8. arrythmias ECG.pptx

Cardiac Arrhythmias Definition An arrhythmia is a problem with the rate or rhythm of the heartbeat. It means that the heart beats too quickly, too slowly, or with an irregular pattern. Clinical Features Tachycardias cause rapid palpitation, dizziness, chest discomfort or breathlessness Brady...

Cardiac Arrhythmias Definition An arrhythmia is a problem with the rate or rhythm of the heartbeat. It means that the heart beats too quickly, too slowly, or with an irregular pattern. Clinical Features Tachycardias cause rapid palpitation, dizziness, chest discomfort or breathlessness Bradycardias cause symptoms that reflect low cardiac output: fatigue, lightheadedness and syncope Extreme tachycardias can cause syncope because the heart is unable to contract or relax properly at extreme rates Extreme bradycardias or tachycardias can precipitate sudden death or cardiac arrest Evaluation of palpitation ARRYTHMIAS Abnormal heart rate or rythm BRADYCARDIAS TACHYCARDIAS Tachycardias Narrow complex tachycardias Tachycardias Broad complex tachycardias Narrow complex tachcardias VT/VF Regular Sinus tachycardia SvT (supra ventricular tachy Irregular AF Atrial flutter Sinus tachycardia Narrow complex Sinus Tachycardia Sinus rate >100/minute Causes Physiological Pathological Sinus tachycardia TACH FEVER: Tamponade/ Thyrotoxicosis Anemia CHF Hypotension Fever Excrutiating pain Volume depletion Exercise Rx (Theo, Dopa, Epi, etc) Supraventricular tachycardia • Paroxysmal supraventricular tachycardia WPW (Wolff–Parkinson–White syndrome ) • Vagal manoeuvres (carotid massage) • Intravenous adenosine ( 6 mg IV ) or verapamil, • AV nodal blockers (β-blockers or calcium channel blockers) • Immediate DC cardioversion is the treatment of choice for all haemodynamically unstable tachycardias. Delta wave The WolffParkinson-White syndrome SVT -AVRT Pre-excitation Syndromes Wolff-Parkinson-White Syndrome WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles Broad Complex Tachycardia - VT Irregular Tachycardias Atrial Fibrillation:Causes Coronary artery disease Valvular heart disease Hypertension Thyrotoxicosis Alcohol Pulmonary embolism Pericardial disease Pneumonia Idiopathic-Lone Atrial Fibrillation:Clinical Can be a symptomatic Complications Precipitate CF Risk of thromboembolism Atrial Fibrillation Atria beat rapidly,chaotically & irregularly Ventricular response irregularly irregular pulse Atrial Fibrillation most common sustained arrhythmia Atria beat rapidly, chaotically, ineffectively Ventricles respond at irregular interval No ‘P’ wave (fibrillatory wave), Normal but irregular QRS complexes (R-R interval) Clinical features Palpitation, breathlessness and fatigue Irregularly irregular pulse Apex Pulse deficit of > 10 / min (HR-PR) Absent ‘a’ wave in JVP Changing intensity of S1 apex Treatment Rate control Control VR () : Digoxin, βblockers,Verapamil Rhythm controlRevert to Normal Sinus Rythm : Amiodarone / DC cardioversion ( after 48 hrs of anticoagulation) Treat the underlying cause Anticoagulation : Warfarin with target INR of 2-3 Aspirin : If age < 65 yrs / If warfarin is contraindicated Atrial Flutter Atrial rate 250 to 350/min Variable AV block ECG saw tooth appearance Cause:organic heart diseasepericarditis, COPD, dig toxicity, AM Atrial Flutter Short lived arrhythmia If persists longer converts to AF Treatment :Conversion to sinus rhythmDC shock 25 to 50 joules or atrial overdrive pacing OR ventricular rate reduction by beta VPB Ventricular Premature Beat • Complexses - Unifocal / Multifocal • Couplet / Triplet – ectopic beats Bigeminy / Trigeminy / Quadrigeminy • Prevalence increases with age; in people with normal heart- disappear with exercise • mostly asymptomatic / palpitation • Pulse - irregular • Aetiology : CAD, HF, Digoxin toxicity, MVP, Escape beat VT Ventricular Tachycardia • most commonly in the settings of acute MI, chronic coronary artery disease, and cardiomyopathy • VT may cause haemodynamic compromise or degenerate into ventricular fibrillation • palpitation or symptoms of low cardiac output, e.g. dizziness, dyspnoea or syncope Treatment ofVentricular Tachycardia Unstable patients with monomorphic VT should be immediately treated with synchronized direct current (DC) cardioversion, usually at a starting energy dose of 100 J (monophasic). Unstable polymorphic VT is treated with immediate defibrillation In stable patients with monomorphic VT and normal left ventricular function, restoration of sinus rhythm is typically achieved with intravenous (IV) procainamide, amiodarone, sotalol, or lidocaine Ventricular fibrillation BRADYCARDIA • Sinus bradycardia • AV block ( Heart block) Sinus bradycardia Ist Degree Heart Block AV Block Disorder of impulse transmission First Degree AV Block Delayed AV conduction Prolonged PR interval A symptomatic- athletes Cause-Rheumatic fever,IHD, Digoxin,Cardiomyopathy Wenckebach’s phenomenon Mobitz type II AV block Second Degree AV Block Some atrial impulse fail to reach ventricle Dropped beats Type I Wenckebach phenomenon (Mobitz Type I) Type II Mobitz AV block Wenckebach’s phenomenon  Progressive lengthening of successi PR intervals.  Dropped beat follows  Repetition of cycle  Not of much significance Mobitz type II AV block PR interval constant Dropped beat at regular intervals Serious condition Mobitz Type II Block Complete Heart Block Complete Third degree failure of AV AV Block conduction Escape rhythm-bundle of His narrow QRS complex or distal conducting tissue-broad QRS complex Complete Heart Block:Cause Congenital Acquired Degeneration AMI Inflammatory Drugs Complete Heart Block Slow pulse(25-50/min) Pulse not varying with exercise Canon waves in JVP Adam-Stokes attacks Stokes Adam AttacksFeature Sudden loss of consciousness without warning Convulsion if prolonged Pallor & death like appearance during the attack Reappearance of pulse &consciousness spont; flushing Adam Stokes Attacks  Episodes v.asystole  Causes Complete heart block Mobitz type II Heart Block Sick Sinus Syndrome CHB Treatment CHB in Acute MIInf wall MI less seriousatropine Ant wall MI-Pacemaker Chronic CHB Symptomatic patientsPacemaker THANK YOU V.Tach:Treatment DC cardioversion Amiodarone infusion Lignocaine-iv bolus, followed by infusion is alternative treatment Torsades De Pointes Type of V.Tachycardia Changing QRS amplitude. Appearance of twist around isoelectric line Sinus Bradycardia Sinus rate <60/minute Causes Physiological Pathological • Causes of sinus bradycardia • Normal physiology in an athelete • Medication (beta-blockers) • Ischemia (typically inferior myocardial infarction with involvement of the sinus node artery) • Hypothermia • Hypothyroidism. • Neuro-mediated bradycardia, such as in a vasovagal reaction AV Block Disorder of impulse transmission First Degree AV Block Delayed AV conduction Prolonged PR interval A symptomatic Cause-Rheumatic fever,IHD, I Degree Heart Block Second Degree AV Block Some atrial impulse fail to reach ventricle Droped beats Type I and II Type I Wenckebach phenomenon Wenckebach’s phenomenon Progressive lengthening of successive PR intervals. Dropped beat follows Repetition of cycle Not of much significance Mobitz type II AV block PR interval constant Dropped beat at regular intervals Serious condition Mobitz Type II Block Complete Heart Block Complete failure of AV conduction Escape rhythm-bundle of His narrow QRS complex or distal conducting tissuebroad QRS complex Distal escape rhythm rate Complete Heart Block:Cause Congenital Acquired Degeneration AMI Inflammatory Drugs Complete Heart Block:Cl/fe Slow pulse(25-50/min) Pulse not varying with exercise Large volume pulse Canon waves in JVP Varying int Ist HS Adam-Stokes attacks Adam Stokes Attacks Episodes v.asystole Causes Complete heart block Mobitz type II Heart Block Sick Sinus Syndrome Adam Stokes Attacks-Feature Sudden loss of consciousness without warning Convulsion if prolonged Pallor & death like appearance during the attack CHB Treatment CHB in Acute MIInf wall MI less seriousatropine Ant wall MI-Pacemaker Chronic CHB Symptomatic patientsPacemaker Cong CHB-No treatment THANK YOU