Signs of atrial arrhythmia on ECG
• Typically early appearance of a slightly deformed R-wave. There is no compensatory pause.
• The frequency of atrial beats in IHD is increased. Relatively often, atrial extrasystoles appear in vegetative-vascular dystonia.
Normally, people with a healthy heart have sinus rhythms. This means that normal physiological arousal occurs automatically in the sinus node and the heart contracts in time with the pulses generated in the sinus node. This phenomenon is called the automaton heart.
At a sinus rhythm normal teeth P and the QRS complexes are registered through identical intervals of time.
Heart rate is normal, as already mentioned, is about 60-80 beats per minute. In sinus bradycardia, the heart contracts with a frequency of less than 60 beats per minute, and in sinus tachycardia, the heart contracts with a frequency of more than 100 beats per minute.
Atrial premature beats are characterized by the premature appearance of individual atrial contractions. Since atrial extrasystoles appear as a result of pathological excitation in some part of the atrium wall, the P wave, which reflects the onset of pathological atrial excitation, is deformed and has not a semilunar shape inherent in it, but a pointed or bizarre and is located above the isoline (positive) ; sometimes the P wave is biphasic.
The remaining intervals and the teeth on the ECG are normal, in particular the atrial extrasystoles, do not affect QRS complexes, since the conduction of arousal from the atria to the ventricles is not disturbed. Only with very early atrial extrasystoles, some deformation of the QRS complexes is possible due to aberrant excitation in the ventricular myocardium.
Another feature of atrial premature beats is that the total duration of the RR interval before and after the extrasystoles is less than twice the RR interval. The RR interval is the time interval between two teeth of R. In atrial extrasystoles, unlike ventricular, there is no compensatory pause. This is due to the fact that the excitation of the sinus node is suppressed in the retrograde direction by the atrial extrasystole and premature atrial excitation occurs.
With very early extrasystoles, the AV node may be still in the period of absolute refractoriness, and the conduction of arousal into the ventricles is blocked. In this case, the P wave is recorded, which, however, is not followed by the ventricular QRS complex (blocked atrial extrasystoles). This is a special form of atrial arrhythmia.
Frequent atrial premature beats, especially with polymorphic P wave, often turns into atrial fibrillation.
Single atrial extrasystoles can also be recorded in people with a healthy heart, especially in vegetative dystonia, while frequent atrial extrasystoles are a sign of pathology (for example, IHD, cardiomyopathy, heart defects).
ECG features in atrial arrhythmia:
• Premature appearance of the P wave on the ECG
• Easy deformation of the P wave
• Lack of compensatory pause
• Background heart disease: vascular dystonia and ischemic heart disease
• Therapy: beta-adrenergic receptor blockers, verapamil, quinidine
ECG with extrasystole of the heart
The terms “ectopic complex”, “extrasystole” and “premature contraction” are synonymous from a practical point of view. They denote the premature impulse that occurs during the cardiac cycle in the atria, the AV connection, or the ventricles.
Atrial ectopic impulse is usually conducted to the ventricles through the AV-junction and along the legs of the bundle of His in the usual way, as a result of which a narrow QRS complex is formed. With a certain degree of prematurity of the atrial ectopic impulse, the P wave may overlap the T wave of the preceding complex.
Ventricular ectopic impulse is not carried out through the ventricles through the His-Purkinye fast-conducting system. As a result, the forming complexes are wide (> 0.12 s) and have an odd shape, and the P wave does not precede them. Ventricular premature beats are often idiopathic, but if it is caused by heart disease, this is associated with an increased risk of cardiovascular death, which does not decrease when antiarrhythmic drugs are prescribed.
By definition, an extrasystole should occur earlier than the next complex in the cardiac cycle is expected. Thus, the interval between the ectopic and anterior complex, i.e. adhesion interval, always shorter than the length of the cycle of the main rhythm. If this fact is ignored, then other complexes of a modified configuration, such as slipping complexes and complexes with an intermittent blockade of the bundle of the bundle of His, can be mistakenly interpreted as an extrasystole.
The location of the source of beats can be established by careful analysis of the ECG. ECG recordings in one lead are not enough for this. Identification of diagnostically important signs requires careful consideration of ECG recordings performed simultaneously in several leads.
What is sinus rhythm and sinus tachycardia on an ECG? Diagnostics
Normal sinus rhythm is the correct rhythm with a frequency of 60-100 per 1 min, originating from the sinus node. If the duration of a heartbeat cycle decreases with inhalation and increases with expiration, this condition is called phase (respiratory) sinus arrhythmia. If duration fluctuations do not depend on the rhythm of breathing – non-phase.
Sinus tachycardia is the result of the automatic discharge of a sinoatrial pacemaker with a frequency exceeding 100 contractions per minute. Characterized by the presence of normal sinus teeth P with a frequency usually not exceeding 130-140 per 1 min at rest, although it is possible and reaching 180-200 per 1 min, especially during exercise.
Sinus tachycardia is a normal physiological response to stress or emotional stress, or a reaction caused by drugs such as adrenaline, ephedrine, or atropine. Alcohol, caffeine or nicotine can also trigger sinus tachycardia. Constant sinus tachycardia usually indicates a latent disease (such as heart failure, pulmonary embolism, hypovolemia, or hypermetabolic state).
Vagal techniques (carotid sinus massage or Valsalva maneuver) help to distinguish sinus tachycardia from other supraventricular tachycardias (NCT). A gradual decrease in elevated frequency, followed by a return to it, is characteristic of sinus tachycardia. In contrast, carrying out vagal samples can abruptly cut off other NZhT or block conduction through the AV node.
Sinus tachycardia usually does not require special treatment; Therapy should be directed towards the underlying disease. B-adrenergic blockers are often effective in slowing the rhythm. However, first of all it is necessary to make sure that tachycardia is not compensatory, as in heart failure.
Performing stress tests
Performing exercise tests is useful for assessing rhythm disturbances caused by physical exercise, especially ventricular extrasystoles (VE) and ventricular tachycardias, for distinguishing pathological mechanisms caused by autonomic dysfunction and structural changes, as well as for diagnosing lesions of the sinus and atrioventricular nodes and for evaluating frequency-dependent cuts arrhythmogenic effects of antiarrhythmic drugs.
Samples with a load are also used for an approximate assessment of the refractory period of additional pathways in patients with Wolff-Parkinson-White syndrome. Intracardiac electrophysiological examination is used to diagnose rhythm and conduction disturbances when ECG imaging from the body surface is insufficient. Multielectrode catheters are located at various points inside the heart, allowing you to find out the sequence in which the excitation is distributed through the atria, the AV connection and the ventricle. It is also possible to identify the localization of pathological pathology, the source of supraventricular tachyarrhythmias and explore the mechanisms of ventricular tachyarrhythmias. In addition, using the electrophysiological study, you can determine the localization of the atrioventricular block (AV-blockade).
During the operation, mapping of the site of origin of both supraventricular and ventricular tachyarrhythmias can be performed using probes guided by the hand of the researcher or special multi-contact electrodes in order to establish the localization of the area for surgical destruction. Previously, the treatment of cardiac arrhythmias was limited to pharmacological and surgical methods.
However, surgical methods for mapping most of the supraventricular arrhythmias and certain types of ventricular arrhythmias are replaced by mapping with a catheter and destruction performed in the electrophysiology department. Implantable devices are often used for long-term treatment of both tachy and bradyarrhythmic conditions.
Principles of heart rhythm analysis – diagnosis of arrhythmias
Effective treatment of cardiac arrhythmias and conduction disorders requires the accurate diagnosis of specific rhythm disturbances, an analysis of the clinical situation in which they occur, and the definition of a safe and effective goal of therapy. Recognition and subsequent correction of any hemodynamic, electrolyte, metabolic and respiratory disorders that aggravate the condition are extremely important for the treatment of arrhythmias.
Rhythm disorders may be primary or secondary. Primary disorders are the result of electrophysiological disorders caused by the pathological process; they are causally not associated with significant changes in the circulatory system.
In contrast, when the pathological process leads to hemodynamic disturbances, which in turn trigger or contribute to the occurrence of electrophysiological disorders, the arrhythmia is called secondary. Prevention or control of secondary arrhythmias is carried out using monotherapy with hemodynamically active agents or their combination with antiarrhythmic drugs.
A standard electrocardiographic study using 12 leads and analysis of longer fragments, taken specifically for rhythm assessment, are the most readily available means of diagnosing cardiac rhythm disorders. The study of the P wave, the morphology of the QRS complex and their relative position may be sufficient for accurate diagnosis of arrhythmia.
If a standard electrocardiogram (ECG) is not sufficiently informative, special lead systems (bipolar esophageal – for recording activity of the left atrium) or an intraatrial catheter with an electrode – for recording right atrial activity can be used to identify the P teeth and obtain additional information.
Constant monitoring of the cardiac rhythm in the inpatient or use of recording devices with simultaneous recording of indicators from two leads (usually II and MCL-1 in the midclavicular line in the outpatient) expands diagnostic capabilities. When rhythm disturbances occurring in this patient only occasionally, the use of recording devices is included, which are switched on as needed by him or by others. This will allow the device to start working during an attack of arrhythmia and will subsequently enable the doctor to process the data obtained.
Signs of sinoatrial blockade on ECG – SA-blockade
Grade I SA blockade: indistinguishable on a surface ECG.
CA blockade II degree:
• Type I: the gradual shortening of the PR interval leading to the loss of the P wave and the QRS complex
• Type II: repeated loss of P teeth and QRS complexes
CA-blockade of III degree: consistent loss of several P-waves and QRS complexes at once
Sinoatrial blockade is a relatively rare arrhythmia. It is characterized by a violation of the conduction between the sinus node and the atrium. As in the case of the AV-blockade, there are 3 types of SA-blockade.
I. SA blockade of I degree
The time of excitation from the sinus node to the atria is extended. However, this elongation on the surface ECG is not visible, and the blockade itself has no clinical significance.
Ii. SA-blockade of the II degree SA-blockade of the II degree, type I (SA-periodics of Wenckebach). Rarely observed. Similar to AV-blockade of the II degree (Wenkebach period), as the time of sinoatrial conduction increases gradually, the heart complex (P wave and QRS complex) falls out. The pause that arises is shorter than the double PP interval.
CA blockade of the II degree, type II. Characterized by occasional loss of sinoatrial conduction. On an electrocardiogram it is shown by loss of a tooth P and the QRS complex corresponding to it.
Sinoatrial blockade of the II degree (type II) is sometimes combined with another rhythm disorder, in particular, with sinus arrhythmia, which complicates the interpretation of the ECG. With a significant reduction in the frequency of ventricular contractions, it is necessary to discuss the issue of implantation of a pacemaker.
Indications for ablation of the heart and its complications
Before and after catheter ablation, it is imperative that an electrophysiological study be performed. Having established the localization of a pathological arrhythmogenic focus, according to strict indications, its ablation is performed with a high frequency current (approximately 500 kHz). In clinical practice, catheter ablation is successfully performed for the following tachyarrhythmic disorders:
• atrial fibrillation;
• atrial flutter;
• an extra bundle of conduction in WPW syndrome;
• reciprocal AV-node tachycardia;
• ventricular tachycardia.
Complications of catheter ablation include: bleeding, thrombosis, embolism, cardiac tamponade. In reciprocal AV-node tachycardia, complete AV-blockade can sometimes develop, in which implantation of a pacemaker is necessary (approximately in 1% of cases).
Catheter ablation is indicated primarily for patients in whom the arrhythmia is resistant to drug therapy and is accompanied by severe clinical symptoms.
Electrophysiological examination (EFI) of the heart is normal
For the first time, the Electrogram of the His bundle (PG) was able to register Puech and Latuor in 1957 in a patient with the Fallot triad. Under the electrophysiological study (EFI) understand a special invasive method for the diagnosis of arrhythmias, namely intracardial electrography, first of all, electrocardiography PG and programmed heart stimulation.
When EFI recorded the following potentials:
• A ‘- high potential of the right atrium;
• A – deep potential of the right atrium;
• CS – coronary sinus – representative of the left atrial potential;
• V – ventricular potential;
• intervals between them.
After recording the indicated potentials and intervals, they proceed to intracardial stimulation of the atria and ventricles with increasing frequency. This allows to clarify the nature of the various tachyarrhythmias. With the help of mapping, it is possible to accurately determine the localization of the arrhythmogenic focus in the following parts of the heart: atrium, AV-node, additional conduction path, ventricles. Then find out whether catheter ablation is possible. When bradyarrhythmia value EFI is small.
Heart rhythm disorders
The mechanisms of the arrhythmia are:
• Ectopic focus of arousal:
– increase automatism
– the appearance of a pathological focus of automatism
– trigger activity
• Conduction disorders: re-entry mechanism (re-entry of excitation waves) Causes of heart rhythm disturbances are diverse and complex:
• myocardial ischemia (CHD)
• infection (myocarditis)
• cardiomyopathy (dilated, hypertrophic)
• electrolyte imbalance (hypo-and hyperkalemia)
• endocrine diseases (hypo-and hyperthyroidism)
• pulmonary heart
• mechanical factors (congenital and acquired heart defects, trauma)
• intoxication (cardiac glycosides, alcohol, nicotine, antiarrhythmic drugs)
• mitral valve prolapse
• mental disorders (depression)
Therapy for cardiac arrhythmias will be discussed separately below. Most of the ECG with a rhythm disturbance listed here was recorded at a speed of movement of a paper tape of 25 mm / s. It is indicated on the ECG itself and in the explanatory notes to the figures. For a better understanding of ventricular tachycardia and ventricular fibrillation, ECG was recorded at a speed of 50 mm / s.
Heart rhythm disorders – causes, mechanisms of development
Diagnosis of cardiac arrhythmias is one of the tasks of electrocardiography since the invention of this method. Usually, a rhythm disturbance can be correctly interpreted by an ECG recorded in one lead, for example, lead II. In recent years, the problem of rhythm disturbances has become increasingly urgent.
With the advent of electrotherapy in the 1960s, carried out, on the one hand, by using an electric defibrillator and implantable pacemaker, on the other, by new antiarrhythmic drugs and interventional electrophysiology, including catheter ablation, the treatment of heart rhythm disturbances acquired a new dimension.
To apply these new treatments, an accurate analysis of the heart rhythm was required. Thus, at present, various methods are used for the study of patients, for example, long-term ECG monitoring, exercise ECG test, GHG electrography and electrical stimulation of the atria and ventricles, as well as electrophysiological research, which will be mentioned separately.
The main prerequisite for successful treatment of cardiac arrhythmias is their correct diagnosis. Often, the rapid recognition of severe arrhythmia allows you to prescribe a salvage therapy; cases of rapid and successful treatment of cardiac arrhythmias are observed in clinical practice more often.
At the same time, even today, ECG is a routine method for diagnosing cardiac arrhythmias, which is of great importance in clinical practice and makes it possible to determine the need for research with more complex and modern diagnostic methods. In the mechanism of arrhythmia, a role is played by a violation of myocardial excitability or a violation of its conductivity.
Currently, a number of theories have been proposed to explain the pathogenesis of cardiac arrhythmias, for example:
• increase of heart automatism (for example, with sympathicotonia);
• activation of the ectopic focus of excitation (for example, during ischemia);
• trigger activity (change in aftereffect potentials);
• re-entry of the excitation wave (re-entry mechanism).
These theories can be divided into 2 groups: one group explains the occurrence of arrhythmia by impaired excitability of a specific area of the myocardium, such as the atrium or ventricle, the other by impaired myocardial conductivity and the formation of a circular excitation wave.