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Electrocardiogram and arrhythmias
PHYSIOLOGY
Electrocardiogram and arrhythmias
Learning objectives After reading this article, you should be able to: C recognize two common variations of each of the normal P, QRS and T waves C distinguish the three atrioventricular blocks C describe three common tachyarrhythmias.
Rajender Singh Jeremy J Murphy
Abstract
the chest wall. Each chest lead records the impulse immediately beneath the electrode because the heart is close to the chest wall. (For detailed discussion about lead position and cardiac depolarization please refer to Anaesthesia and Intensive Care Medicine 2006; 7: 264e6.)
Introduced by Einthoven, electrocardiography remains the most common diagnostic procedure readily available to the physician in primary and secondary care. It is a graphical display of the electrical potential difference as it spreads through the heart and is recorded at the body surface. The electrocardiogram (ECG) is an indispensable tool to screen and monitor cardiac patients. Exercise ECG is used to diagnose coronary artery disease and ambulatory ECG to assess arrhythmias.
ECG waves P wave P waves result from atrial activation by the sinoatrial (SA) node. Because the SA node is situated in the right atrium, right atrial activation begins first and is reflected by the proximal (ascending) limb of the P wave. Left atrial activation begins 0.03 seconds later and is represented by the descending limb of the P wave. Because of the orientation of the leads, this is best seen in standard lead II and lead V1. The P wave in these leads is usually positive, pyramidal and with a slightly rounded apex. It is normally inverted in aVR, and upright in aVF plus the left chest leads (V4e6). Amplitude does not usually exceed 2e3 mm in any lead.
Keywords Atrial fibrillation; atrial flutter; atrioventricular block; bradycardia; ECG waves and their variations; electrical impulse of the heart; tachycardia; ventricular tachycardia Royal College of Anaesthetists CPD Matrix: 1A01
ECG lead system Heart muscle generates an electrical current that can be recorded from the surface of the body by the electrocardiogram (ECG). The 12 conventional ECG leads record the difference in potential between the electrodes on the body surface. ECG leads are divided into two groups: six limb leads and six chest leads. Of the six limb leads, three are bipolar leads and have been in use for more than a century (lead I, lead II and lead III). These leads measure the difference in potential between electrodes at two extremities: lead I, left armeright arm; lead II, left legeright arm; and lead III, left legeleft arm. All leads introduced later are unipolar leads and are termed ‘V’ leads. These measure the voltage (V) at one locus relative to a common central terminal (indifferent electrode) that has approximately zero potential. These comprise the three limb leads aVR, aVL and aVF, where aVR is the right arm, aVL is the left arm and aVF is the left leg (foot). These three limb leads detect only a small deflection of current, which is augmented 50% by the machine. This augmentation of potential is designated by the prefix ‘a’. There are six unipolar chest (precordial) leads that are designated V1eV6; these are placed directly over
Variations of the P wave: Inversion e in leads where it is normally upright (or upright in aVR), an inverted P wave would indicate that the impulse is travelling in an unusual path (e.g. atrial ectopic, atrioventricular (AV) junctional rhythm). Increased amplitude e this is due to right atrial hypertrophy and is seen in cor pulmonale and congenital heart disease. Biphasic (descending limb more negative than the ascending limb) e P waves in leads III and V1 are a sign of left atrial enlargement. P mitrale e notched P waves (distance between two peaks more than 0.04 seconds) owing to left atrial involvement in mitral disease. It is usually notched and taller in lead I than in lead III. QRS complex The QRS complex reflects rapid ventricular depolarization. An initial downward deflection is termed the Q wave and ensuing deflections are labelled in alphabetical order. The first positive deflection is designated R, whereas S is the first negative deflection that follows the R wave. This represents the terminal part of the ventricular activation. The complex ventricular depolarization can be divided into two sequential phases. The first phase is the activation of the ventricular septum from left to right. The second phase is the simultaneous activation of the right and left ventricles, usually dominated by the bulky left ventricle. In the chest leads, as a consequence of this normal depolarization process, the right-oriented leads (V1 and V2) show a small
Rajender Singh MBBS MD MRCP is a Medical Registrar at County Durham & Darlington Foundation Trust, and is also an Honorary Research Associate at the Centre of Integrated Health Care Research, Durham University, UK. Conflicts of interest: none declared. Jeremy J Murphy MSc(Med Ed) MBBS DM FRCP is a Consultant Cardiologist at County Durham & Darlington Foundation Trust, and is also an Honorary Senior Lecturer at Durham University, UK. Conflicts of interest: none declared.
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Ó 2018 Published by Elsevier Ltd.
PHYSIOLOGY
beats per minute is termed bradycardia, whereas the term tachycardia is reserved for rates in excess of 100 beats per minute.
upward deflection (septal R wave), followed by a deep S wave. The same sequence in the left-sided chest leads (V6, aVL, lead I) causes a small downward deflection (physiological Q wave) followed by a tall R wave. In the intermediate chest leads, there is a relative increase in the R wave and a reduction in the S wave amplitude (normal R wave progression) from left to right. R and S waves are approximately equal in the mid-chest leads (V3 and V4); this is called the transition zone. The QRS pattern in the limb leads varies and depends on the mean QRS axis. Lead aVR, which records from the right shoulder, effectively ‘looks’ from the cavity of the heart with all the vectors directed away and thus has all negative deflections. The normal duration of the QRS complex is 0.05e0.10 seconds.
Bradycardia This is normally present during sleep and in fit athletes (athletes’ heart syndrome). Pressure receptors (baroceptors) in the aorta and carotid arteries respond to arterial pressure, altering vagal tone through acetylcholine release. In carotid sinus syndrome, there is increased sensitivity of the baroceptors located in the carotid sinus region of the carotid artery. Therefore, pressure on the neck can result in extreme bradycardia, dizziness and syncope. Sometimes, it can trigger asystole for up to 10 seconds. Heart rate also varies with the phase of respiration; this is called ‘sinus arrhythmia’ (For further description, please refer to Anaesthesia and Intensive Care Medicine 2006; 7: 264e6.)
Variations of the QRS complex: Prolonged QRS duration e a duration of 0.12 seconds or more signifies conduction delay, such as in bundle branch block, but can also be present with pre-excitation of the ventricles via an accessory pathway, such as in WolffeParkinsoneWhite syndrome. Right bundle branch block (RBBB) e this occurs more commonly than left bundle branch block, especially in people with structurally normal hearts. RBBB can also occur in acquired (valvular, ischaemic) and congenital heart disease, especially atrial septal defects. Left bundle branch block (LBBB) e this is usually due to ischaemic heart disease, hypertension, severe aortic stenosis and cardiomyopathy. Bundle branch blocks (QRS duration of 0.12 seconds or more) can be chronic or intermittent and they can be rate related as well. Therefore, some patients with supraventricular tachycardia (SVT) have broad complexes (aberrant conduction).
Atrioventricular (AV) block First-degree block: this is characterized by a prolonged PR interval (> 0.20 seconds), and is due to constant delay rather than a block in conduction of the impulse from the atrium to the ventricle. First-degree block is often present in athletes, but can be associated with ischaemic heart disease, acute rheumatic carditis and drugs such as digitalis and b-blockers. It causes no symptoms and requires no treatment other than observation. Second-degree block: type 1 second-degree AV block (Wenckebach, Mobitz type I); there is progressive prolongation of the PR interval, before a QRS complex fails to appear after a P wave. The block is usually in the AV node and the QRS is of normal duration. Causes are inferior wall myocardial infarction, drug intoxication with beta blockers, digoxin and calcium channel blockers. Type 1 block can be present in normal individuals with increased vagal tone, generally at night. If the ventricular rate is adequate and the patient is asymptomatic, observation is sufficient.
T wave The T wave is a marker of the ventricular recovery period (repolarization) and is normally inscribed in the same direction as the QRS complex. It is, therefore, normally upright in leads I and II and in the left-sided chest leads and is inverted in the aVR lead. It is variable in all other leads.
Type 2 second-degree AV block (Mobitz type II) (Figure 1 shows the 2:1 AV block): the PR interval remains constant before a sudden and unexpected failure of the P wave to conduct. It is usually due to disease of the HisePurkinje system and is often associated with an abnormal QRS wave. When two or more successive P waves are blocked, this is called high-grade AV block. Type 2 block can occur in the setting of anteroseptal myocardial infarction or sclerodegenerative disease of the fibrous skeleton of the heart. This is very likely to progress to symptomatic third-degree block or ventricular standstill, so permanent pacing is indicated. Physiological second-degree block is seen with fast supraventricular rhythms such as atrial tachycardia and atrial flutter.
Variations of the T wave: Tall positive T waves can be a normal variant, but are also seen in hyperkalaemia, hyperacute myocardial ischaemia, cerebrovascular injury and left ventricular volume overload. T wave inversion can be seen with cardiomyopathy, ischaemia, ventricular hypertrophy, myocarditis and intracranial bleeds. U wave U waves usually follow the T wave as a small rounded deflection ( 1 mm). An abnormal increase in the amplitude is seen with hypokalaemia, and with drugs such as quinidine and procainamide. This could be a sign of increased susceptibility to torsades de pointes.
Third-degree block (complete heart block): this is characterized by complete cessation of the electrical impulses from the atrium to the ventricle. P waves are dissociated from the ventricular complex and the two are asynchronously controlled by independent pacemakers. This is the most advanced form of AV block. It is mostly due to chronic degenerative changes in the bundle branches due to Lev’s and Lenegre’s disease. It can also occur with cardiomyopathy and inferior myocardial infarction. Complete heart block can be congenital owing to maternal
Arrhythmias It is beyond the scope of this article to discuss arrhythmias in detail, but a brief overview is provided. The heart normally beats approximately 70 times per minute at rest. A rate less than 60
ANAESTHESIA AND INTENSIVE CARE MEDICINE 19:6
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Ó 2018 Published by Elsevier Ltd.
PHYSIOLOGY
Figure 1 Bradycardia: type II second-degree (Mobitz type II) atrioventricular block. There are two P waves for one QRS complex (2:1 block).
waves on the ECG. The mechanism of AF is unclear, but it is believed that there are numerous micro-re-entry circuits or stimuli that excite the atria, usually from where the pulmonary veins enter the left atrium. The atrial rate is between 350 and 600 beats per minute (bpm), and this activity causes an undulating baseline. Impulses reach the AV node through multiple paths at frequent and irregular intervals. Rapidly entering atrial impulses render the AV node partially refractory to subsequent impulses, so the ventricular rate is somewhat slower and irregularly irregular. Acute AF can be precipitated by infection, alcohol, dehydration, congestive cardiac failure and pulmonary embolism. In acute AF, treating the primary cause usually resolves the arrhythmia. If the patient is compromised, electrical or chemical cardioversion can be performed.
transmission of antinuclear (Ro/SSA and/or La/SSB) antibodies. Treatment is permanent pacing because third-degree block carries significant mortality. Tachycardia Normally, myocardial cells do not discharge spontaneously. Tachyarrhythmias can arise from any part of the heart. These can be disorders of impulse formation (enhanced automaticity) owing to exogenous catecholamines, hyperkalaemia, hypoxia and digitalis; they can also arise from disorders of impulse spread (re-entry), such as in sustained supraventricular tachycardias. Tachyarrythmias can be further classified as (1) regular or irregular and (2) narrow or broad complex, depending on the QRS morphology. An irregular arrhythmia is usually atrial fibrillation (or flutter with variable block), whether narrow or broad complex. Regular narrow complex tachycardia is generally SVT in origin, whereas regular broad complex tachycardia usually originates from the ventricle.
Atrial flutter Atrial flutter (Figure 2) is characterized by rapid and regular atrial activity, causing a saw-tooth or picket-fence appearance, typically in the inferior leads. The mechanism is generally a macro-re-entry circuit in the right atrium. The atrial rate is 250 e350 bpm; the ventricular rate is typically half the atrial rate, usually around 150 bpm. Atrial flutter, when it lasts for more
Atrial fibrillation Atrial fibrillation (AF) can be paroxysmal or persistent and is characterized by disorganized atrial activity with no discrete P
Figure 2 Atrial flutter: regular narrow complex tachycardia showing 2:1 physiological block. P waves (arrows) are best seen in leads V1 and V2.
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PHYSIOLOGY
Figure 3 Regular broad complex ventricular tachycardia.
than a week, frequently converts to AF. Although the risk of systematic emobolization is less than for AF, management is the same for both.
notched downslope of S wave in V1 or V2; Q wave in V6. VT is commonly seen with structural heart disease, especially ischaemic heart disease. It can also occur with prolonged QT syndrome, cardiomyopathies and metabolic and drug disorders. VT without structural heart disease is usually benign; asymptomatic non-sustained VT is not treated, except the longQT syndrome. VT with haemodynamic compromise should be terminated immediately with direct current cardioversion. A
Ventricular tachycardia Ventricular tachycardia (VT) (Figure 3) is defined as three or more consecutive ectopic ventricular QRS complexes occurring at a rate of >100 bpm. It is called sustained VT if it lasts for more than 30 seconds or needs intervention. It is broad complex and quite regular, arising as a result of abnormal automaticity or (more commonly) re-entry distal to the His bundle. Broad complex tachycardia is most commonly VT, particularly if structural heart disease is present. Certain ECG criteria support VT as opposed to SVT with aberrant conduction. ECG features that favour VT are:1 atrioventricular dissociation QRS width: >0.14 seconds with RBBB configuration >0.16 seconds with LBBB configuration QRS axis: left axis with RBBB morphology extreme left axis with LBBB morphology concordance of QRS in precordial leads morphological patterns of QRS complex: RBBB mono- or biphasic complex V1 RS (only with left axis deviation) or QS in V6 LBBB broad R wave in V1 or V2 0.04 seconds onset of QRS to nadir of S wave in V1 or V2 of 0.07 seconds
ANAESTHESIA AND INTENSIVE CARE MEDICINE 19:6
REFERENCE 1 Josephson ME, Zimetbaum P. The tachyarrhythmias. In: Braunwald E, Fauci AS, Kasper DL, et al., eds. Harrison’s principle of internal medicine. 15th edn, vol. 1. New York: McGraw-Hill, 2001; 1303. FURTHER READING Marriott HJL. Practical electrocardiography. 8th edn. Baltimore, USA: Williams & Wilkins, 1988. Schamroth L. An introduction to electrocardiography. 7th edn. Oxford: Blackwell Science, 1990.
Acknowledgement This is an update of the original article by Emrys Kirkman (Kirkman E. The electrocardiogram. Anaesthesia and Intensive Care Medicine 2006; 7: 264e6), which discusses some basic principles of the ECG.
325
Ó 2018 Published by Elsevier Ltd.
Electrocardiogram and arrhythmias
Learning objectives After reading this article, you should be able to: C recognize two common variations of each of the normal P, QRS and T waves C distinguish the three atrioventricular blocks C describe three common tachyarrhythmias.
Rajender Singh Jeremy J Murphy
Abstract
the chest wall. Each chest lead records the impulse immediately beneath the electrode because the heart is close to the chest wall. (For detailed discussion about lead position and cardiac depolarization please refer to Anaesthesia and Intensive Care Medicine 2006; 7: 264e6.)
Introduced by Einthoven, electrocardiography remains the most common diagnostic procedure readily available to the physician in primary and secondary care. It is a graphical display of the electrical potential difference as it spreads through the heart and is recorded at the body surface. The electrocardiogram (ECG) is an indispensable tool to screen and monitor cardiac patients. Exercise ECG is used to diagnose coronary artery disease and ambulatory ECG to assess arrhythmias.
ECG waves P wave P waves result from atrial activation by the sinoatrial (SA) node. Because the SA node is situated in the right atrium, right atrial activation begins first and is reflected by the proximal (ascending) limb of the P wave. Left atrial activation begins 0.03 seconds later and is represented by the descending limb of the P wave. Because of the orientation of the leads, this is best seen in standard lead II and lead V1. The P wave in these leads is usually positive, pyramidal and with a slightly rounded apex. It is normally inverted in aVR, and upright in aVF plus the left chest leads (V4e6). Amplitude does not usually exceed 2e3 mm in any lead.
Keywords Atrial fibrillation; atrial flutter; atrioventricular block; bradycardia; ECG waves and their variations; electrical impulse of the heart; tachycardia; ventricular tachycardia Royal College of Anaesthetists CPD Matrix: 1A01
ECG lead system Heart muscle generates an electrical current that can be recorded from the surface of the body by the electrocardiogram (ECG). The 12 conventional ECG leads record the difference in potential between the electrodes on the body surface. ECG leads are divided into two groups: six limb leads and six chest leads. Of the six limb leads, three are bipolar leads and have been in use for more than a century (lead I, lead II and lead III). These leads measure the difference in potential between electrodes at two extremities: lead I, left armeright arm; lead II, left legeright arm; and lead III, left legeleft arm. All leads introduced later are unipolar leads and are termed ‘V’ leads. These measure the voltage (V) at one locus relative to a common central terminal (indifferent electrode) that has approximately zero potential. These comprise the three limb leads aVR, aVL and aVF, where aVR is the right arm, aVL is the left arm and aVF is the left leg (foot). These three limb leads detect only a small deflection of current, which is augmented 50% by the machine. This augmentation of potential is designated by the prefix ‘a’. There are six unipolar chest (precordial) leads that are designated V1eV6; these are placed directly over
Variations of the P wave: Inversion e in leads where it is normally upright (or upright in aVR), an inverted P wave would indicate that the impulse is travelling in an unusual path (e.g. atrial ectopic, atrioventricular (AV) junctional rhythm). Increased amplitude e this is due to right atrial hypertrophy and is seen in cor pulmonale and congenital heart disease. Biphasic (descending limb more negative than the ascending limb) e P waves in leads III and V1 are a sign of left atrial enlargement. P mitrale e notched P waves (distance between two peaks more than 0.04 seconds) owing to left atrial involvement in mitral disease. It is usually notched and taller in lead I than in lead III. QRS complex The QRS complex reflects rapid ventricular depolarization. An initial downward deflection is termed the Q wave and ensuing deflections are labelled in alphabetical order. The first positive deflection is designated R, whereas S is the first negative deflection that follows the R wave. This represents the terminal part of the ventricular activation. The complex ventricular depolarization can be divided into two sequential phases. The first phase is the activation of the ventricular septum from left to right. The second phase is the simultaneous activation of the right and left ventricles, usually dominated by the bulky left ventricle. In the chest leads, as a consequence of this normal depolarization process, the right-oriented leads (V1 and V2) show a small
Rajender Singh MBBS MD MRCP is a Medical Registrar at County Durham & Darlington Foundation Trust, and is also an Honorary Research Associate at the Centre of Integrated Health Care Research, Durham University, UK. Conflicts of interest: none declared. Jeremy J Murphy MSc(Med Ed) MBBS DM FRCP is a Consultant Cardiologist at County Durham & Darlington Foundation Trust, and is also an Honorary Senior Lecturer at Durham University, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 19:6
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Ó 2018 Published by Elsevier Ltd.
PHYSIOLOGY
beats per minute is termed bradycardia, whereas the term tachycardia is reserved for rates in excess of 100 beats per minute.
upward deflection (septal R wave), followed by a deep S wave. The same sequence in the left-sided chest leads (V6, aVL, lead I) causes a small downward deflection (physiological Q wave) followed by a tall R wave. In the intermediate chest leads, there is a relative increase in the R wave and a reduction in the S wave amplitude (normal R wave progression) from left to right. R and S waves are approximately equal in the mid-chest leads (V3 and V4); this is called the transition zone. The QRS pattern in the limb leads varies and depends on the mean QRS axis. Lead aVR, which records from the right shoulder, effectively ‘looks’ from the cavity of the heart with all the vectors directed away and thus has all negative deflections. The normal duration of the QRS complex is 0.05e0.10 seconds.
Bradycardia This is normally present during sleep and in fit athletes (athletes’ heart syndrome). Pressure receptors (baroceptors) in the aorta and carotid arteries respond to arterial pressure, altering vagal tone through acetylcholine release. In carotid sinus syndrome, there is increased sensitivity of the baroceptors located in the carotid sinus region of the carotid artery. Therefore, pressure on the neck can result in extreme bradycardia, dizziness and syncope. Sometimes, it can trigger asystole for up to 10 seconds. Heart rate also varies with the phase of respiration; this is called ‘sinus arrhythmia’ (For further description, please refer to Anaesthesia and Intensive Care Medicine 2006; 7: 264e6.)
Variations of the QRS complex: Prolonged QRS duration e a duration of 0.12 seconds or more signifies conduction delay, such as in bundle branch block, but can also be present with pre-excitation of the ventricles via an accessory pathway, such as in WolffeParkinsoneWhite syndrome. Right bundle branch block (RBBB) e this occurs more commonly than left bundle branch block, especially in people with structurally normal hearts. RBBB can also occur in acquired (valvular, ischaemic) and congenital heart disease, especially atrial septal defects. Left bundle branch block (LBBB) e this is usually due to ischaemic heart disease, hypertension, severe aortic stenosis and cardiomyopathy. Bundle branch blocks (QRS duration of 0.12 seconds or more) can be chronic or intermittent and they can be rate related as well. Therefore, some patients with supraventricular tachycardia (SVT) have broad complexes (aberrant conduction).
Atrioventricular (AV) block First-degree block: this is characterized by a prolonged PR interval (> 0.20 seconds), and is due to constant delay rather than a block in conduction of the impulse from the atrium to the ventricle. First-degree block is often present in athletes, but can be associated with ischaemic heart disease, acute rheumatic carditis and drugs such as digitalis and b-blockers. It causes no symptoms and requires no treatment other than observation. Second-degree block: type 1 second-degree AV block (Wenckebach, Mobitz type I); there is progressive prolongation of the PR interval, before a QRS complex fails to appear after a P wave. The block is usually in the AV node and the QRS is of normal duration. Causes are inferior wall myocardial infarction, drug intoxication with beta blockers, digoxin and calcium channel blockers. Type 1 block can be present in normal individuals with increased vagal tone, generally at night. If the ventricular rate is adequate and the patient is asymptomatic, observation is sufficient.
T wave The T wave is a marker of the ventricular recovery period (repolarization) and is normally inscribed in the same direction as the QRS complex. It is, therefore, normally upright in leads I and II and in the left-sided chest leads and is inverted in the aVR lead. It is variable in all other leads.
Type 2 second-degree AV block (Mobitz type II) (Figure 1 shows the 2:1 AV block): the PR interval remains constant before a sudden and unexpected failure of the P wave to conduct. It is usually due to disease of the HisePurkinje system and is often associated with an abnormal QRS wave. When two or more successive P waves are blocked, this is called high-grade AV block. Type 2 block can occur in the setting of anteroseptal myocardial infarction or sclerodegenerative disease of the fibrous skeleton of the heart. This is very likely to progress to symptomatic third-degree block or ventricular standstill, so permanent pacing is indicated. Physiological second-degree block is seen with fast supraventricular rhythms such as atrial tachycardia and atrial flutter.
Variations of the T wave: Tall positive T waves can be a normal variant, but are also seen in hyperkalaemia, hyperacute myocardial ischaemia, cerebrovascular injury and left ventricular volume overload. T wave inversion can be seen with cardiomyopathy, ischaemia, ventricular hypertrophy, myocarditis and intracranial bleeds. U wave U waves usually follow the T wave as a small rounded deflection ( 1 mm). An abnormal increase in the amplitude is seen with hypokalaemia, and with drugs such as quinidine and procainamide. This could be a sign of increased susceptibility to torsades de pointes.
Third-degree block (complete heart block): this is characterized by complete cessation of the electrical impulses from the atrium to the ventricle. P waves are dissociated from the ventricular complex and the two are asynchronously controlled by independent pacemakers. This is the most advanced form of AV block. It is mostly due to chronic degenerative changes in the bundle branches due to Lev’s and Lenegre’s disease. It can also occur with cardiomyopathy and inferior myocardial infarction. Complete heart block can be congenital owing to maternal
Arrhythmias It is beyond the scope of this article to discuss arrhythmias in detail, but a brief overview is provided. The heart normally beats approximately 70 times per minute at rest. A rate less than 60
ANAESTHESIA AND INTENSIVE CARE MEDICINE 19:6
323
Ó 2018 Published by Elsevier Ltd.
PHYSIOLOGY
Figure 1 Bradycardia: type II second-degree (Mobitz type II) atrioventricular block. There are two P waves for one QRS complex (2:1 block).
waves on the ECG. The mechanism of AF is unclear, but it is believed that there are numerous micro-re-entry circuits or stimuli that excite the atria, usually from where the pulmonary veins enter the left atrium. The atrial rate is between 350 and 600 beats per minute (bpm), and this activity causes an undulating baseline. Impulses reach the AV node through multiple paths at frequent and irregular intervals. Rapidly entering atrial impulses render the AV node partially refractory to subsequent impulses, so the ventricular rate is somewhat slower and irregularly irregular. Acute AF can be precipitated by infection, alcohol, dehydration, congestive cardiac failure and pulmonary embolism. In acute AF, treating the primary cause usually resolves the arrhythmia. If the patient is compromised, electrical or chemical cardioversion can be performed.
transmission of antinuclear (Ro/SSA and/or La/SSB) antibodies. Treatment is permanent pacing because third-degree block carries significant mortality. Tachycardia Normally, myocardial cells do not discharge spontaneously. Tachyarrhythmias can arise from any part of the heart. These can be disorders of impulse formation (enhanced automaticity) owing to exogenous catecholamines, hyperkalaemia, hypoxia and digitalis; they can also arise from disorders of impulse spread (re-entry), such as in sustained supraventricular tachycardias. Tachyarrythmias can be further classified as (1) regular or irregular and (2) narrow or broad complex, depending on the QRS morphology. An irregular arrhythmia is usually atrial fibrillation (or flutter with variable block), whether narrow or broad complex. Regular narrow complex tachycardia is generally SVT in origin, whereas regular broad complex tachycardia usually originates from the ventricle.
Atrial flutter Atrial flutter (Figure 2) is characterized by rapid and regular atrial activity, causing a saw-tooth or picket-fence appearance, typically in the inferior leads. The mechanism is generally a macro-re-entry circuit in the right atrium. The atrial rate is 250 e350 bpm; the ventricular rate is typically half the atrial rate, usually around 150 bpm. Atrial flutter, when it lasts for more
Atrial fibrillation Atrial fibrillation (AF) can be paroxysmal or persistent and is characterized by disorganized atrial activity with no discrete P
Figure 2 Atrial flutter: regular narrow complex tachycardia showing 2:1 physiological block. P waves (arrows) are best seen in leads V1 and V2.
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Figure 3 Regular broad complex ventricular tachycardia.
than a week, frequently converts to AF. Although the risk of systematic emobolization is less than for AF, management is the same for both.
notched downslope of S wave in V1 or V2; Q wave in V6. VT is commonly seen with structural heart disease, especially ischaemic heart disease. It can also occur with prolonged QT syndrome, cardiomyopathies and metabolic and drug disorders. VT without structural heart disease is usually benign; asymptomatic non-sustained VT is not treated, except the longQT syndrome. VT with haemodynamic compromise should be terminated immediately with direct current cardioversion. A
Ventricular tachycardia Ventricular tachycardia (VT) (Figure 3) is defined as three or more consecutive ectopic ventricular QRS complexes occurring at a rate of >100 bpm. It is called sustained VT if it lasts for more than 30 seconds or needs intervention. It is broad complex and quite regular, arising as a result of abnormal automaticity or (more commonly) re-entry distal to the His bundle. Broad complex tachycardia is most commonly VT, particularly if structural heart disease is present. Certain ECG criteria support VT as opposed to SVT with aberrant conduction. ECG features that favour VT are:1 atrioventricular dissociation QRS width: >0.14 seconds with RBBB configuration >0.16 seconds with LBBB configuration QRS axis: left axis with RBBB morphology extreme left axis with LBBB morphology concordance of QRS in precordial leads morphological patterns of QRS complex: RBBB mono- or biphasic complex V1 RS (only with left axis deviation) or QS in V6 LBBB broad R wave in V1 or V2 0.04 seconds onset of QRS to nadir of S wave in V1 or V2 of 0.07 seconds
ANAESTHESIA AND INTENSIVE CARE MEDICINE 19:6
REFERENCE 1 Josephson ME, Zimetbaum P. The tachyarrhythmias. In: Braunwald E, Fauci AS, Kasper DL, et al., eds. Harrison’s principle of internal medicine. 15th edn, vol. 1. New York: McGraw-Hill, 2001; 1303. FURTHER READING Marriott HJL. Practical electrocardiography. 8th edn. Baltimore, USA: Williams & Wilkins, 1988. Schamroth L. An introduction to electrocardiography. 7th edn. Oxford: Blackwell Science, 1990.
Acknowledgement This is an update of the original article by Emrys Kirkman (Kirkman E. The electrocardiogram. Anaesthesia and Intensive Care Medicine 2006; 7: 264e6), which discusses some basic principles of the ECG.
325
Ó 2018 Published by Elsevier Ltd.