MYOCARDIAL INFARCTION

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4/28/12 -Habiba L. Ali, RN

Myocardial infarction (MI) or acute myocardial infarction (AMI) is the rapid development of myocardial necrosis caused by a critical imbalance between oxygen supply and demand of the myocardium. It is commonly known as heart attack. Inadequate coronary blood flow rapidly results in myocardial ischemia in the affected area. The location and extent of the infarct determine the effects on cardiac function. Ischemia depresses cardiac function and triggers autonomic nervous system responses that exacerbate the imbalance between myocardial oxygen supply and demand. Persistent ischemia results in tissue necrosis and scar tissue formation, with permanent loss of myocardial contractility in the affected area. Cardiogenic shock may develop because of inadequate CO from decreased myocardial contractility and pumping capacity.
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TYPES OF MYOCARDIAL INFARCTION:

(a) Transmural: associated with atherosclerosis involving major coronary artery. It can be subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply. (b) Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular 4/28/12 septum, or papillary muscles.

A 2007 consensus document classifies myocardial infarction into five main types:
Type 1 Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection Type 2 Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension Type 3 Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood Type 4 Associated with coronary angioplasty or stents: Type 4a Myocardial infarction associated with PCI Type 4b Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy 4/28/12 Type 5 Myocardial infarction associated with CABG

RISK FACTORS
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 4/28/12 myocardial infarction as it increases strain on the heart, raises blood pressure, cholesterol levels, and increases the risk of Diabetes.

CAUSES
(a)

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. (b) Coronary Artery Thrombosis this is a blood clot that forms inside 4/28/12 the artery or any of its branches

PATHOPHYSIOLOGY

The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. Blood stream column irregularities visible on angiographies reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium). If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form a cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction. As a result, the patient's heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias. Total occlusion of the vessel4/28/12 than 4-6 for more hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and

SIGNS AND SYMPTOMS

COMMON S/Sx

Chest pain. Classically presents with diffuse, severe chest pain that can occur at rest or with exertion, is heavy in nature, located centrally with radiation to the left arm or jaw, and lasts for at least 20 minutes. Dyspnea. Common feature associated with MI due to pulmonary congestion from diastolic dysfunction. Pallor. due to high sympathetic output. Diaphoresis. due to high sympathetic output. Nausea and/or vomiting. Non-specific for MI, but commonly associated with inferior-wall MI due to increased vagal tone, and can be the only indicator of inferior-wall MI. Dizziness or light-headedness. due to hypotension or bradycardia. Weakness. due to hypotension or bradycardia. More common presentation in women, older people, and those with diabetes. Tachycardia. Especially in anterior-wall MI, due to high sympathetic output. Anxiety. Patients may express anxiety or appear anxious. They may also 4/28/12 report a feeling of impending doom. Additional heart sounds. An audible S3 or S4 on cardiac examination

*Elderly patients and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. The elderly may also present with only altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever. *As many as half of MIs are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. A high index of suspicion should be maintained for MI especially when evaluating women, patients with diabetes, older patients, patients with dementia, and those with a history of heart failure. Patients with a permanent pacemaker in place may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.

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DIAGNOSTIC CRITERIA

2 or more of the following WHO Guidelines may indicate the presence of a definite MI.

I. History of ischemic chest pain lasting for more than 20 minutes; II.Changes in serial / sequential ECG tracings; and III. Instability of cardiac biomarkers such as Troponin 1, Creatine Kinase, and Lactate Dehydrogenase enzymes specific to the heart.
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DIAGNOSTIC TESTS
Lab Studies 1. Troponin is the preferred biomarker for diagnosis. Troponins have the greatest sensitivity and specificity in detecting MI. The test result is both diagnostic as well as prognostic of outcome. Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs. For early detection of myocardial necrosis, sensitivity of this laboratory test is superior to that of the creatine kinase-MB (CK-MB). Troponin I is detectable in serum 3-6 hours after an AMI and its level remains elevated for 14 days. Troponin is also the optimum biomarker for the evaluation of patients with MI who have coexistent skeletal muscle injury. 2. Creatine kinaseMB level. CK-MB levels begin to rise within 4 hours after injury, peak at 18-24 hours, and subside over 3-4 days. A level within the reference range does not exclude myocardial necrosis. Occasionally, very small infarcts can be missed by CK-MB; therefore, a troponin level should be measured for patients suspected of having had MI who have negative serial CK-MBs. 3. Myoglobin levels. Myoglobin, a low-molecular-weight heme protein 4/28/12 found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as

1. Chest radiography. It may provide clues to an alternative or complicating diagnosis (eg, aortic dissection, pneumothorax). Other imaging studies such as a contrast chest CT scan or transesophageal echocardiography should be used to differentiate MI from aortic dissection in patients in whom the diagnosis is in doubt. Stanford type A aortic dissections may dissect in a retrograde fashion causing coronary blockage and dissection, which may result in MI. In one study, 8% of patients with Stanford type A dissections had ST elevation on ECG. Chest radiography also reveals complications of MI such as pulmonary edema secondary to heart failure. 2. Echocardiography. Use 2-dimensional and M-mode echocardiography when evaluating wall motion abnormalities and overall ventricular function. Echocardiography can identify complications of MI (eg, valvular insufficiency, ventricular dysfunction, pericardial effusion). 3. Technetium-99m is a radioisotope that is taken up by the myocardium in proportion to the blood flow and is only minimally redistributed after initial uptake. This allows for time delay between injection of the isotope and imaging. It has potential use in identifying infarct in patients with atypical presentations or in patients with ECGs that are not interpretable. Normal scan findings are associated with an extremely low risk of subsequent cardiac events. 4/28/12 4. Thallium scanning: Thallium accumulates in the viable myocardium. 5. Perfusion imaging has been used in risk stratification after MI and for

Procedures 1. Percutaneous coronary interventions (PCIs) are a group of catheter-based technologies used to establish coronary reperfusion. Angiography provides essential knowledge of the extent of coronary disease and is performed prior to PCI. PCI may then be performed as a primary intervention or as an intervention after thrombolysis failure. Evidence suggests that primary PCI is more effective than thrombolysis and should be performed for confirmed STEMI, new or presumably new left bundle-branch block (LBBB), severe congestive heart failure, or pulmonary edema if it can be performed within 12 hours of symptom onset. Door-to-balloon time should be 90 minutes or less. 2. Percutaneous transluminal coronary angioplasty (PTCA) (balloon angioplasty) is the primary therapeutic modality used at centers where it can provide reperfusion as quickly as fibrinolytic therapy. In other centers, it is used selectively for patients failing to respond to thrombolytics. 3. Coronary artery bypass graft may be indicated based on angiographic findings. 4/28/12

NURSING CARE PLANS

1. Acute pain related to myocardial ischemia resulting from coronary artery occlusion. 2. Activity intolerance related to imbalance between oxygen supply and demand as evidenced by shortness of breath 3. Anxiety/ Fear 4. Decreased cardiac output 5. Ineffective tissue perfusion (cardiopulmonary) 6. Risk for excess fluid volume 7. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs related to lack of understanding of medical condition 8. Imbalanced nutrition: Less than body requirements

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COMPLICATIONS

Congestive heart failure. A myocardial infarction may compromise the function of the heart as a pump for the circulation, a state called heart failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided MI. The incidence of heart failure is particularly high in patients with diabetes and requires special management strategies. Myocardial rupture is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later, in as many as 10% of all MIs. This may occur in the free walls of the ventricles, the septum between them, the papillary muscles, or less commonly the atria. Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular aneurysm, a localized dilation or ballooning of the heart chamber. Life-threatening arrhythmia. Since the electrical characteristics of the infarcted tissue change (see pathophysiology section), arrhythmias are a frequent complication. The re-entry phenomenon may cause too fast heart rates (ventricular tachycardia and even ventricular fibrillation), and 4/28/12 ischemia in the electrical conduction system of the heart may cause a complete heart block (when the impulse from the sinoatrial node, the normal cardiac pacemaker, doesn't reach the heart chambers any more).

PROGNOSIS
MI may be associated with a mortality rate as high as 30%, with more than half of deaths occurring in the prehospital setting. Prognosis is highly variable and depends on a number of factors related to the timing and nature of intervention, success of the intervention, and post-MI management. Better prognosis is associated with the factors including the following: Successful early reperfusion Preserved LV function

Short-term and long-term treatment with beta-blockers, aspirin, and ACE inhibitors Poorer prognosis is associated with the following: Delayed or unsuccessful reperfusion LV function is the strongest predictor of the outcome in the post-MI patient. Ventricular dysrhythmias 4/28/12 Recent experience with amiodarone suggests that it may improve long-term mortality in survivors of MI with ectopy and ventricular tachycardia.

Thank you!
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