Textbook of Clinical Electrocardiography SN Chugh
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1Physiological Mechanisms Governing Electrocardiographic Deflections2

Fundamentals of Electrocardiography1

  • The electrocardiogram—An introduction
  • The Einthoven concept
  • Anatomy and physiology of conduction tissue
  • The modes of activation of the heart
 
THE ELECTROCARDIOGRAM—AN INTRODUCTION
 
Definition
The graphic representation of the electrical events of the heart on a paper, recorded from the body surface electrodes placed at some distance displaying the electrical activity in waveforms in different planes, is called electrocardiogram.
 
Electrical Activity
The electrical activity of the heart depends on the generation of action potentials through the heart muscle by electrical stimulation. The heart muscle possesses an intrinsic property of excitability and conductivity. The electrical potentials generated in the heart propagate through the specialised conducting tissue in a waveform in a co-ordinated manner. Therefore, the electrical activity generated in the sinoatrial (SA) node-the pacemaker, spreads through the conduction pathways, i.e. atria, then to atrioventricular (AV) node, bundle of His and its branches, the Purkinje system and ultimately to the ventricles resulting in an electrocardiographic complex consisting of P-QRS-T during one beat of the heart. The electrical events are followed by mechanical events in the heart; hence, co-ordinated function called electro-mechanical events.
 
Usefulness of Electrocardiogram (ECG)
The ECG is a graphic recording of electrical potentials generated in the heart. It does not represent mechanical events. The ECG should be considered as a laboratory test only and is not a sine-quanon of any heart disease diagnosis. A patient with organic heart disease may have normal ECG; while on the other hand, a perfectly normal healthy individual may show non-specific changes on ECG. Therefore, on the basis of normal ECG, no assurance of the absence of the disease may be given to any one. The ECG should be analysed and interpreted in the light of clinical findings. In general, a physician who is looking after the patient is the most qualified person to interpret the ECG correctly. The ECG interpreted by someone else other than the treating physician may, sometimes, be erroneous and misinterpretation may be sent based on the findings of ECG. The ECG is useful in the following conditions;
  1. Chamber hypertrophy and dilatation. (atrial and/or ventricular hypertrophy and dilatation)
  2. Myocardial ischaemia and infarction.
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  3. Arrhythmias. It serves as a gold standard for diagnosis.
  4. Myopericardial disease or pericarditis.
  5. Conduction disturbances at various stages from the SA node to Purkinje system.
  6. Systemic illnesses affecting the heart.
  7. Effect of drugs and monitoring the drug therapy such as quinine, quinidine and procainamide.
  8. Electrolytes disturbance specially hypo and hyperkalaemia; and hypo and hypercalcaemia. Both are important cations for the heart.
  9. Detection of efficacy of various cardiac intervention procedures, i.e. angioplasty, bypass surgery, etc.
  10. Continuous ambulatory electrocardiography helps in evaluation of symptoms related to daily activity.
 
What does an ECG complex indicate?
An ECG complex of P-QRS –T indicates the total electrical events that occur during one beat. The P wave represents the total electrical activity of the atria. The QRS-T complex represents the electrical events of the ventricles, i.e. both electrical activation (depolarisation) and recovery (repolarisation).
 
What does an ECG complex record?
On ECG, the magnitude and direction of the electrical impulse recorded on the body surface is a resultant action potential produced within the myocardial cells due to depolarisation and repolarisation processes occurring at that point of time after passing through the cancellation of opposing forces from the other cells. Normally, an individual cell is excitable but its activity does not reach to the surface because the opposing cancellation forces make it a weak electrical potential; but cumulative effect of a group or groups of cells can make the electrical potential reproducible on the surface as resultant electrical force or potential which is recorded as deflections or waves. The signals recorded on the surface don't specify their sites of origin, because a given vector (resultant force) at the body surface cannot be accounted for innumerable combinations of cellular signals at their sources in the heart.
 
EINTHOVEN THEORY OF ELECTRICAL ACTIVITY
In 1902, Einthoven recorded an electrical current from the human heart by a galvanometer. He postulated the concept that human body represents as a larger volume conductor having the source of electrical activity at the centre. As an extension of this hypothesis, the net electrical activity at any instant in the cardiac cycle may be viewed as originating from a polarised point source at a theoretical electrical center of the heart. Since this equivalent dipole would have direction and magnitude, one might extend this pattern into a sequence of instantaneous vectors recordable from the body surface.
 
ANATOMY AND PHYSIOLOGY OF CONDUCTION TISSUES OF THE HEART (FIG. 1.1)
Sinoatrial (SA) node: It is the intrinsic natural pacemaker of the heart. It is located in the upper part of the right atrium. There are three internodal-connecting pathways present in atrial musculature which fan out from SA node and converge at AV node. There is an additional interatrial pathway called Bachmann's bundle, which transmits the sinus impulse to the left atrium.
Atrioventricular (AV) node: The three internodal (anterior, middle and posterior) conducting pathways meet at AV node which acts as a way station.
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Fig. 1.1: Conduction system of the heart and spread of excitation wave from SA node to the ventricles is represented by arrows
SA node
=
Sinoatrial node
AV node
=
Atrioventricular node
RBB
=
Right bundle branch
LBB
=
Left bundle branch
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At AV node, the impulses are slowed down and a normal physiological delay occurs, that allows time to the atria to contract and to pump blood to the ventricles (a mechanical event).
Bundle of His: After normal physiological delay in AV node, the impulse enters a short pathway called Bundle of His which runs for a short distance and splits into right and left bundle branches.
Right bundle branch (RBB): It conducts impulses to the right ventricle. It divides into smaller branches and forms a network of conducting fibres called Purkinje system. The Purkinje fibres arborise with fibres from the left bundle branch to complete the Purkinje conduction system. The Purkinje fibres from right bundle branch conduct impulses to the right ventricular muscle cells.
Left bundle branch (LBB): The left bundle divides shortly after its origin into two fascicles (anterior and posterior) that supply the left ventricle. These fascicles supply their respective areas of the ventricles, i.e. anterior supplies the anterosuperior surface and posterior supplies the posteroinferior surface of the left ventricle.
Both the anterior and posterior fascicles branch to form Purkinje fibre system and conduct impulses through this system to the left ventricular wall, thus, completing the process of electrical excitation which is repeated cyclically at an average rate of 72 beats in a minute (bpm).
The right ventricle is activated slight ahead of left ventricle because right bundle branch is activated before the left, but contraction of both the ventricles is synchronous and instantaneous.
 
APPLIED PHYSIOLOGY
 
The P wave
The P wave of ECG complex indicates an atrial depolarisation (an electrical event) which proceeds when AV valves are closed. Spread of electrical excitation to AV node ultimately results in opening of AV valves and discharge of blood from atria to the ventricles. The contraction of atrial muscle to pump blood is a mechanical event, hence, P wave represents an electrical event preceding the mechanical event.
 
The QRS Complex
The QRS complex of ECG indicates ventricular depolarisation, which is followed by recovery, i.e. repolarisation in which there is reversal of activation process resulting in inscription of ST segment and T wave. Occasionally a small deflection due to delayed or secondary repolarisation is seen as a ‘U’ wave, which is prominently visible in hypokalaemia. Normally it is so small that either it is not seen or seen rarely. Its significance is not fully defined.
With arrival of an electrical depolarisation wave in the ventricles, the ventricles contract forcing the AV valves to close and semilunar valves to open so as to pump the blood into aorta and pulmonary circulation. Therefore, this electro-mechanical systole started by the electrical activation of ventricles (QRS complex) is followed physiologically by a mechanical event (cardiac contraction); and in this way, a cardiac cycle is completed in each beat and P-QRS-T complex is recorded during each beat.
 
MODES OF ACTIVATION OF THE HEART (ATRIA AND VENTRICLES, FIGS 1.2A AND B)
Both the atria of the heart are thin-walled structures not equipped with specialised conduction system, are activated longitudinally and by contiguity, i.e. the excitation wave from SA node spreads to the whole chamber, each fibre, in turn, activating the adjacent fibre.
Activation of both the ventricles occurs through the specialised and highly efficient conduction system, which transmits supraventricular impulses from the endocardial to the epicardial surfaces through the terminal ramifications of Purkinje system. Excitation, is therefore, transverse through the ventricular myocardium, and this activates the whole chamber near-synchronously.
The two modes of activation, i.e. longitudinal occurring in the atria and transverse occurring in the ventricles, have following differences and clinical significance (Table 1.1).6
Table 1.1   Modes of activation of atria and ventricles
Longitudinal activation
Transverse activation
• Occurs in the atria
• Occurs in the ventricles
• Proximal parts are activated first followed by distal parts.
• It results in activation of all parts simultaneously, hence, it is sequential.
• This type of activation favours potential Out-of-phase state.
• This favours potential In-phase state.
• It is easy to induce fibrillation in atria due to this type of activation which results in asynchronous state.
• This type of activation results in fibrillation of ventricle due to synchronous or near-synchronous state.
• The longitudinal activation does not reflect the thickness of the atrial wall, thus atrial hypertrophy cannot be reflected electrocardiographically.
• The transverse mode of activation indirectly reflects the thickness or transverse bulk of the ventricular wall, thus hypertrophy of the ventricles can be reflected and expressed electrocardiographically.
zoom view
Fig. 1.2A: Longitudinal activation of atrial wall
zoom view
Fig. 1.2B: Transverse activation of ventricular wall
Suggested Reading
  1. Cranefield PF: The conduction of the cardiac impulse. Futura Publishing Company Inc,  Mount Kisco, NY:  1975.
  1. Einthoven W: Selected papers on Electrocardiography. Snellen, A (Ed). University Press,  Leiden,  1977.
  1. Fisch C: Electrocardiography of arrhythmias, Lea and Febiger,  Philadelphia:  1989.
  1. Fisch C: Evolution of clinical electrocardiogram. J Am Coll Cadiol 14: 1127, 1989.
  1. Fozzard HA, Das Gupta DS: Electrophysiology and the electrocardiogram. Mod Concepts Cardiovas Dis 44: 29, 1975.
  1. Fye WB: A history of origin, evolution and impact of electrocardiography. Am J Cardiol 73:937, 1994.
  1. Fye WB: Disorders of heart beat. A historical overview from antiquity to mid – 20th century. Am J Cardiol 72: 1055, 1993.
  1. Horan IG: Manifest orientation. The theoretical link between the anatomy of the heart and clinical electrocardiogram. J Am Call Cardiol 9:1049, 1987.
  1. Lewis T: The mechanism and graphic registration of the heart beat. Shaw and sons, Ltd.  London,  228, 1920.