logging in or signing up Perioperative Arrhythmias rajeeshh Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 2192 Category: Education License: All Rights Reserved Like it (3) Dislike it (0) Added: July 27, 2009 This Presentation is Public Favorites: 3 Presentation Description No description available. Comments Posting comment... By: Anesthesiadoctor (28 month(s) ago) Thank you Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Slide 1: ., PERI OPERATIVE ARRYHTHMIAS DR.J.RAJESH.,D.A.,DNB Introduction : Introduction Most frequent peri operative cardiac abnormality with high incidence Can occur in a patient with or without cardiac disease During cardiac or non cardiac surgeries During general or regional anesthesia Introduction : Introduction “Abnormality of cardiac rate, rhythm or conduction” Can be either symptomatic (syncope, near syncope, dizziness, or palpitations) or asymptomatic Immediate diagnosis and intervention with appropriate therapy needed Basics : Basics Cardiac cycle Electrical activity Mechanical activity Physiology : Physiology Conduction System: S.A Node Inter Nodal Pathway AV Node HIS Bundle - Right Bundle Branch - Left Bundle Branch - Purkinje System Electro Physiology : Electro Physiology Ions – Sodium, Potassium, Calcium Fibers : Quiescent – Atrial, Ventricular cells Automatic – SA node, Secondary cells Primary pacemaker - SA node Latent pacemakers – atrial tissue, AV junction, HIS bundle, Purkinje system Slide 7: Various parts of the conducting system and under abnormal conditions part of the myocardium produce spontaneous discharge Pathogenesis : Pathogenesis Injury or damage (pathology) to the cardiac conduction systems. Re-entry Automaticity Mutations in ion channels Ectopic foci/ irritable foci Mechanisms of Arrhythmogenesis : Mechanisms of Arrhythmogenesis Arrhythmias Mechanism : Arrhythmias Mechanism Automaticity Abnormal impulse formation Altered Autonomic input, Ischaemia Drug effects alter discharge rate, conduction AV node, HIS bundle may initiate “Escape Rhythm” when SA node discharges slowly or impulse is blocked - Latent pacemakers dominate – Pathological Arrhythmias Mechanism : Arrhythmias Mechanism Re-entry Abnormal Conduction occurs when there are 2 pathways with different conduction properties Criteria – Area of unidirectional Block Recirculation of impulse to origin Interruption of pathway – Eliminate Mechanism of Reentry : Mechanism of Reentry Reentrant Rhythms : Reentrant Rhythms Atrial flutter Atrial fibrillation Paroxysmal SupraVentricular Tachycardia Ventricular tachycardia Slide 14: Triggered Activity Excitation of affected Myocardium – Premature beat occurs due to abnormal ionic currents, hypoxia, digitalis. Whether Arrhythmia is dangerous? : Whether Arrhythmia is dangerous? Haemodynamic Implications : Haemodynamic Implications Due to lack of atrial transport mechanism Inadequate atrial contraction ? Inadequate ventricular filling occurs when there is obstruction between atrium and ventricles, hypertrophied ventricle, sudden stress Brady Arrhythmia Dangerous in patients with low fixed stroke volume – depend on the heart rate for cardiac output Haemodynamic Implications : Haemodynamic Implications Tachy arrhythmias Less time for diastolic filling Increased Myocardial O2 consumption Abnormal ventricular arrhythmia Less effective ventricular contraction leads to decreased cardiac output Whether Arrhythmia is dangerous? : Whether Arrhythmia is dangerous? Yes……when it produces haemodynamic changes Causes : Causes Anaesthetic agents Halogenated hydro carbons like Halothane, Enflurane Drugs blocking reuptake of catecholamine e.g. Ketamine Others like Atropine, Suxamethonium etc Slide 20: 2. Drugs Digoxin, Tricyclic antidepressants 3. Electrolyte abnormalities Potassium, Sodium, Calcium, Magnesium 4. ABG abnormalities Hypo or Hypercarbia Acidosis and Alkalosis – Potassium related Profound Hypoxemia – Bradycardia, Ventricular arrhythmias, asystole Slide 21: 5. Temperature changes Hypothermia – Decreases conduction velocity in all areas of conduction system Hyperthermia – Catecholamine induced arrhythmias 6. Laryngoscopy and intubation Endotracheal intubation is most common cause of arrhythmias during surgery Can also occur at time of extubation Slide 22: 7. Reflexes Vagal stimulation ? Sinus Bradycardia Reflexes arise from pharynx, larynx, abdominal & thoracic organs Direct pressure on vagus during carotid surgery Specific reflexes like ocular cardiac reflex Slide 23: 8. Autonomic disturbances 9. Pre existing cardiac diseases Cardiomyopathy, Myocarditis, CAD, Ventricular hypertrophy, Low cardiac output states 10. Pre existing arrhythmias 11. Central venous cannulation 12. Surgical manipulation of cardiac structures Slide 24: 13. Physical factors High atrial pressure – Atrial arrhythmias High arterial pressure – Ventricular arrhythmias 14. Surgical site 15. Increased catecholamine levels Exogenous - Inotropes, Adrenaline Endogenous release due to pain, hypoxia, light anesthesia, Hypercarbia Slide 25: 16. Intracranial pathology 17. Endocrine disorders Phaeochromoctoma, Thyrotoxicosis, Diabetes, Adreno cortical excess Pre operative arrhythmias (ACC/AHA 2007) : Pre operative arrhythmias (ACC/AHA 2007) Major Clinical Predictors (needs delay & evaluation before proceeding for surgery) Acute coronary syndrome Decompensated HF Significant arrhythmias Severe Valvular Heart disease Significant arrhythmias (ACC/AHA 2007) : Significant arrhythmias (ACC/AHA 2007) High grade AV block Symptomatic ventricular arrhythmias Supraventricular arrhythmias with ventricular rates > 100 at rest Symptomatic bradycardia Newly recognized ventricular tachycardia Intra Operative Arrhythmias : Intra Operative Arrhythmias Sinus Tachycardia Sinus Bradycardia Sinus Arrhythmias Premature Atrial Complex (PAC) Paroxysmal Supra-ventricular Tachycardia (PSVT) Atrial Flutter Atrial Fibrillation Intra Operative Arrhythmias : Intra Operative Arrhythmias Premature Junctional Complex (PJC) Junctional Escape Complex and Junctional Rhythm Premature ventricular complex (PVC) Ventricular Tachycardia Ventricular Fibrillation Ventricular Asystole Approach and diagnosis : Approach and diagnosis Arrhythmia recognized (1) Haemodynamic Disturbances? (2) Treatment Required ? (3) How urgently ? Rule out Pseudo arrhythmias Pseudo arrhythmias : Pseudo arrhythmias Due to Electrocautery ECG lead disconnections Movement of lead wires Muscle artifact Check list : Check list What is the heart rate ? Is the rhythm regular ? Is there one P wave for each QRS ? Is QRS complex normal ? Is the rhythm dangerous ? Does the rhythm require treatment ? Normal Sinus Rhythm : Normal Sinus Rhythm Normal sequence of conduction, originating in the sinus node EKG 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 Sinus Arrhythmia : Sinus Arrhythmia Alternate periods of slower and faster rates Rate increases with inspiration and decreases with expiration Common in children ECG - normal pattern Treatment - None Sinus Tachycardia : Sinus Tachycardia Most common arrhythmia occuring intra operatively Occurs due to increase in rate of discharge of impulses from S.A.node Etiology – Inadequate anesthesia and light plane, anxiety, pain, fever, hypovolemia, hypoxia, hypercarbia,drug effect, heart failure ECG criteria : ECG criteria Rate > 100/ min Rhythm – regular P wave – upright in LI, LII, aVF P : QRS – 1:1 QRS complex – normal ST – depression can occur due to ischaemia Slide 38: Significance - can precipitate heart failure, angina Treatment Treat underlying cause Beta blockers – Esmolol, Metaprolol Atrial Fibrillation/ Atrial Flutter : Atrial Fibrillation/ Atrial Flutter Atrial impulses faster than SA node impulses Atrial fibrillation ? impulse takes multiple, chaotic, random pathways through atria Atrial flutter ? impulse takes a circular course around atria Impulse formation is by ‘re entry’ phenomenon Recommended Therapy - Control Rate : Recommended Therapy - Control Rate Control Rhythm : Control Rhythm Junctional Tachycardia : Junctional Tachycardia Area of ‘automaticity’ develops in AV node Both retrograde and ante grade transmission occurs ECG criteria Rate – 100 – 180/min Rhythm- regular atrial and ventricular firing PR- not measurable or will be short P wave - obscured, may arise before, after or with QRS QRS complex - narrow Slide 47: Key – Position of P wave; show ante grade or retrograde propagation; may arise before, after or with QRS Etiology Digoxin toxicity Acute sequence of acute coronary syndrome Recommended Therapy : Recommended Therapy Diagnosis Unknown ? Vagal stimulation Adenosine ? Preserved heart function Beta blockers Calcium channel blockers Amiodarone NO DC CONVERSION Impaired heart function Amiodarone NO DC CONVERSION Multifocal Atrial Tachycardia : Multifocal Atrial Tachycardia Areas of automaticity originate irregularly and rapidly at different points in atria Etiology Most common cause is COPD (corpulmonale) Impaired and hypertrophied atrium Digoxin toxicity Acute coronary syndromes RHD ECG criteria : ECG criteria Rate- >100bpm Rhythm- irregular atrial firing PR- variable P wave- 3 or more that differ in polarity QRS complex- narrow Key- 3 or more P wave that differ in polarity, shape, size Recommended Therapy : Recommended Therapy Preserved heart function Beta blockers Calcium channel blockers Amiodarone Impaired heart function Amiodarone Diltiazem NO DC cardioversion PSVT ( Paroxysmal SupraVentricular Tachycardia) : PSVT ( Paroxysmal SupraVentricular Tachycardia) Re entry phenomenon – impulse arise and recycle repeatedly in AV node because of unidirectional block in Purkinje fibers Etiology : Etiology Accessory conduction pathway Factors like caffeine, hypoxia, cigarettes, stress, anxiety, sleep deprivation, medications in healthy individuals Unhealthy individuals with CAD, COPD, CHF ECG criteria : ECG criteria Rate – exceeds upper limit of sinus tachycardia (?120bpm ); seldom?150 bpm up to 250bpm Rhythm – regular P waves – seldom seen, rapid rate cause P wave loss in T wave or low origin in atrium QRS complex- narrow Key – Regular, Narrow complex tachycardia without P waves and sudden, paroxysmal onset or cessation or both Recommended Therapy : Recommended Therapy Diagnosis Unknown ? Vagal stimulation Adenosine ? Preserved heart function AV nodal blockade - ? blocker, Calcium channel blocker, Digoxin DC Cardio version Parenteral antiarrhythmics – Procainamide, Amiodarone, Sotalol Recommended Therapy : Recommended Therapy Impaired heart function DC cardioversion Digoxin Amiodarone Diltiazem Premature Ventricular Complex PVC : Premature Ventricular Complex PVC Results from ectopic pacemaker activity from either ventricle Wide, bizarre QRS complex Unifocal- PVCs from same focus; coupling interval is normal Multifocal- coupling interval and QRS morphology vary Types : Types Ventricular bigeminy- every other beat is a PVC Ventricular trigeminy- 2 normal beats and a PVC or 1 normal beat and 2 PVCs Ventricular Bigeminy : Ventricular Bigeminy Management : Etiology Heart diseases Electrolyte abnormalities Blood gas abnormalities Drug inter actions Brainstem stimulation Treatment Lidocaine Esmolol Bretylium Verapamil Atropine Management Premature Atrial Complex - PAC : Premature Atrial Complex - PAC Impulses arise in atria, outside SA node Occurs before next expected sinus beat Etiology Sympathomimetics Hypoxia High atrial pressures Digitalis toxicity ECG criteria : ECG criteria Rate- variable Rhythm- irregular P wave- abnormal with different morphology PR interval – shorter or longer QRS- normal Recommended Therapy : Recommended Therapy Usually not needed If hemodynamically unstable Digitalis Beta blockers Verapamil Sinus Bradycardia : Sinus Bradycardia Occurs due to decrease in rate of discharge of impulses from S.A node Not pathological, not an abnormal arrhythmia, more a physical sign Etiology – Drug effects, acute inferior wall MI, Hypoxia, vagal stimulation, sympathetic blockade, parasympathetic stimulation, sick sinus syndrome ECG criteria : ECG criteria Key – Regular P waves followed by regular QRS complexes at rate < 60/min Recommended Therapy : Recommended Therapy Rarely indicated, treat only if significant Oxygen is always appropriate Intervention sequence Atropine 0.5 to 1mg i.v Transcutaneous pacing if available Catecholamine infusion in severe cases Dopamine 5 to 20 µg/kg/min Epinephrine 2 to 10 µg/min Isoproterenol 2 to 10 µg/min First - degree heart block : First - degree heart block Impulse conduction is slowed (partial block) at AV node by a fixed amount Closer to being a physical sign than an abnormal arrhythmia Etiology – Drugs – Usually AV node blockers, parasympathetic stimulation, inferior AMIs ECG criteria : ECG criteria Rate – bradycardia or tachycardia Rhythm – sinus, regular PR – prolonged, > 0.20 sec, fixed P wave – size & shape normal, each P wave have 1 QRS complex QRS complex – narrow: =0.10 sec in absence of intraventricular conduction defect Key- PR interval > 0.20 sec First degree block : First degree block Second degree heart block Type I(Mobitz I- Wenckebach) : Second degree heart block Type I(Mobitz I- Wenckebach) Site of pathology is AV node Impulse conduction is increasingly slowed at AV node – causing increasing PR interval Occurs till one sinus impulse is completely blocked and a QRS complex fails to follow Etiology : Etiology AV nodal blocking agents- Beta blockers, Calcium channel blockers, Digoxin Stimulation of Para sympathetic system Acute coronary syndrome- right coronary ECG criteria : Key- Progressive lengthening of PR interval until one P wave is not followed by QRS complex ECG criteria Recommended Therapy : Recommended Therapy Intervention sequence Atropine 0.5 to 1mg i.v Transcutaneous pacing if available If signs and symptoms are severe Dopamine 5 to 20 µg/kg/min Epinephrine 2 to 10 µg/min Isoproterenol 2 to 10 µg/min Second degree block Type II(Mobitz II- Non Wenckebach) : Second degree block Type II(Mobitz II- Non Wenckebach) Infra nodal block – site of block most often below AV node Impulse conduction is normal through the node Etiology Acute coronary syndrome – left coronary ECG criteria : ECG criteria Atrial rate- usually 60 to 100 bpm Ventricular rate- slower than atrial rate Rhythm- Atrial- regular; Ventricular- irregular PR- constant, no progressive prolongation P wave- some P waves will not be followed by QRS complex QRS complex- narrow implies high block; wide implies low block Key - No progressive prolongation of P wave Recommended Therapy : Recommended Therapy Prepare for Tran venous pacer Atropine is seldom effective Transcutaneous pacing If signs and symptoms are severe, unresponsive Dopamine 5 to 20 µg/kg/min Epinephrine 2 to 10 µg/min Isoproterenol 2 to 10 µg/min Third degree heart block and AV Dissociation : Third degree heart block and AV Dissociation Injury to cardiac conduction system producing complete block of impulses Block can occur at AV node or Bundle of His or Bundle branches Etiology Acute coronary syndrome- LAD ECG criteria : ECG criteria Atrial rate- usually 60 to 100 bpm, Impulses completely independent from ventricular rate Ventricular rate- depends on rate of escape beats; slower than atrial rate- third degree block; faster- AV dissociation Rhythm- Atrial&Ventricular- regular, independent PR- no relationship between P and R wave P wave- typical in size and shape QRS complex- narrow implies high block; wide implies low block Third degree block : Third degree block Recommended Therapy : Recommended Therapy Prepare for Tran venous pacer Transcutaneous pacing If signs and symptoms are severe, unresponsive Dopamine 5 to 20 µg/kg/min Epinephrine 2 to 10 µg/min Isoproterenol 2 to 10 µg/min Never treat third degree block plus ventricular escape beats with Lidocaine Cardiac arrest : Cardiac arrest Etiology : Etiology 6 Hs Hypovolemia Hypoxia Hydrogen ion- acidosis Hyperkalemia/ Hypokalemia Hypothermia Hypoglycaemia 6 Ts Trauma Tablets Tamponade Tension Pneumothorax Thrombosis, coronary (ACS) Thrombus, Pulmonary Ventricular Fibrillation : Ventricular Fibrillation PEA : PEA Asystole : Asystole No ventricular activity seen P wave seen occasionally, R wave absent Classically presents as a Flat line Conclusion : Conclusion This is just an attempt to discuss cardiac arrhythmias commonly encountered by anesthesiologists Arrhythmias should be recognized immediately Significance should be understood Appropriate therapy can be initiated in need Chapters not discussed – Pacemakers, ICD, Antiarrhythmics Stress Points : Stress Points Intra Operative Arrhymias can occur at any time most commonly during Laryngoscopy and Endotracheal intubation Can occur at any age group With or without cardiac disease Undergoing cardiac or non cardiac surgery Regional or general anesthesia Initiated by one mechanism, sustained by another Slide 96: Impossible to discern mechanism for a particular arrhythmia RECOGNIZE, CONFIRM and TREAT if needed. 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Perioperative Arrhythmias rajeeshh Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 2192 Category: Education License: All Rights Reserved Like it (3) Dislike it (0) Added: July 27, 2009 This Presentation is Public Favorites: 3 Presentation Description No description available. Comments Posting comment... By: Anesthesiadoctor (28 month(s) ago) Thank you Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Slide 1: ., PERI OPERATIVE ARRYHTHMIAS DR.J.RAJESH.,D.A.,DNB Introduction : Introduction Most frequent peri operative cardiac abnormality with high incidence Can occur in a patient with or without cardiac disease During cardiac or non cardiac surgeries During general or regional anesthesia Introduction : Introduction “Abnormality of cardiac rate, rhythm or conduction” Can be either symptomatic (syncope, near syncope, dizziness, or palpitations) or asymptomatic Immediate diagnosis and intervention with appropriate therapy needed Basics : Basics Cardiac cycle Electrical activity Mechanical activity Physiology : Physiology Conduction System: S.A Node Inter Nodal Pathway AV Node HIS Bundle - Right Bundle Branch - Left Bundle Branch - Purkinje System Electro Physiology : Electro Physiology Ions – Sodium, Potassium, Calcium Fibers : Quiescent – Atrial, Ventricular cells Automatic – SA node, Secondary cells Primary pacemaker - SA node Latent pacemakers – atrial tissue, AV junction, HIS bundle, Purkinje system Slide 7: Various parts of the conducting system and under abnormal conditions part of the myocardium produce spontaneous discharge Pathogenesis : Pathogenesis Injury or damage (pathology) to the cardiac conduction systems. Re-entry Automaticity Mutations in ion channels Ectopic foci/ irritable foci Mechanisms of Arrhythmogenesis : Mechanisms of Arrhythmogenesis Arrhythmias Mechanism : Arrhythmias Mechanism Automaticity Abnormal impulse formation Altered Autonomic input, Ischaemia Drug effects alter discharge rate, conduction AV node, HIS bundle may initiate “Escape Rhythm” when SA node discharges slowly or impulse is blocked - Latent pacemakers dominate – Pathological Arrhythmias Mechanism : Arrhythmias Mechanism Re-entry Abnormal Conduction occurs when there are 2 pathways with different conduction properties Criteria – Area of unidirectional Block Recirculation of impulse to origin Interruption of pathway – Eliminate Mechanism of Reentry : Mechanism of Reentry Reentrant Rhythms : Reentrant Rhythms Atrial flutter Atrial fibrillation Paroxysmal SupraVentricular Tachycardia Ventricular tachycardia Slide 14: Triggered Activity Excitation of affected Myocardium – Premature beat occurs due to abnormal ionic currents, hypoxia, digitalis. Whether Arrhythmia is dangerous? : Whether Arrhythmia is dangerous? Haemodynamic Implications : Haemodynamic Implications Due to lack of atrial transport mechanism Inadequate atrial contraction ? Inadequate ventricular filling occurs when there is obstruction between atrium and ventricles, hypertrophied ventricle, sudden stress Brady Arrhythmia Dangerous in patients with low fixed stroke volume – depend on the heart rate for cardiac output Haemodynamic Implications : Haemodynamic Implications Tachy arrhythmias Less time for diastolic filling Increased Myocardial O2 consumption Abnormal ventricular arrhythmia Less effective ventricular contraction leads to decreased cardiac output Whether Arrhythmia is dangerous? : Whether Arrhythmia is dangerous? Yes……when it produces haemodynamic changes Causes : Causes Anaesthetic agents Halogenated hydro carbons like Halothane, Enflurane Drugs blocking reuptake of catecholamine e.g. Ketamine Others like Atropine, Suxamethonium etc Slide 20: 2. Drugs Digoxin, Tricyclic antidepressants 3. Electrolyte abnormalities Potassium, Sodium, Calcium, Magnesium 4. ABG abnormalities Hypo or Hypercarbia Acidosis and Alkalosis – Potassium related Profound Hypoxemia – Bradycardia, Ventricular arrhythmias, asystole Slide 21: 5. Temperature changes Hypothermia – Decreases conduction velocity in all areas of conduction system Hyperthermia – Catecholamine induced arrhythmias 6. Laryngoscopy and intubation Endotracheal intubation is most common cause of arrhythmias during surgery Can also occur at time of extubation Slide 22: 7. Reflexes Vagal stimulation ? Sinus Bradycardia Reflexes arise from pharynx, larynx, abdominal & thoracic organs Direct pressure on vagus during carotid surgery Specific reflexes like ocular cardiac reflex Slide 23: 8. Autonomic disturbances 9. Pre existing cardiac diseases Cardiomyopathy, Myocarditis, CAD, Ventricular hypertrophy, Low cardiac output states 10. Pre existing arrhythmias 11. Central venous cannulation 12. Surgical manipulation of cardiac structures Slide 24: 13. Physical factors High atrial pressure – Atrial arrhythmias High arterial pressure – Ventricular arrhythmias 14. Surgical site 15. Increased catecholamine levels Exogenous - Inotropes, Adrenaline Endogenous release due to pain, hypoxia, light anesthesia, Hypercarbia Slide 25: 16. Intracranial pathology 17. Endocrine disorders Phaeochromoctoma, Thyrotoxicosis, Diabetes, Adreno cortical excess Pre operative arrhythmias (ACC/AHA 2007) : Pre operative arrhythmias (ACC/AHA 2007) Major Clinical Predictors (needs delay & evaluation before proceeding for surgery) Acute coronary syndrome Decompensated HF Significant arrhythmias Severe Valvular Heart disease Significant arrhythmias (ACC/AHA 2007) : Significant arrhythmias (ACC/AHA 2007) High grade AV block Symptomatic ventricular arrhythmias Supraventricular arrhythmias with ventricular rates > 100 at rest Symptomatic bradycardia Newly recognized ventricular tachycardia Intra Operative Arrhythmias : Intra Operative Arrhythmias Sinus Tachycardia Sinus Bradycardia Sinus Arrhythmias Premature Atrial Complex (PAC) Paroxysmal Supra-ventricular Tachycardia (PSVT) Atrial Flutter Atrial Fibrillation Intra Operative Arrhythmias : Intra Operative Arrhythmias Premature Junctional Complex (PJC) Junctional Escape Complex and Junctional Rhythm Premature ventricular complex (PVC) Ventricular Tachycardia Ventricular Fibrillation Ventricular Asystole Approach and diagnosis : Approach and diagnosis Arrhythmia recognized (1) Haemodynamic Disturbances? (2) Treatment Required ? (3) How urgently ? Rule out Pseudo arrhythmias Pseudo arrhythmias : Pseudo arrhythmias Due to Electrocautery ECG lead disconnections Movement of lead wires Muscle artifact Check list : Check list What is the heart rate ? Is the rhythm regular ? Is there one P wave for each QRS ? Is QRS complex normal ? Is the rhythm dangerous ? Does the rhythm require treatment ? Normal Sinus Rhythm : Normal Sinus Rhythm Normal sequence of conduction, originating in the sinus node EKG 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 Sinus Arrhythmia : Sinus Arrhythmia Alternate periods of slower and faster rates Rate increases with inspiration and decreases with expiration Common in children ECG - normal pattern Treatment - None Sinus Tachycardia : Sinus Tachycardia Most common arrhythmia occuring intra operatively Occurs due to increase in rate of discharge of impulses from S.A.node Etiology – Inadequate anesthesia and light plane, anxiety, pain, fever, hypovolemia, hypoxia, hypercarbia,drug effect, heart failure ECG criteria : ECG criteria Rate > 100/ min Rhythm – regular P wave – upright in LI, LII, aVF P : QRS – 1:1 QRS complex – normal ST – depression can occur due to ischaemia Slide 38: Significance - can precipitate heart failure, angina Treatment Treat underlying cause Beta blockers – Esmolol, Metaprolol Atrial Fibrillation/ Atrial Flutter : Atrial Fibrillation/ Atrial Flutter Atrial impulses faster than SA node impulses Atrial fibrillation ? impulse takes multiple, chaotic, random pathways through atria Atrial flutter ? impulse takes a circular course around atria Impulse formation is by ‘re entry’ phenomenon Recommended Therapy - Control Rate : Recommended Therapy - Control Rate Control Rhythm : Control Rhythm Junctional Tachycardia : Junctional Tachycardia Area of ‘automaticity’ develops in AV node Both retrograde and ante grade transmission occurs ECG criteria Rate – 100 – 180/min Rhythm- regular atrial and ventricular firing PR- not measurable or will be short P wave - obscured, may arise before, after or with QRS QRS complex - narrow Slide 47: Key – Position of P wave; show ante grade or retrograde propagation; may arise before, after or with QRS Etiology Digoxin toxicity Acute sequence of acute coronary syndrome Recommended Therapy : Recommended Therapy Diagnosis Unknown ? Vagal stimulation Adenosine ? Preserved heart function Beta blockers Calcium channel blockers Amiodarone NO DC CONVERSION Impaired heart function Amiodarone NO DC CONVERSION Multifocal Atrial Tachycardia : Multifocal Atrial Tachycardia Areas of automaticity originate irregularly and rapidly at different points in atria Etiology Most common cause is COPD (corpulmonale) Impaired and hypertrophied atrium Digoxin toxicity Acute coronary syndromes RHD ECG criteria : ECG criteria Rate- >100bpm Rhythm- irregular atrial firing PR- variable P wave- 3 or more that differ in polarity QRS complex- narrow Key- 3 or more P wave that differ in polarity, shape, size Recommended Therapy : Recommended Therapy Preserved heart function Beta blockers Calcium channel blockers Amiodarone Impaired heart function Amiodarone Diltiazem NO DC cardioversion PSVT ( Paroxysmal SupraVentricular Tachycardia) : PSVT ( Paroxysmal SupraVentricular Tachycardia) Re entry phenomenon – impulse arise and recycle repeatedly in AV node because of unidirectional block in Purkinje fibers Etiology : Etiology Accessory conduction pathway Factors like caffeine, hypoxia, cigarettes, stress, anxiety, sleep deprivation, medications in healthy individuals Unhealthy individuals with CAD, COPD, CHF ECG criteria : ECG criteria Rate – exceeds upper limit of sinus tachycardia (?120bpm ); seldom?150 bpm up to 250bpm Rhythm – regular P waves – seldom seen, rapid rate cause P wave loss in T wave or low origin in atrium QRS complex- narrow Key – Regular, Narrow complex tachycardia without P waves and sudden, paroxysmal onset or cessation or both Recommended Therapy : Recommended Therapy Diagnosis Unknown ? Vagal stimulation Adenosine ? Preserved heart function AV nodal blockade - ? blocker, Calcium channel blocker, Digoxin DC Cardio version Parenteral antiarrhythmics – Procainamide, Amiodarone, Sotalol Recommended Therapy : Recommended Therapy Impaired heart function DC cardioversion Digoxin Amiodarone Diltiazem Premature Ventricular Complex PVC : Premature Ventricular Complex PVC Results from ectopic pacemaker activity from either ventricle Wide, bizarre QRS complex Unifocal- PVCs from same focus; coupling interval is normal Multifocal- coupling interval and QRS morphology vary Types : Types Ventricular bigeminy- every other beat is a PVC Ventricular trigeminy- 2 normal beats and a PVC or 1 normal beat and 2 PVCs Ventricular Bigeminy : Ventricular Bigeminy Management : Etiology Heart diseases Electrolyte abnormalities Blood gas abnormalities Drug inter actions Brainstem stimulation Treatment Lidocaine Esmolol Bretylium Verapamil Atropine Management Premature Atrial Complex - PAC : Premature Atrial Complex - PAC Impulses arise in atria, outside SA node Occurs before next expected sinus beat Etiology Sympathomimetics Hypoxia High atrial pressures Digitalis toxicity ECG criteria : ECG criteria Rate- variable Rhythm- irregular P wave- abnormal with different morphology PR interval – shorter or longer QRS- normal Recommended Therapy : Recommended Therapy Usually not needed If hemodynamically unstable Digitalis Beta blockers Verapamil Sinus Bradycardia : Sinus Bradycardia Occurs due to decrease in rate of discharge of impulses from S.A node Not pathological, not an abnormal arrhythmia, more a physical sign Etiology – Drug effects, acute inferior wall MI, Hypoxia, vagal stimulation, sympathetic blockade, parasympathetic stimulation, sick sinus syndrome ECG criteria : ECG criteria Key – Regular P waves followed by regular QRS complexes at rate < 60/min Recommended Therapy : Recommended Therapy Rarely indicated, treat only if significant Oxygen is always appropriate Intervention sequence Atropine 0.5 to 1mg i.v Transcutaneous pacing if available Catecholamine infusion in severe cases Dopamine 5 to 20 µg/kg/min Epinephrine 2 to 10 µg/min Isoproterenol 2 to 10 µg/min First - degree heart block : First - degree heart block Impulse conduction is slowed (partial block) at AV node by a fixed amount Closer to being a physical sign than an abnormal arrhythmia Etiology – Drugs – Usually AV node blockers, parasympathetic stimulation, inferior AMIs ECG criteria : ECG criteria Rate – bradycardia or tachycardia Rhythm – sinus, regular PR – prolonged, > 0.20 sec, fixed P wave – size & shape normal, each P wave have 1 QRS complex QRS complex – narrow: =0.10 sec in absence of intraventricular conduction defect Key- PR interval > 0.20 sec First degree block : First degree block Second degree heart block Type I(Mobitz I- Wenckebach) : Second degree heart block Type I(Mobitz I- Wenckebach) Site of pathology is AV node Impulse conduction is increasingly slowed at AV node – causing increasing PR interval Occurs till one sinus impulse is completely blocked and a QRS complex fails to follow Etiology : Etiology AV nodal blocking agents- Beta blockers, Calcium channel blockers, Digoxin Stimulation of Para sympathetic system Acute coronary syndrome- right coronary ECG criteria : Key- Progressive lengthening of PR interval until one P wave is not followed by QRS complex ECG criteria Recommended Therapy : Recommended Therapy Intervention sequence Atropine 0.5 to 1mg i.v Transcutaneous pacing if available If signs and symptoms are severe Dopamine 5 to 20 µg/kg/min Epinephrine 2 to 10 µg/min Isoproterenol 2 to 10 µg/min Second degree block Type II(Mobitz II- Non Wenckebach) : Second degree block Type II(Mobitz II- Non Wenckebach) Infra nodal block – site of block most often below AV node Impulse conduction is normal through the node Etiology Acute coronary syndrome – left coronary ECG criteria : ECG criteria Atrial rate- usually 60 to 100 bpm Ventricular rate- slower than atrial rate Rhythm- Atrial- regular; Ventricular- irregular PR- constant, no progressive prolongation P wave- some P waves will not be followed by QRS complex QRS complex- narrow implies high block; wide implies low block Key - No progressive prolongation of P wave Recommended Therapy : Recommended Therapy Prepare for Tran venous pacer Atropine is seldom effective Transcutaneous pacing If signs and symptoms are severe, unresponsive Dopamine 5 to 20 µg/kg/min Epinephrine 2 to 10 µg/min Isoproterenol 2 to 10 µg/min Third degree heart block and AV Dissociation : Third degree heart block and AV Dissociation Injury to cardiac conduction system producing complete block of impulses Block can occur at AV node or Bundle of His or Bundle branches Etiology Acute coronary syndrome- LAD ECG criteria : ECG criteria Atrial rate- usually 60 to 100 bpm, Impulses completely independent from ventricular rate Ventricular rate- depends on rate of escape beats; slower than atrial rate- third degree block; faster- AV dissociation Rhythm- Atrial&Ventricular- regular, independent PR- no relationship between P and R wave P wave- typical in size and shape QRS complex- narrow implies high block; wide implies low block Third degree block : Third degree block Recommended Therapy : Recommended Therapy Prepare for Tran venous pacer Transcutaneous pacing If signs and symptoms are severe, unresponsive Dopamine 5 to 20 µg/kg/min Epinephrine 2 to 10 µg/min Isoproterenol 2 to 10 µg/min Never treat third degree block plus ventricular escape beats with Lidocaine Cardiac arrest : Cardiac arrest Etiology : Etiology 6 Hs Hypovolemia Hypoxia Hydrogen ion- acidosis Hyperkalemia/ Hypokalemia Hypothermia Hypoglycaemia 6 Ts Trauma Tablets Tamponade Tension Pneumothorax Thrombosis, coronary (ACS) Thrombus, Pulmonary Ventricular Fibrillation : Ventricular Fibrillation PEA : PEA Asystole : Asystole No ventricular activity seen P wave seen occasionally, R wave absent Classically presents as a Flat line Conclusion : Conclusion This is just an attempt to discuss cardiac arrhythmias commonly encountered by anesthesiologists Arrhythmias should be recognized immediately Significance should be understood Appropriate therapy can be initiated in need Chapters not discussed – Pacemakers, ICD, Antiarrhythmics Stress Points : Stress Points Intra Operative Arrhymias can occur at any time most commonly during Laryngoscopy and Endotracheal intubation Can occur at any age group With or without cardiac disease Undergoing cardiac or non cardiac surgery Regional or general anesthesia Initiated by one mechanism, sustained by another Slide 96: Impossible to discern mechanism for a particular arrhythmia RECOGNIZE, CONFIRM and TREAT if needed. Slide 97: THANK U any ?s