Acute Myocardial Infarction
Acute myocardial infarction commonly known as “heart attack” results from occlusion of one or more of the coronary arteries leading to necrosis of myocardial tissues..Ischemia develops when there is an increased demand for oxygen or a decreased supply of oxygen.Ischemia can develop within 10 seconds and if it lasts longer than 20 minutes, irreversible cell and tissue death occurs.occurs. Myocardial cell death begins at the endocardium. The area most distal to the arterial blood supplyMI are categorized into two types.they are ST elevated MI (STEMI) and non ST elevated MI (NSTEMI).A STEMI is caused by a sudden complete (100%) blockage of a coronary artery and it accounts for about 70% of MI. A non-STEMI is usually caused by a severly narrowed artery but the artery is usually not completely blocked and its the least serious out of the two.
Presentation
Signs and symptoms are unique to each individual patient..Ranging from no symptoms to sudden cardiac arrest.The basic typical symptom of myocardial infarction is angina.Typical clinical features are mentioned below.
- 3/4 of the clients present with characteristic central or epigastric chest pain radiating to the left arm, shoulders, neck, or jaw.Pain is described by heaviness, pressure, fullness and crushing sensation.
- pain is not relieved by rest, position change or nitrate administration.
- Nausea and Vomiting results as a reflex from severe pain.
- Sweating-temperature increases in first 24 hours
- Pulse and blood pressure increase initially.Later, BP will drop due to decreased cardiac output
- Urine output will decrease
- Lung sounds will change to crackles
- Jugular veins may become distended and have obvious pulsations.
- A third heart sound (S 3) and, most commonly, a fourth heart sound (S 4) on auscultation a systolic murmur can be heard on auscultation.
Causes
Occlusion can stem from atherosclerosis,thrombosis,platelet aggregation,coronary artery spasm or stenosis Predisposing factors can be categorize into Non-modifiable an modifiable factors.
Non Modifiable
Age-Age is the single most important risk factor for MI, For each successive 10 years after age 55, the Heart attack rate more than doubles in both men and women
Gender- men are at greater risk of heart disease than a pre-menopausal woman. But once past the menopause, a woman’s risk is equvalent to a man’s. Risk of Heart attack is similar for men and women.
Family history-Your family’s history of cardiovascular disease indicates your risk. If a first-degree blood relative has had coronary heart disease or stroke before the age of 55 years (for a male relative) or 65 years (for a female relative) your risk increases.
Modifiable
Smoking
Tobacco use increases the risk of coronary artery disease two to six times more than non smokers.Nicotine increases platelet thrombus adhesion and vessel inflammation.
Diabetes not only increases the rate of atherosclerotic formation in vascular vessels but also at an earlier age.The constant stress of high blood pressure has been associated with the increased rate of plaque formation.Shearing Stress and inflammation of endothelial lining begins the process.
Hyperlipidemia
Elevated levels of cholesterol, LDL’s or triglycerides are associated with the increased risk of coronary plaque formation and MI.
Obesity and Physical Inactivity
Mortality rate from CAD is higher in those who are obese.Physically inactive people have lower HDL levels with higher LDL levels and an increase in clot formation.
Investigations
ECG
This is the immediate test to be done soon after a suspected MI diagnosis An ECG records the rhythm and electrical activity of your heart .It is this electrical activity that makes your heart contract, so by measuring it, problems your heart may be having in its rate or rhythm can be identified. . If the ECG shows elevation in ST wave, it is clearly a STEMI. If ST depression is shown it can be a NSTEMI. If the ECG is normal, ECG is repeated in another 2 hours and if it is still normal that can be a stable angina while if ST inverted it can be an unstable angina. (Mayoclinic.org, 2015)
Blood test for cardiac enzymes
Troponin I,a structural protein found in cardiac muscle is elevated,troponin is relesed within 4-6 Hours of myocardial injury and peaks by 12 hours.troponin level remains elevated for 7-10 days after MI.Serum creatinine kinese(CK) levels are elevated especially CK-MB is more specific for MI.It rises within 4-8 hours,peaks at about 18 hours and returns to normal by 48 to 72 hours.C reactive protein(CRP) is positive in myocardial infarction and its negative in ischemic heart disease without myocardial infarction.Myoglobin is also relesed with cardiac muscle damage.
Chest X-ray
Type of photograph of the heart, and It does not show specific details of the heart. It will only show changes in shape and size can be seen.
Echo-cardiogram
In this sound waves are used to get a video imaging of the heart by reflecting the hearts surfaces. A echocardiogram will help to identify whether an area of the heart is damaged by a heart attack and
whether it is pumping normally.
whether it is pumping normally.
Management
1 Obtain ECG
2. CPR and defibrillation if the patient is on an cardiac arrest
3.Administer 5 mg GTN stat sub-lingual or oral spray
4.Morphine sulfate 5-10 mg (IV) given every 5-15 minutes with anti-emetics (if GTN is not adequate)- relieve pain
5.Aspirin 160-325mg (oral)/ Clopidogrel- anti-platelet therapy
6.IV access- to obtain blood samples
7.Oxygen therapy
8.Thrombolytics (IV bolus)- streptokinase and t-PA
9.Anti-coagulation therapy- low molecular weight heparin and Enoxaparin
10.Monitor oxygen saturation and administer oxygen appropriately and continue close clinical monitoring including symptoms, pulse, blood pressure, heart rhythm and oxygen saturation.
11.Angioplasty
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