ECG changes in acute cardiac conditions

1. ECG Interpretation in
Emergency Settings
DR.AYMAN SALEH GMZAWI
MBBS , FEBC (PG Y4)
Presented by
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2.  Identify Common ECG Changes in Emergency settings.
 Interpret Common ECG Strips in Emergency Settings.
 Diagnose Common ECG changes in Emergency Settings.
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Objectives

3.  Arrhythmias
 Acute Coronary Syndrome
 Pulmonary Embolism
 Hyperkalemia
 Pericardial Effusion
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What’s Emergency Conditions
Should Rapidly Identify ?

4. TACHYARRHYTHMIA BRADYARRHYTHMIA
ARRHYTHMIA
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5. TACHYARRHYTHMIA
Supraventricular
Tachycardia
Ventricular
Tachycardia
Atrial
Fibrillation
Atrial
Flutter
Sinus
Tachycardia
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7. Tachycardia
(Rate > 100)
Narrow Complex
Tachycardia
(QRS <120ms)
Wide Complex
Tachycardia
(QRS ≥ 120ms)
Regular Irregular Regular Irregular
• Sinus Tachycardia
• SVT (AVNRT,
AVRT,AT)
• Atrial flutter with
fixed rate
conduction
• AF with rapid
ventricular rate.
• Atrial flutter with
variable rate
conduction
• MAT
• Ventricular
Tachycardia
• SVT with aberrancy
• Antidromic AVRT
• Polymorphic VT
• Preexcited AF
• AF with aberrancy
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8. Sinus Tachycardia
• Regular rhythm with ventricular rate > 100 beat per minute.
• P – wave with constant morphology preceding every QRS
complex.
• The P – wave positive in Lead II.
• The P – wave Negative in aVR.
• The P – wave biphasic in V1.
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9. Sinus Tachycardia
• Sinus tachycardia generally reflect an underlying process,
metabolic state, or medication effect.
• Fever , hypovolemia, shock, CHF, anxiety, PE, anemia,
thyrotoxicosis, caffeine, nicotine, atropine, catecholamine, or
withdrawal from alcohol or drugs can cause sinus tachycardia.
• Sinus tachycardia can be:
• Appropriate: represent normal physiological response
• Inappropriate: represent defects in vagal or sympathetic tone
or an intrinsic problem in SAN itself.
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12. Supraventricular
Tachycardia (SVT)
AV Node
Reentrant
Tachycardia
(AVNRT)
AV Reentrant
Tachycardia
(AVRT)
Atrial
Tachycardia
(AT)
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Remember: whatever the mechanism the
management in ER will be the same.

13. Supraventricular
Tachycardia (SVT)
• Regular Tachycardia.
• Narrow complex, unless pre-existing bundle branch block,
accessory pathway, or rate related aberrant conduction
• P waves may be buried in the QRS complex, visible after the QRS
complex, or very rarely visible before the QRS complex.
• P waves if visible exhibit retrograde conduction with P-wave
inversion in leads II, III, aVF.
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Atrial Fibrillation
• Irregularly irregular rhythm.
• No P waves.
• Fibrillatory waves may be present either fine or coarse
• Fibrillatory waves may mimic P waves leading to misdiagnosis.
• Variable ventricular rate.
• QRS complexes usually < 120 ms .
• Commonly AF is associated with a ventricular rate 110 – 160 .
• AF with rapid ventricular response >100 bpm.
• AF with slow ventricular response <60 bpm.
Remember: Risk of Stroke and Anticoagulation

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• The ventricular response is
irregular and may mimic AF
• On closer inspection, there may
be a pattern of alternating 2:1,
3:1 and 4:1 conduction ratios
Variable AV block
Fixed AV block
Ventricular rate is a fraction of
the atrial rate, e.g.
• 2:1 block = 150 bpm
• 3:1 block = 100 bpm
• 4:1 block = 75 bpm
Atrial Flutter

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Atrial Flutter
• Regular atrial activity
• Narrow complex
• Flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF — may be
more easily spotted by turning the ECG upside down!
• Flutter waves in V1 may resemble P waves

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Wide Complex Tachycardia
SVT with
Aberrancy
Antidromic AVRT
Monomorphic VT
Preexcited AF
AF with
Aberrancy
Polymorphic VT
Regular Irregular

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Ventricular Tachycardia (VT)
ECG Features suggestive of VT:
• Very broad complexes (>160ms)
• Absence of typical RBBB or LBBB Morphology.
• Extreme axis deviation.
• AV dissociation
• Capture beats
• Fusion beats
• positive or negative concordance throughout the
chest leads
• Brugada’s sign, Josephson’s sign

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Ventricular Tachycardia (VT)
Clinical Features Suggestive of VT
• Age > 35 (positive predictive value of 85%)
• Structural heart disease
• Ischemic heart disease
• Previous MI
• Congestive heart failure
• Cardiomyopathy
• Family history of sudden cardiac death (suggesting conditions such as
HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic
right ventricular dysplasia that are associated with episodes of VT)
Remember: If you in doubt, treat as VT!

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Polymorphic (VT)
• Form of ventricular tachycardia in which there are
multiple ventricular foci with the resultant QRS
complexes varying in amplitude, axis and duration.
• Torsades de pointes (TdP) is a specific form of
polymorphic (VT)occurring in the context of QT
prolongation; it has a characteristic morphology in
which the QRS complexes “twist” around the isoelectric
line.
• Bidirectional VT is another type of polymorphic VT
most commonly associated with digoxin toxicity.

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Ventricular Fibrillation
• Chaotic irregular deflections of varying amplitude
• No identifiable P waves, QRS complexes, or T waves
• Rate 150 to 500 per minute
• Amplitude decreases with duration.
Cardiac Arrest
NEXT STEP ?

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BRADYARRHYTHMI
A
Sinus Node
Dysfunction
(SSS)
Sinus
Bradycardia
Junctional
Escape
Rhythm
AF with
Slow
Ventricular
Response
AV Block
AF with
CHB

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Sinus Node Dysfunction (SSS)
• Multiple ECG abnormalities can be seen in sinus node
dysfunction include:
• Sinus bradycardia.
• Sinoatrial Exit Block.
• Sinus Arrest – pause > 3 Seconds
• Atrial fibrillation with slow ventricular response.
• Tachy – Brady syndrome.

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Atrioventricular Block
1st Degree
AV block
2nd
Degree
AV block
3rd
Degree
AV block
Mobitz
Type I
Mobitz
Type II

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1st Degree AV Block
• Fixed prolonged PR interval> 200ms (five small squares)
2nd Degree AV Block (mobitiz type I)
• Progressive prolongation of the PR interval culminating in a
non-conducted P wave
2nd Degree AV Block (mobitiz type II)
• Intermittent non conducted P waves without progressive
prolongation of PR interval.
Atrioventricular Block

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3rd Degree AV block (complete AV Block)
There is a complete AV dissociation - none of the
supraventricular impulses are conducted to the ventricles.
Remember: before Dx look for speed of ECG 25mm/s
Atrioventricular Block

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Myocardial Infarction
ECG Manifestations of Acute Myocardial Ischemia (in Absence of
LVH and LBBB ) are:
ST elevation:
New ST elevation at the J-point in two contiguous leads with the
cut-off points: ≥0.2 mV in men or ≥ 0.15 mV in women in leads
V2–V3 and/or ≥ 0.1 mV in other leads.
ST depression and T-wave changes:
New horizontal or down-sloping ST depression >0.05 mV in two
contiguous leads; and/or T inversion ≥0.1 mV in two contiguous
leads with prominent R-wave or R/S ratio ≥ 1

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Myocardial Infarction
Localization ST elevation
Reciprocal ST
depression
Coronary Artery
Anterior MI V1-V6 None LAD
Septal MI
V1-V4, disappearance of
septum Q in leads V5,V6
none LAD-septal branches
Lateral MI I, aVL, V5, V6 II,III, aVF LCX or OM
Inferior MI II, III, aVF I, aVL
RCA (80%) or RCX
(20%)
Posterior MI V7, V8, V9
high R in V1-V3 with
ST depression V1-V3
> 2mm (mirror view)
RCX
Right Ventricle MI V1, V4R I, aVL RCA

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Myocardial Infarction
In the first hour and day after the onset of a myocardial infarction, several
changes can be observed on the ECG. First, large peaked T wave (or hyperacute T
waves), then ST elevation, then negative T wave and finally pathologic Q
waves develop.
Time from onset of
symptoms
ECG Changes in the heart
minutes
hyperacute T waves (tall T waves), ST-
elevation
reversible ischemic damage
hours
ST-elevation, with terminal negative T
waves, negative T waves (these can last
for days to months)
Ischemic necrosis
days Pathologic Q Waves scar formation

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Hyperkalemia
Serum K >5.5
mEq/L
Serum K >6.5
mEq/L
Serum K >7.0
mEq/L
Serum K >9.0
mEq/L
Repolarization
abnormalities
• Peaked T waves
Progressive paralysis
of atria:
• P wave widens and
flattens
• PR segment
lengthens
• P waves eventually
disappear
Conduction abnormalities
• Prolonged QRS interval
• High-grade AV block with slow
junctional and ventricular
escape rhythms
• BBB or faiscular Block
• Sinus bradycardia or slow AF
• Development of a sine wave
appearance (pre-terminal)
Cardiac Arrest:
• Asystole
• Ventricular
fibrillation
• PEA with
bizarre, wide
complex
rhythm

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v
v

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Pulmonary Embolism
Key ECG finding:
• sinus tachycardia.
• Complete or incomplete RBBB.
• RV strain pattern – T wave inversion in right precordial leads(V1
– 4 ) ± the inferior leads (II, III, aVF)
• Right axis deviation
• Dominant R wave in V1
• Right atrial enlargement (P Pulmonale)
• SI QIII TIII
• Atrial tachyarrhythmias.
• Non specific ST segment and T wave changes

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Massive Pericardial Effuion
Massive pericardial effusion produces a triad of:
• Low voltage ECG
• The amplitudes of all the QRS complexes in the limb leads
are < 5 mm; or
• The amplitudes of all the QRS complexes in the precordial
leads are < 10 mm
• Tachycardia
• Electrical Elternas

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Thank You