Ventricular flutter

Introduction Ventricular flutter is a transitional type between ventricular tachycardia and ventricular fibrillation, or it can be followed by ventricular fibrillation or doping. Ventricular flutter (ventricular flutter) is a severe ventricular ectopic rhythm. The electrocardiogram shows that the QRS complex and the T-wave are difficult to recognize, and are replaced by a relatively regular, high-amplitude sine wave group, 150 to 300 times per minute (an average of about 200 times). Ventricular flutter is indistinguishable from ventricular tachycardia with fast heart rate, which is usually a prelude to ventricular fibrillation. In ventricular fibrillation (ventricular fibrillation), the electrocardiogram shows that the sinusoidal waveform is low and irregular, 200 to 500 times per minute.

Cause

(1) Causes of the disease

Myocardial dysfunction and ventricular fibrillation can be caused by myocardial hypoxia, ischemia, electrolyte imbalance, drug poisoning and physical and chemical factors caused by various organic heart diseases and other diseases. Often a kind of arrhythmia before these patients died. However, it can also be seen that the heart disease is not very serious, or there is no obvious heart disease, and even the heart has no organic disease according to the sudden onset of ventricular flutter or ventricular fibrillation leading to cardiac arrest. The common causes are as follows:

Coronary heart disease

Especially in acute myocardial infarction, unstable angina, ventricular aneurysm, reperfusion after thrombolytic therapy in acute myocardial infarction. Acute myocardial infarction complicated by ventricular fibrillation, without hypotension, shock or heart failure before ventricular fibrillation can be called primary ventricular fibrillation: such as hypotension, shock or heart failure before ventricular fibrillation is called secondary Ventricular fibrillation. The incidence of primary and secondary ventricular fibrillation during hospitalization for acute myocardial infarction was 2.7% and 2.8%, respectively. 71% of primary ventricular fibrillation occurred within 24 hours after acute myocardial infarction, with the highest incidence in the first hour after onset and rapidly decreased in the following hours. No primary ventricular fibrillation occurred after 48 hours of infarction. 41% of secondary ventricular fibrillation occurred 2 weeks after the onset of myocardial infarction. Primary ventricular fibrillation occurs mostly in anterior wall myocardial infarction. When acute myocardial infarction with bradycardia, conduction block or re-myocardial infarction, will increase the incidence of ventricular fibrillation. The survival rate of primary ventricular fibrillation in the acute phase of myocardial infarction was 57%, and the survival rate of secondary ventricular fibrillation was only 18%.

2. Conversion from other arrhythmias to ventricular fibrillation

(1) Complete or high atrioventricular block.

(2) Long QT interval syndrome with torsades de pointes ventricular tachycardia: Brugada syndrome.

(3) QT interval normal polymorphic ventricular tachycardia and extremely short intertemporal polymorphic ventricular tachycardia.

(4) Also seen in pathological paroxysmal persistent ventricular tachycardia.

(5) Pre-excitation syndrome with atrial fibrillation: If the bypass refractory period is <270ms, rapid atrial activation can be transmitted by bypass 1:1, resulting in ventricular fibrillation.

(6) arrhythmogenic right ventricular dysplasia ventricular tachycardia.

3. Other heart disease

(1) Cardiomyopathy: including dilated cardiomyopathy, hypertrophic cardiomyopathy, etc., their incidence of ventricular tachycardia is very high. The sudden deaths were 56% and 19% in the persistent ventricular tachycardia group and 5.4% in the non-sustained ventricular tachycardia group, both of which occurred in dilated cardiomyopathy. Patients with sudden death confirmed by electrocardiogram that ventricular fibrillation accounted for 66%.

(2) valvular disease: such as aortic stenosis and dysfunction with angina or cardiac insufficiency.

(3) Myocarditis, acute pulmonary embolism, some mitral valve prolapse syndrome, aortic aneurysm rupture, cardiac tamponade, heart rupture.

(4) Performance of other patients with severe heart disease or other diseases before dying.

4. The toxicity of various drugs

Such as digitalis, quinidine, procainamide, expectorant, phenothiazine and other drugs poisoning.

5. Electrolyte disorders

Mainly for hypokalemia, or occasionally when hyperkalemia is too high. Severe acidosis.

6. Heart surgery

Especially during the open heart surgery under the low temperature anesthesia block cycle: ventricular fibrillation often occurs when the cardiopulmonary bypass is induced by deep hypothermia. Endotracheal intubation, cardiac trauma, right heart catheter or left cardiac catheter, mitral balloon dilatation catheter failure may also occur.

7. Electric shock or drowning

Ventilation can occur when 300 mA of direct current or 70-80 mA of alternating current passes through the heart during an electric shock. Freshwater drowning people often cause ventricular fibrillation.

8. Other

Myocardial ischemia, hypoxia, cardiac hypertrophy, sympathetic excitation, metabolic acidosis, bradycardia, cerebrovascular accidents, etc. can promote the occurrence of ventricular fibrillation.

(two) pathogenesis

There are two theories:

1. Increased ventricular muscle self-discipline, resulting in single or multiple rapid ectopic excitability in the ventricle.

2. Micro-returning excitement

When myocardial ischemia, hypoxia, myocardial necrosis and severe bradycardia, the repolarization rate of cardiomyocytes is inconsistent with the length and height of refractory period, and one or more micro-returns in the ventricular muscle are formed, which are different in size and direction. The transmission route is transmitted to all parts of the ventricle, causing the myocardial contraction and relaxation of each part to lose consistency.

an examination

Related inspection

ECG dynamic electrocardiogram (Holter monitoring)

The electrocardiogram may have a characteristic change: the electrocardiogram QRS complex and the T wave are difficult to recognize when the ventricle is fluttering, and replaced by a relatively regular, high amplitude wave group, 150 to 250 times per minute. When the ventricular fibrillation is on, the electrocardiogram can have a low and small waveform, 200 to 500 times per minute.

Differential diagnosis

1. Need to differentiate from other polymorphic ventricular tachycardia

The following two points are helpful in the differential diagnosis: on the electrocardiogram before or just after the onset of ventricular tachycardia, if there is a prolongation of the QT interval and the presence of U waves, a relatively long intercostal interval, or a typical induction sequence. (long-short circumference), etc., support TDP; the clinical situation when 2 ventricular tachycardia occurs is helpful for differential diagnosis.

2. This type of arrhythmia should be differentiated from the symptoms of paroxysmal syncope and sudden death.

For example, it should be differentiated from intermittent-dependent TDP, pre-excitation syndrome with extreme atrial fibrillation, idiopathic ventricular fibrillation, Brugada syndrome, sick sinus syndrome, and epilepsy. Secondary QT interval extension should be excluded.

The electrocardiogram may have a characteristic change: the electrocardiogram QRS complex and the T wave are difficult to recognize when the ventricle is fluttering, and replaced by a relatively regular, high amplitude wave group, 150 to 250 times per minute.

When the ventricular fibrillation is on, the electrocardiogram can have a low and small waveform, 200 to 500 times per minute.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.