ECG for Final Prof

Jahinul Anam Fayed

K73
ECG Flowchart

Made by Abrar

Q.How to count
pulse if Irregular
rhythm?

- Number of Qrs in
30 large square
times 10
Heart rate is
30/min
P-P interval is
regular

R-R interval is
regular

There is no relation
between P wave
and QRS complex.
Complete heart block *****
Q.Presentation, finding, cause of complete heart block ?**

Q. Causes of Complete heart block?

Q: Write down three important abnormal findings
in this ECG.
A: As follows:
• Atrial rate is 60/min, P–P interval is constant.
• Ventricular rate is 35/min.
• There is no relationship between P-wave and QRS
complex
Q. It is a complication of what? Inferior MI (RCA also provides AV node, so that is damaged and
causes this heart block)
Q.How to differentiate CHB from sinus bradycardia?
- Sir I will look for some findings ( see presentation)

2 decrease
(hypothyroid,hy
pothermia)
2 increase
(jaundice, ICP)
Q.Why variable intensity of first heart sound and systolic murmur in CHB?
● Variable intensity of first heart sound is due to loss of AV synchrony.
● Systolic flow murmur is due to increased stroke volume.

Q: What is the mechanism of cannon wave?

A:Due to loss of AV synchrony, when atria contracts against closed tricuspid valve, backward pressure produces
cannon wave.

Q:What is the cause of congenital heart block?

Congenital heart block usually occurs, if the mother is suffering from SLE due to the presence of
anti-Ro (SSA) antibody, which crosses the placenta and causes congenital heart block.
Q.Management?
Injection atropine + temporary pacemaker. Then you may need permanent pacemaker.

INF MI With CHB just observe for 7 days with atropine

if extensive anterior MI PPM must, take time with TPM + Epinephrine.

in atropine parasympathetic block.

Type 2 degree HB + CHB treatment same.

in 1st degree HB no treatment, just don't give CCB, B blocker, Digoxin.

Dx- Acute ST elevated Anteroseptal MI **
Q. This is a 12 lead ecg showing ST elevation in V1, V2 and V3, Pathological Q-waves in V1
and V2.
Q.Why anteroseptal? Lead 3,4 (Lead V1-V4 is anteroseptal)
Q.Which artery involved – LAD (left anterior descending branch of LCA)
Q. which chambers are involved – LV (left heart failure)
Q.What intervention do you need to do if you are in CCU? PCI
Q.If Lead 5,6 elevated then dx ? Lateral
Q.If Lead 2,3,avf elevated then? Inferior
Q .If Lead I, avL elevated then? High lateral
Q.Cause of MI in young pt? (vasculitis, Kawasaki disease, hypercoagulability, HOCM,OCP)
Q.Cause of MI in a 20 year old pt? Cocaine abuse (vasospasm), aortic dissection due to
collagen vascular disease (marfan/ ehler danlos syndrome), hypercholesterolemia (due to
familial or in Nephrotic syndrome, anomalous origin of LCA (ALCA)
Q.Acute MI: cause?
Atherosclerosis of major coronary vessels, very rarely aortitis and autoimmune connective
tissue disorders
Q.monitoring of MI?
Cardiac monitoring ECG,BP, Urine output, Sp02, pulse
Q.Complication of MI/ Cause of death in MI? ***
Q. Management of MI?

In periphery
Oxygen if hypoxic
Tab. aspirin 300 mg with clopidogrel 300 mg stat (on new book clopid has been replaced with prasugrel)
Morphine for chest pain
Metoclopramide
Then refer to the higher centre.
Statin stat.

In Higher centre : ( where to send MI patient, Any centre with CCU)

If patient comes to hospital within 12 hour (specially the first 2 hours) of onset of chest pain - Primary PCI LINE
FROM DAVIDSON
If more than 12 hour has passed then give Inj. streptokinase SC (unless any complication)
Even after streptokinase if pain is there then try for delayed PCI. Now alteplase given not streptokinase ( use if
alteplase not available)
● Then
Injection furosemide/ spironolactone if volume overload
Tab statin lifelong (adverse effect is hepatotoxicity and myopathy)
ACEi / ARB to prevent ventricular remodelling.
B-blocker, GTN for angina
Q. Late management of MI? ( ACE/ARB Q. Risk factors of MI?
prevents cardiac remodelling , b blocker
prevents arrythmia

4 DRUGS must be in Discharge paper

Q.Management of cardiogenic shock?
1.Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the
preferred agent in patients with hypotension 2. Immediate PCI if shock due to MI 3. Immediate correction of the
Cause (PCI if MI, correct Arrhythmia, Immediate pericardiocentesis if due to pericardial effusion) 4. Management
of Shock

Q. Indications of streptokinase?
Acute MI, acute PE, DVT, Peripheral vascular disease.
There is ST elevation in lead 2,3,avf with ST depression and T inversion in lead 1,avL
(reciprocal change)
Acute ST Elevated inferior MI **** There may be presence of CHB, so look for it.
Q.Which coronary artery involved in inferior MI (RCA)
Q.Inferior surface of heart formed by which chambers – 2/3 LV 1/3 RV
Q.What type of heart failure occurs in inferior I and why? (biventricular failure) – because of
the chamber RV and LV on the inferior surface
Q.Investigation *
Q.Treatment *
Q.What is dressler syndrome and its treatment? NSAID + Steroid
Q.Is anticoagulant given or not ? yes if patient comes after 12 hour. Fondaparinux
Q. when we do PCI? If patient comes to hospital within 12 hour (specially the first 2 hours) of onset of chest
pain - Primary PCI
-If Facility unavailable then – administer streptokinase
Q.When not to give streptokinase?If there is bleeding disorder,Hx of administration of
streptokinase w/n the previous 5 years
Q.What advice to give to an MI patient? Take medications as prescribed, maintain regular
follow up, manage risk factors (HTN, DM), Reduce cholesterol level, maintain healthy weight,
Don’t strain in constipation.
Q.Character of the pain? *

Severe Retrosternal chest pain with onset rapidly over a few minutes, constricting/ heavy in
character radiating to the arm(s), neck, jaw sometimes epigastrium (if Inf MI), associated with
sweating, nausea , vomiting, breathlessness and feeling of impending death, prolonged in duration,
had no exacerbating factor, not relieved by nitrates or rest.

Q.T inversion involving all leads in subendocardial MI

ST elevation involving both anterior lead ( V2-V6) and Lateral leads (1, avL)
So it is -

Extensive anterior MI

Patient may need Diuretics here for Pulmonary edema as it is extensive anterior MI.

Q. Features of pathological Q wave?

1.Deep > two small squares, except lead 3.
2. Should be present in more than one lead
3.Associated with loss of R wave height
4.Q wave should be > 1/4th of of R wave.

Q. Pathological Q found in ?
● MI
● Ventricular hypertrophy
● Cardiomyopathy
● LBBB
 ● 12 lead ecg showing S wave in V1 (20mm) + R wave in Lead V6 (30mm) equals to 50mm >
35mm.
● ST wave depression and asymmetrical T wave inversion lead 1,2 V3,V4,V5.

So my Dx is LVH with strain pattern

Q.Causes of LVH ** Triple therapy for Heart Failure?

HTN -Acei, B-blocker, spironolactone
AS Digoxin is now third line drug
AR
MR
HOCM

ECG finding of Digoxin Toxicity?

Paroxysmal atrial tachycardia with AV block is pathognomonic
DX- Afib with fast ventricular rate (or slow ventricular rate if HR <100 )
Q. Why is it Afib?
Absent p wave, Irregular R waves, P wave replaced by fibrillatory waves. Don’t say saw tooth appearance in V1
as saw tooth waves are larger and regular and present in all leads. It can be called Coarse fibrillatory waves.
Q. Tell some causes of afib? ***

1.Chronic rheumatic valvular heart disease specially

MS
2.IHD
3. hyperthyroidism
4.Hypertensive heart disease
5.Lone AF

Q.Pulse characteristic? *
- Irregularly irregular pulse ,with high rate with presence of pulse deficit
Q. Heart rate in Afib ?
Usually high
Q. what is it called if there is difference between heart rate and pulse , why is there a discrepancy?
-Pulsus deficit, as there is fibrillation,and high ventricular rate so all the cardiac impulse doesn’t have effective
Stroke volume that is enough to produce a pulse
Q.Findings in heart in afib?
Heart (heart rate to see pulse deficit, mitral valvular or other cardiac disease)
History of IHD (heart failure) and hypertension (palpable A2) , Cardiomegaly and HF (in case of cardiomyopathy)
Presence of any congenital heart disease (ASD), pericardial disease

Q.How to monitor heart rate – by cardiac monitor in CCU, ICU, HDU ?

Q.Complication of AFib? **
● Thromboembolism (systemic and pulmonary).
● Heart failure.

Q.Commonest complication?Stroke
Q.What will you give to prevent complication? Antiplatelet ± anticoagulant drugs
Q.Why thromboembolism develops in AF? As the atria is beating upto 300-600 there is turbulence so it leads
to formation of a thrombus and when the atria contracts hardly against the stenosed valve then the thrombus gets
dislodged leading to thromboembolic manifestation. Also due to LA enlargement there is endocardium injury
Q.AF patient severe abdominal pain + bloody stool – what is the cause (mesenteric ischemia)

Q.Extracardiac cause of Afib – hyperthyroidism, thoracic surgery, Alcohol abuse, pulmonary embolism,
electrolyte imbalance (hypokalemia,hyponatremia), pneumonia

Q.AF and flutter present together. What do you call it?

Flutter fibrillation
Q.Treatment of AF with thyrotoxicosis?
● If paroxysmal AF : occasional attacks that are well tolerated don’t necessarily require treatment. If symptoms
troublesome then B-blocker
● If persistent AF then the 3 headlines :
Rhythm control - Electrical cardioversion (less than 48 hour, unstable patient then DC shock), chemical cardioversion for
stable patient ( no structural heart disease - Flecainide, if underlying heart disease- Amiodarone).
Rate control - B-blocker, rate limiting CCB(verapamil, Diltiazem), Digoxin
To prevent thrombosis : warfarin(needs monitoring, INR 2-3) / Rivaroxaban(more given) If AF more than 48 hours think that
thrombus has formed already.so anticoagulant for 3-4 weeks then rhythm control.
Cardioversion : either by Amiodarone or DC shock
If still not corrected then electrical cardiac-ablation.

1. restoration of sinus rhythm As soon as possible.

2. Rate control
3. Thromboprophylaxis
4. prevention of recurrence
5. Treatment of underlying cause.

For non valvular heart disease- CHA2DS2VASc score wise (it is a score that asses the risk of stroke, HAS-BLED
score estimates the risk of bleeding)
For valvular heart disease- no scoring ,go for direct drugs.
Q.What signs do you want to examine in atrial fibrillation?
- Heart (heart rate to see pulse deficit, mitral valvular or other cardiac disease).
-Thyroid status (warm sweaty hands, tremor of outstretched hands, tachycardia, exophthalmos and thyroid
gland)
-History of IHD and hypertension.
-History of other diseases causing AF

Then features of chest infection, Features of PE :U/L leg swelling(DVT), any redness, dyspnea, tachycardia,
features of alcoholism ( boggy, palmar erythema)

Q: What are the presentations? Must be asked

As follows:
1. Asymptomatic, may be detected during examination of the pulse.
2. Symptomatic:
• Palpitation,
• Breathlessness.
• Weakness, dizziness, giddiness.
• Features of primary disease (MI, thyrotoxicosis)
• Features of complications such as heart failure, embolism (commonly CVD with hemiplegia).
Q.If the patient is young,what are the causes of atrial fibrillation?
1.Chronic rheumatic heart disease with valvular lesions, commonly MS.
2.Thyrotoxicosis.
3.Others: Atrial septal defect (ASD),Acute pericarditis, Myocarditis, Pneumonia.

Q:If the patient is elderly, what are the causes of atrial fibrillation?
● Coronary artery disease (commonly acute myocardial infarction).
● Thyrotoxicosis.
● Hypertension.
● Lone atrial fibrillation (idiopathic in 10% cases).
● Others: See above (unusual or less in chronic rheumatic heart disease.

Q: If a patient with AF is unconscious, what is the likely cause?

- CVD due to cerebral embolism (usually with right sided hemiplegia)
Investigations : CXR, ECHO( LA thrombus).
transesophageal echo can detect even the minor LA thrombus.
TFT, Serum electrolytes

Q.Which CCB to treat AF (cardioselective verapamil, diltiazem)

Q.what are the causes of irregularly irregular pulse

Atrial fibrillation
Multiple ectopics.
Atrial flutter with variable block.
Paroxysmal atrial tachycardia with variable block.
Q.Write down four important findings in this ECG?
Heart rate: 140/min. Q. Presentation
Rhythm: Regular. Palpitation, polyuria,
P-wave: Absent.
syncope, Chest pain
QRS complex is narrow, So it is SVT

Q. Management of SVT?
If patient hemodynamically unstable : DC Shock
If patient hemodynamically stable :
Non pharmacological : carotid sinus massage, vulsalva manuvre
Pharmacological : inj adenosine then IV verapamil
DO Electrophysiological study and radiofrequency ablation of the ectopic beat

Q.What is the complication?

A: Heart failure may occur as a result of reduction of stroke volume (rapid heart rate causes short diastolic
filling time with low diastolic filling).
Tachyarrhythmia :
**Supraventricular (Narrow complex)
(sinus arrhythmia, MAT(COPD), FAT( Digoxin toxicity), SVT (AVRT, AVNRT), nodal rhythm.

in supraventricular tachycardia ONLY in AF rhythm irregular,

Wide complex
VT (regular) all other are irregular ( VF, Torsades, SVT with block, LBBB, multifocal ventricular
ectopic)

Any stimulus that spreads through normal pathway is narrow complex

BCD( Beta blocker, CCB, Digoxin) stops the AVN ( given in AVRT)

● In V.tach there is regular Wide QRS, 3 things needed to say V.tach - fusion beat, capture
beat and AV dissociation
● if irregular Wide QRS it is V.Fib
In AVRT If you stop AVN then
ectopic will contract everything.
then develop VT, V FIB
Carotid massage will show slurring of QRS)
reentry circuit around AVN, no ectopic tissue

in AVNRT ( Carotid will make everything normal)

ectopic pathway in AVNRT.
There is N here so give Node blocker.

permanent is electrophysiological study with catheter ablation