Heart Rhythm disorders Cardiac dysrhythmia (also known as arrhythmia and irregular heartbeat) is any of a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart. The heartbeat may be too fast or too slow, and may be regular or irregular. Coordination of heart work is provided by heart’s main features: automatism, excitation, transmission, and contraction, which disorders cause arrhythmias. 1. Arrhythmias developed at automatism disorder Heart automatism is revealed by sinus node and by transmission system ability to generate impulses. In this regard, the most spontaneously active is sinus node. Other parts of transition system have as less capacity to generate impulses as far they are from sinus node. In normal conditions in these cells action potential is generated by receiving excitation from higher automatism capacity cells. On this basis the transmission system cells “fail” to reveal their automatism. Sinus node (in the right atrium) initiates and regulates the cardiac rhythm, this means, it is the primary hearts' pacemaker. This node discharges electric current (An electrical discharge is the passage of electrical current through a material which normally does not conduct electricity) through the atria causing them to contract. The electric current then passes through the atrioventricular (AV) node which lies within the lower interatrial septum. Electrical impulses pass from here into the Purkinje's network, along the right and left bundles of His, and excite the ventricular muscles causing their contraction. The conduction system and myocardium have a nerve supply and are hormone sensitive (to catecholamines), which allows regulation of the heartbeat according to different activities, stress and excitement. A. Tachycardia and bradycardia An arrhythmia is a disorder of the heart rate (pulse) or heart rhythm, such as beating too fast (tachycardia), too slow (bradycardia), or irregularly. Tachycardia is a fast heart rhythm arising from the sinus node so called P -cells, the normal primary pacemaker of the heart. That is, the heart rhythm is arising from the normal location but at an inappropriately high rate. This symptom is signed e.g. at high temperature of body, at the action of mediators of sympatic nervous system (catecholamines dopamine, adrenaline and noradrenaline). Causes of sinus tachycardia may be: heart inflamative, ischemic, infective or toxic injury. Tachycardia at heart overload is frequently of compensative manner. Tachycardia may be developed by extracardial causes (Anemia, volume depletion, hypoxia etc.) and they also frequently may be compensative. Heart contractions become more frequent at those pathological processes with nervous system activation and catecholamine surplus release. Tachycardia is very characteristic at thyreotoxicosis. It develops also at fever, because warm blood excitates sinoatrial node. As usual, increased temperature for 1 Celsius causes heart beat increase for 8 - 10 in minute. At deceleration of impulse generation in sinoatrial node (e.g. at vagus nerve excitation) impulse generation is decreased and bradycardia is revealed. Heart work slow down – bradycardia can be caused by heart injury as well as by extracardial reasons. Frequently bradycardia is caused by, e.g. vagus nervus centre excitation at intracranial pressure increase or kinetosis. Bradycardia can be developed also by all diseases that cause bile acid transmission to blood (cholemia) because acids excitate vagus nervus and inhibit sinus node function. Tachycardia is characterized by T-P interval decrease on ECG (electrocardiogram), and bradycardia – by increase of this interval. B. Extrasystolic Arrhythmia Extrasystoles are essentially extra beats, or contractions, which interrupt the normal regular rhythm of the heart. They occur when there is electrical discharge from somewhere in the heart other than the sinoatrial node. It may take place when sinus node automatism is decreased or when ectopic sites impulse initiation capacity is increased as well as at potential difference formation, e.g. at non synchronous repolarization at local ischemia, or cardiac glycoside poisoning. Extrasystoles are classified as sinusoidal (nomotopic), atrial, atrioventricular or ventricular extrasystoles (VEs) according to their site of origin. Initiated extra waves are spread towards paradoxical directions that are revealed on the structure of ECG. a) At sinusoidal (nomotopic) extrasystoles pacemaker is in sinus node, QRST complex is preceded by positive atrial P waves. ECG differs from normal only by T-P interval decrease before extrasystole. In response to decreased diastole duration, ventricle is not fully filled with blood that decreases pulse wave of heart. b) Atrial extrasystole is initiated when ectopic excitement site is localized in atrium. They are premature P waves which look different from a normal P wave; are characterized by P wave deformation (two phases, negativity) preceding QRST complex and by prolonged interval after extrasystole. c) At atrio-ventricular extrasystole excitement from the node is spread towards both: atrium and ventricles. As excitement in atrium is spread retrogradely (from bottom to top), P wave is negative. According to the place of impulse generation P wave can precede, combine or follow QRST complex. In this case QRST complex is usually normal because excitement is spread normally trough bundles of Hiss to myocardiocytes. When additional impulse is generated in the middle or upper site of node, diastolic interval after extrasystole is a bit increased. If the impulse is generated in the lower part of the node, compensative pause is signed after the exrtrasystole. d) At ventricular extrasystoles additional impulse is generated in any part of ventricular transmission system. It may be spread differently according to where and which phase of heart it was generated. When impulse is spread in non ordinary manner, Ventricular extrasystoles (VEs) are wide, abnormally-shaped QRS complexes, excitement can not reach atrium and P wave is not observed in ECG. Extrasystoles occurring at every second or third beat are called bigeminy or trigeminy respectively. Seldom we can meet interpolated extrasystole (A ventricular contraction that occurs between two normal heartbeats). It is not followed by compensative pause. When extrasystoles become more frequent compensative pause is observed. This is because, when impulse coming from sinus node reaches ventricle it is in the absolute refraction phase after extrasystole and can not respond to electric current. When frequently repeated, group extrasystoles are initiated, they fully restrain physiological rhythm, and paroxysm tachycardia is developed. Risk factors for extra systoles Can occur in normal hearts, where the prevalence of extrasystoles increases with age Hypertension Heart disease, including acute myocardial infarction, valvular heart disease, cardiomyopathy, ventricular hypertrophy and cardiac failure Electrolyte disturbances, including hypokalaemia, hypomagnesaemia, hypocalcaemia Drugs, including digoxin, tricyclic antidepressants, cocaine Alcohol excess Infection Stress Hyperthyroidism Stimulants such as caffeine may have a role, although this has not been proven for ventricular extrasystoles 2. Arrhythmias developed at transmission disorders Impulse transmission disorder in transmission system is called heart block. Excitement transmission can be interrupted in different parts of the system, according to which heart block following types are differed: A. Sinoauricular block - electric signals are hindered from sinus node to atrium (such kind of block develops at vagus nervus excitation, miocardiodystropies, electrolyte balance disorders in myocardium). B. Atrioventricular block - impulse transmition is hindered in atrioventricular node. They differ full or none full atrioventricular block. The last is divided into 3 types: 1. I degree block – Atrioventricular node transmits every impulse to the ventricles but they are delayed from 0.08 0.12 sec (normally), to 0.2 -0.5 sec P-Q interval on ECG. 2. II degree block – P-Q interval is becoming more and more prolonged until VII – IX wave of excitation is omitted. The next cycle P-Q interval is normal but increasing again gradually until blockage of one of impulses. 3. At III degree none full block every II or III impulse is omitted, on ECG every II or III QRS complex is not observed. 4. Full atrioventruicular block (IV degree block according to some authors) is developed when the node does not transmit any excitation impulse to ventricles. In this case atrium and ventricles contract according to their independent rhythm. Non full block transition to full block is immensely important, when impulses coming from sinus node are totally inhibited. Slow diastolic depolarization in third grade pacemaker appears after some tome after full blockage. This period is called preautomatric pause. At full asystole developed during the pause brain is not provided with blood, loss of consciousness and cramps are signed. (MorganAdams – Stocks Syndrome). In this period death may be signed though frequently ventricles start contraction again by the prevalence of their automatism, symptom disappears. The syndrome may be many times repeated. C. Right or left brunch block of bundle of Hiss – characterized by electric current disorder in any branch of Hiss bundle. (In this case impulse is transmitted to left or right ventricle, to second ventricle impulse can be transmitted to intraventricular partition. That’s why ventricles contract non synchronously. 3. Atrial and ventricular Arrhythmia Heart muscle certain sites non synchronic, chaotic contraction is revealed by palpitation and flutter. Atrial fibrillation: In atrial fibrillation, the electrical activity of the heart is uncoordinated, with electricity traveling about the upper chambers in a chaotic fashion, causing the upper chambers to quiver (like a "bag of worms") and contract inefficiently or not at all. Atrial fibrillation is common particularly in the elderly and those with heart disease. It is also common in patients with heart valve disease who may require surgery to repair or replace the mitral valve. There are a variety of treatment options for atrial fibrillation, including drugs, an ablation -- a non-surgical technique which eliminates the abnormal heart tissue with a catheter, or surgery in some cases. Atrial flutter: Atrial flutter causes a rapid but coordinated electrical stimulation of the upper chamber of the heart, often leading to a rapid pulse. The atria are stimulated so quickly that they can not contract or squeeze. This arrhythmia is due to a loop of electricity in the upper chambers of the heart. It is often curable with ablation. Wolff-Parkinson-White syndrome: This is a special type of supraventricular tachycardia. This syndrome involves episodes of a rapid heart rate (tachycardia) caused by abnormal electrical connection in the heart. In people with Wolff-Parkinson-White syndrome, there is an extra (accessory) connection between the top and bottom chambers of the heart. Wolff-Parkinson-White occurs in approximately 4 out of 100,000 people, and is one of the most common causes of fast heart rate disorders (tachyarrhymthmias) in infants and children. Ventricular Fibrillation is where electrical signals in the ventricles fire in a very fast and uncontrolled manner. This causes the lower chambers to quiver, and not pump blood. If the person does not receive immediate medical attention and a normal rhythm is not restored quickly, the patient will suffer from brain and heart damage and die. Patients who survive this should have a defibrillator (ICD) implanted. Ventricular Tachycardia is a rapid, regular heartbeat arising in the ventricles, the bottom chamber of the heart. When it occurs, it's usually fatal. About 400,000 people a year die from it. The treatment of choice for this invariably includes an implantable defibrillator and or medication and or interventions like ablation to try to minimize or limit the number of shocks.