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ECG and arrhythmia classification

5:39 AM cardiac , cardiovascular , ECG , EKG , heart

ECG and arrhythmia classification :

Narrow complex arrhythmias (arise above bifurcation of the bundle of His) QRS duration
<0.1s (2.5 small squares)
Broad complex arrhythmias (arise from ventricles or are conducted abnormally from a site
above the ventricles so that a delay occurs (rarer). QRS duration is >0.1s (2.5 small squares).
Narrow complex arrhythmias

Sinus arrhythmia

Sinus tachycardia

Sinus bradycardia

Junctional tachycardia

Atrial tachycardia, Atrial flutter

Atrial fibrillation

Atrial ectopics
Broad complex arrhythmias

Ventricular ectopics

Ventricular tachycardia

Supraventricular tachycardia with BBB

Ventricular fibrillation
NARROW COMPLEX ARRHYTHMIAS:
Sinus arrhythmia: Irregular spacing of normal complexes associated with respiration. The PR interval is constant, but there are beat-to-beat changes in R-R interval. Normal, especially
in young people.
- Because in inspiration, the negative pressure sucks more blood into the chest, which
cardiac output. This is detected by baroreceptors which HR).

Sinus tachycardia: Rate over 100bpm. Normal P-QRS-T complexes are present.
Causes include:

Pain

Fever/sepsis

Hypovolemia

Anaemia

Heart failure

Thyrotoxicosis

Drugs atropine, ether, ketamine, catecholamines

Management correction of underlying disease.

-blockers if tachycardia causes myocardial ischemia in patient with IHD

Sinus bradycardia: Heart rate of <60bpm. May be normal in athletic people, or with
increased vagal tone.
Causes:

Drugs - -blockers, digoxin, anticholinesterase drugs, halothane

MI

Sick sinus syndrome (fibrosis of AV node)

Raised intracranial pressure

Hypothyroidism

Hypothermia
Management: Often not necessary in a fit young person (unless rate is <45-50bpm) and/or
there is haemodynamic compromise. You may consider:

Correct underlying cause

Atropine
Arrhythmias due to re-entry

Where there is anatomical branching and re-joining of a conduction pathway.

If one limb is slower than the other, the impulse may pass normally down one limb but be
blocked in the other. Where the pathways rejoin, the impulse can then spread backwards up
the abnormal pathway. If it arrives at a time when the first pathway is no longer refractory to
activation, it can pass right around the circuit repeatedly, activating it and resulting in
tachycardia

Wolf-Parkinson-White syndrome (anatomical accessory pathway between the atria and

ventricles) Macro-reentry circuit (Other macro re-entry circuits can exist in the
atrial/ventricular myocardium and cause paroxysmal atrial flutter, AF, ventricular tachycardia).

In Junctional tachycardia, there are micro re-entry circuits within the AV node itself
Junctional tachycardia: Micro re-entry circuits in or near the AV node (or, as in W-P-W, from
an accessory conduction pathway between the atria and ventricles).

Narrow complex tachycardia with rate of 150-200bpm

SHORT P-R
Slurred upstroke on the R wave (Delta wave in V4 in WPW)

Inverted T waves in V2-5 are characteristic

Management: This arrhythmia may be associated with severe circulatory disturbance

If they are haemodynamically compromised -cardioversion

Carotid sinus massage (rarely converts to sinus rhythm, but slows the rate and will reveal

the underlying rhythm if in doubt) (helps differentiate from atrial flutter/AF)

o The carotid sinus is a small dilatation of the proximal part of the internal carotid artery at the
level of the superior border of the thyroid cartilage. It is vagally innervated and is involved in
the control mechanism for causing a fall in HR and CO in response to rise in arterial pressure.

Gentle pressure here may result in slowing of the heart and occasionally, termination of reentry SVT. Never do on both sides or it can cause asystole and occlusion of the main arterial
blood supply to the brain.

Adenosine (slows AV conduction so is useful for terminating re-entry SVTs of the WPW
type)

Verapamil, -blockers, amiodarone, flecainide may control the rate of convert to sinus
rhythm
Atrial tachycardia and Atrial flutter: Due to an ectopic focus depolarising from anywhere
within the atria. They contract faster than 150bmp and P waves can be seen superimposed
on T waves of the preceding beats.

AV node conducts at a maximum of 200bpm, so if the atrial rate is faster, AV block will occur
(Typically see ventricular rate as 150bpm with atrial flutter)

If the atrial rate is >250bpm, there is no flat baseline between P waves and you get
sawtooth pattern

Can occur with any type of block (2:1, 3:1, 4:1)

Atrial tachycardia is typically a paroxysmal arrhythmia with intermittent tachycardia and

palpitations (may be precipitated by many factors stress, alcohol, caffeine)

o With 2:1 block = characteristic of digitalis toxicity
Management: Very sensitive to direct current cardioversion (almost 100% success rate), so
should be used first line if there is haemodynamic compromise

Carotid sinus massage and adenosine slow AV conduction and reveal underlying rhythm
and block if there is doubt

Other drug treatment as for AF

Atrial fibrillation: Very common. It is a chaotic and uncoordinated atrial depolarisation
(absence of P waves), with an irregular baseline and completely irregular ventricular rate. The
ventricular response rate will normally be rapid about 120-200 bpm.
Common causes:

Ischaemia

Myocardial disease/pericardial disease

Mitral valve disease

Sepsis

Electrolyte disturbance (esp. Hypokalaemia or hypomagnesaemia)

Thyrotoxicosis

Thoracic surgery
Since contraction of the atria contributes 30% to ventricular filling, the onset of AF may result
in significant in CO. Fast AF may precipitate cardiac failure, pulmonary oedema and
myocardial ischaemia and systemic thromboembolism may occur if blood clots in the
fibrillating atria form.
Management: Treatment is aimed at restoration of sinus rhythm if possible and if not,
maintaining the rate to <100bpm and prevention of embolic complications. Management
depends on how long it has been present.

Acute:
Correct precipitating factors where possible

DC cardioversion (for recent onset)

Digoxin to slow ventricular rate

Amiodarone to restore sinus rhythm

Verapamil control ventricular rate

-blockers sometimes used to control ventricular rate

Chronic:
Aim to control ventricular rate to <100bpm allows time for adequate ventricle filling and
maintains CO

Digitalisation

-blockers of verapamil

Amiodarone
When AF has been present for more than a few hours, anticoagulation is necessary before
cardioversion to prevent the risk of embolisation. (Usually warfarin for 3 weeks prior to
elective DCC)
Atrial ectopic beats: An abnormal P wave is followed by a normal QRS. The P wave is not
always easily visible

Ectopic indicates that depolarisation originated in an abnormal place get an abnormally

shaped P wave

If the focus depolarises EARLY, the beat produced is an extrasystole (premature) and may
be followed by a compensatory pause

If the underlying SA node is slow, sometimes an atrial focus takes over escape beat as it
occurs after a SMALL DELAY
Causes:

Any heart disease

Ischaemia, hypoxia

Light anaesthesia

Sepsis

Shock

Anaesthetic drugs
Management: Correction of underlying cause and treatment is not necessary unless runs of
atrial tachycardia occur.
BROAD COMPLEX ARRHYTHMIAS
Ventricular ectopic beats: Depolarisation spreads from a focus in the ventricles by an
abnormal (slow) pathway, so the QRS is wide and abnormal. (T wave is also abnormal in
shape).

Usually benign if there is no structural heart disease

May be associated with abnormalities Hypokalaemia, light anaesthesia (with halothane),

raised CO2, intracranial pressure

The onset of runs of VT should be taken seriously where:

There is a bigeminal rhythm (one ectopic beat with every normal beat)

If they occur in runs of 2 or more (or more than 5/minute)

Where they are multifocal (arising from different foci hence having different shapes)

Where the R wave is superimposed on the T wave

Management:
Small dose of -blocker

If underlying sinus rhythm is slow, increase the rate with IV atropine (as ventricular ectopics
could be a form of escape beat)

Lignocaine is the drug of choice

Alternatives amiodarone
Ventricular tachycardia: A focus in the ventricular muscle depolarises at high frequency.
Excitation spreads through the ventricles by an abnormal pathway. There are no P waves,
wide QRS which may be slightly irregular/vary in shape.
Can be triggered by:

Hypoxia

Hypotension

Fluid overload

Electrolyte imbalance (low K, Mg)

Myocardial ischaemia

Adrenaline injection
Management:

Synchronised direct current cardioversion if the patient is haemodynamically unstable

If they relapse back into VT lignocaine, amiodarone can sustain sinus rhythm
NOT verapamil
Supraventricular tachycardia with bundle branch block: Where there is abnormal conduction
from the atria to the ventricles, a SVT may be broad complex if there is a BBB. Sometimes it
can be due to ischaemia.
BUT all tachycardias should be treated as VT if there is any doubt.

RBBB : V1 looks more at the right side of the heart, so if the right ventricle is the last to
depolarise due to a block, you see the last deflection in V6 will be negative (going away
from the left of the heart) and the last deflection in V1 will be positive (going towards the
right of the heart)

LBBB (much more common): V6 looks at the left heart, so if the left ventricle is the last
depolarising due to a block, you see last deflection in V6 will be positive and the last
deflection in V1 will be negative (going away from the right of the heart)
Ventricular fibrillation: This results in cardiac arrest. There is chaotic and disorganised
contraction of ventricular muscle and no QRS complexes can be identified on the ECG.
Management: Immediate DCC

DISTURBANCES OF CONDUCTION
First degree block: PR interval is >0.2s (delayed). Usually benign, but can progress to
nd

2 degree block.
Second degree block Mobitz type I (Wendebach): Progressive lengthening of the PR
interval and then failure of conduction of an atrial beat. This is followed by a conducted beat

with a short PR interval. The cycle then repeats

Common with inferior MI, tends to be self-limiting and doesnt tend to require treatment
Secondary degree block Mobitz type II: When excitation intermittently fails to pass
through to the ventricles. Most beats are conducted normally, but occasionally, there is atrial

contraction without a subsequent ventricular contraction

Often progresses to complete heart block
Second degree block 2:1 type: Where there is alternate conducted and non-conducted

beats resulting in 2 P waves for every QRS. A 3:1 or 4:1 block may also exist.
May herald complete heart block
Third degree (complete) heart block: Complete failure of conduction from the atria to the
ventricles, so the ventricles are excited by an escape mechanism (slow) from a focus in the
ventricles. There is no relationship between the P waves and the QRS complexes and the

QRS complexes are abnormally shaped.

May be transient due to vagal stimulation (responds to IV atropine)

Acute inferior MI (due to AV nodal ischaemia)

Anterior MI indicates more extensive damage, including the His-Purkinje system

Bundle branch block: If the impulse from the SA and AV nodes reaches the IV septum
normally, the PR interval will be normal, but if there is a subsequent delay in depolarisation of
the L/R bundle branches, there will be a delay in depolarisation of part of the ventricular
muscle and the QRS complex will be wide and abnormal

RBBB often found in normal, may indicate right heart problems

LBBB often indicates heart disease