(3)the position of the P wave with respect to the ventricular complex depends on the rate of propagation of the excitation wave onto the atria and the ventricles;
(4)shape of QRS is normal or slightly deformed;
(5)incomplete compensatory pause.
Ventricular extrasystole (ventricular ectopic beat)
Heart excitation order changes sharply in ventricular extrasystole. The ventricular impulse is not usually transmitted retrogradely through the AV node and the atria are not therefore excited. Second, the ventricles are not excited synchronously (as in normal cases), but one after another, i.e. that ventricle is excited first where the ectopic focus is located. The time of excitation of the ventricles is therefore longer and the QRS complex wider. The ventricular extrasystole is followed by a long (full) compensatory pause (except in interpolated extrasystoles): the atria are only excited by the sinus impulse that follows the extrasystole because the ventricles are refractory at this moment. The P wave corresponding to the atrial excitation is "lost" in the disfigured extrasystolic ventricular complex. Only next (second to the extrasystole) sinus impulse excites both the atria and the ventricles, while the EGG shows a normal cardiac complex.
ECG signs of ventricular extrasystole (Fig. Suppl. 19):
(1)premature appearance of the ventricular complex;
(2)absence of the P wave;
(3)deformation of QRS complex due to increased voltage and length;
(4)the shape and the height of the T wave changes, its direction is opposite to the maximum wave of the QRS complex (T wave is negative if the R wave is high, and positive if the S wave is deep;
(5)сomplete compensatory pause.
Sometimes it is possible to determine in which particular ventricle the ectopic focus is located. This can be done from the configuration of the ventricular complex in various ECG leads. Left-ventricular extrasystole is characterized by a high R wave in III standard lead and the deep S wave in I lead. In right-ventricular extrasystole, the extrasystolic complex is characterized by a high R wave in I lead, and a deep S wave in the III.
Chest leads are very important for the topic diagnosis of ventricular extrasystole. Left-ventricular extrasystoles are characterized by the appearance of the extrasystolic complex with a high R wave in the right chest leads and a broad or deep S wave in the left chest leads. In right-ventricular extrasystole, on the contrary, the deep S wave is recorded in the right chest leads, and a high S wave in the left chest leads.
Paroxysmal tachycardia (PT)
Paroxysmal tachycardia is a sudden acceleration of the regular cardiac rhythm with more than three complexes (to 140-250 beats per min) resulting
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from an abnormal ectopic impulses or re-entry mechanism in the atria, AV junction and ventricles.
At attack of paroxysmal tachycardia may last from several seconds to a few days and terminate just as unexpectedly as it begins. During an attack, all impulses arise from a heterotopic focus because its high activity inhibits the activity of the sino-atrial node. Paroxysmal tachycardia (like extrasystole) may occur in subjects with increased nervous excitability, in the absence of pronounced affections of the heart muscle, but it arises more likely in the presence of a severe heart disease (e.g. myocardial infarction, heart defects or cardiosclerosis).
During an attack of paroxysmal tachycardia, the patient feels strong palpitation, discomfort in the chest, and weakness. The skin turns pale, and if attack persists, cyanosis develops. Paroxysmal tachycardia is characterized by swelling and pulsation of the neck veins, because during accelerated pulse (to 180-200 per min) the atria begin contracting before the ventricular systole ends. The blood is ejected back to the veins from the atria to cause pulsation of the jugular veins. Auscultation of the heart during an attack of paroxysmal tachycardia reveals decreased diastolic pause, whose length nears that of the systolic one, and the heart rhythm becomes fetal (pendulum). The first sound increases due to insufficient ventricular diastolic filling. The pulse is rhythmic, very fast, and small. Arterial pressure may fall. If an attack persists (especially if it develops in the presence of a heart disease) symptoms of cardiac insufficiency develop.
Like in extrasystole, the heterotopic focus in paroxysmal tachycardia may be located in the atria, the atrioventricular node, and the ventricles. It is possible to locate the focus only by electrocardiography: a series of extrasystoles follow on an ECG at regular intervals and at a very fast rate
Classification according to the site of origin:
-atrial, atrioventricular (nodal) (common name of
supraventricular) PT; |
- ventricular PT. |
Supraventricular paroxysmal tachycardia characteristics (Fig. Suppl.
20):
-Sudden acceleration of the regular cardiac rhythm to 140-250 per min and sudden deceleration of HR;
- QRS shape is not changed as rule (or slightly deformed);
-P wave – disfigured (or biphase, negative) prior to QRS in atrial PT or follows QRS in AV nodal PT, or is not differed.
Ventricular paroxysmal tachycardia is characterized (Fig. Suppl. 21): -Sudden acceleration of the regular cardiac rhythm to 140-220 per min
and sudden deceleration of HR;
-QRS shape is changed and broadened (>0.12 s); ventricular complexes are similar to those in ventricular extrasystoles;
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-P waves not correspond to ventricular complexes QRS (atrioventricular dissociation) or are not differed on ECG.
Torsade de pointes is a one of the most serious variants of ventricular PT characterized by a continuously changing vector of QRS, may be as predictor of ventricular flutter, ventricular fibrillation and cardiac arrest.
Ventricular flutter and fibrillation
Ventricular flutter usually appears as a sinusoidal wave with a rate between 150 and 300 per minute. Ventricular fibrillation is a rapid irregular ventricular rhythm due to multiple re-entrant activities associated with essentially zero cardiac output. It is a variant of cardiac arrest (Fig. Suppl. 23). The absence of adequate ventricular systole and contraction of separate ventricular muscles cause pronounced disorders in the hemodynamic and rapidly lead to death. Ventricular fibrillation occurs in grave affections of the myocardium (diffuse myocardial infarction, etc.).
The patient loses consciousness, becomes pallid, the pulse and arterial pressure become indeterminable. The ECG shows abnormal complexes on which separate waves are distinguished with difficulty
Ciliary arrhythmia
Ciliary arrhythmia includes two variants: atrial fibrillation and atrial flutter. According to course of ciliary arrhythmia is divided on paroxysmal and persistent forms of ciliary arrhythmia.
Atrial fibrillation
Atrial fibrillation is rapid irregular atrial rhythm due to multiple reentrant wavelets. Atrial fibrillation otherwise known as complete or absolute arrhythmia. It arises in cases with suddenly increased excitation of the myocardium and simultaneous conduction disorders. The sino-atrial node fails to function as the pacemaker and many ectopic excitation foci (to 600800 per min) arise in the atrial myocardium, which becomes only possible with a marked shortening of the refractory period. Since conduction of these impulses is difficult, each of them only excites and causes contraction of separate muscular fibres rather than the entire atrium. As a result, minor contractions develop in the atrium (atrial fibrillation) instead of adequate atrial systole.
Only part of the impulses is transmitted to the ventricles through the AV node. Since conduction of atrial impulses is irregular, the ventricles contract at irregular intervals to cause complete arrhythmia of the pulse.
Depending on the conductability of the AV node and according to rate of ventricular contractions three forms of atrial fibrillation are distinguished:
-normasystolic form - 60-100 per min; -tachysystolic form ->100 per min;
-bradysystolic form - <60 per min.
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Fibrillation is characteristic of mitral heart diseases (especially of mitral stenosis), coronary atherosclerosis, thyrotoxicosis, etc. Fibrillation may occur as a permanent symptom or in attacks of tachyarrhythmia. Clinically fibrillation (bradyarrhythmia) may cause no subjective symptoms. Tachyarrhythmia is usually characterized by palpitation. Examination of the heart reveals complete irregularity of the heart contractions. Variations in the length of diastole account for variations in ventricular filling and hence in the intensity of the heart sounds. The pulse is also arrhythmic, pulse waves vary in height (irregular pulse), and pulse deficit often develops in frequent heart contractions.
ECG characteristics of atrial fibrillation (Fig. Suppl. 24):
(1)P wave disappears,
(2)multiple small irregular f waves,
(3)QRS ventricular complexes follow are irregular, their shape does not change.
Atrial flutter
Atrial flutter is a rapid regular atrial rhythm due to a constant welldefined macro-reentrant circuit in the right atrium. Atrial flutter is the upset cardiac rhythm, which nears in its pathogenesis to fibrillation. As distinct from fibrillation, the number of impulses arising in fluttering atria does not usually exceed 250-300 per min, and their conduction through the AV node is usually rhythmic. As a rule, not all atrial impulses are conducted to the ventricles. Each other, third or fourth impulse, is only conducted to the ventricles since partial (incomplete) atrioventricular block develops simultaneously. Conduction of the AV node sometimes constantly changes: each other impulse is now conducted; then the rhythm changes to conduction of each third impulse, and the ventricles contract arrhythmically. Like fibrillation, atrial flutter occurs in mitral defects, coronary atherosclerosis, and thyrotoxicosis; flutter sometimes develops in poisoning with quinine or digitalis.
Patients with accelerated heart rate (high conduction of the AV node) complain of palpitation. Examination reveals tachycardia that does not depend on the posture of the patient, exercise or psychic strain, since the sino-atrial node does not function as the pacemaker in atrial flutter (being governed by extracardial nerves). Heart contractions are arrhythmic in patients with varying conduction of the AV node.
ECG characteristics of atrial flutter (Fig. Suppl. 25):
(1)high F waves instead of the normal atrial P waves;
(2)The number of F waves preceding each ventricular complex depends on the AV conduction;
(3)QRS complexes follow at regular intervals.
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Conduction disorders (heart blocks)
Heart blocks are delayed conduction or complete absence of conduction in some department of cardiac conduction system.
Transmission of the impulse may be blocked at any part of the heart's conduction system. Block may develop in inflammatory, dystrophic, and sclerotic affections of the myocardium (e.g. rheumatic and diphtheritic myocarditis or cardiosclerosis). The conduction system may be affected by granulomas, cicatrices, toxins, etc. Conduction is often impaired in disordered coronary circulation, especially in myocardial infarction (the interventricular septum is involved). Block may be persistent and intermittent. Persistent block is usually connected with anatomic changes in the conduction system, whereas intermittent block depends largely on the functional condition of the atrioventricular node and the His bundle and is often connected with increased influence of the parasyrnpathetic nervous system; atropine sulphate is an effective means that restores conduction.
Clinical and ECG signs of block depend on its location. The following types of heart blocks are distinguished:
-sino-atrial block - impairment of conduction between sinus node and atria;
-intra-atrial block - impairment of conduction through the atrial
myocardium;
-atrioventricular block - impairment of conduction between atria to the ventricles;
-intraventricular block (His bundle branch block) - impairment of
conduction through the His bundle and its branches.
Sino-atrial block
Sino-atrial block is characterized by periodic missing of the heart beat and pulse beat.
ECG signs of sino-atrial block (Fig. Suppl. 26):
-periodic missing of the heart complex (PQRST) in the presence of a regular sinus rhythm;
-the length of diastole doubles.
Intra-atrial block
Intra-atrial block can only be detected electrocardiographically because clinical signs are absent.
ECG signs of intra-atrial block (Fig. Suppl. 27):
-P waves are broadened ≥0.11 s and splitted;
-P wave in the V1 lead has two phases.
Atrioventricular block
Atrioventricular block is most important clinically. It is classified into three degrees by gravity.
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