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Arrhythmias
The document provides an overview of arrhythmias, including their etiology, recognition, and management, focusing on common peri-operative arrhythmias. It discusses various types of arrhythmias such as bradyarrhythmias, tachyarrhythmias, AV blocks, and their treatments, along with associated ECG characteristics. Additionally, the document contains clinical questions and answers related to the diagnosis and treatment of specific arrhythmias.
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Arrhythmias
- 1. ARRHYTHMIAS Dr. Rashad Siddiqi FCPS(Anaesthesiology), FCPS (Cardiothoracic Anaesthesia) Associate Prof of Anaesthesiology CMH Lahore Medical College Consultant Cardiac Anaesthetist Army Cardiac Center Lahore
- 2. Learning Objectives Etiologyand recognition of common peri-operative arrhythmias Review management of cardiac arrhythmias, with a focus on the relevant recent literature
- 3. Implies normal sequenceof conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system. ECG Characteristics: Regular narrow-complex rhythm Rate 60-100 bpm Each QRS complex is proceeded by a P wave P wave is upright in lead II & downgoing in lead aVR Normal Sinus Rhythm
- 4. Mechanisms of Arrhythmia Arrhythmias Altered Automaticity EctopicFoci Reentry / Conduction Block
- 5.
- 6.
- 7. Normal Sinus Bradycardia Occurs in normal children and adults (as low as 30/ min during sleep) May also be seen in the absence of heart disease: At rest, in 25 - 35% of asymptomatic individuals < 25 yrs age In well-conditioned athletes In some elderly patients As a manifestation of a rare familial syndrome (mutation in HCN4, one of a family of pacemaker ion channel genes)
- 8. Hypoxia, Hypothermia,Hypothyroidism Intrinsic disease of the SA node (e.g. sick sinus syndrome) Drugs: Digoxin Beta-blockers Quinidine Adenosine Calcium channel blockers Seizure (post-ictal) Infection like Diphtheria, acute rheumatic fever, viral myocarditis Increased intracranial pressure (cushing’s reflex) Electrolyte imbalance e.g., hyperkalemia Sinus Bradycardia - Causes
- 9. Maintain airway; supplementalO2 (if hypoxic) IV access 12 lead ECG (if available) TreatmentofBradycardia Assess appropriateness for clinical condition HR typically less than 50 bpm Hypotension? Acutely altered mental status? Signs of Shock? Ischemic chest discomfort? Acute Heart failure? Atropine 0.5mg IV; or TransCutaneous Pacing; or Dopamine / Adrenaline infusion Monitor & Observe NO YES
- 10. Bradycardia during Anaesthesia • Drugs - inhalational agents - suxamethonium - induction agents - neostigmine • Airway - hypoventilation - hypoxia • Vagal reflexes • Regional anaesthesia • Surgical factors - IVC compression - pneumoperitoneum • Undetected blood loss • Cardiac Event - tension pneumothorax - haemothorax - tamponade - myocardial depression
- 11.
- 12. 1st Degree AVBlock ECG Characteristics: Prolongation of the PR interval, which is constant All P waves are conducted Usually benign but such patients are at higher risk of developing AF or CCF Treatment not warranted except in rare cases of “Pacemaker Syndrome” The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/ Cheng S, et al. JAMA 2009 Magna. Circ Arrhythm Electrophysiol 2013 Crisel RK, et al Eur Heart J 2011
- 13. 2nd Degree AVBlock Mobitz 1 (Wenckebach) ECG Characteristics: Progressive prolongation of the PR interval until a P wave is not conducted. As the PR interval prolongs, the RR interval actually shortens Usually benign unless associated with underlying pathology, i.e. MI Treatment: remove “reversible” causes No treatment for asymptomatic patients atropine / pacemaker for symptomatic
- 14. ECG Characteristics: ConstantPR interval with intermittent failure to conduct • Rhythm is dangerous as the block is lower in the conduction system • May cause syncope or may deteriorate into complete heart block • Causes: drugs, anterioseptal MI • Treatment: permanent pacemaker Mobitz 2 2nd Degree AV Block
- 15. Mobitz Type Ivs Type II Mobitz type I & II can’t be differentiated in 2:1 blocks every other beat is non-conducted so no opportunity to observe PR prolongation a long rhythm strip or a previous ECG examined PR > 300ms or narrow QRS means block at AV node (type I) response to atropine confirms type I block worsening by carotid sinus massage means type I block
- 16. 3rd Degree (Complete)Block ECG Characteristics: No relationship between P waves and QRS complexes Constant PR intervals and RR intervals Block at AV node: 2/3rd narrow QRS Block at bundle of His: narrow QRS Trifascicular block: wide QRS complex • May be caused by inferior MI and its presence worsens the prognosis • May cause syncopal symptoms, angina, or CHF • Treatment: removing “reversible causes” / permanent pacemaker
- 17.
- 18. Increased/Abnormal Automaticity Sinus tachycardia Junctionaltachycardia Ectopic atrial tachycardia www.uptodate.com
- 19. Ectopic Foci &Beats
- 20. Causes of EctopicFoci & Generation of Arrhythmias Hypoxia: Lung disease Ischemia: CAD, Angina (local hypoxia) Sympathetic Stimulation: Anxiety, Exercise, CHF, hyperthyroidism Bradycardia: “Escape” rhythms… Electrolyte Disturbances: K+, Ca++, Mg++ Drugs: Caffeine, stimulants, antiarrhyhtmic Stretch: CHF, hypertrophy, valve disease
- 21. normal ("sinus") beats sinusnode doesn't fire leading to a period of asystole (sick sinus syndrome) p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria. QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal Atrial Escape Beats
- 22. Causes Mitralvalve prolapse / MS Coronary heart disease exercise testing in IHD patients Toxins or chemicals — Smoking, alcohol, and coffee Miscellaneous - acute and chronic pulmonary disease Atrial Escape Beats
- 23.
- 24. • A single ectopicfocus fires near the AV node, which then conducts normally to the ventricles (usually initiated by a PAC) • The rhythm is always REGULAR • Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter • May be terminated by carotid massage • Treatment: carotid massage, adenosine, Ca++ channel blockers, ablation • Adenosine preferred in hypotension, Rhythm usually begins with PAC Note REGULAR rhythm in the tachycardia Paroxysmal SVT
- 25. Paroxysmal SVT • Treatment – vagal maneuvers – adenosine – if not effective • Ca++ channel blockers, beta blockers, digoxin • cardioversion – Ca++ channel blockers, beta blockers, and primary antiarrhythmic agents should not be serially administered because of potential additive negative hypotensive, bradycardic, and proarrhythmic effects. – Class IIa antiarrhythmic drugs • amiodarone, procainamide, sotalol, felcanide – in LV dysfunction • digoxin, amiodarone, diltiazem
- 26. • “wandering pacemaker” • Multiple ectopicfoci fire in the atria, all of which are conducted normally to the ventricles • The rhythm is always IRREGULAR • P-waves of different morphologies (shapes) ± variable PR interval • HR >100 (in COPD patients >90) Note IRREGULAR rhythm in the tachycardia Multifocal Atrial Tachycardia (McCord et al, Chest 1998)
- 27. Causes Pulmonarydisease (60%) COPD, Ac Resp Failure, Pneumonia, embolism Drugs for Resp Diseases (theophylline, salbutamol) Cardiac disease coronary, valvular, hypertensive and other when associated with heart failure Other conditions: Hypokalemia Hypomagnesemia Chronic renal failure (15%) – cause unclear Sepsis Multifocal Atrial Tachycardia
- 28. Treatment correctionof electrolytes treatment of underlying disease removal of cause disappointing results with anti-arrhythmics Ca++ channel blocker (verapamil) beta blockers Multifocal Atrial Tachycardia
- 29.
- 30. there is nop wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction. QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal Junctional Escape Beats
- 31. Causes hypokalemia digitalis toxicity chronic lung disease acute myocardial infarction Treatment No therapy in asymptomatic discontinue or control exposure to offending agents persistent, limiting symptoms: beta blockers Ca++ channel blockers class IA, IC, or III antiarrhythmic Junctional Escape Beats
- 32. • a "retrograde” p-wavemay sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles QRS is wide and much different looking than the normal beats. This indicates that the beat originated somewhere in the ventricles. • no p wave, indicating that the beat did not originate anywhere in the atria Ventricular Escape Beats
- 33. TREATMENT REQUIRED IN • frequent(> 30% of complexes) or are increasing in frequency • come close to or on top of a preceding T-wave (R on T) • 3 or more PVC's in a row (run of V-tach) • Any PVC in the setting of an acute MI • PVC's come from different foci ("multifocal" or "multiformed”) These may result in ventricular tachycardia or fibrillation. sinus beats Unconverted V-tach to V-fibV-tach “R on T phenomenon” time
- 34.
- 35. The Re-entry Mechanism FastConduction Path Slow Recovery Slow Conduction Path Fast Recovery Electrical Impulse Cardiac Conduction Tissue Repolarizing Tissue (long refractory period) Premature Beat Impulse
- 36. Fast Conduction Path SlowRecovery Slow Conduction Path Fast Recovery Electrical Impulse Cardiac Conduction Tissue Tissues with these type of circuits may exist: • in the SA node, AV node, or any type of heart tissue • in a “macroscopic” structure such as an accessory pathway in WPW The Re-entry Mechanism
- 37. Premature Beat Impulse 1.An arrhythmia is triggered by a premature beat 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conductio n Tissue Repolarizing Tissue (long refractory period) The Re-entry Mechanism
- 38. 3. The waveof excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrograde (backwards) up the fast pathway Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue The Re-entry Mechanism
- 39. 4. On arrivingat the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re- enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit Cardiac Conduction Tissue Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery The Re-entry Mechanism
- 40. AV nodalreentrant tachycardia (AVNRT) Supraventricular tachycardia AV reentrant tachycardia (AVRT) Wolf – Parkinson – White syndrome Atrial flutter Ventricular tachycardia Atrial fibrillation Ventricular fibrillation The Re-entrant Rhythm
- 41. Atrio-Ventricular Nodal Re-entry • supraventriculartachycardia Atrial Re-entry • atrial tachycardia • atrial fibrillation • atrial flutter Atrio-Ventricular Re-entry • Wolf Parkinson White Ventricular Re-entry • ventricular tachycardia • ventricular fibrillation
- 42. Ventricular Re-entry • ventricular tachycardia • ventricularfibrillation Atrio-Ventricular Nodal Re-entry • supraventricular tachycardia Atrial Re-entry • atrial tachycardia • atrial fibrillation • atrial flutter Atrio-Ventricular Re-entry • Wolf Parkinson White • supraventricular tachycardia Re-entry Circuits as Ectopic Foci
- 43. Rate 100-270 Normal QRS Aberrancypossible Acute Rx: • Vagal maneuvers • Adenosine 6-12 mg IV push • Ca++ channel blockers AV Nodal Re-entrant Tachycardia
- 44. Atrial flutter iscaused by a reentrant circuit in the wall of the atrium ECG Characteristics: Typical: “sawtooth” flutter waves at a rate of ~ 300 bpm Flutter waves have constant amplitude, duration, and morphology through the cardiac cycle There is usually either a 2:1 or 4:1 block at the AV node, resulting in ventricular rates of either 150 or 75 bpm www.uptodate.com Atrial Flutter
- 45. Unmasking of flutter waveswith adenosine. Acute Rx: • ventricular rate control can be difficult • AV nodal blockers prevent 1:1 conduction • Ibutilide 1-2mg rapid IV infusion – have paddles ready • Rapid pacing or low voltage DC cardioversion is effective • Anticoagulation as per atrial fibrillation Atrial Flutter
- 46. Atrial fibrillation iscaused by numerous waves of depolarization spreading throughout the atria, leading to an absence of coordinated atrial contraction Classifification • Recurrent: when AF occurs on 2 or more occasions • Paroxysmal: episodes that generally last 7 days or less (most last less than 24 hours) • Persistent: AF that lasts more than 7 days • Permanent: paroxysmal or persistent AF with failure to cardiovert or not attempted www.uptodate.com Atrial Fibrillation
- 48.
- 49. Treatment of AtrialFib Haemodnamically Stable Patient: Rate control therapy: β blockers – esmolol, metoprolol, propranolol Ca++ channel blockers – verapamil, diltiazem Amiodarone Digoxin - for AF with CHF, or LV dysfunction (not to be given in patients with paroxysmal AF) Conversion of rhythm: Class I recommendation: flecainide, propafenone, ibutilide Class II a recommendations: amiodarone Class IIb: administration of quinidine/procainamide. Anticoagulation therapy:
- 50. Treatment of AtrialFib Haemodynamically Unstable Patient: life-threatening - emergency electrical cardioversion (irrespective of the duration of AF) non-life-threatening haemodynamic instability where there is a delay in organising electrical cardioversion, intravenous amiodarone should be used known permanent AF (caused mainly by a poorly controlled ventricular rate) beta-blockers (esmolol, metoprolol, propranolol) calcium channel blockers (verapamil, diltiazem) amiodarone (where beta-blockers or calcium antagonists are contraindicated or ineffective)
- 51. Treatment of AtrialFib Haemodynamically Unstable Patient: Antithrombotic therapy for acute-onset AF emergency intervention should be performed ASAP initiation of anticoagulation should not delay any emergency intervention Heparin: heparin should be started at initial presentation continue heparin until full assessment made and appropriate antithrombotic therapy started
- 52. Treatment of AtrialFib Haemodynamically Unstable Patient: Antithrombotic therapy for acute-onset AF Oral Anticoagulation Needed in acute onset AF is uncertain Not needed in confirmed acute onset AF (<48 hours) if converted to sinus rhythm successfully Needed in confirmed acute onset AF if: stable sinus rhythm not successfully restored high risk of recurrence high risk of stroke
- 53. Treatment • Unstable – DCcardioversion • Stable monomorphic – Adenosine, Amiodarone • Stable polymorphic - treat underlying etiology Rate 100-200 Wide QRS Monomorphic vs Polymorphic Ventricular Tachycardia
- 54. Monomorphic common inprevious Q wave MI not caused by acute ischemia Polymorphic (May have long QT interval) Medication Electrolyte imbalance Congenital predisposition Myocardial ischemia Ventricular Tachycardia
- 55. www.uptodate.com Ventricular fibrillation iscaused by numerous waves of depolarization spreading throughout the ventricles simultaneously, leading to disorganized ventricular contraction and immediate loss of cardiac function. ECG Characteristics: Absent P waves Disorganized electrical activity Deflections continuously change in shape, magnitude and direction Ventricular Fibrillation
- 56.
- 57. Question 1 A 25-year-oldpatient presenting with palpitations is noted to have a wide complex, irregular tachycardia at a rate of 260. The upstroke of the QRS is slurred. The blood pressure is normal, and the patient appears well. Most likely diagnosis is: A. Atrial fibrillation with WPW syndrome B. Unstable Ventricular Tachycardia C. Supraventricular Tachycardia D. Atrial Flutter E. Ventricular Fibrillation Answer “A”
- 58. Question 2 A 50years old gentleman is undergoing emergency exploratory laparatomy under GA. On ECG monitors, you notice wide-complexed ectopic beats occurring 3 to 4 times a minute. His heart rate remains 74 bpm and BP is 130/84mmHg. This arrhythmia is considered benign when the ectopic beats: A. come on top of a preceding T-wave B. occur three or more in a row C. happen in an acute MI setting D. are coming from same focus E. are more than 30% of complexes Answer “D”
- 59. Question 3 A 60-year-oldman with a history of prior anterior myocardial infarction develops a monomorphic wide complex tachycardia after non-cardiac surgery. The differential diagnosis includes: A. Ventricular Fibrillation B. Supraventricular Tachycardia C. Torse De Pointes D. Atrial Fibrillation E. SVT with aberrant conduction Answer “E”
- 60. Question 4 First linedrug for rate control in atrial fibrillation is A. amiodarone B. digoxin C. esmolol D. verapamil E. quinidine Answer “C”
- 61. Question 5 A 60years old patient has arrived in emergency department with 6 days history of atrial fibrillation. This type of AF is classified as: A. Chronic B. Recurrent C. Persistent D. Paroxysmal E. Permanent Answer “D”
- 62.