Acute myocardial infarction is the ischemic necrosis of part of the myocardium due to the rapid reduction or interruption of blood flow in the coronary arteries.
The majority of acute myocardial infarction originates from atheromatous lesions, plaque rupture and bleeding in the coronary arteries, on the basis of which blood clots are formed, causing a sudden total blockage of one of the coronary arteries, and the myocardium in the area innervated by that coronary artery is trapped in necrosis.
I. Diagnosis
1.Symptoms
(1) Pressure-like pain in the chest, while the pain radiates to the neck, chin or do arm.
(2) The pain lasts more than 30 minutes.
(3) Some patients present with atypical features and unspecified discomfort in the chest or upper abdomen, such as indigestion.
2. Typical electrocardiographic changes
In the early stage of onset, the ECG may not be abnormal, so the patient should have another ECG after 15-30 minutes if he/she has symptoms of heart pain.
(1) ST segment elevation, more than 1mV in standard leads and more than 2mV in chest leads.
(2) T-wave changes: ST-segment elevation followed by T-wave inversion.
(3) Abnormal Q wave: Q wave >0.04 sec, deeper than 1/4 R wave, Q wave can be permanent, some gradually become smaller and disappear within months to years.
(4) Non-Q-wave infarction: the necrotic myocardium is close to the endomyocardial layer and does not exceed 1/2 thickness of the ventricular wall, the abnormal Q waves do not appear on the ECG, but the R-wave voltage in the corresponding leads decreases progressively, and the ST segment is obviously depressed or inverted. Non-Q-wave infarction is not easily distinguished from severe myocardial ischemia and needs to be diagnosed by combining clinical conditions and serum enzyme changes.
3.Abnormally elevated blood-type cardiac enzymes
(1) Creatine phosphokinase with isoenzyme (CK-MB): it starts to rise in 4-6 hours, reaches the peak in 18-24 hours, and returns to normal in 36-48 hours.
(2) Creatine phosphokinase (CK): starts to rise at 6 hours, peaks at 24-30 hours, and returns to normal in 3-4 days.
(3) Glutathione transaminase (GOT): not high specificity
(4) Lactate dehydrogenase (LDH): LDH activity is increased in liver disease or other systemic diseases, but is only significant in combination with clinical symptoms.
(5) Troponin I and T in the heart: high specificity and sensitivity, troponin I starts to rise at 4-8 hours peaks at 12-16 hours and returns to normal at 7-10 days. Troponin T begins to rise at 3-4 hours, peaks at 12-16 hours, and returns to normal in 7-14 days.
II. Treatment
1.Thrombolysis: streptokinase SK, urokinase UK or tissue fibrinogen activator tPA. reopen the occluded artery, save the myocardium on the verge of necrosis and narrow the infarct.
2.Anticoagulation and antiplatelet therapy: prevent blockage after revascularization.
3.β-blocker therapy: slow down the heart rhythm, lower blood pressure, weaken myocardial contraction, and therefore reduce myocardial oxygen consumption. Due to the negative heart rate and inotropic effect of beta-blockers, sinus bradycardia, low blood pressure, cardiac insufficiency and severe chronic obstructive pneumonia are prohibited.
4.Nitrate therapy: Directly dilate veins, arteries and small veins, reduce cardiac anterior and posterior loads, and reduce myocardial oxygen consumption. It can directly dilate coronary arteries, improve myocardial oxygen supply, reduce myocardial ischemia and narrow the scope of infarction.
5.ACEI improves left ventricular function.
6.Oxygen inhalation: It helps to increase the partial pressure of oxygen, improve myocardial hypoxia, reduce shortness of breath, pain and hypoxia.
7, sedation and pain relief: severe pain makes sympathetic nerves overexcited, which increases myocardial oxygen consumption, expands the infarct range and induces arrhythmias. Morphine has the strongest analgesic effect.
8.Maintain adequate blood pressure to ensure tissue perfusion.
9.Early treatment of complications: closely monitor ECG and blood pressure, and pay attention to the mental status, respiration, sweating and peripheral circulation.
III. Major complications
1.Cardiac arrhythmia
(1) Closely observe the changes of heart rhythm and heart rate.
(2) If ventricular fibrillation occurs, promptly notify the doctor and defibrillate as soon as possible.
(3) Patients with severe atrioventricular block should have immediate external cardiac compressions or temporary pacing if needed.
2.Cardiogenic shock – heart pump failure
(1) Give high-flow oxygen, 4-6 l/min, to improve hypoxia and correct acidosis.
(2) Accurately record the in and out volume, maintain the balance of water, electrolytes and in and out volume.
(3) Closely observe the changes of the mind. Early irritability in cardiogenic shock and failure to correct shock in time may develop into indifference, unresponsiveness or even coma.
3.Acute left heart failure
(1) Give high-flow oxygen, 4-6 l/min, to improve hypoxia and correct acidosis.
(2) Observe the effect and side effects of therapeutic drugs.
(3) When using diuretics, pay attention to the balance of potassium, sodium and other electrolytes.
(4) Pay attention to blood pressure changes and strictly control the input rate.
(5) Pay attention to limiting sodium intake in the diet and prevent constipation to avoid aggravating left heart failure.
4.Heart rupture
(1) Onset is mostly in 2-7 days, after myocardial softening.
(2) Keep blood pressure stable, high blood pressure is a risk factor for heart rupture.
(3) Eliminate emotional stress.
(4) Keep the bowels open and remove the triggers.
IV. Nursing measures
1. Absolute bed rest is required in the first 24 hours after the onset of the disease.
2. Give soft stool or light laxatives to avoid increased physical exertion caused by forceful defecation.
3.Keep the environment quiet and instruct relaxation techniques.
4.Maintain oxygen supply, improve myocardial hypoxia, and adjust oxygen flow rate upwards when pain is increasing.
5.When pain increases, closely monitor changes in ECG, pulse, blood pressure and respiration. Follow the doctor’s prescription for morphine and assess the effect after recording the medication.
6.Assess for signs of decreased cardiac output, such as decreased blood pressure, abnormal heart rate and decreased urine output, fatigue and general weakness, and pale skin.
7.Accurately record the in and out volume.
8.Give an easily digestible diet during the acute period.