Dr Juliette Lee,
Royal Devon And Exeter Hospital, Exeter, UK - Previously: Ngwelezana Hospital, Empangeni, Kwa-zulu Natal, RSA

ECG Monitoring in Theatre		Broad Complex Arrhythmias
The Conducting System of the Heart		Disturbances of Conditions
Graphical Recording		Pre-Operative Prophylactic Pacemaker Insertion
Lead Positions		Detection of Myocardial Ischaemia
Cardiac Arrhythmias		Other ECG Changes Seen in Theatre
Practical Interpretation and Management of Arrhythmias		ECG Appearance of Abnormal Potassium Concentrations
Classification of Arrhythmias		Further Reading and References
Narrow Complex Arrhythmias

ECG Monitoring in Theatre

Cardiac arrhythmias during anaesthesia and surgery occur in up to 86% of patients. Many are of clinical significance and therefore their detection is of considerable importance. This article will discuss the basic principles of using the ECG monitor in the operating theatre. It will describe the main rhythm abnormalities and give practical guidance on how to recognise and treat them.

The continuous oscilloscopic ECG is one of the most widely used anaesthetic monitors, and in addition to displaying arrhythmias it can also be used to detect myocardial ischaemia, electrolyte imbalances, and assess pacemaker function. A 12 lead ECG recording will provide much more information than is available on a theatre ECG monitor, and should where possible, be obtained pre-operatively in any patient with suspected cardiac disease.

The ECG is a recording of the electrical activity of the heart. It does not provide information about the mechanical function of the heart and cannot be used to assess cardiac output or blood pressure. Cardiac function under anaesthesia is usually estimated using frequent measurements of blood pressure, pulse, oxygen saturation, peripheral perfusion and end tidal CO2 concentrations. Cardiac performance is occasionally measured directly in theatre using Swan Ganz catheters or oesophageal Doppler techniques, although this is uncommon.

The ECG monitor should always be connected to the patient before induction of anaesthesia or institution of a regional block. This will allow the anaesthetist to detect any change in the appearance of the ECG complexes during anaesthesia.

Connecting an ECG monitor

Although an ECG trace may be obtained with the electrodes attached in a variety of positions, conventionally they are placed in a standard position each time so that abnormalities are easier to detect. Most monitors have 3 leads and they are connected as follows:

• Red - right arm, (or second intercostal space on the right of the sternum)
• Yellow - left arm (or second intercostal space on the left of the sternum)
• Black (or Green) - left leg (or more often in the region of the apex beat.)

This will allow the Lead I, II or III configurations to be selected on the ECG monitor. Lead II is the most commonly used. (See below for other lead positions and their uses).

The cables from the electrodes usually terminate in a single cable which is plugged into the port on the ECG monitor.

A good electrical connection between the patient and the electrodes is required to minimise the resistance of the skin. For this reason gel pads or suction caps with electrode jelly are used to connect the electrodes to the patients skin. However when the skin is sweaty the electrodes may not stick well, resulting in an unstable trace. When electrodes are in short supply they may be reused after moistening with saline or gel before being taped to the patient's chest. Alternatively, an empty 1000ml iv infusion bag may be cut open to allow it to lie flat (in the form of a flat piece of plastic) on the patient's chest. If 3 small holes are made in 3 of the corners electrodes may be stuck on one side of the plastic allowing the electrode gel to make contact with the skin. This device can be cleaned at the end of the operation and laid on the next patient allowing electrodes to be used repeatedly.

Principles of the ECG

The ECG is a recording of the electrical activity of the heart. An electrical recording made from one myocardial muscle cell will record an action potential (the electrical activity which occurs when the cell is stimulated). The ECG records the vector sum (the combination of all electrical signals) of all the action potentials of the myocardium and produces a combined trace.

At rest the potential difference across the membrane of a myocardial cell is -90mv (figure 1). This is due to a high intracellular potassium concentration which is maintained by the sodium/potassium pump. Depolarisation of a cardiac cell occurs when there is a sudden change in the permeability of the membrane to sodium. Sodium floods into the cell and the negative resting voltage is lost (stage 0). Calcium follows the sodium through the slower calcium channels resulting in binding between the intracellular proteins actin and myosin which results in contraction of the muscle fibre (stage 2). The depolarisation of a myocardial cell causes the depolarisation of adjacent cells and in the normal heart the depolarisation of the entire myocardium follows in a co-ordinated fashion. During repolarisation potassium moves out of the cells (stage 3) and the resting negative membrane potential is restored.
The Conducting System of the Heart The specialised cardiac conducting system (figure 2) consists of : The Sinoatrial (SA) node, internodal pathways, Atrioventricular (AV) node, bundle of HIS with right and left bundle branches and the Purkinje system. The left bundle branch also divides into anterior and posterior fascicles. Conducting tissue is made up of modified cardiac muscle cells which have the property of automaticity, that is they can generate their own intrinsic action potentials as well as responding to stimulation from adjacent cells. The conducting pathways within the heart are responsible for the organised spread of action potentials within the heart and the resulting co-ordinated contraction of both atria and ventricles.
In pacemaker tissue, after repolarisation has occurred, the membrane potential gradually rises to the threshold level for channel opening, at which point sodium floods into the cell and initiates the next action potential (figure 3). This gradual rise is called the pacemaker (or pre-potential) and is due to a decrease in the membrane permeability to potassium ions which result in the inside of the cell becoming less negative. The rate of rise of the pacemaker potential is the main determinant of heart rate and is increased by adrenaline (epinephrine) and sympathetic stimulation and decreased by vagal stimulation and hypothermia. Pacemaker activity normally only occurs in the SA and AV nodes, but there are latent pacemakers in other parts of the conducting system which take over when firing from the SA or AV nodes is depressed. Atrial and ventricular muscle fibres do not have pacemaker activity and discharge spontaneously only when damaged or abnormal.

Graphical Recording

On a paper trace the ECG is usually recorded on a time scale of 0.04 seconds/mm on the horizontal axis and a voltage sensitivity of 0.1mv/mm on the vertical axis (figure 4). Therefore, on standard ECG recording paper,1 small square represents 0.04seconds and one large square 0.2 seconds. In the normal ECG waveform the P wave represents atrial depolarisation, the QRS complex ventricular depolarisation and the T wave ventricular repolarisation.

• The P - R Interval is taken from the start af the P wave to the start of the QRS complex. It is the time taken for depolarisation to pass from the SA node via the atria, AV node and His-Purkinje system to the ventricles.
• The QRS represents the time taken for depolarisationto pass through the His-Purkinje system and the ventricular muscles. It is prolonged with disease of the His-Purkinje system.
• The Q - T interval is taken from the start of the QRS complex to the end of the T wave. This represents the time taken to depolarise and repolarise the ventricles.
• The S - T segment is the period between the end of the QRS complex and the start of the T wave. All cells are normally depolarised during this phase. The ST segment is changed by pathology such as myocardial ischaemia or pericarditis.

Lead Positions

The ECG may be used in two ways. A 12 lead ECG may be performed which analyses the cardiac electrical activity from a number of electrodes positioned on the limbs and across the chest. A wide range of abnormalities may be detected including arrhythmias, myocardial ischaemia, left ventricular hypertrophy and pericarditis.

During anaesthesia, however, the ECG is monitored using only 3 (or occasionally 5) electrodes which provide a more restricted analysis of the cardiac electrical activity and cannot provide the same amount of information that may be revealed by the 12 lead ECG.

The term 'lead' when applied to the ECG does not describe the electrical cables connected to the electrodes on the patient. Instead it refers to the positioning of the 2 electrodes being used to detect the electrical activity of the heart. A third electrode acts as a neutral. During anaesthesia one of 3 possible 'leads' is generally used. These leads are called bipolar leads as they measure the potential difference (electrical difference) between two electrodes. Electrical activity travelling towards an electrode is displayed as a positive (upward) deflection on the screen, and electrical activity travelling away as a negative (downward) deflection. The leads are described by convention as follows:

• Lead I - measures the potential difference between the right arm electrode and the left arm electrode. The third electrode (left leg) acts as neutral.
• Lead II - measures the potential difference between the right arm and left leg electrode.
• Lead III - measures the potential difference between the left arm and left leg electrode.

Most monitors can only show one lead at a time and therefore the lead that gives as much information as possible should be chosen. The most commonly used lead is lead II (figure 5) - a bipolar lead with electrodes on the right arm and left leg as above. This is the most useful lead for detecting cardiac arrhythmias as it lies close to the cardiac axis ( the overall direction of electrical movement ) and allows the best view of P and R waves.
For detection of myocardial ischaemia the CM5 lead is useful (figure 6). This is a bipolar lead with the right arm electrode placed on the manubrium and left arm electrode placed at the surface marking of the V5 position (just above the 5th interspace in the anterior axillary line). The left leg lead acts as a neutral and may be placed anywhere - the C refers to 'clavicle' where it is often placed. To select the CM5 lead on the monitor, turn the selector dial to 'lead I'. This position allows detection of up to 80% of left ventricular episodes of ischaemia, and as it also displays arrhythmias it can be recommended for usein most patients.

The CB5 lead is another bipolar lead which has one electrode positioned at V5 and the other over the right scapula. This results in improved QRS and P wave voltages allowing easier detection of arrhythmias and ischaemia. Many other electrode positions have been described including some used during cardiac surgery, for example oesophageal and intracardiac ECG's. 

Cardiac Arrhythmias

The detection of cardiac arrhythmias and the determination of heart rate is the most useful function of the intraoperative ECG. Anaesthesia and surgery may cause any type of arrhythmia including:

• Transient supraventricular and ventricular tachycardias due to sympathetic stimulation during laryngoscopy and intubation.
• Bradycardias produced by surgical manipulation resulting in vagal stimulation. Severe bradycardia and asystole may result. It is more common in children because the sympathetic innervation of the heart is immature and vagal tone predominates. Bradycardias are most commonly seen in ophthalmic surgery due to the oculocardiac reflex. Generally the heart rate will improve when the surgical stimulus is removed.
• Atrial fibrillation is common during thoracic surgery.

Drugs may also cause changes in cardiac rhythm eg;

• Halothane and nitrous oxide may cause junctional rhythms - (these will be detailed later). Halothane has a direct effect on the SA node and conducting system leading to a slowing in impulse generation and conduction and predisposes to re-entry phenomena. Catecholamines also have potent effects on impulse conduction, so the interaction of halothane and exogenous or endogenous catecholamines may cause ventricular arrhythmias. Ventricular ectopic beats are common. However rhythm disturbances such as ventricular tachycardia or rarely ventricular fibrillation may occur. The presence of cardiac disease, hypoxia, acidosis, hypercarbia (raised CO2 level) or electrolyte disturbances will increase the likelihood of these arrhythmias.
• Arrhythmias occurring during halothane anaesthesia can often be resolved by reducing the concentration of halothane, ensuring adequate ventilation thereby preventing hypercarbia, increasing the inspired oxygen concentration and providing an adequate depth of anaesthesia for the surgical procedure. Tachyarrhythmias in the presence of halothane anaesthesia are uncommon if ventilation is adequate, and the use of adrenaline infiltration for haemostasis is limited to solutions of 1:100,000 or less and the dose in adults is not greater than 0.1mg in 10 minutes or 0.3mg per hour ).
• Drugs increasing heart rate include ketamine, ether, atropine and pancuronium. Drugs decreasing heart rate include opioids, beta blockers and halothane.

Action Plan - when faced with an abnormal rhythm on the ECG monitor

Assess the vital signs - A.B.C.

• Check the airway is patent
• Check the patient is breathing adequately or is being ventilated correctly
• Listen for equal air entry into both lungs
• Circulation - check pulse, blood pressure, oxygen saturation. Is there haemodynamic compromise? Does the abnormal rhythm on the monitor match the pulse that you can feel?

Consider the following:

• Increase the inspired oxygen concentration
• Reduce the inspired volatile agent concentration
• Ensure that ventilation is adequate to prevent CO2 build up. Check end tidal CO2 where this measurement is available
• Consider what the surgeon is doing - is this the cause of the problem? Eg: traction on the peritoneum or eye causing a vagal response. If so ask them to stop while you treat the arrhythmia.
• If the arrhythmia is causing haemodynamic instability, rapid recognition and treatment is required. However, many abnormal rhythms encountered in every day practice will respond to the above basic measures - sometimes even before identification of the exact rhythm abnormality is possible. 

(Continued ...)

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