, accompanied by signs of inadequate blood perfusion, such as restlessness, pallor, cool and clammy skin, and profuse sweating

, accompanied by signs of inadequate blood perfusion, such as restlessness, pallor, cool and clammy skin, and profuse sweating , when the pulse becomes weak and rapid, urine output decreases, and consciousness becomes confused or even leads to syncope, it is classified as cardiogenic shock, caused by extensive myocardial necrosis and a sharp decline in cardiac output. (6) Heart failure Primarily acute left heart failure, resulting from weakened contractility after a large-area myocardial infarction, presenting with dyspnea , cough, irritability, and cyanosis. In severe cases, both lungs are filled with moist rales, leading to pulmonary edema, which can subsequently cause right heart failure. Right ventricular myocardial infarction immediately results in right heart failure. (7) Cardiac signs Tachycardia or bradycardia, diminished first heart sound at the apex, diastolic gallop rhythm, arrhythmias, etc. If a coarse systolic murmur is heard at the apex, it is often due to papillary muscle dysfunction. (4) Laboratory and other examinations

1. Electrocardiogram examination The ECG often shows progressive changes, which are helpful for diagnosing MI, locating the infarct, determining its extent, and estimating disease progression and prognosis. (1) Characteristic changes (Necrotic type): pathological Q wave; (Injury type): ST segment elevation; (Ischemic type): T wave inversion. (2) Dynamic evolution ① Within the first few hours, abnormally tall T waves appear, known as ultra-acute phase changes. ② Several hours later, the ST segment markedly elevates, forming an upwardly convex single curve, and within several hours to 2 days, a pathological Q wave forms, while the R wave diminishes, representing acute-phase changes. If the pathological Q wave remains stable and unchanged for 3 ~ 4 days, it becomes permanent. ③ Over several days to about 2 weeks, the ST segment recovers, and the T wave gradually flattens or inverts, indicating subacute-phase changes. ④ After several weeks to months, the T wave gradually inverts, taking on a "coronary" T wave shape, signifying chronic-phase changes. After several weeks or months, it may gradually return to normal.
2. Radionuclide examination Shows the location and extent of myocardial infarction, observes ventricular wall motion, and measures left ventricular ejection fraction. Helps assess ventricular function and diagnose post-infarction wall motion abnormalities and overall wall function.
3. Echocardiography Understands ventricular wall motion and left ventricular function, diagnoses ventricular aneurysms and papillary muscle function.
4. Laboratory tests (1) Within 24–48 hours of onset, WBC count increases, neutrophil percentage rises, and ESR accelerates, which can persist for up to a week. (2) Serum markers of myocardial necrosis. Elevated levels of myocardial injury markers are closely related to the extent of myocardial necrosis and prognosis. The determination of myocardial necrosis markers should be evaluated comprehensively: For example, myoglobin appears earliest after MI and is highly sensitive, but not very specific; CTnT and CTnl appear slightly later and are highly specific. If the test is negative within 6 hours after symptom onset, then it should be retested after 6 hours. The drawback is that their duration lasts 10–14 days, making it difficult to determine whether there is a new infarction during this period. Although CK-MB is less sensitive than CTnT and CTnl, it is still of considerable value for early ( <4 hours) diagnosis of MI. (4) Diagnosis Typical clinical manifestations, characteristic ECG changes, and laboratory test alterations—meeting any two of these three criteria is sufficient for diagnosis. (5) Treatment
5. Treatment objectives Relieve pain, reduce the infarct size, alleviate cardiac workload, and prevent complications.
6. General treatment and monitoring (1) Monitoring Conduct ECG, blood pressure, and respiratory monitoring in the coronary care unit to promptly address various complications. (2) Rest Complete bed rest for about 2 weeks to eliminate patient anxiety and tension. (3) Oxygen therapy Administer low-flow nasal cannula oxygen in the early stages of illness to improve myocardial hypoxia, relieve pain, and help reduce the size of the myocardial infarct. (4) Nursing care Have others assist with daily living, provide easily digestible, low-salt, low-fat liquid diets, and maintain regular bowel movements.
7. Pain relief Severe pain often makes patients extremely agitated, even leading to shock, serious arrhythmias, or cardiac rupture; therefore, pain should be relieved as soon as possible. Morphine 5 10 mg or pethidine 50 75 mg can be administered via subcutaneous or intramuscular injection, repeating every 1 2 hours if necessary.
8. Antiplatelet and anticoagulant therapy Cyclooxygenase inhibitors (COX) block thromboxane A2 (TXA2) synthesis by inhibiting COX activity, achieving antiplatelet aggregation effects. Aspirin is the cornerstone of antiplatelet aggregation therapy. Unless contraindicated, all patients should routinely receive anticoagulant therapy based on antiplatelet aggregation, with different drugs selected according to treatment strategy and risk of ischemic or bleeding events.
9. Myocardial reperfusion therapy (1) Thrombolytic therapy. (2) Percutaneous coronary intervention (PCI): dilates narrowed vessels, has high recanalization rate, and low reinfarction rate. (3) Coronary artery bypass grafting: for those who are unsuitable for or have failed thrombolytic therapy and PCI.
10. Correction of arrhythmias Prevent progression to severe arrhythmias or even sudden death.
11. Anti-shock treatment Under hemodynamic monitoring, use volume expansion, vasodilators, and other therapies accordingly.
12. Active treatment of heart failure Within 24 hours of infarction, avoid using digitalis; prioritize diuretics and vasodilators.
13. Other therapies The following therapies may help save dying myocardium, prevent infarct enlargement, reduce ischemic area, accelerate healing, though some are not yet fully mature or their efficacy is still debated, and can be considered based on individual patient conditions. (1) Polarizing solution therapy: promotes myocardial cell uptake of glucose, allows K+ to enter cells, restores cell membrane polarization, and reduces occurrence of arrhythmias. (2) Lipid-lowering therapy, β-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers are used. (3) Medications that promote myocardial cell metabolism are applied. (7) Prevention Preventing atherosclerosis and coronary heart disease in the general population is primary prevention; those with a history of coronary heart disease and MI should also prevent recurrent infarction and other cardiovascular events, which is secondary prevention. Secondary prevention should be considered comprehensively; for easy memorization, it can be summarized as five aspects symbolized by ABCDE: ① Antiplatelet, antianginal treatment, and ACEI. ② β blockers to prevent arrhythmias and reduce cardiac load, control blood pressure. ③ Control blood lipids and quit smoking. ④ Control diet and treat diabetes. ⑤ Health education and exercise. Section 3: Arrhythmias Normally, the heart beats regularly at a certain frequency, and the impulse originates from the sinoatrial node (SAN), propagating through the atria and ventricles in a specific sequence and speed, coordinating synchronous contraction of all cardiac parts to form one heartbeat, repeating cyclically—this is the normal rhythm. Arrhythmia refers to abnormalities in the frequency, rhythm, origin, conduction speed, or excitation order of cardiac impulses, resulting in disturbances in the formation and conduction of cardiac impulses, causing the whole heart or part of it to beat too fast, too slow, or irregularly. It can occur under physiological conditions, but is more common in pathological states, including diseases of the heart itself and non-cardiac diseases. Causes
14. Hereditary arrhythmias Currently confirmed hereditary arrhythmias include long QT syndrome, short QT syndrome, Brugada syndrome, catecholamine-sensitive ventricular tachycardia, early repolarization syndrome, etc. Clinically, patients or survivors of sudden cardiac death caused by hereditary arrhythmias, as well as their immediate family members, should undergo enhanced ion channel disease and cardiomyopathy gene testing and risk assessment.
15. Acquired arrhythmias (1) Physiological factors such as exercise and emotional changes can stimulate the sympathetic nervous system, causing rapid-type arrhythmias, or stimulate the vagus nerve during sleep, leading to slow-type arrhythmias. (2) Pathological factors can be further divided into factors related to the heart itself, systemic factors, and other organ-related disorders. Heart-related factors mainly include various organic heart diseases, such as coronary heart disease, hypertensive heart disease, rheumatic heart disease, valvular heart disease, cardiomyopathy, myocarditis, and congenital heart disease; systemic factors include drug toxicity, various causes of acid-base imbalance and electrolyte disturbances, and dysfunction of neural and humoral regulation systems. When the balance between the sympathetic and parasympathetic nervous systems is maintained, the heart functions normally; however, when this balance is disrupted, arrhythmias are more likely to occur. Other organs outside the heart can also trigger arrhythmias when they undergo functional or structural changes, such as hyperthyroidism, anemia, severe infections, and stroke. In addition, chest surgeries (especially cardiac surgery), anesthesia procedures, cardiac catheterization, various interventional cardiac treatments, and drugs and toxins (such as tetrodotoxin) can all induce arrhythmias. II. Clinical classification According to the mechanism of occurrence, arrhythmias are divided into abnormal impulse formation and abnormal impulse origin. 1. Abnormal impulse formation (1) Sinus arrhythmias Including sinus tachycardia, sinus bradycardia, sinus arrhythmia, and sinus arrest. (2) Ectopic arrhythmias ① Passive ectopic arrhythmias: escape beats (atrial, atrioventricular junctional, ventricular), escape rhythm (atrial , atrioventricular junctional, ventricular). ② Active ectopic arrhythmias: premature contractions (atrial, atrioventricular junctional, ventricular), paroxysmal tachycardia ( supraventricular, ventricular), atrial flutter, atrial fibrillation, ventricular flutter, ventricular fibrillation. 2. Abnormal impulse conduction (1) Physiological Interference or interference-induced atrioventricular dissociation. (2) Pathological Sinoatrial block, intra-atrial block, atrioventricular block, intraventricular block (left , right bundle branch, and left bundle branch bifurcation block). (3) Accessory pathways between atria and ventricles Such as pre-excitation syndrome (WPW syndrome, with pre-excitation signs on ECG and paroxysmal tachycardia clinically). III. Western medical diagnosis
16. Medical history Diagnosis of arrhythmias should begin with a thorough collection of medical history, allowing patients to objectively describe their sensations when symptoms occur. Medical history usually provides useful clues for diagnosis. History-taking includes: ① Triggers and frequency of attacks, onset and termination methods, symptoms and signs during attacks. ② Whether there is a previous history of similar arrhythmia attacks, and whether family members have had similar episodes. ③ Whether there is a known history of heart disease. ④ Whether there are systemic diseases that can cause heart lesions, such as hyperthyroidism. ⑤ Whether there is a history of medication use, especially antiarrhythmic drugs, digitalis, and medications affecting electrolytes. Whether there is a history of implanting artificial pacemakers, etc.
17. Cardiac auscultation Includes changes in heart sounds, heart rate, and rhythm.
18. Routine electrocardiogram examination Is the most reliable method for diagnosing arrhythmias; should record 12 or 18-lead ECG, and clearly mark the ECG strip showing the P wave lead for analysis, usually choosing V or II lead. Principles of ECG analysis: Based on the morphological characteristics of the P wave, determine its rhythm,