Arrthmias

Dr.B.Nisahan

Diagnosis and classification of

arrythmia
12 lead ECG
Step 1. L11 or V1 - Sinus rhythm (SR) or Not
P preceding QRS and PR interval
equal
If not in SR

Step 2. Heart rate

> 100- tachyarrhythmia

< 60 - Bradyarrythmia

Step 1
Step 2

Arrythmia

Tachyarrhythmia

Bradyarrythmia

If tachyarrhythmia ( > 100/m)

Step 3. QRS duration
< 120 ms - Narrow Complex Tachycardia
> 120 ms Broad Complex Tachycardia

Narrow complex tachycardia (NCT) is always

Supraventricular in origin

Step 4. Assess whether Regular or Irregular NCT

 Tachyarrythmia

Step 3

Step 4

Narrow QRS

Regular

Irregular

Broad QRS

Regular

Irregular

Vent Tachycardia

 Tachyarrythmia

Step 3

Step 4
Step 5

Narrow QRS

Regular

Irregular

Broad QRS

Regular

Irregular

Vent Tachycardia

Step 5

Regular Narrow-complex
tachycardia
1. Re entrant tachycardia
a) AV nodal (AVNRT) 60 %
b) Atrio ventricular(AVRT) 30 %

2. Atrial flutter with regular AV

block
3. Atrial tachycardia

Regular narrow-complex tachycardia

Atrial flutter
Diagnosed only by the presence of Flutter
waves on the ECG (250-350/min)
Re entrant tachycardia
No P wave ( hidden in ST or T waves)
Atrial tachycardia

conduction

This tracing shows regular narrow QRS tachycardia at 150 bpm. In leads I and
aVL, 2 atrial deflections () are evident that occur regularly at 300 bpm. Regular
atrial rhythm at this rate, or close to it, occurs only with atrial flutter

Types of Atrial flutter

1. Typical Common Ischmus dependent (RA)
Positive flutter waves in V1
Good response to ablation (90%)

2. Atypical - Uncommon , usually scar related

ASD
repair, myocarditis, previous
maze
procedure

Typical counterclockwise flutter will have the

Following :
a) negative P in II, III, aVF
b) positive P in V1
c) negative P in V6
In atrial flutter, there is a continuous circus movement of electrical front
(macroreentry) which spins off an impulse to the AV node. Since the frequency
of this circus movement is around 300/m, which is too fast for the AV node to
transmit 1:1, the end result is 2:1 AV conduction (not 2:1 AV block which implies
there is AV conduction problem. There is no AV conduction problem. It's simply
that the AV node is not made to conduct impulses 300 times per min. Let's not
blame the innocent AV node.). Of course, if the flutter rate slows down to
around 200/m or even 240/m, the AV node can conduct 1:1. This circus
movement always passes thru a narrow isthmus between the oriface of IVC
and tricuspid annulus, providing an easy target for ablation

Atrial tachycardia and atrial flutter are entirely different rhythms

pathogenetically (electrophysiologically). In atrial tachycardia, a
focus in the atrium discharges impulses at a rate of around 150/m
(120-220/m)which are conducted to the ventricles 1:1 (if it is due to
digitalis intoxication, there is 2:1 or variable AV conduction ratio.
In atrial tachycardia, the electrophysiologist has to hunt for the impulse
originating locus when attempting ablation.
Atrial flutter can go in and out of atrial fibrillation but atrial tachycardia
does not. The spectrum of clinical conditions causing atrial fib and
atrial flutter are similar but not atrial tachycardia.
Atrial tachycardia is like a tall building antenna blinking at that rate
while atrial flutter is a searchlight at the air port making circles.

Re - entrant Tachycardia

What is the Significance of Electrical

alternans ?

NCT - Electrical alternans is known to occur in Supra

ventricular and ventricular tachycardia.

Electrical Alternans in sinus rhythm is suggestive of

Pericardial effusion

Step 5

Irregular narrow-complex tachycardia

Atrial fibrillation
Atrial flutter with varying block
Multifocal atrial tachycardia

Atrial fibrillation

Classification of Atrial fibrillation

Acute Atrial fibrillation (<48 hrs)

Chronic Atrial fibrillation

Paroxysmal

Persistent

Permanent

Broad Complex Tachycardia

Clinically
Any cardiac rhythm >100 /min, with QRS
duration of >0.12s

Electro physiologically
Mostly ventricular in origin, involving
automatic focus or re-entry circuit within
the ventricles

Broad Complex Tachycardia

Causes
Ventricular Tachycardia

Supraventricular arrythmia with aberrant

conduction (BBB)
WPW with antidromic pathway
Default diagnosis is VT. Other diagnoses should only be
made on the basis of definite evidence, including adenosine
test.

Ventricular Tachycardia (> 120/min)

Monomorphic Ventricular Tachycardia

>120/min)

Polymorphic Ventricular Tachycardia

a. Acute MI or ischaemia
b. Long QT interval (Torsades)

Ventricular Tachycardia (<120/min)

Accelerated Idioventricular rhythm (< 100/min)
Slow VT (patient already on antiarrythmic)

VT

SVT

P/H IHD,drugs
VA dissociation
QRS>140ms
QRS>160ms
Left axis with
RBBB
Concordance
Fusion or Capture
beat

No cardiac history

BP does not help to differentiate VT/SVT

Accelerated Idioventricular rhythm

AF with LBBB

30 yr male with Syncope

P/H several episodes
F/H

Brugada Syndrome

Long QT Syndrome

A young woman with exercise induced syncope

Long QT Syndrome - congenital

What life threatening abnormality is shown?

QT interval is 800 msecs with T wave alternans. Precursar

for Torsades, P/H DCM, brought in after prehospital arrest

Torsades de points

Management of Torsades de points

Give all patients iv magnesium sulphate (1-2 g IV)

isoprenaline infusion can help suppress TDP

Overdrive atrial pacing (if no AV block) at rate of

100 bpm is treatment of choice. Increase in heart
rate reduces QT interval

DC cardioversion if sustained VT/VF

Ventricular Fibrillation

ICD

ICD Delivering Shock

Bradyarrythmia
SA node disease
AV block
First degree
Second degree Mobitz 1 or Mobitz 11
Third degree or Complete block

Intraventricular block Bifasicular,

Trifasicular

Atrioventricular block
It is a disturbance in the conduction system transient or permanent impairment of electrical activation
from the atria to the ventricles.
There are 3 categories : first-degree, second-degree, and
third-degree AV block.
In first-degree - the conduction is delayed (a PR interval
greater than 200 milliseconds), but all atrial impulses are
conducted to the ventricles.

Second degree Atrioventricular block

Some impulses are conducted, whereas others are not.
2 types
Mobitz type I
Mobitz type II.

Mobitz 1 AV block

Progressive delay in the conduction time to the ventricles until an

impulse is not conducted.

This is an often physiologically mediated state on an area

The block is higher up in the conduction system of the

atrioventricular node.

children and athletes can often be found to have Mobitz type I as an

incidental finding.

Heart rate Improves with exercise or atropine (useful

to differentiate Mobitz 1 from 2 in 2:1 AV block).

Mobitz type II

The block is just below the atrioventricular node.

The PR interval of conducted beats does not change.

QRS is usually widened with BBB.

Lack of conduction of P waves intermittently

Heart rate worsens or unchanged with exercise or atropine (useful

to differentiate Mobitz 1 from 2 in 2:1 AV block).

In third-degree atrioventricular
block, there is no impulse
conduction at any time

Indications for temporary pacing

Cardiac arrest with ventricular asystole

or bradycardia

Asystole due to eletrolyte imbalance

Mobitz11 or CHB in anterior infarct

CHB in INf MI if HRate < 40, Ventricular

arrythmia

Non conducted atrial ectopic

Around the time when the P wave is blocked, the P-P interval significantly lengthens.
This suggests that it is not an intrinsic AV conduction problem but that some "force" extrinsic to the heart is causing
the sinus node to slow down on the one hand and the AV block to occur on the other.
The extrinsic "force" is an increased vagal tone. This phenomenon is seen sometimes in well trained athletes
who usually have an increased vagal tone that is benign. A pacemaker is not necessary.
Thus, during AV block, paying attention to what the P-P interval is doing is useful in understanding what is happening
so that the person can be treated appropriately.

This patient is very unwell. What is the

immediate Rx ?

Diagnosis Hyperkalaemia
Features of hyperkalemia
Bradycardia - Heart rate 23/min
Wide QRS complexes
Symmetric, tall and pointed T waves (in leads V24).
Management

A blood sample should be sent to the laboratory for serum potassium

level.
without waiting for the result, the patient should be treated with
intravenous calcium to counteract the membranous effect of the
high K Glucose insulin infusion.
Bicarbonate

Thank You

Quiz 1

note how sharp the QRS upstroke is in leads I, II, aVF, and V4-V6

Quiz 1
answer is: Atrial flutter with 1:1 A:V conduction with aberrancy.
This is a regular wide, complex tachycardia at 210 bpm.
Although AF can appear fairly regular at very rapid rates,
this is perfectly regular, and also "too fast" for AF.
.
Antidromic tachycardias tend to have a slurred upstroke to the QRS;
note how sharp the QRS upstroke is in leads I, II, aVF, and V4-V6.
This could certainly be either paroxysmal supraventricular tachycardia
or "slow" atrial flutter with 1:1 A:V conduction and aberrancy.
The precordial QRS pattern is right bundle branch block (RBBB);
the frontal plane axis appears to be extreme right-axis deviation.

Quiz 1
After IV AV nodal blocker

Quiz 2

Artifact simulating VT

Quiz 3

NSVT

Differentiating VT from SVT Brugada criteria

If an RS complex cannot be identified in any precordial lead, ventricular

tachycardia can be diagnosed with 100% specificity and 21% sensitivity.

If an RS complex is clearly distinguished in one or more precordial leads,

the interval between the onset of the R wave and the deepest part of the S
wave (RS interval) is measured (if RS complexes are present in several
precordial leads, the longest RS interval is used). If the RS interval is
greater than 100 milliseconds, ventricular tachycardia can be diagnosed
with 98% specificity and 66% sensitivity.

If the RS interval is less than 100 milliseconds, the presence or absence

of atrioventricular (AV) dissociation must be determined. Evidence of AV
dissociation is 100% specific and 82% sensitive for ventricular
tachycardia; this is because atrioventricular dissociation does not occur in
supraventricular tachycardia

Differentiating VT from SVT Other features

An extreme rightward axis (-90 to -180 degrees) is often more suggestive

of ventricular tachycardia.

A slight irregularity of the RR intervals, especially in the early stages

before settling into a regular rhythm, can be suggestive of ventricular
tachycardia

In general, a wide QRS complex greater than 140 milliseconds suggests

VT; however, a QRS duration of less than 140 milliseconds is not helpful
for excluding ventricular tachycardia, because ventricular tachycardia is
sometimes associated with a relatively narrow QRS complex.

A "capture beat" occurs when a supraventricular rhythm briefly conducts

in a normal fashion, with a resultant normal QRS complex also indicate
ventricular tachycardia
.

Fusion" occurs when a supraventricular impulse reaches the

atrioventricular node simultaneously with a ventricular impulse

The most common cardiac manifestation of tricyclic antidepressant (TCA)

overdose is sinus tachycardia. Tricyclic antidepressants are a common
cause of 'unexplained' sinus tachycardia in patients, even when used at
therapeutic doses.

Other cardiac manifestations of TCA toxicity include right axis deviation and
right bundle branch block with a tall R wave in lead aVR (presumably
because of increased sensitivity of the right bundle branch to tricyclic
antidepressant poisoning),

bradyarrhythmias, advanced conduction system disease, and an altered

pattern of repolarization similar to the Brugada pattern (right bundle branch
block with ST-segment elevation in the anterior precordial leads).

In addition, tricyclic antidepressants also inhibit alpha-1 adrenergic

receptors, leading to hypotension and amine uptake (eg, norepinephrine),
and they competitively inhibit muscarinic, histaminic, and gammaaminobutyric acid (GABA)A receptors.

The anticholinergic effects of tricyclic antidepressants and the hypotension

induced by alpha adrenergic blockade result in marked hypotension, which
is a frequent cause of tricyclic antidepressant toxicityrelated mortality.
[5,6,8]

26-year-old man to the A&E with an acute onset of altered mental status

Answer Tricyclic antidepressant overdose-TCA

1. Widened QRS complex
2. Prolonged QT
3. Terminal R-wave greater than 3 mm in lead aVR.
All of these findings are concerning for a TCA overdose
Since a TCA overdose can be lethal, immediate treatment
based on the ECG findings and clinical picture is
warranted
TCAs are thought to exert their principle therapeutic
effects by inhibiting presynaptic uptake of norepinephrine
and serotonin

TCA toxic effect can be divided into 4 main categories:

Inhibition of norepinephrine reuptake,
Direct -adrenergic blockade,
Antimuscarinic-type anticholinergic actions,
Quinidine-like effect on myocardial cells
Deaths from TCA overdose usually result from dysrhythmia,
cardiogenic shock, or status epilepticus with hyperthermia,
and they typically occur within the first few hours of admission

Treatment of Tricyclic overdose cardiac

toxicity

Reverse the competitive antagonism of the fast sodium

channels by administering a bolus of 1-2 mEq/kg of sodium
bicarbonate (NaHCO3), followed by a continuous infusion
(typically, 2-3 ampules of sodium bicarbonate mixed into 1 L
5% dextrose in water [D5W]). This is administered at 2 times
the maintenance rate for intravenous fluids, with the desired
effect of inducing serum alkalemia and a goal pH of 7.5-7.55.
Sodium bicarbonate typically results in rapid improvement of
the ECG abnormalities seen in tricyclic antidepressant
toxicity, sometimes within minutes

Hypotension can initially be treated with aggressive

administration of intravenous fluids.

Refractory cases may require vasoactive agents, such as

norepinephrine or dopamine, although norepinephrine is less
effective than dopamine because patients will have depleted
catecholamine stores.

TCA overdose treatment ct

(CNS) toxicity is typically managed with benzodiazepines as a first-line
treatment for seizures

Seizures are likely result from the inhibition of norepinephrine

reuptake .
Gastric decontamination with activated charcoal is effective and
recommended if a patient presents early enough after
ingestion and has an appropriate mental status
Gastric lavage may be considered for a massive overdose, but it is rarely
justified if it cannot be started within 1 hour of ingestion

Hemodialysis is not effective for TCA treatment.

Because of the extensive tissue and protein binding with a
large volume of distribution, dialysis is not an effective
treatment

Quiz 4

Atrial trigeminy (not Wenchebach)

Heart transplantation; the donor heart is in sinus rhythm while

the atrial "cap" of the recipient heart is fluttering

Is this life threatening ?

Junctional tachycardia with variable block and

underlying atrial fibrillation due to Digoxin
toxicity (70% mortality) if treated promptly 3 %
mortality.

What is the reason for the change in QRS morphology?

ABERRANT CONDUCTION