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Approach to tachyarrhythmia
The document discusses the evaluation and management of tachy-arrhythmias, detailing normal heart rhythm parameters and the causes of arrhythmias, as well as a structured ECG analysis approach. It outlines various types of tachycardia, including sinus tachycardia, supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia, and premature ventricular complexes, along with their management strategies. Key management techniques emphasize patient stability, recognition of adverse features, and appropriate pharmacological and procedural interventions.
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Approach to tachyarrhythmia
- 1. Approach to tachy-arrhythmia DR KTDPRIYADARSHANI REGISTRAR IN EMERGENCY MEDICINE PRIMARY CARE UNIT TEACHING HOSPITAL- PERADENIYA
- 2. What is normalrhythm? HR 60-100 bpm Origin from SA node Propagate through normal conduction pathway With normal velocities
- 3. Causes of arrhythmias Abnormal rhythmicity of pacemaker Shift of the pacemaker from the sinus node to another place in the heart Blocks at different points in the impulse through the heart Abnormal pathways of impulse transmission through the heart Spontaneous generation of spurious impulses in almost any part of the heart
- 4. Lets’ workout.. 7step approach to ECG rhythm analysis 1. Rate 2. Pattern of QRS complexes 3. QRS morphology 4. P waves 5. Relationship between P waves and QRS complexes 6. Onset and termination 7. Response to vagal maneuvers
- 5. Resuscitation A, B-Start Oxygen C- IV access, hemodynamic stability D E If time allows- 12 lead ECG VBG- correct electrolyte imbalance 2 main priorities Is the patient stable? What is nature of the arrhythmia?
- 6. Adverse features ofarrhythmia Shock- SBP < 90mmHg, pallor, sweating, cold extremities, clammy, confusion or impaired level of consciousness Syncope- transient loss of consciousness due to cerebral perfusion Myocardial ischemia- ischemic chest pain, evidence of ischemia on the ECG Heart failure- pulmonary edema and or raised JVP (+/- peripheral edema and liver enlargement)
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- 9. Sinus tachycardia Sinus rhythmwith resting heart rate (HR) > 100 bpm in adults, or above the normal range for age in children Normal heart rates •Newborn: 110 – 150 bpm •2 years: 85 – 125 bpm •4 years: 75 – 115 bpm •6 years+: 60 – 100 bpm
- 10. Management Correct Causes Hypoxia Hypovolemia Fever Thyrotoxicosis Anemia Pain Pharmacological Beta-agonists: adrenaline, isoprenaline, salbutamol, dobutamine Sympathomimetics: amphetamines, cocaine, methylphenidate Antimuscarinics: antihistamines, TCAs, carbamazepine, atropine Others: caffeine, theophylline, marijuana
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- 12. SVT • Regular tachycardia~140-280 bpm • Narrow QRS complexes (< 120ms) • P waves if visible exhibit retrograde conduction with P-wave inversion in leads II, III, aVF.
- 13. Management Unstable patient Unstable + adverse features = synchronized electrical cardio version. Sedate patient 120-150J biphasic Repeat 3 times with stepwise increase in joules
- 14. Stable BP>100mmHg Vagal maneuvers—Valsalva and/or carotid sinus massage. Adenosine = large vein + flush 6 mg as a rapid IV bolus. 12 mg and again and 18 mg if no response. transient sense of impending doom, chest discomfort and shortness of breth Consider verapamil 2.5–5 mg IV over 2 min (if adenosine is contraindicated) or verapamil (continuous slow infusion of 1 mg/min to a maximum of 20 mg or 5 mg IV slowly, which may be repeated). Diltiazem infusion (2 mg/min to a maximum of 50 mg) is an alternativ Flecainide (2 mg/kg over 30–45 minutes) would be considered third-line therapy Catheter ablation may be considered in recurrent episodes not amenable to medical treatment.
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- 16. Atrial flutter • Narrowcomplex tachycardia • Regular atrial activity at ~300 bpm • “Saw-tooth” pattern of inverted flutter waves in leads II, III, aVF • Upright flutter waves in V1 that may resemble P waves • Loss of the isoelectric baseline • Ventricular rate depends on AV conduction ratio
- 17. Handy Tips ForSpotting Flutter • Rapid Recognition Narrow complex tachycardia at 150 bpm (range 130-170)? Yes -> Suspect flutter! • Vagal Manoeuvres +/- Adenosine Atrial flutter will not usually cardiovert with these techniques (unlike AVNRT) • RR intervals In atrial flutter with variable block the R- intervals will be multiples of the P-P interval
- 18. Management administer anantiarrhythmic drug; initiate DC cardioversion low energy 50J; or initiate rapid atrial pacing to terminate the atrial flutter
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- 20. Atrial fibrillation • Irregularlyirregular rhythm • No P waves • Absence of an isoelectric baseline • Variable ventricular rate • QRS complexes usually < 120ms, unless pre- existing bundle branch block, accessory pathway, or rate-related aberrant conduction • Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude > 0.5mm) • Fibrillatory waves may mimic P waves leading to misdiagnosis
- 21. Causes ofAtrial Fibrillation Cardiac causes Non-cardiac causes Common: • Ischaemic heart disease • Rheumatic heart disease • Hypertension • Sick sinus syndrome • Pre-excited syndromes (e.g. WPW) Less common: • Cardiomyopathy • Pericardial disease • Atrial septal defect • Atrial myxoma • Acute infections, especially pneumonia • Electrolyte abnormalities • Lung carcinoma • Other intrathoracic pathology (e.g. pleural effusion) • Pulmonary embolism • Thyrotoxicosis Post-surgery (especially cardiac) • Excessive alcohol or caffeine
- 22. Management Diagnosis ofatrial fibrillation Assessment of duration Assessment for anticoagulation Rate or rhythm control Treatment of underlying / associated diseases
- 24. non-life-threatening hemodynamicinstability, caused by AF, as: Ventricular rate >150 bpm Ongoing chest pain Critical perfusion AF not permanent—electrical cardioversion should be performed. Where there is a delay in organizing electrical cardioversion, intravenous amiodarone should be used. AF permanent—pharmacological rate control strategy should be used. Treatment should be with intravenous β-blockers or rate-limiting calcium antagonists. If these are contraindicated, amiodarone should be used. AF in WPW—flecainide may be used as an alternative for attempting pharmacological cardioversion. AV node-blocking agents (e.g. diltiazem, verapamil, or digoxin) should not be used.
- 25. In stablepatients there are several treatment options: • Rate control by drug therapy (e.g. beta-blocker or rate-limiting calcium antagonist) • Rhythm control by drug therapy (e.g. amiodarone or flecanide) • Rhythm control by electrical cardioversion • Anticoagulation to prevent thromboembolism (should be considered in all patients) NICE recommend that all patients should initially be rate controlled unless: AF is thought to be reversible Presence of heart failure thought to be caused by AF New onset AF Atrial flutter thought to benefit from ablation Rhythm strategy thought to be more suitable based on clinical judgement
- 26. Rate controlis used in those with permanent AF and those with persistent AF, where a rate control treatment strategy has been chosen. Rhythm control may be achieved via electrical or pharmacological cardioversion. It should be considered in patients who remain symptomatic despite rate control, or where a rate control strategy has been unsuccessful. In patients without haemodynamic compromise, this can be performed electively. NICE recommends that a transthoracic echocardiogram is performed prior to elective cardioversion.
- 27. Factors whichmake a patient unsuitable for cardioversion: Contraindication to anticoagulation Structural heart disease that precludes long-term maintenance of sinus rhythm Long duration of AF (>12 months) History of multiple failed attempts/relapses Ongoing reversible cause (e.g. thyrotoxicosis) THROMBOPROPHYLAXIS In AF CHA2DSVASC score 0,1-M, 2-F
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- 29. AV dissociation fusion beats or capture beats wide QRS complexes>140 ms rate>100 bpm: commonly 150–200 bpm rhythm regular constant QRS axis, often with marked left axis deviation or northwest axis deep S wave with r/S ratio<1 in right bundle branch block (RBBB) morphology VT Monomorphic most common associated with MI Polymorphic QRS at 200 beats/min or more which change amplitude and axis so they appear to twist around the baseline
- 30. VT vs SVT Criteria for diagnosis of VT using the 4-step Brugada algorithm:
- 31. Management PULSELESS ACLSprotocol Immediate unsynchronized defibrillation CPR with minimal interruption (30:2, with 2 minute cycles) Intubation O2 IV access Adrenaline 1mg 3min Amiodarone 300mg (following 3rd shock) Exclude reversible causes (4 H’s and T’s)
- 32. CLINICALLY COMPROMISED Haemodynamically unstable, chest pain, ischaemia, heart failure, VR > 150/min -> synchronised shock (x 3) O2 IV access Rapid exclusion of reversible factors (wire, PA catheter in RV, hypoK+ or Mg2+) Synchronised DC Shock (50J Bi, 100 Mono) (150 ->200J-> 360J) Amiodarone 5mg/kg over 20-60 min if patient stable -> infusion Consider: 2nd line drugs procainamide 50mg/min lignocaine 1mg/kg sotalol 1mg/kg Magnesium Inotrope = Dopamine infusion Overdrive pacing
- 33. CLINICALLY STABLE-debate between cardioversion and pharmacological treatment O2 Amiodarone IV amiodarone 150 mg as a slow bolus over 10 minutes. This can be repeated a second time if conversion has not been achieved IV procainamide 100 mg (where available) every 5 minutes to a maximum dose of 10–20 mg/kg body weight IV lignocaine 50–100 mg IV push at a rate not more than 50 mg/min. This can be repeated a second time if conversion is not achieved. Sotolol 1 mg/kg is used as second-line agent. Cardioversion if medical therapy fails (quickly) – will need sedation Consider pacing if cardioversion no effective Evaluation and treatment of cause (usually IHD) If associated with long QT -> consider Mg2+
- 35. Premature ventricular complexes •Broad QRS complex (≥ 120 ms) with abnormal morphology • Premature — i.e. occurs earlier than would be expected for the next sinus impulse • Discordant ST segment and T wave changes. • Usually followed by a full compensatory pause • Retrograde capture of the atria may or may not occur
- 36. Causes Frequentor symptomatic PVCs may be due to: Anxiety Sympathomimetics Beta-agonists Excess caffeine Hypokalaemia Hypomagnesaemia Digoxin toxicity Myocardial ischemia
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- 38. References Diagnosis andmanagement in emergency medicine by Brown and Cardagon 7th edition Text book of Adult emergency medicine 4th edition by peter cameron Life in the fast lane- ECG library
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