Brendan Docherty, MSc, RN, PGCE.
Clinical Manager - Cardiology and Critical Care, Queen Elizabeth Hospital NHS Trust, London, and Honorary Fellow, Healthcare Research Unit, City University, London
This is the first of a three-part cardiac care series comprising:
- February 2003: Interpretation of electrocardiogram rhythm strips.
- March 2003: Atrial arrhythmias.
- April 2003: Ventricular arrhythmias
Electrocardiogram (ECG) monitoring is non-invasive, well tolerated by patients and provides continuous electrical information about the heart. It is frequently used in critical care areas such as the accident and emergency (A&E) department, intensive care units, coronary care units and high-dependency units. However, it is also becoming more common in medical wards for those patients with a cardiac history or unstable medical conditions and in surgical ward areas for those postoperative patients who require more intensive monitoring.In this first paper we look at the background to ECG monitoring, the anatomy and physiology of the heart and recording and interpreting an ECG.
Background to ECG monitoring
Within the National Nursing Strategy (DoH, 1999) there are 10 key roles for nursing, of which three have a direct impact on the patient requiring technological intervention. These are:
- Resuscitation skills (for example defibrillation and arrhythmia management)
- Admission and discharge (for example locating patients in an appropriate, safe environment for care)
- Prescribing/administering therapeutics.All these nursing imperatives relate to the patient with chest pain, ECG interpretation and the ensuing clinical care.
The recent National Service Framework for Coronary Heart Disease standard eight states:
‘People with symptoms of angina or suspected angina should receive appropriate investigation and treatment to relieve their pain and reduce their risk of coronary events’ and that ‘the commonest symptom of coronary heart disease is angina. Each year in the UK more than 20 000 people develop angina for the first time’ (DoH, 2001).
The main reason for placing a patient on a cardiac monitor is for the purpose of early detection of arrhythmias that have an adverse effect on cardiac output or that have the potential to do so. They include atrial, ventricular and atrio-ventricular rhythms associated with ischaemic heart disease, electrolyte imbalance or drug toxicity (Docherty and Roe, 2001).
The aim of this series of three papers is to provide information on how to analyse and interpret this range of cardiac arrhythmias. Equipped with this information, ward nurses should be able to determine the causes, signs and symptoms of cardiac arrhythmias and the nursing interventions required to improve patient outcomes.
For all three papers Medline, Cinahl, Embase and Cochrane databases were searched for the years 1996-January 2003. The key words used were electrocardiogram, arrhythmia, cardiac monitoring and rhythm monitoring. All terms were ‘exploded’ and subsets included. The papers were retrieved and critiqued for robustness using the model provided by Benton and Cormack (2000).
Anatomy and physiology
Cardiac muscle (myocardium) is striated and has involuntary function, and is able to establish its own contraction (depolarisation) and relaxation (repolarisation) cycle - often called autorhythmicity (Tortora and Grabowski, 2001). The atria are the two upper chambers of the heart and they have a connected neural network. This means that when one neurone is stimulated, this will spread rapidly across the network covering the atria. This mechanism is also true for the lower chambers, called ventricles. Neural pathways connect the upper atrial and lower ventricular networks between the sino-atrial node and the atrio-ventricular node (Tortora and Grabowski, 2001). See Figure 1.
The conduction pathway operates by both autorhythmic ability and from the cardiorespiratory centre in the medulla of the brain (Tortora and Grabowski, 2001). The latter can increase neural stimulation (through the glossopharyngeal nerve in the sympathetic nervous system) or biochemical stimulation (through release of norepinephrine (noradrenaline) at the adrenal medulla) to increase the heart rate. These two mechanisms are negative feedback loops that allow more frequent and larger volumes of oxygenated blood to be delivered during times of increased need, for example during exercise.
The normal conduction impulse is generated in the sino-atrial (SA) node that then transmits across the right and left atria - this is shown by a P wave on the ECG. The dividing wall between the atria and ventricles - called the annulus fibrosis - stops this impulse going to the ventricles via any other route except through the specialised conduction network (Tortora and Grabowski, 2001). The impulse then travels down the designated inter-nodal pathway to the atrio-ventricular node (AV) - creating the PR interval - and then through a designated pathway to the bundle of His, down the septum (creating a small Q wave). From there the impulse travels down the right and left fascicles - or bundle branches - to the Purkinje fibres, where it depolarises, causing the ventricles to contract (creating the RS complex). As a result, a cardiac cycle is formed and the normal ECG complex is formed (Paul and Hebra, 1998) (Figure 1/Table 1).
Most ward patients who require monitoring will be attached to a portable three-lead monitor or a telemetry monitor, which sends the ECG signal to a central console. The latter is beneficial in the patient who is pain free and who is mobilising, whereas the former may restrict a patient’s movement and may give a negative sense of illness and dependency for the patient if he or she is able to mobilise (Thompson, 1997). However, most ward patients will be on ECG monitors as part of chest pain management, and will be on bed rest until they have been pain free for 24 hours (Jowett and Thompson, 1996).
The skin should be prepared before attaching electrodes by removing hair (cutting hair short rather than shaving) and by drying the skin (Hand, 2002). ECG electrodes should be changed every 24 to 48 hours (Docherty, 2000) and should be placed on bony areas to prevent muscle movement interfering with the ECG recording (Docherty, 2000; Hand, 2002) as this is potentially a main source of artefact. In one study, it was concluded that the source of an artefact in the ECG during cardiopulmonary resuscitation was the skin-electrode interface and, specifically, that the artefact was related to the electrical abilities of the electrode (Fitzgibbon et al, 2002).
The electrodes should be placed on the right shoulder, the left shoulder and then on the sternum or left rib cage, ensuring that the electrodes do not occupy space where defibrillator paddles may need to be placed (Thompson, 1997). Lead II should be selected on the monitor as it gives the most accurate ECG complex recording and usually the most positive deflection (Docherty and Roe, 2001). All monitor alarms should be set to the individual patient, taking into account his or her medical history. As a general rule staff would want to be alerted by the monitor alarm should the heart rate fall below 50 beats per minute (bpm) or rise above 120bpm.
ECG monitors should have the ability to freeze a particular rhythm for close inspection, be able to record a rhythm strip or store an ECG history should an alarm or arrhythmia be detected. Any changes in ECG rhythm should be followed by a 12-lead ECG and analysed by the appropriate personnel (Docherty and Roe, 2001).
When any arrhythmia presents itself and is known to be a new event (that is, not the patient’s normal rhythm), then oxygen 3-5 litres (28-40%) should be administered (Docherty, 2002a). Those patients with chronic airways disease should have 2 litres (24%). The nurse should then conduct cardiorespiratory assessments and should measure and record the patient’s blood pressure, pulse rate, peripheral oxygen saturation, respiratory rate and observe for any other change in their condition (Docherty, 2002a, 2002b). Cardiorespiratory observations will be essential for determining the final treatment modality used for that specific arrhythmia. In ward patients, the following are some, but not all, of the events that may require intervention should they occur:
- Increasing frequency of ventricular ectopics. These are extra-ventricular contractions that look bizarre: consider hypoxia, hypokalaemia or myocardial irritability as the main causes. Increased ventricular ectopic activity may lead to a cardiac arrest and is associated with an increased risk of cardiovascular disease and mortality (Evenson et al, 2000). Potassium levels should be maintained at 4.0-4.5mmol in cardiac patients, and magnesium levels should be maintained at 0.7-1.1mmol to stabilise the myocardium (Hedges et al, 2001; BMA and RPSGB, 2002)
- ST-segment changes during chest pain. Although not predictive of ischaemia or infarction changes (these should always be checked with a 12-lead ECG), the three-lead ECG may be indicative that ischaemia is occurring (Paul and Hebra, 1998)- Rate changes to being bradycardic. If the rate is less than 60bpm consider hypoxia or vagal stimulation, for example in nausea- Rate changes to being tachycardic. If the rate is greater than 100bpm consider pain and hypovolaemia (Paul and Hebra, 1998).
Heart rate can be calculated by dividing 1500 (the number of tiny squares in one minute of normal speed ECG paper) by the number of tiny squares between each R wave on the ECG (Paul and Hebra, 1998). This works well for regular rhythms. For irregular rhythms, the ECG paper is marked off in six-second intervals. The R waves in every six-second strip should be counted and multiplied by 10 to give the heart rate for a minute.The main questions asked when analysing an ECG are (Paul and Hebra, 1998):
- What is the heart rate?
- Is the rhythm regular or irregular?
- Are there P waves, and are they related to the QRS complex? Are the P waves the same morphology?
- Is the PR interval normal? Is it associated with the QRS complex?
- Is the QRS complex normal or wide?
- What is the rhythm and how is the patient responding?
Possible ECG arrhythmias discussed in this series are summarised in Table 2.
Benton, D.C., Cormack, F.S. (2000)Reviewing and evaluating the literature. In: Cormack, F.S. The Research Process in Nursing (4th edn). Oxford: Blackwell Science.
British Medical Association and Royal Pharmaceutical Society of Great Britain. (2002)British National Formulary (No. 43). London: BMA and RPSGB. Available at: www.bnf.org (Continued on page 323)
Department of Health. (1999)Making a Difference: Strengthening the nursing, midwifery and health visiting contribution to health and healthcare. London: The Stationery Office. Available at: www.doh.gov.uk/ nurstrat.htm
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Docherty, B. (2002a)Cardiorespiratory physical assessment for the acutely ill: part 1. British Journal of Nursing 11: 11, 750-758.
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Evenson, K.R., Lamar Welch, V.L., Cascio, W.E., Simpson, R.J. Jr. (2000)Validation of a short rhythm strip compared to ambulatory ECG monitoring for ventricular ectopy. Journal of Clinical Epidemiology 53: 5, 491-497.
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