Download 179: ekg signs of disordered impulse formation or conduction

179: EKG SIGNS OF DISORDERED IMPULSE FORMATION OR CONDUCTION
Disorders of Impulse Formation

Disorders in SA node
1. Sinus bradycardia
- Slow heart rate
- Features;
i.
Rate less than 60bpm (may be due to reduced automaticity of the sinus
node or blocked conduction)
ii.
P waves upright in lead II (source of impulse is SA node)
iii.
One P wave for every QRS (no AV block)
- Causes;
i.
Athletics hearts
ii.
Drug effects (e.g. beta blockers)
iii.
Electrolyte imbalances
iv.
Sleep
v.
Sick sinus syndrome
2. Sinus tachycardia
- Fast heart rate
- Features;
i.
Rate more than 100bpm (may be due to increased automaticity of the
SA node, or delayed repolarization, or re-entrant circuit)
ii.
P waves upright in lead II (source of impulse is SA node)
iii.
One P wave for every QRS (no AV block)
- Causes;
i.
Anaemia
ii.
Drug effects (e.g. atropine)
iii.
Exercise and stress
iv.
Heart failure
v.
Fluid loss
3. Sick sinus syndrome (SSS)
- Is caused by impaired sinus node activity leading to abnormalities in both
impulse formation and conduction
- Features;
i.
Marked sinus bradycardia (may occur at rates in region of 30bpm)
ii.
Sinoatrial block (is the intermittent failure of the sinus node to activate
the atria resulting in a pause on the ECG)
iii.
Sinus arrest (is the failure of the sinus node to activate the atria
resulting in a pause on the ECG which bears no relationship to the
predominant cycle length)
iv.
Brady-tachy syndrome (is so called because the tachycardias often
alternate with the bradycardia produced by sinus node dysfunction)
v.
Escape beats/rhythms (often seen following a prolonged pause and are
a part of the heart’s “safety net” of subsidiary pacemakers)

Disorders not in SA node (heterotopic)
o Active heterotopic impulse
a. Extrasystoles
 Also known as premature contraction, premature beat, or ectopic
beat
 Most premature contraction result from ectopic foci in the heart,
which emits abnormal impulses at odd times during the cardiac
rhythm. Possible causes of ectopic foci are;
a) Local areas of ischemia
b) Small calcified plaques at different points in the heart, which press
against the adjacent cardiac muscle so that some of the fibres are
irritated
c) Toxic irritation of the AV node, Purkinje system, or myocardium
caused by drugs, nicotine, or caffeine
 Atrial ectopics
a) When the atria are depolarised at any point other than at
the sinus node an ectopic beat is produced demonstrating a
P wave which looks different to the sinus P wave
b) Atrial ectopics are often of no clinical significance and occur
in structurally normal hearts in small numbers
c) Causes;
i. Atrial enlargement
ii. Digitalis toxicity
iii. Ischemic heart disease
iv. Hyperthyroidism
d) Features;
i. P wave is abnormal in shape and occurs early
(because the signal is not from SA node)
ii. Normal QRS conduction
iii. Compensatory pause

Ventricular ectopics
a) Arise from an irritable focus within the ventricular
myocardium and are unmistakably broad and bizarrelooking (because the ventricular impulse is initiated at a
point away from the specialised conduction tissue and hence
the spread of depolarisation is slower)
b) Causes;
i. Myocardial infarction
ii. Coronary artery disease
iii. Drug effects (e.g. digoxin)
iv. Electrolyte disturbances
v. Caffeine and other stimulants
c) Features;
i. Early ventricular beat with no associated P wave
ii. Broad and bizarre QRS
b.
c.
d.
iii. Compensatory pause

AV nodal premature contraction
a) P wave is missing
b) Instead, the P wave is superimposed onto the QRS complex
(because the cardiac impulse travelled backward into the
atria at the same time that it travelled forward into the
ventricles)
c) This P wave slightly distorts the QRS-T complex
Atrial tachycardia

Is formed by a rapid succession of atrial ectopics

Causes are the same as for atrial ectopics

Features;
a) First beat occurs early
b) Abnormally shaped P waves (which may be upright in lead II)
c) Rate greater than 100bpm (but usually greater than
120bpm)
d) Compensatory pause
Ventricular tachycardia

By definition ventricular tachycardia consists of five or more
unifocal ventricular ectopics in a row at a rate in excess of 120140bpm (also called monomorphic ventricular tachycardia)

Causes;
a) Acute causes (e.g. acute myocardial infarction, cardiac
catheterisation, valvular heart disease and etc)
b) Predisposing conditions (e.g. long QT syndrome, cardiac
surgery, arrhythmogenic right ventricular dysplasia and etc)

Features;
a) Broad complex QRS
b) QRS is regular
c) Rate greater than 120bpm

Polymorphic ventricular tachycardia is the result of rapidly
discharging multifocal ventricular ectopics. Most often seen during
acute myocardial infarction or ischemia and occurs in the presence
of a normal QT interval
Atrial flutter

Results from one of two mechanisms;
a) An atrial ectopic focus similar to atrial tachycardia but with a
much faster atrial (P wave) rate
b) A self-perpetuating circular path of atrial depolarisation
which typically forms a continuous circuit between the
inferior and superior vena cavae within the right atrium

Causes are the same as for atrial fibrillation

Features;
a) Sawtooth appearance of baseline
b) Atrial rate 250-350bpm (but typically 300bpm)
e.
f.
c) Presence of AV block
Atrial fibrillation

The basis is multiple ectopic foci within the atria firing off at
rates of up to 600times a minute

Causes;
a) Acute causes and precipitating conditions (acute myocardial
infarction, alcohol intake, electrocution, hyperthyroidism
and etc)
b) Cardiovascular disease associated with a high incidence of
atrial fibrillation (cardiac tumours, cardiomyopathy,
congestive heart failure, cor pulmonale and etc)

Features;
a) Ripple-like oscillations of the baseline (no discernible P
waves)
b) QRS rate irregularly irregular
Ventricular fibrillation

Causes;
a) Acute myocardial infarction
b) Cardiomyopathy
c) Drug toxicity
d) Long QT syndrome
e) Ischemic heart disease

Features;
a) Irregular, chaotic oscillations of the baseline
Disorders of Conduction

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AV Block
Conduction from the atria to the ventricles via the AV node may be
either delayed (as in first degree AV block) or blocked
Causes;
i.
Acute myocardial infarction
ii.
Congenital heart disease
iii.
Fibrosis and sclerosis of the conduction system
iv.
Hyperkalemia
v.
Increased vagal tone
vi.
Ischemic heart disease
Types of block;
i.
First degree AV block (slow conduction)
a) Features;
 PR interval >0.20 secs (and constant) as the impulse
conducted slower than normal through the AV node
 One P wave for every QRS
ii.
Second degree AV block
a) Three types;
 Mobitz type I
 Mobitz type II
 2:1 AV block
Mobitz type I; often occurs during sleep or during periods of high vagal
-
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activity.
There is a cyclic prolongation of the PR interval starting with a normal PR
interval which progressively lengthens until one P wave is not followed by a QRS
complex and a pause ensues. The next beat demonstrates a normal PR interval
and the cycle begins again
Mobitz type II; characterised by occasional non-conducted P waves. The
PR interval constant for conducted beats
2:1 AV block; characterised by a fixed ratio of conducted to nonconducted P waves, where two P waves are seen for every one QRS complex.
The PR interval constant for conducted beats and there is also constant P-P
interval
iii.
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Third degree (Complete Heart Block (CHB))
No conduction from the atria to the ventricles and the two therefore
work entirely independently of each other
The QRS complex may be either broad or narrow depending on
whereabouts the escape rhythm is being generated. Impulse generated high up
the conduction system (around the area of the His bundle or AV junction) will
produce a narrow QRS with a faster escape heart rate and generally better
tolerated by patients. Those generated further down (from the ventricular
myocardium and Purkinje system) will more likely produce a broader complex
with slower resultant heart rates
The features are; no relationship between atrial and ventricular activity
on the ECG, and PR interval appears variable
Bundle Branch Block (BBB)
When a bundle branch or fascicle becomes injured (due to underlying
heart disease, myocardial infarction, or cardiac surgery), it may cease to conduct
electrical impulses appropriately. This results in altered pathways for ventricular
depolarization. Since the electrical impulse can no longer use the preferred
pathway across the bundle branch, it may move instead through muscle fibers in
a way that both slows the electrical movement and changes the direction of the
impulses. As a result, there is a loss of ventricular synchrony, ventricular
depolarization is prolonged, and there may be a corresponding drop in cardiac
output.
Features of Right BBB;
i.
The heart rhythm must be supraventricular origin
ii.
The QRS duration must be = or >120ms
iii.
There should be a terminal R wave in lead V1 (e.g., R, rR', rsR', rSR' or
qR)
iv.
There should be a slurred S wave in leads I and V6
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Features of Left BBB;
i.
The heart rhythm must be supraventricular origin
ii.
The QRS duration must be = or > 120ms
iii.
There should be a QS or rS complex in lead V1
iv.
There should be a monophasic R wave in leads I and V6
Increased conduction
a.
Wolff-Parkinson-White Syndrome (WPWS)
Is a syndrome of pre-excitation of the ventricles of the heart due to an
accessory pathway known as the bundle of Kent. This accessory pathway is an
abnormal electrical communication from the atria to the ventricles.
Both AV re-entry and AV nodal re-entry tachycardias require an
additional conduction pathway. The mechanisms; they form a self-perpetuating
circle of depolarisation either round and around the AV node or through the AV
node and back to the atria via the additional pathway.
Individuals with WPWS have an accessory pathway that connects the
atria and the ventricles, in addition to the AV node. This accessory pathway is
known as the bundle of Kent. This accessory pathway does not share the rateslowing properties of the AV node, and may conduct electrical activity at a
significantly higher rate than the AV node.
Features on the EKG;
i.
It is manifested as a delta wave, which is a slurred upstroke in the QRS
complex
ii.
A short PR interval (The short PR interval and slurring of the QRS
complex is actually the impulse making it through to the ventricles
prematurely (across the accessory pathway) without the usual delay
experienced in the AV node)
iii.
Rate 130-250bpm
References:
1.
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Wikipedia:
http://en.wikipedia.org/wiki/Bundle_branch_block
http://en.wikipedia.org/wiki/Right_bundle_branch_block
http://en.wikipedia.org/wiki/Left_bundle_branch_block
http://en.wikipedia.org/wiki/Wolf_parkinson_white
2.
ECG Complete (by Steven Bowbrick, Alex N. Borg)
PLAGIARISM SOURCES: 50%