercises help reduce the reoccurrence of the controllable risk factors such as cholesterol as its levels are lowered during exercise, obesity – weight loss, and patients can also supplement their exercise by eating a healthy diet and stopping smoking. No strenuous activities (e.g. carrying heavy things or digging etc.) should be done because at this stage the heart can only tolerate light work.

8.5 SECONDARY PREVENTION – Lifestyle modification, management of blood pressure, regular exercise, and stopping smoking can greatly reduce the reoccurrence of an infarction. Long term medication is a recommendation to prevent development of any further complications and may include:

(a) Anti- Platelet Drugs (Aspirin & Clopidogrel) to prevent clot formation.(b) Beta blockers (Metoprolol, Carvedilol) to dilate blood vessels and allowing easy blood flow, thus lowering

oxygen demand, and they also reduce MI mortality by decreasing the incidence of arrhythmogenic death (death by the occurance of dangerous arrhythmias e.g. ventricular fibrillation).

(c) Ace-inhibitors (Diltiazam, Nifedepine) to reduce ventricular remodeling/ hypertrophy, and development of heart failure.

(d) Statins to reduce LDL levels, thus preventing further plaque formation.

8.6 NEW THERAPIES UNDER INVESTIGATION (a) Stem-cell Treatment – involves injection of the patient with stem-cells derived from their bone marrow and

they show improved cardiac output.(b) Progenitor cell infusion and tissue engineering are some of the other therapies still under investigation.

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9. COMPLICATIONS of MI

9.1 Life threatening arrhythmia – conduction disturbances in the heart may indicate damage to the sinu-atrial node/ SA node and re-entry may cause some fast sometimes uncontrollable heart rates such as ventricular tachycardia (VT) or in some cases ventricular fibrillation (VF) and if Nodal damage occurs, this may lead to complete heart block.

www.acc.org/

9.2 Heart failure – myocardial infarction reduces the pumping ability of the heart and depending on the part of the heart that has been affected, the heart failure can either be left/right sided or bilateral (affecting both sides of the heart). But, regardless of which side of the heart is affected, cardiac output is still reduced even though enough blood is coming back to the heart. This causes an increase in preload, therefore leading to volume overload in the ventricles and pulmonary congestion because it’s becoming more difficult to get blood into the heart.

9.3 Cardiogenic shock – this is caused by inadequate cardiac function which in turn results in decreased cardiac output and is characterised by hypotension, tachycardia, and a reduction in urine output. The decrease in cardiac output causes an increase in oxygen demand by the body. Cardiogenic shock is commonly associated with infarction of the anterior wall of the myocardium and loss of left ventricular functioning myocardium.

9.4 Myocardial rupture – it occurs as a result of increased pressure against the weak walls of the heart chambers due to ineffective pumping of the damaged heart muscle. It occurs in three forms, i.e. Papillary muscle rupture usually as a result of right coronary artery occlusion – leading to inappropriate function of the muscle, therefore, valve incompetence/ regurgitation due to improper closure; Septal rupture which may result in shunting of blood from the high pressure chamber (i.e. LV) to the low pressure chamber (i.e. RV) of the heart, and this can lead to right heart failure if volume overload occurs and is sustained; and lastly, External rupture which involves rupture of the myocardium itself, is characterised by a sudden loss of arterial pressures and occurs more frequently in the left ventricular wall because it’s a high pressure chamber.

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Myocardial Rupture. www.usc.edu/

9.5 Pericarditis – occurs as a result of trans-mural infarction which affects all the layers of the heart muscle. Inflammation occurs in the area of the damage as a result of transmural injury, thus inflammation of the pericardium will occur due to inflammatory responses of the heart.

10. PROGNOSIS

The expected outcome varies with the amount and location of damaged tissue. The outcome is worse if there is damage to the electrical conduction system. Approximately one-third of cases are fatal. If the person is alive 2 hours after an attack, the probable outcome for survival is good, but may include complications. Uncomplicated cases may recover fully; heart attacks are not necessarily disabling. Usually the person can gradually resume normal activity and lifestyle.

11. LEGAL IMPLICATIONS At common law, a myocardial infarction is generally a disease, but may sometimes be an injury. This has implications for no-fault insurance schemes such as workers' compensation. A heart attack is generally not covered; however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. Additionally, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person who has suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, for example driving a car, taxi or airplane. www.wikipedia.com/

12. CONCLUSION Myocardial infarction is a life-threatening disease that requires immediate and effective treatment as mentioned previously. For some people it can be a life changing experience as it makes people realize how important it is to live a heart healthy lifestyle. The ongoing research for new ways to treat myocardial infarction and the new

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ways of detecting it before the onset of symptoms can help minimize the number of deaths with of course the cooperation of the patient in terms of them changing their lifestyle and reducing the number of modifiable risk factors.

REFERENCES

1. Hurst’s The Heart, 9th Edition, R.W Alexender, R.C Schlant, V. Fuster, R.A O’Rourke, R. Roberts, E.H

Sonnenblick, Mc GrawHill, NY, 1998.

2. Texbook of Cardiovascular Technology, Lynn Bronson, Lippincot, U.S.A, 1987.

3. Merck Manual of Diagnostic Therapy, 16th Edition, R. Berkow, A.J Fletcher, M.H Beers, Merck

Research Laboratories, S.A, 1992.

4. Heart Attack, www.X-Plain.com, Updated: 08/11/2006, Patient Education Institute inc., © 1995-2006.

5. Myocardial Infarction, Adviware, Wrong Diagnosis.com, Updated: 09/03/2007, © 2000-2007.

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DEPARTMENT of CLINICAL TECHNOLOGYFACULTY of HEALTH SCIENCES

CLINICAL PRACTICE III

MYOCARDIAL INFARCTION

ASSIGNMENT 1

DONE BY: P. SIDLAYI

Reg. No.: 20507412Due Date: 20/04/2007

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