Electrocardiography

Bradyarrhythmias and blocks

Tachyarrhythmias > 100 beats/min

Supraventricular tachyarrhythmias
Ventricular tachyarrhythmias

Bradyarrhythmias < 60 beats/min

384

Sinus bradycardia
Physiological causes
Sleep, increase in vagal tone (sport, sinus carotis, eyeball
pressure)

Pathological causes
Acute inferior MI (right coronary occlusion limited supply of
sinoatrial and AV node), obstructive jaundice, increased
intracranial pressure, sinus node dysfunction, hypothermia,
hypothyroidism
Drugs: digoxin (SA toxicity), amiodarone, blockers, Caantagonists, morphine, quinine, sedato- hypnotics

385

Sinus bradycardia (~36 beats/min) with prominent U waves. Please determine QTc

386

Sinoatrial (SA) block

SA node depolarization is present, but conduction of impulses
to atrial tissue is impaired or blocked
1st-degree SA block
Type I 2nd-degree SA block (SA Wenckebach or SA Mobitz-type1)
Type II 2nd-degree SA block (SA Mobitz-Type-2)
3rd-degree SA block

387

Sinus arrest/pause
Transient sinus pause for seconds to minutes (P waves
disappear). The pause usually triggers escape activity in lower
pacemakers (e.g., atrial, junctional or ventricular)
Escape activity: atrial, junctional or ventricular escape beats or
rhythm
Junctional: narrow QRS and 40-60 beats/min
Ventricular: wide QRS and 15-40 beats/min

Long pauses cause dizziness and syncope

388

389

Sinus node dysfunction (formerly: sick sinus syndrome)

Sinoatrial (SA) dysfunction affects mainly the elderly and
develops as a result of chronic dysfunction of the sinoatrial
node
Patients are usually present with lightheadedness and/or
syncope or dyspnea, and palpitations.
Some degree of AV node dysfunction is seen in ~ 50% of people
with sinus node dysfunction

Sinus node dysfunction can appear in different forms

Inappropriate sinus bradycardia, sinoatrial exit block, sinus pause
or arrest, junctional or ventricular escape beats or rhythm,
tachycardia bardycardia syndrome (atrial tachycardia alternating
with bradycardia), chronic atrial fibrillation or atrial flutter
390

First-degree AV block
Consistently prolonged PR (PQ) interval: > 0.18 sec (child) >
0.2 sec (adult), > 0.22 (elderly)
Every P wave is followed by QRS (not a dysrhythmia)
First-degree AV block may be a normal finding in individuals
with no history of cardiac disease, especially in athletes
Other causes
Increased vagal tone
Ischemia or injury to the AV node or junction (acute inferior wall
MI)
Infiltrative diseases: amyloidosis, sarcoidosis, hemochromatosis
Drugs: digitalis, b-receptor antagonists
Inflammatory diseases: rheumatic heart disease, diphtheria,
Lymes disease
391
Hyperkalemia

PR interval of 360 ms duration in the presence of a heart rate of 62 beats/min.

PR interval of 580 ms duration in the presence of a heart rate of 45 beats/min.

392

Second-degree AV block Mobitz-I or Wenckebach

PR (PQ) interval is increased gradually, then one QRS is
missing and then the cycle starts again (Wenckebach
periodicity) The RR interval of the pause is less than the two
preceding RR intervals, and the RR interval after the pause is
greater than the RR interval before the pause.
Block: at the level of AV node and often associated with AV
nodal ischemia secondary to occlusion of the right coronary
artery (acute inferior wall MI) or due to increased
parasympathetic tone or the effects of medication
Risk of progression to this type of AV block to complete AV
block is low
393

RR ~ 60 beats/min; PR interval 280, 380, 440 ms;

RR ~ 80 beats/min; PR interval 120, 260 ms;

394

Second-degree AV block Mobitz-II

Not as frequent as Mobitz type-I, but more serious and
frequently progresses to complete AV block (prophylactic
pacemaker)
PR interval is constant (normal or increased); P wave is not
followed by QRS and QRS may show wide morphology (bundle
branch block)
If ventricular rate is
Within normal limits the patient may be asymptomatic
More commonly significantly slowed (symptoms: due to
decreased cardiac output)

Block: below the AV node at the bundle of His or bundle

branches (more commonly)
395

 Causes: disease of the left coronary artery or an anterior

myocardial infarction or acute myocarditis or other types of
organic heart disease

Second-degree AV block Mobitz-II 4:3

Regular sinus rhythm at a rate of 56 beats/min (bradycardia), constant PR interval of 188 ms, and nonconducted P
waves.
Wider s wawes may indicate incomplete right bundle branch block

396

Mobitz type II second-degree atrioventricular block (3:2, 2:1) with narrow QRS complex. The patient had
recurrent episodes of syncope. Because of the narrow QRS complex, the block is probably at the level of
the His bundle
397

Mobitz type II second-degree atrioventricular block. There is 3:2 conduction. Normal PR. The
QRS complex has left bundle branch block morphology.

398

Third-degree AV block
The atria and ventricles beat independently of each other (atrioventricular dissociation) Cannon a waves: contraction of the
right atrium against a closed tricuspid valve (jugular pulse)
Impulses are blocked at the AV node, bundle of His, or bundle
branches.
If the QRS is narrow, block is higher in the junction
Rate: 40-60 bpm
If the patient is symptomatic: atropine and/or transcutaneous pacing

If the QRS is wide (> 0.1 sec), block is very low in His bundle or
confined to bundle branches
Potentially lethal (Stokes-Adams-Morgagni syndrome: circulatory
collapse [no pulse and blood pressure], unconsciousness,
convulsions, cyanosis)
399

 If the patient is symptomatic: transcutaneous pacing should be instituted

and permanent transvenous pacemaker should be inserted

Causes
Acute MI
Open heart surgery (valve replacement)
Congenital or acquired abnormality of the intraventricular
conducting system
Cardiomyopathy (CMP)

400

Atrio-ventricular dissociation: atrial tachycardia (~115/min), ventricular bradycardia (~36/min), QRS is narrow

Atrio-ventricular dissociation: atrial tachycardia (~83/min), ventricular bradycardia (~50/min), QRS is wide

401

V1

AV dissociation Atrial rhythm (~72 beats/min); Bidirectional ventricular tachycardia (~160-170 beats/min)

402

AV blocks (summary)
Block degree

Site

Result

AV node

Impulses from the AV node to the ventricles are

consistently delayed. Every P wave is followed by
QRS complex

2nd degree type I

Mobitz-I or
Wenckebach

AV node

Gradual increase in PR (PQ) interval followed by one

missing QRS and then the cycle starts again
(Wenckebach periodicity)

2nd degree type II

Mobitz-II

bundle of His
or bundle
branches

PR interval is constant (normal or increased); P wave

is not followed by QRS; QRS may show wide
morphology (bundle branch block)

3rd degree

AV node or
bundle of
His

AV junction does not conduct any impulses between

the atria and ventricles (atrio-ventricular dissociation)
Potentially lethal (Stokes-Adams-Morgagni syndrome)

1st degree

403

404

Intraventricular conduction blocks (bundle branch

blocks)
Intraventricular conduction blocks can
Occur on the right side or on the left
Left bundle branch block
Right bundle branch block

Affect an entire ventricle (complete block) or only part of it

(divisional/fascicular block)
Left anterior superior fascicular block
Left posterior superior fascicular block

Types of intraventricular conduction blocks

First degree (partial block or conduction delay) when the stimulus conducts
but with delay
Second degree when the stimulus sometimes passes and sometimes does
not
Third degree (advanced block) when passage of the wave front is completely
blocked
405

Left bundle branch block

QRS complex: 0.12 sec, with slurring in the mid-portion of the
QRS
Direction: to left and posterior
Q wave is missing in leads I., V5 and V6
Wide monophasic R wave I. V5 and V6 lead (delayed intrinsicoid
deflection)
V1: QS or rS pattern with a small r wave and a positive T wave
I and V6: a single R wave with its peak after the initial 0.06 s
Lack of R wave progression in precordial leads
aVR: a QS pattern with a positive T wave

ST segments & T waves with their polarity usually opposite to

the slurred component of the QRS complex (secondary ST
segment and T wave changes)
406

V6
3

2 3
1

LV

1
RV

V1

1 3

407

Causes of left bundle branch blocks:

AV node, junction damage, ischemia (eg MI)
Infiltrative and degenerative diseases: amyloidosis, sarcoidosis, Levs disease: senile degeneration of conductive
system, Lengre disease: fibrosis of the conductive system (unknown cause)
Inflammatory causes: rheumatic heart diseases, endocarditis, myocarditis, diphtheria, Lymes disease
Other: WPW, LV hypertrophy, CMP

408

SR (~100/min); Normal QRS axis; PR 160 msec, wide P, Morris index; QRS wide, slurred; ST-T discordant to QRS
Determine QTc time!
409

Right bundle branch block

QRS 0.12 s with slurring in the mid-final portion of the QRS
The first 0.04 sec part of the QRS complex is normal, the terminal
0.04 sec part is directed to the right and anterior direction
Right precordial lead: R wave (V1 and V2)
V1: rsR pattern with a slurred R wave and a negative T wave

Left precordial and limb leads: S wave (I., aVL, V5 and V6)
V6: qRs pattern with s-wave slurring and a positive T wave

aVR: QR with evident R-wave slurring and a negative T wave

ST segment & T wave with polarity opposite to that of the

slurred component of the QRS

410

V1-rsR
QR

qRs
QR

V6

1 3

LV

rsR

qRs

qRs

qRs

qRs

1
3
1

V1
2

RV

rsR
411

QR

qRs

rsR

RR 52/min

Causes of right bundle branch

Brugada syndrome, Ebsteins anomaly, atrial septal defects
Myocarditis, CMP, MI heart failure, cor pulmonale
Duchenne type muscular dystrophy

412

rsR

Regular sinus rhythm (100/min), left axis deviation; PR normal, QRS terminally wide (144 ms), discordant ST-T
Determine QTc time!

413