Arrhythmias and Conduction Disorders

Professor V. Syvolap

Standard ECG Components
By convention, the ECG tracing is divided into the P wave, PR interval, QRS complex, QT interval, ST segment, T wave, and U wave

Normal rhythm 

The resting sinus heart rate in adults is usually 60 to 100 beats/min. Normally, a marked diurnal variation in heart rate occurs, with lowest rates just before early morning awakening. 

Normal rhythm  

A slight increase in rate during inspiration with a decrease in rate during expiration (respiratory sinus arrhythmia) is also normal; it is mediated by oscillations in vagal tone and is particularly common among healthy young people.

in advanced diabetes) or with severe heart failure. .Normal rhythm   The oscillations lessen but do not entirely disappear with age. Absolute regularity of the sinus rhythm rate is pathologic and occurs in patients with autonomic denervation (eg.

although SA node. AV node. The P wave represents atrial depolarization. and the T wave represents ventricular repolarization. The QRS complex represents ventricular depolarization.Normal rhythm   Most cardiac electrical activity is represented on the ECG. and His-Purkinje Hisdepolarization does not involve enough tissue to be detected. .

Normal rhythm  The PR interval (from the beginning of the P wave to the beginning of the QRS complex) is the time from the beginning of atrial activation to the beginning of ventricular activation. . Much of this interval reflects slowing of impulse transmission in the AV node.

Normal rhythm  The R-R interval (time between 2 RQRS complexes) represents the ventricular rate. .

The most common formula (all intervals in sec) is: .Normal rhythm    The QT interval (from the beginning of the QRS complex to the end of the T wave) represents the duration of ventricular depolarization. The QT interval is corrected (QTc) for influence of heart rate. they are also longer with a slower heart rate. Normal values for the QT interval are slightly longer in women.

Sinus bradycardia Slower rates (heart rate less then (heart 60 b/m) occur in young people. b/m) particularly athletes and during sleep. .

b/m) or emotion through sympathetic neural and circulating catecholamine drive. .Sinus tachycardia Faster rates (heart rate more then (heart 100 b/m) occur with exercise. illness.

.  or both.  impulse conduction.Pathophysiology Rhythm disturbances result from  abnormalities of impulse formation.

principally within the AV node or the His-Purkinje Hissystem.Bradyarrhythmias result from decreased intrinsic pacemaker function or blocks in conduction. .

Tachyarrhythmias Most tachyarrhythmias are caused by  reentry.  some result from enhanced normal automaticity  or from abnormal mechanisms of automaticity. .

Reentry is the circular propagation of an impulse around 2 interconnected pathways with different conduction characteristics and refractory periods .

Pathway A has slower conduction and a shorter refractory period. Pathway B conducts normally and has a longer refractory period.Reentry Two pathways connect the same points. .

Reentry I. Conduction through pathway A is slower and finds tissue at 2 already depolarized and thus refractory. . A normal impulse arriving at 1 goes down both A and B pathways. A normal sinus beat results.

A premature supraventricular beat with an increased PR interval results. On arriving at 2. where it is blocked by refractory tissue at 3. the impulse continues forward and retrograde up pathway B. but it can be conducted on pathway A because its refractory period is shorter. . A premature impulse finds pathway B refractory and is blocked.Reentry II.

sending an impulse each cycle to the ventricle (4) and retrograde to the atrium (5). . If pathway A is also past its refractory period. a premature impulse may continue retrograde all the way up pathway B. If conduction over pathway A is sufficiently slow. the impulse may reenter pathway A and continue to circle. producing a sustained reentrant tachycardia. which is now past its refractory period.Reentry III.

are common episodic impulses. alcohol. pseudoephedrine) tea. . coffee. They are common in patients with COPD. or premature atrial contractions (PACs). pseudoephedrine) or may be a sign of a cardiopulmonary disorder.Atrial premature beats Atrial premature beats (APBs). They may occur in normal hearts with or without precipitating factors (eg.

. Aberrantly conducted APBs (usually with right bundle branch block morphology) must be distinguished from premature beats of ventricular origin.Atrial premature beats Diagnosis is by ECG APBs may be normally. or not conducted and are usually followed by a noncompensatory pause. aberrantly.

. the sinus node pacemaker is reset. the T wave is deformed by an APB. Because the APB occurs relatively early during the sinus cycle. and a pause less than fully compensatory precedes the next sinus beat.Atrial premature beats In lead II. after the 2nd beat of sinus origin.

rapid atrial activation from a single atrial focus. with a very rapid atrial rate. however.Atrial tachycardia Atrial tachycardia is a regular rhythm caused by the consistent. Heart rate is usually 150 to 200 beats/min. and ventricular rate may be slower. nodal dysfunction. or digitalis toxicity. . atrioventricular (AV) block may be present.

. Other causes include atrial irritation (eg. digoxin).Atrial tachycardia Mechanisms include enhanced atrial automaticity and intra-atrial reentry. inhalation. drugs (eg. alcohol. pericarditis). intraAtrial tachycardia is the least common form (5%) of supraventricular tachycardia and usually occurs in patients with a structural heart disorder. and toxic gas digoxin).

which differ in morphology from normal sinus P waves. precede QRS complexes but may be hidden within the preceding T wave .Atrial tachycardia Symptoms are those of other tachycardias. Diagnosis is by ECG. P waves.

Atrial tachycardia This narrow QRS tachycardia arises from an abnormal automatic focus or intra-atrial reentry. P waves precede intrathe QRS complexes. . it is a long RP tachycardia (PR < RP).

. Heart rate is 60 to 120 beats/min. acute inferior MI. or digitalis toxicity. myocarditis.Nonparoxysmal junctional tachycardia Nonparoxysmal junctional tachycardia is caused by abnormal automaticity in the AV node or adjacent tissue. symptoms are usually absent. which typically follows open heart surgery. thus.

Nonparoxysmal junctional tachycardia ECG shows regular. normal-appearing normalQRS complexes without identifiable P waves or with retrograde P waves (inverted in the inferior leads) that occur shortly before (< 0. The rhythm is distinguished from paroxysmal supraventricular tachycardia by the lower heart rate and gradual onset and offset. .1 sec) or after the QRS complex.

.Ventricular premature beats (VPBs) are single ventricular impulses caused by reentry within the ventricle or abnormal automaticity of ventricular cells. VPBs may be asymptomatic or cause palpitations. They are extremely common in healthy patients and in patients with a heart disorder. Diagnosis is by ECG.

anxiety. sympathomimetic drugs).Ventricular premature beats Ventricular premature beats (VPBs). stress. caffeine. hypoxia. every 3rd [trigeminy] or 2nd [bigeminy] beat). also called premature ventricular contractions (PVCs). may occur erratically or at predictable intervals (eg. or electrolyte abnormalities. VPBs may increase with stimulants (eg. . alcohol.

. mild hemodynamic symptoms are possible because the sinus rate has been effectively halved.Ventricular premature beats VPBs may be experienced as missed or skipped beats. particularly when they represent every 2nd heart beat. When VPBs are very frequent. the VPB itself is not sensed but rather the following augmented sinus beat. Existing ejection murmurs may be accentuated because of increased cardiac filling and augmented contractility after the compensatory pause.

Ventricular premature beats Diagnosis is by ECG showing a wide QRS complex without a preceding P wave. . typically followed by a fully compensatory pause.

.Prognosis VPBs are not significant in patients without a heart disorder. and no treatment is required beyond avoiding obvious triggers.

.Ventricular tachycardia is 3 consecutive ventricular beats at a rate 120 beats/min. Symptoms depend on duration and vary from none to palpitations to hemodynamic collapse and death. Diagnosis is by ECG.

they are usually benign and are not treated unless associated with hemodynamic symptoms.Ventricular tachycardia Some experts use a cutoff rate of 100 beats/min for ventricular tachycardia (VT). Repetitive ventricular rhythms at slower rates are called accelerated idioventricular rhythms or slow VT. .

. Electrolyte abnormalities (particularly hypokalemia or hypomagnesemia). The long QT syndrome (congenital or acquired) is associated with a particular form of VT. and adverse drug effects contribute. hypoxemia. acidemia. particularly prior MI or a cardiomyopathy.Ventricular tachycardia    Most patients with VT have a significant heart disorder. torsades de pointes.

Ventricular tachycardia VT may be monomorphic or polymorphic and nonsustained or sustained. Monomorphic VT results from a single abnormal focus or reentrant pathway and has regular. identical-appearing identicalQRS complexes. .

.Ventricular tachycardia Polymorphic VT results from several different foci or pathways and is thus irregular. arrest. with varying QRS complexes. VT frequently deteriorates to ventricular fibrillation and thus cardiac arrest. Nonsustained VT lasts < 30 sec. sustained VT lasts 30 sec or is terminated sooner because of hemodynamic collapse.

causing palpitations. symptoms of hemodynamic compromise. . or sudden cardiac death.Symptoms and Signs VT of short duration or slow rate may be asymptomatic. Sustained VT is almost always symptomatic.

12 sec) should be considered VT until proved otherwise.Diagnosis VT is by ECG Any wide QRS complex tachycardia (QRS 0. .

. and a frontalfrontalplane QRS axis in the northwest quadrant. uniformity of QRS vectors in the V leads (concordance) with discordant T-wave vector T(opposite QRS vectors). fusion Por capture beats.Diagnosis VT is by ECG Diagnosis is supported by ECG findings of dissociated P-wave activity.

.Diagnosis VT is by ECG Differential diagnosis includes supraventricular tachycardia conducted with bundle branch block or via an accessory pathway.

. with the polarity of complexes shifting around the baseline. ECG between episodes shows a long QT interval after correction for heart rate (QTc).Torsades de pointes ventricular tachycardia Diagnosis is by ECG showing an undulating QRS axis.44 sec. A family history may suggest a congenital syndrome. Normal values average about 0. although they vary among individuals and by sex.

Ventricular fibrillation (VF) is due to multiple wavelet reentrant electrical activity and is manifested on ECG by ultrarapid baseline undulations that are irregular in timing and morphology .

or Brugada syndrome). hypoxemia. arrhythmogenic right ventricular dysplasia [ARVD]. most patients with VF have an underlying heart disorder (typically ischemic. but also hypertrophic or dilated cardiomyopathies. Overall. or ischemia. . acidosis. Risk of VF in any disorder is increased by electrolyte abnormalities.Ventricular fibrillation (VF) VF is the presenting rhythm for about 70% of patients in cardiac arrest and is thus the terminal event in many disorders.

Ventricular fibrillation (VF) .

irregularly irregular atrial rhythm .Atrial fibrillation  is a rapid.

dyspnea). but many patients have palpitations. vague chest discomfort. particularly when the ventricular rate is very rapid (often 140 to 160 beats/min). lightlightheadedness. weakness. . Patients may also present with symptoms and signs of acute stroke or of other organ damage due to systemic emboli.Symptoms and Signs AF AF is often asymptomatic. or symptoms of heart failure (eg.

. A pulse deficit (the apical ventricular rate is faster than the rate palpated at the wrist) may be present because left ventricular stroke volume is not always sufficient to produce a peripheral pressure wave at fast ventricular rates.Symptoms and Signs AF The pulse is irregularly irregular with loss of a waves in the jugular venous pulse.

Diagnosis is by ECG    Findings include: include: absence of P waves. f (fibrillatory) waves between QRS complexes (irregular in timing. irregular in morphology. baseline undulations at rates > 300/min not always apparent in all leads). and irregularly irregular R-R intervals R- .

Atrial fibrillation .

Atrial flutter Atrial flutter is a rapid regular atrial rhythm due to an atrial macromacroreentrant circuit. .

The atria depolarize at a rate of 250 to 350/min (typically 300/min). or 5:1 block may be present.Atrial flutter  Classical atrial flutter is due to a large reentrant circuit involving most of the right atrium. 4:1. . resulting in a regular ventricular rate of 150 beats/min. a fixed 3:1. Because the atrioventricular (AV) node cannot usually conduct at this rate. Less commonly. Sometimes block varies from moment to moment. typically ½ of the impulses get through (2:1 block). causing an irregular ventricular rhythm.

. there are likely to be few or no symptoms. Faster rates and variable AV conduction usually produce palpitations. If ventricular rate is < 120 beats/min and regular. Close inspection of the jugular venous pulse reveals flutter a waves. dyspnea. chest discomfort. and decreased cardiac output may produce symptoms of hemodynamic compromise (eg. syncope).Atrial flutter Symptoms and Signs Symptoms depend primarily on ventricular rate and the nature of any underlying heart disorder. weakness.

III. which shows continuous and regular atrial activation with a sawtooth pattern.Atrial flutter The diagnosis is by ECG. most obvious in leads II. and aVF .

Conduction Disorders .

The most common cause is idiopathic fibrosis and sclerosis of the conduction system.Atrioventricular (AV) block is partial or complete interruption of impulse transmission from the atria to the ventricles. symptoms and treatment depend on degree of block. usually involves pacing. when necessary. but treatment. . Diagnosis is by ECG.

.FirstFirst-degree AV block FirstFirst-degree AV block may be physiologic in younger patients with high vagal tone and in wellwelltrained athletes. but further investigation may be indicated when it accompanies another heart disorder or appears to be caused by drugs. First-degree AV Firstblock is rarely symptomatic and no treatment is required.

FirstFirst-degree AV block All normal P waves are followed by QRS complexes. but the PR interval is longer than normal (> 0.20 sec) sec) .

block. but some are not. Mobitz type I 2nd-degree AV 2ndblock. High-grade 2nd-degree AV block igh2nd-    . Three types exist: In Mobitz type I 2nd-degree AV 2ndblock.SecondSecond-degree AV block Some normal P waves are followed by QRS complexes.

AV nodal conduction resumes with the next beat. and the sequence is repeated . the 2ndPR interval progressively lengthens with each beat until the atrial impulse is not conducted and the QRS complex is dropped (Wenckebach phenomenon).Mobitz type I 2nd-degree 2ndAV block In Mobitz type I 2nd-degree AV block.

Beats are intermittently nonconducted and QRS complexes dropped.Mobitz type II 2nd2nddegree AV block In Mobitz type II 2nd-degree AV block. 2ndthe PR interval remains constant. usually in a repeating cycle of every 3rd (3:2 block) or (3:2 4th (4:3 block) P wave (4:3 .

High-grade 2nd-degree igh2ndAV block In high-grade 2nd-degree AV block. every high2nd2nd (or more) P wave is blocked .

There is no electrical communication between the atria and ventricles and no relationship between P waves and QRS complexes (AV dissociation). Cardiac function is maintained by an escape junctional or ventricular pacemaker.ThirdThird-degree AV block Heart block is complete. complete. .

in each of the two fascicles. . The result is extensive reorganization of the activation pattern of the left ventricle.Left Bundle Branch Block (LBBB) Left bundle branch block (LBBB) results from conduction delay or block in any of several sites in the intraventricular conduction system. within the fibers of the bundle of His that become the main left bundle branch. less commonly. or. including the main left bundle branch.

. abnormal QRS complexes. and STST-T wave abnormalities.ECG ABNORMALITIES LBBB    LBBB produces a prolonged QRS duration.

broad. . R waves are typically tall and S waves are deep. narrow r waves followed by deep S waves in the right precordial leads. and absent septal q waves. sometimes notched R waves in leads I and aVl and the left precordial leads.Commonly accepted diagnostic criteria for LBBB     Basic requirements include a prolonged QRS duration to 120 msec or beyond.

. it can be normal. Left axis deviation is associated with more severe conduction system disease that includes the fascicles as well as the main left bundle.Commonly accepted diagnostic criteria for LBBB   The mean QRS axis with LBBB is highly variable. whereas right axis deviation suggests dilated cardiomyopathy with biventricular enlargement. deviated to the right. less often. deviated to the left or.

and V6 ). . while the ST segment is elevated and the T wave is upright in leads with negative QRS complexes (leads V1 and V2 ). aVl . V5 . some electrocardiographers require a delayed intrinsicoid deflection (60 msec or greater) to diagnose LBBB. the ST segment is depressed and the T wave is inverted in leads with positive QRS waves (leads I. the ST wave and the T wave are discordant with the QRS complex. STST-T wave changes are also prominent with LBBB. In most cases.Commonly accepted diagnostic criteria for LBBB   In addition to these features. that is.


CLINICAL SIGNIFICANCE LBBB   LBBB usually appears in patients with underlying heart disease. . It is associated with significantly reduced longlong-term survival and with 10-year survival 10rates as low as 50 percent. probably reflecting the severity of the underlying cardiac disease.


Among patients with coronary artery disease, the presence of LBBB correlates with more extensive disease, more severe left ventricular dysfunction, and reduced survival rates. The duration of the QRS complex in LBBB correlates inversely with left ventricular ejection fraction. Patients with associated left or right axis deviation have more severe clinical manifestations.


In addition to the hemodynamic abnormalities produced by these underlying conditions, the abnormal ventricular activation pattern of LBBB itself induces hemodynamic perturbations, including abnormal systolic function with dysfunctional contraction patterns, reduced ejection fraction and lower stroke volumes, and abnormal diastolic function; reversed splitting of the second heart sound and functional mitral regurgitation are common. ECG patterns of LBBB, including low R wave amplitude in the midprecordial leads and ST-T wave STchanges, can simulate anterior infarct patterns.

Right Bundle Branch Block (RBBB)
Right bundle branch block is a result of conduction delay in any portion of the right-sided intraventricular rightconduction system.

Right Bundle Branch Block (RBBB)
The delay can occur in the main right bundle branch itself, in the bundle of His, or in the distal right ventricular conduction system.

Right Bundle Branch Block (RBBB) The latter is the common cause of RBBB after right ventriculotomy performed. to correct the tetralogy of Fallot. for example. The high prevalence of RBBB corresponds to the relative fragility of the right bundle branch. . as suggested by the development of RBBB after minor trauma produced by right ventricular catheterization.

ECG ABNORMALITIES RBBB As with LBBB. while leads I. the QRS complex duration exceeds 120 msec. The right precordial leads show prominent and notched R waves with rsr'. rsR'. and the left precordial leads demonstrate wide S waves that are longer in duration than the preceding R wave. or rSR' patterns. . aVl .

. The ST-T waves are. so T waves are inverted in the right precordial leads (and other leads with a terminal R' wave) and upright in the left precordial leads and in leads I and AVl . The mean QRS axis is not altered by RBBB. as in LBBB.ECG ABNORMALITIES RBBB Septal q waves are preserved because the initial ventricular activation remains unchanged. discordant STwith the QRS complex.


In the group without overt heart disease. . and cardiovascular mortality.CLINICAL SIGNIFICANCE RBBB is a common finding in the general population. congestive heart failure. However. the ECG finding has no prognostic significance. the new onset of RBBB does predict a higher rate of coronary artery disease. and many persons with RBBB have no clinical evidence of structural heart disease.

more extensive multivessel disease and reduced long-term survival in patients with ischemic heart disease. for example. the coexistence of RBBB suggests advanced disease with. .CLINICAL SIGNIFICANCE When cardiac disease is present. An entity known as the Brugada syndrome has been described in which a RBBB-like pattern with persistent ST segment elevation in the right precordial leads is associated with susceptibility to ventricular tachyarrhythmias and sudden cardiac death.

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