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MYOCARDIAL INFARCTION

Definition

When coronary blood flow is interrupted for an extended period of time, myocyte (muscle tissue cell) necrosis occurs. The most common cause is the sudden occlusion of a coronary artery usually the result of rupture of atherosclerotic plague and subsequent thrombus formation.

Risk Factors

As per CAD Metabolic Syndrome if 3 or more of the following are present - abdominal obesity - hyperglycemia (insulin resistance) - Low HDL - High triglycerides for women - Hypertension Increased Homocysteine/C reactive protein Chronic Inflammatory conditions, infections with a variety of bacterias.

Prognosis

During an MI men are more likely to die than women Women have a higher mortality in hospital (may be a result of the manifestations and the differences in treatment) 70,000 heart attacks every year in Canada. Approx. 19,000 die and most of these occurred outside of the hospital (Heart and Strokes Foundation of Canada) The heart attack related hospitalization is on the rise steadily over the past decade.

Etiology
Plaque rupture can be precipitated by

Internal Factors

External Factors strenuous activity emotional stress

- plaque characteristics (size, consistency of the core, thickness of the fibrous cap) - Conditions to which it is exposed to such as coagulation status, degree of arterial constriction

Pathophysiology

Sudden coronary obstruction caused by thrombus formation over a ruptured or ulcerated plague, the acute coronary syndrome results Unstable angina is associated with short-term occlusion, whereas MI results from significant or complete occlusion that lasts more than 1 hour.

Relationships among CAD, Stable Angina, and MI

Fig. 33-7

Etiology and Pathophysiology


Collateral Circulation

Growth of collateral circulation is attributed to two factors: The inherited predisposition to develop new vessels The presence of chronic ischemia

Etiology and Pathophysiology


Collateral Circulation

When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing

Collateral Circulation

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Fig. 33-4

Pathophysiology

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Myocardial Infarction Occurs as a result of sustained ischemia, causing irreversible cellular damage Size of the infarct depends on: - extent, duration and intensity of the ischemia - amount of collateral circulation - Metabolic needs at the time

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Pathophysiology

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Myocardial Infarction The degree of altered function depends on the area of the heart involved and the size of the infarct Contractile function of the heart stops in the areas of myocardial necrosis Most involve the left ventricle (LV) and this affects the stroke volume and cardiac output

Pathophysiology

Myocardial Infarction

Transmural MI: involves the entire thickness of the myocardium Subendocardial infarction: The damage has not penetrated through the entire thickness

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Etiology and Pathophysiology


Healing Process

Within 24 hours, leukocytes infiltrate the area of cell death (necrosis) Enzymes are released from the dead cardiac cells (important indicators of MI)

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Etiology and Pathophysiology


Healing Process

Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by 2nd or 3rd day Development of collateral circulation improves areas of poor perfusion

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Etiology and Pathophysiology


Healing Process

Necrotic zone identifiable by ECG changes and nuclear scanning 10 to 14 days after MI, scar tissue is still weak By 6 weeks after MI, scar tissue has replaced necrotic tissue - area is said to be healed

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Etiology and Pathophysiology


Healing Process

Ventricular remodeling In an attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate. This can result in the development of congestive heart failure.

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Clinical Manifestations
Severe chest pain: knife like, suffocating and heavy pressure Pain can radiate to different locations More severe compared to angina Longer duration compared to angina Pain not relieved by rest and nitro

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Clinical Manifestations

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Nausea and vomiting - Can result from reflex stimulation of the vomiting centre by the severe pain Sympathetic nervous system stimulation catecholamines released during initial phases of MI Results in diaphoresis and vasoconstriction

Clinical Manifestations

Fever Systemic manifestation of the inflammatory process caused by cell death May within first 24 hours May last as long as 1 week

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Clinical Manifestations

Cardiovascular manifestations Increased BP and heart rate initially Later the BP may drop from decreased cardiac output urine output Crackles Hepatic engorgement Peripheral edema

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Clinical Manifestations

Womens signs and symptoms Symptoms may be non-specific Dyspnea fatigue Feeling unwell Symptoms mimicking acid reflux

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Clinical Manifestations

Case Study

Diagnosis

ECG- Changes occur first in the ST segment then the T wave and finally the Q wave. As the myocardium heals the ST and T waves return to normal but the Q wave changes persist.

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Diagnosis

Elevated serum creatine kinase isoenzyme (CK-MB is primarily found in cardiac muscle increase 3-6 hrs after the onset of chest pain . Elevated myoglobin LDH, AST, WBC, ESR. Elevated cardiac troponin T and I identify very small amount of myocardial damage. Troponin T increases within 3-6 hrs after the onset of pain. Troponin I increases 7-14 hrs after the onset of pain. Imaging studies identify presence and location of poor perfusion but do not indicate when.

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Management

Reduce Pain

Improve perfusion
Mechanical/Surgical Interventions

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Pain Management

Morphine is the drug of choice if chest pain is unrelieved by nitrates and oxygen

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Improve Perfusion

Thrombolytic therapy: best results are achieved within 60 to 90 minutes of symptom onset. Some benefit can be achieved for up to 12 hours after the onset of symptoms (e.g. Alteplase, reteplase and tenecteplasetPA) These agents interact with plasminogen to generate plasmin which lyses fibrin clots and digest clotting factors V, VIII, prothrombin and fibrinogen. Antiplatelets: prevent platelet aggregation Anticoagulation therapy (heparin and warfarin) Nitrates (nitroglycerin)

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Beta-adrenergic blocking agents Calcium channel blockers ACE inhibitors

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Mechanical/Surgical Interventions

PTCA Percutaneous transluminal angioplasty with stent placement Pacemaker CABG Coronary artery bypass graft

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Coronary Angioplasty

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Cardiac Rehabilitation

To improve compliance in medical therapies and lifestyle changes Exercise: walking swimming and cycling or individually tailored Nutrition: low salt, low fat Smoking cessation Stress management Medications

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Complications of Myocardial Infarction

Arrhythmias - Most common complication - Present in 80- 90 % of MI clients - Most common cause of death prior to hospital admission Congestive heart failure A complication that occurs when the pumping power of the heart has diminished.

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Complications of Myocardial Infarction

Cardiogenic shock Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure Requires aggressive management 9% of the death

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Complications of Myocardial Infarction

Ventricular aneurysm Results when the infarcted myocardial wall becomes thinned and bulges out during contraction

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Complications of Myocardial Infarction

Pericarditis - An inflammation of the visceral and /or parietal


pericardium - May result in cardiac compression, decrease LV filling and emptying, and cardiac failure - develops in up to 28% of clients This could develop as early as 2- 4 days and as late as 6

weeks
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Complications of Myocardial Infarction

Pulmonary embolism Source of the thrombus may be the roughened endocardium or leg veins

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Complications of MI

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References
Black, J. & Hawks, J. (2009). Medical-surgical Nursing: Clinical management for positive outcomes (8th ed.). St. Louis: MO: Elsevier. Braun, C. & Anderson, C. (2007). Pathophysiology: Functional alterations in human health. Philadelphia: PA: Lippincotts Williams &Wilkins. Brophy, K., Scarlett-Ferguson, H. & Webber, K. (2008). Clinical drug therapy for Canadian practice (1st Canadian edition). Quebec: Lippincott Williamson &Wilkins. Hannon, R. A., Pooler, C. & Porth, C. M. (2010). Porth pathophysiology: Concepts of altered health states (First Canadian Ed.). Philadelphia, PA: Lippincotts Williams &Wilkins . pp. 522-530 Heart & Strokes Foundation of Canada (2009) Tests Retrieved November 16, 2009 from Http://www.heartandstroke.bc.ca/site/c.kpIPKXOyFmG/b.3644463/k.7DB9/Heart_Disease.ht m Lewis, S. Heitkemper, M. & Dirksen, S. (2006) Medical-surgical nursing in Canada: Assessment and management of clinical problems (1st Canadian edition). Toronto, ON: Elsevier Canada. McCance, K. & Huether, S. (2006). Pathophysiology: The biologic basis for disease in adults and children (5th edition). St. Louis, MO: Mosby Elsevier.

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