The Conduction System in the Heart

The conduction system in the heart is an intrinsic system whereby the cardiac muscle is automatically stimulated to contract, without the need for external stimulation (Waugh & Grant, 2007). It comprises specialized cardiac cells, which initiate and conduct impulses, providing a stimulus for myocardial contraction. It is controlled by the autonomic nervous system; the sympathetic nerves increase heart rate, contractility, automaticity and atrioventricular (AV) conduction, while the parasympathetic nerves have an opposite effect.

Irregularities in the conduction system can cause cardiac arrhythmias and an abnormal electrocardiogram (ECG). An understanding of the conduction system and how it relates to myocardial contraction and the ECG is essential for ECG interpretation.
Depolarisation and  repolarisation 
The contraction and relaxation of the cardiac muscle results from the depolarisation and repolarisation of myocardial cells (Meek & Morris, 2008):
Depolarisation : can be deﬁned as the sudden surge of charged particles across the membrane of a nerve or muscle cell that accompanies a physicochemical change in the membrane and cancels out or reverses its resting potential to produce an action potential (McFerran  &  Martin,  2003 ); put simply, it is the electrical discharging of the cell (Houghton  &  Gray,  2003 ). A change in the cell membrane permeability results in electrolyte concentration changes within the cell. This causes the generation of an electrical current, which spreads to neighbouring cells causing these in turn to depolarise. Depolarisation is represented on the ECG as P waves (atrial myocytes) and QRS complexes (ventricular myocytes). 
Repolarisation : Can be deﬁned as the process by which the cell returns to its normal (resting) electrically charged state after a nerve impulse has passed (McFerran  &  Martin,  2003 ); put simply, it is the electrical recharging of the cell (Houghton  &  Gray,  2003 ). Ventricular repolarisation is represented on the ECG as T waves (atrial repolarisation is not visible on the ECG as it coincides with and therefore, is masked by the QRS complex).    
Automaticity is the ability of tissue to generate automatically an action potential or current (Marriott  &  Conover,  1998 ), i.e. electrical impulses can be generated without any external stimulation. It occurs because there is a small, but constant, leak of positive ions into the cell (Waldo & Wit, 2001).
The sinus node normally has the fastest ﬁ ring rate and therefore assumes the role of pacemaker for the heart. The speed of automaticity in the SA node can be determined by a number of mechanisms, including the autonomic nervous system and some hormones, e.g. thyroxin (Opie, 1998). If another focus in the heart has a faster ﬁ ring rate, it will then take over as pacemaker. 
Figure 1     Cardiac ventricular muscle AP.  Reprinted from Aaronson, P.  &  Ward J.,  The Cardiovascular System at a Glance , 3rd edn, copyright 2007, with permission of Blackwell Publishing.  
Cardiac  action  potential 
Action potential can be deﬁned as the change in voltage that occurs across the membrane of a muscle or nerve cell when a nerve cell has been triggered (McFarran  &  Martin, 2003). Cardiac action potential (see Figure 1 ) is the term used to describe the entire sequence of changes in the cell membrane potential, from the beginning of depolarisation to the end of repolarisation.  
Resting cardiac cells have high potassium and low sodium concentrations (140 mmol / l and 10 mmol / l, respectively). This contrasts sharply with extracellular concentrations (4 mmol / l and 140 mmol / l, respectively) (Jowett  &  Thompson,  1995 ). The cell is polarised and has a membrane potential of 90 mV.
Cardiac action potential results from a series of changes in cell permeability to sodium, calcium and potassium ions. Following electrical activation of the cell, a sudden increase in sodium permeability causes a rapid inﬂux of sodium ions into the cell. This is followed by a sustained inﬂux of calcium ions. The membrane potential is now 20 mV. This is referred to as phase 0 of the action potential.
 The polarity of the membrane is now slightly positive. As this is the reverse pattern to that of adjacent cells, a potential difference exists, resulting in the ﬂ ow of electrical current from one cell to the next (Jowett  &  Thompson,  1995 ).
 The cell returns to its original resting state (repolarisation) (phases 1 – 3); phase 4 ensues. Sodium is pumped out and potassium and the transmembrane potential returns to its resting of 90   mV. Table 1  summaries the phases of the cardiac action potential.   
Table 1 Phases of the cardiac action potential.
Upstroke or spike due to rapid depolarisation   
Early rapid depolarisation   
The plateau   
Rapid repolarisation   
Resting membrane potential and diastolic depolarisation 

Action potential in automatic cells  
The action potential in automatic cells differs from that in myocardial cells. Automatic cells can initiate an impulse spontaneously without an external impulse.
Automatic cells can be found in the SA node, AV junction (AV node and Bundle of His), bundle branches and Purkinje ﬁ bres. The rate of depolarisation varies between the sites:
·        SA node : has the shortest spontaneous depolarisation time (phase 4) and therefore the quickest ﬁ ring rate (Julian  &  Cowan,  1993 ), usually approximately 60 – 100 times per minute (Khan,  2004 ). 
·        AV junction (AV node and bundle of His) :  approximately 40 – 60 times per minute (Sharman,  2007).
·        Bundle branches and Purkinje ﬁbres : < 40 times per minute.    
If the SA node ﬁ ring rate signiﬁcantly slows or ceases, e.g. a possible complication following an acute inferior myocardial infarction, a subsidiary pacemaker will (it is hoped) provide an escape rhythm. In general, the lower down the conduction system that the pacemaker is sited, the slower the rate, the wider the QRS complex and the less dependable it is (Jowett &  Thompson,  1995 ). When an ectopic pacemaker takes over control of the electrical activity in the heart it is denoted by the preﬁx ‘idio’, e.g. an idioventricular rhythm is an escape rhythm originating in the ventricles.

Figure 2 The His - Purkinje conduction system.  Reprinted from Morris, F.  et al., ABC of Clinical Electrocardiography, 2nd edn, copyright 2008, with permission of Blackwell Publishing.

The heart possesses specialised cells that initiate and conduct electrical impulses resulting in myocardial contraction. These cells form the conduction system (see Figure 2), which comprises the following:  

Sinoatrial (SA) node 
The SA node is situated at the junction of the right atrium and superior vena cava (Sharman,  2007 ). The blood supply is via the nodal artery, which arises from either the right coronary artery (60%) or the left coronary artery (40%) (Jowett  &  Thompson,  1995 ). The SA node acts as the natural pacemaker and initiates each cardiac cycle (Meek  &  Morris,  2008 ) and is often referred to as the pacemaker (Khan,  2004 ; Waugh  &  Grant,  2007 ). 

Internodal pathways 
The impulse from the SA node is conducted to the atria via four main atrial pathways; three in the right atrium are referred to as internodal pathways because they carry the impulse from the SA node to the AV node (Khan,  2004 ) and one to the left atrium (Bachmann ’ s bundle) (Berne  &  Levy,  1992 ). 

AV node 
The AV node is situated near the inferior aspect of the inter - atrial septum (Sharman, 2007). Blood supply is via the nodal artery, which arises from either the right coronary artery (90%) or the left circumﬂex artery (10%) (Jowett &  Thompson,  1995 ). It acts as a ‘bridge’  connecting the atria to the ventricles, allowing the impulse to cross the atrioventricular ring (a thick layer of ﬁbrous tissue, which electrically insulates the atria from the ventricles) (Khan,  2004 ).
The AV node has a slower conduction speed, which delays the conduction of the impulse from the atria to the ventricles (Waldo  &  Wit,  2001 ). This allows time for the atria to contract, enabling the ventricles to ﬁ ll up before contraction (Khan,  2004 ). Although it does not itself possess the property of automaticity, the AV junction, conduction tissue connecting it to the bundle of His, does (Berne  &  Levy,  1992 ).
 The AV node has a protective feature, blocking the number of atrial impulses reaching the ventricles (Khan,  2004 ). This is only seen when the atrial ﬁ ring rate exceeds 180 – 200 impulses a minute (Berne  &  Levy,  1992 ) which is usually due to an area of abnormal automaticity in the conduction ﬁbres or myocardial in the atria (Huszar,  2001 ), e.g. in atrial ﬁbrillation. 

Bundle of His 
The bundle of His was ﬁrst discovered in 1893 by Wilhelm His Jr a Swiss cardiologist and anatomist. It is divided into right and left bundle branches. The left bundle branch is divided into two or sometimes three branches
Anterior fascicle: radiates anteriorly and superiorly across the ventricular wall. 
Posterior fascicle: radiates inferiorly and posteriorly across the left ventricular wall.
Mid - septal fascicle: present in approximately a third of the population (Kulbertus  &  Demoulin,  1976 ), it usually emerges directly from the left bundle branch but can arise from either the anterior or posterior fascicle, and radiates through the septum (Dhingra  et al. ,  1975 ).
(Source:  Khan, 2004)
Blood supply is via the left anterior descending artery (Jowett  &  Thompson,  1995 ). 

Purkinje ﬁbres 
The Purkinje ﬁ bres were ﬁ rst discovered in 1839 by the Czech physiologist Johannes Evangelist Purkinje (Purkyne). They form the ﬁ nal part of the conduction system and result from subdivisions of the bundle branches (Sharman,  2007 ), enabling ventricular contraction from an inward to outward direction (Khan,  2004 ). 

Control of heart rate 
The heart rate is inﬂuenced by the cardiovascular Centre in the medulla oblongata through the autonomic nervous system (Green, 1991; Waugh  &  Grant,  2007 ):
Parasympathetic or vagus nerve :     supplies mainly the SA node, AV node and atria (Waugh  &  Grant,  2007 ). Continuous vagal activity or vagal tone acts as a brake on the heart. The greater the vagal activity, the slower the heart rate. Increased vagal tone is often associated with an acute inferior myocardial infarction. If vagal activity diminishes, the heart rate will increase. If the vagal tone is completely blocked, the heart rate would be approximately 150 beats per minute (Green,  1991 ). Atropine blocks the action of the vagus nerve. This causes an increase in heart rate.
Sympathetic nerve :     supplies the SA node, AV node, atria and ventricles (Waugh  &  Grant,  2007 ). Sympathetic nerve activity (‘ﬁght and ﬂight’) has a positive chronotropic action on the heart, i.e. it increases the heart rate. It is particularly active in periods of emotional excitement, exercise and stress. Beta blockers shield the heart from sympathetic nerve activity resulting in a decrease in heart rate, blood pressure and myocardial workload.     

The conduction system in the heart comprises specialised cardiac cells, which initiate and conduct impulses, providing a stimulus for myocardial contraction. This chapter has provided an overview to the conduction system. The basic principles of cardiac electrophysiology have been discussed. The conduction system has been described together with how the ECG relates to cardiac contraction.  

Berne R, Levy M ( 1992 )  Cardiovascular Physiology ,  6th edn .  Mosby, St Louis. 
Dhingra   R  ,   Wyndam   C  ,   Ehsani   A  ,   Rosen   K   ( 1975 )  Electrocardiogram of the month: left anterior hemiblock concealing diaphragmatic infarction and simulating anteroseptal infarction .  Chest, 67, 713  –  715 . 
Green   J   ( 1991 )  An Introduction to Human Physiology .  Oxford Medical Publications ,  Oxford . 
Houghton   A  ,   Gray   D   ( 2003 )  Making Sense of the ECG: a Hands on Guide ,  2nd edn .  Hodder Arnold ,  London . 
Huszar   J   ( 2001 )  Basic Dysrhythmias: Interpretation and Management ,  3rd edn .  Mosby ,  St Louis . 
Jowett   NI  ,   Thompson   DR   ( 1995 )  Comprehensive Coronary Care ,  2nd edn .  Scutari Press ,  London . 
Julian   D  ,   Cowan   J   ( 1993 )  Cardiology ,  6th edn .  Bailli è re ,  London .      Khan   E   ( 2004 )  Clinical skills: the physiological basis and interpretation of the ECG .  British Journal of Nursing13  ( 8 ),  440  –  446 .     
Kulbertus   H  ,   Demoulin   J   ( 1976 )  Pathological basis of concept left hemi-block . In:   Wellens   H,   Lie   K  ,   Janse   M   (eds)  The Conduction System of the Heart .  Lea and Febiger ,  Philadelphia . 
McFerran   T  ,   Martin   E   ( 2003 )  Minidictionary for Nurses ,  5th edn ,  Oxford University Press ,  Oxford . 
Marriott   H  ,   Conover   M   ( 1998 )  Advanced Concepts in Arrhythmias ,  3rd edn .  Mosby ,  St Louis . 
Meek   S  ,   Morris   F   ( 2008 )  Introduction. 1 - leads, rate, rhythm and cardiac axis . In:   Morris   F  ,   Brady   W  ,   Camm   J   (eds)  ABC of Clinical Electrocardiography ,  2nd edn .  Blackwell Publishing ,  Oxford . 
Opie   L   ( 1998 )  The Heart: Physiology from Cell lo Circulation ,  3rd edn .  Lippincott Williams  &  Wilkins ,  Philadelphia . 
Sharman   J   ( 2007 )  Clinical skills: cardiac rhythm recognition and monitoring .  British Journal of Nursing16  ( 5 ),  307 . 
Thompson   P   ( 1997 )  Coronary Care Manual .  Churchill Livingstone ,  London .     
Hurst   J   ( 1998 )  Naming of the waves in the ECG, with a brief account of their genesis .  Circulation98 ,  1937  –  1942 .     
Sykes   A  ,   Waller   A   ( 1887 )  The electrocardiogram .  BMJ (Clin Res Ed)294 ,  1396  –  1398 .     
Snellen   H   ( 1995 )  Willem Einthoven (1860 – 1927): Father of Electrocardio-graphy .  Kluwer Academic Publishers ,  Dordrecht, Netherlands . 
Waldo   L  ,   Wit   A   ( 2001 )  Mechanisms of cardiac arrhythmias and conduction disturbance . In:   Fuster   V  ,   Alexander   R  ,   O ’ Rourke   R  ,  et al.  (eds)  Hurst ’ s the Heart .  McGraw Hill ,  New York . 
Waller   A   ( 1887 )  A demonstration on man of electromotive changes accompanying the heart ’ s beat .  J Physiol8 ,  229  –  234 . 
Waugh   A  ,   Grant   A   ( 2007 )  Ross and Wilson Anatomy and Physiology in Health and Illness ,  10th edn  (reprint).  Elsevier ,  Edinburgh .