Airway Management | Patient Monitoring & Diagnostics | Emergency Care A Pocket Guide to Common Arrhythmias Interpretation and Management
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Airway Management | Patient Monitoring & Diagnostics | Emergency Care
A Pocket Guide to Common Arrhythmias
Interpretation and Management
PrefaceIn a patient with suspected or known heart disease, the electrocardiogram should be regarded as an extension of the patient’s history and physical examination. Indeed, electrocardiography is a fundamental part of any cardiovascular assessment. As such, it is an essential tool for accurately diagnosing cardiac-rhythm disorders, ischemic chest pain, and estimating the extent of coronary artery disease. Moreover, the electrocardiogram gives invaluable information about the workload of the individual chambers of the heart, besides being helpful in diagnosing systemic diseases that affect the heart and disturbances in electrolyte metabolism. Because the electrocardiogram is such a powerful tool, it should be well understood for use by medical practitioners, medical students, nurses in intensive and coronary care units, and by paramedics in emergency services.It should be kept in mind, however, that a patient with an organic heart disorder could have a normal electrocardiogram, whereas a perfectly healthy individual may display non-specific electrocardiographic abnormalities. Thus the electrocardiogram should always be interpreted in conjunction with the clinical findings and never in isolation.
This ECG booklet is part of the educational concept ”Professional Advisory” that the Cardiology group from Ambu A/S is offering to provide users and purchasers with greater knowledge by imparting new learning, supplying better clinical documentation and sharing other helpful experiences.Ambu has made this booklet in cooperation with Dr. Christian Lange, Cardiologist, and it can be useful for doctors, nurses, technicians and anybody working within cardiology to analyze ECG patterns.It provides both examples of ECG patterns and diagnosis to match, symptoms and signs to be aware of and what treatment to offer. It also explains the function of the heart and the basic ECG pattern.
Thank you to Lars Ramløse for helping with illustrations in the book.
Another helpful tool Ambu has produced is an ECG ruler for fast and accurate diagnosis based on an ECG pattern. Please contact your local Ambu sales representative for more information.
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ContentsAnatomy and electricity of the heart ............................................4Conduction system ......................................................................5Heart rate, time and voltage ........................................................6The 12-lead ECG .........................................................................8P wave ......................................................................................10PR interval ................................................................................11QRS complex .............................................................................12ST segment ...............................................................................14T wave ......................................................................................15QT interval ................................................................................16U wave .....................................................................................17Sinus rhythm .............................................................................18Sinus bradycardia ......................................................................19Sinus tachycardia ......................................................................20Sinus arrhythmia .......................................................................22Sinoatrial (SA) block ..................................................................23Second-degree SA block ............................................................24Third-degree SA block and sinus arrest ......................................26Atrial fibrillation (AF) .................................................................28
Atrial flutter ..............................................................................32Atrial tachycardia ......................................................................34Multifocal supraventricular tachycardia ......................................36AV nodal re-entry tachycardia ....................................................38Ventricular tachycardia (VT) .......................................................40Ventricular fibrillation (VF) .........................................................44Atrioventricular (AV) block .........................................................46First-degree AV block .................................................................47Second-degree AV block ............................................................48Second-degree AV block – Mobitz type I (Wenckebach) ..............49Second-degree AV block – Mobitz type II ...................................50Advanced second-degree AV block ............................................52Third-degree (complete) AV block ..............................................54Extrasystoles (ectopic beats) ......................................................56Ventricular extrasystoles (ventricular ectopic beats) ....................58Supraventricular extrasystoles (atrial ectopic beats) ....................62Escape rhythms .........................................................................64Common Tracing Problems ........................................................66
Anatomy and electricity of the heartContraction and relaxation of cardiac muscle occurs as a result of electrical changes within the myocardial cells, referred to as depolarisation and re-polarisation. Electrodes attached to the skin on the limbs and chest wall can sense this electrical activity and transmit it to an electrocardiograph. The electrocardiograph then converts this information into waveforms, which are recorded on graph paper to produce an electrocardiogram, commonly known as an ECG.
Although the heart has four chambers, from the electrical point of view it can be thought of as having only two, since the two atria contract simultaneously and the two ventricles contract simultaneously.
The muscle mass of the atria is relatively small and the electrical changes accompanying the contraction are therefore equally small. Contraction (i.e. depolarisation) of the atria causes the ECG wave called P. Since the ventricular mass is large, there is a large deflection of the ECG when the ventricles contract (i.e. depolarise) and this is called the QRS complex. The T wave of the ECG is caused by the return of this ventricular mass to the resting electrical state called re-polarisation. Electrical events and corresponding ECG components.
The SA node depolarises - no deflection
The atria depolarise - P wave
The AV node and the bundle of His depolarise - no deflection
The free walls of the ventri-cles depolarise - QRS complex
The ventricles are totally depolarised - no deflection (ST segment)
The ventricles repolarise - T wave
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Conduction systemThe myocardium contains a system of highly specialised tissue that can conduct impulses faster than the surrounding muscle tissue. Parts of this specialised conducting tissue can discharge spontaneously and set up a wave of depolarisation through the rest of the conducting system of the entire heart.The sinoatrial (SA) or sinus node high in the right atrium, has the highest spontaneous discharge rate of 60–100 beats/min at rest, and therefore acts as a natural pacemaker and initiates atrial depolarisation. The impulse spreads from the sinoatrial node through the muscle mass of the atria to reach the atrioventricular (AV) node.Here the impulse is delayed before rapidly continuing through the bundle of His, which is normally the only pathway between the atria and the ventricles. In the septum between the ventricles, this single pathway divides into the right and left bundle branch. The left bundle branch then divides in two, an anterior and a posterior fascicle. At the lower part of the ventricular septum the conducting branches spread out in a complex network called Purkinje fibres. Therefore, after a delay in the atrioventricular node, atrial contraction is followed by rapid coordinated contraction of the ventricles.
The conduction system.
Sinoatrial node
Atrioventricular node
Right bundle branch
Left posterior hemifascicle
Left anterior hemi-fascicle
Left bundle branch
Electrically inert atrioventricular region
Rightatrium
Left atrium
Right ventricle
Left ventricle
The heart rate can be calculated rapidly by remembering the following sequence:
Number of large squaresbetween 2 QRS complexes
Heart rate(beats/min)
1 3002 1503 1004 755 606 50
Rate rulers are sometimes used to calculate heart rate; these are used to measure two or three consecutive R-R intervals, of which the average is expressed as the rate equivalent. When using a rate ruler, one must take care to count the correct numbers of beats (two or three) and restrict the technique to regular rhythms.
Heart rate, t ime and voltageThe electrocardiogram is recorded on standard paper travelling at a rate of 25 mm/s. The paper is divided into large squares, each is 5 mm wide - the equivalent of 0.2 seconds. Each large square is five small squares wide, and each small square is 1 mm wide - the equivalent of 0.04 seconds.
The heart rate is the number of heartbeats occurring in 1 minute. On an ECG, the heart rate is measured from R wave to R wave to determine the ventricular rate, and P wave to P wave to determine the atrial rate. The QRS complexes represent ventricular depolarisation and the P waves represent atrial depolarisation.The term tachycardia is used to describe a heart rate greater than 100 beats/min and bradycardia is defined as a rate less than 60 beats/min (or < 50 beats/min during sleep).
One large square of recording paper is equivalent to 0.2 seconds, so 5 large squares pass per second and 300 per minute. Thus, when the rhythm is regular and the paper is moving at the standard speed of 25 mm/s, the heart rate can be calculated by counting the number of large squares between two consecutive R waves, and dividing this number into 300.
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When an irregular rhythm is present, the heart rate may be calculated from the rhythm strip. It takes one second to record 2.5 cm of trace; therefore the heart rate per minute can be calculated by counting the number of intervals between QRS complexes every 6 seconds (namely, 15 cm of recording paper) and multiplying by 10.
On the vertical axis, the electrical activity detected by the electrocardiogram machine is measured in millivolts. Machines are calibrated so that a signal with an amplitude or height of 1 mV moves the recording stylus vertically 1 cm (2 large squares). Most commonly and throughout this text, the amplitude of waveforms is expressed as 0.1 mV = 1 mm = 1 small square. Thus each small square is 1 mm high and each large square 5 mm high.
Time and voltage.Vertical axis: • 1smallsquare=1mm(0.1mV)• 1largesquare=5mm(0.5mV)• 2largesquares=10mm(1.0mV)
Horizontal axis:• 1smallsquare=0.04s• 1largesquare=0.2s• 5largesquares=1.0s
P-R Interval
Q-T Interval
QRSDuration
1 sec0.04 sec
0.2 sec
P
R
Q
S
TU
1mm
5mm
1mV
PAPER SPEED - 25mm/sec
The 12- lead ECGTo make sense of an ECG, it is important to appreciate that the various leads “view” the heart from different directions. The term “lead” does not refer to the wires that connect the patient to the ECG machine, but rather to different views of the heart’s electrical activity. An ECG machine uses the information it collects via its four limb and 6 chest electrodes to compile a comprehensive picture of the electrical activity in the heart as observed from 12 different angles.
The six chest leads (V1 to V6) “view” the heart from a horizontal plane. The information from the limb electrodes is combined to produce the six limb leads (I, II, III, aVR, aVL and aVF). The limb electrodes can be thought of as looking at the heart in a vertical plane (that is, from the sides or the feet). The information from these 12 leads is combined to form a standard electrocardiogram.
Position of the six chest electrodes for standard 12-lead electrocardiography.
V1: right sternal border, 4th intercostal space;
V2: left sternal border, 4th intercostal space;
V3: between V2 and V4;
V4: mid-clavicular line, 5th intercostals space;
V5: anterior axillary line, horizontally in line with V4;
V6: mid-axillary line, horizontally in line with V4
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The positions of the leads produces the following anatomical relationships: leads II, III and aVF view the inferior surface of the heart; leads V1 to V4 view the anterior surface; leads I, aVL, V5 and V6 view the lateral surface; and leads V1 and aVR look through the right atrium directly into the cavity of the left ventricle.
Anatomical relations of leads in a standard 12-lead ECG
II, III and aVF Inferior surface of the heart
V1 to V4 Anterior surface
I, aVL, V5 and V6 Lateral surface
V1 and aVR Right atrium and cavity of left ventricle
P waveThe sinoatrial (SA) node is high in the wall of the right atrium and initiates atrial depolarisation which produces the P wave on the electrocardiogram. The P wave thus represents atrial depolarisation and not SA node depolarisation, as is
sometimes mistakenly believed. Although anatomically the atria are two distinct chambers, electrically they act almost as one. They have relatively little muscle and generate a single, small P wave. The duration of the P wave should not exceed 0.12 seconds. P wave amplitude (height) rarely exceeds 0.25 mV. Sinus P waves are usually most prominently seen in leads II and V1.
Characteristics of the P wave• Representsatrialdepolarisation• Positive(upright)inleadsIandII• BestseeninleadsIIandV1
• Duration<0.12s(threesmallsquares)• Amplitude<0.25mV(twoandahalfsmallsquares)
P wave
Sinoatrial node
Atrioventricular node
Right atrium
Wave of depolarisation
Left atrium
Atrial depolarisation gives rise to the P wave.
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PR intervalThe PR interval is the time between the onset of atrial depolarisation and the onset of ventricular depolarisation. It is measured from the beginning of the P wave to the first deflection of the QRS complex; regardless of whether this is a Q wave or an R wave. The normal duration of a PR interval is 0.12 – 0.22 seconds.The “PR segment” represents a brief return of the P wave to the isoelectric line. During this time the electrical impulse is conducted through the atrioventricular node, bundle of His, the bundle branches and the Purkinje fibres.Abnormalities of the conduction system may lead to transmission delays that will prolong the PR interval.
Characteristics of the PR interval• MeasuredfromthebeginningofthePwavetothebeginningofthe
QRS complex• Duration0.12–0.22s(threetofiveandahalfsmallsquares)
P
PR segment
PR interval Q
R
S
TU
QRS complexThe QRS complex represents the electrical forces generated by ventricular depolarisation. Thus, it represents the spread of electrical depolarisation through the ventricular muscle mass. The Q wave is the first negative (downward)
deflection; the R wave is the first positive (upward) deflection in the complex; the S wave is a negative deflection in the complex that follows an R wave.With normal intraventricular conduction, depolarisation occurs in an efficient, rapid fashion. The duration (width) of the QRS complex should not exceed 0.12 seconds or three small squares.
Q
R
S
R
S
R
Q S
The QRS complex:
• ThefirstdownwarddeflectionisaQwave• ThefirstupwarddeflectionisanRwave• AdownwarddeflectionafteranRwaveisanSwave
R wave
S waveQ wave
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Characteristics of the QRS complex• Representsdepolarisationoftheventricles• Duration<0.12s(threesmallsquares) Sinoatrial node
Atrioventricular node
Rightatrium
Left atrium
Right ventricle Left
ventricle
A wave of depolarisation spreading throughout ventricles gives rise to a QRS complex.
ST segmentThe ST segment lies between the terminal portion of the QRS complex and the beginning of the T wave. It represents the period between the end of ventricular depolarisation and the beginning of re-polarisation. The junction between the terminal
portion of the QRS complex and the start of the ST segment is referred to as the J point.The interpretation of subtle abnormalities in the ST segment is one of the more difficult areas of clinical electrocardiography. Nevertheless, any elevation or depression of the ST segment must be explained rather than dismissed.
Characteristics of the ST segment• MeasuredfromtheendoftheSwavetothebeginningoftheTwave• Horizontalline
ST segment
J point
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T waveVentricular re-polarisation produces a T wave. A normal T wave is asymmetrical. The first half has a more gradual slope than the second half.T wave orientation usually corresponds with that of the QRS complex.
Though no widely accepted criteria exist regarding T wave amplitude, as a rule, it correlates with the amplitude of the preceding R wave. Tall T waves may be seen in both acute myocardial ischemia and hyperkalemia. Conversely hypokalemia results in a flatter T wave.
Characteristics of the T wave• Representsre-polarisationoftheventricles• TwaveorientationusuallyfollowsthedirectionoftheQRScomplex
T wave
QT intervalThe QT interval is measured from the beginning of the QRS complex to the end of the T wave and represents the total time taken for depolarisation and re-polarisation of the ventricles.The QT interval lengthens as the heart rate slows, and thus when
measuring the QT interval, the heart rate must be taken into account. As a general guide, the QT interval should be 0.35 – 0.45 seconds and should be no more than half of the interval between adjacent R waves (R – R interval). The QT interval increases slightly with age and tends to be longer in women than in men. Prominent U waves can easily be mistaken for T waves, leading to overestimation of the QT interval.
Characteristics of the QT interval• MeasuredfromthebeginningoftheQRScomplextotheendoftheT
wave• Lengthensastheheartrateslows• Duration0.35–0.45s
QT interval
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U waveThe U wave is a small deflection that follows the T wave. It is generally deflected in the same direction as the preceding T wave. Therefore, inverted U waves usually follow inverted T waves, as a result of the same clinical abnormality.
It has been suggested that U waves result from re-polarisation of the mid-myocardial cells – that is, those cells between the endocardium and the epicardium – and the His-Purkinje system. However, this is by no means certain. Many electrocardiograms have no discernible U waves. Prominent U waves may be found in athletes and are also associated with hypokalemia, hypercalcemia and hyperthyroidism.
Characteristics of the U wave• Smallgenerallyuprightwave• FollowstheTwave• MostprominentinleadsV2 to V4
U wave
Diagnosis• Pwaveshavenormalmorphology• Atrialandventricularrate60–100beats/min• Regularventricularrhythm• EveryPwaveisfollowedbyaQRScomplex• PRinterval0.12–0.22s(threetofiveandahalfsmallsquares)• QRScomplexes<0.12s(threesmallsquares)
Signs and symptomsExercise and emotion are potent accelerators of sinus rhythm through sympathetic, neural and catecholamine stimulation. Resting sinus rates of 60 to 100 beats/min classically represents the limits of a normal rate, but much slower sinus rates occur in young persons, particularly trained athletes. Thus, resting rates of < 60 beats/min (sinus bradycardia) are often not pathologic. Sinus tachycardia describes rates of > 100 beats/min. Normally, a marked diurnal variation in heart rate is common, with the lowest rates just before early morning awakening. Absolute regularity of sinus rhythm is pathologic and occurs with autonomic denervation, as seen in advanced diabetes.
Sinus rhythmA normal heart rhythm is initiated in the sinus node and proceeds to depolarise the atria. P wave are recorded on the ECG, representing atrial depolarisation. The cardiac impulse then travels to the AV node and the bundle of His, traverses the bundle branches and the Purkinje fibres, and a PR interval is recorded. The impulse then reaches the ventricular muscle, and a QRS complex is displayed, representing ventricular depolarisation. This complex is followed by an isoelectric ST segment and a T wave representing ventricular re-polarisation. Altogether, this cycle is called sinus rhythm.
Normal sinus rhythm.
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Signs and symptomsSinus bradycardia is common in individuals during sleep and in those with high vagal tone such as athletes and healthy young adults.Sinus bradycardia frequently occurs during digitalisation, treatment with opiates and beta-blocking agents and is a predominant feature in vasovagal attacks (episodes of bradycardia and hypotension related to pain, arterial puncture, the Valsalva manoeuvre and carotid sinus massage). Sinus bradycardia may also be seen in myxoedema, obstructive jaundice, uraemia, increased intracranial pressure and glaucoma.
TreatmentIf the bradycardia is symptomatic, atropine 0.5 to 1.0 mg can be given intravenously in repeat doses every 3 to 5 minutes.Transcutaneous pacing is always appropriate if the bradycardia is severe and the clinical situation is unstable.
Sinus bradycardiaSinus bradycardia is sinus rhythm with a heart rate of below 60 beats/min. Atrial depolarisation resembles sinus rhythm with normal P waves, and P-P intervals are usually regular. Every P wave is followed by a QRS complex of normal duration and appearance.
Diagnosis• Pwaveshavenormalmorphology• Atrialandventricularrateof<60beats/min• Regularventricularrhythm• OnePwaveprecedeseveryQRScomplex• PRinterval0.12–0.22s(threetofiveandahalfsmallsquares)• NormalQRScomplexes<0.12s(threesmallsquares)
Sinus bradycardia. Heart rate of 51 beats/min.
Sinus tachycardiaSinus tachycardia is a sinus rhythm with a heart rate of greater than 100 beats/min. Atrial depolarisation occurs as in sinus rhythm with normal P waves, and the P-P interval is usually regular.The rate increases gradually and may show beat-to-beat variation but rarely exceeds 140 beats/min in adults except during heavy exercise. A QRS complex follows each P wave, and P wave morphology is normal. The height of the P wave may increase and the PR interval will shorten with the increase in heart rate. With rapid tachycardia, the P wave may become embedded in the preceding T wave, so the rhythm can be mistaken for atrioventricular nodal tachycardia.
Diagnosis• Pwaveshavenormalmorphology• Atrialandventricularrateof100–140beats/min• Regularventricularrhythm• OnePwaveprecedeseveryQRScomplex• PRinterval0.12–0.22s(threetofiveandahalfsmallsquares)• QRScomplexes<0.12s(threesmallsquares)
Signs and symptomsSinus tachycardia is usually a normal physiological response to a need for increased cardiac output, but may be precipitated by symphathomimetic drugs or endocrine disturbances.Common causes of sinus tachycardia include:• Physiological Exertion, anxiety, pain• Pathological Fever, anaemia, hypovolaemia, hypoxaemia, heart failure• Endocrine Thyrotoxicosis, phaeochoromocytoma• Pharmacological Adrenalin, atropine, salbutamol, alcohol, caffeine
Sinus tachycardia. Heart rate of 112 beats/min.
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Recognition of the underlying cause usually facilitates diagnosis of sinus tachycardia. A persistent tachycardia in the absence of an obvious underlying cause should prompt consideration of atrial flutter or atrial tachycardia.
TreatmentTherapy should be directed towards treating the primary disorder. This may involve institution of digitalis and/or diuretics for heart failure, oxygen for hypoxemia, treatment of thyrotoxicosis, volume repletion in dehydration, aspirin for fever, or tranquillisers for emotional upset.When a patient has an appropriate tachycardia (e.g. hypoxia or compensating for low blood pressure such as with fluid loss), slowing it with beta-blockers can lead to disastrous decompensation. The underlying problem needs management. If, however, the sinus tachycardia is inappropriate, as in conditions of anxiety or hyperthyroidism, treatment with a beta blocking agent or verapamil may be helpful.
Sinus arrhythmiaSinus arrhythmia, or irregular sinus rhythm, is characterised by a continuous variation in heart rate.The variation in cycle length is usually related to respiration and exhibits an increase during expiration.The PP and RR cycles usually vary for more than 0.16 of a second.
Diagnosis• Pwaveshavenormalmorphology• Heartratevarieswithrespiration• Atrialandventricularrateof60–100beats/min• EveryPwaveisfollowedbyaQRScomplex• PRinterval0.12–0.22s(threetofiveandahalfsmallsquares)• QRScomplex<0.12s(threesmallsquares)
Signs and symptomsCommonly in children and young adults, this is considered normal in the context of a high vagal tone. The heart rate normally increases during inspiration as a reflex response to an increased volume of blood returning to the heart. Sinus arrhythmia is uncommon after the age of 40.
TreatmentThe condition is completely harmless and no tests or treatment are necessary.
Sinus arrhythmia. Sinus rhythm with continuous variation in the length of the PP (and RR) interval.
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S inoatr ial (SA) blockSinoatrial (SA) block is defined as a reduced or blocked conduction of the normal impulse spreading from the SA node to the surrounding atrial muscle. Similar to AV block, it can be divided into three categories. Of these, only second-degree SA block can be diagnosed using an ordinary ECG. First-degree SA block is not recorded on an ECG because the depolarisation of the SA node is not visible. With third-degree block, no P waves or QRS complexes appear because conduction is totally blocked. Therefore the ECG cannot be differentiated from the ECG of sinus arrest.
Second-degree SA blockSecond-degree sinoatrial block denotes the intermittent failure of conduction of sinus impulses to the surrounding atrial tissue. This is seen as a sudden loss of P waves and corresponding QRS complexes. SA block usually occurs irregularly and unpredictably.
Diagnosis• PwavesandQRScomplexesdonotappearintheexpectedposition• Anescapebeatmayappearlaterinthecycle• ThedurationoftheblockperiodisusuallyamultipleoftheP-Pinterval
of the normal rhythm
Signs and symptomsSA block is seldom clinically significant unless it is a manifestation of drug toxicity with digitalis, quinidine or other antiarrhythmic drugs. It is especially prevalent in athletes and youngsters with an increased vagal tone and is also often associated with uraemia and occasionally hyperaemia.
TreatmentIf the SA block is symptomatic, intravenous atropine may be given.
Second-degree SA block with drop-out of P waves and QRS complex.
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Third-degree SA block and sinus arrestThird-degree SA block and sinus arrest are both characterised by asystole (isoelectric line) on the ECG because activation of the atria does not occur. Usually 2-3 seconds pass before an escape rhythm - usually an AV junctional escape rhythm - supervenes. With SA block, conduction of impulses from the SA node to the atrium is blocked, while in sinus arrest the SA node fails to depolarise. It is difficult to differentiate between the two conditions, but with SA block, the distance between the P waves before and after the dropped beats is a multiple of the P–P interval.
Diagnosis• AbsenceofthreeormorePwaves• Anescapebeatmayappearlaterinthecycle
Signs and symptomsAsymptomatic SA block, with an occasionally dropped P-QRS cycle, is a relatively common phenomenon especially in children, young adults and well-trained athletes.Long periods of sinus arrest may cause fainting attacks but prolonged unconsciousness is rarely seen. The cause may by increased vagal tone due to pain, fear, or procedures such as arterial puncture, gastroscopy, broncoscopy, pleurocentesis etc. SA block is also prevalent during the first hours after acute myocardial infarction. In the elderly, carotid sinus stimulation or the valsalva manoeuvre can trigger SA block. Over doses of digitalis, beta blocking agents or verapamil can be complicated by SA block. In the so-called sick sinus syndrome, a chronic disease usually starting after the age of 60, recurrent attacks of fainting or near-fainting due to third-degree SA block or sinus arrest can be seen.
Third-degree SA block or sinus arrest with missing P waves and QRS complexes.
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TreatmentIn acute episodes, intravenous atropine is given. Recurrent syncope or presyncope is an indication for permanent pacemaker insertion. Digitalis, beta-blocker agents, or verapamil toxicity should be considered.
Diagnosis• Pwavesabsent;oscillatingbaselinewithf(fibrillatory)waves• Atrialrateof350–600beats/min• Irregularventricularrhythm• Ventricularrateof100–180beats/min
Atrial f ibr i l lat ion (AF)Atrial fibrillation (AF) is caused by multiple re-entrant circuits of activation sweeping around the atrial myocardium. It is characterised by irregular depolarisation in the atria at a rate of 350-600 beats/min appearing as an irregular wavy base line made up of f (fibrillatory) waves with absent P waves. Conduction of atrial impulses to the ventricles is variable and unpredictable as only a few of the impulses transmit through the atrioventricular node to produce an irregular ventricular response. This combination of absent P waves, fine baseline f-wave oscillation and irregular ventricular complexes is characteristic of atrial fibrillation. The ventricular rate depends on the degree of atrioventricular conduction, and with normal conduction it varies between 100 and 180 beats/min. Atrial fibrillation is the most common sustained arrhythmia in adult populations.
Atrial fibrillation with a fibrillatory line and irregular ventricular complexes.
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Signs and symptomsBecause of the completely irregular atrial rate, the function of the atria is disorganised and chaotic with no effective systolic contraction. This predisposes to thrombus formation in the atria and consequent systemic emboli. If the ventricular rate is rapid, diastolic filling is reduced and the patient may experience dyspnoea and peripheral or pulmonary oedema.The aetiology of atrial fibrillation is closely associated with myocardial damage and increased atrial pressure. The causes include hypoxaemia, anaemia, hypertension, congestive heart failure, mitral regurgitation, thyrotoxicosis, alcohol misuse, cardiomyopathy and post-cardiac surgery.
TreatmentMajor goals in the management of atrial fibrillation are ventricular rate control, assessment of anticoagulation needs and restoration of sinus rhythm. Reversible and underlying causes of atrial fibrillation should be investigated and, if possible, corrected. Haemodynamically unstable atrial fibrillation with a rapid ventricular rate of (> 120 beats/min) should be electrically cardioverted immediately, regardless of the duration of the arrhythmia.
Sinoatrial node
Atrioventricular node
Right atrium
Left atrium
Atrial fibrillation is the result of multiple wavelets of depolarisation moving around the atria in a chaotic fashion.
Pharmacological rate control is the recommended initial treatment for stable, rapid atrial fibrillation (ventricular rate of > 120 beats/min) regardless of its duration. Specific drug treatment depends on the presence or absence of impaired left ventricular function:• Inpatientswithpreservedleftventricularfunction,beta-blockers,
calcium blockers (verapamil or diltiazem) and digitalis are reasonable agents for rate control.
• Inpatientswithcongestiveheartfailure,(ejectionfractionof<40%),digitalis, diltiazem, and amiodarone are recommended.
Efforts should be made to minimise the risk of thromboembolic complications that are strongly related to the duration of the arrhythmia before cardioversion. If atrial fibrillation has been present for > 48 hours, a risk of systemic embolisation exists with cardioversion to sinus rhythm unless patients are adequately anticoagulated for at least 3 weeks.Electrical cardioversion and the use of antiarrhythmic agents should be avoided unless the patient is unstable or haemodynamically compromised.If pharmacologic measures fail to prevent recurrence of atrial fibrillation or control the ventricular rate, non-pharmacologic strategies should be considered. These include pacemakers, atrial defibrillators, catheter ablation for either rate control or prevention of atrial fibrillation, and surgery.
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Atrial f lutterAtrial flutter is characterised by an atrial rate of between 250 and 350 beats/min. P waves may be obscured by flutter waves. The AV node has a refractory period that prevents it from conducting impulses at more than about 230/min. This results in a degree of atrioventricular block, commonly 2:1 or 3:1 and in a ventricular rate of a half or one third of the atrial rate, typically 150 beats/min.
Diagnosis• AbnormalPwavemorphology,flutterwaves• Atrialrate250–350beats/min• Ventricularrhythmusuallyregular• Variableventricularrate• QRScomplex<0.12s(threesmallsquares)
Signs and symptomsThis arrhythmia occurs most often in patients with organic heart disease. Flutter may be paroxysmal, in which case there is usually a precipitating factor such as pericarditis or acute respiratory failure, or it may be persistent. Atrial flutter is usually more temporary than atrial fibrillation and commonly, if it lasts for more than a week, converts into atrial fibrillation. Systemic embolisation is less common in atrial flutter than in atrial fibrillation.
In contrast to atrial fibrillation, atrial depolarisation in flutter is regular. Atrial flutter is associated with varying degrees of heart failure depending on the ventricular response. The most common symptoms are palpitations and dyspnoea induced by even slight physical exercise.
Atrial flutter showing obvious flutter waves.
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TreatmentThe same applies as for atrial fibrillation.
Sinoatrial node
Atrioventricular node
Right atrium
Left atrium
Atrial flutter is usually the result of a re-entrant circuit in the right atria.
Atrial tachycardiaAtrial tachycardia differs from sinus tachycardia in that the impulses are generated by an ectopic focus somewhere within the atrial myocardium rather than the sinus node.
The P waves are different in configuration to the sinus P wave but usually of the same polarity, as the pacemaker is most often located in the upper part of the right atrium.The atrial (P wave) rate is 140 – 220 beats/min and may be as high as 250 beats/min. At atrial rates of above 200 beats/min, the AV node struggles to keep up with impulse conduction and AV block may occur. Sometimes however, the P waves are hidden within the preceding T wave and are not visible.
Diagnosis• AbnormalPwavemorphology• Atrialrateofusually140–220beats/min• Ventricularrhythmusuallyregular• NormalQRScomplexes<0.12sec.(threesmallcomplexes)
Atrial tachycardia interrupted by sinus complexes.
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Signs and symptomsPeriodic paroxysmal atrial tachycardia can occur in apparently healthy individuals as well as in individuals with cardiac disease. Most forms of heart disease are complicated by atrial tachycardia, including ischemic heart disease, rheumatic heart disease and cardiomyopathy. In addition, it also manifests in severe chronic lung disease, pulmonary embolism or digoxin toxicity.
Patients with significant heart disease, such as severe ischemic heart disease or tight mitral stenosis, may develop congestive heart failure or pulmonary oedema even though the tachycardia is not very rapid. However, unless the ventricular rate is very high, individuals without concomitant heart disease can tolerate atrial tachycardia for longer periods with minimal or no symptoms.
TreatmentDigitalis intoxication should always be suspected in paroxysmal atrial tachycardia with block. If however, digitalis is not the cause then it can be used to control the ventricular response, as can verapamil or a beta-blocker.
Sinoatrial node
Atrioventricular node
Right atrium
Left atrium
Atrial tachycardia is characterised by an ectopic atrial focus.
Multifocal supraventricular tachycardiaMultifocal supraventricular tachycardia is a type of atrial tachycardia that occurs when multiple sites in the atria are discharging due to increased automaticity. It is characterised by P waves of varying morphologies and PR intervals of different lengths. In contrast to atrial fibrillation, distinct P waves are seen, separated by isoelectric periods. Every P wave reflects synchronised atrial depolarisation and a coordinated contraction. The QRS complexes are usually normal, but widened complexes may be seen if the atrial rate is high.
Diagnosis• Pwavesofvaryingshapeanddirectionfrombeattobeat• Pwavefrequencyof120–150beats/min• VaryingPRinterval• Irregularrhythm• NormalQRScomplexesof<0.12s(threesmallsquares)
Signs and symptomsMultifocal supraventricular tachycardia can be confused with atrial fibrillation and is often preceded or followed by atrial fibrillation or atrial flutter.
Multifocal supraventricular rhythm with P waves of changing shape and varying PR intervals.
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This relatively uncommon arrhythmia is most frequently seen in patients with chronic pulmonary disease with cor pulmonale, but may also be seen in patients with pulmonary emboli, left heart failure, acute myocardial infarction and hypoxaemia. It may also occur as a terminal feature in elderly sick patients.Multifocal supraventricular tachycardia is a bad prognostic sign because it usually indicates serious underlying heart disease. At rates < 100 beats/min it is called a multifocal supraventricular rhythm. The ECG picture appears similar to multifocal supraventricular tachycardia but it is harmless and does not usually require treatment.
TreatmentTreat the underlying heart disease. In some cases, careful digitalisation may be warranted, taking note that very ill patients are often sensitive to over digitalisation.
Diagnosis• Rapidregularrhythm• Heartrateof140–220beats/min• NormalQRScomplexes<0.12s(threesmallsquares)• PwavesareoftenhiddenwithintheQRScomplexandarenotvisible
Signs and symptomsEpisodes of atrioventricular nodal re-entrant tachycardia may begin at any age. They tend to start and stop abruptly, can occur spontaneously, or are precipitated by simple movements and may last a few seconds, several hours, or days. The frequency of episodes varies between several a day to
AV nodal re-entry tachycardiaAV junctional tachycardia is defined as three or more consecutive beats originating from the AV node or the surrounding area. This paroxysmal regular, narrow QRS tachycardia involves so-called re-entry either within or beside the atrioventricular node.Retrograde atrial depolarisation occurs (backwards) up through the AV node, which causes the P wave to invert (retrograde). However, since atrial and ventricular depolarisation often occur simultaneously, the P waves are frequently buried in the QRS complex and may be totally obscured. During sinus rhythm the electrocardiogram is normal.
AV junctional (supraventricular) tachycardia with a regular rate of 240 beats/min. P waves visible.
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one episode in a lifetime. Most patients have only mild symptoms such as palpitations or the sensation of a rapidly beating heart. More severe symptoms include dizziness, dyspnoea, weakness, neck pulsation and central chest pain. Some patients report polyuria.
TreatmentVagotonic manoeuvres (Valsalva manoeuvre, carotid sinus massage, swallowing ice cold water), particularly if used before the arrhythmia has stabilised, may terminate the paroxysm. If these methods are ineffective, attacks will often stop during sleep.Acute symptomatic attacks usually respond dramatically to intravenous adenosine or amiodarone, and beta or calcium channel blockers.Prophylaxis is difficult, but beta or calcium channel blockers, alone or in combination, may prove effective. Most patients troubled with this arrhythmia are suitable candidates for electrophysiological testing and possibly radio frequency (RF) pathway ablation.
Ventr icular tachycardiaVentricular tachycardia (VT) is defined as a broad-complex tachycardia consisting of three or more consecutive ventricular beats at a rate of higher than 120 beats/min. Episodes can be self-terminating, sustained or may degenerate into ventricular fibrillation.Impulses originate in pacemakers located distal to the bundle of His, in the bundle branches, Purkinje fibres or, rarely, in the working myocardium of the ventricles. The ventricular complexes are widened and bizarre in
appearance because of the abnormal impulse spreading through the ventricular myocardium. P waves are usually difficult to identify.
Ventricular tachycardia with varying QRS morphology is called polymorphic VT, which is usually irregular in rate, haemodynamically unstable and likely to quickly degenerate into ventricular fibrillation (VF). It is often associated with ischemic heart events, electrolyte imbalance or toxic conditions. A unique form of polymorphic VT is called torsades de pointes, which usually
Fast ventricular tachycardia (rate of 210 beats/min) precipitated by a ventricular extrasystole.
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occurs in a setting of bradycardia and prolongation of the QT interval. Both polymorphic VT and torsades de pointes frequently terminate spontaneously, but the arrhythmia may recur and seldom remains stable.
Diagnosis• Independentactivationoftheatriaandventricles(AVdissociation)• WideQRScomplexes>0.12sofabnormalshape• Ventricularrate>120beats/min• TwavesusuallyinoppositedirectiontotheQRScomplexes
Signs and symptomsSustained VT normally occurs at a rate of 150 – 250 beats/min, but the diagnosis can be difficult. VT can be remarkably well tolerated and may not cause haemodynamic disturbance. Do not assume therefore, that if the patient appears well that it is not VT. Any broad QRS tachycardia (QRS > 0.12 s) should be considered to be VT until proven otherwise.
Sinoatrial node
Atrioventricular node
Right atrium
Left atrium
Ventricular tachycardia showing abnormal direction of wave of depolarisation giving rise to abnormal, bizarre QRS complexes.
Right ventricle
The symptoms of ventricular tachycardia can vary from mild palpitations to dizziness, syncope and cardiac arrest. Always look for an underlying treatable cause. The causes of ventricular tachycardia include:• Acutemyocardialinfarction• Chroniccoronaryarterydisease• Cardiomyopathy• Valvularheartdisease(particularlyaorticvalvedisease)• Mitralvalveprolapse• Myocarditis• Congenitalheartdisease• Electrolytedisturbance(particularlylowandhighserumpotassium)• Antiarrhythmicdrugs
Torsades de pointes ventricular tachycardia with the cardiac axis rotating, changing from one direction to another and back again.
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TreatmentWhen haemodynamic impairment is present, ventricular tachycardia becomes a medical emergency and warrants immediate synchronised cardioversion.However, stable patients can be cardioverted medically. The recommended treatments for haemodynamically stable VT are intravenous procainamide, sotalol, amiodarone, or beta-blockers. Each of these is considered preferable to intravenous lidocaine.Brief salvos of unsustained VT are common in acute myocardial infarction but have no immediate or late prognostic significance and should not be treated.If any doubt exists as to whether the broad complex tachycardia is a genuine VT or in fact a SVT with aberrancy, the therapeutic options should be limited to DC cardioversion, intravenous procainamide or intravenous amiodarone.
The selection of optimal long-term prophylactic treatment requires an understanding of the mechanism of the arrhythmia and the disease process that provides the substrate for the arrhythmia. All patients with sustained VT should be investigated using invasive electrophysiology and therapy selected accordingly. Effective drugs include beta-blockers verapamil,
procainamide, propafenone and amiodarone, but bear in mind that antiarrhythmic agents can produce or exacerbate the very arrhythmias that they are meant to prevent.Radio frequency (RF) catheter ablation or surgery can be used to remove a ventricular focus identified by electrophysiological testing. Finally, automatic implantable cardiovertor defibrillator (ICD) devices can be used to deliver low energy DC shocks for recurrent episodes of VT (and VF).
Ventr icular f ibr i l lat ionVentricular fibrillation (VF) is the most common initial arrhythmia causing cardiac arrest and appears as a chaotic rhythm on the ECG.Ventricular fibrillation can be described as different parts of the ventricular myocardium depolarising in a chaotic manner independently of each other, and at a fast and irregular rate. Coordinated ventricular activity and muscular contraction cease, producing essentially zero cardiac output.
Completely irregular, chaotic and abnormal deflections of varying height and width are seen on the ECG, which has an irregular base line with no real QRS complexes. Ventricular fibrillation, in association with acute myocardial infarction is often provoked by a ventricular extrasystole that
occurs during the first 2/3 of the preceding T wave, the so-called R-on-T phenomenon. In chronic ischemic heart disease, ventricular fibrillation is usually preceded by an episode of ventricular tachycardia that may suddenly degenerate into ventricular fibrillation without warning.
Diagnosis• Rapidirregularroughbaseline• Bizarreventricularpatternsofvaryingsizeandconfiguration• Frequencyof250-600beats/min
Onset of ventricular fibrillation precipitated by a ventricular extrasystole falling on the T wave (R on T phenomenon).
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Signs and symptomsDuring ventricular fibrillation, the heart ceases to pump after approximately 10 seconds and clinical cardiac arrest accompanied by loss of consciousness. If left untreated, death follows after a few minutes. The cause of ventricular fibrillation is mainly coronary artery disease, which occurs most frequent during the first few hours after myocardial infarction (primary VF). Ventricular fibrillation can be caused by electrical accidents, serious electrolyte disturbances, drowning, choking, hypothermia and drug toxicity (digoxin, tricyclic antidepressants, quinidine and others).VF that occurs in the absence of myocardial infarction is usually related to severe underlying coronary artery disease and is likely to recur in patients who survive. Such patients warrant detailed investigation, including exercise testing, coronary angiography and invasive electrophysiology.
TreatmentVF is fatal unless reversed by immediate DC cardioversion. Success rates of 95%arecommonforDCcardioversionofprimaryVF,andshort-termandlong-term prognoses are excellent. The success of defibrillation is time dependentwitha2to10%declineinsuccessrateperminuteofcardiacarrest. Prompt DC cardioversion is far more efficient in resuscitation than pharmacological therapy.
If an immediate DC shock of 200 joules is unsuccessful, a second shock of 200 to 300 joules is given and a third of 360 joules is used if VF persists. These three shocks should be delivered consecutively without interruption for CPR or drug therapy. After three unsuccessful defibrillation attempts, rescuers must move quickly to accomplish tracheal intubation and gain access to the circulation with an intravenous line. Once the intravenous line is established, epinephrine 1 mg is administered, followed by another attempt to defibrillate at 360 joules. The dose of epinephrine may be repeated after intervals of 3 to 5 min. Following each dose of epinephrine, attempts to defibrillate at 360 joules are repeated within 30 to 60 seconds.After the initial unsuccessful defibrillation attempts, or with persistent electrical instability, a rapid infusion of 300 mg amiodarone is given. For persistent or recurrent ventricular fibrillation, a second dose of 150 mg is given intravenously. As an alternative, a bolus of 1.5 mg/kg lidocaine is given intravenously and the dose is repeated after 2 min in those patients who have persistent ventricular arrhythmias or remain in ventricular fibrillation.
Atrioventr icular (AV) blockAtrioventricular (AV) block is characterised by a delay or failure in impulse conduction from the atria to the ventricles. It occurs in three degrees of severity: first-degree AV block simply lengthens the PR interval by delaying conduction through the AV node, in second-degree AV block, some atrial impulses fail to be conducted to the ventricles, and in third-degree AV block, there is no conduction between atria and ventricles.
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F irst-degree AV blockProlongation of the PR interval is a common finding and indicates that conduction through the AV node has been delayed. When this delay is constant for each cardiac cycle, and a QRS complex follows each P wave, it is referred to as first-degree AV block.
Diagnosis• PRinterval>0.22s(fiveandahalfsmallsquares)• NormalPwaveandQRScomplex• AllPwavesarefollowedbyaQRScomplex
Signs and symptomsFirst-degree AV block in itself is asymptomatic and does not generally progress to other more serious sorts of heart block. It is normal when
it accompanies a vagally induced bradycardia, as an increase in vagal tone decreases AV nodal conduction. A prolonged conduction time is frequently found in well-trained athletes and the elderly. First-degree AV block may occur after beta-blocker or digitalis treatment and in electrolyte disturbances such as hyperkalemia. It is also associated with ischemic heart disease, myocarditis, acute rheumatic fever and sarcoid heart disease. Intermittent first-degree AV block often accompanies acute infections.
TreatmentNo specific treatment is necessary for first-degree AV block in its own right, but may suggest further investigation is required.
Sinus rhythm with first-degree AV block (PR interval 0.26 s).
Second-degree AV blockSecond-degree AV block occurs when there is intermittent failure or absence of atrioventricular conduction, which is characterised by some P waves failing to produce a QRS complex. It is subdivided into Mobitz type I block (Wenckebach), Mobitz type II block and advanced AV block.
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Signs and symptomsMobitz type I AV block is thought to result from abnormal conduction through the AV node itself and can simply occur during periods of high vagal activity as it does during sleep. It may also occur in generalised disease of the conducting tissue, is usually periodic and of shorter duration than Mobitz type II AV block and can commonly be seen in digitalis overdose and inferior wall infarction. Haemodynamic compromise is not usually a feature of this condition.
TreatmentMobitz type I AV block is regarded as a relatively benign form of AV block, but in rare cases where it is complicated by severe symptomatic
bradycardia, intravenous atropine given in repeat doses of 0.5 to 1.0 mg every 3 to 5 minutes usually proves effective in immediately accelerating heart rate and alleviating all bradycardia-related symptoms.
Second-degree AV block - Mobitz type I is characterised by a progressive increase in the conduction time over several beats, until an impulse is totally blocked and the corresponding QRS complex does not appear. This phenomenon repeats itself with a gradual prolongation of the PR interval over 3 to 6 beats until a P wave occurs without a following QRS complex.
Diagnosis• NormalPwaveandQRScomplex• GradualincreaseinthePRintervaluntilaPwaveisnotfollowedby
a QRS complex• PRintervalresetstonormalandthecyclerepeatsitself
Sinus rhythm with progressive lengthening of the PR interval until a QRS complex is dropped completely: second-degree AV block Mobitz type I.
Second-degree AV block - Mobitz type I (Wenckebach)
Signs and symptomsThe block in conduction is thought to result from abnormal conduction below the AV node (in the bundle of His or bilaterally in the bundle branches). Haemodynamic upset is common with signs of circulatory disturbance accompanied by a feeling of remoteness. Clinical symptoms include chest pain, shortness of breath and decreased level of consciousness. Common signs are low blood pressure, shock, pulmonary congestion or congestive heart failure.If the block has an acute onset, it is often associated with an acute myocardial infarction (anteroseptal or inferior), while chronic AV block is
Second-degree AV block - Mobitz type IISecond-degree AV block - Mobitz type II - is characterised by an occasional dropped QRS complex without preceding changes in the PR interval. The PR interval may be either normal or slightly prolonged, but remains constant from one P-QRS complex to the next.
Diagnosis• NormalPwavesandQRScomplexes• PRintervalnormalandconstant• SomePwavesarenotfollowedbyaQRScomplex
Sinus rhythm with occasional drop-out of a QRS complex; second-degree AV block Mobitz type II.
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catecholamines such as epinephrine or isoproterenol at rates of 2 to 10 µg/min can be used for short-term therapy.The use of atropine, transcutaneous pacing or intravenous infusion of catecholamines are usually the first line of treatment before the insertion of a temporary pacing electrode for ventricular pacing. Temporary pacing is usually achieved by the transvenous insertion of an electrode catheter, with the catheter positioned in the right ventricular apex and attached to an external pulse-generator.Catecholamines should be used with extreme caution or not at all in patients who have acute myocardial infarction.Drugs do not have any significant role to play in the long-term management of patients with symptomatic AV block. The only final treatment of patients who have an AV block and are symptomatic, is the subcutaneous or retropectoral implantation of a permanent cardiac pacemaker.
often due to degenerative changes in the conduction system. Mobitz type II AV block is often caused by irreversible damage and is considered more serious than Mobitz type I, as it can progress without warning to total AV block.
TreatmentIf the patient has serious signs and symptoms, make sure they are related to the slow rate and not for example, to hypotension due to myocardial dysfunction or hypovolemia. If the bradycardia is severe and the clinical condition is unstable, atropine 0.5 to 1.0 mg can be given intravenously in repeat doses every 3 to 5 minutes. Transcutaneous pacing is always appropriate and should be initiated quickly in patients who do not respond to atropine or who are severely symptomatic, especially when the block is at or below the His-Purkinje level. Dopamine (at rates of 2 to 5 µg/kg per minute) can be added and increased quickly to 5 to 20 µg/kg per minute if low blood pressure is associated with the bradycardia. Alternatively, other
With advanced AV block, a mathematical relationship exists between P waves and QRS complexes, e.g., 2:1, 3:1 or 4:1. It thus encompasses:• 2:1AVblockwithAVconductionofeverysecondPwaveanda
corresponding drop-out of every second QRS complex• 3:1AVblockwithAVconductionofeverythirdPwaveanda
corresponding drop-out of two in every three QRS complexes• 4:1AVblockwithAVconductionofeveryfourthPwavesanda
corresponding drop-out of three in every four QRS complexes
Advanced second-degree AV blockAdvanced AV or high-grade AV block is characterised by an alternate drop-out of the QRS complex, or the drop-out of two or more QRS consecutive complexes. Advanced AV block cannot be categorised as Mobitz type I or type II because it is impossible to say whether the PR interval for the non-conducted P waves would have been the same as, or longer than, the conducted P waves.
Advanced second-degree AV block with AV conduction of every other P wave (2:1 AV block).
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Diagnosis• NormalPwaves• AlternatePwavesarenotfollowedbyaQRScomplex
Signs and symptomsSame as for Mobitz type II AV block.
TreatmentSame as for Mobitz type II AV block.
Diagnosis• NormalPwaveswithregularrhythm• QRScomplexeswithanalmostregularrhythmbutunrelatedtoPwaves• SlowQRSfrequency(<60beats/min)• QRScomplexesnormalorwideneddependingonsiteofventricular
pacemaker
Third-degree (complete) AV blockThird-degree AV block is the most advanced state of AV block in which there is complete absence of conduction of impulses from the atria to the ventricles. Independent pacemakers asynchronously control the arteria and ventricles. In most cases, the ventricular pacemaker function is taken over by a focus below the block, and the heartbeat can then be sustained by impulses from the area around the AV node or the ventricles. A nodal escape rhythm often gives a ventricular rate of 40–60/min and a ventricular escape rhythm a rate of 30–40 beats/min. If an escape rhythm does not develop, it is called ventricular standstill, which is fatal if untreated.
Third-degree AV block with AV junctional escape rhythm. Sinus P waves in a regular rhythm at a rate of 76 beats/min and narrow QRS complexes at a regular but slower rate of 38 beats/min.
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Signs and symptomsClinical symptoms include chest pain, shortness of breath and decreased level of consciousness while common signs are low blood pressure, shock, pulmonary congestion or congestive heart failure.If the cause is acute inferior myocardial infarction, drug toxicity or acute peri/-myocarditis, total AV block is normally a temporary phenomenon. On the other hand, anteroseptal infarctions will lead to irreversible damage. Congenital AV block and blocks seen in elderly patients are also irreversible. Complete AV block may be entirely asymptomatic but is often associated with syncopal attacks. Heart failure develops less commonly, and prolonged ventricular arrest causes sudden death.
TreatmentFor short-term therapy, when the block is likely to be fleeting but still requires treatment or until adequate pacing therapy can be established, isoproterenol infusion can be used transiently. It should be remembered however, that catecholamines cannot be relied on to increase the heart rate for more than several hours to several days in patients with symptomatic heart block without producing significant side effects.Permanent pacemaker implantation is clearly indicated in all symptomatic patients with third-degree AV block, and should be seriously considered in asymptomatic cases.
Extrasystoles (ectopic beats)Extrasystoles or ectopic beats are triggered by premature depolarisation of an ectopic focus outside the sinus node. Usually, a fixed distance exists between the normal beat and the extrasystole, which is called the constant coupling interval. In some cases, the extrasystoles occur irregularly among the normal beats while in others, extrasystoles can be frequent and occur at regular intervals, e.g. every second, third or fourth beat can be an extrasystole termed bigeminy, trigeminy or quadrigeminy, respectively. Depending on its origin, it is possible to differentiate between ventricular and supraventricular extrasystoles.
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configuration, but if those derived from more than one focus have different shapes they are called multifocal ventricular extrasystoles.
Diagnosis• PrematureQRScomplex• Awide,tallandabnormalQRScomplex(>0.12s)• Twave,ofteninverted• Fullycompensatorypostextrasystolicpause
Ventricular extrasystoles or ventricular ectopic beats are caused by an electric impulse from an area in either the right or the left ventricle occurring before the impulse from the SA node has passed the AV node. The impulse conduction through the ventricles becomes abnormal, and the resultant QRS complexes are widened and abnormal. The extrasystoles are followed by a pause (the postextrasystolic pause) but the interval between the preceding and following beat is still twice as long as the normal interval in the basic sinus rhythm. The postextrasystolic pause is said to be fully compensatory. Extrasystoles from the same focus have the same ECG
Sinus rhythm with one ventricular extrasystole.
Ventr icular extrasystoles (ventr icular ectopic beats)
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Signs and symptomsVentricular extrasystoles are very common, especially after acute myocardial infarction or heart surgery and are also associated with hyperkalemia, hypoxemia and digoxin toxicity. Ventricular extrasystoles produce a reduced or impalpable peripheral pulse because of poor diastolic filling, but do not usually cause any haemodynamic upset unless they occur very frequently. In bigeminy the pulse rate and effective cardiac output may be halved,
possibly provoking or worsening heart failure in the sick patient. During ventricular re-polarisation, the heart is electrically unstable for a period corresponding to the first 2/3 of the T wave, also called the vulnerable period. A ventricular extrasystole occurring during this period (“the R-on-T phenomenon”) might lead to ventricular fibrillation in patients with acute myocardial infarction.
Sinus rhythm with ventricular bigeminy.
the ventricular ectopics with antiarrhythmic agents. Beta-blockers may be successful in managing ventricular extrasystoles that occur primarily in the daytime or under stressful situations and in specific cases, such as mitral valve disease or thyrotoxicosis.In the setting of chronic cardiac disease, the presence of multifocal ventricular ectopics, bigeminy, short coupling intervals (R-on-T-phenomenon), and salvos of three or more ectopic beats are suggestive of
TreatmentIn the absence of cardiac disease, isolated asymptomatic ventricular ectopics regardless of their configuration and frequency, need not be treated. Routine treatment with antiarrhythmic drugs has not been shown to decrease risk of sudden death. However, some patients may be significantly troubled by symptoms caused by the ectopic beat, the compensatory pause or the following sinus beat. These symptoms should first be addressed by allaying the patient’s anxiety, or if this is not successful, reducing the frequency of
Sinus rhythm with multifocal ventricular extrasystoles.
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increased risk of sudden cardiac death. In these instances invasive electrophysiologic testing and catheter ablation or implantable cardioverter/defibrillator (ICD) placement should be considered.
originates from a nodal focus, the P wave will usually be inverted and may be seen before or after the QRS complex, or may even be completely hidden. Impulse conduction from the AV node through to the ventricles occurs along the normal pathway, thus producing a normal QRS complex. In this case, the postextrasystolic pause is said to be not fully compensatory.
Diagnosis• ThePwaveandthecorrespondingQRScomplexappearprematurely• ThePwavediffersinshapefromthePwaveinsinusrhythm• NormalQRScomplex<0.12s(threesmallsquares)• Nocompensatorypause
Signs and symptomsSupraventricular extrasystoles are very common, but are rarely of any clinical significance. Common causes are beta 2 agonist therapy, chronic obstructive pulmonary disease or alcohol intake. Three or more consecutive supraventricular extrasystoles are called supraventricular tachycardia and an increase in their frequency may signify impending atrial fibrillation.
Supraventr icular extrasystoles (atr ia l ectopic beats)A supraventricular extrasystole or atrial ectopic beat originates in the atria or around the AV node and is called an atrial or nodal extrasystole, respectively. The P wave appears prematurely and differs in form from the normal sinus P wave. The PR interval is usually shorter. If the extrasystole
Sinus tachycardia with one supraventricular extrasystole.
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TreatmentSupraventricular extrasystoles are usually harmless and do not require treatment unless the patient complains of palpitations. In this case, a beta blocking agent or verapamil may be helpful.
The AV junctional pacemaker will continue until it again starts to be inhibited by impulses from the SA node. If the AV junction pacemaker fails or its impulses are blocked, a ventricular pacemaker will take over. Its rhythm is even slower, at 30 – 40 beats/min, and the QRS complexes will be wide and abnormal.
Escape rhythmsEscape rhythms are a form of a “safety net” for the heart and develop in response to a block or bradycardia. It serves to maintain the vital activation of the ventricles and in turn the pumping activity of the heart. The heart has a number of subsidiary ectopic pacemakers that can assume control if normal impulse generation or conduction fails.
The subsidiary pacemakers are located in the AV junction and the ventricular myocardium. If the AV junction fails to receive impulses as a result of SA arrest or block, or even during severe sinus bradycardia, it will take over as the cardiac pacemaker. The QRS complexes generated will have the same morphology as normal but at a slower rate of around 40 – 60 beats/min.
Sinus rhythm with second-degree SA block and two AV junctional escape beats.
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DiagnosisAV junctional escape rhythm:• NormalQRScomplexes<0.12s(threesmallcomplexes)• Ventricularrate40–60beats/min• Pwavesretrograde(inverted)andmostoftenhiddenwithintheQRS
complexVentricular escape rhythm:• WideQRScomplexes>0.12s(threesmallcomplexes)ofabnormal
shape• Ventricularrate30–40beats/min
Signs and symptomsEpisodes of AV junctional escape rhythm may be induced by high vagal tone and are not uncommon findings in apparently healthy athletes and children. They develop secondarily to sinus bradycardia and AV block but may also occur as an early sign of digitalis over-dosage.The most common cause of ventricular escape rhythm is third-degree AV block.
TreatmentBecause escape rhythms exist as a safety net, they must not be suppressed. Attempts should rather be made to determine the cause of the escape rhythm and correct the underlying problem.
Two sinus complexes followed by third-degree SA block (or sinus arrest) and ventricular escape rhythm.
Alternating current interference. This appears as fluctuations with a constant amplitude and frequency (50Hz) superimposed on the waveform. It can be remedied by:• Ensuringthebestpossibleelectrodecontact.• Switchingoffradiosandlamps.• Movingthepatientawayfromplugsandcablesinthewall.• PlacingtheECGelectrodesparalleltothepatient’sverticalaxis.
Common Tracing ProblemsLarge amplitude deflections. The amplitude of the signal in patients with ventricular hypertrophy may be halved by adjusting the test signal to give deflections of 5 mm (1 mV).
Poor electrode technique. This appears as irregular fluctuations in the recording. Obtain better contact with the skin, change the electrodes or, if using dry (non-gelled) electrodes, apply more electrode paste.
Defective cables. Sharp fluctuations or an isoelectric waveform may be seen. If disturbances can be produced by gently pulling the cable, change the cable.
Muscular activity. This appears as fast irregular fluctuations with an amplitude exceeding that of the ECG. This can be remedied by making the patient more comfortable, and by asking him to relax.The electrodes may be moved so that they are overlying bone. If possible, connect a filter to limit electrical interference.
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