Topic: Myocardial Infraction

MYOCARDIAL INFRACTION
Rathod

Mrs. Suchitra Asst

Prof

A myocardial infraction (MI), commonly known as a heart attack, results in the death of heart muscle.

The affected myocardial cells in the heart are permanently destroyed. An M I occurs from a partial or complete blockage of coronary artery,. which decrease the blood supply to the cells of the heart supplied by the blocked coronary artery

The extent of the cardiac damage varies depending on the location and amount of blockage coronary artery. Cardiac conduction, blood flow and function can be dramatically altered by an M I Definition of M I:- Myocardial Ischemia (MI) is death (coagulative necrosis) of myocardial tissue resulting from an active decrease in coronary blood flow or an abrupt rise in myocardial oxygen demand without sufficient coronary artery perfusion.

M I usually follows the sudden occlusion a coronary artery and the abrupt cessation of blood and oxygen flow to the heart muscle OR

Myocardial infarction occurs when ischemic intracellular changes become irreversible and necrosis results It is also known as heart attack coronary occlusion, is a lifethreatening condition characterized by formation of localized necrotic areas in myocardium It usually follows sudden occlusion of coronary artery and abrupt cessation of blood and oxygen flow to heart muscle.

Etiology of MI:- Same etiology of CAD Direct and risk

factors Classification of M I :- 1.Anterioseptal MI- Involves a portion of the anterior left ventricular wall, the apex and the intraventricular septum and results from occlusion of the left anterior descending artery

2. Anteriolateral MI- this type of MI involves a portion of the anterior as well as a portion of the lateral wall of the left ventricle and results from occlusion of the left circumflex artery.

3. Inferior (Diaphragmatic) MI- This involves the inferior portion of the left ventricle and is usually a results of right coronary artery occlusion.

4. Posterior MI- This involves the posterior portion of the left ventricle and intraventricular septum and can occur from either right coronary or circumflex artery occlusion 5. Right ventricular MI- This kind of MI is usually associated with right coronary artery occlusion and often accompanies an inferior or posterior MI. It is difficult to diagnose.

Development of Plaques:- The stages of development

in atherosclerosis are: I. Fatty Streaks:- soft, yellow, slightly raised lesions on the inner surface of the artery but dont cause vascular obstruction.

It is lipoprotein deposits (mostly cholesterol) these may regress remain static or progress to plaque. Mechanism not understood well. II. Fibrous Plaque:- Develop from fatty streaks. They are grayish-white (yellowish-gray) plaques thicken and extend into the lumen of the artery, interfering with blood flow.

It is made up of three types of martial:- 1. Smooth muscle cells from the middle layer.

2. Collagen. 3. Accumulated lipid within the intimal layer. III. Complicated Lesions:- Develop from the continued accumulation of fat, connective tissue and cells.(Fibrous plaques). They extend into lumen; blood clots develop and form thrombi. Deterioration of the arterial wall may lead to rupture and hemorrhage. Calcium precipitates out of the blood and lipids and forms on plaques. This vessel loses their elasticity and later rupture.

Pathology of MI:- Cellular Changes- Persistent ischemia

(3 to 6 hours) will produce irreversible cellular damage.

Hypoxic cells are forced to find alternative energy substrates. Unable to use free fatty acids, the predominant energy source under normal aerobic conditions, myocardial cells must rely on anaerobic glycogenolysis.

Anaerobic metabolism of glucose is a much less efficient means of energy production. As energy availability falls, metabolites accumulate, pH falls and myocardial function fails.

This result in reduced myocardial contractility, stroke volume, diminished ejection fraction, left ventricular enddiastolic pressure and altered ventricular wall compliance.

Peripheral vascular resistance usually in response to the inevitable catecholamine release and tends to produce both a greater preload and afterload, the burden of the ailing heart

Zones of Infarction- A wave of necrosis spreads across

the ventricular wall from endocardium to epicardium. A central core of coagulative necrosis occurs, in which all cells are dead, including myocardial cells, connective tissue, and capillaries.

This central area of necrosis is surrounded by viable areas of injury and ischemia. Severely ischemic tissue may progress to necrosis if interventions are not implemented within 6 hrs of coronary occlusion.

By 24 to 96 hrs. after MI, there may be a significant in collateral blood flow to revitalize the ischemic area.

Extent of Infarction- Involvement of MI

Transmural Infarction- This involves the full thickness of the myocardium evolving from endocardium to epicardium

Subendocardial Infarction- Generally confined to the area of the subendocardium, producing contraction band necrosis.

The term Non-Q wave MI is sometimes used to describe subendocardial infarction. Severity of damage:- The amount of damage is dependent upon a number of different factors:

Degree of coronary artery occlusion Size and location of the area supplied by the narrowed vessels

Oxygen needs of the poorly perfused myocardium.

Extent of collateral blood vessel development. (An occluded artery need not result in MI if there is extensive collateral circulation present)

Morphology changes:- In the first 12 hrs, the damaged

myocardial tissue appears normal upon gross inspection In 18 to 48 hrs, the infarcted tissue appears pale with focal, redpurple areas of interfiber hemorrhage.

In 2 to 10 days, the necrotic area is very apparent. The tissue appears yellowish and soft and contains areas of hemorrhage. This is the most likely time for ventricular rupture. Within 10 days to 6 weeks, the necrotic tissue is replaced by gray, fibrous, non-contractile scar tissue.

In 2 months, the maximum density of scar tissue is achieved.

Diagnostic evaluation:examination

History and physical

ECG- changes occurs first in the ST segment, then the T wave and finally the Q wave. As the myocardial heals, the ST segment and T wave returns to normal, but Q wave changes remains evident. In subendocardial Infraction, the T wave is also inverted. Non- Q wave MI- Approximately 24% of acute MI patients do not generate pathologic Q waves but have persistent ST- T segment changes. ST segment in V2 and V3 that is isoelectric depressed or minimally elevated (1mm) & T wave inversion in V2 to V5 or V6

Determination of MI:Location of MIWith reciprocal Leads with indicative -

changes

changes
V1, to V3 V5,V6, I, AVL II, III, AVF III II, III, AVF II, III, AVF I, AVL V1, V2

Anteroseptal MI Anterolateral MI Inferior or diaphragmatic Posterior MI -

Right ventricular I, II, AVF, V1, V2 MI V1 to V3 Indicative changes involve abnormal findings in the leads facing the surface of the damaged area Reciprocal changes involve findings in the leads facing the opposite surface of the damaged areas Chest x-ray:- To asses heart size and pulmonary vasculature Routine laboratory tests:- a) CBC to rule out anemia and polycythemia Elevation in WBC may correlate to myocardial tissue damage b) Cardiac enzymes

c) Serum electrolytes- sr. potassium, serum sodium,etc Blood sugar, Renal and Hepatic function

Echocardioum- Evaluates heart size, configuration values and wall motion, hypokinesis, dyskinesis and akinesis Angiography- Identifies the exact location of coronary artery occlusion and assesses efficacy of left ventricular function. Radioisotope studies- Thallium scans, ventriculography, positron emission tomography, MRI are used to assess the location and extent of Myocardial Infraction. ST segment mapping-This procedure is used to predict myocardial necrosis

Clinical manifestations of MI:- Chest pain similar

to angina pectoris but more severe and unrelieved by nitroglycerine

The pain may radiate to the neck, jaw, shoulder, back or left arm Pain may present near the epigastrium, stimulating indigestion. Pain described as heaviness, tightness or constriction located substernally or retrosternally

It may occur during rest, sleep or while awake Commonly occurs in the early morning hours. Pain lasts for up to 30 minutes or more, intensity of pain is variable.

Sometimes may described as epigastric discomfort, weakness or shortness of breath Nausea and vomiting (indigestion) due to severe pain or vagovagal reflexes conducted from area of damaged myocardium to gastro-intestinal tract or decreased cardiac out put.

Diaphoresis skin becomes cold and clammy (cold sweat)catecholamines are released & ses. The increased sympathetic nervous system stimulation results

Fever:- Temperature may increase within 24 hours upto 38 C (100 - 103 F) accompanied by leukocytesis and elevated ESR may last for a week. (Fever WBC increased from destruction of myocardial tissues and inflammatory process)

Fever drops when fibroblasts begin to replace leukocytes and scar tissues starts to form or pulmonary embolism Blood pressure elevated initially, may drop later because of low cardiac output

Pulse rate increases (fast),slow or irregular. In severe conditions, abnormal heart sounds may be heard.

Dyspnea- In some cases left ventricle becomes severely crippled in pumping action owing to Infarction, severe pulmonary congestion results. Respiration rate increased, crackles (pulmonary edema) Oliguria- Urine output decreased. (urine flow of less than 30 ml/hr. Indicates renal hypoxia due to in adequate tissue perfusion resulting from hypotension.

Shock- Systolic BP below 80 mm of Hg, gray facial colour, lethargy, peripheral cyanosis, diaphoresis, tachycardia or bradycardia, weak pulse (severe pain or by severe reduction in cardiac output and inadequate tissue perfusion resulting in tissue hypoxia)

Complications of MI:- Dysrhythmias are the major cause

of MI. Ectopic rhythm arise in or near the borders of intensity Ischemic and damaged myocardial tissues.

Damged myocardium interfere with conduction system, causing dissociation of the atria and ventricles (heart block) Supraventricular tachycardia (SVT)- as a result of heart failure.

Ventricular fibrillation (Vf) Heart block Congestive heart failure

Cardiogenic shock Pulmonary Embolism- may develop to secondary to phlebitis of the leg or pelvic veins (venous thrombosis) or from atrial flutter of fibrillation.

Recurrent Myocardial Infarction- within 6 years after an initial. causes include over exertion, embolization or further thrombotic occlusion of a coronary artery by an atheroma

Papillary muscles dysfunction- cause mitral regurgitation which results in dyspnea, gross pulmonary edema, decreased cardiac output Ventricular aneurysm- Ectopic impulses on palpation, bulges seen in x-ray, persistent long ST segment changes in ECG Pericarditis- In an acute transmural MI will develop early (within 2 - 4 days). The inflamed area of the infarction rubs against the pericardial surface and causes it to lose its lubricating fluid. Chest pain increases with movement, deep inspiration and cough. Pain relieved by sitting up and leaning forward

Comparison of s & s in Angina Pectoris & MI

Sl. Angina pectoris No

MI

1.

Provoked by effort. Exertion, Occur both at rest & during exertion, exposure to cold & heavy meals can often, without any apparent cause. precipitate anginal pain Pain is felt during effort & it is relieved by rest The patient assumes a position of immobility with pain Pain is not relieved by rest. It persists even while resting. MI often comes while the patient is at rest. The pain becomes restless

3 4 5

The pain usually lasts for 5 to 10 Pain lasts longer than 30 minutes minutes Relief is obtained with nitrites No relief with nitrites

Pain is retrosternal. Feels a Pain is similar in character to that of sensation of tightness, constriction angina pectoris, or pressure pain may radiate to the but is more severe and last longer shoulders, lower jaw and upper limbs. Vomiting is absent Dyspnea is absent. Pt. holds the breath at the time of pain Shock is absent Vomiting is often present Dyspnea is common Shock can occur when 40% or more of the myocardium is damaged Sweating may be profuse Fever often occur after 48 to 72 hours of Infarction Pulse may be normal but is often rapid, weak & / or irregular A tendency for the blood pressure to fall Typical changes in the ECG changes occurs during the 1st few days Major goals are:-

7 8 9

10 Sweating is minimal 11 Fever is absent 12 Pulse is normal or rapid 13 Blood pressure is normal or increased 14 Temporarily changes in the ECG occur during the pain

Medical management of M I:-

Successful treatment of acute attack and prompt alleviation of manifestations Prevention of complications and further attacks Rehabilitation and education of the patient and significant others An acute MI needs immediate admission to a hospital with a coronary care unit. The first goal of treatment is to decreased hearts workload and increase oxygen supply to the myocardium to limit the area of infraction.

 Workload is sed through rest, ing preload and eliminating tachycardia Pain control is a priority. Continued pain is a symptom of continuing myocardial ischemia. pain stimulates the autonomic nervous system and es preload and myocardial demands

The drug of choice for MI pain is Morphine Sulphate given in small doses intravenously.

Nitrates are given for their vasodailating effect Oxygen is administered to treat tissue hypoxia because dysrhythmias are common ECG monitoring is essential. Administrating of antiarrythmics drugs

Anticoagulants are given to the risk of embolism

Stool softeners are given to constipation and the risk of bradycardia from straining Standard treatment for acute MI also includes reperfusion therapy to limit infraction size, improve left ventricular function and mortality. Reperfusion can be accomplished through PTCA or medication that lyse or dissolve the clot that is blocking the coronary artery Thrombolytic therapy includes streptokinase, urokinase, tissue- plasminogen activator and acylated plasminogen streptokinase activator complex. Thrombolytic agents should be given within 3 to 6 hours after the onset of chest pain.

 After thrombolytic agent is administered intravenous heparin therapy is usually continued for 5 to 7 days Successful reperfusion of the coronary arteries is evidenced by return of ECG changes to normal, relief of chest pain, presence of reperfusion dysrhythmias usually ventricular and a rapid, early peak of CK-MB enzymes called washout

Complications of thrombolytic therapy include bleeding, allergic reaction and stroke.

Nursing management:- Goals of MI:- 1. Recognition

and treatment of potentially life-threatening dysrhythmias

Monitoring for complications of reduced cardiac output Maintenance of a therapeutic critical care environment Identification of the psychosocial impact of MI on the client and family Education of the client in life-style changes and rehabilitation