Tachycardia

Tachycardia is an increase in heart rate over 100 per minute. The negative effect of tachycardia on the myocardium is explained by the fact that coronary blood flow occurs mainly during diastole. With an excessively high heart rate, the duration of diastole is critically reduced, which leads to a decrease in coronary blood flow and myocardial ischemia. The rhythm frequency at which such disturbances are possible is more than 200 per 1 minute with narrow-complex tachycardia and more than 150 per 1 minute with wide-complex tachycardia. This explains why wide-complex tachycardia is worse tolerated.

Symptoms tachycardias

If tachycardia is registered on the electrocardiogram or ECG monitoring, but there is no pulsation over the arteries, then this condition is assessed as cardiac arrest, and not as periarrest arrhythmia. Treatment of such patients is carried out according to the universal algorithm for resuscitation measures. An exception to this rule is the case when there is tachycardia with narrow QRST complexes with a very high heart rate (over 250 per minute). There are two types of periarrest tachycardia:

• tachycardia with narrow QRS complexes;
• tachycardia with wide QRS complexes.

Typically, tachycardia with narrow QRS complexes causes less disruption to the cardiovascular system than tachycardia with wide QRS complexes.

If pulsation in the arteries is detected, then the presence or absence of the following unfavorable prognostic signs in the patient should be assessed:

• BP below 90 mmHg;
• Heart rate over 150 beats per minute;
• chest pain;
• heart failure;
• disturbances of consciousness.

Forms

Tachycardia with wide QRS complex

The general principle of treating wide QRS complex tachycardia in the periarrest period is that such tachycardia should be considered primarily as ventricular. There is a possibility that such an electrocardiographic picture may be caused by supraventricular tachycardia with aberrant conduction (i.e., developed against the background of bundle branch block), but it is better to treat supraventricular tachycardia as ventricular than vice versa. Especially in a patient who has just suffered a cardiac arrest. Nevertheless, it is recommended to follow certain rules for interpreting such electrocardiographic changes in order to determine with the highest probability the type of cardiac disorder and choose the most rational treatment tactics.

First of all, it is necessary to determine whether the patient has a regular rhythm of tachycardia with wide QRS complexes. Usually, the regularity of the ventricular rhythm is determined by the RR intervals. If the R teeth follow each other with equal intervals, then we can definitely say that the rhythm is regular. If the intervals differ from each other, a conclusion should be made about the irregularity of the rhythm. In tachyarrhythmias with an extended QRS complex, there are sometimes difficulties in identifying individual teeth, so the rhythm can be judged by the regularity of the intervals between the QRS complexes.

Tachycardia with wide QRS and regular rhythm

In the absence of arterial hypotension, chest pain, heart failure and impaired consciousness, the patient should be administered 300 mg of cordarone in a 5% glucose solution intravenously (over 10-20 minutes) followed by a maintenance infusion (900 mg of cordarone over 24 hours).

Careful monitoring of the patient's condition is necessary, a consultation with a cardiologist is required, and one must be prepared to perform electrical cardioversion if the patient's condition worsens or if the attack of tachycardia is prolonged (if the attack lasts several hours).

If there is compelling evidence that the wide QRS complex is due to bundle branch block and supraventricular tachycardia is present, then the treatment algorithm for narrow QRS tachycardia should be followed. In case of uncertainty or any doubt, such tachycardia should be treated as ventricular.

It should always be remembered that in the acute phase of myocardial infarction and in patients with an established diagnosis of coronary heart disease, ventricular tachycardia is most likely to develop.

It is imperative to take into account the underlying disease that caused the cardiac arrhythmia. In all patients, correction of hypoxia, hypercapnia, acid-base and water-electrolyte imbalance is important. It is possible to stop tachycardia with a wide QRS and regular rhythm using esophageal competing frequent stimulation.

Tachycardia with wide QRS and irregular rhythm

Tachycardia with a wide QRS and irregular rhythm may be caused by:

• atrial fibrillation (AF) with concomitant blockade of one of the bundle branches of His;
• atrial fibrillation with premature ventricular excitation (Wolff-Parkinson-White syndrome);
• polymorphic ventricular tachycardia (the probability of its development without significant disturbances of systemic hemodynamics is extremely low).

All patients should be consulted by a cardiologist and a specialist in functional therapy. After diagnosis, treatment of atrial fibrillation with concomitant bundle branch block is carried out according to the algorithm for the treatment of atrial fibrillation. In patients with atrial fibrillation and Wolff-Parkinson-White syndrome, zlenosine, digoxin, verapamil, or diltiazem should not be used. These drugs cause atrioventricular node block and may worsen existing disorders. Optimal treatment for such patients is electrical cardioversion.

Treatment of polymorphic ventricular tachycardia should begin with discontinuing all drugs that prolong the QT interval. Correction of existing electrolyte imbalances (especially hypokalemia) should be performed. Magnesium sulfate at a dose of 2 g (intravenously over 10 minutes) is indicated. If complications develop, immediate synchronized electrical cardioversion is indicated. If the patient does not have arterial pulsation, electrical defibrillation should be performed immediately and a universal resuscitation algorithm should be used.

Narrow QRS complex tachycardia

Variants of tachycardia with a narrow QRS complex and regular rhythm:

• sinus tachycardia;
• atrial tachycardia;
• atrioventricular tachycardia;
• atrial flutter with regular atrioventricular conduction (usually 2:1).

The most common causes of tachycardia with a narrow QRS complex and irregular rhythm are atrial fibrillation or atrial flutter with different atrioventricular conduction.

Tachycardia with narrow QRS and regular rhythm

Sinus tachycardia is an increase in the number of heartbeats originating in the sinus node. It may be caused by increased sympathetic or suppressed parasympathetic influences on the sinus node. It may occur as a normal reaction to physical exertion, as a compensatory reaction to myocardial damage, hypoxic conditions, hormonal changes (thyrotoxicosis), pain, fever, blood loss, etc.

The electrocardiogram for sinus tachycardia is characterized by a shortening of the RR, PQ, QT interval, an enlarged and slightly sharpened P wave. Sinus tachycardia can occur in the form of paroxysms, but it differs from paroxysmal tachycardia in its gradual (not sudden) normalization of the rhythm. Treatment should be aimed at the cause of this condition (pain relief, lowering temperature, replenishing the volume of circulating blood, etc.).

Paroxysmal supraventricular tachycardia

In clinical practice, supraventricular paroxysmal tachycardias are often observed (atrial and atrioventricular paroxysmal tachycardias are combined into this group).

The heart rate is from 140 to 260 per minute. Supraventricular tachycardia is less dangerous in terms of developing ventricular fibrillation compared to ventricular tachycardia. The shape of ventricular complexes on the electrocardiogram in supraventricular arrhythmia differs little from that in normal rhythm. The P wave is usually difficult to distinguish. If the ectopic focus is located in the upper atria, then positive deformed P waves are observed on the electrocardiogram; if the ectopic focus is in the lower atria, then negative P waves are observed in leads II, III and aVF. If the paroxysm originates from the atrioventricular junction, the P waves on the electrocardiogram are negative, they can merge with the unchanged QRS complex or follow it.

Paroxysmal supraventricular tachyarrhythmias, like ventricular ones, are subject to termination, especially if they entail disturbances of ventral hemodynamics.

Atrial fibrillation

In atrial flutter, the flutter focus impulses (270-350 per minute) “interrupt” the frequency of sinus impulse generation (60-100 per minute). Therefore, the absence of sinus rhythm (absence of P waves) is a sign of flutter.

The electrocardiogram records "flutter waves" - uniform, saw-toothed (similar to saw teeth), with a gradual rise and a sharp fall, low-amplitude (no more than 0.2 mV) teeth. They are best determined in lead aVF. The frequency of these "flutter waves" is within 250-370 per minute, and the atrioventricular junction is not able to pass all the impulses to the ventricles, so some of them are missed. If atrial flutter occurs with a frequency of 350 per minute, and only every fifth impulse passes to the ventricles, then we speak of a functional atrioventricular block 5: 1 (the excitation frequency of the ventricles will be equal to 70 per minute, the RR interval will be the same).

Since the flutter impulses reach the ventricles in the usual way (through the ventricular conduction system), the shape of the ventricular QRS complex is not changed or widened (does not exceed 0.12 s).

The most common "flutter wave" rate is 300 bpm and a 2:1 functional block. This results in tachycardia with a ventricular rate of 150 bpm. A more rapid rhythm (170 or more) is not characteristic of atrial flutter with a 2:1 block.

In some cases, the functional atrioventricular block rapidly changes, becoming 5:1, then 4:1, then 3:1, etc. In this situation, the atrial flutter waves will overcome the atrioventricular junction arrhythmically and the interval between the ventricular QRS complexes will be different. This variant is called irregular atrial flutter. The combination of atrial flutter with bundle branch block leads to the appearance of an electrocardiographic picture that is difficult to differentiate from ventricular tachycardia.

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Treatment tachycardias

In parallel with the initial examination, the patient should:

• establish oxygen supply;
• ensure reliable intravenous access;
• record a 12-lead electrocardiogram.

Compared with electrical cardioversion, antiarrhythmic drugs act more slowly and convert tachycardia to sinus rhythm less effectively when used. Therefore, drug therapy is used in patients with a stable condition without adverse symptoms, and electrical cardioversion is more preferable in patients with an unstable condition and adverse symptoms.

If the patient has hemodynamic instability with progressive deterioration of the condition in the periarrest period (the presence of threatening signs, systolic blood pressure less than 90 mm Hg, ventricular rate more than 150 per 1 minute, heart failure or other signs of shock) caused by severe tachycardia, then synchronized cardioversion must be urgently performed. If it is ineffective, 300 mg of cordarone should be administered intravenously (over 10-20 minutes) and an attempt at cardioversion should be repeated. Subsequently, a maintenance infusion of 900 mg of cordarone is indicated for 24 hours.

Scheme of electropulse therapy:

• oxygen therapy;
• premedication (fentanyl 0.05 mg or promedol 10 mg intravenously);
• sedation (diazepam 5 mg intravenously and 2 mg every 1-2 minutes until falling asleep);
• heart rate control;
• synchronization of the electrical discharge with the R wave on the ECG;
• cardioversion with the recommended dose (for tachycardia with wide QRS complexes or atrial fibrillation, the initial shock is 200 J monophasic or 120-150 J biphasic; for atrial flutter and tachycardia with regular narrow QRS complexes, the initial shock is 100 J monophasic or 70-120 J biphasic);
• if there is no effect, an antiarrhythmic drug indicated for this arrhythmia should be administered;
• if there is no effect, cardioversion should be repeated, increasing the discharge energy;
• If there is no effect, the EIT should be repeated with a maximum power discharge.

For emergency restoration of sinus rhythm, the following initial discharge energies are recommended:

• ventricular fibrillation and polymorphic ventricular tachycardia - 200 J;
• monomorphic ventricular tachycardia - 50-100 J;
• atrial fibrillation - 200 J;
• atrial flutter and paroxysmal supraventricular tachycardia - 50-100 J.

If tachyarrhythmia is not accompanied by significant hemodynamic disorders, then, first of all, it is necessary to determine whether there is a widening of the QRS complex (normally, the width of the QRS complex is less than 0.12 seconds).

Treatment of tachycardia with narrow QRS and regular rhythm

If the patient has unstable hemodynamics and progressive deterioration of the condition, then immediate synchronized electrical cardioversion is indicated. While preparations for this procedure are underway, adenosine can be administered intravenously by bolus (adenosine is an antiarrhythmic drug that is highly effective in paroxysmal supraventricular tachycardias; it is available as an injection solution containing 6 mg in 2 ml vials). Cardioversion should not be delayed; there is no immediate effect after the drug administration (sinus rhythm is not restored).

If the patient's condition is stable, then therapeutic measures should begin with a reflex effect on the vagus nerve (straining the patient at the height of a deep breath, massage of the carotid sinus, pressure on the eyeball). If tachycardia persists and atrial fibrillation is excluded, intravenous bolus administration of 6 mg of adenosine is indicated. It is advisable to record an electrocardiogram during the administration of the drug and monitor changes in it. If the ventricular contraction rhythm becomes slower for a short time, but then increases again, then atrial fibrillation or other atrial tachycardia should be considered. If the administration has no effect at all, then 12 mg of adenosine should be administered as a bolus (then 12 mg should be administered again if there is no effect). According to the 2010 AHA guidelines, adenosine can now be used for the initial evaluation and treatment of stable, undifferentiated, regular wide-complex monomorphic tachycardia in the presence of a regular heart rhythm. It is important to note that adenosine should not be used for irregular wide-complex tachycardia because it may precipitate ventricular fibrillation.

Successful termination of tachycardia by vagal tests or adenosine indicates its atrial or atrioventricular origin (usually termination occurs in a matter of seconds). If there are contraindications to the administration of adenosine or atrial flutter is detected, the following should be administered:

• verapamil intravenous bolus 2.5-5 mg (over 2 minutes), or
• diltiazem intravenous bolus 15-20 mg (over 2 minutes).

Treatment of tachycardia with narrow QRS and irregular rhythm

Tachycardia with a narrow QRS and irregular rhythm is most likely due to atrial fibrillation or atrial flutter with varying degrees of atrioventricular conduction. A 12-lead electrocardiogram is required to identify the rhythm.

If the patient has unstable hemodynamics and progressive deterioration of the condition, then immediate synchronized - electrical cardioversion is indicated. If the patient's condition is stable, then the following treatment options are available:

• drug therapy to regulate heart rate;
• performing drug-induced (chemical) cardioversion;
• restoration of rhythm by electrical cardioversion;
• prevention of complications (anticoagulation therapy, etc.).

Treatment tactics depend on the duration of atrial fibrillation, since the longer it lasts, the greater the chance of thrombus formation in the right atrium. Chemical or electrical cardioversion should not be performed if atrial fibrillation has existed for more than 48 hours until anticoagulation therapy has been administered or the absence of a thrombus in the right atrium has been proven (using transesophageal echocardiography).

To achieve and maintain an acceptable ventricular rate (slowing down to 70-90 beats/min), beta-blockers, cardiac glycosides (digoxin), calcium antagonists (diltiazem), or combinations of these drugs are usually used:

• Verapamil 5-10 mg (0.075-0.15 mg/kg) intravenously over 2 minutes.
• Diltiazem 20 mg (0.25 mg/kg) intravenously over 2 minutes (continuous infusion - 5-15 mg/h).
• Metoprolol 5.0 mg intravenously over 2-5 minutes (up to 3 doses of 5.0 mg can be administered at 5-minute intervals).
• Propranolol 5-10 mg (up to 0.15 mg/kg) intravenously over 5 minutes.
• Esmolol 0.5 mg/kg intravenously over 1 minute (continuous infusion - 0.05-0.2 mg/kg/min).
• Digoxin 0.25-0.5 mg intravenously, then for rapid saturation 0.25 mg can be administered intravenously every 4 hours up to a total dose of no more than 1.5 mg.
• Cordarone 300 mg intravenously over 10 minutes, then intravenous infusion at a rate of 1 mg/min for 6 hours, then continued infusion at a rate of 0.5 mg/min.
• Calcium antagonists (verapamil, diltiazem) and beta blockers are first-line drugs for emergency reduction of heart rate. Sustained slowing of ventricular rate with digoxin administration is achieved within 2-4 hours.

In case of decreased contractile function of the left ventricle, it is recommended to slow the heart rate with cardiac glycosides or cordarone. If the duration of the paroxysm of atrial fibrillation is less than 48 hours, cordarone in a dose of 300 mg (for 10-20 minutes) can be used to stop it, followed by maintenance infusion (900 mg cordarone for 24 hours).