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CARDIAC ARRYTHMIA AND ITS MANAGEMENT.pptx

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CARDIAC ARRYTHMIA AND ITS MANAGEMENT.pptx

  1. 1. CARDIAC ARRYTHMIAAND ITS MANAGEMENT Dr. Sandeep Singh Jadon MBBS MD Anaesthesiology Gajraraja Medical College Gwalior madhyapradesh
  2. 2. DEFINITION Arrythmia also known as dysrythmia, refers to any disturbance in the rate, regularity, site of origin, or conduction of the cardiac electrical impulse.  Arrhythmias may cause sudden death, syncope, heart failure, dizziness, palpitations or no symptoms at all.
  3. 3. Arrhythmia pathogenesis  Disorder of impulse formation:  Automaticity.  Triggered activity • Early after depolarization. • Delayed after depolarization.  Disorder of impulse conduction:  Impulse Block  Re - entry phenomena
  4. 4. Abnormal automaticity • The SA node is the heart’s natural pacemaker. • Any impulses fired from elsewhere in the heart before or concurrently with SA node firing can lead to premature heartbeats or sustained abnormal heartbeats. • Problems associated are: 1. Sinus tachyarrhythmia 2. Sinus bradyarrhythmia 3. Abnormality in site of impulse generation (ectopic loci) 4. Escape rhythms
  5. 5. Triggered automaticity • This is an abnormal secondary upstroke which occur only after a normal initial or “triggering “ upstroke or action potential. • These secondary upstrokes are called after depolarization.This may be of two types: 1. Early after depolarization 2. Delayed after depolarization
  6. 6. Abnormal impulse conduction Conduction block may occur due to depression of impulse conduction at AV node & bundle of His, due to vagal influence or ischaemia . Types : • 1st degree heart block – slowed conduction • 2nd degree block – some supraventricular complex not conducted • 3rd degree block – no supraventricular complex are conducted
  7. 7. Re-entry phenomena It can be of two types: I. Anatomically defined re-entry - Wolf Parkinson White syndrome(WPW). II. Functionally defined re-entry -Mostly seen in patients with ischemic heart disease.
  8. 8. Two features of arrhythmias • Site of origin 1. Atria 2. Atrioventricular node (AV node) 3. Ventricles • Affect on heart rate 1. Too slow heart rate (bradycardia) 2. Too fast heart rate(tachycardia)
  9. 9. Contributing factors and causes 1. Patient related factors- • preexisting cardiac disease • central nervous system disease • Old age 2.Anaesthesia related factors • Tracheal intubation • General anaesthesia • Regional anaesthesia • Electrolyte imbalance and abnormal arterial blood gases • Central venous cannulation 3.Surgery related factors-cardiac and non cardiac surgery
  10. 10. Reversible cause of arrhythmia • Hypovolemia • Hypoxia • Hypo/Hyperkalemia • Hypomagnesaemia /Hypocalcaemia • Hypoglycemia • Hypothermia • Acidosis • Mechanical Irritation (e.g. central venous lines, pulmonary artery catheter,chest tube) • Cardiac ischaemia • Light plane of anaesthesia/pain • Toxins/ Drugs • Cardiac Tamponade • Tension pneumothorax • Thrombosis (Coronary or pulmonary) • Trauma
  11. 11. Anaesthetic considerations • All patients undergoing anaesthesia and surgery should have ECG monitoring. • Lead II and V 5 are superior for arrhythmia detection and diagnosis before the appearance of physical signs.
  12. 12. Routine measure for all intraoperative arrythmias • Assure adequate oxygenation and ventilation • Assure adequate depth of anaesthesia • Assure optimum Po2,pco2, acid base, electrolyte and temperature • Re-evaluate cardiac history/pathology Get ready for • Anti-Arrythmic drug • Anti-Ischemic drug • Pacing and DC shock
  13. 13. Normal Sinus Rhythm • SA Node is the primary pacemaker • One upright uniform p-wave for every QRS • Rhythm is regular • Rate is between 60-100 beats per minute • PR interval = 0.12 – 0.20 sec • QRS interval <0.12 sec
  14. 14. ARRYTHMIA CLASSIFICATION 1. Bradyarrhythmia 2. Ectopics/ Premature systoles 3. Tachyarrhythmias
  15. 15. Bradyarrhythmias A. SA node Dysfunction 1) Sinus bradycardia 2) Sinus Arrhythmias 3) Sinoatrial block 4) Sick Sinus Syndrome B. Atrioventricular (AV) node and bundle of His Atrioventricular block 1) First degree AV block 2) Second degree block a. Mobitz I b. Mobitz II 3) Third degree heart block
  16. 16. Mechanism of Bradyarrhythmias A. Slowed SA node pacemaker activity  Sinus bradycardia, in excessive parasympathetic (vagal) tone.  Hypothyroidism  Drugs like β-adrenergic blockers and some L-type calcium channel blockers. B. Impaired impulse conduction (block) 1. SA Block 2. AV Block a. In the AV node b. In the AV bundle, both bundle branches, or all three fascicles
  17. 17. Sinus bradycardia • Defined as a heart rate of less than 60 beats per minute. • In patients on chronic beta-blocker, defined as a heart rate of less than 50 beats/min.
  18. 18. Sinus bradycardia Perioperative causes of Sinus Bradycardia are: 1.Vagal stimulation- Oculocardiac reflex, Celiac plexus stimulation (traction on mesentry),laryngoscopy, Abdominal insufflation. 2. Drugs- Beat blocker, Cal channel blocker,opioids(fentanyl/sufentanyl) 3. Succinylcholine 4.Hypothermia 5. Hypothyroidism 6. Athelets 7. Cholestatic jaundice or raised intracranial pressure 8. During the early stages of MI
  19. 19. Sinus bradycardia Perioperative management • In asymptomatic pt. no treatment is required. • In Mildly symptomatic pts, underlying factors should be eliminated. • In severly symptomatic pts, those with chest pain or syncope, immediate transcutaneous/transvenous pacing is required. • Atropine 0.5 mg i.v. every 3-5 min(max 3mg) may be given. • An epinephrine or dopamine infusion may be titrated while awaiting cardiac pacing.
  20. 20. Sinus arrhythmia Inspiration accelerates the heart rate, and expiration slows it down.
  21. 21. Sick sinus syndrome CAUSES: • Conditions leading to fibrosis of the sinoatrial (SA) node, such as increased age, atherosclerotic heart disease, hypertension, and cardiomyopathy • Trauma to the SA node caused by open heart surgery • Autonomic disturbances • Cardioactive medications such as digoxin, beta adrenergic blockers, and calcium channel blockers.
  22. 22. Sick sinus syndrome Sometimes called the bradycardia-tachycardia syndrome. When severe, sinus slowing can cause syncope, but rarely sudden death.
  23. 23. Sick sinus syndrome • No treatment required unless symptomatic • If the patient is symptomatic, however, treatment aims to alleviate signs and symptoms and correct the underlying cause of the arrhythmia. • Atropine or epinephrine may be given initially for symptomatic bradycardia. • A temporary or permanent pacemaker may be used. • Tachyarrhythmias may be treated with antiarrhythmic medications, such as metoprolol and digoxin.
  24. 24. AV BLOCK • Atrial impulse is conducted with delay or is not conducted at all to the ventricle when the AV junction is not physiologically refractory. • Block can occur in the AV node , bundle of his or bundle branches
  25. 25. First Degree Heart Block Causes: Increased vagal tone, digitalis toxicity, inferior wall MI and myocarditis. Usually asymptomatic and rarely require T/t.
  26. 26. Second Degree AV Block Type 1 (Wenckebach) • Often seen in post inferior MI with AV node ischemia • No pacing as long as no bradycardia.
  27. 27. Second Degree AV Block Type 2 • Diseased bundle of HIS with BBB. • May be precursor to complete heart block and needs pacing.
  28. 28. Third Degree AV Block Complete heart block where atria and ventricles beat independently and atria beat faster than ventricles. Pacemaker is the treatment.
  29. 29. Bundle branch blocks • RBBB: More common and associated with ASD, IHD, valvular heart disease ECG : wide QRS, terminal R wave in lead V1(rSR’) , deep S wave in lead I and V6 Bifascicular HB- RBBB +left anterior /posterior hemiblock • LBBB : wide QRS, predominantly negative QRS in V1,V2,V3 and absence of Q waves in lead I and V6. • Treat underlying causes
  30. 30. Bundle branch block
  31. 31. Premature systoles 1) Atrial 2) Junctional 3) Ventricular APC
  32. 32. Premature Atrial Contraction (PAC) • PACs arises from ectopic foci in atria. • May produce palpitation, pt. complain of skipped beat/irregular pulse. • Precipitated by excessive caffeine, alcohol, nicotine , anxiety, hyperthyroidism. • Often occur at rest and become less frequent by exercise. • Frequent PAC forerunner of atrial fibrillation, flutter, • Treatment : Avoidance of ppt. factors and sympathetic stimulation. • Pharmacological T/t required only if the PACs trigger secondary dysrhythmias. • Usually suppressed by calcium channel blocker or Beta blocker.
  33. 33. Premature Atrial Contraction (PAC)
  34. 34. Junctional Rhythms • Rhythms that originate at the AV junction • Junctional rhythms do not have characteristic p-waves • P-wave can come before or after the QRS complex or lost within the QRS entirely • If a p-wave is seen it will be inverted • Junctional rhythm often result in AV dys-synchrony and a junctional tachycardia can severly impaired cardiac output.
  35. 35. Premature Junctional Contraction
  36. 36. Junctional Rhythms Perioperative T/t- • Junctional rhythm is not frequent during GA,usually requires no T/t • Loss of AV synchrony during a junctional rhythm may result in MI, heat failure or hypotension • Atropine 0.5 mg can be used to treat hemodynamically significant junctional rhythms • Temporary or permanent pacemaker may be required.
  37. 37. Premature Ventricular Contraction (PVC)
  38. 38. Premature Ventricular Contraction (PVC) Two major characteristics of PVCs: 1. They are premature, occurring before the next normal beat is expected 2. QRS complex is abnormally wide and T wave and QRS complex usually points in opposite direction. PVC are significant for two reason- 1. They can lead to more serious arrhythmia- VT/VF( R- on –T phenomenon)- PVC occur so early that it fall on the T wave because the cells are not fully repolarized, VT/VF can result. 2. Also decreases CO esp. if ectopic beats are frequent or sustained
  39. 39. Premature Ventricular Contraction (PVC) • Classify as unifocal, or multifocal PVC’s • – Unifocal-originating from same area- same morphology • – Multifocal-originating from different area-different morphology • Causes of PVCs • Arterial hypoxemia • MI • Myocarditis • Hypokalemia/Hypomagnesemia • Digitalis toxicity • Caffeine, cocaine, Alcohol • Mechanical irritation-(CV or Pulm. Artery catheter)
  40. 40. Premature Ventricular Contraction (PVC) • If pt. asymptomatic- the arrythmia won’t req. t/t • During anaesthesia, if pt exhibits 6 or more PVCs per minute and repetitive or multifocal forms, there is increased risk of developing life-threatening dysrhythmia. • T/t include identification of possible cause and t/t of that cause. While t/t of cause, the immediate availability of a defibrillator should be confirmed. • Beta blockers are the most successful drug, • Amiodarone, lidocaine and other antiarrhythmic are indicated if the PVCs progress to VT or VF to cause hemodynamic instability
  41. 41. TACHYARRYTHMIAS
  42. 42. Sinus Tachycardia • Sinus rhythm with HR > 100 beats/min. • Causes-exercise, pain, stress, anxiety, fever, intravascular volume loss, shock, anaemia, embolism, sepsis, hyperthyroidism, drugs- atropine, isoproterenol, aminophylline, dobutamine, epinephrine, • With sinus tachycardia at very fast rate, P wave may be merge with the preceding T wave and become difficult to distinguish. • Myocardial demands for O2 increased can bring episode of chest pain in CAD pt. • Can lower C.O by reducing ventricular filling time leads to hypotension and decrease perfusion.
  43. 43. Sinus Tachycardia
  44. 44. Sinus Tachycardia Treatment • Focus on determining and correcting underlying cause. • In symptomatic pt. maintaining the adequate C.O and tissue perfusion. • Beta blockers may be used to slow the heart rate and decrease myocardial O2 demand(if pt is not hypovolemic). • Supplemental O2 to increase supply in response to increase demand. • Avoidance of vagolytic drug (pancuronium) intraoperatively
  45. 45. Paroxysmal Supraventricular Tachycardia (PSVT) • Narrow QRS complex tachycardias • m.c. PSVT is AV nodal re-entrant tachycardia (AVNRT) • ECG- narrow complex tachycardia with regular rhythm, no visible P wave. • Treatment- • Carotid sinus massage and Valsalva manoeuvre. • Adenosine-6 mg rapid IV injection.If response inadequate repeat 12mg • When PSVT not respond to adenosine – CCB-diltiazem/verapamil can be effective
  46. 46. ATRIAL FLUTTER • Supra ventricular tachycardia.- atrial rate around 300 cycles/min. • Commonly associated with second degree block. • Mechanism-Reentrant circuit revolves around the tricuspid valve in the right atrium. • Conditions that enlarge atrial tissue and elevate atrial pressure.-sev. Mitral valve ds., hyperthyroidism, pericardial ds., pt. after cardiac surgery, pt with MI/ COPD • AF and flutter can occur in the same patient, transitioning from one to the other( at a given time usually one or other rhythms present)
  47. 47. ATRIAL FLUTTER
  48. 48. ATRIAL FLUTTER • T/t depends on hemodynamic stability of patient. • If pt. is hemodynamically unstable - T/t is synchronized electrical Cardioversion starting at 50 J is indicated. • If pt.is Hemodynamically stable-With normal cardiac function and duration< 48 hrs. -Direct current (DC) cardioversion. • If duration >48 hrs. DC cardioversion would not be considered b/c increases the risk of thromboembolism unless pt is adequately anti coagulated. • Pharmacological control of ventricular response with IV amiodarone, diltiazem or verapamil may be tried, if vital signs are stable.
  49. 49. Atrial Fibrillation (AF) • Most common cardiac arrhythmia in general population. • AF is a supraventricular arrhythmia characterized by complete absence of coordinated atrial contractions. • Originate in the area of pulmonary vein- left atrial junctions. • Causes- occurs following cardiac sx., long standing hypotension, pulmonary embolism, COPD, electrolyte imbalance, MR/MS, hyperthyroidism, CAD, acute MI, pericarditis. • Usually, the single best lead to identify the diagnostic irregular atrial activity of AF is- lead V1 • If AF/flutter can occur with Complete heart block ECG- shows regular slow ventricular response
  50. 50. Atrial Fibrillation (AF)
  51. 51. Atrial Fibrillation (AF) • AF or flutter have two major clinical implications- 1. Increase in thromboembolism risk( whenever AF is present –anticoagulant status of pt. should be reviewed and appropriate t/t promptly initiated). 2. development of chronic heart failure. • Treatment- • Thromboprophylaxis- based on CHADS2 score • Score=0 no anticoagulation needed • Score=1 dabigatron 150 mg bd • Mitral stenosis /coronary ds. = Warfarin target INRof2-3
  52. 52. Atrial Fibrillation (AF) • Rate control can achieved by AV nodal blockings agents( beta blocker, CCB, digoxin) or AV junction ablation. • Rhythm control- cardioversion(rhythm restoration)- chemical cardioversion- limited value, ibutilide (convert up to 50% of AF) cause QT prolongation • Rhythm maintenance by anti arrhythmic drugs class 1 agents-flecainide, propafenone,) class 3 drugs- sotalol, amiodarone, dofetilide, • If patient is hemodynamically stable and, if duration of AF< 48 hrs- pharmacological cardioversion (amiodarone, ibutilide), if duration of AF >48 hrs -anticoagulation 3 wks prior to an elective cardioversion and continue anticoagulation for 4 wks after procedure. • Pt. is hemodynamic unstable- anticoagulation with heparin should be initiated as soon as possible prior to cardioversion followed by 4 wks of anticoagulation after the procedure
  53. 53. Wolf Parkinson White Syndrome (WPW) syndrome • Extra pathway between atria and ventricle that would bypass the AV junction(bundle of kent) preexcite the ventricles. • ECG shows: - Short PR interval - Delta wave on the upstroke of the QRS complex Incidental finding of WPW syndrome- usually do not require specific intervention. • Drug treatment includes Procainamide, amiodarone • Pt who are symptomatic Tachycardia cured by radiofrequency ablation. • Major concern risk of sudden onset atrial fibrillation lead to ventricular fibrillation. • When AF is associated with WPW- drugs that block the AV node(CCB, Beta blocker, digoxin) is contraindicated.
  54. 54. WPW syndrome
  55. 55. Ventricular Tachycardia (VT) • Three or more PVCs occur in a row and the ventricular rate >100 beats/min. • Classification -based on duration (non-sustained-<30 sec, sustained> 30 sec) • Based on appearance on lead(Monomorphic/Polymorphic) • Mechanism - Increased myocardial irritability triggered by enhanced automacity/re entry in purkinje system or PVCs initiating the R-on- T phenomenon. • Monomorphic VT in patient with prior MI is caused by re-entry around the areas of myocardial scar. • Torsades pointes is special variant of polymorphic VT
  56. 56. Ventricular Tachycardia (VT)
  57. 57. Ventricular Tachycardia (VT) • Treatment: • In hemodynamically compromised patients- emergency electrical cardioversion indicated. • If there is no hemodynamic compromise and diagnosis of VT is certain- I.V amiodarone used to terminate arrhythmia • If no hemodynamic compromise diagnosis of VT is uncertain – response to adenosine helpful(terminate paroxysmal SVT) • DC cardioversion is necessary if medical therapy is unsuccessful • Sustained monomorphic VT in pt. structural heart ds. Is indication for implantable cardioverter defibrillator.
  58. 58. Torsades de Pointes • French term-Means twisting around the points. • Special form of polymorphic ventricular tachycardia. • Usually initiated by VPB starting at the peak of T wave ( R on T phenomenon) • Cause-usually reversible-drugs which lengthen QT interval, myocardial ischemia, electrolyte abn. • Hereditary long QT syndrome- abn. Ion channel function in the heart result in prolong repolarization – Treatment- • Correcting the underlying causes • I.V Magnesium 2 gm bolus followed by infusion at 2-4mg/min • Sustained polymorphic VT requires nonsynchronized cardioversion(defibrillation)
  59. 59. Ventricular Fibrillation (VF) • Chaotic pattern of electrical activity in the ventricles in which electrical impulse arise from many different foci. • It produces no effective muscular contraction and no cardiac output. If VF continues, it leads to ventricular standstill and death. • Causes- myocardial ischemia, infarction, untreated VT, underlying heart ds., acid base imbalance, sev. Hypothermia, electric shock, sev. Hypoxia, • Successful resuscitation requires rapid recognition of the problem and prompt defibrillation. • Defibrillation is most effective t/t for VF. • During cardiac surgery internal paddles are used
  60. 60. Treatment

Editor's Notes

  • ). However, it should be used cautiously in pa­tients with CAD, since excessive increase in heart rate may worsen ischaemia because of increased myocardial oxygen consumption or reduced diastolic filling time
  • Atrial and Junctional Premature Beats
    Single ectopic supraventricular beats can originate in the atria or in the vicinity of the AV node. The former are called atrial premature beats (or premature atrial contractions); the latter, junctional premature beats. These are common phenomena, neither indicating underlying cardiac disease nor requiring treatment. They can, however, initiate more sustained arrhythmias. An atrial premature beat can be distinguished from a normal sinus beat by the contour of the P wave and by the timing of the beat.
    Contour. Because an atrial premature beat originates at an atrial site distant from the sinus node, atrial depolarization does not occur in the usual manner, and the configuration of the resultant P wave differs from that of the sinus P waves. If the site of origin of the atrial premature beat is far from the sinus node, the axis of the atrial premature beat will also differ from that of the normal P waves.
    Timing. An atrial premature beat comes too early; that is, it intrudes itself before the next anticipated sinus wave. With junctional premature beats, there is usually no visible P wave, but sometimes a retrograde P wave may be seen. This is just like the case with the junctional escape beats seen with sinus arrest.
    What is the difference between a junctional premature beat and a junctional escape beat? They look exactly alike, but the junctional premature beat occurs early, prematurely, interposing itself into the normal sinus rhythm. An escape beat occurs late, following a long pause when the sinus node has failed to fire.
    (A) A junctional premature beat. The third beat is obviously premature, and there is no P wave preceding the QRS complex. (B) The third beat is a junctional escape beat, establishing a sustained junctional rhythm. It looks just like a junctional premature beat, but it occurs late, following a prolonged pause, rather than prematurely.
    Both atrial and junctional premature beats are usually conducted normally to the ventricles, and the resultant QRS complex is therefore narrow.


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