5384182 Myocardial Infarction Assignment

8/14/2019 5384182 Myocardial Infarction Assignment

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7.5 Air travel 8. Treatment 13 8.1 First line 8.2 Reperfusion 8.2.1 Thrombolytictherapy 8.2.2 Percutaneous coronary intervention 8.2.3 Coronary artery bypasssurgery 8.3 Monitoring for arrhythmias 8.4 Rehabilitation 8.5 Secondary prevention8.6 New therapies under investigation 9. Complications 16 9.1 Congestive heartfailure 9.2 Myocardial rupture 9.3 Life-threatening arrhythmia 9.4 Pericarditis9.5 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 anddeadly end results of heart disease, and is usually the result of some underlyingdisease such as coronary artery disease (which is a disease of occluded coronaryblood vessels).

The disease limits and eventually stops blood flow to the particular area of theheart muscle/myocardium supplied by the occluded coronary artery, thus resultingin a reduced amount of oxygen and other essential nutrients needed by the heartmuscle in order for it to be able to function as an effective pump. The lack ofoxygenated blood to the myocardium results in death of cardiac cells andmyocardial damage which causes loss of cardiac contractility therefore decreasedcardiac output. One of the most common symptoms of myocardial infarction is chestpain and the extent of myocardial cell death determines the size of theinfarction.

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1.

EPIDEMIOLOGY

1.1RISK FACTORS The risk factors are what predisposes the person to getting heartdisease in the first place as they make the person more prone to being ill. Someof the risk factors can be modified (meaning they can be reversed/changed) bylifestyle changes (e.g. eating healthy), and physical exercise, thus reducing the

chances of infarction. They may include any of the following: 1. Age the diseaseoccurs most commonly in old age (i.e. > 65 years). 2. Gender males are more atrisk of coronary artery disease, especially after the age of 65, and females aremore at risk between the ages of 20 to 65 years. 3. Family history thispredisposes the person to a higher risk of coronary artery disease. 4. Smoking cigarette smoke is known to have certain substances/gases that cause damage toblood vessel walls, thereby increasing the risk of myocardial infarction. 5. Highblood pressure (Hypertension) this is a common risk factor in many disorderse.g. Diabetes Mellitus and also increases the risk of myocardial infarction as itcan lead to the development of atherosclerosis, and the risk is associated withboth systolic dysfunction (which occurs as a result of loss of contractilefunction of the damaged myocardium) and diastolic dysfunction (which occursstraight after systolic dysfunction leads to an increased left ventricular end

diastolic distensibility which may cause hypertrophy. 6. Obesity increases therisk of coronary artery disease, stroke and hence myocardial infarction as itincreases strain on the heart, raises blood pressure, cholesterol levels, andincreases the risk of Diabetes. 7. Diabetes Mellitus this disorder is morecommon in obese people who are also more likely to develop hypertension, and itincreases the risk of myocardial infarction because it increases the progressionrate of arthrosclerosis and adversely affects blood cholesterol levels.

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

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

2.

PATHOPHYSIOLOGY of MYOCARDIAL INFARCTIONMyocardial infarction as was mentioned previously is the irreversible damage ofthe heart muscle, caused by a prolonged oxygen shortage (Hypoxia) as a result ofcoronary artery occlusion.

MECHANISM of OCCLUSION

The occlusion usually occurs as a result of the formation of a plaque on the innerwall of the blood vessel, thereby decreasing the diameter of the blood vessel inthat area. Eventually the atherosclerotic plaque raptures, leading to theformation of a blood clot/thrombus that may lead to partial or total occlusion ofthe 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 sometime fibrotic scar formation occurs in the area of the damage. The infracted areacan also serve as a source for the formation of life threatening arrhythmias suchas ventricular tachycardia/VT and ventricular fibrillation/VF. The damage to themyocardium also causes a disruption in the electrical activity of the heart andcauses 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 arterialsupply and the longer the duration of the occlusion, the greater the area ofdamage. From the endocardium, the damage spreads to the myocardium and then to theepicardium, which is the closest layer of heart muscle to the arterial supply. Itthen 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 timeof the occlusion i.e. the longer the period of time of occlusion, the moreirreversible the damage becomes, and (c) The presence/absence of collateralcirculation (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 arteryis occluded (blocked) there is no blood supply to that region. dark red = arteryblue = 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 arteryor any of its branches causing an obstruction to blood flow and it is the mostcommon cause of a myocardial infarction. Blood clotting does not usually form innormal arteries; however they do form in the presence of an atherosclerotic plaque(fatty deposit) that forms in the lining of the coronary artery. These plaquesform over a number of years in one or sometimes more than one branch of a coronaryartery 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 theinner layer to blood, which in turn stimulates the clotting mechanism leading tothe formation of blood clots that eventually cause an obstruction in theartery/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 ifit persists. It may occur at rest and can also occur in people without significantcoronary artery disease. If coronary artery spasm occurs for a long period oftime, a heart attack can occur.

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

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CLASSIFICATION

6.2 ST ELEVATION MYOCARDIAL INFARCTION / STEMI This type of infarction is causedby a prolonged period of blood supply to the heart muscle and it is an indicationthat a large area of heart muscle is affected by the infarction, thus causing thenoted electrocardiographic (ECG) changes. 6.2 NON-ST ELEVATION MYOCARDIALINFARCTION / NSTEMI This type of MI does not normally cause ECG changes. Theblockage of an artery in this case is

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usually partial or temporary, thus meaning that the extent of the damage to themyocardium is not large enough to cause notable ECG changes. 6.2 UNSTABLE ANGINA /UA Angina is a clinical syndrome caused by myocardial ischemia characterized bychest discomfort/pain. It is referred to as coronary insufficiency or Pre-Infarctangina and follows a progressive pattern. The discomfort / pain experienced by thepatient may be of varying intensity, last for a longer period of time, may bebrought about by less effort, or occur spontaneously at rest and can also occur inany 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 WAVEMYOCARDIAL INFARCTION (Previously referred to as Transmural MI) This type ofinfarction includes necrosis (tissue death) of the whole affected area of cardiacmuscle 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 increasedadrenergic/ sympathetic activity as well as increased blood fibrinogen (aglycoprotein & precursor of fibrin which is involved in blood clotting) levels andincreased platelet adhesiveness. 6.2 NON-Q WAVE MYOCARDIAL INFARCTION (Previouslyreferred to as Subendocardial MI) In this case, necrosis does not affect all thelayers of the heart muscle i.e. it might affect only the myocardium or both theendocardium and myocardium. Non- Q wave MI usually causes ST segment and T waveabnormalities. Early spontaneous reperfusion usually occurs with this type of MImostly 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 suppliedby 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.

SYMPTOMSChest pain this is the most common symptom and is usually characterized by chesttightness. Shortness of breath (dyspnea) this is due to decreased cardiac output

(therefore increased oxygen demand) as a result of compromised left ventricularfunction (LV failure), thus pulmonary congestion and/ edema. Nausea and vomitingPalpitations this is because the heart is trying to compensate for the poorventricular contraction by increasing the heart rate to try and pump out enoughblood. Sweating (diaphoresis) Syncope (dizziness) poor LV function lowerscardiac output, and therefore blood supply to the brain will be decreased anddizziness 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.

DIAGNOSISThe diagnosis of MI varies from one patient to the next with regard to theirindividual symptoms. A straight forward diagnosis can be made for those patientswho 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 medicalemergency and a person suspected of having an MI undergoes the followingprocedures and tests: ECG, Blood Tests, and Coronary Angiography.

6.1 DIAGNOSTIC CRITERIA 2 or more of the following WHO Guidelines may indicatethe presence of a definite MI. (a)history of ischemic chest pain lasting for morethan 20 minutes; (b)changes in serial / sequential ECG tracings; and(c)Instability of cardiac biomarkers such as Troponin 1, Creatine Kinase, andLactate Dehydrogenase enzymes specific to the heart. 6.2 PHYSICAL EXAMINATION Patients do not always present with the same symptoms, therefore on physicalexamination the presentation will be different for each patient. For example, onepatient might be restless with anxiety resulting in an increase in respiratoryrate (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 perspirationcan also be experienced. And since long-term infarction results in decreasedcardiac contractility, heart failure can also develop.

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6.3 ELECTROCARDIOGRAM / ECG The main aim of the ECG is to determine the presenceof ischemia or coronary injury because it is sensitive to detecting ischemia andinfarction and there are certain ECG changes that will indicate the presence ofdisease. These changes can include early ECG changes of T wave inversion and STdepression which may indicate infarction. The hallmark of acute myocardialinfarction is the development of abnormal Q waves (their presence is usuallyindicative of tissue death) which may appear a few hours after the onset ofsymptoms. 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 ShowingReciprocal ST Segment Depression None None None

Wall Affected

Suspected Culprit Artery

Septal Anterior Anteroseptal Anterolateral Extensive anterior (Sometimes calledAnteroseptal with Lateral extension) Inferior Lateral

Left Anterior Descending (LAD) Left Anterior Descending (LAD) Left AnteriorDescending (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 ObtuseMarginal Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX))

Posterior (Usually associated with V7, V8, V9 Inferior or Lateral but can beisolated) 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 determinethe area of damaged myocardium, but also helps in by making it easier to identifythe occluded artery. The following table shows the ECG changes that take place aswell as the affected area of the heart wall. www.wikipedia.com/ 6.4 CARDIACMARKERS / ENZYMES These are proteins from cardiac tissue released into the bloodstream when damage to the heart muscle occurs. These enzymes are contained in thecardiac cells within membranes associated with 11


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specialized cellular function such as contraction and they include- CreatinePhosphokinase (CK-MB), Myoglobin, and Troponin. Once they are outside the cell,they are cleared from the interstitial by cardiac lymphatics. And once they exceedthe capacity of the cardiac lymphatics to clear them, they become detectable incirculation. (a) Creatine Kinase-MB is a biomarker that is highly sensitive andspecific for to the heart. When infarction occurs, MB2 which is the tissue form ofcreatine kinase is initially released in small amounts so that CK-MB remainswithin 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 skeletaland cardiac muscle and also happens to bind to oxygen. It is a sensitive indicatorof muscle injury and its rise can help determine the infarct size and although itis not specific for cardiac muscle, it helps in the diagnosis of MI. (c) TroponinT & I These are regulatory muscle proteins released by damaged myocardial cellsand are more specific for MI than MB-CK. They increase plasma levels a few hoursafter an infarction occurs. (d) Lactate Dehydrogenase This is another proteinwhich becomes elevated with the occurance of a myocardial injury. It increases afew days after the onset of symptoms and lasts up to 10 days. It is less commonlyused nowadays. 6.5 ANGIORAPHY This is a percutaneous procedure that involves themaking of an incision in the groin area for the insertion of a cardiac catheterinto the femoral artery which helps to gain access to the heart and its coronaryarteries. 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. Thishelps to see the extent of the occlusion and which branches are affected, therebymaking it easier for the Cardiac Surgeon to decide whether that vessel should beopened up by insertion of a balloon or stent to keep it open (CoronaryAngioplasty).

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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 thattake place during the occurrence of an infarction. The histologicalcharacteristics of an infarction are usually examined in specimens obtained frominfarct-related coronary artery lesions in patients with initial infarction whoundergo directional coronary atherectomy (removal of an atheroma by the use of asingle-blade balloon) following intracoronary thrombolysis within 6 hours after

the onset of chest pain. Removed tissues were fixed in buffered formaldehyde andembedded in paraffin, and the thick paraffin sections are then stained withhematoxylin-eosin and examined by light microscopy which revealed the presence ofthrombus and/ intramural hemorrhage in the samples. High incidences of cholesterolcleft, foam cell, calcium deposit and intimal proliferation are also observedwhich further suggest that thrombus and/ intramural hemorrhage are importantfactors 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 71year old Asian male. The features are those of acute myocardial infarction showingneutrophilic infiltrate along with areas of necrosis, diffuse interstitial edemaand pale myocytes with fading nuclei and decreased striations.www.histopathologyindia.net/Heart5.htm

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Since myocardial infarction is regarded as a common medical emergency, theemergency medical principles that apply in First Aid courses also apply with amyocardial infarction.

FIRST AID

6.2 IMMEDIATE CARE In the case of severe chest pain/ infarction, it is advisableto call for immediate help to prevent / minimize further damage to the heart. Thepatient should sit in a position that will allow them to be able to breathenormally without too much effort/ trouble (e.g. half sitting with knees bent). Incase of unconsciousness, it is important to have an external defibrillator at hand(if possible). Aspirin dissolved or given sublingually (for quicker absorption bythe body) also helps prevent further clot formation in the arteries. Glyceril

Trinitrate/TNT can also be give as it helps dilate (relax) blood vessels andtherefore allows for more blood flow, thus reducing the chest pain. The person whois with the patient before the Medics arrive is responsible for getting thepatients particulars as well as any other information that might help acceleratethe treatment of the patient such as the severity/ nature of the pain, patientactivities at the time of onset. 6.2 AUTOMATIC EXTERNAL DEFIBRILLATION/ AED Installation of external defibrillators in public places may help reduce thenumber of deaths due to sudden 14


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heart attacks as they are able to monitor and analyze cardiac rhythm and determinewhether the patient can be shocked. 6.2 EMERGENCY SERVICES They differ in theirway of treating patients of suspected MI. Even so, all emergency services make iteasier for patients to gain medical treatment. The treatment may include Aspirin; TNT (given sublingually); Thombolytic therapy; Oxygen; and Morphine. A 12Lead ECG can help in recognizing patients with ST elevation MI, thereforeproviding a basis for medical staff at a hospital to perform emergency coronaryangioplasty and open the occluded vessel. 6.2 WILDERNESS FIRST AID Under these

circumstances, it is important to remove the person whos suspected of having aheart attack to an area that provides easy access to medical care. This saves timeand the trouble of having to carry the person in the event of them losingconsciousness. 6.2 AIR TRAVELL It is wise to have First Aid kits with differentmedication in this type of public transport as you never know when they might beneeded. Having staff that is well equipped in terms of dealing with these kinds ofemergencies and in the event of an MI, the pilot can land in the nearest Airportand notify them of the emergency in order to get faster access to medicaltreatment. It is also important for the person who knows they suffer from heartdisease to carry their medication as this might prove helpful in the case of themhaving chest pain or even a heart attack.

8.

Myocardial Infarction is a serious medical emergency that requires immediate andeffective medical therapy in order to prevent extended myocardial damage. Anydelay 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 amedical facility and to get proper treatment. It also helps to reduce the pain andmay 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; andAspirin to prevent further clotting of blood and damage to the heart, hencereducing mortality.

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8.2 REPERFUSION This is an important part of the treatment of myocardialinfarction and includes 3 types Thrombolytic therapy; Angioplasty; and Bypasssurgery. Reperfusion is important mainly in patients with STEMI or those showingrecent bundle branch blocks on a 12 Lead ECG. 8.2.1 Thrombolytic Therapy Thistreatment is indicated mainly in ST elevation MI and is usually more effectivewithin the first 2 hours of the onset of symptoms. Thrombolytics prevent furtherformation of thrombi/ clots and allow for blood flow to occur. They may includethe 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 optionfollowing thrombolytic therapy that is used to open occluded coronaries. As incoronary angiography, Angioplasty includes the insertion of a catheter (with aballoon) into the femoral artery to gain access to the heart and its coronaryarteries. During this procedure, dye is also injected in order to locate theoccluded vessel and X-Ray photos are also taken and the balloon or stent or bothare 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 ofthe procedure to prevent blood from clotting. TNT is also sometimes given tominimize 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 patientsthat have a high risk of left main coronary artery thrombosis during a coronaryintervention and those who are more prone to Cardiogenic shock and is usually 16


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done a few weeks after the occurance of an acute myocardial infarction. Itinvolves implantation of an artery/ vein (usually taken from the internal mammaryartery or the saphenous vein) into the aorta to bypass the occlusion. Thisprocedure is more successful in patients that have a less number of occludedvessels.

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

8.3 MONITORING for ARRHYTHMIAS This is done to prevent the occurance of lifethreatening arrhythmias and treatment such as anti-arrhythmic agents is given toprevent development of arrhythmias especially after an acute infarction. After theprocedure, monitoring of the patients condition/ improvement is continued in thehospital ward or Cardiac ICU. 8.4 REHABILITATION - The aim of cardiacrehabilitation is to optimize/ produce effective cardiac function and improvequality of life of the patient. Light exercises help reduce the reoccurrence ofthe controllable risk factors such as cholesterol as its levels are lowered duringexercise, obesity weight loss, and patients can also supplement their exerciseby 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 theheart can only tolerate light work. 8.5 SECONDARY PREVENTION Lifestylemodification, 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 preventdevelopment 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 loweringoxygen demand, and they also reduce MI mortality by decreasing the incidence ofarrhythmogenic death (death by the occurance of dangerous arrhythmias e.g.ventricular fibrillation). (c) Ace-inhibitors (Diltiazam, Nifedepine) to reduceventricular 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 injectionof the patient with stem-cells derived from their bone marrow and they showimproved cardiac output. (b) Progenitor cell infusion and tissue engineering aresome of the other therapies still under investigation.

9.

COMPLICATIONS of MI

9.1 Life threatening arrhythmia conduction disturbances in the heart mayindicate 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 maylead to complete heart block.

www.acc.org/ 9.2 Heart failure myocardial infarction reduces the pumping abilityof the heart and depending on the part of the heart that has been affected, theheart failure can either be left/right sided or bilateral (affecting both sides ofthe heart). But, regardless of which side of the heart is affected, cardiac outputis 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 andpulmonary congestion because its becoming more difficult to get blood into theheart. 9.3 Cardiogenic shock this is caused by inadequate cardiac function whichin turn results in decreased cardiac output and is characterised by hypotension,tachycardia, and a reduction in urine output. The decrease in cardiac outputcauses an increase in oxygen demand by the body. Cardiogenic shock is commonlyassociated with infarction of the anterior wall of the myocardium and loss of leftventricular functioning myocardium. 9.4 Myocardial rupture it occurs as a resultof increased pressure against the weak walls of the heart chambers due toineffective 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 volumeoverload occurs and is sustained; and lastly, External 19


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rupture which involves rupture of the myocardium itself, is characterised by asudden loss of arterial pressures and occurs more frequently in the leftventricular wall because its 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. Inflammationoccurs in the area of the damage as a result of transmural injury, thusinflammation of the pericardium will occur due to inflammatory responses of the

heart.

10. PROGNOSISThe expected outcome varies with the amount and location of damaged tissue. Theoutcome 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 afteran attack, the probable outcome for survival is good, but may includecomplications. Uncomplicated cases may recover fully; heart attacks are notnecessarily disabling. Usually the person can gradually resume normal activity andlifestyle.

11. LEGAL IMPLICATIONS

At common law, a myocardial infarction is generally a disease, but may sometimesbe 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 emotionalstress or unusual exertion. Additionally, in some jurisdictions, heart attackssuffered by persons in particular occupations such as police officers may beclassified as line-of-duty injuries by statute or policy. In some countries orstates, 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 exampledriving a car, taxi or airplane. www.wikipedia.com/ Myocardial infarction is alife-threatening disease that requires immediate and effective treatment asmentioned previously. For some people it can be a life changing experience as itmakes people realize how important it is to live a heart healthy lifestyle. Theongoing research for new ways to treat myocardial infarction and the new ways ofdetecting it before the onset of symptoms can help minimize the number of deathswith of course the cooperation of the patient in terms of them changing theirlifestyle and reducing the number of modifiable risk factors.

REFERENCES1.Hursts The Heart, 9th Edition, R.W Alexender, R.C Schlant, V. Fuster, R.A

ORourke, 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.HBeers, 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 INFARCTIONASSIGNMENT 1

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

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Documents

5384182 Myocardial Infarction Assignment