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The Heart - Part 2:

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The heart’s electrical system consists of three parts of specialised myocardium - the sino-atrial (SA) node, the atrioventricular (AV) node and the bundle of His network (Tortora and Grabowski, 2002) (Fig 1). The starting point of the cardiac electrical cycle is the SA node. This is the heart’s natural/dominant pacemaker, which can create impulses at 60-100 beats per minute. Its ability to spontaneously generate and discharge an electrical impulse is called automaticity.

Abstract

VOL: 101, ISSUE: 32, PAGE NO: 26

Brendan Docherty, MSc, PGCE, RN, nurse manager patient access and nursing services, Prince of Wales Hospital, Sydney, Australia

The heart’s electrical system consists of three parts of specialised myocardium - the sino-atrial (SA) node, the atrioventricular (AV) node and the bundle of His network (Tortora and Grabowski, 2002) (Fig 1). The starting point of the cardiac electrical cycle is the SA node. This is the heart’s natural/dominant pacemaker, which can create impulses at 60-100 beats per minute. Its ability to spontaneously generate and discharge an electrical impulse is called automaticity. The SA node is located in the wall of the right atrium, near the superior vena cava entry to the atrium (Tortora and Grabowski, 2002). The atria contract almost simultaneously and before the ventricles. The impulse is transmitted to the left atrium by a pathway or internodal tract known as Bachmann’s bundle (Lemery et al, 2003), giving rise to a P wave on the electrocardiogram (ECG) (Fig 2). The impulse travels from the atria to the ventricles via the AV node through three internodal tracts (Lemery et al, 2003). This is the PR interval on the ECG (Fig 2). From the AV node, the impulse travels down the His-Purkinje system, carrying the electrical signals throughout the ventricles. The septal area contracts before the main ventricle muscle (Tortora and Grabowski, 2002) - giving rise to a very small negatively deflected Q wave on the ECG. The His-Purkinje system consists of the following parts (Tortora and Grabowski, 2002): - His bundle; - Right bundle branch; - Left bundle branch; - Purkinje fibres. The Purkinje fibres conduct impulses through the muscle to assist in depolarisation and contraction. Both ventricles then contract almost simultaneously (Philip and Kowey, 2001), giving rise first to the positive R-wave deflection on the ECG (that is the force of contraction of the left ventricle as the main muscle mass, travelling towards the ECG electrode), followed by an S wave as the ECG then detects the right ventricle muscle movement. The ventricles then relax following contraction giving rise to the T wave on the ECG (Philip and Kowey, 2001). Nervous system and contraction
The heart’s conduction and contractility can be adapted by two branches of the autonomic nervous system - which is controlled by the cardiorespiratory centre in the medulla oblongata at the base of the brain (Tortora and Grabowski, 2002). The sympathetic (adrenergic) nervous system increases the heart rate, contractibility, automaticity and AV conduction (Cohn, 2002). Two related hormones are triggered: epinephrine (adrenaline) and norepinephrine (noradrenaline) (Cohn, 2002). The parasympathetic (cholinergic) nervous system works in the opposite way, and decreases the heart rate and AV conduction via the vagus nerve at the SA node (Philip and Kowey, 2001). The vagus nerve sits behind the oesophagus, so when patients vomit they may stimulate the nerve and have a decrease in heart rate and blood pressure, and complain of light-headedness or fainting (Tortora and Grabowski, 2002). Impulses (electrical energy) lead to ions crossing the myocardial cell membranes, creating an action potential - called depolarisation (mechanical or kinetic energy) (Philip and Kowey, 2001). The main ions concerned are potassium, sodium and calcium, which are in different concentrations on either side of the cell membranes. Their movement across ion-specific channels creates the energy to depolarise/contract (Tortora and Grabowski, 2002). Repolarisation is the relaxation of the myocardium muscle and the ionic movement back to the original resting state (polarisation). This process is demonstrated in more detail in the action potential curve of the cardiac cycle. It must be remembered that the ECG only shows electrical conduction (Docherty and Douglas, 2003a; Philip and Kowey, 2001). Mechanical transmission/capture to ensure that there is adequate connection between the electrical cycle and the muscle can only be assessed by pulse, blood pressure and levels of consciousness (RCUK, 2004). Arrhythmias
Regular sinus complexes of 60-100bpm are classified as sinus rhythm. In the normovolaemic person with a normal haemoglobin level (10-14g/dl) this is adequate to maintain a normal blood pressure and cardiac output to ensure tissue oxygenation (Philip and Kowey, 2001). However, electrical disturbances caused by ion/electrolyte changes (for example hypokalaemia) or hypoxaemia may lead to a changed or irregular rhythm, which may affect cardiac output (Philip and Kowey, 2001; RCUK, 2004). Tachycardia is a fast heart rhythm, which will often not allow for adequate ventricular filling or time to eject blood efficiently from the ventricles (Philip and Kowey, 2001). Examples of these rhythms include narrow complex tachycardia such as atrial tachycardia, flutter or fibrillation, and broad complex tachycardia such as ventricular tachycardia or flutter. Narrow complex tachycardias tend to be less life-threatening as the conduction is following the normal pathway. They can often be resolved using chemical cardioversion (for example amiodarone) or electrical cardioversion in severe cases (synchronised cardioversion) (Docherty and Douglas, 2003b; RCUK, 2004). Broad complex tachycardias tend to be more critical as the impulse is transmitted across the ventricle wall and not down the His bundle. This means the ventricles do not contract simultaneously, significantly reducing the ejection force at the septal wall (Docherty and Douglas, 2003c). Heart rhythms defined as slow may be <60bpm (<35bpm is defined as severe) or uncoordinated between the atria and ventricles due to SA node or internodal tract ischaemia slowing or interrupting the passage of impulses (Philip and Kowey, 2001). This leads to a reduced cardiac output creating hypotension and poor perfusion (RCUK, 2004). Examples of these include sinus bradycardia and complete heart block (Fig 3), which can be managed chemically (for example with atropine or adrenaline) or mechanically/electrically with external transcutaneous or internal transvenous pacing (RCUK, 2004). Common signs and symptoms of arrhythmias include fatigue, chest pain, being light-headed, fear or sense of impending doom, breathlessness, palpitations, chest pain, lethargy and fainting (Philip and Kowey 2001; Docherty and Douglas, 2003a). Any patient with these symptoms should be placed on an ECG monitor, have their pulse and blood pressure recorded, venous blood taken for electrolyte analysis and a 12-lead ECG (RCUK, 2004). This article has been double-blind peer-reviewed. For related articles on this subject and links to relevant websites see www.nursingtimes.net

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