Cardiac Conduction Disorders PDF

Cardiac Conduction Disorders NICK HURST Conduction system of the heart https://www.s lides hare.net/Firedemon13/cardiac-conduction-system https://s ocratic.org/ questions/5a7be0f411ef6b64d c211c76 SA node and AV node SA node – ‘Natural pacemaker’ ◦ Elec...

Cardiac Conduction Disorders NICK HURST Conduction system of the heart https://www.s lides hare.net/Firedemon13/cardiac-conduction-system https://s ocratic.org/ questions/5a7be0f411ef6b64d c211c76 SA node and AV node SA node – ‘Natural pacemaker’ ◦ Electrical discharge starts ◦ 60-80 beats/min AV node – ‘Gatekeeper’ between the atria and ventricles ◦ Delays depolarization – allows atrium to fully empty ◦ Can generate beat 40/min if SA node fails ◦ But can cause chest pain, SOB, weakness – reduced blood volume to body  Calculate rate The standard paper speed is 25mm/sec: 1 SMALL square (1mm) = 0.04 sec (40ms) 5 SMALL squares (5mm) = 1 LARGE square = 0.2 sec (200ms) 5 LARGE squares = 1 second 300 LARGE squares = 1 minute 1500 SMALL squares = 1 minute Small square method 1500 is divided by the number of SMALL squares between consecutive R waves For example, 10 small squares between R-R interval implies a rate of 150 bpm, 15 implies a rate of 100 bpm, and so forth: Blocks at the Atrioventricular node Atrioventricular block (‘HEART BLOCK’) A block in the conduction pathway between the sinoatrial node and the ventricles Also known as ‘heart block’ 3 levels of severity: ◦ First degree AV block ◦ Second degree AV block ◦ Two subtypes: ◦ Mobitz type I (Wenckebach) ◦ Mobitz type II ◦ Third degree AV block (‘total’ or ‘complete’ heart block) First degree AV block ◦ First degree AV block: Prolonged PR interval (>200msec – 5 small squares) ◦ Delayed conduction through the atria and AV node ◦ Every atrial depolarisation is followed by conduction to the ventricles but with a delay ◦ May progress to higher degrees of heart block ◦ Be careful treating these patient with medications, such as beta blockers ◦ If asymptomatic – no treatment? Causes of First Degree AV Block Increased vagal tone Athletic training Inferior MI Mitral valve surgery Myocarditis (e.g. Lyme disease) Electrolyte disturbances (e.g. Hyperkalaemia) AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone) May be a normal variant Second degree AV block Two types of second degree AV block: ◦ Mobitz type 1 (Wenckebach) ◦ Mobitz type II Second degree AV block – Mobitz type 1 (Wenckebach) Mobitz type I (Wenckebach): ◦ PR interval gets progressively longer until the P wave does not transmit to the ventricles (the QRS is absent) ◦ Appears on the ECG as a ‘skipped beat’ (the Wenckebach phenomenon) ◦ Sometimes occurs during the night in patients with high vagal tone. ◦ If present during the day, may be a sign of degenerative conductive problems ◦ May also be present in children on 24 hour ECG monitoring ◦ Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia) produced by progressive fatigue of the AV nodal cells  The P-P interval remains relatively constant The greatest increase in PR interval duration is typically between the first and second beats of the cycle. The RR interval progressively shortens with each beat of the cycle. Treatment ◦ Symptomatic → may be treated by implantation of a pacemaker ◦ Reversible conditions – rectify/treat ◦ Electrolyte abnormalities ◦ Lyme disease ◦ Enhanced vagal tone ◦ Medications ◦ Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk of progression to third degree heart block. Second degree AV Block - Mobitz type II Mobitz type II: ◦ PR interval is normal - does not have progressive prolongation ◦ Some P waves do not result in a QRS complex. ◦ Can be expressed as a ratio of number of P waves to the number of resulting QRS complexes (e.g. 2:1, 3:1) ◦ Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis). ◦ Mobitz II is an “all or nothing” phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse. ◦ May lead to complete heart block ◦ More likely that Mobitz type 1 to cause Haemodynamic instability ◦ 35% chance of asystole – immediate cardiac monitoring and admission Causes Anterior MI (due to septal infarction with necrosis of the bundle branches). Idiopathic fibrosis of the conducting system (Lenegre’s-Lev’s disease). Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair) Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease). Autoimmune (SLE, systemic sclerosis). Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis). Hyperkalaemia. Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone. Treatment ◦ Symptomatic → may be treated by implantation of a pacemaker ◦ Reversible conditions – rectify/treat ◦ Electrolyte abnormalities ◦ Lyme disease ◦ Enhanced vagal tone ◦ Medications Third degree AV block (‘total’ or ‘complete’ heart block) Third degree AV block (‘total heart block’): ◦ No P waves are conducted from the atria to the ventricles ◦ Ventricles depolarise as the result of lower pacemaker activity in the heart (at about 40bpm) ◦ Broad QRS complexes and bradycardia ◦ No consistent relationship between the P waves and the QRS complexes on the ECG ◦ Always more P waves than QRS complexes  The atrial rate is approximately 100 bpm. The ventricular rate is approximately 40 bpm. The two rates are independent; there is no evidence that any of the atrial impulses are conducted to the ventricles.  Higher risk of ventricular standstill and sudden cardiac death Urgent admission for cardiac monitoring, backup temporary pacing and usually insertion of a permanent pacemaker. Causes of complete heart block: Same as for 2nd degree type 1 and 2 Important causes: Inferior myocardial infarction AV-nodal blocking drugs (e.g. calcium channel blockers, beta-blockers, digoxin) Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease) Likely to respond to atropine Blocks to the Bundle Branches Bundle Branch Block ❑The right and left bundle branches come off the bundle of His ❑The left bundle branch subdivides into the anterior and posterior divisions ❑Complete block of a bundle branch is associated with a widened QRS complex ❑The shape of the QRS complex depends on whether the right or left bundle is blocked Right Bundle Branch Block (RBBB) The right ventricle is activated later than normal (as the bundle branch that would activate the right ventricle quickly is blocked) QRS is greater than 120msec (3 small squares) Deep S wave in leads I and V6 Tall late R wave or second R wave (R’) in the QRS of lead V1 (‘rabbit ear’ pattern) Causes of RBBB May include: ◦ Congenital heart disease (ASD, VSD, tetralogy of Fallot) ◦ Pulmonary disease (pulmonary hypertension, pulmonary embolism) ◦ Myocardial disease (MI, cardiomyopathy) New RBBB with chest pain: May indicate occlusion of left anterior ascending artery New RBBB with dyspnoea: May indicate pulmonary embolism Presentation and assessment May be incidental finding Asymptomatic individuals – no correlation with adverse outcomes and usually benign Patients may present with episodes of syncope ECG Echocardiogram Treatment Asymptomatic – none required Symptomatic ◦ Pacemaker ◦ Cardiac resynchronization therapy – biventricular pacing  Left Bundle Branch Block (LBBB) The left ventricle is activated later than normal (as the bundle branch that would activate the left ventricle quickly is blocked) QRS is wider than 120msec (3 small squares) Deep S wave in lead V1 Tall late R wave in leads 1 and V6 Abnormal Q waves (as left bundle branch usually initiates ventricular contraction)  LBBB always affects cardiovascular system and increases mortality More common in people with structural and ischaemic heart disease Causes may include: ◦ Left ventricular outflow obstruction (e.g. hypertension, aortic stenosis) ◦ Coronary artery disease (MI, severe coronary artery disease) Danger – LBBB patients with chest pain – high probability of acute coronary occlusion Assessment of LBBB Assessment of ischaemia on an ECG is difficult: Results in ST changes – may mimic or mask ischemia Increased referral for STEMI with patients with new onset of LBBB Bifascicular Block Bifascicular block: ◦ Combination of a right bundle branch block with either a left anterior fascicular *Fascicular fibres of the heart block or a left posterior fascicular block – specialised muscle fibres that conduct electrical ◦ Indicates widespread damage to the impulse through the heart. Ie bundle of HIS* conductive system ◦ ECG shows RBBB + left or right axis deviation  Lead 1 positive Rabbit ears Lead aVF negative Cardiac axis – average direction of Deep S wave depolarisation of the ventricles. Left ventricle larger muscle mass has greater effect of the axis. Right bundle branch block and left axis deviation Axis deviation https://elentra.healths ci.queensu.ca/assets/mo dules/ECG/s tep_3c_calculate_the_electrical_axis.html Causes Ischaemic heart disease (40-60% cases) Hypertension (20-25%) Aortic stenosis Anterior MI (occurs in 5-7% of acute AMI) Primary degenerative disease of the conducting system (Lenegre’s / Lev’s disease) Congenital heart disease Hyperkalaemia (resolves with treatment) Treatment of Bifascicular Block Asymptomatic - no treatment required Symptomatic (ie syncope) – pacemaker recommended Trifascicular Block Trifascicular block: ◦ May be ‘incomplete’ or ‘complete’ ◦ Incomplete: ◦ Combination of either: ◦ Bifascicular block and 1st degree AV block ◦ Bifascicular block and 2nd degree AV block ◦ RBBB with alternating LAFB/LPFB ◦ Complete: ◦ Bifascicular block and a 3rd degree (Complete) AV block  RBBB, Left axis deviation, 1st degree AV block Positive deflection lead 1 Rabbit ears 1st degree block Negative deflection Deep S wave lead aVF https://litfl.com/trifascicular-block-ecg-library/ Clinical implications Incomplete may progress to complete heart block (low risk though) Symptomatic with syncope – refer for cardiology monitoring May be having episodes of complete heart block Asymptomatic bifascicular block with 1st degree AV block Not an indication for pacing Causes Ischaemic heart disease Hypertension Aortic stenosis Anterior MI Primary degenerative disease of the conducting system (Lenègre-Lev disease) Congenital heart disease Hyperkalaemia (resolves with treatment) Digoxin toxicity Treatment Class I – Pacemaker recommended ◦ Bifascicular block + complete heart block, even in the absence of symptoms (1b) ◦ Bifascicular block + 2nd degree AV Block Type 2, even in the absence of symptoms (1b) ◦ Alternating bundle branch blocks, even in the absence of symptoms (1c) Class II – Pacemaker possible ◦ Bifascicular block + syncope + alternative causes ruled out (e.g. orthostasis, arrhythmia) (2a) Class III - pacemaker not recommended ◦ Bifascicular block without symptoms ◦ Bifascicular block + 1st degree AV Block, without symptoms Premature Beats Premature atrial contractions Premature heartbeats originating in the atria Often occur in healthy people Cardiomyocytes in the atria depolarise before the sinoatrial node, triggering a premature beat Patients are likely to be asymptomatic but may perceive a ‘skipped’ heartbeat Unlikely to be picked up on a 12 lead ECG unless they are occurring regularly ◦ May be evident on a cardiac monitor or on 24hr ECG monitoring Rhythm will appear irregular P waves of ectopic beats may look different (as originating elsewhere in the atrium) QRS will appear normal as the premature contraction is transmitted through the AV node  In most patients, there is no risk associated with premature atrial contractions Younger patients may ‘grow out of it’ In patients with underlying heart conditions, PACs may trigger atrial flutter or atrial fibrillation Management: Reassurance of the patient In patients with recurring or symptomatic PACs, beta blocker therapy to reduce the frequency of the PACs may be indicated Premature Ventricular Contractions (PVC’s) Premature heartbeats initiated by the purkinje fibres in the ventricles Often occur in healthy people May also be caused by: Drugs (e.g. digoxin, cocaine, caffeine) Ischaemia Structural defects Electrolyte disturbances (hypokalaemia, hypercalcaemia) Smoking Stress Thyroid disease Patients may be symptomatic. Where symptoms occur, they may include: ◦ Palpitations ◦ ‘Skipped’ heartbeats or ‘forceful’ heartbeats ◦ Chest pain, fatigue, pre-syncope and hyperventilation after exercise PVC’s Normal sinus rhythm originates in the SA node In PVC, an ectopic heartbeat is generated by cells within the ventricles Usually a one of event, but can occur regularly If they occur regularly, they can be defined by the frequency of their occurrence: ◦ Bigeminy: one sinus beat between each PVC ◦ Trigeminy: two sinus beats between each PVC ◦ Quadrigeminy: three sinus beats between each PVC  Bigeminy: Trigeminy: Quadrigeminy https://www.practicalclinicalskills.com/ ekg-reference-type/30/Premature-Ventricular-Complex-Bigeminy https://www.practicalclinicalskills.com/ ekg-reference-type/31/Premature-Ventricular-Complex-Trigeminy https://ekg.academy/learn-ekg?courseid=315&s eq=4 Premature ventricular contractions Unifocal PVC Multifocal PVCs can occur in which multiple sites in the ventricles trigger depolarisation. If PVCs start to occur in a row, ventricular tachycardia (VT) occurs Multifocal PVC  Unlikely to be picked up on a 12 lead ECG unless they are occurring regularly May be evident on a cardiac monitor or on 24hr ECG monitoring ECG findings: Premature beats will lack a preceding P wave QRS and T wave will look clearly abnormal QRS shape will depend upon the origin site in the ventricle The ectopic beat occurs before the normal sinus beat is expected The sinus beat following the ectopic beat will be delayed through a compensatory pause Significance of the PVCs is not fully understood ◦ In the absence of structural heart disease, occasional PVCs are believed to be benign ◦ PVCs may be associated with underlying heart pathology leading to increased mortality risk Management will depend upon the underlying pathology. May include: ◦ Lifestyle advice (e.g. stress management) ◦ Beta blockers or calcium channel blockers to reduce the frequency of the PVCs ◦ Electrolyte replacement (e.g. magnesium or potassium) ◦ Radiofrequency catheter ablation to destroy abnormal conduction pathways that may be leading to regular PVCs Tachycardia Fast heart rate (>100 bpm) Sympathetic cardiac nerves increase the spontaneous depolarisation of the nodes May be a physiological (sinus tachycardia) or pathological (a tachyarrhythmia)  Narrow or broad complex tachycardia? Narrow complex tachycardia has QRS complexes of less than 120msec (3 small squares) Almost always originate above the ventricles (AKA supraventricular tachycardia) Broad complex tachycardia has QRS complexes of greater than 120msec (3 small squares)  Types of tachycardia Narrow complex tachycardia Broad complex tachycardia Sinus tachycardia ◦ Ventricular tachycardia Atrial flutter ◦ SVT (e.g. AT, AVRT, AVNRT) with abberant conduction (e.g. bundle branch block) Atrial tachycardia ◦ SVT conducted through an accessory pathway Atrial fibrillation with fast ventricular rate ◦ Polymorphic VT (torsades de pointes) ◦ Paced rhythms Atrioventricular nodal re-entrant tachycardia (AVNRT) ◦ Hyperkalaemia Atrioventricular re-entrant tachycardia (AVRT) Narrow complex tachycardias Narrow complex tachycardias The key features of sinus Causes of sinus tachycardia tachycardia are: Exercise ◦ The heart rate is more than 100 Emotion/stress/pain beats per minute Pyrexia ◦ Each P wave is followed by a QRS complex Hypotension and Hypovolaemia ◦ The P wave is positive (upright) Anaemia in lead II and negative (inverted) Drugs in lead aVR Heart failure Hyperthyroidism Sinus tachycardia rarely exceeds 200 beats per minute ❑ Sinus tachycardia at rest is not normal ❑ The cause should be identified and treated Narrow complex tachycardias Supraventricular Tachycardia (SVT) Abnormally fast heart rate originating from the atria's 4 main types: Atrial fibrillation Paroxsymal supraventricular tachycardia (PSVT) Atrial flutter Wolff-Parkinson-White syndrome Presentation: ◦ May go unnoticed in some patients ◦ May be perceived as discomfort/palpitations ◦ If persistent, patient may present in heart failure ◦ May cause angina attacks in patients with underlying coronary perfusion problems ◦ May present as faint/loss of consciousness Atrial fibrillation Common (affects 1-2% of the population) Continuous rapid activation of the atria (300-600/min) driven by depolarising cells predominantly located in the region of the pulmonary veins Fibres contract independently – ‘Fibrillating’ Not all are transmitted to the ventricles  AF Cardiac causes Non-cardiac causes ❑Hypertension ❑Thyrotoxicosis ❑Heart failure ❑Phaeochromocytoma ❑Coronary artery disease ❑Pulmonary disease ❑Valvular heart disease ❑Electrolyte abnormality ❑Cardiomyopathy ❑Alcohol misuse ❑Cardiac surgery ❑Caffeine ❑Smoking ❑Recreational drugs AF Symptoms ◦ May be asymptomatic ◦ May present with chest pain, palpitations and shortness of breath Signs ◦ Very irregular pulse ECG ◦ No visible P waves ◦ Rapid and irregular QRS complexes ◦ Ventricular rate ~120-180/min Fine AF – difficulty detecting P-waves Irregularly irregular pattern  Complications: Increased mortality (sudden death, heart failure or stroke) Strokes (20-30% of all strokes are due to AF) Hospitalisations (10-40% of AF patients hospitalised each year) Left ventricular dysfunction (found in 20-30% of AF patients) Vascular dementia Diagnosis If paroxysmal, 24 hour ECG monitoring or an event recorder may be needed Consider an Echo to examine underlying heart structure and function  Management of chronic AF: Medications to control heart rate and rhythm (beta-blocker or calcium-channel blocker) Assess the patient’s risk of having a stroke. Offer anticoagulation therapy to reduce the risk of strokes if indicated (Warfarin or Novel Oral AntiCoagulant). CHA2DS2-VASc If paroxysmal, consider a ‘pill in the pocket’ approach If AF is persisting, consider electrical cardioversion If drug treatment unsuccessful – consider catheter ablation of the left atrium Anticoagulant therapy? Offer anticoagulation with an overall score ≥2 Consider offering anticoagulation to men with a score ≥1 Management of acute AF: ◦ Synchronised DC cardioversion if the patient is haemodynamically unstable ◦ If stable: ◦ Start rate control medication (Beta-blocker 1st line medication) ◦ Anticoagulate with DOAC or Warfarin (Check HAS-BLED score) ◦ Consider pharmacological cardioversion or synchronised DC cardioversion once anticoagulation established NICE guidance - READ https://cks.nice.org.uk/atrial-fibrillation#!scenario Atrial flutter Organised atrial rhythm with atrial rate between 250-300 Depolarisation oscillates around the atria ECG shows regular saw-toothed atrial flutter waves (F waves) between the QRS complexes Not all atrial depolarisation is transmitted through the AV node (degree of AV block) HR at 150/min Recurrent atrial flutter may be treated with radiofrequency ablation of the pathways responsible for the oscillating depolarisation Atrial Flutter Atrial tachycardia Abnormal, rare, narrow complex tachycardia (usually 100-250 bpm) May be paroxysmal or sustained Heart rate will be regular Arises from an ectopic source in the atrial myocardium rather than the SA node Usually slower than atrial flutter May be associated with AV block if the rate is >200bpm P wave often abnormally shaped (as depolarisations are not coming from the SA node) Atrial tachycardia May be difficult to distinguish from atrial flutter. In atrial flutter, depolarisations will occur at ~300bpm with a 2:1 or 3:1 block reducing the heart rate to 100-150bpm If P wave is positive in V1 and negative in aVL or 1, it is likely to be originating from the left atrium Patient may present with palpitations. In the long term, a tachycardia induced cardiac failure may develop. If no haemodynamic compromise, may be treated with a beta blocker, calcium channel blocker or antiarrhythmic medication If haemodynamically compromised, cardioversion may be indicated Atrial Tachycardia Re-entrant tachycardias: AVRT and AVNRT Re-entry allows a wave of depolarisation to cycle around the heart tissue, causing tachycardia AVRT ◦ Part of the re-entry circuit lies outside of the AV node. This can lead to a narrow or broad complex tachycardia depending on whether the cycle is clockwise or anticlockwise AVNRT ◦ The re-entry circuit is within the AV node, leading to a narrow complex tachycardia AVRT and AVNRT Usually paroxysmal tachycardias (they start and stop suddenly) Usually regular with heart rate >150bpm Wolff-Parkinson White syndrome is an example of an AVRT with an accessory called the bundle of Kent Do not occur commonly as cells are often in refractory stage when they receive the following depolarisation so are unable to ‘pass the message on’ When arrhythmia occurs, often triggered by an ectopic beat that propagates through the system. May be associated with thyrotoxicosis as this increases the likelihood of ectopic beats AVRT: atrioventricular re-entrant tachycardia Re-entrant circuit due to the presence of an accessory pathway between the atria and ventricles 2 types: orthodromic and antidromic: Orthodromic is anterograde down the AV node pathway and retrograde up the accessory pathway, leading to a narrow complex tachycardia. P wave is often present after the QRS complex. Usually generated by a premature atrial complex Antidromic is anterograde down the accessory pathway and retrograde up through the AV node, leading to a broad QRS complex tachycardia. Usually generated by a premature ventricular complex AVRT: atrioventricular re-entrant tachycardia ECG may show ‘delta wave’: a slurred upstroke on the QRS complex associated with a shortened PR interval AVRT: atrioventricular re-entrant tachycardia Patient may present with palpitations, pounding in the neck, dizziness and chest discomfort Tachycardia is usually between 110 and 250 beats per minute AVRT: atrioventricular re-entrant tachycardia Wolff-Parkinson White syndrome: Congenital malformation leads to incomplete separation of atria and ventricles in utero Patients may present with paroxysmal SVT Resting ECG may show a shortened PR interval, a delta wave and a prolonged QRS complex If patient’s blood pressure is normal, can be managed with vagal manoeuvres, adenosine, calcium-channel blockers or beta blockers (in the presence of resuscitation equipment as fast AF can result) Patients who are haemodynamically unstable may require DC cardioversion or drugs such as flecainide, procainamide or amiodarone which slow/block the accessory pathway  WPW syndrome https://elentra.healths ci.queensu.ca/assets/modules/ts-ecg/wolffparkinsonwhite_s yndrome.html https://www.cardiocases.com/en/ecg/traces /rhythm-disorders-junctional-tachycardias/acces sory-pathway-bundle-kent-and-wolff AVNRT: Atrioventricular Nodal Re-entrant Tachycardia Regular, paroxysmal narrow complex tachycardia Short circuit occurs within the AV node One P wave per QRS but usually not visible due to simultaneous contraction or atria and ventricles (if visible, usually just after the QRS complex) Most common cause of palpitations in pts with NO structural heart disease women > men May present with palpitation, chest discomfort, dizziness and rapid pounding in the neck Heart rate is usually between 110-250bpm AVNRT No P wave visible Acute management of narrow complex tachycardia Assess if the patient is haemodynamically stable ◦ Signs of haemodynamic instability would include low BP and tachycardia. The patient may complain of breathlessness, chest pain, light-headedness or fainting If the patient is haemodynamically unstable, synchronised DC cardioversion should be considered If the patient is haemodynamically stable, you can try momentarily blocking the AV node with the valsalva manoeuvre, carotid sinus massage or with certain medications (this stops re-entrant tachycardias which occur when the electrical stimulation cycles around the heart, rather than going from one end of the heart to the other) Acute management of narrow complex tachycardia ◦ The valsalva manoeuvre describes forced expiration over a closed glottis. Patients can be asked to blow through the hole in the end of a syringe ◦ Carotid sinus massage (NB: do not do!): Massage the carotid artery medial to the sternocleidomastoid for five seconds (not in the elderly, patients with carotid artery bruits or other carotid disease) ◦ IV adenosine or IV verapamil (‘chemical cardioversion’) if there are no contraindications (asthma, COPD, sick sinus syndrome, long QT syndrome, severe hypotension or decompensated cardiac failure) Broad Complex Tachycardia  Ventricular tachycardia Usually seen in patients with underlying Can cause hypotension and collapse heart muscle disease, especially previous MI Without prompt cardioversion may lead to ventricular fibrillation, cardiac arrest Scar tissue forms an arrhythmogenic and death substrate leading to a short circuit in the ventricle Associated with a high mortality rate out of hospital Ectopic beats (especially if multifocal) can trigger a tachycardia circuit Sympathetic stimulation during exercise or anxiety is more likely to trigger this  Ventricular tachycardia Signs of VT on an ECG ◦ AV dissociation: P wave activity independent of ◦ Precordial concordance: all the chest lead QRS and a ventricular rate higher than the atrial complexes are in the same direction (either rate positive or negative) ◦ Capture beats: normal narrow complex beats ◦ VT often produces left axis deviation within the broad complex ventricular ◦ Almost always associated with a history of tachycardia heart disease, especially ischaemia ◦ Fusion beats: QRS complexes with features of normal and broad complex QRS VT Rapid ventricular rhythm with broad, abnormal QRS complexes VT May present with pre-syncope, syncope, hypotension and cardiac arrest Pulse rate will be between 120-220 bpm Immediate action needed: ◦ If haemodynamically stable: chemical cardioversion with IV amiodarone ◦ If haemodynamically unstable: synchronised DC cardioversion If no pulse: ◦ CPR and defibrillation Ventricular flutter A form of VT with a loss of organised electrical activity Leads to haemodynamic compromise Rapidly deteriorates to VF (ventricular fibrillation) Advanced Life Support required Ventricular Flutter Ventricular fibrillation (VF) Rapid and irregular ventricular activation with no mechanical effect (i.e. no cardiac output) Often provoked by a ventricular ectopic beat Patient has no pulse, will become rapidly unconscious and stop breathing Requires immediate action: ◦ BLS/ALS/defibrillation ◦ Treatment of the underlying cause VF Shapeless rapid oscillations with no sign of any organised complexes Further resources Life in the fast lane https://lifeinthefastlane.com/ NICE AF guidelines https://www.nice.org.uk/guidance/cg180/ https://mollyfletcher.com/ top-4-reasons-to-ask-ques tions-stay-curious/