At the heart of all arrhythmias is a violation of the formation or conduction of an impulse, or a simultaneous disorder of both functions of the conducting system. Arrhythmias such as sinus tachycardia and bradycardia are associated, respectively, with an increase or inhibition of the automatism of the cells of the sinus node. In the origin of extrasystole and paroxysmal rhythm disturbances, there are 2 main mechanisms: increased automatism of ectopic foci, re-entry of excitation (re-entry) and circular movement of the impulse.
An increase in the automatism of ectopic foci may be associated with an acceleration or deceleration of spontaneous diastolic depolarization, fluctuations in the excitation threshold and resting potential, as well as with trace subthreshold and suprathreshold oscillations.
The mechanism of re-entry of excitation (re-entry) consists in repeated or repeated excitation of a part of the myocardium with the same impulse making a circular motion. To implement this mechanism, two conduction pathways are required, and along one of them, the passage of the impulse is disrupted due to a local unidirectional blockade.
The part of the myocardium, to which the next impulse did not reach in time, is excited in a roundabout way with some delay and becomes a source of extraordinary excitement. It spreads to neighboring areas of the myocardium, if these areas managed to get out of the state of refractoriness.
The macro re-entry mechanism is possible due to the functional division of the atrioventricular node into two parts, conducting impulses at different speeds due to functioning additional pathways (in WPW syndrome), and the micro re-entry mechanism is implemented mainly by anastomoses in the branches of the conducting system.
Disruption of impulse conduction is facilitated primarily by a decrease in the action potential, which may be associated with a decrease in the resting potential. Conduction disorders can develop as a result of lengthening the period of refractoriness (slowing down of repolarization) in areas of the conducting system.
One of the mechanisms of conduction disturbance is the so-called decremental conduction, which consists in a progressive decrease in the rate of depolarization and the action potential during the propagation of an impulse from one fiber to another. An important role in the mechanism of parasystolic arrhythmias is played by the so-called blockade of entry and exit in the area of the ectopic focus.
The blockade of the entrance means the impossibility of penetration into the ectopic focus of the impulses of the main rhythm, and the blockade of the exit- the impossibility of leaving this focus of part of the ectopic impulses.
Combinations of the above and some other mechanisms may underlie the development of combined arrhythmias.
"Practical electrocardiography", VL Doshchitsin
Cardiac arrhythmias are one of the most common manifestations of cardiovascular diseases. In recent years, significant advances have been made in the diagnosis of rhythm and conduction disturbances due to the use of new methods of long-term recording of ECG, electrohisography and programmed cardiac stimulation. These methods obtained new data on the anatomy and electrophysiology of the cardiac conduction system, on the pathogenetic mechanisms of rhythm and conduction disturbances. As a result ...
I. Disturbances of impulse formation: sinus tachycardia. sinus bradycardia. sinus arrhythmia. rhythm source migration. extrasystoles: supraventricular and ventricular; single, group, allorhythmic; early, middle and late; paroxysmal tachycardia: supraventricular and ventricular; by the re-entry mechanism and ectopic; non-paroxysmal tachycardia and accelerated ectopic rhythms: supraventricular and ventricular; by the re-entry mechanism, parasystolic and elusive; atrial flutter: paroxysmal and persistent; correct ...
If in the process of decoding the ECG, signs of any rhythm or conduction disturbance are revealed, then a special technique should be used. The analysis of rhythm disturbances should begin with the identification of P waves, assessment of their regularity and atrial rate, which is determined in the same way as the ventricular rate. In this case, it is possible to detect changes in the frequency of the atrial rhythm: its decrease (sinus bradycardia, sinoauricular ...
It is necessary to proceed to the analysis of the ventricular rhythm: its frequency (if it has not been determined earlier) and the regularity of the R - R intervals. Individual premature QRS complexes are possible against the background of the correct rhythm (extrasystoles), separate ventricular complex prolapse due to sinoauricular or atrioventricular blockade, or completely irregular, disorderly rhythm characteristic of atrial fibrillation. It is also necessary to determine the width of the QRS complexes, the position of the electrical ...
5572 0
The majority of monomorphic VTs are based on the re-entry mechanism. Unlike automatic arrhythmias, the conditions for re-entry are associated with chronic rather than acute illness. With the help of endocardial and intraoperative mapping, it was shown that these arrhythmias occur within or on the border of the zone of the altered myocardium. The size of the re-entry circle can be large (especially in patients with LV aneurysm) or limited to a small area.
A number of conditions are required for a re-entry to occur:
- two or more potential pathways;
- a unidirectional block that occurs in one of the paths;
- an excitation wave propagating around the zone of the unidirectional conduction block through an alternative path;
- further excitation of the myocardium distal to the zone of the unidirectional block with a delay (i.e., with slow conduction);
- retrograde entry of the excitation wave into the block zone and re-excitation of those tissues where it originated initially.
The zones of slow conduction in the myocardium can be detected by endocardial mapping in the form of fractionated and (or) average diastolic electrograms (Fig. 1) of constant electrical activity, or by recording a long delay between the stimulus artifact and the resulting QRS complex. Not all slow-moving zones participate in the re-entry chain, as there may be dead-end paths or "observer paths".
Thus, for a successful ablation procedure, evidence must be provided that the mapped area is indeed located within the re-entry circle and is critically related to the maintenance of the arrhythmia. If VT is not induced during the ablation procedure or is poorly haemodynamically tolerated, electroanatomical mapping systems are used to locate areas of critical narrowing, such as the mitral isthmus (Fig. 2), to facilitate successful ablation.
Rice. 1. ECG of a patient with anterior myocardial infarction and recurrent sustained VT: mapping (A) and subsequent catheter ablation (B) were performed. Presents leads I, III, V1 and V6, intracardiac signals from the apex of the RV (RV); An ablation catheter is positioned in the anterior septal LV basal region at the point of successful ablation. Attention should be paid to the fragmented diastolic potential at the ablation site where VT was terminated a few seconds after the initiation of radiofrequency (RF) ablation (B).
Rice. 2. A - an episode of VT (cycle length - 400 ms) in a patient with a previous inferior MI and episodes of recurrent VT was diagnosed and treated with an implanted cardioverter-defibrillator.
B - VT on 12-lead ECG in the same patient.
B - rear view of the LV on an electroanatomical map (Carto): electroanatomical mapping is used to determine the boundaries of the "ring" of tachycardia, which allows for successful ablation. The color distribution characterizes the amplitude of local potentials. Dense scar tissue is shown in gray. A linear ablative treatment was applied from the mitral annulus to the edge of the scar tissue to prevent the development of re-entry tachycardia involving the mitral annulus (around the MV or posterior scar).
It should be noted that in HF, re-entry in the His-Purkinje system (re-entry in the bundle of His; Fig. 3) causes a significant number of monomorphic VTs. The front of the re-entry wave travels down one bundle branch (mainly on the right) and up the contralateral leg. This creates a QRS complex with signs of LBBB and normal or deviated to the left in the frontal plane of the EOS. That is why catheter ablation of PNBG makes it easy to eliminate such VT.
Rice. 3. ECG from a patient with dilated cardiomyopathy and sustained recurrent VT. A - shows stable re-entry tachycardia in the bundle branch with LBBB morphology. Intracardiac signals (B) indicate ventricular-atrial dissociation (RV - right atrial catheter; RV - apex of the RV) and excitation of PNPG from the proximal part (PNPG prox) to distal (PNPG dist). The tachycardia was treated with radiofrequency ablation.
Arrhythmias due to ventricular automatism
Pathological automatism is considered a more rare mechanism of VT. Automatic VT is typically associated with conditions such as acute MI, hypoxia, electrolyte disturbances, and high adrenergic tone. Automatic VT, which is recorded within the first 24-48 h after acute MI, is the main cause of SCD. They are probably associated with residual ischemia that occurs in the infarction zone. In the stage of infarction scarring, the substrate of such arrhythmias disappears, but the substrate remains for the development of arrhythmias by the re-entry mechanism. Since automatic arrhythmias usually occur secondary to metabolic disturbances, treatment should be directed towards detecting and eliminating the underlying causes.
Lars Eckardt, Günter Breithardt and Stefan Hohnloser
Ventricular tachycardia and sudden cardiac death
FSBEI HE Samara State MedicalUniversity of the Ministry of Health of the Russian Federation
Department of Cardiology and Cardiovascular Surgery IPO
TACHYCARDIA ON MECHANISM RE-ENTRY
Speaker:
student VI
course, medical faculty,
group L604, Abramova Z.V. Re-entry mechanism
- re-entry
excitement
myocardial site
the same
impulse,
committing
circular
traffic.
RE-ENTRY MECHANISM TYPES (1)
1. Macro-rental(ordered)
A loop
macro-reentry
formed in the myocardium
around
anatomical
plots not conducting
electrical impulses
(mouth
vessels,
fibrous tissue), or
at
stock
additional
conducting
ways.
The loop size is
more than 1 cm, the macrorientry rotor is usually one and
It has
permanent
localization.
RE-ENTRY MECHANISM TYPES (2)
2. Micro-rental(random)
Formed in
myocardium around
plot
electric
inhomogeneity, i.e.
not related to
anatomical
structures of the heart.
Size of one loop
1 mm.
THE MAIN TACHYCARDIA WITH THE MACRO RE-ENTRY MECHANISM ARE:
BACK TO MAINTACHYCARDIA WITH
MACRO REENTRY MECHANISM
RELATE:
1.
WPW - Syndrome
2. Atrial flutter
3. AVURT
4. Paroxysmal
tachycardia
REASONS OF TACHYCARDIA WITH THE MACRO RE-ENTRY MECHANISM
coronary heart diseaserespiratory distress
arterial hypertension
heart injury
chronic cardiac
failure
amyloidosis of the heart
hemochromatosis
heart tumors
heart defects
pericarditis
hypertrophic
cardiomyopathy
dilated
cardiomyopathy
pulmonary thromboembolism
arteries
thyrotoxicosis
toxic myocardiodist
rophy
valve prolapse with
regurgitation
mitral calcification
rings
idiopathic dilatation
right atrium
premature syndrome
ventricular excitation
complications
cardiac surgery
operations
WOLF-PARKINSON-WHITE SYNDROME (WPW)
WOLFAPARKINSON-WHITE SYNDROME (WPW)Syndrome with preexcitation of the ventricles of the heart by
accessory atrioventricular junction
(VPZhS) and supraventricular tachyarrhythmia
WPW syndrome clinic
Seizuresrapid rhythmic or
less often irregular heartbeat
- feeling of "fluttering" of the heart in
breasts with a very high frequency,
accompanied by:
weakness, dizziness;
loss of consciousness and attacks of suffocation
(at extremely high heart rate
may be rare).
Attack
may stop when
taking a deep breath and holding your breath.
ECG SIGNS OF WPW SYNDROME
ECG SIGNS WPW SYNDROMEShortening the P-Q interval
At the beginning of the QRS complex, an additional delta wave
excitement
Increased duration and slight deformation
complex QRS
Discordant to the QRS complex displacement of the S-T segment and
reversal of the polarity of the T wave (intermittent signs)
Treatment of WPW syndrome
The method of choice - catheter ablation of DPPIf catheter ablation is not possible
drugs of choice for the prevention of paroxysms
tachycardias with preexcitation syndromes are
class I antiarrhythmic drugs, primarily IC
class: etacizine and propafenone. Appointment
Class I drugs are contraindicated in patients with
signs of structural damage to the heart, cardiac
failure, with a decrease in the left ejection fraction
ventricle up to 40% or less, as well as with hypertrophy
myocardium (wall thickness of the left ventricle 1.5 cm and
more)
In the presence of structural damage to the heart
Class III drugs (sotalol and amiodarone)
ATRIAL FLUSH
Atrial flutter (AT) refers to atrial tachycardias caused by the circulation of the excitation wave alongtopographically extensive contour (the so-called "macro-reentry"), as
usually around large anatomical structures in the right or
left atrium.
Clinic
Palpitations
Dyspnea
Dizziness
Frequent, correct pulse (at a constant rate
holding)
ECG SIGNS OF ATRIAL FLUTD
Frequent up to 200-400 per minute, regular,sawtooth similar to each other
atrial F waves in leads II, III, aVF,
V1-2;
complexes, each of which is preceded by
a certain number of atrial waves F
Regular ventricular rhythm with
equal R-R intervals (can
temporarily lose regularity when changing
atrioventricular conduction - with
atypical irregular form)
Atrial flutter treatment
To stop the attacks of TP, useintravenous administration of procainamide,
propafenone, sotalol and amiodarone,
atria.
In the presence of a hemodynamic disorder, the method of choice is an emergency electrical
cardioversion.
When treating patients with repeated paroxysms of typical TP and with
persistent typical atrial fibrillation method of choice catheter ablation of cavotricuspid
isthmus.
ATRIOVENTRICULAR RECIPROCAL NODULAR TACHYCARDIA (AVURT)
AVURT is a stable circulation of impulses (re-entry) in the AV node and the adjacent septal region of the atrial myocardium.Classification
1) a typical variant is "slow-fast" or "slowfast":
the impulse moves along the AV node anterograde (from the atrium to
ventricles) along the "slow" path, and from the ventricles to
atria (retrograde) along the "fast" path;
2) atypical variant - "fast-slow" or "fastslow":
the impulse moves along the AV node anterograde along the "fast"
path, and retrograde along the "slow" path;
3) atypical variant - "slow-slow" or "slowslow": the impulse moves along the AV node anterograde and
retrograde along two "slow" paths.
ECG - SIGNS OF AVURT
Tachycardia with ventricular ratecuts from 140 to 250 per minute
Retrograde P wave of 40 duration
ms superimposed on the QRS complex or
occurs immediately after it (less than 70 ms), which
often leads to the appearance of pseudo-r 'in
lead V1
AVURT treatment
To stop an attack of AVURTuse "vagal" samples, when they
intravenous inefficiencies are used
adenosine (ATP) or isoptin,
transesophageal electrical stimulation
atria.
By selection method when re
recurrent AVNRT is
catheter ablation of the "slow" pathway of the AV node
If it is impossible to conduct a catheter
ablation drug of choice is
verapamil
PAROXISMAL TACHYCARDIA
Attackrapid heartbeat with
Heart rate from 130 to 200 and more per minute,
starts suddenly and just as suddenly
ends. Duration of an attack from
several seconds to several hours and
days.
Allocate:
-Ventricular paroxysmal
tachycardia
-Paroxysmal tachycardia from the A-V node
- Atrial paroxysmal
tachycardia
CLINIC OF PAROXISMAL TACHYCARDIA
-dizzinessheartbeat
- a feeling of constriction of the heart
-noise in the head
-phasia, hemiparesis
-sweating
-nausea
-flatulence
ECG - SIGNS OF VENTRICULAR PAROXISMAL TACHYCARDIA
Activity independent of QRS complexesatria in the form of P waves
"Drainage" complexes (occur frequently) with
the appearance of QRS complexes other than
previous, due to the imposition of the supraventricular
and ventricular complexes
The presence before and after a ventricular attack
extrasystoles
ECG SIGNS OF NODULAR PAROXISMAL TACHYCARDIA
In leads II, III and aVF negative P waves ",located behind the QRS complexes "or
merging with them and not recorded on the ECG
Normal unchanged ventricular complexes
QRS
ECG SIGNS OF ATRIAL PAROXISMAL TACHYCARDIA
Presence in front of each ventricularcomplex QRS "reduced,
deformed, two-phase or
negative P wave ".
Normal unchanged ventricular
QRS complexes
Treatment of paroxysmal tachycardia
Emergency I / O antiarrhythmics,effective in all forms of paroxysms.
With prolonged paroxysms of tachycardia, not
drug-controlled
conduct electro-pulse therapy.
Long-term anti-relapse therapy
paroxysmal tachycardia is performed
antiarrhythmic drugs
disopyramide, etmosine, etacizin,
amiodarone (cordarone), verapamil, etc.),
as well as cardiac glycosides (digoxin,
celanide).
Installation of a pacemaker, RFA at
severe course
Interventional research and treatment methods in arrhythmology
Intracardiac electrophysiologicalstudy.
Radiofrequency catheter ablation.
Nonfluoroscopic 3D
mapping of the heart.
Standard placement of EFI catheters
Standard placement of EFI cathetershigh PP
bundle of His
right ventricle
coronary sinus
RFA
RFA method
Used electrical unmodulatedsinusoidal current 300-750 kHz.
Monitoring of temperature, impedance,
electrograms from the tip of the ablative electrode.
Damage generated is controllable, causing
limited damage at the point of contact of the tip
an electrode with a myocardium 3-4 mm around it.
The procedure is painless, the size of the damage is not
increase over time.
Damage size is proportional to size
catheter, power and duration of the supplied
energy.
If you have played a poker tournament at least once in your life, you have probably come across such a concept as "re-entry". Moreover, it exists both in online poker and in live tournaments, and it is used quite often. So what is poker re-entry? What is it for, and is it worth using it during a tournament? Let's figure it out ...
Definition of the term
Poker re-entry (English "re-entry" - "re-entry")- this is the player's opportunity to make an additional purchase of chips in the event that he loses his entire initial stack. Basically, this term means the same thing as. But is it really useful to buy additional chips in a tournament? Or is it better to get up and leave the tournament if you're not so lucky today?
In fact, poker re-entries are useful for tournaments for two reasons:
- The prize fund of the tournament is accelerated.
- Professionals' chances of success increase.
Let's take a closer look at each of these reasons.
Prize fund growth
Of course, if players can buy additional chips every time they lose their stack, then the prize pool of the tournament will slowly but surely grow, which means that the interest of other participants in this tournament will also increase. Moreover, interestingly, as the prizes in the tournament increase, the number of players who have made a purchase also increases.
The logic here is quite simple. Players see the tournament prize pool growing, and even if they lose their starting stack, they try again by re-entering and buying more chips. Moreover, in modern tournaments, an unlimited number of additional purchases is most often introduced, which means that you can buy additional chips over and over again, accelerating the tournament prize pool.
Improving the chances of professionals
Today, even beginner poker players know that any hand can win a hand. You can go all-in with two aces and end up losing to someone with 7-2 offsuit. And this happens much more often than you used to think. And that is why re-entry in poker can increase the chances of professionals who play according to strategy, and reduce the chances of successful beginners, since luck cannot smile at them forever.
Accordingly, the mathematical expectation grows between a beginner player and a regular who acts according to a previously developed strategy.
What's in practice?
However, everything that we have said above is purely theoretical. In practice, the situation is somewhat different. After all, it is human nature to make mistakes, and even experienced players can sometimes start looking for the reasons for their failures in themselves, even if they lost solely by chance. Therefore, we do not recommend doing re-entry more than twice in one tournament. Because the more “additional purchases” you make, the greater your desire to “recoup” will be. Accordingly, you yourself will start tilting, which in the end will not bring anything good to your bankroll.
On the other hand, the size of the re-buy is always the same, and usually it is equal to the size of the player's starting stack at the beginning of the tournament. That is, if at the very beginning of the tournament each of the players received a thousand chips, then for the additional purchase you will also receive a thousand game chips. However, it should be understood that at the beginning of the tournament the blinds were much smaller, and the players' stacks were approximately the same.
And if you buy in the middle of the tournament, then your thousand chips will cost, at most, several big blinds, while your opponents will have stacks of tens of thousands of chips. Accordingly, you are unlikely to be able to perform well with such a limited stack.
Fortunately, you can only re-enter in poker until a certain period, after which the game "knockout" begins.
Excitation wave re-entry (mechanism re-entry ) - this term denotes a phenomenon in which an electrical impulse, making a movement in a closed circle (loop, ring), returns to the place of its origin (circus movement).
Distinguish macro re-entry(macrorientry) and micro re-entry(microrientry). With this division, the dimensions of the circle (loop) in which the pulse is re-entered are taken into account.
To form macro re-entry certain conditions are required:
1.existence of 2 channels separated functionally or anatomically (one-sided blockade of one of them);
2.the presence of a potentially closed loop of impulse movement... The circular movement of impulses occurs mainly in the places of branching of the fibers of the conducting system, the presence of anastomoses between them, the zones of contacts of the ends of the Purkinje fibers with muscle cells.
3.deceleration of the pulse propagation speed, so that at no point in the loop does the excitation wave meet the refractory zone.
The incoming wave of excitation slowly moves along branch 1, but does not enter branch 2 (Fig. 3), where there is a section of unilateral blockade.
A slow moving impulse causes depolarization of the entire muscle segment with the formation of an action potential. Then it penetrates retrogradely into branch 2, exciting it all over.
By this moment, the refractoriness of branch 1 disappears, into which the impulse enters again. A repeated circle begins with premature excitation of the muscle segment.
If such a process is limited to one re-entry , then an extrasystole is recorded on the ECG.
If the circular motion of the impulse exists for a long time, a series of premature ECG complexes occurs (i.e., an attack of tachycardia).
With electrical pacing of the heart section, where the re-entry loop exists, the entire myocardium is simultaneously transferred to a state of absolute refractoriness, and the circulation of the impulse stops. This is most clearly manifested during cardiac defibrillation.
Described mechanism macro re-entry is believed to be the basis of atrial flutter.
Rice. 3. Mechanism diagram re-entry. The site of the myocardium - the posterior wall of the left ventricle: 1 - orthograde propagation of the impulse; 2 - unilateral blockade of conduction; 3 - zone of damaged myocardium with delayed retrograde propagation of excitation
With another kind of re-entry - micro re-entry - the movement of the impulse occurs along a small closed ring, not associated with any anatomical obstacle. Apparently, many complex tachyarrhythmias, in particular fibrillations, are associated with a mechanism micro re-entry.
Thus, the essence of the mechanism re-entry consists in the fact that the excitation impulse re-enters the area of the myocardium or the conducting system. Circulation of the excitation wave is created.
Abnormal conduct... Abnormal conduction occurs when excitation to the ventricles comes in two ways: 1. through the AV node and 2. along the Kent's bundle (an abnormal additional pathway of impulse conduction between the atria and ventricles). Excitation spreads faster along the Kent's bundle and reaches the ventricles before the impulse passing through the AV node. In this case, there is a mutual overlap of the conducted impulses and in half of the cases, ventricular tachyarrhythmia occurs ( with Wolff-Parkinson-White indrome ) .
Arrhythmias as a result of a violation of automatism
Types of arrhythmias. Depending on the place (topography) of the generation of an abnormal excitation pulse, nomotopic and heterotopic arrhythmias are distinguished.
Nomotopic arrhythmias... Occur in the CA node. These include sinus tachycardia, sinus bradycardia, and sinus arrhythmia.
Heterotopic arrhythmias... They arise outside the CA-node and are caused by a decrease in the automatism of the overlying centers of rhythmogenesis. Manifestations: nodal (atrioventricular), idioventricular (ventricular) rhythms, etc. (migration of the supraventricular pacemaker; atrioventricular dissociation).
Nomotopic arrhythmias.
Sinus tachycardia- an increase at rest in the frequency of generation of excitation pulses in the CA-node more than 90 per minute with equal intervals between them (Fig. 4).
Electrophysiological mechanism: acceleration of spontaneous diastolic depolarization of CA-node cell membranes.
1. Activation of the effect on the heart of the sympathetic-adrenal system: stress, physical activity, acute arterial hypotension, heart failure, hyperthermia, fever.
2. Reducing the effect of the parasympathetic nervous system on the heart: damage to parasympathetic nerve formations or myocardial cholinergic receptors.
3. Direct action of damaging factors of various nature on the cells of the CA-node (myocarditis, pericarditis, etc.).
Rice. 4. Sinus tachycardia. Normal P waves and QRS complexes Heart rate is more than 100 beats / min.
The value of sinus tachycardia. On the one hand, it is a compensatory-adaptive reaction aimed at maintaining the IOC adequate to the needs of the body under conditions of stress, acute blood loss, hypoxia, etc.
On the other hand, tachycardia contributes to an increase in myocardial oxygen demand and a decrease in the duration of heart diastole (prolonged severe sinus tachycardia can lead to insufficiency of the coronary arteries and ischemic damage to the myocardium).
Sinus bradycardia- a decrease in the frequency of generation of excitation pulses by the CA-node at rest below 60 per minute with equal intervals between them (Fig. 5).
Electrophysiological mechanism: slowing down of spontaneous diastolic depolarization of CA-node cell membranes.
- Activation of the effects of the parasympathetic nervous system on the heart. Under physiological conditions, this is observed in trained athletes. It can be observed with stomach and duodenal ulcers, intestinal and renal colic; due to increased intracranial pressure with meningitis, encephalitis. Strengthening of vagal influences can occur reflexively when straining (Valsalva test); pressure on the eyeballs (Aschner's reflex), as well as in the area of the carotid artery bifurcation (Hering's reflex) and in the area of the solar plexus.
- Reducing sympathetic-adrenal effects on the heart. Sinus bradycardia can develop with a decrease in the adrenoreactive properties of the heart (for example, the action of β-blockers), disruption of higher nervous activity (neurosis), damage to brain structures (for example, the hypothalamus), pathways, intracardiac ganglia and the endings of sympathetic nerve fibers in the myocardium.
- Direct effect of damaging factors on the cells of the CA-node (mechanical injury, ischemia in the CA-node zone, intoxication).
Hemodynamic disturbances in severe sinus bradycardia are due to a decrease in cardiac output.
Rice. 5. Sinus bradycardia. Normal P waves and QRS complexes; decreased heart rate< 60 уд/мин.
Sinus arrhythmia- violation of the heart rhythm, characterized by uneven intervals between individual excitation impulses emanating from the CA-node (Fig. 6).
Electrophysiological mechanism: fluctuations in the rate (increase / decrease) of slow spontaneous diastolic depolarization of pacemaker cells.
Reasons: fluctuation or violation of the ratio of sympathoadrenal and parasympathetic effects on the heart.
Sinus arrhythmia associated with the phases of breathing is called respiratory arrhythmia, observed in newborns, in healthy young people.
Rice. 6. Sinus arrhythmia. Normal P waves and QRS complexes.
SA-node weakness syndrome(bradycardia – tachycardia syndrome) - the inability of the CA-node to provide a heart rhythm adequate to the level of vital activity of the body.
Electrophysiological mechanisms: violation of the automatism of the CA-node, especially the phases of repolarization and spontaneous diastolic depolarization, the emergence against this background of heterotopic (ectopic) foci of rhythmic activity.
Reasons: imbalance of sympathetic-adrenal and parasympathetic influences on the heart with a predominance of the latter (for example, in neurotic conditions), as well as death or dystrophy of CA-node cells (for example, in heart attack, inflammation).
It is manifested by periodic or constant sinus bradycardia, alternating with sinus tachycardia, flutter or atrial fibrillation, slow restoration of sinus rhythm after the cessation of sinus tachycardia, episodes of stopping the CA node (Fig. 7).
Rice. 7. Syndrome of weakness of the CA-node. The episode of stopping the CA-node.
Sinus bradycardia is accompanied by a decrease in cardiac output, a decrease in blood pressure and loss of consciousness due to cerebral ischemia at a heart rate of less than 35 beats per minute. Cessation of the generation of impulses by the SA-node (syndrome of stopping the SA-node) for more than 10-20 seconds causes loss of consciousness. A significant decrease in cardiac output in severe bradycardia can lead to a decrease in perfusion pressure in the coronary arteries and the development of coronary insufficiency.
Heterotopic arrhythmias. Ectopic arrhythmias (heterotopic rhythms) occur outside the CA-node, due to the predominance of automatism of the underlying centers of rhythmogenesis. Decrease in activity or cessation of activity of the CA-node as a result of its functional or organic damage creates conditions for the activation of automatic centers of the second and third orders. The ectopic (in relation to the SA-node) focus with its more rare rhythm assumes the function of a pacemaker. In this regard, rhythm disturbances of this type are called heterotopic or replacement (sinus rhythm) arrhythmias.
Heterotopic arrhythmias: slow atrial rhythm, junctional rhythm (AV rhythm), idioventricular rhythm.
Knot rhythm - this is a disorder in which the role of the pacemaker is taken over by the atrioventricular node (Fig. 8). With this pathology, the heart rate decreases to 40-60 beats / min. The causes of such a violation of automatism are most often intoxication, which leads to weakness of the sinus node, or blockade of the intra-atrial impulse conduction. The degree of bradycardia that occurs depends on which part of the AV node (upper, middle or lower) becomes a pulse generator: the lower the pulses are generated, the less frequent their frequency. General hemodynamics is also disturbed, for which a rare atrioventricular rhythm may be insufficient.
Rice. 8. Atrioventricular rhythm. P wave inversion, heart rate 40-60 beats / min.
Idioventricular rhythm(ventricular, Fig. 9) - this is a violation in which the role of the pacemaker is taken by the legs of the bundle of His or Purkinje fibers. The rhythm is cut down to 10-30 bpm. Such a violation of automatism develops when the sinus and atrioventricular nodes are damaged and leads to a violation of central hemodynamics, which can result in the death of the patient.
Rice. 9. Idioventricular rhythm. Absence of P wave, PQ interval; Heart rate 10-30 beats / min.
