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Contents

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1a. Introduction 1b. Epidemiology 1.1 Risk factors 2. Pathophysiology 3. Causes 4.


Classification 5. Symptoms 6. Diagnosis 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
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3 4

5 6 7 8 9
7.5 Air travel 8. Treatment 13 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

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12. Conclusion 18 13. References 18

INTRODUCTION

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.

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1.

EPIDEMIOLOGY

1.1RISK 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). 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.

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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 OCCLUSION

The 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 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.

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MECHANISM of MYOCARDIAL DAMAGE

Cell 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,
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 occlusion, the more
irreversible the damage becomes, and (c) The presence/absence of collateral
circulation (circulation in two branches that parallel to each other/side by side)
– the larger the infarction, the greater 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 the the run the

Circumflex occlusion back of heart

Left anterior descending (LAD) occlusion front 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 rapture
http://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

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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. 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 Subendocardial 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/

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

5.
1. 2.

SYMPTOMS
Chest pain – this is the most common symptom and is usually characterized by chest
tightness. 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. Nausea and vomiting
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. Sweating (diaphoresis) Syncope (dizziness) – poor LV function lowers
cardiac output, and therefore blood supply to the brain will be decreased and
dizziness results. Fatigue – this is also due to the great oxygen demand.

3. 4.

5. 6. 7.

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The above is an example of a patient presenting with chest pain. www.wvhsta.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; (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.

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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.
Leads Showing ST Segment Elevation V1, V2 V3, V4 V1, V2, V3, V4 Leads Showing
Reciprocal ST Segment Depression None None None

Wall Affected

Suspected Culprit Artery

Septal Anterior Anteroseptal Anterolateral Extensive anterior (Sometimes called


Anteroseptal with Lateral extension) Inferior Lateral

Left Anterior Descending (LAD) Left Anterior Descending (LAD) Left Anterior
Descending (LAD) Left Anterior Descending (LAD), Circumflex (LCX), or Obtuse
Marginal

V3, V4, V5, V6, II, III, aVF I, aVL

V1,V2,V3, V4, V5, V6, I, aVL

II, III, aVF

Left main coronary artery (LCA)

II, III, aVF I, aVL, V5, V6

I, aVL II, III, aVF

Right Coronary Artery (RCA) or Circumflex (LCX) Circumflex (LCX) or Obtuse


Marginal Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX))

Posterior (Usually associated with V7, V8, V9 Inferior or Lateral but can be
isolated) Right ventricular (Usually associated with Inferior)

V1,V2,V3, V4

II, III, aVF, V1, I, aVL V4R

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/ 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 11
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).

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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
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.

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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.histopathologyindia.net/Heart5.htm

7.

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.

FIRST AID

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 14
heart attacks as they are able to monitor and analyze cardiac rhythm and determine
whether the patient can be shocked. 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.

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.

TREATMENT

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.

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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.
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 16
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

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

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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.

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

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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 19
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.

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

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12. CONCLUSION

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/ 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 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.

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5.

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


2007.

__________________________________________________________________________________
____

DEPARTMENT of CLINICAL TECHNOLOGY FACULTY of HEALTH SCIENCES

CLINICAL PRACTICE III

MYOCARDIAL INFARCTION
ASSIGNMENT 1

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DONE BY: P. SIDLAYI Reg. No.: 20507412 Due Date: 20/04/2007

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