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Cardiac Arrhythmias

Arrhythmias are pathological changes in cardiac impulse generation or conduction that can be visualized by ECG. Disturbances of impulse generation change the sinus rhythm. Sinus tachycardia A2): The sinus rhythm rises to 100 min-1 or higher e.g., due to physical exertion, anxiety, fever (rise of about 10 beats/min for each 1 °C) or hyperthyroidism. Sinus bradycardia: The heart rate falls below 60 min1 (e.g., due to hypothyroidism). In both cases the rhythm is regular whereas in sinus arrhythmias the rate varies. In adolescents, sinus arrhythmias can be physiological and respiration-dependent (heart rate increases during inspiration and decreases during expiration).

Ectopic pacemakers. Foci in the atrium, AV node or ventricles can initiate abnormal ec-topic (heterotopic) impulses, even when normal (nomotopic) stimulus generation by the SA node is taking place (^ A). The rapid discharge of impulses from an atrial focus can induce atrial tachycardia (serrated baseline instead of normal P waves), which triggers a ventricular response rate of up to 200 min-1. Fortunately, only every second or third stimulus is transmitted to the ventricles because part of the impulses arrive at the Purkinje fibers (longest APs) during their refractory period. Thus, Purkinje fibers act as impulse frequency filters. Elevated atrial contraction rates of up to 350 min-1 are defined as atrial flutter, and all higher rates are defined as atrial fibrillation (up to 500 min-1). Ventricular stimulation is then totally irregular (absolute arrhythmia). Ventricular tachycardia is a rapid train of impulses originating from a ventricular (ectopic) focus, starting with an extrasystole (ES) (^ B3; second ES). The heart therefore fails to fill adequately, and the stroke volume decreases. This can lead to ventricular fibrillation (extremely frequent and uncoordinated contractions; ^ B4). Because of failure of the ventricle to transport blood, ventricular fibrillation can be fatal.

Ventricular fibrillation mainly occurs when an ectopic focus fires during the relative refractory period of the previous AP (called the "vulnerable phase" synchronous with T wave on the ECG; ^ p. 193 A). The APs triggered during this period have smaller slopes, lower propagation velocities, and shorter durations. This leads to re-excitation of myocardial areas that have already been stimulated (re-entry cycles). Ventricular fibrillation can be caused by electrical accidents and can usually be corrected by timely electrical defibrillation.

Extrasystoles (ES). The spread of impulses arising from an supraventricular (atrial or nodal) ectopic focus to the ventricles can disturb their sinus rhythm, leading to a supraventricular arrhythmia. When atrial extrasystoles occur, the Pwave on the ECG is distorted while the QRS complex remains normal. Nodal extrasystoles lead to retrograde stimulation of the atria, which is why the Pwave is negative and is either masked by the QRS complex or appears shortly thereafter (^ B1 right). Since the SA node often is discharged by a supraventricular extrasystole, the interval between the Rwave of the extrasystole (RES) and the next normal R wave increases by the amount of time needed for the stimulus to travel from the focus to the SA node. This is called the post-extrasystolepause.The RRintervalsareasfollows: RESR > RR and (RRes + ResR) < 2 RR (^ B1).

Ventricular (or infranodal) ES (^ B2, B3) distorts the QRS complex of the ES. If the sinus rate is slow enough, the ES will cause a ventricular contraction between two normal heart beats; this is called an interpolated (or interposed) ES (^ B2). If the sinus rate is high, the next sinus stimulus reaches the ventricles while they are still refractory from the ectopic excitation. Ventricular contraction is therefore blocked until the next sinus stimulus arrives, resulting in a compensatory pause, where RRES + RESR = 2 RR.

Disturbances of impulse conduction: AV block.

First-degree AV block: prolonged but otherwise normal impulse conduction in the AV node (PQ interval > 0.2 sec); second-degree AV block: only every second (2:1 block) or third (3:1 block) impulse is conducted. Third-degree AV block: no impulses are conducted; sudden cardiac arrest may occur (Adam-Stokes attack or syncope). Ventricular atopic pacemakers then take over (ventricular bradycardia with normal atrial excitation rate), resulting in partial or total disjunction of QRS complexes and Pwaves (^ B5). The heart rate drops to 40 to 55 min-1 when the AV node acts as the pacemaker (^ B5), and to a mere 25 to 40 min-1 when tertiary (ventricular) pacemakers take over. Artificial pacemakers are then used.

Bundle branch block: disturbance of conduction in a branch of the bundle of His. Severe QRS changes occur because the affected side of the myocardium is activated by the healthy side via abnormal pathways.

I— A. Nomotopic impulse generation with normal conduction

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