Bradycardia

Bradycardia - reduction of heartbeats less than 60 beats per minute. In some cases, this and a smaller number of heartbeats are considered a variant of the norm (trained athletes).

[1], [2], [3], [4], [5], [6], [7], [8]

Causes Bradycardia

What causes bradycardia?

The main causes of life-threatening bradycardia: syndrome of weakness of the sinus node, atrioventricular blockade of the 2nd degree (especially atrioventricular blockade of the II degree, type Mobits II), atrioventricular blockade of the third degree with a wide complex of QRS.

Forms

Types of bradycardia

In connection with the degree of danger, there are:

• marked bradycardia (heart rate <40 per minute), which is rarely physiological and rarely asymptomatic, almost always requires treatment;
• moderate bradycardia (heart rate 40-60 per minute), which requires immediate medical treatment only with arterial hypotension (ADS <90 mm Hg), hemodynamic disorders and heart failure.

Treatment Bradycardia

How is the bradycardia treated?

Severe bradycardia or disorders of central hemodynamics with moderate bradycardia is treated by intravenous injection of 0.5 mg (0.5 ml of 0.1% solution) of atropine. If necessary, repeated administration of atropine to a maximum dose of 3 mg (3 ml of 0.1% solution) is performed. In patients with myocardial infarction, atropine should be administered with caution, since atropine-induced tachycardia can aggravate myocardial ischemia and increase lesion size.

With a positive effect of atropine and the absence of hemodynamic disorders, an assessment of the risk of asystole should be conducted. The main risk criteria for asystole:

• already had an asystole in recent times;
• atrioventricular blockade of the second degree Mobitz II, complete transverse block with wide QRS complexes;
• cessation of ventricular activity (ventricular pause), exceeding 3 seconds.

If there is a significant risk of asystole, a resuscitation team or specialist should be called in for pacing.

Optimal timing of endocardial stimulation. It is carried out by conducting the endocardial electrode in the right heart through the lumen of the catheter (by catheterization of the superior vena cava by subclavian or jugular access). With the impossibility of temporary endocardial stimulation, percutaneous pacemaking is indicated. If it is not possible to use cardiac stimulation or its ineffectiveness, intravenous adrenaline is recommended at a rate of 2-10 μg / min (by titration until an adequate hemodynamic response is obtained).

The method of "mechanical pacemaker" (fist pacing) can be used as a temporary measure of treatment of such conditions as: ventricular activity or pronounced bradycardia while there is preparation for other methods of stimulation of cardiac activity.

If the treatment is ineffective, the introduction of a beta-adrenostimulant isoprenaline capable of stimulating the myocardium is shown. The drug is administered intravenously dropwise by titration at a rate of 2-20 μg / min. In cases where severe bradycardia is caused by the use of beta-blockers or calcium antagonists, intravenous glucagon is indicated. The drug is able to exert a foreign and chronotropic effect on the heart due to an increase in the formation of cAMP, that is, it produces an effect similar to beta-adrenergic receptor agonists, but without their involvement.

When beta-adrenoblockers are intoxicated, glucagon is administered at a rate of 0.005-0.15 mg / kg with the transition to a maintenance infusion of intravenous drip at a rate of 1-5 mg / h.

In case of intoxication with calcium antagonists, the drug is administered intravenously bolus in a dose of 2 mg. Supportive doses are selected individually depending on the patient's condition. There is no sense in administering atropine in patients after heart transplant. Due to denervation of the myocardium, the administration of atropine in them will not lead to an increase in the number of cardiac contractions, but can cause a paradoxical atrioventricular block.

A complete atrioventricular block with non-extended QRS complexes does not serve as an absolute indication for pacemaking. In these cases, the rhythm comes from the atrioventricular junction and can provide sufficient hemodynamic stability and organ perfusion. As a rule, such patients have a good effect from the administration of atropine, and the risk of developing asystole in them is regarded as low.

Sometimes cardiac arrest is caused by Adams-Stokes-Morgagni syndrome, in which there is a cessation or sharp decrease in the effective contractile activity of the heart. There is an attack during the period of extinction of the conduction of the bundle of His with the transition of incomplete atrioventricular blockade to full, as well as with severe depression of ventricular automatism or the occurrence of asystole and ventricular fibrillation in patients with a permanent form of complete blockade. In this case, pronounced bradycardia is observed, ventricular contractions sharply decrease, reaching 20-12 per 1 minute, or stop completely, which leads to a violation of blood supply to organs, especially the brain.

The syndrome is manifested by attacks of loss of consciousness, sharp pallor, stopping breathing and convulsions. Attacks last from a few seconds to several minutes and pass independently or after appropriate treatment measures, but sometimes end up lethal.

Adams-Stokes-Morgani syndrome is most often observed in patients with atrioventricular blockade of II-III degree, but sometimes also with syndromes of sinus node weakness, premature ventricular excitation, paroxysmal tachycardia, attacks of ciliary tachyarrhythmia.

With the development of an attack of Adams-Stokes-Morgani syndrome, resuscitation is necessary, as with any stop of blood circulation. At the same time, there is rarely a need for full-scale resuscitation, since cardiac activity is most often restored after an indirect heart massage.