Acute myocardial infarction plus bradycardia, acute myocardial infarction complicated by ventricular

Hello, I am an intern doctor and I have just finished studying cardiology. Here are some suggestions for your reference. First of all, a heart rate of 40+ below 60 is definitely bradycardia.

As for whether this is an arrhythmia caused by structural heart disease, it remains to be determined, but I think it is still impossible to rule out the old myocardial infarction scar (for example, like the scar that will form after trauma), which affects the normal heartbeat.

I suggest that you find a tertiary hospital, or the cardiology department of the hospital that will be followed up regularly after your intervention**, or see a specialist outpatient clinic, which may make your father memorize a Holter electrocardiogram, or a cardiac enzyme test, cardiac ultrasound, and even CTA coronary angiography are possible.

Do you ask about drug conflicts? Presumably, you always have antiarrhythmic drugs, antihypertensive drugs or statin lipid-lowering drugs at home, right? The pharmacological effects of drugs for myocardial infarction and arrhythmia are very intertwined, but it is still necessary to individualize the medication, and now no one can give you an accurate answer through the Internet.

If conditions permit, it is recommended that you can supplement the past medical history of the elderly, what are the main discomforts, symptoms and signs, and medications taken here.

I hope the old man's physical condition will improve soon!!

Slow heartbeat is likely to be related to a heart attack, a 24-hour Holter ECG is required, and a pacemaker is needed if there is a long interval or your father has symptoms of blackness or even fainting in front of his eyes. There is no conflict between the use of drugs for myocardial infarction and the use of drugs to raise the heart rate, but it is necessary to go to the hospital for examination first.

Answer] :d 1Once myocardial infarction is detected, premature ventricular contractions or ventricular tachycardia are detected, lidocaine 50 100 mg intravenously is immediately given, repeated every 5 to 10 minutes, and amiodarone can be used repeatedly if ventricular arrhythmia occurs.

2.Accelerated ventricular autonomic rhythm, also known as bradycardia, occurs by increasing automaticity, with the onset and termination of tachycardia progressive, and the two pacemakers of the ventricle and sinus node alternately controlling the ventricular rhythm and the synthesis. If hemodynamics are affected, atropine can be used to increase sinus rhythm or atrial pacemaker frequency, which can be eliminated.

3.Amiodarone prolongs the refractory period of the atrioventricular bypass, slows the bypass or conduction only, and slows the ventricular rate in patients with atrial fibrillation.

The prognosis of acute myocardial infarction has a great relationship with the size of the infarction, complications, and **. Most of the deaths occur within the first week, especially within 1 to 2 hours, and a significant proportion of patients die of ventricular fibrillation before hospitalization. In addition to severe arrhythmias, the causes of death after hospitalization include cardiogenic shock, heart failure, and cardiac rupture.

The acute inpatient mortality rate was above 30% in the 60s of the last century, dropped to about 15% after widespread use of monitoring**, and dropped to 4% to 6% after the application of direct PCI in recent years.

Acute myocardial infarction is a very serious disease, and the condition may be worsened by improper treatment and random movement of the patient at the time of onset. For patients with acute myocardial infarction, lying down and resting and stopping activities are extremely important measures for on-site first aid. At the onset of myocardial infarction:

1. Absolute bed rest, stop exercise, reduce the load on the heart, and limit the injury area to a certain range. 2. Early and rapid medication can significantly increase the survival rate and limit the further development of myocardial infarction. Drugs that stop new blood clots, such as heparin, are also very necessary.

3. Continuous low-flow oxygen inhalation can be used to increase blood oxygen concentration, reduce cardiac load, and increase tissue perfusion. 4. Relieve pain to relieve the patient's pain, because severe pain can cause sympathetic nerve excitation, increase heart rate and vascular resistance. Increases heart rate and vascular resistance.

5. It can reduce venous return, dilate arteries, reduce the preload and afterload of the heart, and increase coronary blood flow. 6. Proper rest and exercise should be carried out in the first stage of myocardial infarction. Regular living can reduce the occurrence of atherosclerosis and high blood pressure.

Medications for various ** heart diseases should be used appropriately.

The rapid death of myocardial infarction is related to malignant arrhythmias, cardiogenic shock and other factors. Myocardial infarction can lead to death within 1 hour, because malignant arrhythmias occur within 1 hour, if ventricular tachycardiac infarction will deteriorate into ventricular fibrillation, and if effective assistance is not received within 4 minutes, the patient will enter the stage of biological death. The mortality rate of patients caused by cardiogenic shock is also relatively fast, the mortality rate of cardiogenic shock is more than 50%, the risk of death is relatively high within 1 week, there is a 1-month risk period after 1 week, and there is a half-year risk period after 1 month, and then the risk degree will decrease.

**Method: Medication**.

1.Nitroglycerin.

It is a vasodilator, which mainly dilates the coronary arteries, increases coronary blood flow and increases venous volume, reduces the amount of blood returning to the heart, and reduces the left ventricular end-diastolic pressure and pulmonary vascular pressure.

2.Metoprolol.

It is a receptor antagonist, reduces myocardial oxygen consumption, improves the imbalance of oxygen supply in the myocardial ischemic area, reduces the area of myocardial infarction, reduces complications, reduces the mortality rate, and should be taken routinely as soon as possible within 24 hours without contraindications.

3.Aspirin plus ticagrelor or clopidogrel.

Antiplatelet drugs to prevent thrombosis.

4.Heparin. Anticoagulants, whether or not the patient is treated with thrombolysis**, should be routinely combined with antiplatelet anticoagulation**.

5.Statins.

It is a lipid-lowering drug, such as atorvastatin, rosuvastatin, etc.

Surgery**. 1.Percutaneous coronary intervention**.

If the patient can be transferred to a hospital with PCI conditions within 120 minutes, the PCI strategy can be preferred, and reperfusion can be completed within 90 minutes, and all patients with acute ST-elevation myocardial infarction within 12 hours of onset should undergo direct PCI**.

2.Coronary artery bypass grafting.

For patients with failed intervention** or ineffective thrombolysis** and surgical indications are indicated, it is advisable to strive for emergency coronary artery bypass grafting (CABG) within 6 to 8 hours.

Hypertension or hypotension "Heart disease" is maintained or controlled for a long time. are prone to outbreaks of late-stage heart disease.

A myocardial infarction can lead to death within 1 hour at the earliest, because malignant arrhythmias, ventricular tachycardia, and ventricular fibrillation occur within 1 hour. If ventricular tachycardia** is not received in time, it will easily deteriorate into ventricular fibrillation, at which point the heart will lose its effective contraction, that is, the heart will stop, and if it is not effectively rescued within 4 minutes, the patient will enter the stage of biological death. Therefore, most myocardial infarctions lead to relatively rapid death, which is related to malignant arrhythmias caused by myocardial ischemia and myocardial infarction.

In addition to deaths directly attributable to malignant arrhythmias, patients with cardiogenic shock due to massive myocardial infarction also die at a relatively rapid rate. Cardiogenic shock has a mortality rate of more than 50%, and the risk of death within 1 week is relatively high, and there is a 1-month risk period after 1 week, and a 6-year risk period after 1 month, after which the risk level decreases. Therefore, patients need to focus on preventing myocardial infarction, otherwise the consequences will be more serious.

Myocardial infarction is caused by acute occlusion of the coronary arteries, resulting in local necrosis of part of the conduction system due to severe and persistent ischemia. Therefore, the arrhythmia associated with acute myocardial infarction is caused by myocardial ischemia and necrosis of the conduction system. Many metabolites are released after myocardial avascular necrosis.

A large amount of potassium ions can form extracellular local hyperkalemia, which can make the local quiescent membrane potential close to the threshold potential, shorten the duration of the action potential, and form an injury current between the ischemic and non-ischemic areas. Due to the increase of potassium in the local necrotic area, conduction can be delayed and the refractory period can be shortened, which is conducive to the occurrence of agonistic reentry. In acute myocardial infarction, catecholamines in the blood increase, which excitates receptors, thereby improving the automaticity of pacemaker cells and causing tachyarrhythmias.

In addition, catecholamines can lower the threshold of ventricular fibrillation, causing the development of ventricular fibrillation. Acute myocardial infarction can cause severe impairment of cardiac function, and metabolic acidosis may occur, which lowers the threshold current of ventricular fibrillation. If respiratory ventilation is impaired, hypoxemia with respiratory alkalosis may occur.

It can change the distribution of ions inside and outside the pacemaker cell, reduce the extracellular liquid alkali reserve, and potassium and sodium ions enter the cell, enhance the automaticity of the pacemaker cell, and can cause ventricular and supraventricular tachyarrhythmia. In addition, myocardial ischemia can cause hyperarrhythmias, which in turn can cause tachyarrhythmias. Myocardial ischemia can reduce myocardial contractility and increase left ventricular terminal diastolic pressure, which in turn strengthens the automaticity of pacemaker cells, turns non-pacemaker cells into slow fibers with pacing performance, and can make the refractory period and conductivity of various parts of the myocardium inconsistent, thus causing arrhythmia.