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ARRHYTHMIA Edited by Yingmin Chen

Definition of Arrhythmia: The Origin, Rate, Rhythm, Conduct velocity and sequence of heart activation are abnormally .

Anatomy of the conducting system

Pathogenesis and Inducement of Arrhythmia Some physical condition Pathological heart disease Other system disease Electrolyte disturbance and acid-base imbalance Physical and chemical factors or toxicosis

Mechanism of Arrhythmia Abnormal heart pulse formation Sinus pulse Ectopic pulse Triggered activity Abnormal heart pulse conduction Reentry Conduct block

Classification of Arrhythmia Abnormal heart pulse formation Sinus arrhythmia Atrial arrhythmia Atrioventricular junctional arrhythmia Ventricular arrhythmia Abnormal heart pulse conduction Sinus-atrial block Intra-atrial block Atrio-ventricular block Intra-ventricular block Abnormal heart pulse formation and conduction

Diagnosis of Arrhythmia Medical history Physical examination Laboratory test

Therapy Principal Pathogenesis therapy Stop the arrhythmia immediately if the hemodynamic was unstable Individual therapy

Anti-arrhythmia Agents Anti-tachycardia agents Anti-bradycardia agents

Anti-tachycardia agents Modified Vaugham Williams classification I class: Natrium channel blocker II class: ß-receptor blocker III class: Potassium channel blocker IV class: Calcium channel blocker Others: Adenosine, Digital

Anti-bradycardia agents ß-adrenic receptor activator M- cholinergic receptor blocker Non-specific activator

Clinical usage Anti-tachycardia agents: Ia class: Less use in clinic Guinidine Procainamide Disopyramide: Side effect: like M- cholinergic receptor blocker

Anti-tachycardia agents: Ib class: Perfect to ventricular tachyarrhythmia 1. Lidocaine 2. Mexiletine

Anti-tachycardia agents: Ic class: Can be used in ventricular and/or supra-ventricular tachycardia and extrasystole. 1. Moricizine 2. Propafenone

Anti-tachycardia agents: II class: ß-receptor blocker Propranolol: Non-selective Metoprolol: Selective ß 1 -receptor blocker, Perfect to hypertension and coronary artery disease patients associated with tachyarrhythmia.

Anti-tachycardia agents: III class: Potassium channel blocker, extend-spectrum anti-arrhythmia agent. Amioarone: Perfect to coronary artery disease and heart failure patients Sotalol: Has ß-blocker effect Bretylium

Anti-tachycardia agents: IV class: be used in supraventricular tachycardia Verapamil Diltiazem Others: Adenosine: be used in supraventricular tachycardia

Anti-bradycardia agents Isoprenaline Epinephrine Atropine Aminophylline

Proarrhythmia effect of antiarrhythmia agents Ia, Ic class: Prolong QT interval, will cause VT or VF in coronary artery disease and heart failure patients III class: Like Ia, Ic class agents II, IV class: Bradycardia

Non-drug therapy Cardioversion: For tachycardia especially hemodynamic unstable patient Radiofrequency catheter ablation (RFCA): For those tachycardia patients (SVT, VT, AF, AFL) Artificial cardiac pacing: For bradycardia, heart failure and malignant ventricular arrhythmia patients.

Sinus tachycardia Sinus rate > 100 beats/min (100-180) Causes: Some physical condition: exercise, anxiety, exciting, alcohol, coffee Some disease: fever, hyperthyroidism, anemia, myocarditis Some drugs: Atropine, Isoprenaline Needn’t therapy

Sinus Bradycardia Sinus rate < 60 beats/min Normal variant in many normal and older people Causes: Trained athletes, during sleep, drugs ( ß-blocker ) , Hypothyriodism, CAD or SSS Symptoms: Most patients have no symptoms. Severe bradycardia may cause dizziness, fatigue, palpitation, even syncope. Needn’t specific therapy , If the patient has severe symptoms, planted an pacemaker may be needed.

Sinus Arrest or Sinus Standstill Sinus arrest or standstill is recognized by a pause in the sinus rhythm. Causes: myocardial ischemia, hypoxia, hyperkalemia, higher intracranial pressure, sinus node degeneration and some drugs (digitalis, ß-blocks) . Symptoms: dizziness, amaurosis, syncope Therapy is same to SSS

Sinoatrial exit block (SAB) SAB: Sinus pulse was blocked so it couldn’t active the atrium. Causes: CAD, Myopathy, Myocarditis, digitalis toxicity, et al. Symptoms: dizziness, fatigue, syncope Therapy is same to SSS

Sinoatrial exit block (SAB) Divided into three types: Type I, II, III Only type II SAB can be recognized by EKG.

Sick Sinus Syndrome (SSS) SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node automaticity and SA conduction. Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, tumor, trauma and congenital disease. With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythms Bradycardia-tachycardia syndrome

Sick Sinus Syndrome (SSS) EKG Recognition: Sinus bradycardia, ≤40 bpm ; Sinus arrest > 3s Type II SAB Nonsinus tachyarrhythmia ( SVT, AF or Af). SNRT > 1530ms, SNRTc > 525ms Instinct heart rate < 80bmp

Sick Sinus Syndrome (SSS) Therapy: Treat the etiology Treat with drugs: anti-bradycardia agents, the effect of drug therapy is not good. Artificial cardiac pacing.

Premature contractions The term “premature contractions” are used to describe non sinus beats. Common arrhythmia The morbidity rate is 3-5%

Atrial premature contractions (APCs) APCs arising from somewhere in either the left or the right atrium. Causes: rheumatic heart disease, CAD, hypertension, hyperthyroidism, hypokalemia Symptoms: many patients have no symptom, some have palpitation, chest incomfortable. Therapy: Needn’t therapy in the patients without heart disease. Can be treated with ß-blocker, propafenone, moricizine or verapamil.

Atrial tachycardia Classify by automatic atrial tachycardia (AAT); intra-atrial reentrant atrial tachycardia (IART); chaotic atrial tachycardia (CAT). Etiology: atrial enlargement, MI; chronic obstructive pulmonary disease; drinking; metabolic disturbance; digitalis toxicity; electrolytic disturbance.

Atrial tachycardia May occur transient; intermittent; or persistent. Symptoms: palpitation; chest uncomfortable, tachycardia may induce myopathy. Auscultation: the first heart sound is variable

Intra-atrial reentry tachycardia (IART) ECG characters: Atrial rate is around 130-150bpm; P’ wave is different from sinus P wave; P’-R interval ≥ 0.12” Often appear type I or type II, 2:1 AV block; EP study: atrial program pacing can induce and terminate tachycardia

Automatic atrial tachycardia (AAT) ECG characters: Atrial rate is around 100-200bpm; Warmup phenomena P’ wave is different from sinus P wave; P’-R interval ≥ 0.12” Often appear type I or type II, 2:1 AV block; EP study: Atrial program pacing can’t induce or terminate the tachycardia

Chaotic atrial tachycardia (CAT) Also termed “Multifocal atrial tachycardia”. Always occurs in COPD or CHF, Have a high in-hospital mortality ( 25-56%). Death is caused by the severity of the underlying disease. ECG characters: Atrial rate is around 100-130bpm; The morphologies P’ wave are more than 3 types. P’-P’, P’-R and R-R interval are different. Will progress to af in half the cases EP study: Atrial program pacing can’t induce or terminate the tachycardia

Therapy IRAT: Esophageal Pulsation Modulation, RFCA, Ic and IV class anti-tachycardia agents AAT: Digoxin, IV, II, Ia and III class anti-tachycardia agents; RFCA CAT: treat the underlying disease, verapamil or amiodarone. Associated with SSS: Implant pace-maker.

Atrial flutter Etiology: It can occur in patients with normal atrial or with abnormal atrial. It is seen in rheumatic heart disease (mitral or tricuspid valve disease), CAD, hypertension, hyperthyroidism, congenital heart disease, COPD. Related to enlargement of the atria Most AF have a reentry loop in right atrial

Atrial flutter Symptoms: depend on underlying disease, ventricular rate, the patient is at rest or is exerting With rapid ventricular rate: palpitation, dizziness, shortness of breath, weakness, faintness, syncope, may develop angina and CHF.

Atrial flutter Therapy: Treat the underlying disease To restore sinus rhythm: Cardioversion, Esophageal Pulsation Modulation, RFCA, Drug (III, Ia, Ic class). Control the ventricular rate: digitalis. CCB, ß-block Anticoagulation

Atrial fibrillation Subdivided into three types: paroxysmal, persistent, permanent. Etiology: Morbidity rate increase in older patients Etiology just like atrial flutter Idiopathic Mechanism: Multiple wavelet re-entry; Rapid firing focus in pulmonary vein, vena cava or coronary sinus.

Atrial fibrillation Manifestation: Affected by underlying diseases, ventricular rate and heart function. May develop embolism in left atrial. Have high incidence of stroke. The heart rate, S1 and rhythm is irregularly irregular If the heart rhythm is regular, should consider about (1) restore sinus rhythm; (2) AF with constant the ratio of AV conduction; (3) junctional or ventricular tachycardia; (4) slower ventricular rate may have complete AV block.

Atrial fibrillation Therapy: Treat the underlying disease Restore sinus rhythm: Drug, Cardioversion, RFCA, Maze surgery Rate control: digitalis. CCB, ß-block Antithrombotic therapy: Aspirine, Warfarin

Atrioventricular Junctional arrhythmia

Atrioventricular junctional premature contractions Etiology and manifestation is like APCs Therapy the underlying disease Needn’t anti-arrhythmia therapy.

Nonparoxysmal AV junctional tachycardia Mechanism: relate to hyper-automaticity or trigger activity of AV junctional tissue Etiology: digitalis toxicity; inferior MI; myocarditis; acute rheumatic fever and postoperation of valve disease ECG: the heart rate ranges 70-150 bpm or more, regular, normal QRS complex, may occur AV dissociation and wenckebach AV block

Nonparoxysmal AV junctional tachycardia Therapy: Treat underlying disease; stopping digoxin, administer potassium, lidocaine, phenytoin or propranolol. Not for DC shock It can disappear spontaneously. If had good tolerance, not require therapy.

Paroxysmal tachycardia Most PSVT (paroxysmal supraventricular tachycardia) is due to reentrant mechanism. The incidence of PSVT is higher in AVNRT (atrioventricular node reentry tachycardia) and AVRT (atioventricular reentry tachycardia), the most common is AVNRT (90%) Occur in any age individuals, usually no structure heart disease.

Paroxysmal tachycardia Manifestation: Occur and terminal abruptly. Palpitation, dizziness, syncope, angina, heart failure and shock. The sever degree of the symptom is related to ventricular rate, persistent duration and underlying disease

Paroxysmal tachycardia ECG characteristic of AVNRT Heart rate is 150-250 bpm, regular QRS complex is often normal, wide QRS complex is with aberrant conduction Negative P wave in II III aVF, buried into or following by the QRS complex. AVN jump phenomena

Paroxysmal tachycardia ECG characteristic of AVRT Heart rate is 150-250 bpm, regular In orthodromic AVRT, the QRS complex is often normal, wide QRS complex is with antidromic AVRT Retrograde P’ wave, R-P’>110ms.

Paroxysmal tachycardia Therapy: AVNRT & orthodromic AVRT Increase vagal tone: carotid sinus massage, Valsalva maneuver.if no successful, Drug: verapamil, adrenosine, propafenone DC shock Antidromic AVRT: Should not use verapamil, digitalis, and stimulate the vagal nerve. Drug: propafenone, sotalol, amiodarone RFCA

Pre-excitation syndrome (W-P-W syndrome) There are several type of accessory pathway Kent: adjacent atrial and ventricular James: adjacent atrial and his bundle Mahaim: adjacent lower part of the AVN and ventricular Usually no structure heart disease, occur in any age individual

WPW syndrome Manifestation: Palpitation, syncope, dizziness Arrhythmia: 80% tachycardia is AVRT, 15-30% is AFi, 5% is AF, May induce ventricular fibrillation

WPW syndrome Therapy: Pharmacologic therapy: orthodrome AVRT or associated AF, AFi, may use Ic and III class agents. Antidromic AVRT can’t use digoxin and verapamil. DC shock: WPW with SVT, AF or Afi produce agina, syncope and hypotension RFCA

Ventricular Premature Contractions (VPCs) Etiology: Occur in normal person Myocarditis, CAD, valve heart disease, hyperthyroidism, Drug toxicity (digoxin, quinidine and anti-anxiety drug) electrolyte disturbance, anxiety, drinking, coffee

VPCs Manifestation: palpitation dizziness syncope loss of the second heart sound

PVCs Therapy: treat underlying disease, antiarrhythmia No structure heart disease: Asymptom: no therapy Symptom caused by PVCs: antianxiety agents, ß -blocker and mexiletine to relief the symptom. With structure heart disease (CAD, HBP): Treat the underlying diseas ß -blocker, amiodarone Class I especially class Ic agents should be avoided because of proarrhytmia and lack of benefit of prophylaxis

Ventricular tachycardia Etiology: often in organic heart disease CAD, MI, DCM, HCM, HF, long QT syndrome Brugada syndrome Sustained VT (>30s), Nonsustained VT Monomorphic VT, Polymorphic VT

Ventricular tachycardia Torsades de points (Tdp): A special type of polymorphic VT, Etiology: congenital (Long QT), electrolyte disturbance, antiarrhythmia drug proarrhythmia (IA or IC), antianxiety drug, brain disease, bradycardia

Ventricular tachycardia Accelerated idioventricular rhythm: Related to increase automatic tone Etiology : Often occur in organic heart disease, especially AMI reperfusion periods, heart operation, myocarditis, digitalis toxicity

VT Manifestation: Nonsustained VT with no symptom Sustained VT : with symptom and unstable hemodynamic, patient may feel palpitation, short of breathness, presyncope, syncope, angina, hypotension and shock.

VT ECG characteristics: Monomorphic VT: 100-250 bpm, occur and terminate abruptly,regular Accelerated idioventricular rhythm: a runs of 3-10 ventricular beats, rate of 60-110 bpm, tachycardia is a capable of warm up and close down, often seen AV dissociation, fusion or capture beats Tdp: rotation of the QRS axis around the baseline, the rate from 160-280 bpm, QT interval prolonged > 0.5s, marked U wave

Treatment of VT Treat underlying disease Cardioversion: Hemodynamic unstable VT (hypotension, shock, angina, CHF) or hemodynamic stable but drug was no effect Pharmacological therapy: ß-blockers, lidocain or amiodarone RFCA, ICD or surgical therapy

Therapy of Special type VT Accelerated idioventricular rhythm: usually no symptom, needn’t therapy. Atropine increased sinus rhythm Tdp: Treat underlying disease, Magnesium iv, atropine or isoprenaline, ß -block or pacemaker for long QT patient temporary pacemaker

Ventricular flutter and fibrillation Often occur in severe organic heart disease: AMI, ischemia heart disease Proarrhythmia (especially produce long QT and Tdp), electrolyte disturbance Anaesthesia, lightning strike, electric shock, heart operation It’s a fatal arrhythmia

Ventricular flutter and fibrillation Manifestation: Unconsciousness, twitch, no blood pressure and pulse, going to die Therapy: Cardio-Pulmonary Resuscitate (CPR) ICD

Cardiac conduction block Block position: Sinoatrial; intra-atrial; atrioventricular; intra-ventricular Block degree Type I: prolong the conductive time Type II: partial block Type III: complete block

Atrioventricular Block AV block is a delay or failure in transmission of the cardiac impulse from atrium to ventricle. Etiology: Atherosclerotic heart disease; myocarditis; rheumatic fever; cardiomyopathy; drug toxicity; electrolyte disturbance, collagen disease, lev’s disease.

AV Block AV block is divided into three categories: First-degree AV block Second-degree AV block: further subdivided into type I and type II Third-degree AV block: complete block

AV Block Manifestations: First-degree AV block: almost no symptoms; Second degree AV block: palpitation, fatigue Third degree AV block: Dizziness, agina, heart failure, lightheadedness, and syncope may cause by slow heart rate, Adams-Stokes Syndrome may occurs in sever case. First heart sound varies in intensity, will appear booming first sound

AV Block Treatment: I or II degree AV block needn’t antibradycardia agent therapy II degree II type and III degree AV block need antibradycardia agent therapy Implant Pace Maker

Intraventricular Block Intraventricular conduction system: Right bundle branch Left bundle branch Left anterior fascicular Left posterior fascicular

Intraventricular Block Etiology: Myocarditis, valve disease, cardiomyopathy, CAD, hypertension, pulmonary heart disease, drug toxicity, Lenegre disease, Lev’s disease et al. Manifestation: Single fascicular or bifascicular block is asymptom; tri-fascicular block may have dizziness; palpitation, syncope and Adams-stokes syndrome

Intraventricular Block Therapy: Treat underlying disease If the patient is asymptom; no treat, bifascicular block and incomplete trifascicular block may progress to complete block, may need implant pace maker if the patient with syncope

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