Dr. A. M.

Jahangir Alam, Registrar |1

ECG of acute MI
Acute ST elevated inferior MI (myocardial infarction).

This is 12 leads ECG tracing with rhythm strip showing that

1. ST segment elevation in lead II, III & aVF with reciprocal ST depression in lead I, aVL
2. So my ECG diagnosis is Acute ST elevated inferior MI.

Question-1: How will you localize culprit artery in acute MI ?

Localization of Culprit artery in acute MI

Leads Surface Culprit artery
II, III, aVF Inferior Right coronary artery (80%) / Left
circumflex artery (20%)
V1-V6 Anterior Left anterior descending (LAD)
I, aVL High lateral Left circumflex artery (LCx)

Causes of ST elevation in ECG

ST elevation in ECG
1. Acute MI
2. Acute pericarditis
3. Prinzmetal angina/vasospasmic angina
4. LV aneurysm (persistent ST elevation)
5. Benign early repolarization (BER)
 Dr. A. M. Jahangir Alam, Registrar |2

Question-2: Describe clinical features of acute MI ?

Clinical features of acute MI:

Clinical features of acute MI

• Chest pain ( sudden, severe, central retrosternal chest pain which is constricting, squeezing
chocking, tightening in nature & persists more than 1hour , radiates to throat, neck, jaw, inner
aspect of left upper arm, aggravated by physical exersion, emotion, heavy meal, anxiety, cold
exposure not relieved by rest or nitroglycerine & associated with nausea, vomiting, sweating and
fear of impending death (angor animi).
• Silent MI (no chest pain-DM, Old age)
• Features with complication like cardiogenic shock leads to death.
• Breathlessness (Acute LVF) & body swelling (CCF)

Question-3: How will you manage a case of acute MI ?

Streptokinase:
Dose: 1.5 million IU in 100ml N/S IV over 60 mins (1 hour).
Adverse effects: Allergic reaction, hypersensitivity, hypotension, bleeding
Indication: Typiocal chest pain, ST elevation MI (ECG) & cardiac enzymes high.
Other recombinant tissue type plasminogen activators (rt-PA): Alteplase, Reteplase, Tenecteplase
& Anistreplase.
 Dr. A. M. Jahangir Alam, Registrar |3

Contraindications of thrombolysis:
Absolute contraindication:( very important to know)
1. Active internal bleeding
2. Suspected aortic aneurysm
3. Recent head trauma and/or intracranial neoplasm
4. Previous haemorrhagic stroke at any time
5. Previous ischaemic stroke within the past 1 year
6. Previous allergic reaction to fibrinolytics agent.
7. GI bleeding within the last month
Relative contraindications:
Contraindicated or failed thrombolysis
• TIA in the preceding 6 months then do PCI.
• Oral anticoagulant therapy
• Heavy vaginal bleeding, pregnancy
• Severe hypertension Menstrual bleeding not a contraindication
• Previous SAH, intracerebral hemorrhage
• High probability of active PUD.

Question-4: How will you investigate a case of acute MI ?

Investigations-
1. Cardiac enzyme markers
• Troponin – I & T
• CK-MB
• LDH
• Myoglobin
• AST
2. Echocardiography
3. CXR (heart failure/ pulmonary oedema)
4. Coronary angiogram
5. CBC (leucocytosis)
6. ESR/ CRP – raised
7. Lipid profile & RBS (Risks factors)

Enzymes Rise (Hours) Peaks (hours) Persists

Troponin I & T 3-6 hours 36 hours 2 weeks
CPK 4-6 hours 12 2 days
LDH 12 4 days 7-10 days
 Dr. A. M. Jahangir Alam, Registrar |4

Questions-5: What are the complications arises from acute MI ?

Complications of Acute MI:

Early complications ( within 24 hours)

Late complications: After 24 hour

• Ventricular aneurysm 10% ( persistent ST elevation in ECG)

• Post MI syndrome (Dressler’s syndrome)
• Post infarct angina
• Frozen shoulder (adhesive capsulitis)

Dressler’s syndrome:
It is a late complication of acute MI that occurs usually a few weeks or even months (2-10 weeks) after
acute MI. it is characterized by 5P’s –
• Pain (chest pain)
• Pyrexia
• Pleurisy
• Pericarditis (or pericardial effusion)
• Pneumonitis (or pulmonary infiltrates)
It is due to autoimmune reaction to necrosed myocardium. Antimyocardial antibody may be found in
the blood. Recurrence is common, confuses with new MI or unstable angina.
Treatment:
Mild to moderate: High dose aspirin (600-900 mg) every 4-6 hours or other NASIDS
Severe case or recurrent : Corticosteroids
Anticoagulant shoid be discontinued (unless strong evidence for high risk of thromboembolism)
 Dr. A. M. Jahangir Alam, Registrar |5

Question-6: What is your ECG diagnosis ?

This is 12 leads ECG tracing showing that..

1. ST elevation in lead V1-V5
2. ST depression in II, III, aVF
3. T inversion in V1-V5
4. Tall R in V1
So my ECG diagnosis is acute ST elevated anterior myocardial infarction.
Culprit artery is Left anterior descending artery (LAD) .

Question-7: How will you differentiate acute MI from acute pericarditis ?

Acute MI versus acute pericarditis

Points Acute MI Acute pericarditis

ST segment shape Convexity upwards Concavity upwards

Reciprocal ST depression Present Absent

ST elevation Segmental Global

PR segment in aVR Depression Elevation

Scenario: A 55 years old male, smoker , comes to you with the complaints of sudden severe chest
pain with sweating and vomiting.
What is your provisional diagnosis?
How will you investigate & manage ?
What are the complications arising from this ?
 Dr. A. M. Jahangir Alam, Registrar |6

This is 12 leads ECG tracing showing that-

ST elevation in lead I, Avl & reciprocal ST depression in lead III, aVF & left axis deviation.
So my ECG diagnosis is Acute ST elevated high lateral MI.

Culprit artery: Left circumflex artery (LCx), branch of left coronary artery (LCA)

This is 12 leads ECG tracing with rhythm strip showing that

• ST elevation in lead II, III, aVF
• Reciprocal ST depression in lead I, aVL
• Pathological Q wave in Lead II, III, aVF
• ST elevation in V1-V3
So my ECG diagnosis is acute ST elevated inferior MI (with RV infarction ).
Culprit artery is Right coronary artery .
 Dr. A. M. Jahangir Alam, Registrar |7

This is 12 leads ECG tracing with rhythm strip showing that

1. ST elevation in lead II, III, aVF
2. Reciprocal ST depression in lead I & aVL
3. Also ST depression in V1 & V2
So my ECG diagnosis is acute ST elevated inferior Myocardial infarction (with posterior extension).

Risk factors for IHD/MI

NON MODIFIABLE MODIFIABLE
Age Smoking / Alcohol

Sex : Male & Post menopausal women Hypertension

Genetics: +ve Family history Hypercholesterolaemia

DM

Hyperfibrinogenaemia
Lack of physical activity
Diet ( Mediterranean diet reduce CV disease)

Social deprivation
 Dr. A. M. Jahangir Alam, Registrar |8

NICE TO KNOW :

The serial evolution of ECG changes in transmural MI :

A. B. C. D. E.

Minutes Hours Days Several

weeks/months
Normal ECG Acute ST elevation Progressive loss of the Deep Q wave and T- Old or established
R wave, developing Q wave inversion infarct pattern;
wave, resolution of the Q wave tends to
the ST elevation and persist
terminal T-wave
inversion.

Definition :
Angina pectoris Angina pectoris is a symptom complex caused by transient myocardial ischaemia, which occurs
whenever there is an imbalance between myocardial oxygen supply and demand.
Stable Angina Ischaemia due to fixed atheromatous stenosis of one or more coronary arteries.
Unstable angina Ischaemia caused by dynamic obstruction of a coronary artery due to plaque rupture or erosion with
superimposed thrombosis.
Unstable angina is characterised by new-onset or rapidly worsening angina (crescendo angina), angina
on minimal exertion or angina at rest in the absence of myocardial damage.
Myocardial Myocardial necrosis caused by acute occlusion of a coronary artery due to plaque rupture or erosion
Infarction with superimposed thrombosis.
The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis
in a clinical setting consistent with acute myocardial ischaemia.
Acute coronary Acute coronary syndrome is a term that encompasses both unstable angina and myocardial infarction
syndrome (ACS)

Diagnostic Criteria for Acute MI:

Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin (cTn)), with at least one
value above the 99th centile upper reference limit (URL) and with at least one of the following:
1. Symptoms of ischaemia
2. New or presumed new significant ST segment–T wave (ST–T) changes or new left bundle branch block (LBBB)
3. Development of pathological Q waves in the ECG
4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
5. Identification of an intracoronary thrombus by angiography or postmortem • Cardiac death with symptoms
suggestive of myocardial ischaemia.
 Dr. A. M. Jahangir Alam, Registrar |9

Percutaneous Percutaneous coronary intervention (PCI) involves

passing a fine guidewire across a coronary stenosis
coronary under radiographic control and using it to position a
intervention balloon, which is then inflated to dilate the stenosis.
(PCI) A guidewire is advanced from the radial (or femoral)
artery to the coronary artery under radiographic
control (1). A fine balloon catheter is then advanced
over the guidewire to the stenotic coronary artery and
the balloon is inflated to dilate the stenosis (2). When
this has been achieved, a stent is usuallyplaced at the
site of the stenosis to maintain patency of the artery
(3)

Antiplatelet with mechanism of action

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ECG FOR FINAL PROF (M-53)

ECG-1: Complete Heart Block (CHB)

ECG

This is 12 leads ECG tracing with rhythm strip showing that –

1. P-P interval is regular & fixed
2. R-R interval is regular & fixed
3. P-R interval is variable (not fixed)
4. Heart Rate is 34 bpm

So my ECG diagnosis is Complete heart block (CHB) .

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Question-1: Classify block

Ans:

Question-2: Define Sinoatrial (SA) Block.

Ans:
In SA exit block, the sinus node continues to discharge at regular intervals, but some impulses are
blocked and are unable to reach the surrounding atria, as a result of this there complete absence of
an entire P-QRS-T complex.

Fig: SA block
 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 12

Question-3: Define AV block .

1st degree AV block:
ECG criteria:
1. P-R interval is prolonged (>0.20s or 5mm)
2. Every P wave is followed by a QRS complex ( No drop beat)

Fig: ECG of 1st degree AV block

2nd Degree AV Block: Mobitz type-1 (Wenckebach)
ECG criteria:
1. Progressive prolongation of PR interval followed by absence of QRS complex ( Drop
beat)
2. The PR interval always shortest immediately after the drop beat & longest just before
the drop beat ( Pause).
3. Two or more consecutive P waves are conducted, only single P wave is blocked (
Drop).
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2nd Degree A-V block: Mobitz Type-II (M-II)

ECG Criteria :
1. P-R interval of the conducted beats are Constant (Constant/ fixed PR)
2. One P wave is not followed by QRS complex ( Drop beat).
3. No progressive prolongation of PR intervals.

Complete heart block (CHB)

ECG Criteria of CHB
1. P-P interval is regular & fixed
2. R-R interval is regular & fixed
3. P-R interval is variable (not fixed)
4. Heart Rate is <40 bpm
 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 14

Question-3: What are the causes of CHB?

Ans:
1. IHD (Acute inferior MI)
2. Drugs: Digoxin/beta blocker/Calcium Channel Blocker/amiodarone
3. Progressive fibrosis of Bundle of His
4. Cardiomyopathies ( Ischamic/Dilated/ Idiopathic)
5. Infiltrative (Sis group) : Sarcoidosis/Amyloidosis/Haemochromatosis
6. Infectious: Infective endocarditis/Chagas disease/Lyme disease
7. Connective Tissue Disorders: SLE/RA/ Ankylosing spondylitis
8. Congenital : Child who’s mother is SLE (Anti-Ro positive)

1. Progressive fibrosis of distal His bundle system (Lev’s disease): Elderly

2. Progressive fibrosis of proximal his bundle system (Lenegre’s disease): Young
 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 15

Question-4: What are the presentation of CHB?

Ans:
Due to Low circulation Stoke’s Adams syndrome: It is an abrupt, transient loss
■ Dizziness
of consciousness due to a sudden but pronounced
■ Syncope
decrease in the cardiac output without warning sign.
■ Blackout
■ Stoke’s Adams syndrome

Question: What are the examination findings of CHB ?

Ans: Examination findings of CHB/ signs of CHB
Pulse: Bradycardia & High volume & Rate not increased by exercise or atropine.

BP: High systolic, Normal diastolic & High pulse pressure ( Wide pulse pressure)
JVP: Raised & “Cannon a” wave present , This wave due to atria contracts against a
closed TV, backward pressure produce “cannon a” wave.

Precordium:
Heart sound: Variable intensity of S1 (AV Asynchronous)
Added sound/ murmur: Systolic flow murmur ( due to increased stroke volume)

Question: How will you manage CHB ?

Management CHB:
If symptomatic: PACEMAKER
Acute stage (Stoke Adams): CPR followed by Transcutaneous Pacing (temporary pacemaker)
then PP (Permanent Pacemaker ).
Atropine doesn’t help to increase ventricular rate in case of CHB
 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 16

Causes of Bradycardia (HR<60 bpm) High volume pulse:

➢ Physiological: Athlets, sleep • Aortic regurgitation

➢ Pathological: • Hyperdynamic circulation due to any
1. Complete Heart block/Inferior MI cause
2. Sick sinus syndrome (SSS) • PDA
3. Carotid hypersensitivity • Hypertension
4. Drugs: BB, CCB, Digoxin • CHB
5. Hypothyroidism/myxoedema
6. Obstructive jaundice
7. Raised intracranial pressure (ICP)
8. Hypothermia
9. Enteric fever (Relative Bradycardia)

Pulse pressure: SBP-DBP (120-80) mm of Hg Hyperkinetic circulations :

=40 mm Of Hg 1. Severe anaemia
2. Pregnancy
Wide pulse pressure: >60 mm of Hg 3. High fever
4. Thyrotoxicosis
1. Aortic Regurgitation (AR) 5. Wet beriberi (Thiamine def)
2. Patent ductus arteriosus (PDA) 6. Pagets disease of bone
3. Complete Heart block (CHB) 7. A-V fistula
4. Hyperkinetic circulations

Causes of syncope:
➢ Cardiogenic:
1. CHB
2. Aortic stenosis
3. Left ventricular dysfunction
4. HOCM
5. Arrhythmias (AF/SVT)
6. IHD
7. Cardiac tamponade
➢ Neurocardiogenic syncope:
1. Vasovagal syncope
2. Carotid hypersensitivity
3. Cough syncope
4. Micturition syncope
5. Orthostatic syncope
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Question : Describe this ECG .

 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 18

Ecg for final prof (M-53)

ECG of Atrial fibrillation

This is 12 leads ECG tracing with rhythm strip showing that…

1. Absent of ‘”P” wave & replaced by fibrillatory “f” wave
2. R-R interval is irregularly irregular
3. Heart rate is 70 bpm
4. T-wave inversion in lead I & aVL
So my ECG diagnosis is atrial fibrillation with slow ventricular rate & high lateral ischaemia.

Causes of Absent P wave :

1. Atrial fibrillation
2. Atrial flutter
3. SVT
4. Hyperkalaemia
5. Ventricular tachycardia (VT)
6. SA block
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It is an arrhythmia where atria beat rapidly, chaotically & ineffectively, while the ventricules
respond at irregular intervals, paucing the characteristic irregular pulse.
Any conditions causing raised atrial pressure, increased atrial muscle mass, atrial fibrosis,
inflammation & infiltration of the atrium can cause atrial fibrillation.

Atrial rate is very high than ventricular rate= Pulsus deficit >10

Question-1: What are the types of atrial fibrillation ?

Types of atrial fibrillation:

1. Paroxysmal AF Self termination within 7 days (<7 days)

2. Persistent AF If cardioverted to sinus rhythm by any means or lasts > 7days regardless
of how it terminates.
3. Permanent AF If cardioverted to sinus rhythm is not possible by chemical (drugs).

4. Lone AF In the absence of underlying structural heart diseases or idiopathic (in the
absence of any disease).
Question no-2: What are the causes of atrial fibrillation ?
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Common causes
1. Chronic rheumatic valvular heart disease ( MS)
2. Coronary heart diseases (IHD / MI)
3. Hypertension (HTN)
4. Thyrotoxicosis
5. Chest infection (pneumonia)
6. Cardiomyopathies (DCM & HOCM)
Less common causes:
7. Myocarditis
8. Acute pericarditis & chronic constrictive pericarditis
9. Pulmonary embolism
10. Electrolyte imbalance
11. Alcoholism
12. ASD
13. Lone atrial fibrillation (idiopathic)

Investigations of Atrial fibrillation CXR in atrial fibrillation

1. CBC 1. MS ( straight left border)
2. CXR
2. Oneumonia
3. Se. Electrolytes
4. Se. Creatinine, Urea 3. LV type hypertrophy (HTN)
5. Echocardiogram 4. Pulmonary embolism
6. Thyroid function tests
7. Others: According to aetiology
 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 21

Question-3: How will you manage a case of atrial fibrillation ?

Management of AF

1. Rate control Rate limiting drugs (if fast AF)

Betablocker, calcium channel blocker, digoxin

2. Rhythm control Anti arhythmic drugs

Amiodarone, flecainide, BB, CCB
Catherter & surgical ablation
Pacemaker
3. Prevention of thromboembolism: Stroke Antiplatelets/anticoagulant

4. Treatment of aetiology MS, Thyrotoxicosis , ASD

Question-4: What are the anti-arrhythmic drugs used in AF?

 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 22

Question-5: How will you prevents thrombo-embolism/stroke in case of AF?

Question-6 : How will manage underlying causes in case of AF ?

 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 23

Question -7: What are the complications arises from atrial fibrillation ?

Complications of atrial fibrillation:

1. Thrombo-embolic manifestations: Stroke (ischaemic) & Pulmonary embolism (Pul infarction)

2. Heart failure

This is 12 leads ECG tracing with rhythm strip showing that…

1. Absent of ‘”P” wave & replaced by fibrillatory “f” wave
2. R-R interval is irregularly irregular
3. Heart rate is 140 bpm
So my ECG diagnosis is atrial fibrillation with Fast ventricular rate .
 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 24

Question -8: What are the examination findings of AF ?

Examination findings in AF

1. Pulse Irregularly irregular, Pulsus deficit

2. Blood pressure Normal (if HTN- raised BP)

3. JVP Raised if MS with right heart failure & absence of “a” wave in JVP

4. Precordium (MS) Visible apex beat

Tapping apex beat (MS) & heaving (HTN)
Palpable P2 (Pul HTN if mitral stenosis)
Left parasternal heave ( if mitral stenosis)
Diastolic thrill in mitral / apical area (if MS)
Auscultation:
S1 variable intensity (AF), S2 normal
Murmur: Mid diastolic murmur (MS) & Pansystolic murmur (TR)
Added sound: Opening Snap

Dr. A.M. Jahangir Alam

MRCP UK
Registrar , Medicine, MMCH
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ECG for FINAL PROF ( M-55)

Supraventricular Tachycardia (SVT)

This is 12 leads ECG tracing with rhythm strip showing that-

1. Heart rate is 225 bpm
2. R-R interval is regular (Rhythm regular)
3. Absent of P wave (P wave buried with QRS complex)
4. QRS complex is narrowed
So my ECG diagnosis is Supraventricular Tachycardia (SVT).

Question-1: What are the causes of SVT ?

Causes of SVT
1. Physiological : Anxiety / tension/ Tea/ Coffee/ Alcohol
2. Ischaemic Heart diaseses ( IHD)
3. WPW syndrome
4. Thyrotoxicosis
5. Digoxin toxicity
 D r . A . M . J a h a n g i r A l a m , R e g i s t r a r | 26

Question-2: How patient presents to you with SVT ?

Presentation of SVT / Clinical Features of SVT

1. Palpitation (rapid HR)
2. Dizziness/ presyncope/ syncope (Low CO)
3. Hypotension / shock (low BP)
4. Dyspnoea ( acute LVF)
5. Polyuria ( due to release of ANP causing diuresis & natriuresis)
6. Chest pain

Question-3: What are complications arises from SVT?

Complications of SVT

• Cardiogenic shock
• Heart failure (LVF) due to decreased
diastolic filling time (tachycardia)

Question-4: What are the difference between SVT & sinus tachycardia ?

Points Sinus tachycardia SVT

1. Onset Gradual Abrupt

2. Pulse Usually <160 bpm >160 bpm
3. P wave in ECG Present Usually absent
4. QRS duration Normal Narrow
5. Symptoms Palpitation Palpitation, polyuria, syncope, SOB
6. Carotid sinus/ valsalva maneuver No response May response abruptly
7. Prognosis Not serious Haemodynamically instability is
common

Question no-5: What are the difference between SVT & VT?

SVT VT
Narrow complex tachycardia (QRS) Wide complex tachycardia
No fusion beats Fusion beats present
No capture beats Capture beats present
No AV dissociation AV dissociation present
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Question-6: How will you manage a case of SVT ?

Management of SVT:
1. Acute management
2. Prophylactic management
I would like to asses first vitals (Pulse, BP, RR) whether patient is haemodynamically
stable or not..

If asthma/COPD: Adenosine Contraindicated

Carotid sinus massage: After exclusion of carotid bruit (atherosclerotic plug which dislodged
after massage and causes ischemic stroke ) & avoid massage simultaneously in both side ( cardiac
arrest).

Valsalva manuvre: Forceful expiration with closed glottis OR ( Forceful expiration with closed
mouth & nostril) which increase vagal stimulation and cardioinhibitory effect.

IV adenosine bolus dose: Initially 3 mg IV bolus (rapid infusion/IV flush/2s) then wait for 2 mins
Then assesses the HR & if unsuccessful then again IV adenosine 6mg bolus & wait 2 mins
Then reassess the HR , if unsuccessful : Again IV adenosine 12mg bolus dose
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Question-7: What you will do next after reversion to sinus rhythm ?

Ans:

• After restoration to sinus rhythm, I will do repeat ECG to find out or exclude WPW syndrome
& electrophysiological (EP) study to confirm WPW syndrome.
• WPW syndrome: RF (Radio frequency ) ablation of bypass tract (bundle of Kent )

Question-8: What are the side effects of adenosine ?

Ans:

➢ Flushing of face
➢ Broncho constriction so contraindicated in asthma
/ COPD
➢ Chest pain

Wolff-Parkinson-White syndrome

Question no-09: What are the ECG findings of WPW syndrome ?

Ans:
1. Presence of “Delta” wave
2. Wide QRS complex
3. Short PR interval

Treatment :

RFA (radiofrequency ablation) of Bundle of Kent.

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PRACTICE:

Question no-10: What is your ECG findings ? What is your ECG diagnosis ?

Dr. A. M. Jahangir Alam

Registrar
Dept of medicine . MMCH
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ECG for Final Prof Exam (M-55)

Ventricular Tachycardia (VT)

Question-1: Describe this ECG findings .

This is 12 leads ECG tracing with rhythm strip showing that..

1. Heart rate >150 bpm (Tachycardia) SVT

2. P wave absent
3. QRS complex wide ( very broad QRS complex >160ms) 1. Absent P
4. Extreme axis deviation ( lead I & lead III negative ) 2. Narrow QRS complex
5. Presence of ‘Fusion beat’ & ‘Capture beat’. 3. R-R regular
6. QRS V1-V6 : Negative ventricular concordance
So my ECG diagnosis is Ventricular Tachycardia (VT).
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Question no-2: What are the causes of VT ?

Ans:

1. Acute myocardial infarction.

2. Myocarditis.
3. Hypertensive heart disease
4. Cardiomyopathy.
5. Chronic ische mic heart disease with poor left ventricular function (Heart failure).
6. Ventricular aneurysm.
7. Mitral valve prolapse.
8. Electrolyte imbalance (mainly hypokalemia and hypomagnesemia).
9. Digitalis intoxication

Question No-3: What are the causes of wide complex tachycardia (WCT) ?
Ans:

Wide complex (QRS) tachycardia are-

1. Ventricular tachycardia ( VT)

2. SVT with bundle branch block
3. SVT with abberrancy

Question No-4: How will you differentiate VT from SVT ?

Points VT SVT

1. QRS duration Wide Narrow

2. AV dissociation Present Absent

3. Capture beat Present Absent

4. Fusion beat Present Absent
5. Concordance (+/-) Present Absent
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Question No-5: How will you manage a case of VT ?

A) Acute Management : Ventricular Tachycardia

During acute attack

Haemodynamical status

Stable BP >90/60 mmHg Unstable <90/60 mmHg or Heart failure

Amiodarone: IV amiodarone 150-300 mg bolus DC cardioversion (DC shock)

push followed by IV infusion for 24 hrs.
Or IV lignocaine 100 mg bolus (1 to 2 mg/kg). It
is followed by lignocaine infusion 2- 4 mg/min for
24 to 36 hours.
Or Slow infusion of IV Procainamide / Sotalol

If Fail or not improve

B) Prophylactic management / prevention of recurrence

Oral beta blocker or amiodarone & If recurrence : AICD (Implantation of automatic Cardioverter -
Defibrillator
Or Surgical or catheter ablation of focus.

Question-6: How will you prevent recurrence of VT ?

Ans:
1. Medicine : Amiodarone, Sotalol, beta-blocker, disopyramide, procainamide, flecainide .
2. EPS (Electrophysiological study ) + RFA ( Radio frequency ablation )
3. AICD
4. Surgery
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Question-7 : What are the types of VT / classify VT ?

Ans:

A) Based on its morphology (Monomorphic VT & polymorphic VT)

B) Based on its duration ( Sustained VT & non sustained VT).
Mono morphic VT Means that the appearance of all the beats match each other in each lead of
a surface ECG .
Poly morphic VT Means as a wide complex ventricular rhythm at rate over 100 with rapidly
changing QRS axis and / or morphology.
Sustained VT Sustained ventricular tachycardia (lasts > 30 sec.)

Non sustained VT Non sustained ventricular tachycardia (lasts < 30 sec.), consists of short salvos s
(> 3 or more).

Question-8: What are the symptoms of VT ?

• Palpitation (usually sudden onset like ‘switching on a light”.
• Faintness / dizziness
• Syncope
• Breathlessness / SOB ( due to heart failure)
• Chest pain

Signs of VT: Investigation

Pulse: Rapid regular but small pulse 1) ECG

BP: Low 2) Cardiac enzyme: Troponin I
Neck vein : Irregular canon wave 3) Echo
Auscultation: Variable S1 4) CBC & ABG
5) EP study
6) S electrolyte & magnesium

VERY IMPORTANT:
Tachycardia + Irregular RR + Absent “P” = Atrial fibrillation
Tachycardia + Regular RR + Absent “P” + Narrow QRS = SVT
Tachycardia + regular RR + “P” present = Sinus tachycardia
Tachycardia + absent “P” + wide QRS = VT
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Question No-09: What are the complications of VT ?

Ans:

1. Heart failure
2. Hypotension
3. Syncope
4. Cardiac arrest & cardiogenic shock
5. VF ( Ventricular fibrillation)
6. Torsedes De pontes (TdP)

Question No-10: What are the ECG findings ? What is your ECG diagnosis & management ?

Dr. A. M. Jahangir Alam

Registrar
Dept of Medicine , MMCH
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ECG of LVH

Final professional Exam (M-53)

1. What is your ECG findings? What is your ECG diagnosis ?

This is 12 leads ECG tracing with rhythm strip showing that

1. Tall R in V5/V6 which is 37 mm & Depp S in V1 which is 15 mm & summation of them
is 52 mm ( more than 35 mm)
2. ST Depression & T wave inversion in V5/V6 & also T wave inversion in I, aVL
3. Left axis deviation
So my ECG diagnosis is Left ventricular hypertrophy (LVH) with strain & high lateral ischaemia.
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Question-2: What are the causes of LVH ?

Causes of LVH:

1. Systemic HTN
2. Aortic stenosis
3. MR/AR
4. Coarctation of aorta
5. Hypertrophic cardiomyopathy

3. What are the precordium examination findings of LVH ?

Precordium examination findings of LVH
Inspection: Visible apex beat
Location: Slightly shifted and heaving (forceful, sustain, lift-up)
Heart sound:
S2 soft if severe AS
S4

4. What are the complications arises from LVH ?

Complications of LVH
1. Angina/ MI ( Chest pain)
2. LVF (Breathlessness)

LVH with strain + SOB= Acute LVF ( Bibasal creps/Pulsus alternans/gallop rhythm)

Treatment:

LVH with strain + Chestpain = Acute Myocardial infarction

Treatment:
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This is 12 leads ECG tracing with rhythm strip showing that,

1. Tall R in V5/V6 which is 37 mm
2. Deep S in V1 which is 32 mm & summation of them is 69 mm
3. ST depression in V6
So my ECG diagnosis is Left ventricular hypertrophy (LVH) with strain.

Classify hypertension
Endocrine causes of hypertension
Signs for secondary hypertension
Complications of hypertension
Management of hypertension
Name some anti hypertensive medications with side effects .

Dr. A. M. Jahangir Alam

Registrar
Dept of Medicine , MMCH