ECG diagnosis

you dont want

to miss
Acute Medicine Conference
Dr Noel Thomas Ross
Acute Medicine Fellow,
Hospital Kuala Lumpur

Introduction
A Basic tool
So readily available
Cheap but so informative
If you make the right decision and
recognize the pattern/pathology
accurately it will SAVE a LIFE

MISS RATE ?

Case 1
24 year old lady, Post LSCS D 26 for breech
Presents with lightheadedness, new onset
seizures/LOC 1 week, extension of both UL and LL,
uprolling of eyes.
Blood pressure 116/84 mmHg. Taking Gamat

Questions
What is the diagnosis
What are the causes of
Seizures/syncope in a young patient

On arrival to the ward

seizures 5 secs

What investigation to order?

Go through drugs patient is/has taken
Mg+, Ca++, K+

Corrected QT interval
The Bazett formula is the formula most
commonly used to calculate the QTc, as
follows: QTc = QT/square root of the R-R
interval (in seconds).
QT interval corrected for heart rate (QTc)
that is longer than 0.44 seconds is
generally considered to be abnormal,
although a normal QTc can be more
prolonged in females (up to 0.46sec).

Remember ECG Causes of

Seizures/Syncope
Long QT syndrome,
Brugada Syndrome,
WPW syndrome
Aryhythmogenic RV
cardiomyopathy(ARVC)
Sick sinus syndrome
HOCM

Progress
Refered to Cardiology same day
Diagnosis: Long QT syndrome
AICD inserted
Propranolol 40 mg bd.

Case 2
70 year old man, brought to hospital with c/o
palpitation and giddiness, long standing DM,
Hypertension and gout. Blood pressure
110/66mmHg
In the ward patient has an ECG done

HR
100/m

Important Questions you

should ask
Is this VT?
- too fast for VT
- too slow for VT
Is the QRS complex really wide?
Mimic of VT?
-toxic, metabolic

Decisions

Registrar wants to amiodarone / shock NO!

Senior MO whats wrong with our boss

maybe he bought his degree.
SN think maybe about time we should get a
new boss.
Junior specialist called his cardiologist
friend asking whats wrong with my boss.
5th year medical students wondering whats
going on here?

History
No chest pain
No traditional medications
Did you take a lot of bananas - NO NO,
NOOO
Not on any K supplements
Not on ACE inhibitors

Our Boss gives the patient

Give Calcium gluconate, Insulin,

dextrose 50% and Sodium bicarbonate

Regular really wide complex

tachycardia (RRWCT)
Think of metabolic causes
Think of Sodium channel toxicity

Regular really wide complex

tachycardia
Consider Calcium chloride and Sodium
bicarbonate first
Rather than Antiarrhythmics

Furthur information
K 8.8mmol/l
Patients son said father has Advanced
Renal Failure
Son confesses patient had a durian feast
last 2 days

ECG Spectrum Hyperkalemia

P-wave flattening,
PR-interval,
QRS prolongation,
ST elevation
High-grade AV blocks,
Intraventricular conduction abnormalities
(including fascicular blocks and bundle
branch blocks), and
Finally a sine-wave appear- ance on the
rhythm.

K
7.5mmol/l

K 6.8mmol/l

Hyperkalemia

Great mimicker in ECG

Remember
Hyperkalemia is a Na channel poison
Amiodarone, lignocaine, procainamide
are Na channel blockers

Pointers
Hyperkalemia can mimic VTach
Suspect when QRS is very wide or when
rate is too slow for VT

Pointers

Regular really wide complex tachycardia

- Consider sodium channel toxicity and
metabolic causes
- Consider calcium and sodium
bicarbonate trial
- Antiarrhythmics can kill these patients

Case 3
29 year old gentleman.
Presents with palpitation, Blood pressure is
108/74mmHg

What are questions should

you ask?
Regular or Irregular
Broad complex or narrow complex
Hemodynamics

What is the treatment of

choice here?
Adenosine
Dilteazam
Amiodarone
Digoxin
Beta blockers
???
Electrical Cardioversion

Drugs that are

contraindicated in WPW with
AF
Class II drugs(BBl) are contraindicated
Class III drugs are also contrindicated.
Although classified as a potassium
channel blocker, amiodarone also has
electrophysiologic characteristics of
sodium channel blockers, beta blockers,
and calcium channel blockers.
Class IV drugs (CCB) are also
contraindicated

WPW with Atrial

Fibrillation
Treatment with amiodarone resulted in
patient decompensation
Boriani et al(Am Heart J, 1996)
Gaita et al, (Drugs,1992)
Shutzenberger et al(Int J Cardiol, 1987)
Sheinman et al(BMJ, 1982)
Tijunelis et al (Can J Emerg Med, 2005)

WPW with AF
Irregular WCT
Electrical Cardioversion

Case 4
84 year old man who presented with chest pain,
he was given thrombolytics earlier in the
morning , now is pain free. BP 116/78mmHg, HR
110/m You come in as the in charge senior MO to
CCU in the morning

His current ECG

Rate 110/m

What
is this
ryth
m

What questions you should

ask?
Is this VT?
What is the treatment?
Patient is stable.

ECG report says VT

MO in the ward decided to follow
Amiodarone is given
Asystole
Could not be revived

Ventricular rhythm
Ventricular rate 20-40 ventricular
escape rhythm (Idioventricular rhythm)
Ventricular rate 60-120 (accelerated
idioventricular rhythm) AIVR
Ventricular rate >120 Ventricular
tachycardia (130-250)

Caveat

Ventricular tachycardia can be slower if

patient is already on an antiarrythmic,
eg flecainide or amiodarone

Remember
Other mimics of Ventricular
tachycardia(rate < 120)
Hyperkalemia
Sodium channel blocker toxicity

Accelerated Idioventricular
rhythm (AIVR)
Sometimes called slow VT
Suggests successful reperfusion of an
occluded coronary artery in AMI. Cause?
Other presentation digoxin toxicity,
post cardiac arrest rhythm, severe
electrolyte abnormalities

Accelerated Idioventricular
rhythm (AIVR)
Usually transient
Unlikely to cause hemodynamic
instability
Supression can lead to instability and
asystole
Treatment: Observe!

Case 5
47 year old man presents with atypical chest pain,
BP 80/50 mmHg, tachypneic

Diagnosis?

Story goes
Diagnosed Inferior lateral MI
Given Loading Aspirin 300mg,
Clopidogrel 300mg, Fondaparinux 2.5
mg and Thrombolysed with Metylase
Shortly after patient collapsed and could
not be revived

What did they miss

Small complexes
Saddleback ST elevation
Electrical alternans
PR segment depression
= Pericardial Tamponade

Small complexes

Saddleback ST
elevation

Depressed
PR seg

Electrical alternans

Low Blood
Pressure

Diagnosis

Pericardial Tamponade - Hemorragic

Case 6
29 year old man
Found unconscious
Presumed intoxicated

T wave changes. It Must

Be Cardiac Ischemia!
Treated as non stemi
Do you agree?

Questions
Intoxicated patient
Found unconscious
ARE the ECG changes territorial?

Subarachnoid
hemorrage

ECG changes in CNS Pathology

Severe ECG changes mimicking acute

myocardial infarction frequently
complicate presentations of acute
intracranial pathology, such as
thrombotic or hemorrhagic stroke,
subdural hematoma, epidural
hematoma, seizures, and/or
subarachnoid hemorrhage.

ECG changes in CNS

Pathology

Most commonly, ECG changes in these

processes manifest as alterations in the
pattern of repolarization, such as in the
QT interval, ST segment, and/or T
waves. A prolonged QT interval and
prominent peaked or deeply inverted
and symmetric T waves are commonly
seen.

Mayer SA, LiMandri G, Sherman D, et al.

Electrocardiographic markers of abnormal left ventricular
wall motion in acute subarachnoid hemorrhage. J
Neurosurg. 1995;83:889-96.

Mayer et al described a pattern of QT

prolongation and deep T-wave
inversions in patients with acute
subarachnoid hemorrhage.

Goldstein DS. The electrocardiogram in

stroke: relationship to pathophysiological
type and comparison with prior tracings.
Stroke. 1979;10:253-9.
Described the ECG changes in 150
patients and age- and sex-matched
controls.
92% of patients with stroke had some
sort of ECG changes, with 45% of
patients developing a prolonged QT
interval and 35% exhibiting ischemicappearing T-wave inversions..

Goldstein DS et al

The changes may occur soon after the

neurologic event, or they can evolve
over a few days

Not all T wave inversions are

Cardiac Ischemia
Clinical scenario
Territorial distribution

Case 7
A 57-year-old woman, with a history of
hypertension, was admitted to the CCU due to an
atypical, non-compressing, excruciating chest
pain of recent origin (30 minutes) with radiation
to the back.

Case presentation

The patient was hemodynamically

stable, with no peripheral pulse deficit.
Auscultation of the heart revealed a 2/6
systolic murmur at the right base and
apex and an early diastolic murmur at
the right base without pericardial
friction.

What is
your
diagnosis?

What is your next step?

Thrombolysis?
Get an urgent Chest radiograph?
Get urgent Echocardiography?

Pt was treated as an acute

Inferior Myocardial
Infarction and
thrombolysed

Patients chest radiograph

Computed Tomography CT):

Median plane depicts the
extended dissection from the
ascending aorta, passing
through the origins of celiac
trunk (black arrow) and
superior mesenteric artery
(arrow head) down to the iliac
arteries (white arrow).

Cases which we hope

we missed

Some ECGs we hoped we

missed
Made the wrong diagnosis because did
not have enough knowledge/did not
take adequate history
Gave the right treatment for the
diagnosis
Results in adverse outcome or expose
the patient to a lethal consequence

Case 1
78 year old Man
DM, HTN
Presents with presyncopal attack
Also has chest pain 4/10 the same day,
no autonomic symptoms,
Pain score reduced to 1/10 with GTN

ECG

Progress
Diagnosis Inferior Myocardial Infarction
Metylyse 60,000 u given
2 hours later patient complaints of
headache, vomited
DAPT not continued and LMWH not
started.
Urgent CT brain ordered

Further History and

Progress
INR 1.06
AF on warfarin
Warfarin stopped 2 weeks ago fall
diagnosed ? ICB at another hospital
Neurosurgical consult- conservative
Patient succumbs in next 24 hours

Take Home Point

Nothing replaces good history takingalways makes the day
We should not compromise on this asset
Contraindication for thrombolysis
It may be all that is required to save a
life

Case 2
40 year old male
Homeless
Hypertensive but defaulted treatment
Body weakness for 7 days
Shortness of breath 1 day

Clinical
Blood pressure193/139mmHg
Lungs; Crepitations bibasal to mid
Troponin T 0.3
ECG ST elevation V1-4
Started on IVI GTN
BP reduced to 180/110 mmHg

Patient received thrombolysis

Progress
90 minutes later patient vomited few
times
GCS dropped 3 hours later
Urgent CT brain
Creatinine 182umol/l

Progress

Patient succumbs in the next 48 hours

Non cononary causes of ST

elevation

Pericarditis
Benign early repolarization
Left bundle branch block
Left ventricular hypertrophy
Ventricular aneurysm
Brugada syndrome
Ventricular paced rhythm
Raised intracranial pressure

Less common causes

Pulmonary embolismand acute cor pulmonale

(usually in lead III)
Acute aortic dissection (classically causes
inferior STEMIdue to RCA dissection)
Hyperkalaemia
Sodium-channel blocking drugs(secondary
to QRS widening)
J-waves(hypothermia,hypercalcaemia)
Following electrical cardioversion
Others: Cardiac tumour, myocarditis,
pancreas or gallbladder disease

Conclusion
Consider Clinical scenario
Take a good history
Dont rush unless it is hemodynamically
unstable

Conclusion
Just because Electrocardiography is a
basic skill it doesnt mean our skills
should be basic
A ton we have not learnt about ecgs
Every day we learn something new
YOU must strive be the experts in
Electrocardiography
Saves lives

REMEMBER

END
THANKS

ECG

What is the
diagnosis?

ECG