Abstract
Arrhythmias are disturbances in normal cardiac electrical activity. They occur in structurally normal hearts, but are sometimes indications of underlying congenital or acquired abnormalities. Arrhythmia can be a mild or transient problem; however, the potential exists for severe life-threatening pathology - even death. It is important that primary care practitioners can recognise various arrhythmias and understand their management. The GP’s role in arrhythmia care ranges from primary diagnosis, through initiation of treatment or monitoring to long-term management of some conditions e.g. atrial fibrillation. Patients require advice about driving or employment, and occasionally the GP may act as a critical link in the ‘chain of survival’ when responding to a cardiac arrest. This article highlights the key findings that can be identified from history and examination, and how these can guide subsequent investigation and diagnosis. The features of common, major arrhythmias and their immediate and subsequent treatment are discussed.
The GP curriculum and arrhythmia
Accurately diagnose symptoms that may potentially be caused by cardiovascular causes Be able to manage cardiovascular conditions, including arrhythmias Appreciate the importance of the social and psychological impact of cardiovascular problems on the patient and their family, friends, dependants and employers Be competent in the management of cardiovascular emergencies in primary care
Pathophysiology
Arrhythmias are categorised based on rate, site of origin, duration, and importantly, whether or not the arrhythmia is immediately life-threatening. Bradyarrhythmias result from reduced automaticity or slowed conduction, commonly due to ischaemia or fibrosis of the conducting system, whereas tachyarrhythmias arise through three mechanisms:
Increased automaticity: Repeated spontaneous depolarisation of a specific myocardial focus Re-entry phenomena: Sustained by a re-entry circuit after starting with a normal or ectopic beat Triggered activity: Often in patients with underlying ischaemic heart disease; it happens when secondary depolarisation occurs in incompletely repolarised cardiac myocytes
History
Given the breadth of possible diagnoses, patients should explain symptoms in their own words, as this provides valuable insight into the underlying cause and enables the impact of their illness on their life to be considered. Symptoms of an arrhythmia are variable, due to the multitude of rhythms, which can present in different ways. Chest pain, palpitations, breathlessness, nausea, dizziness, pre-syncope or syncope are all well-recognised symptoms. Patients can also present with complications of their arrhythmia, e.g. embolic events such as stroke, limb and gut ischaemia.
It is helpful to elicit whether symptoms are paroxysmal or have specific triggers (e.g. exertion). Aggravating and relieving factors are useful to note, and taking a thorough past medical history is important. It is crucial to consider how symptoms can affect the individual’s life, so that appropriate and timely intervention can occur. The implications for a patient’s employment, ability to function as a carer and their mental wellbeing should be considered. Always ask about medications, especially any new prescriptions, as some drugs cause QT interval prolongation, which predisposes to life-threatening arrhythmias.
Check smoking and alcohol history, and ask about recreational drug use. In younger patients it may be helpful to ask sensitively about sudden unexpected or cardiac deaths in relatives: especially younger family members. A ‘systems review’ may identify other systemic features, e.g. weight gain/loss, sweating, diarrhoea or constipation, hunger or anorexia as these may relate to a systemic cause such as hyper- or hypothyroidism.
Examination
Where the patient’s symptoms suggest arrhythmia, physical examination helps to determine:
Is the patient currently experiencing the arrhythmia, and if so, are they compromised by it? Are there additional features that give clues towards the specific arrhythmia?
Adverse clinical features necessitating emergency intervention.
Adapted from Abbas et al. (2006).
A lack of positive findings is reassuring, but dangerous arrhythmias such as ventricular tachycardia (VT) might exhibit no hard clinical signs unless they are ‘caught in the act’. Pulse assessment provides valuable initial information about the possible arrhythmia: is it regular (e.g. supraventricular tachycardia (SVT)), regularly irregular (e.g. second-degree heart block) or irregularly irregular (e.g. atrial fibrillation)? Pulse volume and character help when assessing for haemodynamic compromise.
Focussed cardiovascular examination may identify both the causes and effects of arrhythmias. Elevated jugular venous pressure, fine pulmonary crepitations and peripheral oedema all suggest cardiac failure, which could be the cause or consequence of profound tachyarrhythmia or bradyarrhythmia.
A displaced apex beat suggests cardiomegaly or left ventricular hypertrophy (LVH) – and perhaps underlying cardiomyopathy or ischaemic heart disease, which can predispose to arrhythmias including VT and ventricular fibrillation (VF). LVH also manifests as an easily palpable apex beat.
One rare, but important, physical sign to be alert for in younger patients is the ‘double apical impulse’. It is caused by palpable contraction of both atria and ventricles, and is a feature of established hypertrophic cardiomyopathy, which can predispose to life-threatening arrhythmias (e.g. VF/VT) and sudden cardiac arrest.
Auscultation of the heart sounds may reveal murmurs and altered or added sounds. This can point towards the cause of some arrhythmias (e.g. patients with mitral valve murmurs often have a dilated left atrium, which predisposes to atrial fibrillation (AF)). Checking for signs of anaemia or goitre and other signs of thyroid disease may point towards any underlying systemic problem.
Investigation
Some pathological causes of sinus bradycardia and tachycardia.
Reproduced from Colledge N, Walker B, & Ralston S. Davidson’s Principles & practice of medicine, 21st Edition. Churchill Livingstone, London. Copyright Elsevier (2010).
Other patients are not acutely unwell, but nevertheless suffer significant morbidity or functional impairment due to their symptoms. Others are asymptomatic, despite a sustained arrhythmia. These patients might reasonably be investigated and/or managed in a primary care setting.
Perform blood tests to check for infection/acute inflammatory processes, thyroid disease and electrolyte disturbances (consider calcium and magnesium levels). If possible, obtain a 12-lead electrocardiogram (ECG). A normal ECG provides some reassurance, however, life-threatening arrhythmias cannot be completely excluded by this test (e.g. paroxysmal VT), as a standard ECG is only a brief snapshot of cardiac activity. Some practices perform ECGs in-house and GPs interpret the data. If there is uncertainty regarding findings, routes exist to discuss with secondary care colleagues (‘e-cardiology’ referrals are possible in some localities) or GPs with a special interest.
Ambulatory ECG monitoring can identify the correlation between a patient’s symptoms and their ECG rhythm. It is most effective when the patient is motivated to keep a symptom diary. Ambulatory monitoring can be arranged for various time durations e.g. 24 or 72 hours. When deciding on the timescale, consider that infrequent arrhythmias could be missed if monitoring occurs for a short time, so a false negative result might be obtained.
Some practices own monitoring devices and interpretation software, some own devices but out-source analysis, some have open access to ambulatory services and some require secondary care referral for these investigations.
A newer concept is the ‘implantable loop recorder’. These small devices are about the size of a flash memory stick. They are implanted below the skin in a similar position to a traditional pacemaker. They continuously monitor the heart rate for up to 3 years, recording loops of ECG data. When an episode occurs, the patient or a bystander can hold a small device over the implanted device to trigger a wireless transfer of the data captured from before, during and following the episode. This can be transmitted onwards for analysis or presented on the device. Some devices store and periodically transmit data in case a patient does not note symptoms or cannot correlate symptoms with arrhythmia.
Patients should perform their usual activities (insofar as is safe) when undergoing monitoring. Some patients believe they must limit their activity, so that recordings are not disturbed or prevented. Ironically, such inactivity may prevent the arrhythmia being precipitated – yielding a false negative result. Echocardiography should be considered for the extra information it provides patients in whom structural heart disease is suspected e.g. valve pathology or chamber enlargement.
Psychosocial considerations
The anxiety that some patients experience while a suspected arrhythmia is investigated should not be underestimated. They may fear being alone when acute episode occurs, or fear sudden death (at the initial stages of investigation it might not be clear if this is a significant risk). They may be unable to drive, and this has implications for family life and employment. Issues associated with arrhythmias can therefore pose a significant psycho-social burden for those affected and their families.
Information and support for patients and relatives often helps. GPs can signpost to reliable (printed or online) information and support groups. The Driver and Vehicle Licensing Agency (DVLA) publishes frequently updated guidance regarding whether patients with suspected or proven arrhythmia may drive (DVLA, 2015).
Sinus arrhythmia
Sinus arrhythmia is a common physiological arrhythmia, in which the ECG demonstrates sinus rhythm but the heart rate varies (slowing during expiration, increasing during inspiration). This is more pronounced in fit, healthy individuals and children, whereas it is diminished in those with autonomic neuropathy (which is in itself noteworthy).
Tachycardia
Sinus tachycardia
Sinus tachycardia is a heart rate greater than 100 beats per minute (bpm) that is otherwise normal (Figure 1(a)) (Abbas et al., 2006). It may be a physiological response to anxiety, distress or pain, but other causes are possible. Treatment depends upon the underlying cause (See Table 1).
Rhythm strips identifying: (a) sinus rhythm; (b) supraventricular tachycardia, e.g. atrio-ventricular nodal tachycardia or atrial tachycardia; (c) atrial flutter; (d) atrial fibrillation; (e), ventricular tachycardia; and (f) torsade des pointes.
Atrial ectopic beats
Atrial ectopic beats are common. Some patients are asymptomatic, this being an incidental finding. Other patients experience chest heaviness due to missed beats or awareness of stronger beats. Ectopic P waves have abnormal morphology compared with sinus rhythm. These are obvious in some cases and subtler in others, depending on where in the atria the P wave has arisen.
The ectopic P wave and associated QRS complex (which is unchanged in shape as conduction via the rest of the conducting system is normal) occurs earlier than expected based on the next beat. Reassurance is adequate for most patients, although atrial ectopic beats can herald a future progression into AF. In patients with troublesome symptoms, beta blockers can help. Cardiologists can advise when more invasive treatment, such as catheter ablation of an ‘irritable focus’ is appropriate.
Atrial tachycardia
Atrial tachycardia (AT) is an uncommon tachycardia; usually it is associated with normal heart structure. It often causes symptoms, but is occasionally asymptomatic. It arises from a small focus of atrial tissue that depolarises faster than the sino-atrial node (SAN) – the usual pacemaker - ‘overriding’ the SAN causing rapid atrial depolarisation. This can occur intermittently (paroxysmal AT) or persist for days or months. Several ectopic foci can exist.
Causes include an abnormal congenital focus, valvular disease (causing dilated atria that are more prone to ectopic activity), and damaged or weakened myocardium, e.g. after myocardial infarction (MI). Triggers in susceptible patients include drug or alcohol ingestion and metabolic disturbances, e.g. hyperthyroidism or catecholamine excess. In many patients no precipitant is identified. Capture of the arrhythmia during an episode confirms the diagnosis, but sometimes electrophysiology studies are needed to demonstrate and ‘map out’ the abnormality when it cannot be ‘caught in the act’.
Although distressing and debilitating, AT is not usually dangerous in younger patients with healthy hearts, as rapid heart rates can be tolerated for a significant amount of time. For patients with underlying ischaemic heart disease (which could be undiagnosed) myocardial ischaemia could ensue, manifesting as an acute coronary syndrome.
Individuals who remain tachycardic for prolonged periods (weeks) may develop ‘tachymyopathy’ where myocardial tissue weakens, reducing the heart’s ejection fraction. This can result in heart failure, which is often at least partly reversible if rate/rhythm control is achieved. Treatment for AT is indicated if patients suffer cardiac instability, experience troublesome symptoms due to the rhythm, or develop complications of tachymyopathy.
Urgent treatment should follow Resuscitation Council (UK) (RCUK) tachycardia guidelines (Figure 2). Specialist equipment and medication is required for much of this treatment, so it often requires a hospital setting. Pre-hospital interventions can include giving oxygen, acute coronary syndrome (ACS) treatment (if required), or vagal manoeuvres if ECG monitoring is available. In the longer term, rate-limiting medication is used first line, and catheter ablation considered if the patient accepts the associated risks and is inadequately treated by (or does not wish for) longer-term medication.
Resuscitation Council UK tachycardia guidelines (Abbas et al., 2006). Prior to hospital, initial assessment can be made and vagal manoeuvres could be attempted e.g. in known AVNRT, or rate control in new diagnosis of AF. Emergency and other treatments may require ambulance support and hospital admission.
Atrio-ventricular nodal re-entrant tachycardia
Atrio-ventricular nodal re-entrant tachycardia (AVNRT) is a regular rhythm ranging from 140 to 200 bpm. It is common, affecting women more than men. It frequently occurs in those with normal heart structure (Cadogan, 2015). Some patients experience paroxysms, whereas in others, caffeine, stress or alcohol can be precipitants. Symptoms start suddenly and sometimes hypotension can occur, causing syncope or pre-syncope. As for AT, AVNRT is not directly life-threatening; however, it can precipitate ACS in patients with ischaemic heart disease. In common with other ATs, patients sometimes report polyuria. This results from increased atrial pressures; the atria beat too rapidly to allow proper ejection of blood, which causes atrial natriuretic peptide release, reducing reabsorption of renal filtrate. AVNRT can self-terminate or continue until intervention occurs.
The most-common AVNRT variant is ‘slow-fast’ AVNRT. In this, a ‘slow’ atrio-ventricular (AV) node pathway conducts electrical activity in the normal direction, but then retrograde conduction occurs within the AV node via a ‘fast’ pathway, creating a re-entry circuit with rapid ventricular depolarisation. P waves are usually absent, as atrial activity is obscured by the rapid QRS complexes (Figure 1(b)). Sometimes abnormal P waves, which reflect retrograde conduction within the AV node, are seen towards the end of the QRS complex.
Treatment for acute episodes should again follow the RCUK tachycardia guidelines and the same initial measures are appropriate as for AT. AVNRT may be successfully terminated by vagal manoeuvres or intra-venous (IV) adenosine, both of which slow or block AV nodal conduction. Patients with known AVNRT who suffer an acute episode are often safely discharged from hospital after a few hours of observation. Longer-term treatments for AVNRT include beta blocker or verapamil prophylaxis or definitive intervention with radiofrequency ablation, which is usually highly successful.
Atrial flutter
Atrial flutter is caused by a re-entry circuit within the right atrium around the tricuspid valve (Colledge, Walker, & Ralston, 2010). The atrial rate is usually 300 bpm in adults. It occurs with ‘two-to-one’ or ‘three-to-one’ block, i.e. only every second or third impulse is transmitted down the AV conducting system to generate ventricular depolarisation. The corresponding pulse rate is therefore 150 or 100 bpm. Patients can experience ‘variable block’ alternating between ‘two-to-one’ and ‘three-to-one’ patterns. This results in a variable heart rate making atrial flutter harder to diagnose.
A typical rhythm strip demonstrates ‘saw tooth’ flutter waves (Figure 1(c)). Patients present with similar symptoms as for other tachycardias. RCUK tachycardia guidelines again outline emergency treatment (Abbas et al., 2006). For non-compromised patients, vagal manoeuvres or IV adenosine administration can unmask atrial activity by transiently slowing/blocking AV conduction (therefore slowing or halting QRS complexes), but this does not terminate the arrhythmia.
Beta blockers are used for medical rate control, and catheter ablation therapy offers a 90% chance of definitive cure (Lee, Sanders, & Kallman, 2012). Anticoagulation should be considered on a case-by-case basis, balancing risks against benefits for patients who remain in atrial flutter for greater than 48 hours.
AF
AF is the most-common sustained cardiac arrhythmia, becoming increasingly common with advancing age. It is caused by multiple interacting atrial re-entry circuits. Episodes usually begin with abnormal electrical activity in myocytes surrounding the inlet of the pulmonary veins into the left atrium. It can be sustained by persistent discharges from these diseased areas, or due to re-entry circuits within the atria – more likely in dilated atria. AF can be paroxysmal, persistent (episodes being terminated by medical intervention) or permanent.
AF has three classic ECG features: absent P waves, baseline fibrillation ‘f’ waves, and irregularly irregular QRS complexes. A fourth feature is very subtle variation between the morphologies (particularly height) of the QRS complexes (Figure 1(d)). Treatment is complex, and was recently discussed in detail in an InnovAiT article by McCartney, Lomas, and Cahill (2015).
In summary, rate and rhythm control strategies are possible. Rhythm control is preferable for younger patients, who are more likely to have structurally normal hearts and therefore have a greater chance of maintaining sinus rhythm after cardioversion. Rate control is preferred in patients more likely to revert to AF – older patients with irreversible causes e.g. ischaemic or dilated hearts. It is also preferred for asymptomatic or minimally symptomatic patients. Greater details of each strategy are outlined in the recent InnovAiT article (McCartney et al., 2015).
Warfarin was the mainstay of anticoagulation therapy, aspirin having lost favour following evidence that it produces a bleeding risk without significant protection from cerebro-vascular accidents. Increasingly, however, novel oral anticoagulants (NOACs) are being utilised with their benefit of not requiring regular monitoring. NOACs still confer a bleeding risk, and at the time of writing there is no licensed antagonist. Anticoagulation is again considered on a case-by-case basis, balancing risks and benefits.
Wolff–Parkinson—White syndrome
In Wolff–Parkinson–White syndrome (WPW) patients possess an abnormal band of conducting tissue that forms an electrical connection termed an ‘accessory pathway’. Atria and ventricles are normally insulated from each other with the only conducting pathway being via the AV node. The accessory pathway conducts impulses rapidly, unlike the AV node where there is intrinsic delay (responsible for the PR interval on the ECG). The pathway gives rise to an abnormal resting ECG with a shortened PR interval and slurred QRS upstroke, as some electrical impulses spread through the pathway bypassing the AV node’s intrinsic delay. Rarely, the resting ECG may be normal, the accessory pathway only becoming apparent when arrhythmia occurs.
A re-entry circuit can develop involving the accessory pathway and the AV node, causing tachycardia. It can be hard to distinguish this from AVNRT unless the patient’s history is known. Pre-hospital assessment and treatment should again follow the RCUK tachycardia guidelines (Abbas et al., 2006).
AF can occur in combination with WPW, and this can be dangerous, as each electrical impulse can rapidly pass from the atria to the ventricles through the accessory pathway, avoiding the AV node. This causes rapid ventricular contraction, which is incompatible with adequate filling or emptying. Cardiac output may deteriorate resulting in collapse and unless rapidly treated, possible death.
Prophylactic medication, which prevents episodes of tachycardia in patients with known WPW, includes amiodarone and flecainide. Both prolong the accessory pathway’s refractory period and slow the rate of AV nodal conduction. Digoxin and verapamil should be avoided; they block AV node conduction while reducing the accessory pathway’s refractory period, and therefore, increasing the risk of conduction across it and favouring initiation of a re-entry circuit. Definitive treatment is catheter ablation therapy of the accessory pathway. The success rate approaches 100% when this is performed by experts (Knight, 2013).
VT
VT is a distinctive regular, broad complex tachycardia (Figure 1(e)). SVT with a co-existing bundle branch block appears similar to VT due to the broad QRS. It arises from abnormal automaticity or triggered activity in ventricular myocardial tissue, which is often ischaemic or scarred from previous infarction. VT can occur in otherwise healthy patients (‘normal heart VT’) and is treated with catheter ablation with excellent prognosis.
VT is life-threatening and emergency treatment is required to restore sinus rhythm and prevent further episodes. Unresponsive patients in VT with no pulse are in cardiac arrest and should be treated urgently with cardio-pulmonary resuscitation (CPR) and defibrillation. Early defibrillation maximises survival chances. For every minute defibrillation is delayed, the chance of survival falls by between 10 and 12% (Abbas et al., 2006).
In hospital, aggravating factors such as cardiac ischaemia, electrolyte imbalance or acidosis will be sought and treated. RCUK guidelines advise IV amiodarone, or synchronised electrical cardioversion for patients in VT with a pulse, depending on whether they are ‘stable’ (pharmacological treatment) or ‘unstable’ (electrical cardioversion).
Preventative treatment includes oral beta blockers or amiodarone to suppress myocyte automaticity and to reduce conduction through scar-related re-entry circuits. After electrophysiological mapping, catheter ablation can eliminate re-entry circuits. Patients with significant risk of arrhythmia-related sudden death (those with poor left ventricular function who suffer marked haemodynamic compromise in VT) are offered an implantable cardiac defibrillator to treat future episodes.
Torsade de pointes
Torsade de pointes is a specific VT variant. The QRS morphology alters each beat due to changes in the cardiac axis giving a distinctive appearance (Figure 1(f)) – it literally translates as ‘twisting of the spikes’. This rhythm can arise when the QT interval is prolonged, either due to congenital abnormalities (e.g. channelopathy or long QT syndromes) or acquired issues such as electrolyte disturbance or medications. Acute treatment is again outlined in the RCUK tachycardia guidelines (Abbas et al., 2006). General measures are identical to those for other tachy arrhythmias, however with cardiac monitoring, IV magnesium can be given because it shortens the QT interval and may successfully treat the rhythm. Magnesium can itself cause arrhythmia and muscle weakness including respiratory failure, so it should only be given in a monitored hospital environment.
VF
VF appears as bizarre irregular electrical activity on a rhythm strip (Figure 3(a)). It is a shockable cause of cardiac arrest, and more likely to present pre-hospital than within hospital; hence, the increasing popularity of pre-hospital defibrillators. Prompt CPR and early defibrillation are critical in maximising the chance of survival. Onset often follows acute MI. Once cardiac output is returned, the underlying cause should be sought and treated (e.g. angiography and other investigation).
Rhythm strips identifying: (a) VF; (b) sinus bradycardia; (c) first-degree block; (d) Mobitz type-1 block; (e) Mobitz type-2 block; and (f) third-degree block.
Bradycardia
Sinus bradycardia
Bradycardia is a heart rate under 60 bpm (Figure 3(b)) (Abbas et al., 2006). Sometimes it is a normal variant e.g. in athletic individuals. Some pathological causes are listed in Table 1. Asymptomatic sinus bradycardia often needs no treatment, but anyone who has a ventricular pause of greater than 3 seconds, i.e. greater than 3 seconds between each palpated pulse (likely to be symptomatic) should also be treated, as they are at increased risk of asystolic cardiac arrest.
The initial approach for any bradycardia is outlined in the RCUK bradycardia guidelines shown in Figure 4 (Abbas et al., 2006). Sometimes observation is appropriate, however, adverse features or increased risk of 3asystole should result in IV atropine (500 micrograms) being given. This can be repeated at intervals to a maximum dose of 3 milligrams. Further treatment with pharmacological or electrical pacing may follow while the underlying cause for the bradycardia is identified and treated. Symptomatic or ‘at risk’ patients therefore receive hospital-based treatment. Cardiac pacemaker insertion may be required where no underlying reversible cause can be identified.
Resuscitation Council UK bradycardia guidelines (Abbas et al., 2006). Initial assessment is possible in primary care. If further treatment required, call 999 and send to hospital. Be alert for the ‘risks of asystole’ in otherwise stable patients - intervention is still required.
First-degree heart block
First-degree block describes PR interval prolongation to 0.2 seconds or greater (Figure 3(c)). This represents delayed AV nodal conduction – usually due to fibrosis. It is generally asymptomatic, and therefore needs no treatment. It can be associated with aortic stenosis, and so it may be seen in the context of an ejection systolic murmur.
Second-degree heart block
There are two forms of second-degree heart block, both involving ‘dropped ventricular beats’ – absent QRS complexes on the ECG. Mobitz type-1 block (Wenckebach phenomenon) demonstrates progressive elongation of the PR interval until a QRS/ ventricular beat is missed (Figure 3(d)). It is usually caused by impaired AV nodal conduction, which may be a pathological finding or physiological phenomenon, especially in athletic patients with high resting vagal tone. Treatment is generally not required for healthy asymptomatic individuals (unless they have a ventricular pause greater than 3 seconds). When in doubt, discussion with a cardiologist helps to identify individuals who should have interval monitoring to ensure they do not progress to a Mobitz type-2 block.
A Mobitz type-2 block occurs when the PR interval remains fixed, but some P waves fail to conduct, resulting dropped QRS complexes (Figure 3(e)). This is usually due to ischaemia or fibrosis of the distal conducting system. It is important to recognize, as it is unpredictable and carries a risk of asystole. A ‘Two-to-one block’ occurs if two p waves are present for each QRS complex and a ‘three-to-one’ block is present when three p waves exist for each QRS. The degree of block can vary or increase, giving rise to longer ventricular pauses. Increasing lengths of ventricular pause increases the risk of asystolic cardiac arrest.
Mobitz type-2 block requires emergency treatment with atropine and electrical or pharmacological pacing as per RCUK bradycardia guidelines (Abbas et al., 2006), due to the risk of asystole. Definitive treatment depends on the underlying cause such as ischaemia or medications, which may be adjusted. Patients without a reversible cause may require insertion of a permanent pacemaker.
Third-degree heart block
A third-degree block occurs when AV conduction completely fails. The atria and ventricles continue to beat, but do so independently. This occurs because ventricular myocytes can generate an ‘escape rhythm’ that functions as a back-up pacemaker. The more distal in the His–Purkinje system this occurs, the slower the ventricular rate, and the broader the QRS appears on ECG.
Escape rhythms from high in the His–Purkinje system produce near-normal QRS complexes, and the risk of asystolic arrest is lower. It can be difficult to recognise heart block in this instance, but identifying asynchrony between P and QRS confirms the diagnosis (Figure 3(f)).
There is a significant risk of asystole for patients who have a broad QRS in third-degree block, because this reflects a more distal, slower, less reliable back-up pacemaker. Those patients should therefore have emergency treatment as per RCUK bradycardia guidelines (Abbas et al., 2006). Many patients have third-degree block due to underlying cardiac ischaemia or fibrosis, and definitive treatment is permanent pacemaker insertion.
Asystole
This is the absence of organised electrical activity. However, the baseline still wanders on the rhythm strip. A completely flat line raises the suspicion of monitoring lead disconnection. It is not compatible with cardiac output and urgent CPR is appropriate.
Cardiac arrest
Shockable rhythms, i.e. VF and VT are more common in the pre-hospital environment and rapid defibrillation is crucial. These patients have a better chance of survival than those with asystole and pulseless electrical activity (PEA), any other rhythm discussed without a palpable pulse, which are non-shockable.
In asystole and PEA, good CPR and adrenaline administration sometimes results in return of output or rhythm change to a shockable rhythm. Where a defibrillator and arrest drugs are available, the RCUK guidelines for adult cardiac arrest can help to guide treatment. These are updated periodically and available online via the RCUK website.
Key points
RCUK guidelines assist the assessment and emergency management of patients with tachycardia, bradycardia and cardiac arrest Clinical assessment helps to determine whether emergency treatment, primary-care-led treatment, or shared care with hospital services is appropriate Patients present with varied symptoms; a thorough history and clinical examination with appropriate investigations help to guide further management The psychosocial impact of arrhythmia can be significant, including fitness to drive Many investigations exist to investigate symptoms – picking the most suitable investigations maximises yield and avoids false negatives.
