The abnormal pacemaker from the ventricle cannot affect the sinoatrial node, so it is a fully compensated pause.

Contrast memory Atrial premature contractions are incomplete compensatory pauses

Types of premature ventricular contractions: Premature ventricular contractions may occur isolatedly or regularly.

When each sinus beat is followed by a ventricular contraction, it is called bigeminy; when every two sinus beats are followed by a premature ventricular contraction, it is called tripony; and so on.

Two consecutive ventricular premature contractions are called paired ventricular premature contractions. Three or more consecutive premature ventricular contractions are called ventricular tachycardia.

If the premature ventricular contraction happens to be inserted between two sinus beats and does not cause a pause after the premature contraction, it is called metastatic ventricular contraction. In the same lead, ventricular premature contractions with the same shape are called monomorphic premature ventricular contractions; those with different shapes are called polymorphic or polymorphic premature ventricular contractions.

Preventricular contractions are followed by a long pause,

The second heart sound of premature ventricular contractions is weakened,

Only the first heart sound can be heard,

Radial artery pulse weakens or disappears.

Those with asymptomatic or mild symptoms do not need treatment

For those with obvious symptoms, eliminate the symptoms and remove the inducements.

If symptoms are severe, ß-blockers, non-dihydropyridine calcium channel blockers, and amiodarone may be used

For acute myocardial ischemia or infarction combined with premature ventricular contractions, reperfusion therapy is the first choice, and preventive use of antiarrhythmic drugs is not recommended.

Frequent ventricular premature contractions originating from the right ventricular outflow tract or left ventricular posterior septum. If the symptoms are obvious, antiarrhythmic drugs are ineffective or cannot tolerate drug treatment, and there are no obvious organic heart disease patients, the success rate is higher.

The most common is coronary heart disease, especially in patients who have had myocardial infarction

Followed by cardiomyopathy, heart failure, and valvular heart disease

Others include metabolic disorders, electrolyte disorders, long QT syndrome, etc.

Occasionally seen in patients without structural heart disease - idiopathic ventricular tachycardia

The rhythm of the abnormal ventricular pacemaker plus the rhythm of the sinus node becomes irregular.

Ventricular fusion wave: The shape is between sinus and ectopic ventricular beats, which is a partial capture of the ventricle.

The presence of ventricular capture and ventricular fusion waves is the most important basis for establishing the diagnosis of ventricular tachycardia.

According to the shape of the QRS wave during ventricular tachycardia, ventricular tachycardia can be divided into monomorphic ventricular tachycardia and polymorphic ventricular tachycardia. Those in which the direction of the main QRS wave changes alternately are called bidirectional ventricular tachycardia.

If non-sustained ventricular tachycardia occurs in patients without structural heart disease, if there are no symptoms and hemodynamic effects, treat intraventricular premature contractions;

Those with structural heart disease or clear triggers should be given targeted treatment first

Sustained episodes of ventricular tachycardia, regardless of whether there is structural heart disease, should be treated

(1) Termination of ventricular tachycardia attack

(2) Prevention of recurrence

Non-sustained VT (<30 seconds, terminates spontaneously) is often asymptomatic

Sustained VT (>30s, requiring drugs or electrical cardioversion to terminate) is often accompanied by significant hemodynamic disturbance and myocardial ischemia. Clinical symptoms include hypotension, oliguria, shortness of breath, angina, syncope, etc.

Mildly irregular heart rhythm, S1 and S2 split, affecting systolic blood pressure

Stimulating the vagus nerve can slow or stop attacks

atrial presystole triggering

The P wave is related to the QRS complex in a 1:1 ratio

ventricular fusion wave;

ventricular capture;

interventricular separation;

The main wave direction of the QRS complex in all leads is in the same direction, all upward or downward

Is a special type of polymorphic ventricular tachycardia

During the attack, the amplitude and peak of the QRS wave complex change periodically, as if they are continuously twisting around the equipotential line, hence the name.

Frequency 200-250bpm

It is also characterized by a usually prolonged QT interval, often complicated by high U waves, etc.

Premature ventricular contractions can be induced when they occur in late diastole and fall on the terminal part of the preceding T wave (R-on-T).

May progress to ventricular fibrillation and sudden death

Causes: congenital, electrolyte disorders (hypokalemia, hypomagnesemia), antiarrhythmic drugs (Class IA or Class III), tricyclic antidepressants, etc.

treat:

Definition: Also known as slow ventricular tachycardia, the mechanism of occurrence is increased automaticity.

Electrocardiogram: 3-10 QRS complexes originating from the ventricles occur continuously, with a heart rate of 60-110 beats/min. Begins and ends gradually

Often occurs in patients with heart disease, especially during reperfusion of acute myocardial infarction, cardiac surgery, etc.

The attacks are brief or intermittent, generally asymptomatic, and do not affect the prognosis. Antiarrhythmic treatment is usually not required.

The duration is short. If rescue is not carried out in time, the general electrical activity will disappear quickly within a few minutes.

There is a QRS wave after the P wave

P-R is greater than 0.20 seconds

Mostly intranodal block

Also known as Wenck's block, it is the most common second-degree atrioventricular block

The PR interval progressively lengthens until the P wave is blocked and cannot pass down to the ventricle;

The RR interval including the obstructed P wave is less than twice the normal sinus PP interval.

The most common atrioventricular conduction ratios are 3:2 and 5:4

1. After the P wave that appears regularly, the P-R interval is constant, but there are periodic P waves that cannot be transmitted down to the ventricle, and ventricular leakage occurs;

2. The long R-R interval when ventricular leakage occurs is equal to twice or an integral multiple of the short R-R interval.

In second-degree atrioventricular block, two or more consecutive P waves that cannot be transmitted down to the ventricle are often called high-grade atrioventricular block.

1. P waves and QRS complexes are rhythmic and unrelated to each other.

2. The room rate is faster than the room rate;

3. The ventricular pacing point is usually below the block site

In the first degree, there are usually no symptoms; in the second degree, there may be palpitations, fatigue, and a sense of missing heartbeats;

The third degree depends on the original disease and the speed of the ventricular rate, and often includes palpitations, cardiac insufficiency, angina, dizziness or syncope.

First degree of constant weakening of the first heart sound

Second degree type I progressively weakens, from strong to weak

Second degree type II constant weakening

The first heart sound of the third degree varies in intensity and can be heard like the sound of a cannon.

Obvious symptoms: significantly slow ventricular rate, accompanied by obvious symptoms or hemodynamic disorders, or even AS syndrome

V1 is on the right

1. QRS time limit ≥0.12s; complete block

2. Lead V1 has an rsR’ shape, and the R’ wave is thick and blunt;

4. The T wave is opposite to the main QRS wave.

Left on V5

1. QRS time limit ≥0.12s; complete block

2. The R wave in leads V5 and V6 is wide, with a notch or blunt top and no Q wave in front;

3. Leads V1 and V2 show broad QS waves or rS waves;

4. The T wave is opposite to the main QRS wave.

Ia: Slow down the rise rate of action potential phase 0 (Vmax), prolong APD, quinidine, procainamide, disopyramide

Ib: Do not slow down Vmax, shorten APD

Ic: Significantly slows Vmax, significantly slows conduction and slightly prolongs APD