16 arrhythmias2009

Cardiac ArrhythmiasLiu Pin-Ming, M.D., Ph.D.

Professor of MedicineDepartment of CardiologySun Yat-sen Memorial HospitalSun Yat-sen University

Master the causes, clinical manifestations, ECG characteristics and management principles of common arrhythmias

Be familiar with the classification of arrhythmias, and its relevant cardiac electrophysiological mechanisms, and pharmacological treatment of tachyarrhythmias

Learning Objectives

The Cardiac Conduction System

Normal sinus rhythm Sinoatrial node is cardiac

pacemaker Normal sinus rhythm 60-

100 beats/min Depolarisation triggers

depolarisation of atrial myocardium (‘forest fire’)

Conducts more slowly through AV node

Conducts rapidly through His bundles and Purkinje fibres

Arrhythmias Definition: An arrhythmia is an abnormality of rate,

regularity, or site of origin of the cardiac impulse or a disturbance in conduction that causes an abnormal sequence of activation.

Irregular rhythm Abnormal Rate Conduction abnormality

Clinical classification of arrhythmias

Heart rate (increased/decreased)

Heart rhythm (regular/irregular) Site of origin

(supraventricular/ventricular) QRS complexes on ECG

(narrow/broad)

Mechanisms Responsible for Arrhythmias

Abnormalities of impulse generation A. Alterations of normal automaticity B. Abnormal automaticity C. Triggered activity Early/Delayed afterdepolarization Abnormalities of impulse conduction A. Reentry: 1. Unidirectional block; 2.

Anatomic or functional reentrant circuit ; 3. wavelength

B. Conduction block Combined abnormalities of impulse generation

and conduction

A: Contractile cellB: Autorhythmic cell:spontaneous depolarization at phase 4

Transmembrane Potentials of Myocardial Cells

Alterations of normal automaticity

Autonomic neurotransmitters

Triggered activity: Early/Delayed afterdepolarization

Re-Entry Mechanism Branch 2 has a unidirectional block Impulses can travel retrograde (3 to 2) but not

orthograde. An AP will travel down the branch 1, into the

common distal path (br 3), then travel retrograde through the unidirectional block in branch 2.

When the AP exits the block, if it finds the tissue excitable, it will continue by traveling down (reenter) the branch 1.

If it finds the tissue unexcitable (ERP) the AP will die.

Timing is critical –AP exiting the block must find excitable tissue to propagate.

If it can re-excite the tissue, a circular pathway of high frequency impulses (tachyarrhythmia) will become the source of APs that spread throughout a region of the heart (ventricle) or the entire heart.

Reentrant Arrhythmias

Anatomic or

functional

reentrant circuit

Unidirectional

block on one

path;

Slow conduction

on the other path

Necessitating 3 requirements

Diagnostic Approaches to Arrhythmias

History and physical examination ECG Ambulatory ECG recording: Holter

recording Exercise ECG: treadmill test Trans-esophageal

electrophysiological study Invasive electrophysiological study

(EPS)

Management of Arrhythmias Antiarrhythmic drugs Cardiac pacemakers DC cardioversion/defibrillation Implantable cardioverter/defibrillater (ICD) Radiofrequency catheter ablation Surgical operation

Non-pharmacological Pharmacological (All

antiarrhythmic agents may also be proarrhythmic)

Vaughan Williams classification of antiarrhythmic drugs

Class I: block sodium channels Ia (quinidine, procainamide,

disopyramide) AP Ib (lignocaine) AP Ic (flecainide) AP

Class II: β-adrenoceptor antagonists (propranolol, sotalol)

Class III: prolong action potential and prolong refractory period (suppress re-entrant rhythms) (amiodarone, sotalol)

Class IV: Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil, diltiazem)

Phase 4

Phase 0

Phase 1

Phase 2

Phase 3

0 mV

-80mV

II

IIII

IV

How about others: adenosine, digoxin?

Atrial fibrillation: Common Causes

Coronary artery disease Hypertensive heart disease Valvular heart disease, mitral stenosis Cardiomyopathy Thyrotoxicosis Occasionally, no structural heart

disease, especially paroxysmal atrial fibrillation

Atrial Fibrillation: ECG Characteristics

Absence of P waves Very irregular baseline, f waves, with a

rate of 350-600 bpm, best seen in V1, Ⅱ Irregular QRS complex rate, usually

normal shape

Atrial Fibrillation

Atrial Fibrillation: Auscultation Features

Variation in the intensity of S1 Extremely irregular heart rate Pulse deficit (because each

contraction is not sufficiently strong to open the aortic valve or transmit an arterial pressure wave through the peripheral arteries)

Atrial fibrillation: Clinical Considerations Decreased hemodynamic functions —— rapid ventricular rates —— the loss of atrial contraction Risk of systemic embolism 5 to 7 times greater than that in

controls

Atrial fibrillation: Classification and Management Strategies

Paroxysmal (<24-48hr): preventing further attacks

Persistent: attempting restoration of sinus rhythm

Permanent: offering good control of ventricular rate

Atrial Fibrillation: Treatment Etiological therapy Restoration of sinus rhythm paroxysmal: beta-blocker, propafenone,

cedilanid, amiodarone persistent: drugs, DC cardiovertion Control on the ventricular rate digoxin, betablocker Prevention of thromboembolism aspirin or clopidogrel, warfarin

Atrial flutter: Characteristics Regular sawtooth like wave with a

rate of 250-350 bpm Ventricular response may be 1:1

(300), 2:1 (150), 3:1 (100) or 4:1 (75), etc

Severity of the symptoms depends on the ventricular rate

Causes are similar to atrial fibrillation

Atrial flutter: ECG

Paroxysmal SVT—— AVNRT & AVRT: ECG Features

Sudden initiation and termination Fixed relationship between p wave

and QRS complex, with p often superimposed in ORS-T

Regular rate of 150-250 bpm Narrow QRS complexes unless there

is an aberrant ventricular conduction or pre-existing bundle branch block

Paroxysmal SVT—— AVNRT & AVRT: ECG Features

Mechanism Responsible for AVNRT

Pre-excitation syndrome

Abnormal connection between the atrium and the ventricle

Pre-excitation syndrome ECG Features

Short PR interval Slurred upstroke of

QRS complexes (the delta wave)

broad QRS complexes Secondary ST-T

abnormalities (reflecting modified ventricular repolarization secondary to abnormal depolariozation 11111

Mechanism Responsible for AVRT

Pre-excitation Syndrome (WPW)

Paroxysmal SVT: Treatment Vagal maneuvers: Valsalva maneuver or

carotid sinus massage First choice of drugs: adenosine 6-12

mg iv, or verapamil 5 mg iv Preferred choice of drugs: propafenone

70 mg iv; cedilanid 0.4-0.6 mg iv Synchronized DC cardioversion (shock

delivery that is timed within the QRS complex

Radiofrequency catheter ablation

Radiofrequency Catheter Ablation

Premature Beats Atrial AV junctional Ventricular Clinical considerations ECG features Management

strategies

Normal AP Conduction in Ventricles

Initiation site

Normal conduction

VPB conduction

Ventricular Premature Beats

Atrial Premature Beats

Ventricular Tachycardia ECG: ≥3 VPBs in succession at a rate of

100-250 bpm; suggesting VT: ventricular captures, fusion complexes

Clinical: coronary heart disease, AMI; dilated cardiomyopathy; signifying myocardial damage

Treatment: drugs (lidocaine, amiodarone) DC cardioversion (synchronized)

Ventricular Tachycardia ECG: ≥3 VPBs in

succession at a rate of 100-250 bpm;

Non-sustained VT ( ＜ 30 sec), sustained VT

suggesting VT: ventricular captures, fusion complexes

Ventricular Tachycardia A wide QRS tachycardia is VT until proven otherwise. Features suggesting VT include: evidence of AV dissociation independent P waves (shown by arrows here) capture or fusion beats beat to beat variability of the QRS morphology very wide complexes (> 140 ms) same morphology in tachycardia as in ventricular

ectopics history of ischaemic heart disease absence of any rS, RS or Rs complexes in the chest leads concordance (chest leads all positive or negative)

Ventricular Tachycardia

A54 year-old woman collapsed 24 hours post MI

Torsades de Pointes (TDP) ECG: an irregular rapid ventricular

rhythm with a periodic twisting axis seen on ECG; long QT interval

Etiology: congenital long QT syndrome; acquired long QT syndrome, as antiarrhythmic drugs (ClassⅠa, ClassⅢ); hypokalamia, hypomagnesemia

Torsades de Pointes (TDP)

Torsades de Pointes Management

Identifying and treating any precipitating factors

MgSO4, IV; avoidance of drugs lengthening APD

Atropine, isoprenaline infusion or ventricular pacing to increase heart rate

Beat-blocker for congenital long QT sydrome

Ventricular Flutter / Fibrillation

Irregular rapid ventricular depolarization No organized ventricular contractions,

no pulse, loss of consciousness Most common cause: AMI, drug toxicity,

electrolyte disturbances, electric shock, end stage of many disease processes

Management: non-synchronized DC defibrillation, cardiopulmonary resuscitation

Ventricular Fibrillation

Chaotic ventricular electrical activity which causes the heart to lose the ability to function

as a pump.

DC Defibrillation

Defibrillator: used to "shock" the heart from an abnormal

rhythm pattern back into a normal rhythm

Sick Sinus Syndrome (SSS) Definition:characterized by intrinsic

inadequacy of sinus node pacemaking and /or conduction failure between sinus node and the rest of the atrium

Etiology: coronary heart disease, degenerative process, cardiomyopathy

Clinical manifestations: insufficiency of blood supply to important organs

Sick Sinus Syndrome (SSS) ECG Features

Marked sinus bradycardia < 50 bpm measured as SNRT, SACT and IHR

Sinus arrest / sinoatrial block Holter recording

Bradycardia-tachycardia syndrome atrial tachyarrhythmias

Probable coexistence with atrioventricular block

Sick Sinus Syndrome (SSS)

Atrioventricular Block

Pacemaker Implantation

Failure to generate enough impulses on time Pauses may last for several seconds and cause syncope Definitive therapy for symptomatic bradyarrhythmias

requires pacemaker implantation

.

Cardiac Arrhythmias Questions?

What are the common causes, ECG features, auscultation characteristics and management strategies of atrial fibrillation?

Please list the management protocols of paroxysmal supraventricular tachycardia

Please list the concept and ECG findings of sick sinus syndrome

Please consider the differential diagnosis of wide QRS tachycardia

Cardiac Arrhythmias

Thank you!

16 arrhythmias2009

Education

Transcript of 16 arrhythmias2009