Table of Contents Initial approach Narrow complex tachycardiasSinus tachycardiaAV nodal re-entry tachycardia/’AVNRT’AV re-entry tachycardia/‘AVRT’Ectopic atrial tachycardaAtrial flutterAtrial fibrillationBroad complex tachycardias Ventricular tachycardiaTorsades de pointesSupraventricular tachyarrhythmia with aberrant conductionAtrial fibrillation/flutter with pre-excitationTypes of bradyarrhythmiaSinus bradycardiaSA node dysfunction (‘sick sinus syndrome’)AV node dysfunction (‘heart block’)Management of bradyarrhythmiasDrug doses to memorisePlacement of 3-lead cardiac monitoring and anterior-posterior (AP) defibrillator pads Synchronised DC cardioversionTranscutaneous pacingTest yourself with some questions Reference: UK Resuscitation Council ‘Adult advanced life support’ 2021 Initial approach No pulse – follow cardiac arrest ALS algorithm Life threatening features Shock (SBP <90) Syncope Myocardial ischaemia (chest pain on ECG) Severe heart failure Arrythmia Tachyarrhythmia → synchronised DC cardioversion Bradycardia → atropine ± pacing No life threatening features – see specific sections below All arrhythmias Apply 3-lead cardiac monitoring Identify and treat cause, e.g. electrolyte abnormalities, ACS, hypoxaemia, sepsis, thyroid dysfunction, drug toxicity Review ECG – determine type of arrhythmia Tachycardia (HR > 100 bpm) Narrow complex tachycardia (QRS < 120 ms/3 small squares) Broad complex tachycardia (QRS > 120 ms/3 small squares) Bradycardia (HR < 60 bpm) Tachycardias Unmasking rhythm If the cause of a regular narrow complex tachycardia is unclear, you can unmask the rhythm by transiently increasing AV node block with vagal manoeuvres or adenosine while an recording a 3-lead cardiac tracing. Narrow complex tachycardias Caused by supraventricular tachyarrhythmias. Sinus tachycardia ECG: regular with P waves before each QRS complex; variable rate) Management: treat cause AV nodal re-entry tachycardia/’AVNRT’ Occurs due to an entire re-entry conduction circuit in AV node ECG: regular, often without discernible P waves because they may be buried in the QRS; fast, e.g. 150-200bpm Management: vagal manoeuvres (1st), adenosine (2nd; not in severe asthma – use Ca2+ channel blocker, e.g. verapamil), β-blocker (3rd) AV re-entry tachycardia/‘AVRT’ Occurs due to an accessory conduction pathway allowing conduction re-entry between atrium and ventricle, e.g. in Wolff-Parkinson-White syndrome ECG: regular, often without discernible P waves because they may be buried in the QRS or retrograde; fast, e.g. 150-200bpm NB: this refers to orthodromic AVRT. Antidromic AVRT looks more like VT. Management: vagal manoeuvres (1st), adenosine (2nd; not in severe asthma – use Ca2+ channel blocker, e.g. verapamil), β-blocker (3rd) Ectopic atrial tachycarda Occurs due to abnormal depolarising focus in atrium ECG: regular with abnormal P waves; variable rate; irregular with abnormal p waves with differing morphology if ‘multifocal’ atrial tachycardia Atrial flutter Occurs due to fluttering atria ECG: regular with saw-tooth baseline; usually around 150bpm; irregular if ‘variable block’ Management: rate or rhythm control and treating cause and therapeutic anticoagulation (offer if CHA2DS2-VASc score ≥2 and consider if male with score of 1) Atrial fibrillation Occurs due to fibrillating atria ECG: irregular with no P waves Management: rate or rhythm control and treating cause and therapeutic anticoagulation (offer if CHA2DS2-VASc score ≥2 and consider if male with score of 1) Rate vs. rhythm control Rate control if: patient is >65 years and has IHD/no Sx/is not suitable for cardioversion β-blocker (e.g. bisoprolol) generally first line Rate-limiting Ca2+ channel blocker (e.g. diltiazem) if contraindicated Digoxin if acute heart failure/hypotension/sedentary lifestyle (others negatively inotropic). Amiodarone is also an alternative in acute heart failure/hypotension Rhythm control if the above does not apply Acutely if clear onset <48 hours ago, or after 4 weeks therapeutic anticoagulation and rate control if not Options include electrical cardioversion or pharmacological cardioversion (amiodarone if structural/ischaemic heart disease, or flecainide if not) Broad complex tachycardias Caused by ventricular tachyarrhythmias, or supraventricular tachyarrhythmias with abnormal conduction. Ventricular tachyarrhythmias Ventricular tachycardia Occurs due to an abnormal depolarising focus in ventricles or a re-entry circuit within the ventricles ECG: regular broad complex tachycardia Management: amiodarone if haemodynamically stable; synchronised DC cardioversion if unstable or adverse signs NB: may be due to ACS Torsades de pointes Torsades de pointes is rhythmic polymorphic VT related to ↑QT, due to prolonged ventricular repolarisation ECG: VT with rhythmic varying amplitude Management: magnesium sulphate Broad complex tachycardias of supraventricular origin Supraventricular tachyarrhythmia with aberrant conduction Examples: SVT or AF with L/RBBB ECG: looks like VT but see box for how to distinguish; irregular if due to AF Management: treat as supraventricular if definitely sure. If any doubt, treat as VT if regular or below if irregular. Atrial fibrillation/flutter with pre-excitation Example: in Wolff-Parkinson-White syndrome ECG: irregular broad complex tachycardia and with different size complexes due to different AV conduction pathways) Management: usually managed with synchronised DC cardioversion (don’t use AV nodal blocking medications – they will increase accessory path conduction and may cause VF) Broad complex tachycardias of supraventricular origin Mimic VT The broad complex is caused by a pre-existing condition such as BBB The tachycardia is of supraventricular origin More likely supraventricular if: previous ECG with bundle branch block, delta waves (Wolff-Parkinson-White syndrome), same shape QRS or irregular QRS More likely ventricular if: QRS >160ms, left axis deviation, AV dissociation, capture/fusion beats Bradycardias Types of bradyarrhythmia Sinus bradycardia May be caused by: drugs (e.g. β-blockers, digitalis), neutrally mediated syndromes (e.g. carotid sinus hypersensitivity, vasovagal syncope), hypothermia, hypothyroidism, SA node dysfunction SA node dysfunction (‘sick sinus syndrome’) Occurs when the SA node fails to depolarise. May result in: sinus bradycardia, sinus pauses, or sinoatrial arrest with an ‘escape rhythm’ Escape rhythms may be initiated by the AV node (ECG: ‘ junctional rhythm’ – no p waves but normal QRS at 40-60bpm) or ventricles (ECG: ‘ventricular escape rhythm’ – no p waves and abnormal broad QRS at 20-40bpm) AV node dysfunction (‘heart block’) Occurs when the AV note fails to conduct electric depolarisations between the atria and ventricles. Examples: 2nd degree or complete heart block Learn more about this in the ECG interpretation section Management of bradyarrhythmias Treat cause If life threatening features present → atropine If ongoing haemodynamic compromise or there is risk of asystole → transvenous/permanent pacing is required In the interim: further atropine, transcutaneous pacing, or isoprenaline/adrenaline infusion may be required If no life threatening features and not at risk of asystole → observe and treat cause if possible Drug doses to memorise Adenosine 6mg IV (can be followed by 12mg then 18mg if unsuccessful) flushed quickly wide-bore cannula in the antecubital fossa Amiodarone 300mg IV over 10-60 minutes followed by 900mg over 24 hours through a large vein (900mg should be via central venous line) Atropine 500micrograms IV (repeat every 3-5 minutes to maximum of 3mg if needed; avoid if cardiac transplant, use aminophylline) Magnesium sulphate 2g IV over 10 minutes Placement of 3-lead cardiac monitoring and anterior-posterior (AP) defibrillator pads 3-lead cardiac monitoring (clockwise from right arm: Ride Your Green Bicycle) Red: anterior aspect of right shoulder Yellow: anterior aspect of left shoulder Green: left anterior superior iliac spine Black: not present on defibrillation machine (would go on right anterior superior iliac spine) AP defibrillation pads ‘Right’ pad: place longitudinally on left sternal edge ‘Left’ pad: place longitudinally on left paraspinal muscles (in line with anterior pad) Synchronised DC cardioversion Anaesthetist/sedation-trained doctor should be present to sedate patient Apply 3-lead cardiac monitoring and connect lead to external monitor or defibrillator machine Apply defibrillator pads (AP position if atrial dysrhythmia; in anterolateral position if ventricular) after shaving chest if required Connect pads lead to defibrillator machine Set defibrillator machine monitoring trace to ‘pads’ Set defibrillator to synchronised mode (synchronises shock with R wave to avoid inducing VF) Set energy level (increase as shown if unsuccessful) – energy protocols vary depending on defibrillator and hospital policy AF: 200J → 200J → 200J (biphasic) Broad-complex tachycardia: 150J → 200J → 200J (biphasic) Regular narrow complex tachycardia or atrial flutter: 70J → 100J → 150J (biphasic) Ask anaesthetist to sedate patient and wait until they are happy to proceed Ask for oxygen to be removed and everybody to move away from the patient Press ‘charge’, then move hand away from button Re-check everybody (and oxygen) is away from the patient, announce you are about to shock and, while looking at the patient, hold down the ‘shock’ button until the shock is delivered – it will wait for the R wave Re-assess the rhythm and pulse (even if patient reverts to sinus rhythm, ensure you feel pulse to check it is not PEA) If unsuccessful, repeat at next energy (up to 3 attempts) NB: some defibrilators automatically turn off synchronisation after shock. If successful, reassess patient (ABCDE) and perform another ECG to check rhythm and for any signs of ischaemia If cardioversion fails and the patient is unstable, give amiodarone 300 mg IV over 10-20 min and re-attempt electrical cardioversion Give all patients who are not anticoagulated therapeutic LMWH or heparin infusion, and continue anticoagulation for at least 4 weeks NB: the above is for patients with a pulse. If pulseless, follow cardiac arrest ALS algorithm. Transcutaneous pacing A conscious patient will require some sedation (ask anaesthetist/sedation-trained doctor) Apply the defibrillator machine’s 3-lead cardiac monitoring and defibrillator pads (in standard position) after shaving chest if required Ask sedating doctor to sedate patient and wait until they are happy to proceed Set defibrillator to pacing (NB: synchronous/demand mode means pacing will only occur if no complex is sensed within given time period; asynchronous/fixed rate mode means pacing will occur at programmed rate regardless of complexes – demand mode usually used) Set onscreen pacing rate (default usually 70bpm) and energy (default starting energy usually 30mA) Press button to start pacing Observe the monitor to see if QRS complexes follow every pacing spike. If not, gradually increase the energy until they do – electrical capture (usually occurs at 50-100mA). Next check the patient’s pulse corresponds to the induced QRS complexes – mechanical capture. Now increase the energy by 10mA further. Now seek definitive management NB: you can touch the patient during pacing Test yourself with some questions What are the indications for a permanent pacemaker? Oops! This section is restricted to members. What does the CHA2DS2‑VASc score take into account? Oops! This section is restricted to members. Patients with prolonged QT interval are at risk of Torsade de pointes. What can cause a long QT? Oops! This section is restricted to members.