(1)electrophysiological inhomogeneity (i.e., differences in conduction and/or refractoriness) in two or more regions of the heart connected with each other to form a potentially closed loop;
(2)unidirectional block in one pathway;
(3)slow conduction over an alternative pathway, allowing time for the initially blocked pathway to recover excitability;
(4)reexcitation of the initially blocked pathway to complete a loop of activation.
Classification of cardiac rhythm disorders (arrhythmias):
1.Arrhythmias associated with altered automaticity of the sino-atrial node (sinus arrhythmia).
2.Ectopic (heterotopic) arrhythmias.
3.Arrhythmias due to disordered myocardial conduction (heart blocks).
4.Combined cardiac rhythm disorders.
Sinus arrhythmia
Sinus arrhythmia -arrhythmias associated with altered automaticity of
the sinus (sinoatrial) node.
When automaticity of the sino-atrial node is upset, the rate of impulse generation may either accelerate (sinus tachycardia) or slow down (sinus bradycardia), or the sequence of impulses may be changed with their generation at irregular intervals (sinus arrhythmia).
Normal sinus rhythm characteristics (Fig. Suppl. 13):
-HR (heart rate) equals 60-80 in min, regular rhythm (differences between minimal and maximal R-R intervals is not more than 15%);
-P wave - positive in I, II, aVF, P wave – negative in aVR, PQ ≥0.12 s.
Sinus tachycardia
Sinus tachycardia is directly connected with effects of biologically active substances which increase excitability of the sinoatrial node. This phenomenon may also depend on the change in the tone of the vegetative nervous system. It develops with intensified effect of the sympathetic nervous system. The rate of cardiac contractions in sinus tachycardia usually varies from 90 to 120 and sometimes to 150-160 per min. Sinus tachycardia develops during meals, physical exertion and emotional stress. At elevated body temperature, the heart rate increases by 8-10 per min per each degree over 37 °C. Sinus tachycardia is a frequent symptom of myocarditis, heart defects, and other diseases. It develops by reflex mechanism in heart failure and in response to the increased pressure in the orifices of venae cavae. Tachycardia often develops in neurosis, anemia, hypotension, and in many infectious diseases and toxicosis; it can be provoked by some pharmacological preparations (adrenaline, caffeine, atropine sulphate, etc.), and in thyrotoxicosis.
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The clinical signs of sinus tachycardia are heart palpitation and accelerated pulse.
ECG signs of sinus tachycardia (Fig. Suppl. 14):
-acceleration of heart rate from 90-100 up to 160-180 in one minute;
-Р-wave of the normal form precedes complex QRS;
-regular accelerated rhythm (all intervals R-R are identical).
Sinus bradycardia
Sinus bradycardia is connected with slowed excitation of the sino-atrial node, which in turn depends mostly on the increased influence of the parasympathetic nervous system on the heart (or decreased influence of the sympathetic nervous system). Automaticity of the sino-atrial node decreases in sclerotic affections of the myocardium and in the cold. The cardiac rate in sinus bradycardia decreases to 50-40 (in rare cases to 30) beats per min, Bradycardia may occur in well-trained athletes. It is not permanent and the heart rhythm is accelerated during exercise as distinct from pathological bradycardia in atrioventricular block when bradycardia persists during and after exercise. If automaticity of the sino-atrial node sharply decreases (sicksinus syndrome), the secondor third-order centres may function as the pacemaker, i.e. ectopic arrhythmias develop (see below).
Sinus bradycardia occurs in increased intracranial pressure (tumour and edema of the brain, meningitis, cerebral hemorrhage), in myxedema, typhoid fever, jaundice, starvation, lead and nicotine poisoning, and due to effect of quinine and digitalis preparations. It may develop by reflex during stimulation of baroreceptors of the carotid sinus and the aortic arch in essential hypertension, and can be provoked by pressure on the eye-ball (Dagnini-Aschner reflex), or by irritation of receptors of the peritoneum and the internal organs.
Mild bradycardia is not attended by any subjective disorders, nor does it produce any effect on the circulation. Marked bradycardia (under 40 beats per min) may cause nausea and loss of consciousness due to cerebral anemia. Objective examination reveals slow pulse.
ECG signs of sinus bradycardia (Fig. Suppl. 15):
-decrease of a heart rate less than 60 in one minute;
-Р-wave has a normal form;
-regular infrequent rhythm.
Sinus (respiratory) arrhythmia
Sinus arrhythmia characterized by irregular generation of impulses is due to variations in the tone of the vagus. It would commonly be associated with respiratory phases (respiratory arrhythmia): the cardiac rhythm accelerates during inspiration and slows down during expiration. Sinus arrhythmia is observed in children and adolescents (juvenile arrhythmia), in
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patients convalescing from infectious diseases, and in certain diseases of the central nervous system. It can be a sign of pathology in rare cases when arrhythmia is not connected with respiration or when it develops in the aged during normal respiration.
Clinically sinus arrhythmia is not attended by any subjective disorders.
ECG signs of sinus arrhythmia
-different intervals R-R;
-Р always precedes complex QRS;
-cardiac rhythm accelerates during inspiration and slows down during expiration.
Ectopic arrhythmias
Additional (heterotopic or ectopic) foci of excitation can arise at any site of the conduction system (in the atria, ventricles, atrioventricular region). They can cause premature contraction of the heart before termination of the normal diastolic pause. This premature contraction is called extrasystole, and the disorder of the cardiac rhythm is called extrasystolic arrhythmia. If the activity of the ectopic focus is very high, it can become a temporary pacemaker, and all impulses governing the heart will during this time be emitted from this focus. The cardiac rhythm is then markedly accelerated. The condition is known as paroxysmal tachycardia. Ectopic arrhythmias are often due to increased excitability of the myocardium. The phenomenon known as re-entry can be another mechanism of ectopic arrhythmia. If an impulse meets an obstacle in the pathway of its conduction (local conduction disorder), the excitation wave can return from this obstacle to excite the myocardium.
Extrasystolic arrhythmia (Ectopic beats, Extrasystoles)
Extrasystoles are premature cardiac beats resulting from an abnormal electrical focus or re-entry mechanism in the atria, AV (atrio-ventricular) junction and ventricles (Fig. Suppl. 16).
Extrasystole usually develops during normal contractions of the heart governed by the sino-atrial node (nomotopic contractions). Ectopic foci of excitation can arise at any site of the conduction system. Usually excitations arise in the ventricles, less frequently in the atria, the atrioventricular node, and in the sino-atrial node (sinus extrasystole). A nomotopic contraction of the heart that follows extrasystole occurs in a longer (than normal) interval of time. This can be explained as follows. During the atrial extrasystole, excitation from the ectopic focus is transmitted to the sino-atrial node to "discharge" it, as it were. The next impulse arises in the sino-atrial node only in a lapse of time that is required to "discharge" the node and to form a new impulse.
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In ventricular extrasystole, the time between the extrasystolic contraction and subsequent nomotopic contraction is even longer. The impulse from the heterotopic focus, located in the ventricles, propagates only over the ventricular myocardium; it would not be usually propagated to the atria via Aschoff-Tawara (AV) node. The impulse occurs in normal time in the sino-atrial node but it is not transmitted to the ventricles because they are refractory after the extrasystolic excitation. The next impulse from the sinoatrial node will only excite and contract the atria and the ventricles. A long "compensatory" pause therefore follows the ventricular extrasystole which lasts till the next nomotopic contraction.
Extrasystolic arrhythmia is quite common. Functional extrasystole may occur in practically healthy individuals as a result of overexcitation of certain sites of the conduction system due to the action of the extracardiac nervous system in heavy smokers and in persons abusing strong tea or coffee; it can occur by reflex in diseases of the abdominal organs, or it may be due to hormonal disorders (thyrotoxicosis, menopause), various intoxications, disorders of electrolyte metabolism, etc. Organic extrasystole often attends various cardiovascular pathological conditions due to inflammatory or dystrophic affections of the myocardium or its deficient blood supply.
Patients with extrasystole can feel their heart missing a beat (escape beat) and a subsequent strong stroke. Auscultation of the heart reveals its premature contraction with a specific loud first sound (due to a small diastolic filling of the ventricles). Extrasystole can be easily revealed by feeling the pulse: a premature weaker pulse wave and a subsequent long pause are characteristic. If extrasystole follows immediately a regular contraction, the left ventricle may be filled with blood very poorly and the pressure inside it may be so small that the aortic valve would not open during the extrasystolic contraction and the blood will not be ejected into the aorta. The pulse wave on the radial artery will not be then detectable (missing pulse).
ECG characteristics of all extrasystoles:
(1)premature appearance of the cardiac complex;
(2)elongated pause between the extrasystolic and subsequent normal contraction;
(3)Compensatory pause - the sum of pre-extrasystolic and postextrasystolic intervals. Complete compensatory pause equals to 2 normal R-R intervals. Incomplete compensatory pause is lesser than 2 normal R-R intervals.
If excitability of the myocardium is high, several (rather than one) ectopic foci may exist. Extrasystoles generated in various heart chambers and having different configuration then appear on the ECG (polytopic extrasystole).
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Wherever an ectopic focus may arise, its impulses may alternate in a certain order with the normal impulses of the sino-atrial node. This phenomenon is known as allorhythmia. Extrasystole may alternate with each sinus impulse (bigeminy), or it may follow two normal impulses (trigeminy), or three normal impulses (quadrigeminy). If the heterotopic focus is even more active, a normal contraction may be followed by several extrasystoles at a run (group extrasystole), which sometimes precedes an attack of paroxysmal tachycardia.
Classification of extrasystolic arrhythmia
1.According to the origin: functional and organic extrasystoles.
2.According to the site of origin: -atrial, atrioventricular (nodal) (common name of supraventricular); - ventricular (leftand rightventricular).
3.According to quantity of ectopic beats:
-single, group, paired, frequent extrasystoles;
-allorhythmia - alternaton of extrasystoles with sinus beats - bigemeny (1:2), trigeminy (1:3), quadrigeminy (1:4).
4. According to quantity of ectopic foci:
- monotopic and polytopic (polymorphic) extrasystoles.
Atrial extrasystole
Excitation of the atria only changes in atrial extrasystole because the impulse is generated not in the sino-atrial node, and the ventricles are excited by the usual way.
ECG signs of atrial extrasystole (Fig. Suppl. 17):
(1)premature appearance of the cardiac complex;
(2)P wave - normal shape or slightly disfigured and superimposed on the preceding T wave;
(3)normal shape of QRS;
(4)slight elongation of the diastolic pause (T-P interval) following the extrasystolic contraction (incomplete compensatory pause.
Atrioventricular (nodal) extrasystole (premature atrioventricular junctional complex)
In atrioventricular (nodal) extrasystole the excitation of the atria differs from normal more substantially than in atrial extrasystole. The AV node impulse is transmitted to the atria retrogradely, from bottom to top. The ventricles are excited in nodal extrasystole in the usual way.
ECG signs of atrioventricular extrasystole (Fig. Suppl. 18):
(1)premature appearance of the cardiac complex;
(2)negative P wave because of the retrograde atrial excitation (may be absence of P wave);
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