Arrhythmias
The cardiac conduction system
Cardiac action potential
The resting cardiac myocyte is electrically negative, with a transmembrane voltage of between -50 mV and -95 mV. This is due to the distribution of K+, Na+, Cl–, and Ca2+ ions across the cell membrane. The negativity is maintained by the energy-consuming Na+/K+ pump, which transports three Na+ ions out of the cell for two K+ ions inward. During phase 4 of the action potential, the voltage slowly increases until a threshold of -60 mV is reached, which opens voltage-gated Na+ channels and triggers depolarization. The voltage changes in one cell are spread to adjacent cells via gap junctions between them, such that a wavefront of electrical activation is propagated. At least ten distinct ion channels modulate the voltage changes that occur in the action potential (Figs. 10.1 and 10.2).
Automaticity
This is the ability of all cardiac cells to spontaneously depolarize. It is caused by the inward flow of positive ions during diastole. At potentials more negative than -60 mV, ion channels open allowing a slow influx of cations. The slow influx of Ca2+ in the sinoatrial node (SAN) allows it to depolarize more rapidly and therefore suppress other potential pacemaker sites.
Sinoatrial node
The SAN sits high in the lateral right atrium (RA) just below the superior vena cava (SVC). It is 1-2 cm in length, 2-3 mm wide, and less than 1 mm from the epicardial surface. It is the dominant site of impulse generation; impulses are conducted out of the sinus node to depolarize the surrounding RA. The SAN is richly innervated with both adrenergic and cholinergic receptors, which alter the rate of depolarization hence controlling the heart rate. Activation spreads out from the SAN to the rest of the RA and left atrium (LA) via specialized interatrial connections including Bachmann’s bundle.
Atrioventricular node
The atrioventricular node (AVN) is found in the RA anterior to the mouth of the coronary sinus and directly above the insertion of the septal leaflet of the tricuspid valve. It is the only electrical connection to the ventricle, via the bundle of His, which, like the SAN it is also densely innervated with sympathetic and parasympathetic fibres.
His-Purkinje system
The electrical impulse conducts rapidly through the bundle of His into the upper part of the interventricular septum, where it splits into two branches: the right bundle branch, which continues down the right side of the septum to the apex of the right ventricle and the base of the anterior papillary muscle, and the left bundle branch, which further splits into two fascicles, anterior and posterior. The terminal Purkinje fibres connect with the ends of the bundle branches, forming an interweaving network on the endocardial surface so that a cardiac impulse is transmitted almost simultaneously to the entire right and left ventricles.
 Fig. 10.1 The cardiac action potential. The action potential has five parts: 0 rapid influx of Na+ causing fast depolarization 1 rapid early repolarization due to efflux of Na+ 2 plateau phase where repolarization is slowed by an influx of Ca2+ 3 repolarization due to the the efflux of K+ 4 diastole with a steady-state resting transmembrane voltage. The plateau phase distinguishes the cardiac from neuronal action potential. The release of Ca2+ during phase 2 triggers mechanical contraction of the cell. |
Bradycardia: general approach
Ask specifically about previous cardiac disease, palpitations, blackouts, dizziness, chest pain, symptoms of heart failure, current medication.
Investigations
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Emergency nanagement
Haemodynamically unstable patients
Severe haemodynamic compromise (cardiac arrest, asystole, systolic blood pressure (SBP)<90 mmHg, severe pulmonary oedema, evidence of cerebral hypoperfusion) needs immediate treatment.
Give oxygen via face mask if the patient is hypoxic on air.
Keep nil by mouth (NBM) until definitive therapy has been started, to reduce the risk of aspiration in case of cardiac arrest or when the patient lies supine for temporary wire insertion.
Secure peripheral venous access.
Give atropine 1 mg IV (MiniJet®) bolus; repeat if necessary up to a maximum 3 mg.
Give isoprenaline 0.2 mg IV (MiniJet®) if there is a delay in pacing and the patient remains unstable. Set up an infusion (1 mg in 100 mL 1 M saline starting at 1 mL/min titrating to heart rate (HR)).
Insert temporary pacing wire (technique described in
Temporary ventricular pacing, p. 808). If this is not possible immediately, set up an external pacing system and transfer to a screening room for transvenous pacing.
Look for and treat reversible causes; drug overdose (β-blockers, verapamil, diltiazem, digoxin), hypothyroidism, hypothermia, myocardial infarction (MI), infective endocarditis).
Long-term management
Ensure all possible underlying causes have been identified and removed.
Regardless of aetiology if symptomatic bradycardia remains refer for permanent pacing (see
p. 530).
Complete heart block should always be referred for a permanent pacemaker, whether symptomatic or not.
External cardiac pacing
In emergencies, external cardiac pacing (via an external defibrillator that can pace) may be used first, but this is only a temporary measure until a more ‘definitive’ transvenous pacing wire can be inserted.
The defibrillator ECG electrodes need to be attached.
Attach the defibrillation patches to the anterior and posterior chest wall. Turn the output up (in volts or amperes) until ventricular capture with QRS complexes is seen. This will also cause extremely unpleasant thoracic muscular capture, so the patient must be sedated with benzodiazepam
External cardiac pacing is useful as a standby in patients, e.g. post-MI, when the risks of prophylactic transvenous pacing after thrombolysis are high.
Haemodynamically stable patients with anterior MI and bifasicular block may be managed simply by application of the external pacing electrodes and having the pulse generator ready if necessary.
Familiarize yourself with the machine in your hospital when you have some time—a cardiac arrest is not the time to read the manual for the apparatus!
Sinus bradycardia
In sinus bradycardia, the SAN discharges <60/min. P waves are normal but slow. It may be normal (e.g. in sleep, healthy resting hearts).
Causes
Young athletic individual
Healthy resting heart, e.g. sleep
Chronic degeneration of sinus or AV nodes or atria
Drugs—β-blockers, morphine, amiodarone, calcium-channel blockers, lithium, propafenone, clonidine
Increased vagal tone
vasovagal attack
nausea or vomiting
carotid sinus hypersensitivity
Hypothyroidism
Hypothermia
MI or ischaemia of the sinus node
Cholestatic jaundice
Raised intracranial pressure
Sinus pause
The SAN fails to generate impulses (sinus arrest) or the impulses are not conducted to the atria (SA exit block). A single dropped P wave with a PP interval that is a multiple of the basic PP interval suggests exit block. A period of absent P waves suggests sinus arrest. Causes include, excess vagal tone, acute myocarditis, MI, aging (fibrosis), stroke, digoxin toxicity, and anti-arrhythmic drugs.
Sick sinus syndrome
This syndrome encompasses a number of conduction system problems: persistent sinus bradycardia not caused by drugs, sinus pauses, AV conduction disturbances, and paroxysms of atrial arrythmias. It is usually diagnosed by ambulatory cardiac monitoring.
Atrioventricular block
This can occur at the AVN (nodal) or His-Purkinje system (infranodal). Common causes are ischaemic heart disease (IHD), conduction system fibrosis (aging), calcific aortic stenosis, congenital, cardiomyopathy, hypothermia, hypothyroidism, trauma, radiotherapy, infection, connective tissue disease, sarcoidosis, and anti-arrhythmic drugs. AV block is further classified:
First-degree AV block
Every impulse conducts to the ventricle but the conduction time is prolonged. Every P wave is followed by a QRS but with a prolonged PR interval (>200 ms). If the QRS width is normal then the block is at the AV node, if the QRS shows aberration (right (RBBB) or left bundle branch block (LBBB)), then the block may be at the AV node or the His-Purkinje system.
Second-degree AV block
Mobitz 1 (Wenckebach): ECG shows the PR interval prolongs until a P wave is not conducted. The PR interval following the dropped P wave must be the shortest. The RR interval is therefore irregular. This block is characteristic of the AVN.
Mobitz 2: ECG shows a fixed P to QRS ratio of 2:1, 3:1, or 4:1. Block is predominantly at the His bundle and there is often an aberrant pattern to the QRS complex.
Third-degree AV block (complete heart block)
There is no conduction to the ventricle. The ECG shows dissociation between the P and QRS complexes. An escape pacemaker rhythm takes over. A narrow QRS indicates AVN block, and the His bundle is the pacemaker, which is faster and more stable than more distal sites. A wide QRS indicates infranodal block and a distal ventricular pacemaker site. Asystole may occur; therefore, this carries a worse prognosis. This type of heart block always requires implantation of a permanent pacemaker.
Causes of atrioventricular block
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Bundle branch block
This is due to disease in the His-Purkinje system causing a QRS >120 ms. Common causes are conduction system fibrosis (aging), IHD, hypertension, cardiomyopathies, cardiac surgery, infiltrative diseases (e.g. amyloid).
LBBB (Fig. 10.3): LV depolarization is delayed, giving a wide QRS, large notched R waves in leads I and V6, and a deep S wave (may be preceded by small R wave) in V1. Block confined to the anterior or posterior fascicles of the left bundle gives left-axis or right-axis deviation respectively on the ECG. BBB leads to asynchronous contraction of the left and right ventricle, which reduces cardiac output, important in heart failure.
RBBB: RV depolarization is delayed, giving wide QRS, an RSR pattern in V1, and a slurred S wave in I and V6. This can be a normal variant but more commonly as a result of causes listed above and, in addition, ASD, pulmonary embolism (PE), cor pulmonale.
Bifasicular block (Fig. 10.4) = RBBB + left anterior hemiblock (left-axis deviation on ECG), RBBB + left posterior hemiblock (right-axis deviation on ECG), or LBBB. All of these may progress to complete AV block.
Trifasicular block = bifasicular block + 1st-degree AV block.
Management
Conventional teaching is that LBBB is always pathological, and thorough investigation for an underlying cause is needed (echocardiogram, cardiac MR, coronary angiography); however, a cause may not be found. RBBB may occur in otherwise completely normal hearts.
Common causes of bundle branch block
Hypertensive heart disease
Valve disease (especially aortic stenosis)
Conduction system fibrosis (aging)
Myocarditis or endocarditis
Cardiomyopathies
Pulmonary hypertension
Trauma or post-cardiac surgery
Neuromuscular disorders (myotonic dystrophy)
Polymyositis.
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 Fig. 10.4 ECG showing bifasicular block. There is a wide QRS complex with an rSr pattern in V1 and deep slurred S wave in V6 (=RBBB). The QRS in lead 1 is positive and lead aVF negative (=left anterior hemiblock). There is also 2nd-degree AV nodal block (Mobitz type 1 or Wenkebach). Observing the rhythm strip from the first P wave, there is a gradually prolonging PR interval and the P wave that follows the 6th QRS complex is blocked. |
Tachycardia: general approach
Tachyarrhythmias may present with significant symptoms and haemodynamic compromise. The approach to patients depends upon the following factors:
The effect of the rhythm on the patient
Patients with cardiac arrest—immediate unsynchronized DC shock (follow advanced life support (ALS) guidelines)
Patients with signs of severe haemodynamic compromise:
shock; low BP, cool peripheries, sweating
cerebral hypoperfusion; confusion, agitated, depressed conscious level
pulmonary oedema
chest pain
Patients without haemodynamic compromise: record an ECG and diagnose tachyarrhythmia. Follow the treatment algorithm outlined here. If they deteriorate, treat as above.
Diagnosing the arrhythmia
The main distinctions to make are:
tachy- (>120/min) vs. brady- (<60/min) arrhythmia
narrow (≤120 ms or 3 small squares) vs. broad QRS complex
regular vs. irregular rhythm.
Investigations for patients with tachyarrhythmias
Tachycardia: emergency management
History
Previous cardiac disease, palpitations, dizziness, chest pain, symptoms of heart failure and recent medication. Ask specifically about conditions known to be associated with certain cardiac arrhythmias (e.g. AF—alcohol, thyrotoxicosis, mitral valve disease, IHD, pericarditis; VT—previous MI, LV aneurysm).
Management (Fig. 10.5)
Haemodynamically unstable patients
Tachyarrhythmias causing severe haemodynamic compromise require urgent correction, usually with external defibrillation. Drug therapy requires time and haemodynamic stability.
The only exception is a patient in chronic AF with an uncontrolled ventricular rate—defibrillation is unlikely to cardiovert to sinus rhythm (SR). Rate control and treatment of precipitant is first-line.
Sedate awake patients with midazolam (2.5-10 mg IV) ± diamorphine (2.5-5 mg IV + metoclopramide 10 mg IV) for analgesia. Beware respiratory depression and have flumazenil and naloxone to hand.
Formal anaesthesia with propofol is preferred, but remember the patient may not have an empty stomach and precautions should be taken to prevent aspiration (e.g. cricoid pressure, endotracheal (ET) intubation).
Start at 200 J synchronized shock and increase as required.
If tachyarrhythmia recurs or is unresponsive try to correct ↓PaO2 (partial pressure of oxygen in the arterial blood), ↑PaCO2 (partial pressure of carbon dioxide in the arterial blood), acidosis or ↓K+. Give Mg2+ (8 mmol IV stat) and shock again. Amiodarone 150-300 mg bolus IV may also be used.
If there is ongoing ventricular tachycardia (VT) in the context of cardiac arrest or recurrent VT episodes, causing haemodynamic compromise, requiring repeated DC cardioversions then give IV amiodarone (300 mg IV bolus, followed by 1.2 g IV over 24 hours via central venous line). Follow Resuscitation Council periarrest arrhythmia guidelines.1
Haemodynamically stable patients
Try vagotonic manoeuvres (e.g. Valsalva/carotid sinus massage).
If diagnosis is clear, introduce appropriate treatment.
If there is doubt regarding diagnosis, give adenosine 6 mg as a fast IV bolus followed by 5 mL saline flush. If there is no response, try 9, 12, and 18 mg in succession with continuous ECG rhythm strip.
Definitive treatment should start as soon as diagnosis is known (see
Treatment options in tachyarrhythmias, p. 721).
First episodes of atrioventricular node re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), or focal atrial tachycardia may need no further treatment. All other diagnoses and Wolff-Parkinson-White syndrome (WPW) should be referred to a cardiologist for further investigation and management.
 Fig. 10.5 Guidelines to the safe management of arrhythmias in the emergency department (adapted from Barts and the London NHS Trust A+E guidelines). CV = cardioversion; UEs = urea and electrolytes. |
Tachyarrhythmias: classification
Fast heart rates can be classified in various ways; however, an anatomical approach should be used, which can then be subdivided mechanistically. This provides a simple foundation for understanding the ECG appearance and the tachycardia mechanism.
Atrial tachyarrhythmias
These are contained completely in the atria (or SAN) and are characterized by:
Atrioventricular tachyarrhythmias
These are dependent on activation between the atrium and ventricle (or AV node). They are characterized by:
junctional tachycardia.
Ventricular tachyarrhythmias
These are contained completely in the ventricle and are characterized by:
Features of a broad complex tachycardia suggesting ventricular origin
independent P waves.
capture and fusion beats
QRS axis <-30 or >+90.
Concordance of QRS complexes in precordial leads (all positive or all negative)
Absence of RS or RS >100 ms in precordial leads
ECG diagnosis of tachyarrhythmias
By following simple rules when interpreting the ECG, any tachycardia can be classified to the categories described earlier; however, the ECG should always be considered in the clinical context. A broad complex tachycardia (BCT) must always be diagnosed as VT in the acute setting, as treating such patients incorrectly may be fatal. View the ECG in both tachycardia and the patients’ usual rhythm to make a diagnosis (e.g. may see features of WPW). For narrow complex tachycardias (NCTs), use carotid sinus massage or adenosine boluses to see the underlying atrial rhythm.
A simple approach follows (Fig. 10.6):
1. Is the tachycardia regular?
Grossly irregular RR intervals regardless of other ECG features indicate AF (or VF; however expect the patient to be unconscious!). A slight irregularity can occur in other tachycardias, particularly at their onset. Alternatively, multiple atrial and/or ventricular ectopic beats or atrial tachycardia with variable AV block can give irregularity.
2. Is the QRS complex broad (>120 ms)?
Yes—ventricular in origin, no—supraventricular.
SVT should only be considered for a BCT when there is strong clinical suspicion (e.g. young patient, no previous cardiac history, normal RV and LV function, no accompanying cardiovascular compromise) and after discussion with senior colleagues. NB: Look at the SR ECG (if available) for pre-existing bundle branch block or pre-excitation (suggesting an accessory pathway).
3. Identify P waves, their morphology and P:R ratio
1:1 P:R, normal P-wave morphology: sinus tachycardia, focal atrial tachycardia originating from close to the SA node (high crista terminalis or right superior pulmonary vein) or, rarely, SNRT.
1:1 P:R, abnormal P-wave morphology: focal atrial tachycardia. AVRT or AVNRT (if slow activation from ventricle to atrium = long RP tachycardia).
P waves not visible: AVRT or AVNRT (with fast activation from ventricle to atrium). Compare QRS morphology in tachycardia with SR, as a slight deflection in the tachycardia QRS complex not seen in SR may represent the P wave,
P:R 2:1,3:1 or greater: focal or macro-re-entrant atrial tachycardia with AV nodal block.
P-wave rate >250/min: this defines atrial flutter (macro-re-entrant atrial tachycardia). Usually there will be 2:1 or 3:1 P:R ratio. In typical atrial flutter, a characteristic saw-tooth baseline is seen in the inferior leads.
4. Response to AV block (adenosine or carotid massage)
If a rapid P-wave rate persists despite induced AV nodal block, then the tachycardia is independent of the AV node, i.e. macro-re-entrant or focal atrial tachycardia and SNRT. If tachycardia is terminated by AV nodal block, it is either AVRT or AVNRT (rarely, junctional tachycardia). Focal atrial tachycardia and SNRT may also be terminated by adenosine, not due to AV nodal block, but because they are adenosine sensitive.
 Fig. 10.6 ECG diagnosis of tachycardia. |
Supraventricular tachycardia (see Fig. 10.7)
This section deals with the diagnosis and pharmacological management of individual SVTs. Their mechanisms and ablation are discussed in detail in Chapter 11.
 Fig. 10.7 Types of supraventricular tachycardia. Reproduced with permission from Ramrakha P, Moore K, and Sam M (2010). Oxford Handbook of Acute Medicine. 3rd ed. Oxford: Oxford University Press. |
Sinus tachycardia
Defined as a sinus rate >100/min, this may be physiological (e.g. exercise or emotion) or pathological. Look for and treat the underlying cause— anaemia, drug related (e.g. caffeine, cocaine, salbutamol, etc.) hyperthyroidism, pain, hypoxia, pyrexia, or hypovolaemia. If no underlying cause is found, consider SNRT or focal atrial tachycardia as alternative diagnoses. These will be paroxysmal in nature, have sudden onset or offset and are usually terminated by IV adenosine. If no underlying cause is found, it may be termed inappropriate sinus tachycardia. β-blockers are useful for symptomatic persistent inappropriate sinus tachycardia, and vital in controlling the sinus rate in hyperthyroidism or heart failure, or post MI.
Sinus nodal re-entrant tachycardia
This is a rare cause of narrow complex tachycardia due to a micro re-entry circuit within the SAN. ECG is identical to sinus tachycardia, making diagnosis difficult. β-blockers or calcium-channel antagonists are the first-line treatment. Modification of the SA node by radiofrequency ablation (RFA) is reserved for drug-refractory cases or those not wishing to take drugs.
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Atrial tachycardia
The term atrial tachycardia describes all regular atrial rhythms with a P rate >100/min, regardless of the mechanism, and this should be prefixed by either focal or macro-re-entrant, unless the mechanism is unknown.
Focal atrial tachycardia
This is due to an automatic focus of atrial cells firing faster than the SA node. The P-wave morphology and axis during tachycardia can be used to predict the location of the source. They are characteristically paroxysmal with short bursts at a rate of 150-250/min, but may be incessant, risking tachycardia-induced cardiomyopathy. They occur in normal hearts but are also associated with many forms of cardiac disease. It may be terminated with IV adenosine.
Treatment is needed only for symptomatic patients or incessant tachycardia. β-blockers and calcium-channel antagonists can be used to slow the atrial rate and the ventricular response by AV nodal blockade. Class 1c (flecainide and propafenone) or class 3 (amiodarone and sotalol) may suppress the tachycardia, but their use is limited by toxicity. RFA is the most effective therapy and is a cure.
Macro-re-entrant atrial tachycardia (atrial flutter)
Atrial flutter (AFL) is an ECG definition of a P-wave rate > 240/min, and an absence of an isoelectric baseline between deflections. It is caused by a re-entry circuit over large areas of the right or left atrium (see 
Atrial arrhythmias: mechanism, p. 564). The circuit is not influenced by adenosine, and the AVN block reveals the underlying rhythm. It is usually (but not always) associated with structural heart disease. AFL exacerbates heart failure symptoms and, if incessant, will worsen LV function.
Atrial arrhythmias: mechanism, p. 564). The circuit is not influenced by adenosine, and the AVN block reveals the underlying rhythm. It is usually (but not always) associated with structural heart disease. AFL exacerbates heart failure symptoms and, if incessant, will worsen LV function.
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