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Understanding Cardiac Arrhythmias S Chakrabarti, a G Stuart

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Understanding Cardiac Arrhythmias S Chakrabarti, a G Stuart 1086 Arch Dis Child: first published as 10.1136/adc.2005.076984 on 21 September 2005. Downloaded from REVIEW Understanding cardiac arrhythmias S Chakrabarti, A G Stuart ............................................................................................................................... Arch Dis Child 2005;90:1086–1090. doi: 10.1136/adc.2005.076984 This review highlights the applied science intrinsic to the impulse. When the sinus node is diseased, secondary pacemaker cells initiate the heart- interpretation of the electrocardiogram and cardiac beat—usually at the atrioventricular junction. arrhythmias in children. The autonomic nervous system also plays a ........................................................................... role in the myocyte action potential. When cholinergic vagal fibres to nodal tissue are stimulated, acetylcholine is liberated. This results n 1887, Augustus Waller published the first in an increase in the permeability of nodal 1 human electrocardiogram (ECG). The early tissues to K+ (via muscarinic receptors) and Istudies were carried out using Waller’s dog, reduces conductance in the Ca2+ channel. The Jimmy, who would stand for hours with paws effect is to reduce and occasionally transiently immersed in saline filled jars! Since then the abolish spontaneous discharge. This effect is seen electrocardiogram has become an essential clin- in vasovagal syncope. Conversely, stimulation of ical tool that has revolutionised our assessment the cardiac sympathetic system makes the of cardiac electrophysiology and disorders of membrane potential fall more rapidly. cardiac rhythm. An understanding of the scien- Noradrenaline increases the rate at which K+ tific basis of the ECG enables a logical inter- declines between action potentials and increases pretation of the ECG findings and an conductance in the Ca2+ channel. The overall appreciation of abnormalities that may occur. effect is to increase the amplitude of the action The aim of this review is to highlight the applied potential, the rate of spontaneous discharge, and science intrinsic to the interpretation of the the strength of each cardiac contraction. electrocardiogram and arrhythmias in infants Similarly, increased temperature increases the and children. rate of discharge of conduction tissues. The action potential of the myocyte has a far BASIC CARDIAC ELECTROPHYSIOLOGY longer duration than nerve or skeletal muscle. Like all living cells, the inside of the cardiac This long action potential, mediated by slow myocyte has a negative charge. This results in a calcium channels, is essential to allow regular voltage difference across the cell membrane independent beats to occur. It also allows called the transmembrane potential. Unlike most modulation of the strength of contraction and other cells, cardiac myocytes are excitable. When is one reason why tetany cannot occur in the http://adc.bmj.com/ appropriately stimulated, channels in the cell cardiac muscle. Abnormalities of the various ion membrane open, allowing ions to flow across the channels give rise to serious cardiac arrhyth- cell membrane. This results in the cardiac action mias2–5 (table 1). potential (fig 1). There are three main three Each myocyte is connected to its neighbour by components to the action potential: depolarisa- an intercalated disc at the end of the cell. These tion, repolarisation, and a resting phase. During discs include gap junctions that contain areas of depolarisation, sodium channels in the cell high conductance called nexi. Each nexus is membrane open and positively charged sodium formed by two half channels, known as connex- on September 30, 2021 by guest. Protected copyright. ions enter the cell, causing a rapid change in the ons, which protrude into adjacent cell cytoplasm transmembrane potential. This depolarisation and link to a mirror image connexon in the spreads to adjacent cells. During repolarisation, neighbouring cell. Connexons are composed of the cardiac membrane potential returns to six protein subunits arranged around a high normal by complex interactions involving conductance fluid filled pore. This allows the sodium, potassium, and calcium. During this heart to behave electrically as if it were a single phase, the myocytes cannot contract (refractory cell. Thus, an electrical impulse can spread period). The resting phase is the period between through the heart muscle in a similar way to action potentials. During the resting phase most conduction through a nerve cell. Gap junction myocytes have no net movement of ions across permeability is increased by ATP and cyclic AMP See end of article for the cell membrane. In some cells, however, the dependant kinases. This quality enables the gap authors’ affiliations ....................... resting phase is associated with a gradual junction to close if ATP levels fall, thus limiting increase in transmembrane potential (phase 4 cell death when one area of the myocardium is Correspondence to: activity). When this potential is high enough, the damaged. Similarly, conduction increases in Dr A G Stuart, Congenital Heart Unit, Bristol Royal appropriate channels open and spontaneous response to adrenergic stimulation. Hospital for Children, depolarisation begins. The property of cells to Abnormalities of gap junctions are associated Upper Maudlin St, Bristol increase transmembrane potential during the with a variety of serious cardiac diseases includ- BS2 8BJ, UK; AGStuart@ resting phase is called automaticity. This is the ing arrhythmias.6 blueyonder.co.uk mechanism whereby the normal cardiac impulse Spontaneously depolarising pacemaker cells Accepted 17 June 2005 is generated. Cells in the sinus node usually have within the sinus node lead to propagation of ....................... the fastest phase 4 and initiate the cardiac depolarisation throughout atrial myocardium www.archdischild.com Understanding cardiac arrhythmias 1087 Arch Dis Child: first published as 10.1136/adc.2005.076984 on 21 September 2005. Downloaded from ICa = calcium current Ionic contributions to cardiac action potential Ih = hyperpolarisation activated current IK1 = inward rectifier K+ current IKr = rapid component of delayed rectifier current IKur = ultrarapid K current INa = sodium current IKs = slow component of IK Phase 1 Ito = transient outward K+ current +30 mV Ito Phase 2 ICa IKur 0 mV Phase 3 Phase 0 IKr IKs INa EAD LAD Phase 4 IK1 IK1 Ih –80 mV Figure 1 Summary of ionic currents involved in the production of the cardiac action potential. Phase 0, rapid depolarisation; phase 1, initial repolarisation; phase 2, plateau; phase 3, repolarisation; phase 4, slow spontaneous depolarisation (only in pacemaker cells). and atrial systole. The action potential is then conducted means that the more rapid the atrial contraction, the longer throughout the heart. This conduction is facilitated by the conduction time through the AV node. This is an specific conduction pathways. These cells are, in general, important safety feature, which prevents very rapid atrial muscle cells which have become specialised for rapid tachycardia or fibrillation leading to rapid ventricular rates. conduction rather than contraction. In the normal heart, At rapid atrial rates the AV node conduction time will the only electrical connection between atria and ventricles is increase, leading to prolonging of the PR interval and via the atrioventricular (AV) node. After traversing the AV eventually non-conducted P waves. This is known as the node, the action potential is propagated rapidly through the Wenkebach phenomenon. bundle of His and into the Purkinje fibres located on the endocardium of the left and right ventricles. Rapid conduc- THE ELECTROCARDIOGRAM tion through the atrium causes synchronous contraction of The electrocardiogram (ECG) is based on the property of the most of the atrial muscle (within 60–90 ms). Similarly, rapid body to act as a volume conductor. Fluctuations in electrical http://adc.bmj.com/ conduction throughout the ventricle leads to synchronous potential recorded on the body surface represent the algebraic contraction of the bulk of the ventricular myocardium sum of myocardial action potentials. The ECG may be (within 60 ms). This synchrony may be lost in pathological recorded using an active electrode connected to an indifferent states (for example, left bundle branch block), leading to electrode at zero potential (unipolar recording) or between inefficient myocardial contraction and reduced cardiac out- two active electrodes (bipolar recording). In a volume put. A recent development in heart failure treatment is the conductor with a current source at the centre, the sum of restoration of synchrony using multisite pacing.7 Delay in the potentials at the points of an equilateral triangle is zero. A propagation of the action potential through the AV node triangle with the heart at the centre can be created by placing on September 30, 2021 by guest. Protected copyright. (120–140 ms) leads to sequential contraction of the atrium electrodes on both arms and the left leg (Einthoven’s followed by the ventricle. This facilitates atrial filling of the triangle). If these electrodes are connected to a common ventricle. Slow conduction in the AV node is associated with terminal, an indifferent electrode at zero potential is created. a smaller number of gap junctions between cells leading to Cardiac depolarisation moving towards the active electrode slowly rising action potentials. The AV node has a unique will produce a positive deflection
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