Right Atrial Enlargement

AKA: Right atrial hypertrophy, right atrial abnormality Attention! Before reading this page, check out our introduction to the P wave for an explanation of the basics of atrial enlargement. Electrocardiographic Criteria Right atrial enlargement produces a peaked P wave (P pulmonale) with amplitude: > 2.5 mm in the inferior leads (II, III and AVF) > 1.5 mm in V1 and V2

Causes The principal cause is pulmonary hypertension due to: Chronic lung disease (cor pulmonale)

Tricuspid stenosis Congenital heart disease (pulmonary stenosis, Tetralogy of Fallot) Primary pulmonary hypertension

Examples

Right atrial enlargement: P wave amplitude > 2.5mm in leads II, III and aVF

Right atrial enlargement: P wave amplitude > 1.5 mm in V2

Right Axis Deviation

Right Axis Deviation Definition

QRS axis between + 90 and + 180 degrees

Right axis deviation: +90 to +180 degrees How To Recognise Right Axis Deviation

QRS is positive (dominant R wave) in leads III and aVF QRS is negative (dominant S wave) in leads I and aVL

Right axis deviation: leads III and aVF are positive; leads I and aVL are negative Causes

Left posterior fascicular block Lateral myocardial infarction Right ventricular hypertrophy Acute lung disease (e.g. PE) Chronic lung disease (e.g. COPD) Ventricular ectopy Hyperkalaemia Sodium-channel blocker toxicity WPW syndrome Normal in children or thin adults with a horizontally positioned heart

Right Bundle Branch Block

RBBB Background

In RBBB, activation of the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle. The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged. The delayed right ventricular activation produces a secondary R wave (R) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads. Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, with ST depression and T wave inversion in the right precordial leads. In isolated RBBB the cardiac axis is unchanged, as left ventricular activation proceeds normally via the left bundle branch.

Tall R' wave in V1 ("M" pattern) with wide, slurred S wave in V6 ("W" pattern) ECG Changes In RBBB Diagnostic Criteria Broad QRS > 120 ms

RSR pattern in V1-3 (M-shaped QRS complex) Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

Associated Features

ST depression and T wave inversion in the right precordial leads (V1-3)

Variations Sometimes rather than an RSR pattern in V1, there may be a broad monophasic R wave or a qR complex.

Typical RSR' pattern ('M'-shaped QRS) in V1

Wide slurred S wave in lead I

Typical pattern of T-wave inversion in V1-3 with RBBB

Causes Of RBBB

Right ventricular hypertrophy / cor pulmonale Pulmonary embolus Ischaemic heart disease Rheumatic heart disease Myocarditis or cardiomyopathy Degenerative disease of the conduction system Congenital heart disease (e.g. atrial septal defect)

More ECG Examples Of RBBB Example 1

Example 2

Example 3

Incomplete RBBB

Incomplete RBBB is defined as an RSR pattern in V1-3 with QRS duration < 120ms. It is a normal variant, commonly seen in children (of no clinical significance).

Incomplete RBBB (RSR' pattern in V1) in a 2-year old child

Differential Diagnosis Of RBBB

An RSR pattern in V1-3 may also be caused by Brugada syndrome an ECG pattern associated with malignant ventricular arrhythmias.

Brugada syndrome

Right Ventricular Hypertrophy

Electrocardiographic Features Diagnostic criteria Right axis deviation of +110 or more.

Dominant R wave in V1 (> 7mm tall or R/S ratio > 1). Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1). QRS duration < 120ms (i.e. changes not due to RBBB).

Supporting criteria Right atrial enlargement (P pulmonale).

Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads. S1 S2 S3 pattern = far right axis deviation with dominant S waves in leads I, II and III. Deep S waves in the lateral leads (I, aVL, V5-V6).

Other abnormalities caused by RVH Right bundle branch block (complete or incomplete).

NB. There are no universally accepted criteria for diagnosing RVH in the presence of RBBB; the standard voltage criteria do not apply. However, the presence of incomplete / complete RBBB with a tall R wave in V1, right axis deviation of +110 or more and supporting criteria (such as RV strain pattern or P pulmonale) would be considered suggestive of RVH. Causes

Pulmonary hypertension Mitral stenosis Pulmonary embolism Chronic lung disease (cor pulmonale) Congenital heart disease (e.g. Tetralogy of Fallot, pulmonary stenosis) Arrhythmogenic right ventricular cardiomyopathy

Example ECGs Example 1

Typical appearance of RVH: Right axis deviation (+150 degrees).

Dominant R wave in V1 (> 7 mm tall; R/S ratio > 1) Dominant S wave in V6 (> 7 mm deep; R/S ratio < 1). Right ventricular strain pattern with ST depression and T-wave inversion in V1-4.

Example 2

RVH in an adult with uncorrected Tetralogy of Fallot: Right axis deviation. P pulmonale peaked P wave in lead II > 2.5 mm. Dominant R wave in V1 (> 7 mm tall; R/S ratio > 1) Dominant S wave in V6 (> 7 mm deep; R/S ratio < 1). Right ventricular strain pattern in V1-3.

Example 3

Right axis deviation (+150 degrees) P pulmonale (P wave in lead II > 2.5 mm) Incomplete RBBB Right ventricular strain pattern with T-wave inversion and ST depression in the right precordial (V1-3) and inferior (II, III, aVF) leads.

This ECG was originally posted by Johnson Francis on Cardiophile.org. Example 4

Right ventricular hypertrophy in a patient with arrhythmogenic right ventricular cardiomyopathy: Right axis deviation.

R/S ratio in V1 > 1 Right ventricular strain pattern with T-wave inversion and ST depression in the right precordial (V1-3) and inferior (II, III, aVF) leads.

This ECG was originally posted by Jayachandran Thejus on the website HeartPearls.com.

Right Ventricular Infarction

Clinical Significance

Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon. Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents. Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.

The ECG changes of RV infarction are subtle and easily missed! How To Spot Right Ventricular Infarction The first step to spotting RV infarction is to suspect it in all patients with inferior STEMI! In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of: ST elevation in V1 - the only standard ECG lead that looks directly at the right ventricle.

ST elevation in lead III > lead II - because lead III is more rightward facing than lead II and hence more sensitive to the injury current produced by the right ventricle.

Other useful tips for spotting right ventricular MI (as described by Amal Mattu and William Brady in ECGs for the Emergency Physician): If the magnitude of ST elevation in V1 exceeds the magnitude of ST elevation in V2.

If the ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed. NB. The combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI.

Right ventricular infarction is confirmed by the presence of ST elevation in the rightsided leads (V3R-V6R). Right-Sided Leads There are several different approaches to recording a right-sided ECG: A complete set of right-sided leads is obtained by placing leads V1-6 in a mirror-image position on the right side of the chest (see diagram, below). It may be simpler to leave V1 and V2 in their usual positions and just transfer leads V3-6 to the right side of the chest (i.e. V3R to V6R). The most useful lead is V4R, which is obtained by placing the V4 electrode in the 5th right intercostal space in the midclavicular line. ST elevation in V4R has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% in the diagnosis of RV MI.

Reproduced from Morris and Brady, 2002. Click image for link to original reference. NB. ST elevation in the right-sided leads is a transient phenomenon, lasting less than 10 hours in 50% of patients with RV infarction. Example ECGs Example 1a

Inferior STEMI. Right ventricular infarction is suggested by: ST elevation in V1 ST elevation in lead III > lead II Example 1b

Repeat ECG of the same patient with V4R electrode position: There is ST elevation in V4R consistent with RV infarction

Example 2

Another example of right ventricular MI: There is an inferior STEMI with ST elevation in lead III > lead II. There is subtle ST elevation in V1 with ST depression in V2. There is ST elevation in V4R.

Example 3

This ECG shows a full set of right-sided leads (V3R-V6R), with V1 and V2 in their original positions. RV infarction is diagnosed based on the following findings: There is an inferior STEMI with ST elevation in lead III > lead II.

V1 is isoelectric while V2 is significantly depressed. There is ST elevation throughout the right-sided leads V3R-V6R.

Right Ventricular Outflow Tract (RVOT) Tachycardia

Introduction

Right ventricular outflow tract (RVOT) tachycardia is a form of monomorphic VT originating from the outflow tract of the right ventricle or occasionally from the tricuspid annulus. It is usually seen in patients without underlying structural heart disease, although may also occur in the context ofarrhythmogenic right ventricular dysplasia (ARVD). Diagnostic Features

Heart rate > 100 bpm. QRS duration > 120 ms. LBBB Morphology. Rightward / inferior axis (around +90 degree). Atrioventricular dissociation. Other general features of VT, such as fusion and capture beats may also be present. Causes

RVOT tachycardia is associated with two conditions: Idiopathic VT Occurs in structurally normal hearts.

Accounts for 10% of all VT. 70% of idiopathic VT will have a RVOT morphology. Underlying mechanism of c-AMP mediated triggered activity. May respond to adenosine.

Arrhythmogenic Right Ventricular Dysplasia An inherited myocardial disease associated with paroxysmal ventricular arrhythmias and sudden cardiac death.

Characterized pathologically by fibro-fatty replacement of the right ventricular myocardium. RVOT may be precipitated in both patient groups by catecholamine excess, stress, and physical activity. Example ECGs Example 1

RVOT tachycardia: Broad complex tachycardia. LBBB-like morphology. Inferior axis (+ 90 degrees). Example 2

RVOT tachycardia: Broad complex tachycardia.

LBBB-like morphology. Inferior axis (+ 90 degrees).

Right Ventricular Strain

Definition = Repolarisation abnormality due to right ventricular hypertrophy or dilatation. Electrocardiographic Features ST depression and T wave inversion in the leads corresponding to the right ventricle, i.e The right precordial leads: V1-3, often extending out to V4 The inferior leads: II, III, aVF, often most pronounced in lead III as this is the most rightward-facing lead.

NB. Compare this to the left ventricular strain pattern, where ST/T-wave changes are present in the left ventricular leads (I, aVL, V5-6). Causes Associated with increased pulmonary artery pressures in the setting of acute or chronic right ventricular hypertrophy or dilatation: Pulmonary hypertension

Mitral stenosis Pulmonary embolism Chronic lung disease (cor pulmonale) Congenital heart disease (e.g. Tetralogy of Fallot, pulmonary stenosis) Arrhythmogenic right ventricular cardiomyopathy

ECG Examples Example 1 Right ventricular hypertrophy

Typical right ventricular strain pattern: ST depression and T-wave inversion in V1-4 (plus lead III), in this case due to right ventricular hypertrophy.

Example 2 Acute right ventricular dilatation due to massive PE

Right ventricular strain pattern involving both the precordial and inferior leads: T-wave inversions are seen in the right precordial (V1-4) and inferior leads (III, aVF) in this patient with acute right ventricular dilatation due to massivepulmonary embolism.

R Wave Peak Time

AKA Intrinsicoid deflection Definition

The time from the onset of the earliest Q or R wave to the peak of the R wave in the lateral leads (aVL, V5-6). Represents the time taken for excitation to spread from the endocardial to the epicardial surface of the left ventricle. R-wave peak time is said to be prolonged if > 45ms.

Causes Of Prolonged RWPT

Left anterior fascicular block Left ventricular hypertrophy Left bundle branch block

Prolonged R-wave peak time in aVL due to left anterior fascicular block

Sgarbossa Criteria
Background

In patients with left bundle branch block (LBBB) or ventricular paced rhythm, infarct diagnosis based on the ECG is difficult. The baseline ST segments and T waves tend to be shifted in a discordant direction (appropriate discordance), which can mask or mimic acute myocardial infarction. However, serial ECGs may show dynamic ST segment changes during ischemia. A new LBBB is always pathological and can be a sign of myocardial infarction.

Electrocardiographic Criteria The three criteria used to diagnose infarction in patients with LBBB are: Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5) Concordant ST depression > 1 mm in V1-V3 (score 3) Excessively discordant ST elevation > 5 mm in leads with a negative QRS complex (score 2). This criterium is sensitive, but not specific for ischemia in LBBB. It is however associated with a worse prognosis, when present in LBBB during ischemia. A total score of 3 has a specificity of 90% for diagnosing myocardial infarction.

During right ventricular pacing the ECG also shows left bundle brach block and the above rules also apply for the diagnosis of myocardial infarction during pacing, however they are less specific.

In the GUSTO-1 trial the ECG criterion with a high specificity and statistical significance for the diagnosis of an acute MI was: Excessively discordant ST segment elevation 5 mm (in leads with a negative QRS complex). Two other criteria with acceptable specificity were: Concordant ST elevation 1 mm in leads with positive QRS Concordant ST depression 1 mm in leads V1, V2, or, V3 ECG Example

Positive Sgarbossa criteria in a patient with LBBB and troponin-positive myocardial infarction: This patient presented with chest pain and had elevated cardiac enzymes. Baseline ECG showed typical LBBB. There is 1mm concordant ST elevation in aVL (= 5 points). Other features on this ECG that are abnormal in the context of LBBB (but not considered positive Sgarbossa criteria) are the pathological Q wave in lead I and the concordant ST depression in the inferior leads III and aVF. This constellation of abnormalities suggests to me that the patient was having a high lateral infarction. Video Amal Mattu presents a case of acute myocardial infarction in the presence of left bundle branch block.

ECG Motion Artefacts

Introduction

Motion artefact due to tremor or shivering can obscure the waveforms of the ECG or simulate pathology, making ECG interpretation difficult. In certain circumstances (e.g. hypothermia), the presence of shivering artefact may actually aid diagnosis. Causes Of Tremor

Benign Essential Tremor (physiological tremor) Parkinsons Disease (resting tremor) Cerebellar disease (intention tremor) Alcohol / Benzodiazepine withdrawal Anxiety Thyrotoxicosis Multiple sclerosis Drugs: Amphetamines, cocaine, beta-agonists (adrenaline, salbutamol), theophylline, caffeine, lithium. Other Types Of Motion Artefact

Fever (rigors) Hypothermia (shivering) Cardiopulmonary resuscitation (chest compressions) A non-compliant, mobile, talkative patient (= the most common cause)!

ECG Examples Example 1

Hypothermia: This ECG displays the classic features of hypothermia: bradycardia, Osborn waves and shivering artefact. Example 2

Parkinsonian tremor: The irregular baseline in this ECG gives the appearance of atrial fibrillation. The slow regular rhythm even suggests the possibility of atrial fibrillation with complete heart block and a junctional escape rhythm. However, on closer inspection there are visible P waves in V3 (circled). This patient had sinus bradycardia and a resting tremor due to Parkinsons disease. Example 3

Chest compressions during CPR: The high amplitude oscillations at the start of the rhythm strip are produced by movement artefact due to chest compressions during cardiopulmonary resuscitation. The second half of the rhythm strip shows ventricular fibrillation presumably at this point the resuscitating team have stopped CPR to reassess the rhythm! Example 4

Precordial thump: This ECG demonstrates the movement artefact produced by a precordial thump!

Short QT Syndrome

Image reproduced from Schimpf et al. (See references below for link) Description

Short QT syndrome is a recently-discovered arrhythmogenic disease associated with paroxysmal atrial and ventricular fibrillation, syncope and sudden cardiac death. It is a genetically-inherited cardiac channelopathy on the same spectrum as other familial arrhythmogenic diseases such as Long QT Syndrome (LQTS), Brugada Syndrome and Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT). Patients are typically young and healthy, with no structural heart abnormalities; age at first presentation ranges from a few months to the sixth decade of life (median age = 30 years). The most common initial presenting symptom is cardiac arrest (in one-third of cases); other patients may present with palpitations or syncope due to rapid atrial fibrillation or selfterminating ventricular arrhythmias. Witnessed cardiac arrest within the first year of life and unexplained infant deaths have been observed in patients and families with SQTS, making it a possible cause of sudden infant death syndrome (SIDS). SQTS is still a relatively new disease: It was first described in 2000, and elucidation of the genetic, electrophysiological and clinical abnormalities associated with the disease has only taken place over the past few years. Mechanism Arrhythmogenesis in SQTS is thought to result from: Extremely short atrial and ventricular refractory periods (manifest on the ECG as a short QT interval).

Transmural dispersion of repolarisation, i.e., the different layers of the myocardium (endocardium, epicardium and the mid-myocardial M-cells) repolarise at different rates. Both these repolarisation abnormalities convey an increased susceptibility to re-entrant atrial and ventricular arrhythmias. Genetic Basis

SQTS is a genetically heterogenous disease, with multiple mutations producing a similar clinical picture. Five mutations have been characterised so far, all of which seem to be inherited in an autosomal dominant fashion. SQTS genotypes 1-3 are produced by a gain-of-function mutation in myocardial potassium channels (the opposite to LQTS), with increased potassium efflux during various stages of the action potential leading to more rapid atrial and ventricular repolarisation with marked shortening of the QT interval (<320 ms). SQTS genotypes 4 and 5 are produced by a loss-of-function mutation in the L-type cardiac channel, with reduced influx of calcium during the plateau phase of the action potential leading to modest shortening of the QT interval (<360ms) associated with a Brugadasyndrome-like QRS complex morphology. Potassium fluxes in SQTS 1-3

A. Schematic representation of the normal action potential and the flux of ions. B. With gainof-function mutations in any of 3 different potassium channels (SQTS 1-3), the cardiac action potential shortens and the QT interval decreases. (Reproduced from Brugada et al) Classification of SQTS according to genotype

Classification of SQTS according to genotype. (Reproduced from Moreno-Reviriego & Merino) Diagnosis At present, there are no diagnostic criteria for SQTS. The diagnosis is based upon the patients symptoms (e.g. syncope, palpitations), family history (of syncope, sudden death or atrial fibrillation at an early age) and characteristic findings on the 12-lead ECG.

Clinical Features So far, there have only been a handful of cases of SQTS reported in the literature. The true prevalence of the disease is unknown. The largest case series to date reported on 29 patients with the disease: The most common presenting symptom was cardiac arrest (in one-third of cases). Cardiac arrest occurred in the first months of life in two patients. Syncope was the presenting symptom in 24% of cases, thought to be secondary to selfterminating episodes of ventricular fibrillation. Up to 31% of patients complained of palpitations, and 80% of patients had documented episodes ofatrial fibrillation. All patients had a QT < 320ms and a QTc < 340ms with no evidence of structural heart disease(NB. This case series did not include the more recently-described SQTS genotypes 4 & 5) ECG Features

The main electrocardiographic abnormalities seen in SQTS are: Short QT interval Lack of the normal changes in QT interval with heart rate Peaked T waves, particularly in the precordial leads Short or absent ST segments Episodes of atrial or ventricular fibrillation QT, ST and T-wave changes in SQTS Short QT interval, peaked T waves and short ST segments in two patients with SQTS 1.

Reproduced from Crotti et al. Short QT Interval There is currently no universally accepted lower limit of normal for the QT interval that can be used to diagnose SQTS. Known patients with SQTS genotypes 1-3 all had QTc intervals < 300-320 ms Known patients with SQTS genotypes 4 & 5 all had QTc intervals < 360 ms A recent review by Viskin suggested the following approach: QTc intervals < 330 ms in males or < 340 ms in females should be considered diagnostic of SQTS QTc intervals < 360 ms in males or < 370 ms in females should only be considered diagnostic of SQTS when supported by symptoms or family history A QT interval scale for diagnosing SQTS and LQTS

A 'QT interval scale' for diagnosing SQTS and LQTS. (Reproduced from Viskin) Lack Of The Normal Changes In QT With Heart Rate

Patients with SQTS demonstrate fixed QT intervals which remain constant over a range of heart rates. At fast heart rates, the calculated QTc may appear normal (= pseudonormal QTc) However, as the heart rate slows, the QTc typically fails to prolong. Serial ECGs or Holter monitoring at rest may be used to try and capture short QT intervals during periods of relative bradycardia (heart rate 60-80bpm). Exercise testing may demonstrate lack of adaptation of QT interval with different heart rates. Fixed QT interval seen on Holter monitoring in a patient with SQTS

Holter strip from a patient with SQTS at heart rates of 68 and 119 bpm. QT interval of 280 ms remains constant at both heart rates. (Reproduced from Short QT Syndrome.org)

Electrophysiological Studies Electrophysiological studies in SQTS demonstrate: Extremely short atrial and ventricular refractory periods High rates of inducible atrial and ventricular fibrillation Marked vulnerability to mechanical induction of ventricular fibrillation The role of EP studies in diagnosing and risk-stratifying patients with SQTS has not yet been established. Treatment Options

At present, the only effective treatment is implantation of an ICD. The main problem with this is T-wave oversensing and inappropriate shocks due to the tall, narrow T waves seen in SQTS. Efforts to find a suitable pharmacological treatment have focused on potassium blocking antiarrhythmic agents (classes Ia and III). Class III agents ibutilide and sotalol, while having theoretical benefits in prolonging QT and suppressing arrhythmias, have been shown to be ineffective due to reduced drug binding to mutated potassium channels. Class Ia agents quinidine and disopyramide have shown more promising effects. Quinidine is currently the agent of choice, having been shown in SQTS 1 patients to markedly prolong both the QT interval and ventricular refractory period, with normalisation of ST segments and T waves and prevention of VF induction.

Normal Sinus Rhythm

Definition

The default heart rhythm. Pacemaking impulses arise from the sino-atrial node and are transmitted to the ventricles via the AV-node and His-Purkinje system. This results in a regular, narrow-complex heart rhythm at 60-100 bpm.

Characteristics Of Normal Sinus Rhythm

Regular rhythm at a rate of 60-100 bpm (or age-appropriate rate in children). Each QRS complex is preceded by a normal P wave. Normal P wave axis: P waves should be upright in leads I and II, inverted in aVR. The PR interval remains constant. QRS complexes are < 100 ms wide (unless a co-existent interventricular conduction delay is present). Normal heart rates in children Newborn: 110 150 bpm 2 years: 85 125 bpm 4 years: 75 115 bpm 6 years+: 60 100 bpm

Sinus rhythm

Variations On Sinus Rhythm

Sinus tachycardia = sinus rhythm with resting heart rate > 100 bpm in adults, or above the normal range for age in children. Sinus bradycardia = sinus rhythm with resting heart rate < 60 bpm in adults, or below the normal range for age in children. Sinus arrhythmia = sinus rhythm with a beat-to-beat variation in the P-P interval (the time between successive P waves), producing an irregular ventricular rate. Example ECG

Normal sinus rhythm in a healthy 18-year old male: Regular rhythm at 84 bpm. Normal P wave morphology and axis (upright in I and II, inverted in aVR). Narrow QRS complexes (< 100 ms wide). Each P wave is followed by a QRS complex. The PR interval is constant.

Sinus Arrhythmia
Definition
Sinus rhythm with a beat-to-beat variation in the P-P interval (the time between successive P waves), producing an irregular ventricular rate.

Characteristics

Variation in the P-P interval of more than 120 ms (3 small boxes). The P-P interval gradually lengthens and shortens in a cyclical fashion, usually corresponding to the phases of the respiratory cycle. Normal sinus P waves with a constant morphology (i.e. no evidence of premature atrial contractions). Constant P-R interval (i.e. no evidence of Mobitz I AV block).

Mechanism

Sinus arrhythmia is a normal physiological phenomenon, most commnonly seen in young, healthy people. The heart rate varies due to reflex changes in vagal tone during the different stages of the respiratory cycle. Inspiration increases the heart rate by decreasing vagal tone. With the onset of expiration, vagal tone is restored, leading to a subsequent decrease in heart rate. The incidence of sinus arrhythmia decreases with age, presumably due to age-related decreases in carotid distensibility and baroreceptor reflex sensitivity. NB. Non-respiratory sinus arrhythmia (not linked to the respiratory cycle) is less common, typically occurs in elderly patients and is more likely to be pathological (e.g. due to heart disease or digoxin toxicity).

Differential Diagnosis
There are several other entities that cause sinus rhythm with an irregular ventricular rate:

Frequent premature atrial contractions Second-degree AV block, Mobitz I (Wenckebach phenomenon) Type I Sinoatrial Exit Block Follow the links to find out more about these conditions.

Example ECG

Sinus arrhythmia:

Normal sinus P waves (upright in leads I and II) with a constant morphology albeit with an appearance suggestive of left atrial enlargement. P-R interval is constant (no evidence of AV block). The P-P interval varies widely from 1.04 seconds (heart rate ~57 bpm) down to 0.60 seconds (heart rate ~100 bpm); a variability of over 400ms. For irregular rhythms such as this, the ventricular rate is best estimated by multiplying the total number of complexes in the rhythm strip by 6. This gives an overall rate of 12 x 6 = 72 bpm.

Sinus Bradycardia
Definition

Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children. Normal heart rates in children

Newborn: 110 150 bpm 2 years: 85 125 bpm 4 years: 75 115 bpm 6 years+: 60 100 bpm

Causes
Non-pharmacological

Normal during sleep Increased vagal tone (e.g. athletes) Vagal stimulation (e.g. pain) Inferior myocardial infarction Sinus node disease Hypothyroidism Hypothermia Anorexia nervosa Electrolyte abnormalities hyperkalaemia, hypermagnesaemia Brainstem herniation (the Cushing reflex) Myocarditis Pharmacological

Beta-blockers Calcium-channel blockers (verapamil & diltiazem) Digoxin Central alpha-2 agonists (clonidine & dexmedetomidine) Amiodarone Opiates GABA-ergic agents (barbiturates, benzodiazepines, baclofen, GHB) Organophosphate poisoning

Differential Diagnosis

Sinus bradycardia may be indistinguishable from type II sino-atrial block.

ECG Example
Sinus bradycardia secondary to anorexia nervosa

Sinus bradycardia (35 bpm) in a 15-year old girl with anorexia nervosa. Note the prominent U waves in the precordial leads, a common finding in sinus bradycardia.

Sinus Node Dysfunction (Sick Sinus Syndrome)

Definition

A disease characterised by abnormal sinus node functioning with resultant bradycardia and cardiac insufficiency.

Causes

May be multi-factorial in origin. Causes can be considered either intrinsic or extrinsic. Intrinsic

Idiopathic Degenerative Fibrosis (commonest). Ischaemia. Cardiomyopathies. Infiltrative Diseases e.g. sarcoidosis, haemochromatosis. Congenital abnormalities. Extrinsic Causes

Drugs e.g. digoxin, beta-blockers, calcium channel blockers. Autonomic dysfunction. Hypothyroidism. Electrolyte abnormalitites e.g. hyperkalaemia.

ECG In Sinus Node Dysfunction

ECG abnormalities can be variable and intermittent. Multiple ECG abnormalities can be seen in sinus node dysfunction including:

Sinus Bradycardia. Sinus Arrhythmia associated with sinus node dysfunction in the elderly in the absence of respiratory pattern association. Sinoatrial Exit Block. Sinus Arrest pause > 3 seconds. Atrial fibrillation with slow ventricular response. Bradycardia tachycardia syndrome. Bradycardia tachycardia syndrome

Alternating bradycardia with paroxysmal tachycardia, often supraventricular in origin.

On cessation of tachyarrhythmia may be a period of delayed sinus recovery e.g. sinus pause or exit block. If significant this period of delayed recovery may result in syncope.

Clinical Manifestations

Commonly seen in the elderly but sinus node dysfunction can affect all age groups. Symptoms are due to decreased cardiac output and end-organ hypoperfusion associated with cardiac rhythm abnormality. Wide range of clinical symptoms including syncope, near-syncope, dizziness, fatigue and palpitations.

Treatment

Correction / removal of extrinsic causes e.g. non-essential drugs. Pacemaker insertion requires correlation of both ECG abnormalities and clinical symptoms.

Recommendation For Pacing In Sinus Node Dysfunction

Class I Evidence and/or agreement that permanent pacing is useful and effective.

Sinus node dysfunction with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms. In some patients, bradycardia is iatrogenic and will occur as a consequence of essential long-term drug therapy of a type and dose for which there are no acceptable alternatives.

Symptomatic chronotropic incompetence. Class IIa Conflicting evidence/ divergence of opinion but weight of evidence / opinion in favour

Sinus node dysfunction occurring spontaneously or as a result of necessary drug therapy, with heart rate less than 40 bpm when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented.

Syncope of unexplained origin when major abnormalities of sinus node function are discovered or provoked in electrophysiological studies. Class IIb Conflicting evidence/divergence of opinion where usefulness / efficacy is less well established

In minimally symptomatic patients, chronic heart rate less than 40 bpm while awake. Class III Permanent pacing is not useful/effective and in some cases may be harmful.

Sinus node dysfunction in asymptomatic patients, including those in whom substantial sinus bradycardia (heart rate less than 40 bpm) is a consequence of longterm drug treatment.

Sinus node dysfunction in patients with symptoms suggestive of bradycardia that are clearly documented as not associated with a slow heart rate. Sinus node dysfunction with symptomatic bradycardia due to nonessential drug therapy.

ECG Examples
Example 1: Sinus arrest

Sinus arrest:

Prolonged absence of sinus node activity (absent P waves) > 3 seconds.

Example 2: Bradycardia-tachycardia syndrome

Bradycardia-tachycardia syndrome:

Runs of tachycardia interspersed with long sinus pauses (up to 6 seconds). The sinus rate is extremely slow, varying from 40 bpm down to around 10 bpm in places. Sinus beats are followed by paroxysms of junctional tachycardia at around 140 bpm.

Sinoatrial Exit Block

Sino-atrial exit block is due to failed propagation of pacemaker impulses beyond the SA node. The sino-atrial node continues to depolarise normally. However, some of the sinus impulses are blocked before they can leave the SA node, leading to intermittent failure of atrial depolarisation (dropped P waves).

Type II sino-atrial exit block

Anatomical Basis
The SA node consists of two main groups of cells:

A central core of pacemaking cells (P cells) that produce the sinus impulses. An outer layer of transitional cells (T cells) that transmit the sinus impulses out into the right atrium. Sinus node dysfunction can result from either:

Failure of the P cells to produce an impulse. This leads to sinus pauses and sinus arrest. Failure of the T cells to transmit the impulse. This leads to sino-atrial exit block.

Patterns Of Conduction

The patterns of conduction in SA exit block are identical to the different types of AV block. However, as the initial sinus impulse is not visible on the ECG, the relationship between impulse generation and transmission must be inferred from the P waves alone (analogous to examining only the R waves in AV block).

Only second degree SA block (types I and II) can be diagnosed from the 12-lead ECG. First Degree SA block = Delay between impulse generation and transmission to the atrium.

This abnormality is not detectable on the surface ECG. Second Degree SA block, Type I (Wenckebach) = Progressive lengthening of the interval between impulse generation and transmission, culminating in failure of transmission.

The gradually lengthening transmission interval pushes successive P waves closer together. This results in grouping of the P-QRS complexes. Pauses due to dropped P waves occur at the end of each group. The P-P interval progressively shortens prior to the dropped P wave. This pattern is easily mistaken for sinus arrhythmia. Second Degree SA block, Type II = Intermittent dropped P waves with a constant interval between impulse generation and atrial depolarisation.

This pattern is the equivalent of Mobitz II. There is no clustering of P-QRS complexes. Intermittent P waves drop out of the rhythm, while subsequent P waves arrive on time. The pause surrounding the dropped P wave is an exact multiple of the preceding P-P interval. Third Degree SA Block = None of the sinus impulses are conducted to the right atrium.

There is a complete absence of P waves. The onset of 3rd degree SA block may produce long sinus pauses or sinus arrest (may lead to fatal asystole). Rhythm may be maintained by a junctional escape rhythm. Third degree SA exit block is indistinguishable from sinus arrest due to pacemaker cell failure. It can only be diagnosed with a sinus node electrode during electrophysiological evaluation.

Causes

Sick sinus syndrome

Increased vagal tone (athletes) Vagal stimulation (surgery, pain) Inferior myocardial infarction Myocarditis Drugs: digoxin, beta-blockers, calcium channel blockers, amiodarone.

ECG Examples
Example 1

Type I SA block:

This pattern of grouped beating is characteristic of type I SA block. There is progressive shortening of the P-P interval, followed by an absent P wave-QRS complex.

Example 2

Type II SA block:

Arrows indicate the presumed timing of each sinus impulse. The blue arrows represent normally transmitted impulses, i.e. resulting in P waves. The black arrows represent blocked sinus impulses (dropped P waves). The pauses around the dropped P waves (2.1 seconds) are exactly double the preceding P-P interval (1.05 seconds) Also note:

The 4th QRS complex is a junctional escape beat followed by a non-conducted P wave (occurring just prior to the T wave). The 8th QRS complex is a junctional escape beat. The following P wave is conducted to the ventricles, albeit with an extremely long PR interval (400ms).This second ECG example is reproduced from Dr Steve Smiths excellent ECG Blog. Click here for a more indepth analysis of this fascinating ECG.

Supraventricular Tachycardia (SVT)

Background
The term supraventricular tachycardia (SVT), whilst often used synonymously with AV nodal re-entry tachycardia (AVNRT), can be used to refer to any tachydysrhythmia arising from above the level of the Bundle of His.

Different types of SVT arise from or are propagated by the atria or AV node, typically producing a narrow-complex tachycardia (unless aberrant conduction is present).

Paroxysmal SVT (pSVT) describes an SVT with abrupt onset and offset characteristically seen with re-entrant tachycardias involving the AV node such as AVNRT or atrioventricular re-entry tachycardia (AVRT).

Supraventricular tachycardia

Classification

SVTs can be classified based on site of origin (atria or AV node) or regularity (regular or irregular). Classification based on QRS width is unhelpful as this is also influenced by the presence of pre-existing bundle branch block, rate-related aberrant conduction or presence of accessory pathways. Classification of SVT by site of origin and regularity Regular Irregular Atrial Sinus tachycardia Atrial fibrillation Atrial tachycardia Atrial flutter with variable block Atrial flutter Multifocal atrial Inappropriate sinus tachycardia tachycardia Sinus node re-entrant tachycardia

Atrioventricular Atrioventricular re-entry tachycardia (AVRT) AV nodal re-entry tachycardia

(AVNRT) Automatic junctional tachycardia AV Nodal Re-Entry Tachycardia (AVNRT)

This is the commonest cause of palpitations in patients with structurally normal hearts. AVNRT is typically paroxysmal and may occur spontaneously or upon provocation with exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines).

It is more common in women than men (~ 75% of cases occurring in women) and may occur in young and healthy patients as well as those suffering chronic heart disease. Patients will typically complain of the sudden onset of rapid, regular palpitations. The patient may experience a brief fall in blood pressure causing presyncope or occasionally syncope.

If the patient has underlying coronary artery disease the patient may experience chest pain similar to angina (tight band around the chest radiating to left arm or left jaw). The patient may complain of shortness of breath, anxiety and occasionally polyuria due to elevated atrial pressure releasing atrial natriuretic peptide. The tachycardia typically ranges between 140-280 bpm and is regular in nature. It may cease spontaneously (and abruptly) or continue indefinitely until medical treatment is sought.

The condition is generally well tolerated and is rarely life threatening in patients with pre-existing heart disease.

Pathophysiology

In comparison to AVRT, which involves an anatomical re-entry circuit (Bundle of Kent), in AVNRT there is a functionalre-entry circuit within the AV node.

Different types of re-entry loops: Functional circuit in AVNRT (left), anatomical circuit in AVRT (right)

Functional Pathways Within The AV Node

In AVNRT, there are two pathways within the AV node:

The slow pathway (alpha): a slowly-conducting pathway with a short refractory period. The fast pathway (beta): a rapidly-conducting pathway with a long refractory period.

Mechanism of re-entry in "slow-fast" AVNRT (ERP = effective refractory period)

Initiation Of Re-Entry

During sinus rhythm, electrical impulses travel down both pathways simultaneously. The impulse transmitted down the fast pathway enters the distal end of the slow pathway and the two impulses cancel each other out.

However, if a premature atrial contraction (PAC) arrives while the fast pathway is still refractory, the electrical impulse will be directed solely down the slow pathway (1).

By the time the premature impulse reaches the end of the slow pathway, the fast pathway is no longer refractory (2) hence the impulse is permitted to recycle retrogradely up the fast pathway.

This creates a circus movement whereby the impulse continually cycles around the two pathways, activating the Bundle of His anterogradely and the atria retrogradely (3). The short cycle length is responsible for the rapid heart rate.

This is the most common type of re-entrant circuit and is termed Slow-Fast AVNRT. Similar mechanisms exist for the other types of AVNRT.

Electrocardiographic Features
General Features of AVNRT

Regular tachycardia ~140-280 bpm. QRS complexes usually narrow (< 120 ms) unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction. ST-segment depression may be seen with or without underlying coronary artery disease. QRS alternans phasic variation in QRS amplitude associated with AVNRT and AVRT, distinguished from electrical alternans by a normal QRS amplitude. P waves if visible exhibit retrograde conduction with P-wave inversion in leads II, III, aVF. P waves may be buried in the QRS complex, visible after the QRS complex, or very rarely visible before the QRS complex. Subtypes of AVNRT Different subtypes vary in terms of the dominant pathway and the R-P interval. The RP interval represents the time between anterograde ventricular activation (R wave) and retrograde atrial activation (P wave). 1. Slow-Fast AVNRT (common type)

Accounts for 80-90% of AVNRT Associated with Slow AV nodal pathway for anterograde conduction and Fast AV nodal pathway for retrograde conduction. The retrograde P wave is obscured in the corresponding QRS or occurs at the end of the QRS complex as pseudo r or S waves ECG features:

P waves are often hidden being embedded in the QRS complexes. Pseudo R wave may be seen in V1 or V2.

Pseudo S waves may be seen in leads II, III or aVF. In most cases this results in a typical SVT appearance with absent P waves and tachycardia

Cardiac rhythm strips demonstrating (top) sinus rhythm and (bottom) paroxysmal SVT. The P wave is seen as a pseudo-R R wave (circled in bottom strip) in lead V1 during tachycardia. By contrast, the pseudo-R pseudo wave is not seen during sinus rhythm (it is absent from circled area in top strip). This very short ventriculo ventriculo-atrial time is frequently seen in typical Slow-Fast Slow AVNRT.

2. Fast-Slow AVNRT (Uncommon AVNRT)

Accounts for 10% of AVNRT Associated with Fast AV nodal pathway for anterograde conduction and Slow AV A nodal pathway for retrograde conduction. Due to the relatively long ventriculo-atrial ventriculo atrial interval, the retrograde P wave is more likely to be visible after the corresponding QRS. ECG features:

QRS-P-T complexes. Retrograde P waves are visible between the QRS QR and T wave.

3. Slow-Slow AVNRT (Atypical AVNRT)

1-5% AVNRT Associated with Slow AV nodal pathway for anterograde conduction and Slow left atrial fibres as the pathway for retrograde conduction. ECG features:

Tachycardia with a P-wave seen in mid-diastole effectively appearing before the QRS complex. Confusing as a P wave appearing before the QRS complex in the face of a tachycardia might be read as a sinus tachycardia.

Summary of AVNRT subtypes

No visible P waves? > Slow-Fast P waves visible after the QRS complexes? > Fast-Slow P waves visible before the QRS complexes? > Slow-Slow

Management Of AVNRT

May respond to vagal maneuvers with reversion to sinus rhythm. The mainstay of treatment is adenosine. Other agents which may be used include calcium-channel blockers, beta-blockers and amiodarone. DC cardioversion is rarely required. Catheter ablation may be considered in recurrent episodes not amenable to medical treatment.

Other Types Of SVT

Most of the other types of SVT are discussed elsewhere (follow links in table above). Two less-common types are discussed below.

Inappropriate Sinus Tachycardia

Typically seen in young healthy female adults. Sinus rate persistently elevated above 100 bpm in absence of physiological stressor. Exaggerated rate response to minimal exercise. ECG indistinguishable from sinus tachycardia.

Sinus Node Reentrant Tachycardia (SNRT)

Caused by reentry circuit close to or within the sinus node. Abrupt onset and termination. P wave morphology is normal. Rate usually 100 150 bpm.

May terminate with vagal manoeuvres.

ECG Examples
Example 1a

Slow-Fast (Typical) AVNRT:

Narrow complex tachycardia at ~ 150 bpm. No visible P waves. There are pseudo R waves in V1-2.

Pseudo R' waves in V1-2

Example 1b

The same patient following resolution of the AVNRT:

Sinus rhythm. The pseudo R waves have now disappeared.

Pseudo R' waves in V1-2 have resolved

Example 2a

Slow-Fast AVNRT:

Narrow complex tachycardia ~ 220 bpm. No visible P waves. Subtle notching of the terminal QRS in V1 (= pseudo R wave). Widespread ST depression this is a common electrocardiographic finding in AVNRT and does not necessarily indicate myocardial ischaemia, provided the changes resolve once the patient is in sinus rhythm.

Example 2b

The same patient following resolution of the AVNRT:

Sinus rhythm.

Pseudo R waves have disappeared. There is residual ST depression in the inferior and lateral leads (most evident in V4-6), indicating that the patient did indeed have rate-related myocardial ischaemia ( NSTEMI).

Example 3

Patient with Slow-Fast AVNRT undergoing treatment with adenosine:

The top section of the rhythm strip shows AVNRT with absent P waves and pseudo R waves clearly visible. The middle portion of the strip shows adenosine acting on the AV node to suppress AV conduction there are several broad complex beats which may be aberrantlyconducted supraventricular impulses or ventricular escape beats (this is extremely common during administration of adenosine for AVNRT).

The bottom section shows reversion to sinus rhythm; the pseudo R waves have resolved.

Example 4a

Fast-Slow (Uncommon) AVNRT:

Narrow complex tachycardia ~ 120 bpm. Retrograde P waves are visible after each QRS complex most evident in V2-3.

Retrograde P waves

Example 4b

The same patient following resolution of the AVNRT:

Now in sinus rhythm. The retrograde P waves have disappeared.

Retrograde P waves resolved

Example 5a

Fast-Slow AVNRT:

Narrow complex tachycardia ~ 135 bpm. Retrograde P waves following each QRS complex upright in aVR and V1; inverted in II, III and aVL.

Upright retrograde P waves in aVR

Inverted retrograde P waves lead II

Example 5b

The same patient following resolution of the AVNRT:

Sinus rhythm. The retrograde P waves have disappeared.

Retrograde P waves in aVR resolved

Retrograde P waves in lead II resolved

Example 6a

Fast-Slow AVNRT:

Narrow complex tachycardia at ~ 125 bpm. Retrograde P waves follow each QRS complex: upright in V1-3; inverted in II, III and aVF.

Upright retrograde P waves in V2

Inverted retrograde P waves in lead II

Example 6b

The same patient following resolution of the AVNRT:

Sinus rhythm. Retrograde P waves have disappeared.

Retrograde P waves in V2 have resolved

Retrograde P waves in lead II have resolved

Example 7

SVT with QRS Alternans:

Narrow complex tachycardia ~ 215 bpm. Retrograde P waves are visible preceding each QRS complex (upright in V1, inverted in lead II). There is a beat-to-beat variation in the QRS amplitude without evidence of low voltage (= QRS alternans). The PR interval is ~ 120 ms, so this could be either a low atrial tachycardia or possibly an AVNRT with a long RP interval (i.e. either Fast-Slow or Slow-Slow varieties).

Sinus Node Dysfunction (Sick Sinus Syndrome)

Definition

A disease characterised by abnormal sinus node functioning with resultant bradycardia and cardiac insufficiency.

Causes

May be multi-factorial in origin. Causes can be considered either intrinsic or extrinsic.

Intrinsic

Idiopathic Degenerative Fibrosis (commonest). Ischaemia. Cardiomyopathies. Infiltrative Diseases e.g. sarcoidosis, haemochromatosis. Congenital abnormalities.

Extrinsic Causes

Drugs e.g. digoxin, beta-blockers, calcium channel blockers. Autonomic dysfunction. Hypothyroidism. Electrolyte abnormalitites e.g. hyperkalaemia.

ECG In Sinus Node Dysfunction

ECG abnormalities can be variable and intermittent. Multiple ECG abnormalities can be seen in sinus node dysfunction including:

Sinus Bradycardia. Sinus Arrhythmia associated with sinus node dysfunction in the elderly in the absence of respiratory pattern association. Sinoatrial Exit Block. Sinus Arrest pause > 3 seconds. Atrial fibrillation with slow ventricular response. Bradycardia tachycardia syndrome. Bradycardia tachycardia syndrome

Alternating bradycardia with paroxysmal tachycardia, often supraventricular in origin. On cessation of tachyarrhythmia may be a period of delayed sinus recovery e.g. sinus pause or exit block. If significant this period of delayed recovery may result in syncope.

Clinical Manifestations

Commonly seen in the elderly but sinus node dysfunction can affect all age groups. Symptoms are due to decreased cardiac output and end-organ hypoperfusion associated with cardiac rhythm abnormality. Wide range of clinical symptoms including syncope, near-syncope, dizziness, fatigue and palpitations.

Treatment

Correction / removal of extrinsic causes e.g. non-essential drugs. Pacemaker insertion requires correlation of both ECG abnormalities and clinical symptoms.

Recommendation For Pacing In Sinus Node Dysfunction

Class I Evidence and/or agreement that permanent pacing is useful and effective.

Sinus node dysfunction with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms. In some patients, bradycardia is iatrogenic and will occur as a consequence of essential long-term drug therapy of a type and dose for which there are no acceptable alternatives.

Symptomatic chronotropic incompetence. Class IIa Conflicting evidence/ divergence of opinion but weight of evidence / opinion in favour

Sinus node dysfunction occurring spontaneously or as a result of necessary drug therapy, with heart rate less than 40 bpm when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented.

Syncope of unexplained origin when major abnormalities of sinus node function are discovered or provoked in electrophysiological studies. Class IIb Conflicting evidence/divergence of opinion where usefulness / efficacy is less well established

In minimally symptomatic patients, chronic heart rate less than 40 bpm while awake.

Class III Permanent pacing is not useful/effective and in some cases may be harmful.

Sinus node dysfunction in asymptomatic patients, including those in whom substantial sinus bradycardia (heart rate less than 40 bpm) is a consequence of longterm drug treatment.

Sinus node dysfunction in patients with symptoms suggestive of bradycardia that are clearly documented as not associated with a slow heart rate. Sinus node dysfunction with symptomatic bradycardia due to nonessential drug therapy.

ECG Examples
Example 1: Sinus arrest

Sinus arrest:

Prolonged absence of sinus node activity (absent P waves) > 3 seconds.

Example 2: Bradycardia-tachycardia syndrome

Bradycardia-tachycardia syndrome:

Runs of tachycardia interspersed with long sinus pauses (up to 6 seconds). The sinus rate is extremely slow, varying from 40 bpm down to around 10 bpm in places. Sinus beats are followed by paroxysms of junctional tachycardia at around 140 bpm.

Sinus Tachycardia
Definition

Sinus rhythm with a resting heart rate of > 100 bpm in adults, or above the normal range for age in children.

Normal heart rates in children

Newborn: 110 150 bpm 2 years: 85 125 bpm 4 years: 75 115 bpm 6 years+: 60 100 bpm

Causes
Non-pharmacological

Exercise Pain, anxiety Hypoxia, hypercarbia Acidaemia Sepsis, pyrexia Pulmonary embolism Hyperthyroidism

Pharmacological

Beta-agonists: adrenaline, isoprenaline, salbutamol, dobutamine Sympathomimetics: amphetamines, cocaine, methylphenidate Antimuscarinics: antihistamines, TCAs, carbamazepine, atropine Others: caffeine, theophylline, marijuana

Handy Tip
With very fast heart rates the P waves may be hidden in the preceding T wave, producing a camel hump appearance.

Hidden P waves in sinus tachycardia ("camel hump" appearance)

Example ECG

Sinus tachycardia:

Heart rate 150 bpm. P waves are hidden within each preceding T wave.

Tricyclic Overdose (Sodium-Channel Blocker Toxicity)

Background
The ECG is a vital tool in the prompt diagnosis of poisoning with sodium-channel

blocking medications such as:

Tricyclic antidepressants (= most common) Type Ia antiarrhythmics (quinidine, procainamide) Type Ic antiarrhythmics (flecainide, encainide) Local anaesthetics (bupivacaine, ropivacaine) Antimalarials (chloroquine, hydroxychloroquine) Dextropropoxyphene Propranolol Carbamazepine Quinine The two main adverse effects of sodium-channel blocker poisoning are seizures and ventricular dysrhythmias (due to blockade of sodium channels in the CNS and myocardium) Handy tip: An ECG should be taken in all patients who present with a deliberate self-poisoning (or altered GCS of unknown aetiology) to screen for TCA overdose.

Typical example of TCA toxicity

Electrocardiographic Features Of Sodium-Channel Blockade

Features consistent with sodium-channel blockade are:

Interventricular conduction delay QRS > 100 ms in lead II Right axis deviation of the terminal QRS: Terminal R wave > 3 mm in aVR R/S ratio > 0.7 in aVR

o o

Dominant secondary R wave (R') in aVR > 3mm

Patients with tricyclic overdose will also usually demonstrate sinus

tachycardia secondary to muscarinic (M1) receptor blockade.

Clinical Features Of Tricyclic Overdose

In overdose, the tricyclics produce rapid onset (within 1-2 hours) of:

Sedation and coma Seizures Hypotension Tachycardia Broad complex dysrhythmias Anticholinergic syndrome Tricyclics mediate their cardiotoxic effects via blockade of myocardial fast sodium channels (QRS prolongation, tall R wave in aVR), inhibition of potassium channels (QTc prolongation) and direct myocardial depression. Other toxic effects are produced by blockade at muscarinic (M1), histamine (H1) and 1-adenergic receptors. The degree of QRS broadening on the ECG is correlated with adverse events:

QRS > 100 ms is predictive of seizures QRS > 160 ms is predictive of ventricular arrhythmias (e.g. VT)

Management Of Significant Tricyclic Overdose (> 10mg/Kg) With Signs Of Cardiotoxicity (ECG Changes)

Patients need to be managed in a monitored area equipped for airway management and resuscitation. Secure IV access, adminster high flow oxygen and attach monitoring equipment. Administer IV sodium bicarbonate 100 mEq (1-2 mEq / kg); repeat every few minutes until BP improves and QRS complexes begin to narrow. Intubate as soon as possible. Hyperventilate to maintain a pH of 7.50 7.55. Once the airway is secure, place a nasogastric tube and give 50g (1g/kg) of activated charcoal. Treat seizures with IV benzodiazepines (e.g. diazepam 5-10mg). Treat hypotension with a crystalloid bolus (10-20 mL/kg). If this is unsuccessful in restoring BP then consider starting vasopressors (e.g. noradrenaline infusion). If arrhythmias occur, the first step is to give more sodium bicarbonate. Lidocaine (1.5mg/kg) IV is a third-line agent (after bicarbonate and hyperventilation) once pH is > 7.5.

Avoid Ia (procainamide) and Ic (flecainide) antiarrhythmics, beta-blockers and amiodarone as they may worsen hypotension and conduction abnormalities. Admit the patient to the intensive care unit for ongoing management.

Example ECGs
Example 1a TCA overdose

Typical ECG of TCA toxicity demonstrating:

Sinus tachycardia with first-degree AV block (P waves hidden in the T waves, best seen in V1-2). Broad QRS complexes. Positive R wave in aVR.

Example 1b Worsening TCA toxicity

A second ECG of the same patient showing worsening TCA cardiotoxicity with marked QRS broadening producing a sine wave appearance reminiscent of hyperkalaemia.

Example 1c Resolution of TCA toxicity with treatment (bicarbonate and hyperventilation)

Third ECG of the same patient after serum alkalinisation with sodium bicarbonate, intubation and hyperventilation.

The QRS duration has narrowed back to normal and the R wave in aVR has disappeared.

Example 2 Massive TCA overdose

Another example of severe TCA cardiotoxicity after ingestion of 35 mg/kg doxepin. There is marked QRS widening with tachycardia and a positive R wave in aVR.

Example 3 Flecainide overdose

Similar ECG changes are seen with other sodium-channel blocking agents. This ECG demonstrates QRS widening and positive R wave in aVR consistent with sodium-channel blockade in a patient with flecainide poisoning.

Example 4 Flecainide overdose

Another example of flecainide cardiotoxicity.

ST Elevation In AVR LMCA Occlusion?

This ECG demonstrates the classical pattern of left main coronary artery (LMCA) occlusion:

Widespread horizontal ST depression, most prominent in leads I, II and V4-6 ST elevation in aVR 1mm ST elevation in aVR V1

However, ST elevation in aVR is not entirely specific to LMCA occlusion. It may also be seen with:

Proximal left anterior descending artery (LAD) occlusion Severe triple-vessel disease (3VD)

Mechanism Of STE In AVR

Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR. Lead aVR also directly records electrical activity from the right upper portion of the heart, including the right ventricular outflow tract and the basal portion of the interventricular septum; infarction in this area could theoretically produce ST elevation in aVR. ST elevation is aVR is thought to result from two possible mechanisms:

Diffuse subendocardial ischaemia (producing reciprocal change in aVR) Transmural ischaemia / infarction of the basal interventricular septum (e.g. due to a proximal occlusion within the left coronary system)

NB. The basal septum is supplied by the first septal perforator artery (a very proximal branch of the LAD), so ischaemia/infarction of the basal septum would imply involvement of the proximal LAD or LMCA.

Predictive Value Of STE In AVR

In the context of widespread ST depression + symptoms of myocardial ischaemia:

STE in aVR 1mm indicates proximal LAD / LMCA occlusion or severe 3VD STE in aVR 1mm predicts the need for CABG STE in aVR V1 differentiates LMCA from proximal LAD occlusion Absence of ST elevation in aVR almost entirely excludes a significant LMCA lesion In the context of anterior STEMI:

STE in aVR 1mm is highly specific for LAD occlusion proximal to the first septal branch In patients undergoing exercise stress testing:

STE of 1mm in aVR during exercise stress testing predicts LMCA or ostial LAD stenosis Magnitude of ST elevation in aVR is correlated with mortality in patients with acute coronary syndromes:

STE in aVR 0.5mm was associated with a 4-fold increase in mortality STE in aVR 1mm was associated with a 6- to 7-fold increase in mortality STE in aVR 1.5mm has been associated with mortalities ranging from 20-75% For a more in-depth look at the literature on aVR, click here

More ECG Examples

Example 2 LMCA occlusion

Another typical example of LMCA occlusion:

Widespread ST depression, most prominent in the lateral leads (V4-6, I, aVL) ST elevation > 1mm in aVR ST elevation in aVR V1

Example 3 LMCA occlusion

The ECG shows:

Marked ST elevation in aVR >> V1 ST depression in mulitple leads (V2-6, I, II, aVL, aVF), to some extent masked by a non-specific interventricular conduction delay This patient presented to our ED recently with severe ischaemic chest pain, vomiting, syncope (due to runs of VT) and cardiogenic shock. He was taken for emergent angiography and found to have a complete ostial occlusion of his left main coronary artery.

Example 4 Proximal LAD occlusion

This ECG shows:

ST elevation in aVR and V1 of similar magnitude. Widespread ST depression (V3-6, I, II, III, aVF) This patient had a severe ostial LAD thrombus that was close to the left main. (This ECG is reproduced from Dr Smiths ECG Blog click here to see the ECG in its original context)

Example 5 Severe Multi-Vessel Disease

This ECG shows:

ST elevation in aVR and V1, of similar magnitude ST depression in multiple leads (V5-6, I, II, aVL, aVF) Evidence of anteroseptal STEMI ST elevation with Q wave formation in V1-3 It would be reasonable to suspect a proximal LAD occlusion based on this ECG. However, this patient actually had severe multi-vessel disease. Angiography demonstrated a chronic total occlusion of his circumflex artery, with critical stenoses of his proximal LAD, RCA and ramus

intermedius. Surprisingly, in this case the culprit vessel was thought to be the RCA, which had been collateralising his chronically occluded circumflex.

Implications For Therapy In Acute Coronary Syndromes

Given the ability of STE in aVR to predict critical coronary lesions and death, this ECG pattern is increasingly being recognised as a STEMI equivalent that requires emergent reperfusion therapy to prevent cardiogenic shock and death. Furthermore, the presence or absence of STE in aVR may potentially inform the decision to give thienopyridine platelet inhibitors (e.g. clopidogrel, prasugrel) during an acute coronary syndrome:

Clopidogrel treatment 7 days before CABG is associated with an increase in major bleeding, haemorrhage-related complications, and transfusion requirements. Prasugrel is associated with even more bleeding than clopidogrel. If urgent CABG (within 7 days) is likely, then there is an argument for omitting thienopyridines during the initial management of an acute coronary syndrome (or at least using clopidogrel instead of prasugrel). In the recent study by Kosuge et al. (2011)

STE in aVR 1 mm was a strong predictor of severe LMCA / 3VD requiring CABG. Conversely, patients with < 1mm ST elevation in aVR had a negligible risk of severe LMCA / 3VD requiring CABG. Based on this data:

Patients with < 1mm STE in aVR may safely receive clopidogrel/prasugrel during the initial treatment of their ACS as they are unlikely to proceed to urgent CABG. Patients with 1 mm STE in aVR may potentially require early CABG; therefore these patients should ideally be discussed with the interventional cardiologist ( cardiac surgeon) before thienopyridines are given.

High Lateral STEMI

High lateral STEMI

Definitions

ST elevation primarily localised to leads I and aVL is referred to as a high lateral STEMI. It is usually associated with reciprocal ST depression and T wave inversion in the inferior leads.

Culprit Vessels

Occlusion of the first diagonal branch (D1) of the left anterior descending artery (LAD) may produce isolated ST elevation in I and aVL Occlusion of the circumflex artery may cause ST elevation in I, aVL along with leads V5-6.

Acknowledgements
This ECG was reproduced from Dr Smiths ECG Blog.

Inferior STEMI
Cinical Significance

Inferior MIs account for 40-50% of all myocardial infarctions. Generally have a more favourable prognosis than anterior myocardial infarction (inhospital mortality only 2-9%), however certain factors indicate a worse outcome. Up to 40% of patients with an inferior STEMI will have a concomitant right ventricular infarction. These patients may develop severe hypotension in response to nitrates and generally have a worse prognosis.

Up to 20% of patients with inferior STEMI will develop significant bradycardia due to second- or third-degree AV block. These patients have an increased in-hospital mortality (>20%).

Inferior STEMI may also be associated with posterior infarction, which confers a worse prognosis due to increased area of myocardium at risk.

How To Recognise An Inferior STEMI

ST elevation in leads II, III and aVF Progressive development of Q waves in II, III and aVF Reciprocal ST depression in aVL ( lead I)

Which Artery Is The Culprit?

Inferior STEMI can result from occlusion of all three coronary arteries:

The vast majority (~80%) of inferior STEMIs are due to occlusion of the dominant right coronary artery (RCA). Less commonly (around 18% of the time), the culprit vessel is a dominant left circumflex artery (LCx). Occasionally, inferior STEMI may result from occlusion of a type III or wraparound left anterior descending artery (LAD). This produces the unusual pattern of concomitant inferior and anterior ST elevation. While both RCA and circumflex occlusion may cause infarction of the inferior wall, the precise area of infarction in each case is slightly different:

The RCA territory covers the medial part of the inferior wall, including the inferior septum. The LCx territory covers the lateral part of the inferior wall and the left posterobasal area.

This produces subtly different patterns on the ECG:

The injury current in RCA occlusion is directed inferiorly and rightward, producing ST elevation in lead III > lead II (as lead III is more rightward facing). The injury current in LCx occlusion is directed inferiorly and leftward, producing ST elevation in the lateral leads I and V5-6. These differences allow for electrocardiographic differentiation between RCA and LCx occlusion.

RCA occlusion is suggested by:

ST elevation in lead III > lead II Presence of reciprocal ST depression in lead I Signs of right ventricular infarction: STE in V1 and V4R

Circumflex occlusion is suggested by:

ST elevation in lead II = lead III Absence of reciprocal ST depression in lead I Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-6 (NB. Relative Q-wave depth in leads II and III is not useful in determining the culprit artery. Both RCA and LCx occlusion produce a similar pattern of Q wave changes, often with deeper Q waves seen in lead III)

Example ECGs
Example 1

Early inferior STEMI:

Hyperacute (peaked) T waves in II, III and aVF with relative loss of R wave height.

Early ST elevation and Q-wave wave formation in lead III. Reciprocal ST depression and T wave inversion in aVL. ST elevation in lead III > lead II suggests an RCA occlusion; the subtle ST elevation in V4R would be consistent with this. Note how the ST segment morphology in aVL is an exact mirror image of lead III. This reciprocal change occurs because these two leads are approximately opposite to one another (150 degrees apart). The concept of reciprocal change can be further highlighted by taking lead aVL and inverting it see how the ST morphology now looks identical to lead III.

(For or more about lead aVL and its utility in diagnosing subtle inferior STEMI, check out this post from Dr Smiths ECG G Blog) Blog Example 2

Inferior STEMI:

ST elevation in II, III and aVF. Q-wave wave formation in III and aVF. Reciprocal ST depression and T wave inversion in aVL ST elevation in lead II = lead III and absent reciprocal change in lead I (isoelectric ST segment) suggest a circumflex artery occlusion

Example 3

Inferior STEMI:

Marked ST elevation in II, III and aVF with early Q-wave formation. Reciprocal changes in aVL. ST elevation in lead III > II with reciprocal change present in lead I and ST elevation in V1-2 suggests RCA occlusion with associated RV infarction: This patient should have right-sided leads to confirm this.

Example 4

Hyperacute inferior STEMI:

Hyperacute T waves in II, III and aVF. Early ST elevation and loss of R wave height in II, III and aVF. Reciprocal change in aVL and lead I. Example 5

Inferior STEMI:

The concave ST elevation in II, III and aVF may be mistaken for pericarditis. However, the fact that the ST elevation is localised to the inferior leads with reciprocal changes in aVL confirms that this is an inferior STEMI. Example 6

Massive inferolateral STEMI:

Marked ST elevation in II, III and aVF with a tombstone morphology. Reciprocal change in aVL. ST elevation is also present in the lateral leads V5-6, indicating an extensive infarct of the inferior and lateral walls. In patients with inferior STEMI, ST elevation of 2mm or more in leads V5 and V6 is predictive of extensive coronary artery disease and a large area of infarction. Example 7

Recent inferolateral STEMI:

Well-formed Q waves in III and aVF suggest that this STEMI is not acute. The T waves in III and aVF are beginning to invert. There is still some residual ST elevation in the inferior (II, III, avF) and lateral (V5-6) leads. ST elevation may take 2 weeks to resolve after an acute inferior MI (even longer for an anterior STEMI). NB. If this patient had ongoing chest pain you would still treat them as an acute STEMI!

Bradycardia And AV Block In Inferior STEMI

Up to 20% of patients with inferior STEMI will develop either second- or third degree heart block. There are two presumed mechanisms for this:

Ischaemia of the AV node due to impaired blood flow via the AV nodal artery. This artery arises from the RCA 80% of the time, hence its involvement in inferior STEMI due to RCA occlusion.

Bezold-Jarisch reflex = increased vagal tone secondary to ischaemia. The conduction block may develop either as a step-wise progression from 1st degree heart block via Wenckebach tocomplete heart block (in 50% of cases) or as abrupt onset of second or third-degree heart block (in the remaining 50%).

Patients may also manifest signs of sinus node dysfunction, such as sinus bradycardia, sinus pauses, sinoatrial exit block and sinus arrest. Similarly to AV node dysfunction, this may result from increased vagal tone or ischaemia of the SA node (the SA nodal artery is supplied by the RCA in 60% of people).

Bradyarrhythmias and AV block in the context of inferior STEMI are usually transient (lasting hours to days), respond well to atropine and do not require permanent pacing. Example 8

Inferior STEMI with third degree heart block and slow junctional escape rhythm. Example 9

Inferior STEMI with sinus node dysfunction (either sinus arrest or extreme sinus bradycardia) and a slow junctional escape rhythm.

Video
Amal Mattu presents a subtle case of inferior MI portended by downsloping ST segment depression in aVL. Sometimes the reciprocal changes occur first in STEMIs.