Overview of non-ST-segment elevation myocardial infarction
Non-ST-segment elevation myocardial infarction is a type of acute coronary syndrome, usually caused by atherosclerotic plaque rupture, clinical manifestations of sudden chest pain, prolonged unresolved, electrocardiogram suggests acute myocardial ischemic damage, but does not accompany the ST-segment elevation. The incidence of non-ST-segment elevation myocardial infarction is higher than that of ST-segment elevation myocardial infarction.
Etiology
Most of the clinical consequences are due to rupture of unstable coronary atherosclerotic plaques with subsequent local thrombosis or coronary vasospasm at the site of plaque lesions, causing a sudden and severe decrease in coronary blood flow. There are also a few patients who do not have an underlying coronary atherosclerosis and may belong to the category of trauma, large artery entrapment, arteritis, and complications of catheterization.
Symptoms
Typical clinical symptoms of non-ST-segment elevation myocardial infarction include prolonged resting angina, new onset of severe angina, recent exacerbation of stable angina, and post myocardial infarction angina. There is also retrosternal crushing pain with radiation to the left shoulder, neck and palate, often accompanied by cold sweat, nausea, abdominal pain, dyspnea, and syncope.
Examination
1. Electrocardiogram
The electrocardiogram of non-ST-segment elevation myocardial infarction shows:
(1) Sudden and significant depression of the ST segment, which is gradually aggravated and can be gradually restored to the original state after a few days or weeks.
(2) Symmetrical inversion of T waves in the leads of ST-segment depression, showing coronary T waves, which gradually deepens, and the inversion may gradually become shallower or return to its original state after a few days.
(3) No significant QRS wave group changes.
2. Laboratory examination
Serum phosphocreatine kinase begins to rise 4-6 hours after the onset of the disease, reaches a peak in about 20 hours, and falls to normal in 48-72 hours. Phosphocreatine kinase must exceed the upper limit of normal value by more than two times.
Diagnosis
1. Typical precordial pain consistent with acute myocardial infarction, lasting >> 30 minutes.
2. Serum enzyme changes consistent with acute myocardial infarction.
3. No ST-segment elevation on ECG, only ST-segment depression and/or T-wave inversion.
Treatment
Early conservative treatment strategy is to start with aggressive antimyocardial ischemia, anticoagulation, antiplatelet therapy, rational application of antiplatelet agents, anticoagulants, β-blockers, nitrates, non-dihydropyridine calcium channel blockers, and elective coronary angiography and revascularization according to the condition.
For patients with non-ST-segment elevation myocardial infarction who are not well treated with drugs, it is advisable to implement coronary intervention as early as possible. The strategy of early intervention is to undergo coronary angiography and revascularization on 1 to 3 days.
Nursing care
1. Life care
Within 2 weeks after the onset of the disease, patients should be absolutely bedridden, assisted by nursing staff to do passive limb movement to prevent thrombosis. 2 weeks later, patients should be instructed to move around in bed, and the movement should be slow to prevent upright hypotension. 3 weeks later, patients can leave the bed to stand up and walk around the room slowly, and those who are seriously ill or have complications need to prolong the time of bedridden.
2.Dietary care
Give low-fat and easy-to-digest light diet, and limit the intake of cholesterol-rich food, such as eggs and fatty meat. To avoid aggravating the burden on the heart, it is not advisable to be too full, and meals should be small and frequent.
3. Maintain smooth bowel movement
Encourage patients to consume vegetables, honey and bananas to promote intestinal lubrication, keep defecation once every 1 to 2 days, and use laxatives if necessary.