Artificial pacemakers

Artificial pacemakers (IVR) are electrical devices that produce electrical impulses sent to the heart. Permanent electrodes of artificial pacemakers are implanted during thoracotomy or through extreme venous access, however, electrodes of some temporary emergency artificial pacemakers can be applied to the chest.

There are several indications for the use of artificial pacemakers, but mostly they include clinically significant bradycardia or high-grade AV blockade. Some tachyarrhythmias can be terminated by exceeding signals that capture the ventricles by creating short discharges of higher frequency; then artificial pacemakers slow down to the selected frequency. In any case, ventricular arrhythmias are more amenable to instrumental treatment with devices that can perform cardioversion, defibrillation, and serve as a source of rhythm (implantable cardioverter-defibrillators). Types of artificial pacemakers are recorded in three to five letters indicating the following parameters:

• which chambers of the heart are stimulated; which cameras perceive the impulse;
• how an artificial pacemaker responds to its own impulse (supports or suppresses arousal);
• whether it can increase heart rate during exercise (heart rate modifying);
• is multi-chamber stimulation (in both atria, both ventricles, or more than one electrode in the same chamber).

Indications for implantation

Arrhythmia	Revealed (confirmed by research)	Possibly shown and supported by research or experience.
Sinus node dysfunction	Bradycardia with clinical manifestations, including frequent, accompanied by symptoms of sinus node omission and bradycardia when using the necessary medicines (alternative approaches are contraindicated). Symptoms-associated chronotropic insufficiency (heart rate cannot meet physiological needs, that is, it is too small to perform physical activity)	Heart rate <40 per minute, when clinical manifestations are reliably associated with bradycardia. Syncope of obscure nature with severe sinus node dysfunction, fixed on an electrocardiogram or caused by an electrophysiological study
Therapy	Continuous pause-dependent VT with or without a prolonged QT  interval, when the pacemaker efficiency is documented	High-risk patients with congenital long QT syndrome
After acute myocardial infarction	Permanent AV block of the II degree in the His-Purkinje system with a double-dip block or III degree of blockade at the level of the His-Purkinje system or below. Transient AV-blockade of II or III degree at the level of the AV node, combined with blockade of the bundle of the His bundle. Permanent AV block II or III degree, accompanied by book symptoms	Not
Multifascicular blockade	Intermittent AV blockade of III degree. AV blockade II degree type Alternating bifascicular blockade	It is not proven that syncope occurs due to AV blockade, but other possible causes (especially VT) are excluded. Highly prolonged HB * interval (> 100 ms) in asymptomatic patients, detected by chance during an electrophysiological study. Non-physiological intraventricular blockade induced by a pacemaker, detected by chance during an electrophysiological study
Hypersensitive carotid sinus syndrome and neurocardiogenic syncope	Repeated syncope for stimulation of the carotid sinus. Ventricular asystole with a duration of> 3 s with pressure on the carotid sinus in patients who do not take drugs that suppress the sinus node or AV-conduction	Repeated syncope without obvious triggering events and with a pronounced decrease in heart rate. Repeated neurocardiogenic syncope with marked clinical manifestations associated with bradycardia, which is confirmed clinically or when performing a test with an oblique table
After heart transplantation	Bradyarrhythmias with clinical symptoms, suspected chronotropic insufficiency or other established indications for permanent cardiostimulation	Not
Hypertrophic Cardiomyopathy	Indications are the same as in the case of dysfunction of the sinus node or AV-blockade	Not
Dilated cardiomyopathy	Indications are the same as in the case of dysfunction of the sinus node or AV-blockade	Refractory to drug therapy, accompanied by clinical symptoms, idiopathic dilatation or ischemic cardiomyopathy with NYHA functional class III or IV in heart failure according to NYHA and an extended QRS complex (130 ms), with a final LV diastolic diameter of 55 mm and a LV ejection fraction of <35% (biventricular stimulation)
AV blockade	Any variant of AV blockade of the II degree, accompanied by bradycardia with clinical manifestations. AV-blockade of III degree or II degree of high gradations at any anatomical level, if it is associated with the following: Clinical symptoms of bradycardia (including those with heart failure), if they are considered to be associated with a blockade; Arrhythmias and other conditions that require the use of drugs that cause bradycardia; Documented asystole of 3.0 s or any rhythm <40 per minute in awake patients without clinical manifestations; Abdominal catheter ablation; Postoperative blockade, which was not resolved after the intervention; Neuromuscular diseases for which uncontrolled progression of conduction disorders is possible (for example, myotonic muscular dystrophy, Cairns-Sayre syndrome, Erb dystrophy, Charcot-Marie-Tut disease with or without clinical manifestations)	Asymptomatic third-degree AV blockade at any anatomical level, when the number of ventricular contractions when walking is 40 per minute, especially with cardiomegaly or LV dysfunction. Asymptomatic blockade of the II degree of type 2 with a narrow QRS complex (the pacemaker is shown with a wide complex). Asymptomatic blockade of the II degree of type 1 at or below the feet of the bundle of His, identified during an electrophysiological study performed for other indications. AV block I or II degree with clinical manifestations in favor of pacemaker syndrome

* HB - the interval from the beginning of the appearance of a signal in the Hiss system to the beginning of the first ventricular signal. Source: Gregoratos G. Et al. ACC / AHA / NASPE 2002 Guideline update for implantation of cardiac pac Vol. 106. -Suppl. 16. - P. 2145-2161.

For example, a PSI encoded by WIR generates (V) and conducts (V) a pulse in the ventricle, suppresses self-excitation (I), and may increase the frequency during exercise (R).

Rhythm drivers like WI and DDD are used most often. They have the same effect on survival, but physiological pacemakers (AAI, DDD, VDD) compared with WI reduce the risk of atrial fibrillation and heart failure and somewhat improve the quality of life.

Progress on pacemakers involves creating devices with less power consumption, new batteries and electrodes with micro-release of glucocorticoids, which reduces the stimulation threshold, and all this together increases the lifetime of the pacemaker. The switch-on option affects the automatic change of the type of stimulation in response to the impulses sent (for example, a change from DDDR to WIR during atrial fibrillation).

Pacemaker malfunction can occur in the form of an increase or decrease in the sensory impulse's perception threshold, lack of stimulus or capture, as well as stimulation with an abnormal frequency. The most common anomaly are tachycardias. Variable frequency pacemakers can generate pulses in response to vibration, muscle activity, or when they enter a magnetic field during an MRI. With pacemaker-induced tachycardia, a normally functioning two-chamber pacemaker catches a premature ventricular impulse or sends an impulse to the atrium through the AV node or in the opposite direction along an additional conductive pathway, which leads to stimulation of the ventricles with a high frequency, cyclically. Another complication associated with a normally functioning pacemaker is the cross-inhibition, in which the ventricular conduction is perceived by an impulse of atrial stimulation using a two-chamber stimulator. This leads to inhibition of ventricular stimulation and the development of "pacemaker syndrome", in which a violation of the AV-node conduction due to ventricular stimulation leads to dizziness, unsteadiness of gait, cerebral, cervical (cervical veins swelling) or respiratory (dyspnea) symptoms.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]

Encoding artificial pacemakers

One	II	III	IV	V
Stimulated	Perceiver	The answer to the event	Frequency change	Multi-chamber stimulation
A - atrium V - ventricle D - both cameras	A - atrium V - ventricle D - both cameras	0 - no 1 - inhibits the pacemaker T-stimulates the pacemaker to stimulate the ventricles D - both chambers: stimuli perceived in the ventricle inhibit; enhances incentives Perceived in the atrium	0 - non-programmable R - with the possibility of changing the heart rate	0 - no A - atrium V - ventricle D - both cameras

Environmental exposure implies the influence of sources of electromagnetic radiation, such as a surgical electrocautery or MRI, although MRI may be safe if the pacemaker and electrodes are not inside the magnet. Cell phones and e-security systems are potential sources of exposure; phones can not be placed next to the pacemaker, but their conversation on them is quite safe. Passing through metal detectors does not lead to disruption of the pacemaker’s performance if the patient does not linger in them.

Complications during implantation of artificial pacemakers are rare, but myocardial perforations, bleeding and pneumothorax are possible. Postoperative complications include infection, displacement of the electrodes and the pacemaker itself.

[11], [12], [13], [14], [15], [16]