judge whether the basic rhythm is sinus rhythm or ectopic rhythm; ② Measure PP or RR

judge whether the basic rhythm is sinus rhythm or ectopic rhythm; ② Measure PP or RR intervals to calculate atrial or ventricular rate, checking for tachycardia or bradycardia, as well as arrhythmia; measure PR interval and QT interval to judge whether they are prolonged or shortened; ④ Compare PP intervals and RR intervals, looking for the relationship between atrial rhythm and ventricular rhythm. 4. Ambulatory ECG Can observe 24-hour dynamic cardiac electrical activity. 5. Electrophysiological examination Taking the whole heart or a part of the heart as the object, recording intracardiac ECG, mapping ECG and applying various specific electrical pulse stimulations, as a method for diagnosing and studying arrhythmias. IV. Premature contractions Premature contractions refer to premature impulses originating from ectopic pacemakers below the sinoatrial node, causing the heart to beat earlier—commonly called “premature beats”—and are the most common type of arrhythmia. According to the origin of the premature beat, they are divided into atrial, atrioventricular junctional, and ventricular types, with ventricular premature beats being the most common, followed by atrial ones. Premature beats can occur sporadically or frequently, irregularly or regularly. For example, if one premature beat occurs after every or every two sinus beats, it’s called a couplet or triplet; if two premature beats follow each sinus beat consecutively, it’s called paired premature beats. (---) Causes (1) Functional: Related to mental stress, fatigue, emotional excitement, etc. (2) Organic heart disease. (3) Effects of certain medications: Such as digitalis, quinidine, etc. (4) Electrolyte disturbances: Low potassium , low calcium. (5) Direct stimulation of the heart: Such as cardiac surgery, etc. (II) Clinical manifestations (1) Symptoms: Sporadic premature beats generally have no obvious clinical symptoms; some patients feel palpitations or pauses in heartbeat; frequent or continuous premature beats can cause dizziness, fatigue, and other discomforts, even triggering angina and cardiac insufficiency. This is due to reduced cardiac output. (2) Clinical auscultation can reveal that the heartbeat suddenly occurs earlier, followed by a longer pause. During premature beats, the reduced ventricular filling leads to an increased first heart sound, while the decreased cardiac output causes the second heart sound to weaken or disappear. Short pulses may also occur. (III) ECG examination

1. Atrial premature beats ① There is an early appearing atrial P wave, whose morphology differs from the sinus P wave. ② P'-R interval > 0.12 seconds. ③ Normal or deformed QRS complex (with intraventricular differential conduction ). ④ Mostly incomplete compensatory pauses.
2. Atrioventricular junctional premature beats ① An early appearing supraventricular QRS complex without a corresponding P wave beforehand. ② May have retrograde P waves. ③ Mostly complete compensatory pauses.
3. Ventricular premature beats ① An early appearing wide ( > 0.12 seconds ) deformed QRS complex without a prior early P wave. ② The T wave is wide and opposite in direction to the main QRS wave. ③ Mostly complete compensatory pauses. (IV) Treatment (1) Eliminate the cause; for various premature beats without evidence of organic heart disease, special treatment is generally not required. If there is obvious discomfort, administer mild sedatives such as diazepam (Valium). (2) For frequent premature beats caused by cardiovascular disease, consider using verapamil, propafenone, β - blockers, digitalis, etc. (3) Ventricular premature beats induced by myocardial ischemia should be taken seriously, especially those that are multiple, frequent, paired, or consecutive, to prevent them from developing into ventricular fibrillation and endangering life. Usually, lidocaine is preferred for intravenous administration, followed by oral medication ( mexiletine or propafenone) for maintenance once effective. For ventricular premature beats caused by cardiac insufficiency, it is advisable to use digitalis-based cardiac glycosides for treatment. However, for ventricular premature beats induced by digitalis poisoning, digitalis should be immediately discontinued, and phenytoin and potassium chloride should be administered. (4) For ventricular premature beats occurring with bradycardia, consider using atropine, scopolamine, etc., as appropriate. V. Atrial fibrillation Atrial fibrillation (often abbreviated as AFib) is when the atria generate rapid, irregular impulses, reaching 350 ~ 600 times per minute, causing the atrial muscle fibers to tremble erratically, thereby losing the atria's effective pumping function. (---) Causes (1) Those with organic cardiovascular diseases, such as rheumatic heart disease, coronary heart disease, pulmonary heart disease, hypertensive heart disease, and hyperthyroid heart disease, etc. (2) Cardiac catheterization and thoracic surgery. (3) Digitalis poisoning. (4) Paroxysmal cases often have no organic cardiovascular disease, seen in situations of hypoxia, low potassium, emotional excitement, smoking, and drinking. (II) Clinical manifestations Related to the severity of pre-existing heart disease and the speed of ventricular rate. Generally, there are palpitations, dizziness, and chest tightness, among other discomforts; if the ventricular rate is too fast, it can trigger angina or heart failure. The rhythm is absolutely irregular, with varying strength of the first heart sound, accompanied by short pulses. (III) ECG examination (1) The P wave disappears, replaced by f waves of varying sizes, ranging from 350 to 600 times per minute. (2) The ventricular rhythm (R-R interval) is absolutely irregular. (3) The morphology of the QRS complex and T wave is supraventricular, but can be deformed; for example, if there is intraventricular differential conduction, wide deformations may occur, especially after long pauses before the next premature beat, resembling left bundle branch block. (IV) Treatment Treatment of atrial fibrillation emphasizes long-term comprehensive management: on the basis of treating the primary disease and inducing factors, actively preventing thromboembolism, converting to and maintaining sinus rhythm, and controlling ventricular rate—these are the basic principles of AFib treatment.
4. Anticoagulant therapy Patients with AFib have a higher risk of embolism, so anticoagulant therapy is an important part of AFib treatment. Warfarin is an effective anticoagulant for AFib, while newer oral anticoagulants (NOACs), such as dabigatran etexilate, rivaroxaban, apixaban, etc., are currently mainly used for anticoagulation in non-valvular AFib. NOACs are characterized by not requiring routine coagulation index monitoring, being less affected by food or medications, and having better safety.
5. Slowing down the ventricular rate When the ventricular rate is too fast or accompanied by cardiac insufficiency, digitalis-based cardiac glycosides should be used for treatment, striving to keep the ventricular rate below 70 ~ 80 times per minute. If necessary, verapamil or propranolol can be added.
6. Conversion to and maintenance of sinus rhythm

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Methods for converting atrial fibrillation back to sinus rhythm include pharmacological cardioversion, electrical cardioversion, and catheter ablation. These are suitable for patients in the acute phase who are expected to maintain sinus rhythm for a prolonged period. Amiodarone has the lowest incidence of arrhythmia induction and is currently a commonly used drug for maintaining sinus rhythm, especially in patients with organic heart disease. When pharmacological cardioversion fails, electrical cardioversion can be considered. For paroxysmal atrial fibrillation with obvious symptoms that does not respond to drug therapy, catheter ablation can be used as first-line treatment.

Indications for cardioversion: ① Atrial fibrillation lasting no more than 1 year with mild cardiac lesions. ② Persistent atrial fibrillation after removal of the underlying cause. ③ Atrial fibrillation accompanied by hypertrophic cardiomyopathy.

VI. Paroxysmal Tachycardia Paroxysmal tachycardia is a paroxysmal, rapid, and regular ectopic rhythm, which is essentially three or more consecutive premature beats, with a heart rate often ranging from 160 to 220 beats per minute. Based on the origin of the ectopic impulse, it is classified into three types: supraventricular, junctional, and ventricular. However, supraventricular and junctional tachycardias are difficult to distinguish and are collectively referred to as supraventricular tachycardia, which is more common than ventricular tachycardia.

(---) Etiology

1. Supraventricular Tachycardia It is commonly seen in individuals without obvious cardiovascular disease, but can also occur in patients with various heart diseases, pre-excitation syndrome, hyperthyroidism, hypokalemia, and digitalis toxicity.
2. Ventricular Tachycardia The vast majority occurs in patients with severe myocardial damage, most commonly in coronary heart disease. Other heart diseases, electrolyte disturbances, and drug poisoning (such as digitalis and quinidine) can also lead to ventricular tachycardia.

(III) Clinical Manifestations

1. Paroxysmal Supraventricular Tachycardia It often starts and stops suddenly, with varying durations—from a few seconds, minutes, hours, to even days. During an episode, patients may experience palpitations, restlessness, polyuria, and other discomforts; a small number may develop dizziness, syncope, angina pectoris, or even heart failure. Physical examination reveals a fast and regular heart rhythm, with a heart rate of 160–220 beats per minute, unequal intensity of the first heart sound, and a rapid, weak pulse.
2. Paroxysmal Ventricular Tachycardia During an episode, due to the loss of normal contraction sequence between the atria and ventricles, cardiac output decreases, leading to acute heart failure, syncope, shock, cardiogenic cerebral ischemia syndrome, and even sudden death. Physical examination shows an irregular heart rhythm, with a heart rate of 150–200 beats per minute, and uneven intensity of the first heart sound at the apex.

(IV) Electrocardiographic Examination

1. Paroxysmal Supraventricular Tachycardia ① Heart rate of 160–220 beats per minute, with regular R-R intervals. ② The P wave morphology differs from the sinus P wave. If the P wave is upright and the P-R interval is >0.12 seconds, it is supraventricular tachycardia; if the P wave is retrograde and the P-R interval is <0.12 seconds or the R-P interval is <0.20 seconds, it is junctional tachycardia. ③ Secondary T-wave changes may occur.
2. Paroxysmal Ventricular Tachycardia ① Heart rate of 150–200 beats per minute, with slightly irregular rhythm. ② The QRS complex is wide and deformed, >0.12 seconds. ③ The P wave may be buried within the ventricular complex or unrelated to the QRS complex (atrioventricular dissociation).

(V) Treatment

1. Paroxysmal Supraventricular Tachycardia (1) Mechanical stimulation of the vagus nerve If the patient's cardiac function and blood pressure are normal, vagal stimulation methods can be tried first, such as stimulating the pharynx to induce a gag reflex, pressing on the eyeballs, or compressing the carotid sinus. (2) Pharmacological vagal stimulation This can terminate the tachycardia. Patients with a history of hypertension or coronary heart disease should avoid this method. (3) Antiarrhythmic drugs Verapamil is the first choice, administered intravenously after dilution, or propafenone, also given intravenously after dilution. Medication should be stopped once the attack subsides. For cases caused by digitalis toxicity, potassium salts and phenytoin should be administered. (4) Digitalis preparations These are suitable for patients with reduced cardiac function. Digoxin is often administered intravenously. However, patients with pre-excitation syndrome should avoid them. (5) Catheter ablation technique This technique is highly mature, safe, effective, and can cure tachycardia, so it should be prioritized. For those who cannot undergo catheter ablation at present but experience frequent attacks and significant symptoms, long-acting β-blockers, long-acting calcium channel blockers, or digitalis can be considered for prophylactic use. For patients with infrequent attacks, good tolerance, short duration, self-termination, or easy termination by the patient themselves, prophylactic medication is not necessary.
2. Paroxysmal Ventricular Tachycardia First, we need to determine which patients should receive treatment. Currently, apart from β-blockers and amiodarone, no other antiarrhythmic drugs have been proven to reduce the incidence of sudden cardiac death. Moreover, antiarrhythmic drugs themselves can cause or exacerbate existing arrhythmias. Therefore, the general principle for treating ventricular tachycardia is: patients with organic heart disease or clear precipitating factors should receive targeted treatment first; persistent ventricular tachycardia, regardless of whether there is organic heart disease, should also be treated.

VII. Atrioventricular Block Atrioventricular block refers to a delay in the conduction of impulses from the atria to the ventricles, or the inability of some or all impulses to reach the ventricles. According to the degree of block, it is usually divided into first-degree, second-degree, and third-degree (complete) atrioventricular block.