Analysis of Holter monitoring of ECG with a pacemaker. How does a heart pacemaker work?

To treat heart blocks, electrodes are installed in the right atrium or right ventricle, or in both cavities (Fig. 3, 4).

Fig. 3 (electrode in the cavity of the right ventricle).

Fig. 4 (electrodes in the cavity of the right atrium and right ventricle).

The atrial electrode is usually fixed to the interatrial septum, and the ventricular electrode to the apex of the right ventricle. This fixation option may not be optimal from the point of view of the spread of electrical excitation and contraction of the heart chambers, but the mechanical fastening of the electrodes (which is extremely important) is as reliable as possible. When implanting an IPC with a cardioverter-defibrillator function, the localization of the ventricular electrode will be the same.

With resynchronization therapy, the location of the “right” electrodes is the same; into the left ventricle, the electrode is passed through the coronary sinus located in the right atrium (the mouth of the venous system of the left ventricle), then through the venous system the electrode is brought to the optimal (from the point of view of cardiac stimulation) place of the left ventricle and fixed (Fig. 5).

Fig. 5 (electrodes in both ventricles and in the right atrium).

As for the fixing elements of the electrodes, they can be passive (antennae) and active (“like a corkscrew for a bottle”); the latter are screwed into the endocardium (Fig. 6, 7).

Fig.6.
Fig.7.

To understand how IPCs work, let’s look at specific examples. In Fig. 8 shows an ECG of a patient who suffered from unexplained fainting. After Holter monitoring ECG The cause of syncope was established - sporadically occurring heart blocks.

Fig.8.

She had a pacemaker implanted, after which the fainting stopped. Figure 9 shows an ECG fragment of the same patient at the moment the pacemaker is activated “on demand”.

Fig.9.

Another fragment of an ECG (Fig. 10) of a patient who suffered from fainting before implantation of the pacemaker.

Fig. 10.

Currently everything pacemakers programmed in the “safety net” mode (on demand, Demand). That is, the pacemaker turns on only at the moment of a cardiac pause of a certain duration, and the priority (for the pacemaker itself) is the heart’s own contractions, which are much more beneficial for intracardiac hemodynamics (Which is better: the natural propagation of the impulse or from the apex of the right ventricle? The answer is obvious). Another thing is that one’s own cardiac conduction can be so depressed (total or subtotal heart block) that almost all the time the heart’s work will be subordinated to the pacemaker. In addition, complete dependence on the pacemaker is observed in the case of targeted ablation of some critical section of the conduction system (for example, ablation of the AV node in tachysystolic atrial fibrillation), which leads to the absolute impossibility of the natural propagation of the electrical impulse.

Trigger cardioverter-defibrillator occurs at the moment of occurrence ventricular tachycardia(contraction of the ventricles with an unmotivated high frequency) or ventricular fibrillation (“cardiac chaos”, clinical death). These arrhythmias are caused by the circulation of one or more electrical waves in the ventricle. A cardioverter-defibrillator stops the resulting tachyarrhythmia using 2 possible ways: a packet of impulses (8-10 each) with a frequency exceeding the frequency of tachycardia (one of the impulses penetrates the circulating electrical loop and breaks it), orsingle discharge of high voltage electric current (Fig. 11, 12).

Fig. 11.

Fig. 12.

The indication for resynchronization therapy is the mandatory combination of severe CHF with an ECG picture of complete blockade of the left bundle branch. The more pronounced the blockade, the higher the likelihood of a positive clinical effect from resynchronization therapy. Figure 13 depicts the moment when resynchronization therapy is turned on: before it is turned on, a blockade of the left leg is recorded (the width of the complex is 150 ms), at the moment of inclusion, the blockade disappears (the width of the complex is 100 ms), which reflects the emerging synchronism in the contraction of the right and left ventricles.

Fig. 13.

Implantation of modernpacemakers leads to minimal restrictions in the patient’s life. While maintaining the pumping function of the heart, a patient with a pacemaker can lead a normal lifestyle: cottage, any household chores, work, physical education, travel, driving, etc. Those restrictions that existed earlier (the ban on the use of various electronic devices by patients) were due to the use monopolar cardiac pacing systems. In this case, upon contact with high voltage sources, the phenomenon of intermagnetic interference developed, which led to incorrect operation of the pacemaker. Mono polar and bipolar device configurationdetermines the potential difference between the two poles of the electrodes; at mono polar sensitivity, the second pole of the electrode is the body pacemaker. Therefore, with mono in the polar version, due to the large interelectrode distance of 30-50 cm, the pacemaker can perceive all signals falling within these limits (skeletal muscle contractions, electrical activity of other cardiac chambers, etc.), whereas in the bipolar version configuration anode and cathode are at the end of the electrode(distance between them: 1-2 cm) - in this case extraneous electricalsignals are not perceived.

Currently, bipolar stimulation systems are used, which practically eliminate the manifestation of intermagnetic interference, and the IPCs themselves work properly even after external defibrillation. Restrictions remain only for professional activities that involve constant contact with high voltage sources (electrical substations, electrical switchboards, electrical installation work, welding, jackhammer). The only absolute contraindication for patients with a pacemaker is magnetic resonance imaging and direct application of a magnet to the attached device. Some foreign manufacturers of pacemakers are introducing IPCs that allow for the possibility of MRI. However, until the safety of this diagnosis is proven in a randomized trial, performing MRI in patients with a pacemaker will remain prohibited. The basis of the normal life of a patient with a pacemaker is scheduled checks of the system by a specialist who programs the IPC. The equivalent of such checks could be regular (every 6-12 months) Holter ECG monitoring, allowing timely identification of problems with the pacemaker. However, visits to an arrhythmologist still cannot be avoided, if only to know the approximate service life of the IPC battery and the time of its scheduled replacement.

Cardiac stimulation is carried out in the “on demand” mode. With correct programming of the device, priority is given to the heart’s own contractions.

Modern cardiac stimulation is unthinkable without the frequency adaptation function ().

The key to reliable functioning of the ECS is regular (once every 6-12 months) assessment of the effectiveness of its operation using 24-hour ECG monitoring; it will confirm the correct choice of stimulation mode and promptly identify.

Each patient with IPC is given a so-called pacemaker passport. It can be compared to the instructions for use of some electrical appliance. This document specifies all the most important information regarding the operating parameters of the device: from the localization of the electrodes to the subtle electrophysiological parameters of cardiac stimulation. It would seem that the patient cared: he trusted the doctor, who did everything right. This is actually what the vast majority of patients think. However, there is always a small percentage of subjects with pacemakers from the “I want to know everything” category; or linking their poor health with “incorrectly configured stimulation parameters” (as they themselves believe), which forces them to spend time “searching for the truth.”

After a scheduled check of the pacemaker by an arrhythmologist surgeon, the patient is given a brief report reflecting the current pacemaker parameters (what was done and what was changed); in fact this conclusion is a simplified equivalent of a pacemaker passport. If the latter is lost, such conclusions are the only source of information about the current pacemaker settings. Regardless of what the patient has on hand (a passport or a report after a routine check of the device), when studying this documentation, one can see a variety of Russian-language or English-language (depending on the country of the pacemaker manufacturer) specific terms or, even worse, an incomprehensible abbreviation. Something like:

Let's look at the most important concepts.

Mode - reflects the basic characteristics of the pacemaker. Represented as a sequence of capital English letters; usually 3-4, for example: for example DDDR. What is hidden under them?

The first letter indicates which chamber is being stimulated (that is, where the stimulating electrode is located): in the atrium (A - atrium), in the ventricle (V - ventricle) or in both chambers (D - dual).

The second letter means information about the electrical activity of which chamber of the heart is transmitted to the pacemaker (detection / recognition / perception function). In other words, which chamber is detected by the stimulator: the atrium (A - atrium), the ventricle (V - ventricle) or both chambers (D - dual).

The third letter means the type of reaction of the pacemaker to the information received from the detecting electrode: I - inhibited (inhibition), T - triggered (stimulation), D - dual (double response), combinations of inhibiting and stimulating reactions are possible.

The fourth letter, if present, indicates the presence of the heart rate stimulation function ( R - Rate modulation) - the ability of a pacemaker to produce impulses not at a fixed frequency, but according to the needs of the body (accelerate the heart rate).

The fifth letter, if present, indicates the presence cardioverter-defibrillator functions: P (Pase - anti-tachycardia stimulation), S (shock - defibrillation, shock) or D (P+S).

If we talk about the currently widespread mode of cardiac stimulation DDDR, then analyzing this abbreviation, we can say the following: “In both chambers of the heart there is a stimulating electrode (D - dual, both) - that is, both the atria and ventricles are stimulated; it is detected (perceived) information about the electrical activity of both (D - dual) chambers of the heart; depending on the information received from the detection electrodes, the pacemaker can prohibit itself from delivering stimulation (and continue to monitor the electrical activity of the heart) or carry out stimulation (D - dual, both answers); pacemaker has a frequency adaptation function (R)".

To fully understand what has been written, let’s consider another stimulation mode that is widely used for bradycardic atrial fibrillation - VVI. Analyzing this abbreviation, we can say the following: “The stimulating electrode is located in the ventricle (V - ventricle); the sensing electrode is in the ventricle (V - ventricle); if the stimulator detects its own contraction of the ventricles, it does not produce an impulse (I - inhibited, prohibition) , thereby giving priority to spontaneous (natural) electrical activity of the ventricles."

Thus, a pacemaker can be single-chamber (an electrode in one chamber, for example VVI) or dual-chamber (in both chambers along an electrode, for example DDDR).

Important note: there can only be one electrode in one cardiac chamber; Depending on the mode, this electrode performs either stimulation or detection, or both.

Base stimulation frequency ( Base Rate, Lower Rate, Basic Rate) - the frequency with which the heart is stimulated in the absence of its own contractions. Typically programmed at 55 or 60 beats per minute.

Secondly, from the total percentage of ventricular stimulation - the more often the ventricles contract from the stimulator, the higher the risk of developing pacemaker syndrome. It is for this purpose that various algorithms are used that reduce the overall percentage of imposed contractions or reduce the base frequency of stimulation - everything so that the heart contracts naturally as often as possible, and the pacemaker is triggered only in rare episodes on backup (Demand).

Thirdly, if the stimulator does not use an algorithm. If it is not there, the risk of developing pacemaker syndrome is extremely high.

Fourthly, if a long one is programmed (300-350 ms).

Fifthly, on the duration of cardiac stimulation: even with an absolutely correct pacemaker setting (for example, DDDR mode), no one can guarantee that over the years the patient will not develop pacemaker syndrome.

Manifested pacemaker syndrome is actually a symptom complex of heart failure caused by prolonged cardiac stimulation. Its manifestations: weakness, swelling of the legs, fast fatiguability, dizziness, blood pressure lability, shortness of breath with minimal exertion, tendency to low blood pressure.

The pacemaker electrode implanted into the chambers of the heart is foreign to the environment in which it finds itself. When the electrode is inserted into the right ventricle, it inevitably comes into contact with the tricuspid valve leaflets, and this contact remains the entire time the electrode is in the heart. At the point of contact between the valve leaflet and the electrode, aseptic inflammation occurs, which leads to irreversible deformation of the leaflet and the development of tricuspid valve insufficiency. However, the severity of electrode-induced tricuspid insufficiency can be completely different: from minor or moderate (common) to severe (rare). It is important to understand that it is initially impossible to predict how severe valve insufficiency will be with an implanted lead. Only one thing can be stated unequivocally: every patient will have it (valvular regurgitation). Fortunately, practical experience shows that electrode-induced tricuspid regurgitation rarely becomes severe and has little effect on hemodynamics. If, nevertheless, it reaches a severe stage, it will be accompanied by characteristic symptoms of heart failure (weakness, shortness of breath, swelling of the legs). Any degree of lead-induced tricuspid regurgitation is not an indication for lead replacement (reimplantation).

Details Published: 10/27/2018, A pacemaker (pacemaker) is implanted when the heart rate decreases so much that it no longer provides stable hemodynamics. This may manifest as sudden deterioration in exercise capacity, syncope, or death.

Most often, a pacemaker is installed in case of disruption of the sinus node (SSSU) or AV node (2nd-3rd degree AV block). In this case, depending on the specific pathology and age of the patient, a single-chamber or double-chamber pacemaker is implanted.

Let's look at the most common stimulation modes (click for quick navigation):

AAI mode - single chamber atrial pacing

In this mode, the chamber being stimulated and detected is the right atrium. Typically, such stimulation is used when the sinus node is unable to maintain a sufficient heart rate, but with intact AV conduction. These are different symptomatic variants of SSSS: sinus arrest, pauses, SA blockade, severe sinus bradycardia.

A stimulator operating in AAI mode monitors intrinsic atrial activity and fires when the time after the last QRS exceeds 1 second (or other programmed interval). Stimulation mode AAI can be either a consequence of the operation of a single-chamber pacemaker with an electrode in the right atrium, or a consequence of the operation of a dual-chamber pacemaker in the DDD or AAI mode.

On the ECG with such stimulation, spikes are visible, immediately followed by an induced P wave with the QRS complex (remember, AV conduction is preserved: this is a prerequisite for the correct operation of the AAI mode).

AAI on ECG:

Example 1: Atrial pacing, AAI mode

• The pacemaker rhythm is exactly 60 beats per minute.
• The stimulator spike initiates the P wave, which has a changed morphology.
• AV conduction and QRS complex are the same as during normal supraventricular contraction.

VVI mode - single chamber stimulation

In this mode, the chamber being paced and detected is the right ventricle. Most often, a stimulator in VVI mode is installed in elderly patients with a bradysystolic form of atrial fibrillation or with SSSS in order to avoid long pauses between heartbeats.

The VVI mode assumes that the stimulator is triggered when the time after the last QRS exceeds 1 second. The pacemaker detects ventricular contractions and counts 1000 ms. after each of them - in the absence of independent contraction, an impulse is sent and a stimulated contraction occurs.

VVI on ECG:

• Morphologically, the stimulated QRS complex is similar to that seen in LBBB, but in the lateral leads V5-V6 the complex is also negative.
• If the electrodes are monopolar, then the pacemaker spike is high and clearly visible in all leads. Modern bipolar electrodes create only a miniature spike in leads close to the implantation point at the apex of the pancreas (V2-V4).
• Depending on the initial problem, the patient's own contractions may be noted (most often narrow supraventricular QRS). Stimulated contractions will have a characteristic morphology and occur exactly after 1 second. after the last contraction.
• If spontaneous activity is weak and less than 60 beats per minute, the ECG will show only stimulated contractions.
• If the patient has his own activity, then the so-called. "drain" contractions - when an impulse from one's own pacemaker and an impulse from a pacemaker trigger a contraction simultaneously. Morphologically, such contractions are somewhere between normal and stimulated QRS.
• Note that recording filters (high-pass and network) can completely hide stimulation spikes ().

Example 2: Single-chamber stimulation with a monopolar electrode

• The pacemaker rhythm is 65 beats per minute.
• Note the clearly visible spike on the monopolar lead that initiates ventricular contraction.

Example 3: Single-chamber stimulation with a bipolar electrode

• Pacemaker rhythm with a frequency of 60 beats per minute (the ECG machine on which the recording was made does not feed the tape correctly.)
• The stimulator spike is visible in leads V4-V6 as a small dash before the QRS.
• Against the background of the stimulated rhythm, P waves are visible (best in V1), which do not cause a ventricular response. In this patient, a stimulator was implanted due to complete AV block.

Example 4: No stimulator spikes with recording filters enabled

• The pacemaker rhythm is 60 beats per minute.
• The ECG looks very "smooth" because All recording filters are enabled. This is why spikes from the bipolar electrode are not visible - they were filtered out as “electrical noise” ( ).
• The fact that this is a stimulated rhythm is indicated only by the frequency of exactly 60 beats per minute and the typical morphology of the complexes (compare all three examples above).

VVIR mode - single-chamber stimulation with adaptive frequency

Mode similar to VVI mode, but with frequency adaptation. Sometimes the stimulator is labeled SSIR (S = single), which does not change the essence.

Pacemakers that support this mode have a built-in accelerometer that responds to the patient’s movements and increases the stimulation frequency during prolonged movements. This allows the pacemaker to operate more physiologically and improves the patient’s tolerance to physical activity.

VVIR on ECG:

The morphology of stimulated complexes does not differ from that in VVI.

The frequency of the complexes will change: at rest it decreases to the minimum threshold (usually 60 beats per minute), after exercise it can be higher and reach the maximum threshold (up to 180 beats per minute, but usually no more than 120-130 beats per minute). The frequency does not change immediately, but a minute or two after changing the activity mode.

Example 5: Three different heart rates in a patient with a pacemaker in VVIR mode

• Pacemaker rhythm with three different frequencies: 60 beats/min., 68 beats/min. and 94 beats/min.
• Classic small spike of a bipolar electrode.
• Typical morphology of stimulated complexes.

DDD mode

The most common mode is dual-chamber stimulation, in which one electrode is installed in the right atrium and the second in the right ventricle.

Moreover, both electrodes are capable of detecting independent contractions of their chamber and sending an impulse only in their absence.

That is, if the atria contract on their own (the pacemaker detects the P wave), but AV conduction is impaired, then only the ventricles will be stimulated. If independent contractions of the ventricles also occur, then the stimulator “wait” for disturbances and does not work, while the rhythm that is normal for the patient is recorded on the ECG.

DDD on ECG:

Depending on how well the heart’s own functions are preserved, the ECG may show both completely normal P-QRS and completely stimulated ones - with two spikes.

When stimulating the atria, the first spike will be recorded before the P wave. The P wave will have a slightly changed morphology.

After natural or stimulated P there will be a PQ interval.

When ventricular stimulation occurs, after the PQ interval a spike and a classic paced QRS will be visible. With normal AV conduction, there is a normal, self-conducted QRS.

Example 6: Dual-chamber stimulator with monopolar electrodes

• The rhythm of a dual-chamber pacemaker is approximately 75 beats per minute.
• Note that the atria are not stimulated in every beat. The first two contractions have their own P wave, then the spike before the QRS. The second, third and fourth beats - with two spikes - for the atria and ventricles.
• The spikes are clear and high - typical for monopolar electrodes.

Example 7: Dual-chamber stimulator with bipolar electrodes

The chapter discusses current problems of electrocardiotherapy of heart failure (installation of cardiac resynchronization devices), including in patients at high risk of sudden cardiac death (use of pacemakers, cardioverter-defibrillators). The etiology, pathogenesis, classification, clinical manifestations, possibilities of clinical, instrumental and interventional diagnostic methods, indications and contraindications for electrocardiotherapy are discussed.

Keywords: pacing, sinus node dysfunction, heart blocks, cardioverter defibrillators, sudden cardiac death, cardiac arrest, ventricular tachycardia, ventricular fibrillation, heart failure, ventricular desynchronization, cardiac resynchronization devices.

permanent pacing

Implantation of pacemakers

Permanent cardiac pacing is implemented by implanting a cardiac pacing system consisting of a pacemaker (pacemaker) and electrodes. Usually, surgery performed using combined anesthesia (local anesthesia and parenteral sedatives). Before surgery, the condition of the pacemaker battery is assessed using a programmer. For electrode implantation, the endocardial technique is used in most cases. Electrodes under fluoroscopic control are installed and fixed in the right atrium and/or right ventricle, and they are tested using an external stimulator (impedances, stimulation thresholds and amplitude of spontaneous bioelectric potentials are assessed). The bed of the pacemaker device is formed in the subclavian region, subcutaneously or subfascially. To prevent infectious complications, antibiotics are prescribed intravenously.

Unified nomenclature code

Currently, in international practice, a five-letter nomenclature code is used to designate implantable pacemakers and cardioverter defibrillators, which was developed by the working group of the North American Society for Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) (see Table 2.1) .

The letter in the first position of the code indicates the chamber of the heart to which the stimulating impulse is received. The second letter indicates the chamber of the heart from which the spontaneous bioelectrical signal is sensed by the pacemaker. The letter in the third position of the code illustrates the mode in which the stimulation system

Table 2.1

Unified EKS code nomenclature NBG NASPE/BPEG (1987)

responds to spontaneous electrical activity of the heart (I - stimulation is inhibited by a spontaneous signal from the heart, i.e. if there is spontaneous electrical activity, the device does not work; T - stimulation is triggered by a spontaneous signal from the heart, i.e. spontaneous electrical activity of the atria triggers P -synchronized ventricular stimulation with dual-chamber pacemaker). The fourth position of the code characterizes the possibilities of external (non-invasive) programming of stimulation parameters, as well as the presence of a frequency-adaptive function in the pacemaker system. The letter in the fifth position indicates the presence of an antitachycardia pacing function in the pacemaker system, including cardioversion or defibrillation.

In October 2001, the NASPE and BPEG working groups proposed an updated version of the five-letter nomenclature code for antibradycardia devices shown in Table. 2.2.

As a rule, the first three letters of the code are used to designate the type and mode of cardiac pacing (for example: VVI, AAI, DDD), and the letter R (IV position) is used to designate programmable pacemakers with cardiac rate adaptation function

rhythm (for example, VVIR, AAIR, DDDR).

Frequency adaptation or modulation should be understood as the ability of the device to increase or decrease the frequency of stimulation within programmed values ​​when the load sensor is activated during an increase or cessation of physical activity, or a change in the psycho-emotional status of the patient.

Continuous pacing modes

VVI - single-chamber ventricular pacing in the “on demand” mode. This stimulation mode is understood as single-chamber “demand” stimulation of the ventricles, which is carried out when the frequency of the spontaneous heart rhythm decreases below the set value of the fixed stimulation frequency and stops if the spontaneous heart rhythm exceeds the established frequency limits (I - inhibitory control mechanism of the pacemaker). In Fig. Figure 2.1 shows a fragment of an ECG illustrating the electrical

Table 2.2

Updated unified EX code- NBG nomenclature - NASPE/BPEG (2001)

Rice. 2.1. ECG fragment illustrating single-chamber ventricular on-demand pacing (VVI pacing) with a base pacing rate of 60 ppm.

Note. V-V interval - the interval between two successive ventricular stimulating impulses - the interval of ventricular pacing (for example, with a base pacing frequency of 60 imp/min, the V-V interval is 1000 ms); V-R interval - the interval between the stimulating impulse and the subsequent spontaneous contraction of the ventricles of the heart (with a base stimulation frequency of 60 imp/min, the V-R interval is less than 1000 ms); R-V interval - the interval between the spontaneous contraction of the ventricles of the heart and the subsequent stimulating impulse if the frequency of spontaneous contractions of the ventricles decreases below the base stimulation frequency (with a base stimulation frequency of 60 imp/min, the R-V interval is 1000 ms)

trocardiostimulation in the VVI-60 pulse/min mode (basic pacing frequency).

Base pacing rate(lower limit of stimulation frequency) - the frequency with which the ventricles or atria are stimulated in the absence of spontaneous contractions (spontaneous rhythm). As shown in Fig. 2.1, when the spontaneous frequency of ventricular contractions decreases to less than 60 beats/min (R-R interval more than 1000 ms), single-chamber ventricular stimulation begins with a frequency of 60 beats/min (V-V interval 1000 ms). If, after the applied pulse, spontaneous ventricular contraction is detected within 1000 ms,

the work of the pacemaker is inhibited (an inhibitory mechanism for controlling the work of the pacemaker), and the patient is in a spontaneous heart rhythm (with a heart rate of more than 60 beats/min). If, after spontaneous contraction of the ventricles, no detection of the next spontaneous QRS complex occurs within 1000 ms, ventricular stimulation is resumed at a frequency of 60 imp/min. It should be noted that the V-V and R-V intervals are equal to and exceed the V-R interval (see Fig. 2.1).

The point of application of stimulation and detection of spontaneous bioelectric signals is located in the right ventricle of the heart. The disadvantages of this type of electrocardiotherapy are that adequate atrioventricular synchronization is disrupted during stimulation, which causes clinical signs of chronotropic insufficiency. According to most authors, this is the main mechanism for the development of pacemaker syndrome.

AAI - single-chamber atrial pacing in the “on demand” mode (Fig. 2.2). This stimulation mode is understood as single-chamber “demand” stimulation of the atria, which is carried out when the frequency of the spontaneous atrial rhythm decreases below the set value of the fixed stimulation frequency and stops if the spontaneous heart rhythm exceeds the established frequency limits (I - inhibitory control mechanism of the pacemaker).

With a decrease in the frequency of spontaneous atrial rhythm(Fig. 2.2) below the base stimulation frequency (P-P interval is greater than the programmed stimulation interval (A-A interval), with a base stimulation frequency of 60 imp/min, the A-A interval is 1000 ms) single-chamber atrial stimulation is performed with a base frequency. In a situation where, after a pacing pulse is applied to the atria during the pacing interval, spontaneous atrial contraction is recorded, the pacemaker is inhibited and the patient is in spontaneous sinus rhythm (with the heart rate exceeding the baseline pacing rate). If, after a spontaneous atrial contraction, no further spontaneous P wave is detected during the pacing interval, atrial pacing is resumed at a fixed rate. It should be noted that the A-A and P-A intervals are equal to and exceed the A-P interval (Fig. 2.2).

Rice. 2.2. ECG fragment illustrating single-chamber atrial on-demand pacing (AAI pacing) with a base pacing rate of 60 ppm.

Note. A-A interval - the interval between two successive atrial pacing pulses - the atrial pacing interval (for example, with a base pacing rate of 60 imp/min, the A-A interval is 1000 ms); A-P interval - the interval between the stimulating impulse and the subsequent spontaneous contraction of the atria of the heart (at a base stimulation frequency of 60 imp/min, the A-P interval is less than 1000 ms); P-A interval - the interval between the spontaneous contraction of the atria of the heart and the subsequent stimulating impulse in the case of a decrease in the frequency of spontaneous contractions of the atria below the base stimulation frequency (with a base stimulation frequency of 60 imp/min, the P-A interval is 1000 ms)

The point of application of stimulation and detection of spontaneous bioelectric signals is located in the right atrium of the heart. With this type of electrocardiotherapy, adequate atrioventricular synchronization is maintained, which allows it to be defined as physiological. The disadvantages of the AAI pacemaker are the lack of possibility of frequency adaptation of the heart rhythm in patients with chronotropic insufficiency, since there is no frequency modulation function (R in the fourth position of the code), as well as the inability to use this type of pacemaker in patients with impaired atrioventricular conduction.

VVIR - single-chamber ventricular rate-adaptive pacing. With this type of stimulation, single-chamber frequency-adaptive stimulation of the ventricles is carried out with an inhibitory mechanism for controlling the operation of the pacemaker. The inhibitory control mechanism implies the absence (cessation) of stimulation

with adequate electrical activity of the heart, sensed by a device in the specified chamber of the heart (V - ventricle, i.e. R-inhibitory stimulation of the ventricles, where R is the wave of the QRS complex, not to be confused with R - frequency modulation function). The point of application of stimulation and detection of spontaneous bioelectric signals is located in the right ventricle of the heart. This type of electrocardiotherapy, as well as in VVI-EC, leads to disruption of adequate atrioventricular synchronization.

AAIR - single-chamber atrial rate-adaptive pacing. With this type of stimulation, single-chamber frequency-adaptive stimulation of the atria is carried out with an inhibitory mechanism for controlling the operation of the pacemaker. The inhibitory control mechanism implies the absence (cessation) of stimulation with adequate electrical activity of the heart, sensed by a device in the specified chamber of the heart (A - atrium, i.e. P-inhibitory stimulation of the atria, where P is a wave illustrating the electrical activation of the atria). The point of application for stimulation and detection of spontaneous bioelectric signals is located in the right atrium of the heart (cannot be used in patients with AV conduction disorders). With this type of electrocardiotherapy, adequate atrioventricular synchronization is maintained and there is the possibility of frequency adaptation (modulation) of the heart rhythm in patients with signs of chronotropic insufficiency.

VDD is single-chamber P-synchronized pacing, which stimulates the ventricles while maintaining adequate atrioventricular synchronization. With this type of pacemaker, both inhibitory (R-inhibitory stimulation of the ventricles, where R is the wave of the QRS complex, not to be confused with R is the frequency modulation function) and trigger mechanisms for controlling the operation of the pacemaker are used. The trigger control mechanism involves the initiation of ventricular stimulation in response to adequate electrical activity of the heart, sensed in the atria (P-induced ventricular stimulation, where P is a wave illustrating the electrical activation of the atria).

In Fig. Figure 2.3 shows an ECG fragment illustrating cardiac pacing in VDD mode with a base stimulation frequency of 60 pulses/min. A necessary condition for effective stimulation in the VDD mode is to exceed the frequency of spontaneous pre-sermon

Rice. 2.3. ECG fragment illustrating single-chamber atrial-synchronized ventricular pacing (VDD pacing). Note. P - spontaneous contraction of the atria (spontaneous P-wave); AV - atrioventricular (atrioventricular) delay; V - stimulating impulse applied to the ventricles (synchronized with the spontaneous P-wave)

bottom rhythm of the base stimulation frequency. After the perception of the spontaneous atrial signal, the atrioventricular (AV) delay interval begins. Atrioventricular (AV) delay is the interval that begins with an atrial event (artificially induced or spontaneous) and ends with the application of a stimulus to the ventricle, provided that no spontaneous ventricular contraction is sensed during this time period. In most cases, the AV delay value is set between 150 and 180 ms. Thus, if spontaneous ventricular contraction does not occur during the AV delay period, P-synchronized ventricular pacing is performed. Adequate atrioventricular synchronization will be maintained until the spontaneous atrial rhythm reaches a frequency equal to the set value of the maximum synchronization frequency. Maximum Clock Frequency(upper limit of stimulation frequency) - the frequency up to which ventricular stimulation synchronized with spontaneous atrial activity is carried out in a 1:1 ratio, and if it is exceeded, it begins pacemaker periodicals by Wenckebach.

With VDD stimulation, the point of application of the pacemaker is located in the right ventricle of the heart, and the detection points of spontaneous bioelectric signals are in the right atrium and right ventricle.

A significant disadvantage of this type of pacemaker is that when the frequency of the spontaneous atrial rhythm decreases below the established values ​​of the basic stimulation frequency, atrioventricular synchronization is disrupted (VDD mode switches to VVI mode), since there is no possibility of atrial stimulation. This type Continuous electrocardiotherapy is not applicable in patients with signs of chronotropic sinus node insufficiency.

DDD - dual-chamber pacing. This type of stimulation allows you to maintain adequate atrioventricular synchronization at all times, since when the frequency of the spontaneous atrial rhythm decreases below the established values ​​of the minimum (basic) stimulation frequency, sequential stimulation of both the atria and ventricles is carried out. In a situation where the spontaneous atrial rate exceeds the minimum pacing rate, single-chamber P-synchronized (i.e., atrial-synchronized) ventricular pacing (VDD-pacing) is performed.

With DDD-EC, both inhibitory (P- and R-inhibitory stimulation, where R is the wave of the QRS complex, not to be confused with R - the frequency modulation function, and P is the wave illustrating the electrical activation of the atria), and trigger (P -induced stimulation of the ventricles, where P is a wave illustrating the electrical activation of the atria) control mechanisms for the operation of the pacemaker. If the spontaneous atrial rate is below the set baseline pacing rate, a pacing pulse is delivered to the atria. If no spontaneous contraction occurs during the period of the programmed AV delay, the stimulator applies an impulse to the ventricles (Fig. 2.4).

With DDD-EX, the points of application of stimulation and detection of spontaneous bioelectric signals are located in two chambers of the heart (in the right atrium and right ventricle). The disadvantage of this type of pacemaker is the lack of possibility of frequency adaptation of the heart rate in patients with signs of chronotropic insufficiency.

Depending on the frequency of spontaneous atrial rhythm and the state of atrioventricular conduction, several options for dual-chamber DDD stimulation are possible.

Rice. 2.4. ECG fragment illustrating dual-chamber pacing (DDD) with a base pacing rate of 60 ppm.

Note. A - stimulating impulse applied to the atria; AV - atrioventricular (atrioventricular) delay; V - stimulating impulse applied to the ventricles; A-A interval - the interval between two consecutive atrial stimulating impulses - the atrial pacing interval (at a base pacing rate of 60 imp/min, the A-A interval is 1000 ms); V-V interval - the interval between two successive ventricular stimulating impulses - the ventricular pacing interval (at a base pacing frequency of 60 imp/min, the V-V interval is 1000 ms); V-A interval - the interval between the ventricular impulse and the subsequent stimulating impulse to the atria (V-A equals V-V (A-A) minus AV delay))

If the spontaneous atrial rate is low (below the base pacing rate) and impaired atrioventricular conduction, dual-chamber “sequential” pacing will be performed at a set base rate (Fig. 2.5).

In a situation where the frequency of the spontaneous atrial rhythm is lower than the base pacing rate, and AV conduction is not impaired (i.e., spontaneous ventricular contractions occur during the established atrioventricular delay), atrial pacing is performed at the established base rate (Fig. 2.6).

If adequate spontaneous atrial activity is preserved (atrial rhythm frequency exceeds the base frequency of the atrium),

Rice. 2.5. ECG fragment illustrating dual-chamber pacing (DDD pacing).

Note. A - stimulating impulse applied to the atria; V - stimulating impulse applied to the ventricles

Rice. 2.6. ECG fragment illustrating dual-chamber pacing with preserved normal AV conduction (AAI pacing).

Note. A - stimulating impulse applied to the atria

mulation), but in conditions of impaired AV conduction (during the period of the established AV delay, no spontaneous contractions of the ventricles occur), atrial-synchronized stimulation of the ventricles will be implemented in the VDD mode (Fig. 2.7). Adequate atrioventricular synchronization will be maintained until the spontaneous atrial rhythm reaches a frequency equal to the set value of the maximum synchronization frequency.

If there are episodes where the atrial rate of the heart exceeds the baseline pacing rate and there is no evidence of atrioventricular conduction disturbance, complete inhibition of the pacemaker will occur.

DDDR - dual-chamber frequency-adaptive pacing. This type of permanent cardiac pacing is the most modern and completely eliminates the disadvantages of the pacemaker modes described above.

Rice. 2.7. ECG fragment illustrating dual-chamber pacing (VDD pacing)

Heart blocksDefinition

Heart blocks are understood as complete or partial disturbances in the conduction of impulses that occur at different levels of the conduction system of the heart due to changes of a functional or organic nature (see Table 2.3).

General classification

By localization:

1. Sinoatrial blockades.

2. Intra- and interatrial blockades.

3. Atrioventricular blockade.

4. Fascicular blockades. By severity: First degree blockade (incomplete). Second degree blockade (incomplete). Third degree blockade (complete). By durability: Transient. Intermittent. Constant.

Latent.

Sinus node dysfunctionDefinition

Sinus node dysfunction is a heterogeneous clinical syndrome of various etiologies associated with disruption of the chronotropic function of the structural components that make up the sinoauricular node area.

Classification

Clinical forms of sinus node dysfunction (M.S. Kushakovsky, 1992):

Sick sinus syndrome (SSNS) is dysfunction of the sinus node of an organic nature.

Regulatory (vagal) dysfunctions of the sinus node.

Drug-induced (toxic) dysfunction of the sinus node. Electrocardiographic equivalents of SSSU:

1. Sinus bradycardia with a rate of less than 40 beats/min at rest.

2. Sinus arrest (sinus node arrest).

Criteria for determining the minimum duration of sinus pause that could be classified as an episode of sinus arrest have not been defined. However, the occurrence of pauses of more than 3 s suggests with a high degree of probability that the sinus node has stopped.

3. Sinoatrial (SA) blockade according to the degree of severity is divided into:

SA blockade of the first degree - characterized by a slowdown in the conduction of impulses from the sinoatrial node to the atria, which is not reflected on the ECG;

SA blockade of the second degree, type I (with the Samoilov-Wenckebach periodicity) - in this case, a gradual shortening of the P-P intervals preceding the loss of the P wave is observed;

SA blockade of the second degree, type II - loss of one or more waves is noted on the ECG R, which leads to pauses that are multiples of two or more P-P intervals;

SA blockade of the third degree - not a single impulse from the sinoatrial node is carried out to the atria.

4. Alternation of slow sinus rhythm or slow escape rhythm with paroxysms of tachycardia, usually of supraventricular origin (bradycardia-tachycardia syndrome).

The most commonly observed paroxysmal supraventricular cardiac arrhythmia in patients with SSS is atrial fibrillation (Short's syndrome). However, it is also possible to verify atrial flutter, accelerated rhythm from the AV junction, and reciprocal AV nodal tachycardia. In rare cases, ventricular tachycardia may also occur.

5. Slow recovery of sinus node function (the appearance of sinus pauses) after electrical or drug cardioversion.

Atrioventricular blocksDefinition

Atrioventricular block - slowing or complete disruption of the conduction of impulses from the atria to the ventricles. Classification By severity:

1. First degree AV block - defined as an abnormal prolongation of the P-Q interval (more than 210-220 ms).

2. Second-degree AV block, type Mobitz I (with Samoilov-Wenckebach periodicity) - it is characterized by a progressive lengthening of the P-Q interval until conduction blockage occurs. The maximum increase in the P-Q interval is observed between the first and second contractions in the Wenckebach cycle. P-Q interval has the longest duration in the contraction preceding blocking of AV conduction, and the shortest duration after the dropped QRS complex. In most cases, this type of block is associated with a narrow QRS complex.

3. Second degree AV block type Mobitz II - P-Q intervals before and after conduction blocking have a fixed duration. This type of AV block in most cases is characterized by a wide QRS complex. In case of second degree AV block with 2:1 conduction, it cannot be classified into the first or second type, however, the type of blockade can be indirectly judged by the width of the QRS complex.

4. Third degree AV block - AV conduction is completely absent, ECG shows signs of complete AV dissociation.

According to the anatomical level of conduction disturbance:

supragisial AV block;

Intragisial AV blocks;

Infragisial AV block.

Fascicular blocksDefinition

Fascicular block - Impairment of impulse conduction in the His-Purkinje system.

Classification

I. Monofascicular blocks:

1. Right bundle branch block.

2. Block of the anterosuperior branch of the left bundle branch.

3. Block of the posteroinferior branch of the left bundle branch.

II. Bifascicular blocks:

1. Unilateral - blockade of the left bundle branch.

2. Double sided:

a) the right bundle and the anterosuperior branch of the left bundle branch.

b) the right leg and the posteroinferior branch of the left bundle branch.

III. Trifascicular blocks- combination of AV block with any of the above bifascicular blocks.

IV. Peripheral blockades(His-Purkinje system).

Pathophysiology of heart blocks

Sinus node dysfunction and AV block are characterized by clinical manifestations of chronotropic incompetence due to delayed or absent conduction of impulses from the sinus node to the atria or from the atria to the ventricles. Clinical symptoms are caused by hypoperfusion of vital organs, especially the brain and heart, as a result of low cardiac output syndrome due to bradysystole (see Table 2.4).

Violation of inter- and intraventricular impulse conduction leads to desynchronization of the right and left ventricles, which contributes to the progression of heart failure and increases the risk of developing paroxysmal ventricular arrhythmias.

Table 2.3

Etiology of heart block

Table 2.4

Patients with SSSS may have clinical symptoms caused by tachycardia, bradycardia, or a combination of these forms of cardiac arrhythmias. To determine the indications for continuous electrocardiotherapy in this category of patients, it is necessary to identify a clear connection between clinical symptoms and arrhythmia. Determining this relationship may be difficult due to the transient nature of cardiac arrhythmias and conduction disturbances.

Clinical manifestations of atrioventricular conduction disturbances are similar to those of SSSU. The most typical complaints are general weakness, fatigue,

the presence of pre- and syncope, as well as full-blown Morgagni-Adams-Stokes attacks (see Table 2.4).

Patients with bi- or trifascicular blockades often experience weakness, dizziness, decreased exercise tolerance, and syncope. The main causes of syncope in these patients may be transient high-grade atrioventricular conduction disturbances and paroxysmal ventricular arrhythmias.

for sick sinus syndrome (ACC/AHA/NASPE, 2002)

Class I:

1. Sinus node dysfunction with documented symptomatic sinus bradycardia, including frequent pauses causing symptoms. In some patients, bradycardia is iatrogenic and occurs as a result of long-term drug therapy and/or overdose.

2. Symptomatic chronotropic insufficiency. Class IIa:

1. Sinus node dysfunction, occurring spontaneously or as a result of necessary drug therapy with a heart rate of less than 40 per minute, when a clear connection between symptoms and bradycardia is not documented.

2. Syncope of unknown origin with significant dysfunction of the sinus node, identified or provoked during an electrophysiological study.

Class IIb:

1. Constant heart rate upon awakening of less than 40 per minute in patients with minor symptoms.

Class III:

1. Sinus node dysfunction in asymptomatic patients, including those with sinus bradycardia (heart rate less than 40 per minute) is a consequence of long-term drug therapy.

2. Sinus node dysfunction in patients with symptoms similar to bradycardia, when their lack of connection with a rare rhythm is clearly documented.

3. Sinus node dysfunction with symptomatic bradycardia as a result of inadequate drug therapy.

In our opinion, the indications for continuous electrocardiotherapy for patients with sick sinus syndrome, developed by D.F., deserve attention. Egorov et al. (1995).

Clinical and electrophysiological indications:

1) the presence of Morgagni-Adams-Stokes attacks against the background of bradyarrhythmia or when stopping paroxysms of supraventricular tachycardia;

2) progressive circulatory failure due to bradyarrhythmia;

3) lack of effect or impossibility of drug therapy for SSS in the presence of clinical manifestations of bradyarrhythmia;

4) spontaneous asystole according to ECG monitoring data lasting 2000-3000 ms or more;

5) stop or failure of the sinus node;

6) sinoatrial blockade with periods of asystole greater than 2000 ms;

7) periodic decrease in the number of ventricular contractions to less than 40 beats/min, especially at night.

Electrophysiological indications:

Sinus node function recovery time (SVFSU) - 3500 ms or more;

Corrected sinus function recovery time

node (KVVFSU) - 2300 ms or more;

The time of true asystole after atrial stimulation is 3000 ms or more;

Sinoatrial conduction time (SCAP) is more than 300 ms in the presence of:

Signs of “secondary” pauses during EPI;

- “paradoxical” reaction to the administration of atropine during

Signs of sinoatrial block on ECG;

Negative test with atropine (increase in heart rate less than 30% from the original, decrease in VVFSU by less than 30% from the original).

It should also be added that permanent pacing is absolutely indicated for patients with permanent form atrial fibrillation with rare conduction to the ventricles, symptomatic bradycardia and clinical manifestations of heart failure. On the contrary, pacemaker implantation has not yet

is prescribed in the absence of clinical symptoms against the background of bradyarrhythmia in atrial fibrillation (with a heart rate of less than 40 per minute), even if the duration of individual R-R intervals exceeds 1500 ms.

in adults (ACC/AHa/nASPE, 2002)

Class I:

1. Third degree AV block and advanced second degree AV block at any anatomical level associated with any of the following conditions:

1) symptomatic bradycardia (including heart failure) presumably due to AV block;

2) arrhythmia or other medical circumstances requiring the prescription of medications that cause symptomatic bradycardia;

3) documented periods of asystole equal to 3.0 seconds or more, as well as any escape rhythm less than 40 beats/min on awakening, in asymptomatic patients;

4) status after catheter radiofrequency ablation of the AV junction (there are no studies assessing the outcome without pacing; pacing is always planned in these situations, except in cases where the procedure for modifying the AV junction has been performed);

5) AV block after cardiac surgery, when spontaneous resolution is not expected;

6) neuromuscular diseases in combination with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (herpes zoster), and peroneal muscular atrophy, with or without symptoms, as unexpected deterioration of AV conduction may occur.

2. Second degree AV block, regardless of the type and level of damage when combined with symptomatic bradycardia.

Class IIa:

1. Asymptomatic third-degree AV block at any anatomical level with a mean ventricular rate on awakening of 40 beats/min or more, especially in the presence of cardiomegaly or left ventricular dysfunction.

2. Asymptomatic second-degree AV block type Mobitz II with a narrow QRS complex (when there is a wide QRS complex in second-degree AV block type Mobitz II, the recommendation class becomes the first).

3. Asymptomatic first-degree AV block at the intra- or infragisial level, identified during an electrophysiological study performed for another reason.

4. AV block of the first or second degree with symptoms similar to pacemaker syndrome.

Class IIb:

1. Significant first-degree AV block (P-Q greater than 300 ms) in patients with left ventricular dysfunction and symptoms of congestive heart failure in whom shortened AV delay leads to improved hemodynamics, presumably by reducing left atrial filling pressure.

2. Neuromuscular diseases, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (shingles), and peroneal muscular atrophy, with any degree of AV block, symptomatic or not, as unexpected deterioration of AV conduction may occur.

Class III:

1. Asymptomatic AV block of the first degree.

2. Asymptomatic AV block of the first degree at the supragisial level (AV node level) or in the absence of data on the intra or infrahisial level of the block.

3. Expected resolution of AV block and/or low likelihood of recurrence (eg, drug toxicity, Lyme disease, hypoxia due to asymptomatic sleep apnea).

for chronic bifascicular and trifascicular blockade

(ACC/AHA/NASPE, 2002)

Class I:

1. Transient third degree AV block.

2. Second degree AV block type Mobitz II.

3. Alternating bundle branch block.

Class IIa:

1. Syncope with an unproven connection with AV block, when other causes are excluded, especially ventricular tachycardia.

2. A significant lengthening accidentally detected during an electrophysiological study H-V interval(more than 100 ms) in asymptomatic patients.

3. A non-physiological infragisial block caused by stimulation was accidentally detected during an electrophysiological study.

Class IIb:

Neuromuscular diseases, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (shingles) and peroneal muscular atrophy, with any degree of fascicular block, with or without symptoms, as there may be unexpected deterioration of atrioventricular conduction.

Class III:

1. Fascicular block without AV block and clinical symptoms.

2. Asymptomatic fascicular block in combination with 1st degree AV block.

Indications for permanent pacing during atrioventricular blockade in acute myocardial infarction

(ACC/AHA/NASPE, 2002)

If symptomatic bradycardia occurs due to impaired atrioventricular conduction in the acute period of myocardial infarction, incurable with medication, temporary endocardial pacing is indicated. It is advisable to use this type of electrocardiotherapy for 12-14 days. According to the ACC/AHA guidelines for the treatment of patients with acute myocardial infarction, the need for temporary pacing is acute period Myocardial infarction alone does not determine the indications for permanent pacing. After the above period of time, the degree of impairment of AV conduction, its irreversibility is established, and indications for continuous electrocardiotherapy are determined.

Indications for permanent cardiac pacing in patients who have suffered a myocardial infarction complicated by impaired atrioventricular conduction are largely due to impaired intraventricular conduction. In contrast to the indications for chronic electrocardiotherapy for AV conduction abnormalities, the selection criteria for patients with myocardial infarction are often independent of the presence of symptomatic bradycardia. When considering the indications for permanent cardiac pacing in this category of patients, the type of atrioventricular conduction disturbance, the localization of myocardial infarction should be taken into account, and the cause-and-effect relationship of these electrical disturbances with it should be established.

for acquired atrioventricular conduction disorders

after acute myocardial infarction (ACC/AHA/NASPE, 2002)

Class I:

1. Persistent second-degree AV block in the His-Purkinje system with bilateral bundle branch block or third-degree AV block at or below the His-Purkinje system after acute myocardial infarction.

2. Transient, advanced (2nd or 3rd degree AV block) infranodal AV block in combination with bundle branch block. If the level of AV block is unclear, an electrophysiological study is indicated.

3. Persistent and symptomatic AV block of the second or third degree.

Class IIb:

1. Persistent AV block of the second or third degree at the level of the atrioventricular junction.

Class III:

1. Transient AV block in the absence of intraventricular conduction disturbances.

2. Transient AV block with isolated blockade of the anterior branch of the left bundle branch.

3. Appearing blockade of the anterior branch of the left bundle branch in the absence of AV block.

4. Persistent AV block of the first degree with a previously existing bundle branch block of unknown duration.

5. Echocardiography.

6. Teal t-test.

8. Transesophageal electrophysiological study.

IMPLANTABLE CARDIOVERTER DEFIBRILLATORS IN PATIENTS AT HIGH RISK OF SUDDEN CARDIAC DEATH

Implantation of cardioverter-defibrillators

Technically, the procedure for installing an implantable cardioverter-defibrillator (ICD) differs little from the implantation of permanent pacemakers. Before surgery, the device's battery status and capacitor function are assessed using the programmer, and antibradycardia pacing and ICD therapy functions are disabled. After installing the electrodes in the chambers of the heart, they are tested using an external stimulator. In the pectoral region, a bed of the ICD device is formed subcutaneously or subfascially, which is connected to the implanted electrodes. Using the programmer, detection and therapy parameters are set. Then the defibrillation threshold and the effectiveness of the programmed ICD therapy algorithm are determined. To do this, the patient is given short-term intravenous anesthesia and, using a programmer, ventricular fibrillation is induced (T-shock (defibrillator discharge synchronized with T-wave) or 50 Hz burst-pacing modes). With optimal therapy parameters set, the device should deliver a shock and stop ventricular fibrillation. The ICD discharge energy set in the device must be 2 times the defibrillation threshold. In case of ineffective therapy

ICD emergency measures are carried out using an external defibrillator.

Basics of cardioverter-defibrillator therapy

A modern ICD is a system consisting of a device enclosed in a small titanium housing and one or more electrodes installed in the chambers of the heart. The device contains a power source (lithium-silver-vannadium battery), a voltage converter, resistors, a capacitor, a microprocessor, heart rate analysis and shock release systems, and a database of electrograms of arrhythmic events. IN clinical practice ventricular and atrial electrodes with both passive and active fixation mechanisms are used for defibrillation, antitachycardia, antibradycardia pacing and resynchronization therapy. Today, one-, two-, and three-chamber (biventricular) systems are used. In most systems, the device itself, enclosed in a titanium housing, is part of the defibrillator discharge circuit (Fig. 2.8).

Rice. 2.8. Implantable cardioverter-defibrillator. Note.(1) titanium body, (2) intracardiac electrode. The discharge circuit of the implantable cardioverter-defibrillator is located between the device body and the coil (3) located on the electrode. Using the distal tip of the electrode (4), arrhythmic events are detected and antitachy and antibradystimulation is performed

Table 2.5

Antitachycardia pacing modes

Functions of implantable cardioverter-defibrillators

1. Antitachycardia pacing (ATS).

Modes of suppressive ventricular stimulation in the detection zone of ventricular tachycardia are presented in Table. 2.5.

2. Cardioversion - low-voltage shock (high-energy direct electric current discharge), which is applied outside the vulnerable phase cardiac cycle(20-30 ms after the apex of the R wave) in the detection zone of ventricular tachycardia (VT).

3. Defibrillation - high-voltage shock (discharge of high energy direct electric current) in the detection zone of high-frequency VT and ventricular fibrillation (VF).

4. Antibradycardia stimulation - electrocardiostimulation in the bradycardia detection zone.

The detection of arrhythmias is based on the analysis of R-R intervals, the shape of the ventricular signal, the stability of R-R intervals, the ratio of the characteristics of atrial and ventricular activity (in dual-chamber systems). The incoming signal undergoes filtering, as a result of which low-frequency (due to the T-wave) and high-frequency components (due to the activity of skeletal muscles) are eliminated and not detected. Detection parameters and therapy algorithms for each zone are set intraoperatively during testing of the device using a programmer (Fig. 2.9). Depending on the clinical situation of the drug therapy, these values ​​can be adjusted in the future.

Rice. 2.9. Detection zones and possible operating modes of the cardioverter defibrillator

To prevent unnecessary discharges during supraventricular arrhythmias and sinus tachycardia, functions are used to analyze the stability of R-R intervals (in the tachysystolic form of atrial fibrillation), the morphology of the ventricular signal recorded by the ventricular electrode, the suddenness of the onset of tachyarrhythmia (when VT or VF occurs, the value of the R-R interval suddenly decreases), and also dual-chamber recording of signals in the atria and ventricles. The treatment algorithm is selected by the doctor based on the patient’s tolerance of clinical tachycardia. In case of VF or rapid VT, the first step in therapy is defibrillation with a power of 10 J exceeding the intraoperative defibrillation threshold, followed by an automatic increase in the discharge power to maximum values ​​(30 J), as well as a change in the polarity in the defibrillation circuit from the ICD body to the intracardiac electrode and vice versa.

Prevention of sudden cardiac deathDefinitions

Sudden cardiac death (SCD)- death that developed immediately or occurred within an hour from the moment of acute changes in the clinical status of the patient.

Cardiac arrest is a condition accompanied by loss of consciousness due to asystole, ventricular tachycardia or ventricular fibrillation. A prerequisite for the diagnosis of cardiac arrest is the registration of these episodes using the electrocardiographic method.

Sustained ventricular tachycardia - This is a tachycardia lasting more than 30 seconds.

Unsustained ventricular tachycardia - This is a tachycardia from 3 complexes to 30 s, which is interrupted on its own.

Risk factors - these are clinical signs indicating the percentage probability of developing SCD in a particular patient in the current year.

Prevention of sudden cardiac death - This is a set of measures carried out in people who have experienced cardiac arrest (secondary prevention), or in patients at high risk of developing SCD without a history of cardiac arrest (primary).

Pathophysiology of sudden cardiac death

The most common electrophysiological mechanisms for the development of SCD are ventricular tachycardia and ventricular fibrillation. In approximately 20-30% of cases, the causes of SCD are bradyarrhythmia and asystole. It is often difficult to determine the primary mechanism of SCD in patients with documented bradyarrhythmia, since asystole may be a consequence of sustained VT. On the other hand, the initial bradyarrhythmia caused by myocardial ischemia can provoke VT or VF. Below is the etiology of sudden cardiac death according to J. Ruskin (1998)

Coronary heart disease Dilated cardiomyopathy Left ventricular hypertrophy Hypertrophic cardiomyopathy Acquired heart defects Congenital heart defects Acute myocarditis

Arrhythmogenic right ventricular dysplasia

Anomalies of the development of the coronary arteries

Sarcoidosis

Amyloidosis

Heart tumors

Left ventricular diverticula

WPW syndrome

Long QT syndrome Drug proarrhythmia Cocaine intoxication Severe electrolyte imbalance Idiopathic ventricular tachycardia

In most cases, SCD develops in patients with structural myocardial pathology. Patients with congenital arrhythmic syndromes in the absence of morphological changes in the heart make up a small percentage of the SCD structure. On the Molecule-

Table 2.6

Efficiency of therapy with implantable cardioverter-defibrillators

Note. HRV - heart rate variability; IHD - coronary heart disease; MI - myocardial infarction; VT - ventricular tachycardia; PVC - ventricular extrasystole; CHF - chronic heart failure; EF - ejection fraction; HR - heart rate; endo-EPI - endocardial electrophysiological study; FC - functional class

At the lar level, the causes of electrical instability of the myocardium can be changes in the concentration of potassium and calcium ions, neurohormonal changes, mutations causing dysfunction of sodium channels, which leads to increased automaticity and the formation of re-entry.

Selection of patients for implantation of cardioverter-defibrillators

In 1984 J.T. Bigger analyzed the probabilistic characteristics of the development of SCD in each clinical case. He identified groups of people with high and moderate risk factors for developing SCD. The data is presented in table. 2.7.

Table 2.7

Risk factors for sudden cardiac death

Note. AMI - acute myocardial infarction; EF - ejection fraction; PVC - frequent ventricular extrasystole; VT - ventricular tachycardia; SCD - sudden cardiac death.

It is important to note that these data were reflected in the AVID study, which was conducted 13 years after the work of J.T. Bigger. Thus, the most significant predictors of SCD are: left ventricular dysfunction, a history of cardiac arrest, myocardial hypertrophy, as well as a number of diseases based on the presence of electrically unstable myocardium (see Table 2.6).

Class I:

1. Persons who have experienced cardiac arrest due to VF or VT, which were caused by non-transient and reversible causes (AVID patients).

2. Patients with spontaneous, sustained VT, verified by ECG or Holter monitoring in combination with structural heart pathology.

3. Patients with syncope of unknown etiology and with identified, hemodynamically significant, sustained VT or VF induced during EPS. In this case, permanent AAT is ineffective, poorly tolerated, or the patient himself does not want to receive it.

4. Patients with coronary artery disease, a history of AMI and non-sustained VT with a moderately reduced left ventricular EF (below 35%), as well as induced VF or sustained VT during EPI, which is not suppressed by class Ia antiarrhythmic drugs (MADIT I ​​patients ).

5. Patients with left ventricular EF below 30% at least one month after AMI and three months after myocardial revascularization surgery (MADIT II- and SCD-HF patients).

6. Patients with spontaneous, sustained VT, verified by ECG or Holter monitoring without structural heart pathology, and which is not eliminated by other treatment methods.

Class II:

1. Patients with a history of VF, for whom EPS is contraindicated.

2. Patients with poorly tolerated, hemodynamically significant sustained VT while awaiting heart transplantation.

3. Patients with hereditary or acquired diseases that are accompanied by a high risk of developing cardiac arrest due to VF or VT (long QT syndrome, hypertrophic cardiomyopathy, Brugada syndrome, arrhythmogenic right ventricular dysplasia).

4. Patients with syncope in combination with left ventricular dysfunction and VT induced during endo-EPI, with the exclusion of other causes of syncope.

5. Patients with widespread structural heart pathology and syncope in whom previous studies have not been definitive in identifying the cause.

Class III:

1. Patients without structural heart pathology and syncope of unknown etiology without detected VT during EPI, and when other causes of syncope are not completely excluded.

2. Patients with persistently recurrent VT.

3. Patients with idiopathic VT that can be successfully eliminated by radiofrequency catheter destruction (idiopathic VT from the area of ​​the outflow tracts of the right and left ventricles, VT with impulse circulation through the conduction system of the heart (bundle branch re-entry), etc.

4. Patients with ventricular rhythm disturbances resulting from transient and reversible causes (electrolyte imbalance, acute poisoning, endocrine disorders, use of adrenergic agonists, etc.).

5. Patients with severe mental disorders, which may interfere with monitoring the patient in the early and late postoperative periods.

6. Patients with terminal diseases whose expected life expectancy is less than 6 months.

7. Patients with coronary disease hearts without VT induced during endo-EPI, with left ventricular dysfunction, for which revascularization measures are planned.

8. Patients with functional class IV heart failure according to NYHA, refractory to drug therapy, and patients who cannot be candidates for heart transplantation.

Program for instrumental examination of patients

2. Daily ECG monitoring.

3. Test with physical activity.

4. X-ray of the chest organs.

5. Echocardiography.

6. Tilt test.

7. Doppler ultrasound of the brachiocephalic arteries.

8. Coronary angiography.

9. Endocardial electrophysiological study (if necessary).

USE OF RESYNCHRONIZING ELECTROCARDIOTHERAPY IN PATIENTS WITH HIGH FUNCTIONAL CLASS OF CHRONIC HEART FAILURE

Implantation of cardiac resynchronization devices

With the exception of installing an electrode to stimulate the left ventricle of the heart, the technique of implanting a cardiac resynchronization device (CRSD) is not much different from the surgical technique of implanting a dual-chamber pacemaker. At the first stage of CRSU implantation, atrial and right ventricular endocardial electrodes are installed (Fig. 2.10, panel B). When implanting a ventricular electrode with a passive fixation mechanism, the latter must be installed in the apical region, closer to the interventricular septum, so that the tip of the electrode is projected close to the shadow of the diaphragm, which ensures the best fixation. Ventricular electrodes with an active fixation mechanism can be positioned in the area of ​​the interventricular septum or the outflow tract of the right ventricle of the heart.

Endocardial J-shaped atrial leads with passive fixation are placed in the right atrial appendage. When implanting atrial electrodes with an active fixation mechanism, it is possible to position them both in the right atrial appendage and in the area of ​​the interatrial septum.

At the next stage of the operation, catheterization and contrast enhancement of the coronary sinus are performed (Fig. 2.10, panel A). The most pronounced clinical effect of biventricular stimulation can be achieved by positioning the left ventricular electrode in the lateral, anterolateral or posterolateral veins of the heart (Fig. 2.10, panel B). Installation of an electrode in the great or middle vein of the heart leads to stimulation of the anterior or

Rice. 2.10. Implantation of cardiac resynchronization device electrodes. Panel A: contrast enhancement of the coronary sinus. Panel B: implantation of the left ventricular lead via transvenous access through the coronary sinus into the lateral cardiac vein. Panel B: diagram of the arrangement of cardiac resynchronization device electrodes

apical segments of the left ventricle, which is associated with an increase in the degree of mitral regurgitation and, therefore, accompanied by a negative hemodynamic effect. For conducting and installing the left ventricular electrode in venous vessels coronary sinus systems use a special set of instruments - a coronary sinus electrode delivery system.

Ventricular desynchronization as a link in the pathogenesis of chronic heart failure

Chronic heart failure syndrome (CHF) is based on diastolic and/or systolic dysfunction

left ventricle. CHF is characterized by a progressive course and is accompanied by the process of left ventricular remodeling, which is manifested by a change in the geometry of the heart chambers in the form of their hypertrophy and/or dilatation. Emerging mechanical disturbances in the functioning of the heart as a pump contribute to the maintenance and progression of remodeling processes, and are also accompanied by complex compensatory and pathophysiological changes, including disturbances in the phase structure of the cardiac cycle (Fig. 2.11).

Rice. 2.11. Disturbance of the phase structure of the cardiac cycle. Note: Panel A: schematic representation of the disturbance in the phase structure of the cardiac cycle during left bundle branch block. Noteworthy is the increase in the pre-discharge period and the decrease in left ventricular filling time. Panel B: Normalization of the phase structure of the cardiac cycle as a result of resynchronization therapy. There is synchronization of the systole of the right and left ventricles, an increase in the filling time of the left ventricle and a reduction in the pre-firing period

Intraventricular conduction disturbances (in 90% of cases in the form of left bundle branch block (LBBB)) occur in 35% of patients with CHF. Moreover, there is a direct correlation between the duration of the QRS complex and mortality among this group of patients with CHF (Fig. 2.12).

Rice. 2.12. Survival among patients with chronic heart failure depending on the duration of the ventricular complex

Impaired conduction along the branches of the His-Purkinje system leads to mechanical inter- and intraventricular desynchronization. This is most pronounced in LBBB. In this case, there is an alternation of active contraction and passive stretching of the contralateral areas of the left ventricle: early-systolic contraction of the interventricular septum with stretching of the lateral wall of the left ventricle and subsequent late-systolic contraction of the lateral wall with pronounced end-systolic hyperextension of the interventricular septum. As a result, there is a passive displacement of the interventricular septum towards the right ventricle, erroneously called “paradoxical”. The existing sequence of depolarization of the left ventricular myocardium leads to a decrease in the duration of the rapid filling phase of the left ventricle, a delay in contraction of the left ventricle and a slowdown in the total duration of systolic ejection from it, a decrease in the time of diastolic relaxation and filling of the left ventricle, an increase in the pre-filling period.

persecution (see Fig. 2.11). Changes in the phases of the cardiac cycle under conditions of desynchronization lead to an increase in end-systolic and end-diastolic pressures in the cavities of the heart, a decrease in the ejection fraction and shortening fraction of left ventricular fibers, and an increase in pressure in the pulmonary artery, reflecting the progression of systolic and diastolic dysfunction in patients with CHF.

The appearance of pathological mitral regurgitation in patients with CHF is an unfavorable prognostic sign. A significant contribution to its formation is made by the presence of subvalvular dysfunction of the left ventricle, discoordination of the movement of groups of papillary muscles and overstretching of the fibrous ring. In the presence of LBBB, early active movement of the interventricular septum, occurring before the mitral valve leaflets close, also leads to blurring of the boundary between diastole and systole, which can increase the degree of mitral regurgitation.

Pathological systolic stretching of the transverse muscle bridges of the left ventricle creates conditions for maintaining re-entry and increases the likelihood of life-threatening ventricular arrhythmias.

The presented mechanisms of desynchronization in patients with CHF reduce the efficiency of the contractile function of the heart and are accompanied by an increase in energy consumption, which worsens it functional state regardless of the etiological factor of heart failure.

Desynchronization consists of several components: atrioventricular, interventricular and intraventricular.

The first component reflects the dissociation of coordination of the systole of the atria and ventricles. In clinical practice for verification atrioventricular desynchronization assessment of transmitral flow using the Doppler method is used when performing transthoracic echocardiography (Echo-CG). The fusion of peaks E (passive diastolic filling of the atria) and A (atrial systole) illustrates atrioventricular desynchronization (Fig. 2.13).

Indicators interventricular desynchronization are the duration of the QRS complex more than 120 ms, the delay in the movement of the lateral wall of the left ventricle relative to the movement of the interventricular septum is more than 140 ms, recorded during

Rice. 2.13. Determination of transmitral blood flow using the Doppler method in a patient with an implanted CRSU and a set AV delay value of 140 ms.

Note. On the left side of the figure, flows E and A, characterizing passive diastolic filling and atrial systole, are indistinguishable. The right side of the figure shows Doppler data from the same patient when the AV delay was changed (it was set to 110 ms). There is a discrepancy between peaks E (first, low-amplitude) and A (second, high-amplitude), indicating optimization of diastolic filling

conducting Echo-CG in M-mode, an increase in the cumulative asynchrony index of more than 100 ms during tissue Doppler scanning, the difference in intervals from the beginning of the QRS complex to the beginning of flow in the aorta and pulmonary artery exceeding 40 ms (Fig. 2.14, 2.15, see inset).

Intraventricular desynchronization can be verified by tissue Doppler ultrasound. The use of various tissue Doppler modes makes it possible to reflect the delay between the onset of the QRS complex on the surface ECG and the appearance of the tissue Doppler signal, displaying the systolic wave in the corresponding segments of the left ventricular myocardium (Fig. 2.16, see inset).

Intraventricular desynchronization is an independent predictor of unfavorable course of cardiovascular diseases in patients who have suffered myocardial infarction.

Rice. 2.14. Signs of interventricular desynchronization. Note. M-mode transthoracic echocardiography: delayed contraction of the lateral wall of the left ventricle relative to the interventricular septum in a patient with left bundle branch block is verified

Table 2.8

Clinical effects of resynchronization therapy

Selecting a mode and determining the parameters of resynchronizing cardiac pacing

The procedure for testing KRSU differs little from testing a conventional pacemaker. Additionally, during the check of the CRSU, parameters related to the left ventricular electrode (pacing threshold, impedance) are determined. In devices that do not have the function of separate programming of the left ventricular pacing channel, it is advisable to monitor a 12-lead ECG when determining the pacing threshold. If during this test there is a change in the morphology of the stimulated ventricular complex on the surface ECG while ventricular uptake persists, this indicates that the stimulation threshold in one of the ventricular channels has been reached. In this case, ventricular “captures” are carried out due to the lower value of the stimulation threshold in the second ventricular channel. Based on the analysis of 12 ECG leads, it is possible to determine which stimulation mode is used in the patient (Table 2.9 and Fig. 2.17, see inset).

Table 2.9

Morphology of the QRS complex in leads I, III and V1 when performing various types of cardiac pacing

Patients in sinus rhythm

If a patient with an implanted CRSU does not have chronic atrial fibrillation, an important point is to optimize atrioventricular resynchronization using the method of

selection of optimal AV delay parameters. There are several methods for determining this value. The most commonly used formula is Ritter, which allows you to calculate the optimal value of AV delay based on the registration of the shape of the transmitral flow recorded in M-mode during transthoracic echocardiography:

ABopt. - ABdl. + QAdl. - QA.short

AB for - the value is set on the programmer and is 75% of the PQ interval.

AB short - the value is set on the programmer and is 25% of the PQ interval.

QA dl - measured from the beginning of the ventricular pacing complex (Q) to the end of the A peak at a programmed extended AV delay (AV dl).

QA short - measured from the beginning of the ventricular pacing complex (Q) to the end of the A peak at a programmed short AV delay (AV short).

In some cases, the AV delay is programmed based on visual registration of the optimal shape of the transmitral flow peaks (Fig. 2.13). We especially emphasize that the value of the programmable AV delay should be less than the value of the interval P.Q. since only in this case will constant biventricular stimulation be provided.

Optimization of interventricular resynchronization parameters is possible only in devices that have the function of separate programming of the left and right ventricular channels. Setting the interventricular delay in the range of 5-20 ms with left ventricular advance is optimal in hemodynamic terms, compared with simultaneous right and left ventricular stimulation. In this case, it is advisable to select the value of the interventricular delay under echocardiographic control by calculating the difference in intervals from the beginning of the QRS complex to the beginning of flow in the aorta and pulmonary artery (no more than 40 ms) and the delay in the movement of the lateral wall of the left ventricle relative to the interventricular septum (no more than 40 ms).

Patients with chronic form atrial fibrillation

In this category of patients, selection of AV delay is impossible, since atrial systole is absent as such. Therefore, the key point is to achieve constant biventricular stimulation by setting the pacemaker frequency at least 70-80 per minute and controlling the ventricular rate. Normosystole is achieved either by drug suppression of AV conduction, or by modifying the atrioventricular connection using radiofrequency destruction. The principles for optimizing interventricular resynchronization are no different from those that apply to patients in sinus rhythm.

According to clinical studies, it has been established that approximately 25-30% of patients with a high functional class of CHF do not experience a positive effect from cardiac resynchronization for a number of reasons. Firstly, this is the absence of pronounced signs of desynchronization of the right and left ventricles before implantation of the system. Secondly, inadequate positioning of the electrode for left ventricular stimulation. Electrical stimulation of the lateral wall of the left ventricle is more effective through an electrode inserted into the lateral or posterolateral veins of the heart. However, electrical stimulation from the heart or great cardiac vein often does not have a positive effect on left ventricular systolic function. Thirdly, incorrect setting of cardiac resynchronization parameters. Improvement in clinical symptoms occurs only with constant biventricular stimulation.

Indications for implantation of cardiac resynchronization devices (ECC/ACC/AHA, 2005)

Class I:

1. Heart failure III/IV FC (NYHA), despite optimal drug therapy.

2. Duration of the QRS complex >130 ms.

3. Left ventricular ejection fraction<35%.

4. End-diastolic size of the left ventricle >55 mm.

5. Echocardiographic signs of ventricular desynchronization.

Program for instrumental examination of patients

2. Daily ECG monitoring.

3. Test with physical activity.

4. 6-minute walk test.

5. X-ray of the chest organs.

6. Echocardiography.

7. Coronary angiography.

The main types of pacemakers are described by a three-letter code: the first letter indicates which chamber of the heart is being paced (A - A trium - atrium, V - V entricle - ventricle, D - D ual - both atrium and ventricle), the second letter - the activity of which chamber is perceived (A, V or D), the third letter indicates the type of response to the perceived activity (I - I nhibition - blocking, T - T riggering - launch, D - D ual - both). Thus, in the VVI mode, both the stimulating and sensing electrodes are located in the ventricle, and when spontaneous ventricular activity occurs, its stimulation is blocked. In DDD mode, two electrodes (stimulating and sensing) are located in both the atrium and ventricle. Response type D means that when spontaneous atrial activity occurs, its stimulation will be blocked, and after a programmed period of time (AV interval) a stimulus will be issued to the ventricle; when spontaneous ventricular activity occurs, on the contrary, ventricular stimulation will be blocked, and atrial stimulation will start after the programmed VA interval. Typical single-chamber pacemaker modes are VVI and AAI. Typical dual-chamber pacemaker modes are DVI and DDD. Fourth letter R ( R ate-adaptive - adaptive) means that the pacemaker is able to increase the pacing frequency in response to changes motor activity or load-dependent physiological parameters (eg, QT interval, temperature).

A. General principles of ECG interpretation

Assess the nature of the rhythm (own rhythm with periodic activation of the stimulator or imposed).

Determine which chamber(s) are being stimulated.

Determine the activity of which chamber(s) is perceived by the stimulator.

Determine programmed pacemaker intervals (VA, VV, AV intervals) from atrial (A) and ventricular (V) pacing artifacts.

Determine the EX mode. It must be remembered that ECG signs of a single-chamber pacemaker do not exclude the possibility of the presence of electrodes in two chambers: thus, stimulated contractions of the ventricles can be observed with both single-chamber and dual-chamber pacemaker, in which ventricular stimulation follows at a certain interval after the P wave (DDD mode) .

Eliminate imposition and detection violations:

A. imposition disorders: there are stimulation artifacts that are not followed by depolarization complexes of the corresponding chamber;

b. detection disturbances: there are pacing artifacts that must be blocked for normal detection of atrial or ventricular depolarization.

B. Individual EX modes

AAI. If the natural rhythm frequency becomes less than the programmed pacemaker frequency, then atrial stimulation is started at a constant AA interval. When spontaneous atrial depolarization (and its normal detection) occurs, the pacemaker time counter is reset. If spontaneous atrial depolarization does not recur after the specified AA interval, atrial pacing is initiated.

VVI. When spontaneous ventricular depolarization (and its normal detection) occurs, the pacemaker time counter is reset. If, after a predetermined VV interval, spontaneous ventricular depolarization does not recur, ventricular pacing is initiated; otherwise, the time counter is reset again and the entire cycle starts over. In adaptive VVIR pacemakers, the rhythm frequency increases with increasing level of physical activity (up to a given upper limit Heart rate).

DDD. If the intrinsic rate becomes less than the programmed pacemaker rate, atrial (A) and ventricular (V) pacing is initiated at the specified intervals between pulses A and V (AV interval) and between a V pulse and the subsequent A pulse (VA interval). When spontaneous or induced ventricular depolarization (and its normal detection) occurs, the pacemaker time counter is reset and the VA interval begins to count. If spontaneous atrial depolarization occurs during this interval, atrial pacing is blocked; otherwise, an atrial impulse is issued. When spontaneous or induced atrial depolarization (and its normal detection) occurs, the pacemaker time counter is reset and the AV interval begins to count. If spontaneous ventricular depolarization occurs during this interval, ventricular pacing is blocked; otherwise, a ventricular impulse is issued.

IN. Pacemaker dysfunction and arrhythmias

Violation of imposition. The stimulation artifact is not followed by a depolarization complex, although the myocardium is not in the refractory stage. Causes: displacement of the stimulating electrode, cardiac perforation, increased stimulation threshold (with myocardial infarction, taking flecainide, hyperkalemia), damage to the electrode or disruption of its insulation, disturbances in pulse generation (after defibrillation or due to depletion of the power source), as well as incorrectly set pacemaker parameters.

Detection failure. The pacemaker time counter is not reset when its own or imposed depolarization of the corresponding chamber occurs, which leads to the occurrence of an incorrect rhythm (the imposed rhythm is superimposed on its own). Reasons: low amplitude of the perceived signal (especially with ventricular extrasystole), incorrectly set pacemaker sensitivity, as well as the reasons listed above. Often it is enough to reprogram the sensitivity of the pacemaker.

Pacemaker hypersensitivity. At the expected point in time (after the appropriate interval has passed), no stimulation occurs. T waves (P waves, myopotentials) are misinterpreted as R waves and the pacemaker timer is reset. If the T wave is detected incorrectly, the VA interval begins counting from it. In this case, the sensitivity or refractory period of detection must be reprogrammed. You can also set the VA interval to start from the T wave.

Blocking by myopotentials. Myopotentials arising from arm movements may be misinterpreted as potentials from the myocardium and block stimulation. In this case, the intervals between the imposed complexes become different, and the rhythm becomes incorrect. Most often, such disorders occur when using unipolar pacemakers.

Circular tachycardia. An imposed rhythm with the maximum frequency for the pacemaker. Occurs when retrograde atrial excitation after ventricular stimulation is sensed by the atrial electrode and triggers ventricular stimulation. This is typical for a two-chamber pacemaker with detection of atrial excitation. In such cases, it may be sufficient to increase the detection refractory period.

Tachycardia induced by atrial tachycardia. An imposed rhythm with the maximum frequency for the pacemaker. It is observed if atrial tachycardia (for example, atrial fibrillation) occurs in patients with a dual-chamber pacemaker. Frequent atrial depolarization is sensed by the pacemaker and triggers ventricular pacing. In such cases, they switch to the VVI mode and eliminate the arrhythmia.

Depending on the pacemaker mode, it can reach 0.02-0.06 s, and the amplitude can vary from almost imperceptible to domm.

From the point of view of the cryptographer, we need to answer three questions when deciphering such ECGs:

1. Understand where the stimulating electrode is located in the atrium, ventricle, or both if the pacemaker is two- or three-chamber.

2. Does the pacemaker force stimulation or run idle?

3. Try to determine the background rhythm.

Without delving into the “wild”, for beginners we can formulate the following provisions:

1. Normally, a spike is always followed by a response from the atria or ventricles, so we understand that the pacemaker imposes a rhythm, that is: after each spike, the ECG “picture” is always identical. There should be no isolated spikes after which a long isoline is recorded.

2. Depending on which part of the heart is excited after the spike, the localization of the stimulating electrode(s) can be determined. If the lead only stimulates the ventricles (single-chamber pacemaker), then you need to look for what is the pacemaker for the atria, usually it is either sinus rhythm or atrial fibrillation/flutter.

3. Considering that the ECS usually leads to significant deformation of the complexes, we can say nothing more except: the ECS works or not. In conclusion we usually write, for example, like this: “EX Rhythm ... per minute” or “The rhythm for the atria is sinus, for the ventricles the ECS rhythm is ... per minute.” Usually there is nothing more to add.

In this course we will not go into details of the interpretation of such ECGs; I want you to simply learn to recognize the pacemaker rhythm and not be afraid of such recordings.

Below we will consider several typical examples of pacemaker with IVR.

▼ ECG 1 ▼

In this recording we see ECS spikes, after which a small wave similar to a P wave appears; after a certain delay, which is the same in all complexes, the ventricles are excited.

Thus, we can say that most likely the patient has a single-chamber pacemaker and in this case, the pacemaker stimulates the excitation of only the atrium, after which the impulse proceeds in its normal course - through the AV node to the ventricle. There is no QRS deformation on this ECG (since the ventricles are excited in the usual way - from top to bottom), so its interpretation is not much different from any other ECG.

▼ ECG 2 ▼

Here we see ECS adhesions, after which a deformed ventricular complex immediately appears. That is, here the ECS stimulates the ventricles, while the impulse goes from bottom to top, which does not allow us to decipher the ECG according to the standard plan. It is difficult to assess the rhythm for the atria in such a short period, however, pay attention to the last two complexes - they arose spontaneously, without the participation of an pacemaker. That is, this is a “native” rhythm, the heart rate of which has become, while clear r values ​​are not visible (one of the waves is similar, but further and earlier, on the isoline between the imposed QRS, it is not traceable). It seems that there is no sinus rhythm, otherwise the stimulator would have adapted to “issue” a spike for the ventricles at a certain distance after the native R.

It can be assumed (but this may not be the case) that the pacemaker was implanted due to sick sinus syndrome of the tachy-brady type (sinus bradycardia alternating with paroxysms of AF tachysystole). That is, when there was bradycardia, the pacemaker was working, when the heart rate exceeded the threshold of 75 per minute, the pacemaker turned off and then we saw the native rhythm. It is not possible to assess conductivity, ischemic changes and other characteristics on this ECG.

The conclusion looks like this: “Exciter rhythm 75 per minute, single-chamber stimulation from the ventricular position”

▼ ECG 3 ▼

Here we see the operation of a dual-chamber pacemaker, that is, the pacemaker first stimulates the atria through one electrode, then simulates a delay in the AV node and then provides a stimulus to excite the ventricles through the second electrode. In fact, we see here a combined picture from ECG 1 and ECG 2.

We do not see P waves anywhere, therefore this is either sick sinus syndrome or bradyform AF. In addition, if there was a need to install a dual-chamber pacemaker, then there was a problem with AV conduction, that is, there was also a complete AV block. But these are just guesses.

The conclusion looks like this: “EX pacer rhythm 60 per minute, dual-chamber stimulation”

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Pacemaker on ECG

The operation of a pacemaker significantly changes the picture of the electrocardiogram (ECG). At the same time, a working stimulator changes the shape of the complexes on the ECG in such a way that it becomes impossible to judge anything from them. In particular, the work of the stimulator can mask ischemic changes and myocardial infarction. On the other hand, since modern stimulators work “on demand”, the absence of signs of the stimulator on the electrocardiogram does not mean that it is broken. Although there are often cases when nursing staff, and sometimes doctors, without proper grounds, tell the patient “your stimulator is not working,” which greatly irritates the patient. In addition, the long-term presence of right ventricular stimulation also changes the shape of its own ECG complexes, sometimes simulating ischemic changes. This phenomenon is called “Chaterje syndrome” (more correctly, Chatterjee, named after the famous cardiologist Kanu Chatterjee).

Rice. 77. Artificial heart pacemaker, heart rate = 75 per 1 min. The P wave is not detected; each ventricular complex is preceded by a pacemaker impulse. The ventricular complexes in all leads are deformed according to the type of blockade of the left bundle branch of His, i.e. excitation is imposed through the apex of the right ventricle.

Thus: interpretation of the ECG in the presence of a pacemaker is difficult and requires special training; if acute cardiac pathology (ischemia, heart attack) is suspected, their presence/absence should be confirmed by other methods (usually laboratory). The criterion for correct/incorrect operation of the stimulator is often not a regular ECG, but a test with a programmer and, in some cases, daily ECG monitoring.

Now let’s briefly consider the main ECG characteristics of patients with pacemakers and sequentially study: a) stimulators: types and interpretation code;

b) electrocardiology of stimulators.

1. Pacemakers: types and interpretation code. The stimulator consists of a generator (energy source or battery), an electronic circuit and a system that connects the generator to the heart, and a system that delivers the energy (the stimulating electrode).

Currently, lithium batteries are the most commonly used source. An electronic circuit supplies the catheter with energy and changes the duration and intensity of the impulse. The catheter is connected at one end to the generator and the other end to the heart through an electrode (unipolar or bipolar), which is connected transvenously to the endocardium.

Endocardial pacing of the ventricles, less commonly of the atria, is the most commonly used type of pacing. Endocardial access, often used during the early days of electrical stimulation, is now used only in exceptional cases. Bipolar pacing creates small spikes that are sometimes difficult to recognize, while unipolar electrodes create large spikes that distort the QRS complex and can shift the isoelectric line, sometimes resembling the QRS complex without pacing. This can lead to serious errors.

To avoid errors, check whether the expected QRS complex is followed by a T wave.

The simplest stimulator is one that generates pulses at a fixed frequency and is not affected by the activity of the patient’s heart. Such stimulators cannot sense electrical activity (readout function) and are called fixed-rate stimulators, or asynchronous stimulators (VVO).

In this case, if spontaneous electrical activity occurs, there is competition between spontaneous and stimulatory electrical activity, which leads to discomfort due to uneven frequency and some danger ventricular fibrillation, if the stimulator pulse coincides with the patient’s T wave, although this is hardly possible in the newest low-power stimulators.

To avoid such effects, non-competing pacemakers have been developed that sense the electrical activity of the heart using an electrode. This ability to recognize electrical activity is called the readout function of the stimulator. The pulse generator is designed to remain unresponsive for some time after the signal or pulse has been read.

There are two ways in which the stimulator can respond to a cardiac signal that occurs outside the refractory period:

a) the cardiac signal causes the stimulator to change the triggering of a new control interval. The stimulator functions only if the discharge peak is longer than the spontaneous R-R interval (the stimulator acts in an inhibitory manner) (VVI) (ventricular demand pacing);

b) the cardiac signal creates an immediate release of an impulse, which subsequently occurs during the refractory period of the heart: if there is no spontaneous activity, then from this moment a programmed increase in rhythm begins. The stimulant is believed to function in a trigger way (VVI). The trigger pulse does not cause a cardiac response because it occurs during the absolute refractory period, but it does cause a shift in the QRS complex known as pseudoconfluent complexes (a complex that is shifted but not triggered by the stimulator pulse).

There are stimulators that trigger the stimulator for some time after the cardiac signal before the pulse is released (delayed triggering). The stimulator provides stimulation of the atria and/or ventricles.

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ECG with pacemaker description

With a two-chamber, or bifocal, mode of (sequential) stimulation (DDD), physiological hemodynamic conditions are created for cardiac activity, in which contractions of the atria and ventricles are separated in time. The main indication for this pacing regimen is AV block while maintaining sinus node function.

DDD type pacemakers are multifunctional devices with several built-in programs. Stimulation is carried out by two electrodes, which are inserted into the RA and RV, respectively. This makes it possible to detect its own rhythm in both the atria and ventricles, and stimulate “on demand” the atria and/or ventricles.

The following changes are detected on the ECG recorded during stimulation in DDD mode. First, after atrial detection, an atrial pacemaker spike appears, causing atrial depolarization. This is manifested by the appearance of an atypical P wave on the ECG. After a certain, pre-programmed AV interval (approximately 150 ms), a ventricular spike of the pacemaker follows, causing ventricular depolarization, which is manifested on the ECG by a QRS complex, reminiscent of LAP block.

After a fixed period of 0.16 s, the atrial spike of the pacemaker is followed by a ventricular spike and a QRS complex resembling LBP block. ECG with dual-chamber cardiac stimulation (DDD).

The ECG shows variability in the pattern, in particular, intrinsic waves, ventricular extrasystoles, VAT and DDD modes. Belt speed 10 mm.

If the excitation of the sinus node and atrium occurs in a timely manner, then the atrial activity of the pacemaker is suppressed, and its own P wave is recorded on the ECG. If the propagation of excitation from the atria to the ventricles is delayed and exceeds the programmed AV interval, then the pacemaker stimulates the RV.

On the ECG, after the P wave and the PQ interval, a ventricular spike appears and, after it, a QRS complex, reminiscent in configuration of LBP blockade. This mode of stimulation is referred to as VAT. This picture after implantation of a pacemaker for dual-chamber stimulation in the DDD mode is often observed in everyday practice both at rest and during exercise.

If the activity of the atria is disturbed or they do not contract at a normal frequency, but AV conduction and ventricular excitability are not impaired, then an atrial spike of the pacemaker appears on the ECG followed by a deformed P wave. This is followed by the PQ interval and, finally, a normal non-broadened ventricular complex. This stimulation mode is referred to as AAI.

The frequency of complications after implantation of a DDD type pacemaker, as already mentioned, is small, however, it exceeds the frequency of complications after cardiac pacing in the VVI mode. The nature of complications in both stimulation modes is the same: premature depletion of the pacemaker power source, impaired detection of electrical activity of the heart cavities, dislocation and fracture of electrodes, as well as infection of the bed.

Training video for decoding an ECG with a pacemaker (artificial pacemaker)

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Types of pacemakers - Electrocardiogram with artificial pacemaker

AND STIMULATION MODES

The international three-letter code nomenclature developed by the Intersociety Commission for Heart Disease Resources is used to designate the pacing mode and types of pacemakers (pacers). The code is called ICHD. The first letter of the code indicates the cardiac chamber being paced; the second letter of the code indicates the chamber of the heart from which the control signal is perceived (V - ventricle, A - atrium, D - dual, 0 - the control signal is not perceived from any chamber); the third letter of the code indicates the way the pacemaker reacts to the perceived signal (Table 2).

With the development of more complex pacing systems, the introduction of programming, and the use of pacemakers to treat tachycardias, the three-letter code was expanded to a five-letter code; the fourth letter indicates the nature of programming (P - simple programming of frequency and/or output parameters, M - multiple programming of frequency parameters, output parameters, sensitivity, stimulation mode, etc., O - lack of programmability); the fifth letter indicates the type of stimulation when affecting tachycardia [B - Burst stimuli

(application of a “pack of impulses”), N - normal rate competition (competitive stimulation), S - single or doubletimed stimuli (application of a single or paired extrastimulus), E - externally controlled (stimulator regulation is carried out externally).

Table 2. Types of pacemakers according to letter code

Paced heart chamber

Chamber of the heart from which the control signal is received

The way the pacemaker reacts to a perceived signal

Fixed rate stimulation, asynchronous stimulation

Sequential fixed-rate atrioventricular pacing

Atrial pacing inhibited by P wave

Ventricular pacing inhibited by R wave

Ventricular pacing, R-repetitive

Ventricular pacing synchronized with P wave

Ventricular pacing synchronized with P wave and inhibited by I wave

Sequential atrioventricular pacing inhibited by R wave

Sequential atrioventricular pacing inhibited by P and R waves

Abbreviations when designating the chambers of the heart: V - ventricle, A - atrium, D - ventricle and atrium.

The way the pacemaker reacts to the perceived signal: 0 - the signal from the heart is not perceived by the device, I - stimulation is prohibited by the signal from the heart, T - stimulation occurs synchronously with the signal from the heart (trigger mode), D - a combination of prohibited and trigger modes.

The three-letter code, however, remains the most common and generally accepted, so in the future we will use it.

Currently, the following types of pacemakers and stimulation modes are known: A00, V00, D00, AAI, VVI, WT, VAT, VDD, DVI, DDD.

Let's consider the basic principles of operation of each of these ECS.

The V00 type stimulator (asynchronous) stimulates the ventricles in a fixed mode, i.e., regardless of the patient’s spontaneous rhythm (Fig. 17).

a - imposed complexes (1, 2, 8, 9) alternate with sinus ones (4, 5, b, 7). Stimuli 4, 5, b did not cause ventricular depolarization, since they fell into the absolute refractory period; b - asynchronous stimulation during atrial fibrillation. Forced complexes (8, 10) alternate with spontaneous (2-7, 9, 11, 13-16) and pseudoconfluent complexes (1, 12).

This stimulation mode was first used in humans in 1952 by R. M. Zoll; we can consider that it was from this time that the era of cardiac stimulation began.

For the functioning of such a pacemaker, only one electrode per ventricle is required. Through this electrode, the stimulating function of the ECS is carried out. The pacemaker generates impulses with a set fixed frequency, regardless of the frequency of the spontaneous heart rhythm. The time between stimuli is called the interpulse interval, also the automatic interval or stimulation interval, expressed in milliseconds.

seconds (ms) and inversely the stimulation frequency (Fig. 18). If, against the background of such stimulation, atrioventricular conduction is restored, then competition between the intrinsic and instrumental rhythms appears (Fig. 19, a, b). Since pacemaker pulses are generated at a constant interval, they can fall into any phase of depolarization of the spontaneous ventricular complex. If the impulse falls outside the refractory period of the spontaneous ORS complex, then it, in turn, will also cause a response, i.e., an artificially induced, imposed contraction will occur; If the pulse falls into the refractory period, it will remain idle. Competition can occur not only in the presence of a spontaneous rhythm (sinus or atrial fibrillation), but also in the occurrence of extrasystole, as well as in a combination of both (Fig. 20, a, b). Competition between artificially induced and spontaneous rhythms creates conditions for ventricular arrhythmias , including ventricular fibrillation, when the stimulating impulse enters a vulnerable period of the cardiac cycle. Arrhythmias associated with pacing are discussed in the chapter.

Asynchronous pacemakers can be used with relative safety in patients with prolonged atrioventricular (AV) block when restoration of conduction through the AV node is unlikely. Nevertheless, even in such a situation, restoration of AV conduction is possible after a long time. S. S. Sokolov et al. (1985) showed that within a period of up to 1.5 years, restoration of sinus rhythm is observed in 21% of patients with persistent third-degree AV block. We observed patients with restoration of sinus rhythm 4-8 years after the initial pacemaker implantation.

Type V00 pacemakers are still widely used in the USSR, but abroad their use is limited only to the fight against myopotential inhibition; It is believed that in the near future the production of ECS of this type will be completely discontinued.

EX VVI is a pacemaker inhibited by the R wave (Fig. 21). Otherwise, this type of ECS is called “demand” and “standby”, which means “working on demand” and “spare”. Just like the V00 pacemaker, its operation requires implantation of one electrode into the ventricle, but in addition to stimulating, it also plays a detector role.

Rice. 20. Options for rhythm competition.

a - monitor recording, lead Vj. Frequent ventricular extra asystole with asynchronous stimulation. The extrasystolic complex is located between the two imposed ones; b - rhythm competition associated with the restoration of sinus rhythm and the presence of ventricular extrasystoles.

Rice. 21. Functioning of the pacemaker in VVI mode (diagram). An asterisk in a circle indicates perception of the control signal and stimulation.

EX type WI has two operating modes: native and fixed.

In the absence of its own heart contractions, the pacemaker generates impulses at the frequency set for it. When spontaneous ventricular depolarization occurs outside the refractory period of the stimulator, the device perceives it and the generation of a stimulating impulse is blocked (Fig. 22). The next impulse can occur only after a set interval, which determines the frequency of stimulation. In other words, if within a certain time the spontaneous wave R is not perceived by the stimulator, then a stimulating impulse will be generated; if this situation persists for a long time, the pacemaker will begin to work constantly at its inherent base frequency. This operating mode is called native (Fig. 23). Explaining the principle of operation of the pacemaker, we do not specifically say that “the stimulator begins to generate impulses when the natural heart rate is lower than the stimulation frequency,” although such an explanation is often found in the literature.

Rice. 23. Functioning of the pacemaker in its own operating mode. Alternation of spontaneous complexes (atrial flutter with different conduction coefficients) with imposed ones. Stimulation frequency 73 pulses/min (stimulation interval 848 ms). The interval between spontaneous contractions is less than 848 ms.

This is not entirely correct, since the frequency of natural contractions may be lower, but individual contractions falling within the above-mentioned interval will be perceived by the ECS and block the application of the stimulating impulse (Fig. 24).

In type VVI pacemakers, the following intervals are distinguished: automatic, pop-up and asynchronous stimulation interval.

Automatic interval, or stimulation interval: the interval between two consecutive imposed complexes.

Pop-up pacing interval: the interval between a spontaneous (sinus or extrasystolic) beat and the subsequent imposed beat.

In most VVI pacemakers, the pop-up pacing interval corresponds to the automatic interval.

However, in practice, when analyzing an ECG, the stimulation interval that pops up may turn out to be slightly larger than the automatic one (Fig. 25). This is due to the fact that it is very difficult to determine from the configuration of the QRS complex the moment when the amplitude of the R wave will be sufficient for the sensory mechanism to perceive the pacemaker [E1-Sherif N. et al., 1980]. Since the counting is made from the beginning or top of the QRS complex, there may be a discrepancy in determining the true value of the automatic interval.

Upper curve - ECG in II standard lead; lower curve - transesophageal recording of atrial potentials (t/p). Stimulation frequency 70 imp/min (stimulation interval 850 ms), sinus rhythm frequency 60 per 1 min (P - P interval 1000 ms).

Automatic interval 920 ms. The jump interval, measured from the beginning of the QRS complex after the first and third extrasystoles, is 960 ms, after the second extrasystoles - 920 ms.

Rice. 26. Changing the value of the pop-up interval when introducing a hysteresis value.

a - initial ECG (hysteresis value not entered). Automatic and pop-up intervals are equal; b - a hysteresis value of 375 ms is entered. The pop-up interval increased to 1255 ms (880-t375).

In recent years, programmable ECS have been produced here and abroad, in particular based on the hysteresis value. Hysteresis, when applied to stimulation, means the difference between frequency. at which the pacemaker begins to generate impulses, and the frequency with which this stimulation occurs. As we mentioned above, in most cases the automatic and pop-up pacing intervals are equal. If hysteresis is introduced into the ECS, then it will make the difference between the pop-up and automatic intervals. In other words, in the case of positive hysteresis, the pop-up stimulation interval will be greater than the automatic one (Fig. 26, a, b). The significance of hysteresis is that it allows maximally maintaining a more favorable hemodynamically sinus rhythm (Fig. 27). Recognizing hysteresis is very important to avoid misdiagnosis of a problem in the stimulation system. In the USSR, EKS-500 devices are produced, which have a hysteresis value. To simplify the analysis of the ECG in table. Figure 3 shows the correspondence between the frequency of the start of stimulation and the frequency with which this stimulation is carried out, at different values ​​of hysteresis.

Asynchronous pacing interval: This is an automatic interval that is recorded when the pacemaker enters a fixed mode under the influence of magnetic fields. The device is switched to a fixed operating mode when an external magnet is brought to the site of pacemaker implantation.

Table 3. Change in stimulation frequency when introducing hysteresis

True stimulation frequency at different hysteresis values

In this case, the asynchronous stimulation interval may become shorter than the automatic one, which leads to an increase in the stimulation frequency. This change in stimulation frequency when a magnet is applied is called a magnetic test. The frequency of stimulation during a magnetic test depends on the pacemaker model. For example, with EX-222, the stimulation frequency does not change much, and this difference can only be detected using special monitoring equipment. For EX-500 and Siemens - Elema-668 (Siemens - Elema), the stimulation frequency increases to 100 pulses/min (Fig. 28, a, b). With the Spectrax-5985 device [Medtronic], the frequency changes only in the first three complexes, increasing to 100 pulses/min, the remaining complexes follow with a frequency equal to the base one (Fig. 29, a, b).

Rice. 28. Transfer of EKS-500 to fixed mode. When a magnet is applied (arrow), the device operates in a fixed stimulation mode with a frequency of 100 pulses/min.

a - the initial rhythm is sinus; b - the original rhythm is imposed.

The stimulation frequency of the magnetic test depends on the state of the power supply, and therefore this test is used to determine the energy state of the power supply. During the operation of the pacemaker, the frequency of stimulation when performing a magnetic test decreases (Fig. 31). A decrease in the frequency of generated impulses below the critical value specified in the passport indicates an threatening depletion of the power source and, even with effective stimulation, requires replacement of the pacemaker.

Rice. 29. Transferring Spectrax-5985 pacemaker to fixed mode.

a - initial sinus rhythm. When a magnet is applied, the first artificially evoked complex appears 600 ms after the spontaneous one. The first three imposed complexes follow at a frequency of 100 imp/min. Subsequent pacemaker pulses are recorded with a frequency of the basic stimulation rhythm of 69 imp/min, falling into the refractory period of the ventricles, they do not cause their depolarization. The asynchronous stimulation interval of 600 ms is recorded only twice, since the countdown starts from the sinus complex; b - the initial rhythm is imposed by the pacemaker. The base stimulation frequency is 70 pulses/min. When a magnet is applied, the first artificially evoked complex appears after 600 ms. The next three complexes follow with a frequency of 100 impulses/min, after which stimulation is again carried out with a frequency of 70 impulses/min.

In some types of pacemaker operating in VVI mode, when a magnet is applied to the pacemaker area or removed, the automatic interval increases due to the pacemaker inhibition (Fig. 32). This fact is explained by a change in the difference in electromechanical potentials between the intracardiac electrode and the ground plate. Each time a magnetically controlled contact circuit opens or closes in response to a magnet, this potential difference changes and the pacemaker senses it and is inhibited. It is believed that similar

The arrows indicate the moment of application and removal of the magnet. An increase in rhythm up to 100 imp/min is recorded only in two complexes (and not in three, as one would expect). Starting from the sixth complex, the pacemaker functions in the R-inhibited mode, as evidenced by the absence of a stimulus when a ventricular extrasystole occurs.

Arrows indicate the moment of application and removal of the magnet. When applying a magnet, the stimulation frequency increases only to 89 pulses/min (the initial frequency during the magnetic test is 100 pulses/min). This result indicates depletion of the power source, but not the need to replace the pacemaker, since reimplantation is indicated when the stimulation frequency is reduced to 85 pulses/min.

This picture occurs only in those ECS whose magnetically controlled contact circuit is connected to the sensor circuit; in models where these circuits are isolated, the application or removal of a magnet does not lead to pauses.

Each type VVI pacemaker has a refractory period, i.e., a time during which it does not perceive any signals. The pacemaker remains refractory to intracardiac potentials not only after each imposed, but also after each “caught” spontaneous complex.

Stimulation increases to 90 pulses/min after a pause, the value of which can vary.

a - pause duration 108 ms; b - pause duration 156 ms.

As a rule, the refractory period in various ECS models ranges from 200 to 500 ms. A spontaneous ventricular complex that occurs in the interval corresponding to the refractory period will not be detected by the device, and the next imposed complex will appear after a specified automatic interval. The device perceives only those complexes in which the amplitude of the intracardiac potential is at least 2-2.5 mV. If the amplitude of the R wave is less than the specified value (this often happens when a low-amplitude ventricular complex is recorded on the ECG), this complex will not be perceived by the pacemaker and the next impulse will appear after a specified automatic interval.

VVI pacing is the mainstay of treatment for sick sinus syndrome (SSNS) and AV conduction disorders.

The VVT ​​stimulator is an R-repetitive pacemaker; stimulator synchronized with the wave (Fig. 33).

This type of pacemaker, like the VVI type pacemaker, has both sensory and stimulating mechanisms. Both sensory and stimulating functions are carried out through a single electrode implanted in the ventricle.

The VVT ​​type pacemaker has the same intervals as the VVI type pacemaker. Just like the R-inhibited pacemaker, the R-repeat pacemaker senses cardiac activity, but does not block the generation of a stimulating impulse, but, on the contrary, the stimulating impulse appears in response to the “captured” intracardiac ventricular potential. Stimuli, as a rule, fall into the initial part of the QRS complex, but they cannot cause depolarization of the ventricles, since the ventricles at this time are in a state of absolute refractoriness (Fig. 34). If spontaneous depolarization of the ventricles does not occur during the automatic interval, then the next complex will be imposed by the pacemaker (Fig. 35). If the frequency of the spontaneous rhythm is close to the base frequency, then confluent contractions may occur (Fig. 36). Sometimes a stimulating impulse may not occur at the beginning of the QRS complex, but a little later, in cases of splitting of the ventricular complex due to intraventricular conduction disorders.

The device has a refractory period during which it does not perceive any signal, so no impulses are generated in response to potentials recorded in this interval. The peculiarity of the operation of this type of pacemaker is that the occurrence of an impulse in response to a spontaneous complex occurs only up to a certain frequency, the value of which depends on the refractory period. For example, with a refractory period of 400 ms, this frequency will correspond to 150 pulses/min.

Complexes 2, 3, 7 were imposed by the pacemaker, since no spontaneous contractions occurred in the automatic interval of 880 ms. The remaining complexes are spontaneous; at the beginning of each of them a stimulating impulse is recorded.

1, 2, 3, 4, 7, 9, 10 - spontaneous complexes; 5 and 8 - artificially caused; 6 - drain. The distance between the drain and the previous imposed one is 860 ms, i.e., close to the value of the automatic interval, equal to 880 ms.

Spontaneous ventricular contractions follow at a frequency of 83 to 120 per minute. At the beginning of each QRS complex, pacemaker stimuli are visible.

The variant of R - repeating pacemaker discussed above belongs to the devices of the first generations. In them, the value of the stimulation interval is composed of the value of the refractory period of the pacemaker and the interval in which the synchronized impulse was applied,

Rice. 37. Functioning of VVT type ECS of the first and last generations(scheme). Explanation in the text.

the so-called synchronization period (Fig. 37, a). The next imposed ventricular complex always occurred at a fixed interval equal to the stimulation interval. In modern foreign ECS of this type, the stimulation interval consists of three intervals: the refractory period, the inhibition period, i.e., the period in which the ECS is inhibited by the perceived signal, and the synchronization period (Fig. 37.6). The inhibition period is always shorter than the synchronization period and together they constitute the so-called readiness interval. The next imposed complex will not necessarily occur after a time corresponding to the value of the automatic interval. If the ventricular signal is sensed during the inhibition period, the pacemaker will not produce a synchronous pacing pulse; on the contrary, it will discharge and a new cycle will begin, but during this cycle there will be no period of inhibition and after the refractory period the synchronization period will begin (Fig. 37, c), therefore the resulting interpulse interval will be greater than the stimulation interval. For example, the pacing rate is set to 60 ppm. Accordingly, the stimulation interval is 1000 ms. Let's assume that the refractory period is 332 ms, the inhibition period occupies 145 ms of the entire readiness interval. This means that the synchronization period is the remaining 523 ms. If any signal occurs during the inhibition period, 143 ms after the refractory period, the pacemaker will perceive it, as a result, the ventricular chain will be inhibited and the cycle will begin again: the refractory period is 332 ms and the synchronization period is 523 ms. If no signal is received in this cycle, then at the end of it a stimulating impulse will be applied to the ventricle. As a result, it turns out that the distance between two subsequent stimulating pulses is 1330 ms (Fig. 37, d).

Pacemaker

Material from Wikipedia - the free encyclopedia

An electrical pacemaker (ECS), or artificial pacemaker (APV) is a medical device designed to influence the rhythm of the heart. The main task of pacemakers is to maintain or impose a heart rate in a patient whose heart either does not beat fast enough or has an electrophysiological disconnection between the atria and ventricles (atrioventricular block). There are also special (diagnostic) external pacemakers for performing stress functional tests.

History of the creation of pacemakers

The ability of electric current pulses to cause muscle contractions was first noticed by the Italian Alessandro Volta. Later, Russian physiologists Yu. M. Chagovets and N. E. Vvedensky studied the effects of electrical impulses on the heart and suggested the possibility of using them to treat certain heart diseases. In 1927, Hyman G. created the world's first external pacemaker and used it in the clinic to treat a patient suffering from a rare pulse and loss of consciousness. This combination is known as a Morgagni-Edams-Stokes attack (MES).

In 1951, American cardiac surgeons Callaghan and Bigelow used a pacemaker to treat a patient after surgery, as she developed complete transverse heart block with a rare rhythm and attacks of MES. However, this device had a big drawback - it was located outside the patient’s body, and impulses to the heart were carried through wires through the skin.

In 1958, Swedish scientists (in particular Rune Elmqvist) created an implantable pacemaker, that is, completely under the skin. (Siemens-Elema). The first stimulants were short-lived: their service life ranged from 12 to 24 months.

In Russia, the history of cardiac stimulation dates back to 1960, when Academician A. N. Bakulev approached the country's leading designers with a proposal to develop medical devices. And then at the Precision Engineering Design Bureau (KBTM) - a leading enterprise in the defense industry, headed by A. E. Nudelman - the first development of implantable ECS began (A. A. Richter, V. E. Belgov). In December 1961, the first Russian stimulator, EX-2 (“Mosquito”), was implanted by Academician A. N. Bakulev into a patient with complete atrioventricular block. EKS-2 was in service with doctors for more than 15 years, saved the lives of thousands of patients and established itself as one of the most reliable and miniature stimulators of that period in the world.

Indications for use

• Cardiac arrhythmias
• Sick sinus syndrome

Stimulation techniques

External pacing

External cardiac pacing can be used to initially stabilize the patient, but it does not exclude the implantation of a permanent pacemaker. The technique involves placing two stimulator plates on the surface of the chest. One of them is usually located on the upper part of the sternum, the second is on the left back, almost at the level of the last ribs. When an electrical discharge passes between two plates, it causes contraction of all muscles located in its path, including the heart and muscles chest wall.

A patient with an external stimulator should not be left unattended for long periods of time. If the patient is conscious, this type of stimulation will cause discomfort due to frequent contraction of the chest wall muscles. In addition, stimulation of the muscles of the chest wall does not mean stimulation of the heart muscle. In general, the method is not reliable enough, so it is rarely used.

Temporary endocardial stimulation (TECS)

Stimulation is performed through a probe-electrode passed through a central venous catheter into the heart cavity. The operation of installing the probe-electrode is carried out under sterile conditions, the best option is to use disposable sterile kits for this, including the probe-electrode itself and its delivery means. Distal end The electrode is placed in the right atrium or right ventricle. The proximal end is equipped with two universal terminals for connection to any suitable external stimulator.

Temporary pacing is often used to save the patient's life, incl. as the first step before implantation of a permanent pacemaker. Under certain circumstances (for example, in the case of acute myocardial infarction with transient rhythm and conduction disturbances or in the case of temporary rhythm/conduction disturbances due to drug overdose), the patient will not be transferred to permanent stimulation after temporary stimulation.

Implantation of a permanent pacemaker

Implantation of a permanent pacemaker is a minor surgical intervention and is performed in the cath lab. The patient is not given general anesthesia; only local anesthesia is given in the area of ​​the operation. The operation includes several stages: an incision in the skin and subcutaneous tissue, isolation of one of the veins (most often - head, she's the same v.cephalica), passing through a vein one or more electrodes into the chambers of the heart under X-ray control, checking the parameters of the installed electrodes using an external device (determining the stimulation threshold, sensitivity, etc.), fixing the electrodes in the vein, forming subcutaneous tissue bed for the pacemaker body, connecting the stimulator to the electrodes, suturing the wound.

Typically, the stimulator body is placed under the subcutaneous fatty tissue of the chest. In Russia, it is customary to implant stimulators on the left (right-handed people) or on the right (left-handed people and in a number of other cases - for example, in the presence of skin scars on the left), although the issue of placement is decided in each case individually. Outer shell the stimulant rarely causes rejection, because it is made of titanium, or a special alloy that is inert to the body.

Transesophageal pacing

For diagnostic purposes, the transesophageal pacing (TEPS) method, otherwise called non-invasive electrophysiological study of the heart, is also sometimes used. This technique is used in patients with suspected dysfunction of the sinus node, in patients with transient disturbances of atrioventricular conduction, paroxysmal rhythm disturbances, suspected presence of accessory pathways (APP), and sometimes as a replacement for the exercise bicycle ergometer or treadmill test.

The study is carried out on an empty stomach. The patient lies on the couch. Through the nose (less often through the mouth), a special two- or three-pole electrode probe is inserted into the esophagus; this probe is installed in the esophagus at the level where the left atrium comes into contact with the esophagus. In this position, stimulation is carried out with pulses of voltage, usually from 5 to 15 V; the proximity of the left atrium to the esophagus allows the rhythm to be imposed on the heart.

Special external pacemaker devices, such as TEEKSP, are used as a pacemaker.

Stimulation is carried out using different methods for different purposes. In principle, there is increased stimulation (frequencies close to the frequencies of the natural rhythm), frequent (from 140 to 300 imp/min), ultra-frequent (from 300 to 1000 imp/min), and also programmed (in this case, not a “continuous series” of stimuli is given, and their groups (“packs”, “volleys”, in English terminology burst) with different frequencies, programmed using a special algorithm).

Transesophageal stimulation is a safe diagnostic method because the effect on the heart is short-lived and stops instantly when the stimulator is turned off. Stimulation with frequencies of more than 170 pulses/min is carried out for 1-2 seconds, which is also quite safe.

The diagnostic effectiveness of TEES for various diseases varies. Therefore, the study is carried out only according to strict indications. In cases where TEES does not provide complete and/or exhaustive information, the patient has to undergo invasive EPI of the heart, which is much more difficult and expensive, is carried out in a cath lab and involves the insertion of a catheter-electrode into the heart cavity.

The method of transesophageal electrical stimulation is sometimes used for treatment: relief of paroxysmal atrial flutter (but not atrial fibrillation) or some types of supraventricular paroxysmal tachycardias.

Basic functions of a pacemaker

A pacemaker is a small, sealed steel device. The case contains a battery and a microprocessor unit. All modern stimulators perceive the heart’s own electrical activity (rhythm), and if a pause or other rhythm/conduction disturbance occurs for a certain time, the device begins to generate impulses to stimulate the myocardium. Otherwise, if there is an adequate natural rhythm, the pacemaker does not generate impulses. This function was previously called “on demand” or “on demand”.

Pulse energy is measured in joules, but in practice a voltage scale (in volts) is used for implantable pacemakers and a voltage (in volts) or current (in amperes) scale for external stimulators.

There are implantable pacemakers with frequency adaptation function. They are equipped with a sensor that perceives physical activity patient. Most often, the sensor is an accelerometer, an acceleration sensor. However, there are also sensors that determine physical activity in accordance with minute ventilation or changes in electrocardiogram parameters (QT interval) and some others. Information about the movement of the human body received from the sensor, after processing by the stimulator processor, controls the frequency of stimulation, allowing it to be adapted to the needs of the patient during physical activity.

Some models of pacemakers can partially prevent the occurrence of arrhythmias (atrial fibrillation and flutter, paroxysmal supraventricular tachycardia, etc.) due to special stimulation modes, incl. overdrive pacing (forced increase in rhythm relative to the patient’s own rhythm) and others. But it has been shown that the effectiveness of this function is low, therefore the presence of a pacemaker in general case does not guarantee elimination of arrhythmias.

Modern pacemakers can accumulate and store data on heart function. Subsequently, the doctor, using a special computer device - a programmer, can read these data and analyze the heart rhythm and its disorders. This helps to prescribe adequate drug treatment and select adequate stimulation parameters. The operation of an implanted pacemaker with a programmer should be checked at least once every 6 months, sometimes more often.

Stimulant labeling system

Pacemakers are single-chamber (to stimulate only the ventricle or only the atrium), two-chamber (to stimulate both the atrium and the ventricle) and three-chamber (to stimulate the right atrium and both ventricles). In addition, implantable cardioverter defibrillators are used.

In 1974, a system of three-letter codes was developed to describe the functions of stimulants. According to the developer, the code was named ICHD (Intersociety Commission on Heart Disease).

Subsequently, the creation of new pacemaker models led to the emergence of the five-letter ICHD code and its transformation then into the five-letter code for implantable systems of electrical influence on the heart rhythm - pacemakers, cardioverters and defibrillators in accordance with the recommendations of the British Pacing and Electrophysiology Group – BREG) and the North American Society of Pacing and Electrophysiology (NASPE). The final code currently in use is called NASPE/BREG (NBG).

In Russia, something like a combined encoding is traditionally used: for stimulation modes that do not have frequency adaptation, the three-letter ICHD code is used, and for modes with frequency adaptation, the first 4 letters of the NASPE/BREG (NBG) code are used.

According to NBG code:

The designations in this table are abbreviations of English words. A – atrium, V – ventricle, D – dual, I – inhibition, S – single (in positions 1 and 2), T – triggering, R – rate-adaptive.

For example, according to this system, VAT will mean: a stimulator in atrial rhythm detection mode and ventricular stimulation in biocontrol mode, without frequency adaptation.

The most common pacing modes: VVI - single-chamber ventricular pacing on demand ( according to the old Russian nomenclature “R-inhibited ventricular stimulation”),VVIR – the same with frequency adaptation, AAI – single-chamber atrial stimulation on demand ( according to the old Russian nomenclature “P-inhibited atrial stimulation”),AAIR – the same with frequency adaptation, DDD – dual-chamber atrioventricular biocontrolled stimulation, DDDR – the same with frequency adaptation. Sequential stimulation of the atrium and ventricle is called sequential.

VOO/DOO – asynchronous ventricular stimulation/asynchronous sequential stimulation (in clinical practice, it is not used as a constant, it occurs in special cases of stimulator operation, for example, during a magnetic test or in the presence of external electromagnetic interference. Transesophageal pacing is most often performed in the AOO mode (formally this is not contradicts standard designations, although the atrium during endocardial stimulation is meant to be the right one, and with TEES - the left one)).

It is quite obvious that, for example, a DDD type stimulator can in principle be switched programmatically to the VVI or VAT mode. Thus, the NBG code reflects both the fundamental ability of a given pacemaker and operating mode device at any given time. (For example: IVR type DDD operating in AAI mode). Dual-chamber stimulators from foreign and some domestic manufacturers have, among other things, a “mode switching” function (switch mode is a standard international name). So, for example, if atrial fibrillation develops in a patient with an implanted IVR in DDD mode, the stimulator switches to DDIR mode, etc. This is done to ensure patient safety.

A number of IVR manufacturers are expanding these coding rules for their stimulants. For example, Sorin Group uses a mode designated as AAIsafeR (as well as AAIsafeR–R) for Symphony type IVR. Medtronic designates a fundamentally similar mode for its IVR Versa and Adapta as AAI<=>DDD, etc..

Biventricular pacing (BVP, biventricular pacing)

With some heart diseases, a situation is possible when the atria, right and left ventricles contract asynchronously. Such asynchronous work leads to a decrease in the performance of the heart as a pump and leads to the development of heart failure and circulatory failure.

With this technique (BVP), stimulating electrodes are placed in the right atrium and to the myocardium of both ventricles. One electrode is located in the right atrium, in the right ventricle the electrode is located in its cavity, and it is supplied to the left ventricle through the venous sinus.

This type of stimulation is also called cardiac resynchronization therapy (CRT).

By selecting parameters for sequential stimulation of the atrium and the left and right ventricles, in some cases it is possible to eliminate dyssynchrony and improve the pumping function of the heart. As a rule, to select truly adequate parameters for such devices, it is necessary not only to reprogram and monitor the patient, but also to simultaneously monitor echocardiography (with determination of cardiac output parameters, including VTI - volumetric blood flow velocity integral).

Nowadays, combined devices can be used that provide PCT, ICD functions, and, of course, stimulation for bradyarrhythmias. However, the cost of such devices is still very high, which limits their use.

Implantable cardioverter-defibrillators (ICD, IKVD)

A patient’s circulatory arrest can occur not only when the cardiac pacemaker stops or when conduction disturbances (blockades) develop, but also when ventricular fibrillation or ventricular tachycardia occurs.

If a person is at high risk of circulatory arrest for this reason, a cardioverter-defibrillator is implanted. In addition to the stimulation function for bradysystolic rhythm disturbances, it has the function of interrupting ventricular fibrillation (as well as ventricular flutter, ventricular tachycardia). For this purpose, after recognizing a dangerous condition, the cardioverter-defibrillator delivers a shock of 12 to 35 J, which in most cases restores normal rhythm, or at least stops life-threatening rhythm disturbances. If the first shock was ineffective, the device can repeat it up to 6 times. In addition, modern ICDs, in addition to the discharge itself, can use various schemes for delivering frequent and burst stimulation, as well as programmed stimulation with various parameters. In many cases, this makes it possible to stop life-threatening arrhythmias without applying a shock. Thus, in addition to the clinical effect, greater comfort for the patient is achieved (no painful discharge) and saving the device’s battery.

Pacemaker danger

A pacemaker is a high-tech device that implements many modern technical and software solutions. In it, incl. provision of multi-stage security is provided.

When external interference appears in the form of electromagnetic fields, the stimulator switches to an asynchronous operating mode, i.e. stops responding to these interferences.

With the development of tachysystolic rhythm disturbances, the dual-chamber stimulator switches modes to ensure ventricular stimulation at a safe frequency.

When the battery is low, the stimulator disables some of its built-in functions to provide life-saving stimulation (VVI) for some time until the battery is replaced.

In addition, other mechanisms are used to ensure patient safety.

In recent years, the possibility of deliberately causing harm to a patient with a pacemaker that has the ability to remotely exchange with the programmer has been widely discussed in the media. In principle, such a possibility exists, which has been convincingly shown. However, please note:

• Most of the currently used foreign and all domestic pacemakers require close contact with the programmer head for programming, i.e. not susceptible to remote influence at all;
• a potential hacker must have at his disposal information about the exchange codes with the pacemaker, which are the technological secret of the manufacturer. An attempt to influence the stimulator without these codes will lead to the fact that, as with any other non-deterministic interference, it will go into an asynchronous mode and cease to perceive external information at all, and therefore will not cause harm;
• the very possibilities of the stimulator’s effect on the heart are structurally limited for safety reasons;
• the hacker must know that this patient has a stimulant in general, a specific brand in particular, and that specific effects are harmful to this patient due to his state of health.

Thus, the danger of such an attack on the patient seems low. It is likely that IVR manufacturers will take further measures to cryptographicly protect remote exchange protocols.

Pacemaker failure

In principle, like any other device, a pacemaker can fail. However, taking into account the high reliability of modern microprocessor technology and the presence of duplicated safety systems in the stimulator, this happens extremely rarely, the probability of failure is hundredths of a percent. The likelihood of refusal causing harm to the patient is even less. You should ask your doctor how the failure of a particular stimulant will manifest itself and what to do in this case.

However, the very presence in the body foreign body– especially an electronic device – still requires the patient to comply with certain safety measures.

Rules of conduct for a patient with a pacemaker

Any patient with a pacemaker must follow certain restrictions.

• DO NOT be exposed to powerful magnetic and electromagnetic fields, microwave fields, as well as direct exposure to any magnets near the implantation site.
• DO NOT expose yourself to electrical current.
• DO NOT perform magnetic resonance imaging (MRI).
• It is PROHIBITED to use most methods of physiotherapy (heating, magnetic therapy, etc.) and many cosmetic interventions associated with electrical influence (the specific list should be checked with cosmetologists).
• It is PROHIBITED to conduct an ultrasound examination (ultrasound) with the beam directed towards the stimulator body.
• It is PROHIBITED to strike the chest in the area where the stimulator is implanted, or try to dislodge the device under the skin.
• It is PROHIBITED to use monopolar electrocoagulation when surgical interventions(including endoscopic), the use of bipolar coagulation should be limited as much as possible, and ideally, not used at all.

It is advisable not to bring a mobile or other wireless phone closer than 20–30 cm to the stimulator; it should be held in the other hand. It is also better to place the audio player not close to the stimulator. You can use a computer and similar devices, incl. portable. You can perform any X-ray examinations, incl. computed tomography (CT). You can work around the house or on the site, use tools, incl. power tools, provided they are in good working order (so that there is no risk of electric shock). The use of rotary hammers and electric drills, as well as lawn mowers, should be limited. Mowing and chopping wood by hand should be done with caution and should be avoided if possible. You can engage in physical education and sports, avoiding contact-traumatic types and avoiding the above-mentioned mechanical impact on the stimulator area. Large loads on the shoulder girdle. In the first 1–3 months after implantation, it is advisable to limit arm movements on the implantation side, avoiding sudden lifts above the horizontal line and sudden abductions to the side. After 2 months, these restrictions are usually lifted. Swimming is permitted.

Controls in stores and airports (“frameworks”) essentially cannot spoil the stimulator, but it is advisable either not to go through them at all (for which you need to show the pacemaker owner’s card to security), or to reduce your stay in their area of ​​effect to a minimum.

A patient with a pacemaker must promptly visit a doctor to have the device checked using a programmer. It is highly advisable to know about yourself: the brand (name) of the implanted device, the date and reason for implantation.

Pacemaker on ECG

The operation of a pacemaker significantly changes the picture of the electrocardiogram (ECG). At the same time, a working stimulator changes the shape of the complexes on the ECG in such a way that it becomes impossible to judge anything from them. In particular, the work of the stimulator can mask ischemic changes and myocardial infarction. On the other hand, because modern stimulators work “on demand”; the absence of signs of stimulator operation on the electrocardiogram does not mean that it is broken. Although there are often cases when nursing staff, and sometimes doctors, without proper grounds, tell the patient “your stimulator is not working,” which greatly irritates the patient. In addition, the long-term presence of right ventricular stimulation also changes the shape of its own ECG complexes, sometimes simulating ischemic changes. This phenomenon is called “Chaterje syndrome” (more correctly, Chatterjee, named after the famous cardiologist Kanu Chatterjee).

Thus: interpretation of an ECG in the presence of a pacemaker is difficult and requires special training; if acute cardiac pathology (ischemia, heart attack) is suspected, their presence/absence should be confirmed by other methods (usually laboratory). The criterion for correct/incorrect operation of the stimulator is often not a regular ECG, but a test with a programmer and, in some cases, daily ECG monitoring.

ECG conclusion in a patient with a pacemaker

When describing an ECG in a patient with an implanted IVR, the following is indicated:

• presence of a pacemaker;
• its operating mode, if this is known or unambiguous (it should be taken into account that dual-chamber stimulators have different operating modes, the transition between which can be carried out continuously, including beat-to-beat, i.e. in each contraction);
• description of your own complexes (if any) according to the standards of a regular ECG (it is necessary to indicate with the transcript that the interpretation is carried out using your own complexes);
• judgment about the malfunction of the IVR (“violation of the detection function”, “violation of the stimulation function”, “violation of the electronic circuit”), if there are grounds for this.

When describing a 24-hour ECG in a patient with IVR, the following is indicated:

• ratio of rhythms (how long each rhythm was recorded, including the IVR rhythm in the mode.);
• rhythm frequencies according to the usual rules for describing a Holter monitor;
• standard decoding of monitor data;
• information about identified violations of the operation of the IVR (“violation of the detection function,” “violation of the stimulation function,” “violation of the electronic circuit”), if there are grounds for this, all types of identified violations, and in the case of a small number of episodes, all episodes must be illustrated in conclusion printout of ECG fragments at the described moment in time. If there are no signs of dysfunction of the IVR function, it is acceptable to record “no signs of dysfunction of the IVR function were identified.”

It should be taken into account that when analyzing the operation of modern IVRs, a number of functions (hysteresis, pseudo-Wenckebach, mode switching and other responses to tachycardia, MVP, etc.) can simulate incorrect operation of the stimulator. Moreover there are no ways distinguish correct from incorrect operation using the ECG. A functional diagnostics doctor, if he does not have special training in programming stimulators and does not have at his disposal comprehensive data on the programmed modes of this particular IVR for a given patient, does not have the right to make final judgments about the adequacy of the IVR operation (except in cases of obvious dysfunction of the device). In cases of doubt, patients should be referred for consultation at the site of IVR programming/verification.

see also

• Cardiology
• Conduction system of the heart

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