ecg workshop

ECG Workshop

Dr. Zohair Alaseri, MD

FRCPc, Emergency Medicine

FRCPc, Critical Care Medicine

Assistant Professor

Chairman, Department of Emergency Medicine

King Saud University Hospitals, Riyadh, KSA

60 Y. O. F. presented with sever palpitation and waeaknessArrested in 3 minutes from arrival to your department

Severe hyperkalemiaprolonged PR interval and

widened QRS complex

Arrest ECG

60 year old with sever crushing, heavy chest pain started 45 m. agowith BP of 85/45

Family want to know what is going on & what do you want to do for their relative??

Elderly man with this rhythm and with previously normal ECG??State your intervention please??

Electrical Alternans

Spot DX please????D/D???

Wolff-Parkinson-White pattern

Explain what do you see????

The short PR interval is due to a bypass track, also known as the Kent pathway. By bypassing the AV node the PR shortens .

The delta wave represents early activation of the ventricles from the bypass tract. The fusion QRS is the result of two activation sequences, one from the bypass tract and one

from the AV node .The ST-T changes are secondary to changes in the ventricular activation sequence .

54 year old lady history of hyperthyroidism presented with palpitation and sweating

Med inderal and digoxin & carbimazol

50 y.o. m. with sever submental pain,redness and tenderness ass with chest pain

50 y.o. m. with sever submental pain,redness and tenderness ass with chest pain

“danger” (post to retropharyngeal space from skull base to diagphragm)

Peritonsillar, Parapharyngeal (contains carotids, jug vein, cerv symp chain and CN IX XII)

Retropharyngeal (skull base to mediastinum – T2)

Prevertebral spaces (skull ,coccyx)

Prolonged QT

Elderly bed ridden man with increased weakness & fatigabulity with BP of 90/50

What do you want to give??

The deep S waves in the inferior leads and a left axis deviation indicates Left Anterior hemiblock+ poor R wave progression .

70 y o m sever chest typical ischemic pain for 30 minutes

The rhythm is atrial flutter sawtoothed pattern.

The conduction ratio is variable between 12:1 and 6:1

60 year old lady with suden onset of Palpitation

PR interval is short at about 100ms. QRS is broad even running into the P wave in lead II. Initial slurring of the QRS is evident. This is a case of WPW, and it seems to be intermittent with a recovery to normal in the last 3 beats of the rhythm strip.

18 year old with sudden onset of sever dizziness for 15 minutes

Anteroseptal InfarctionThe elevated S-T segements in leads

V1,V2,V3

69 y o f with sever pleuritc chest pain and diaphoresis for 30 minutes PMH DM IHD HTN

acute anterolateral myocardial infarctio & left anterior hemiblock

65 year old male with sever chest pain radiating to his back similar to his pain when he had MI 1 year agoHis bp is 90/30

Complete heart block third degree AV block & PVC QS complexes are commonly found in leads V1, and V2 as a normal variant.

45 year o. f. head of emergency department with sever headache, nausea & vomiting

Mobitz type II AV block

80 y. o. 2 hours after streptokinase for anterior wall MI

The ventricular rate is 75. The atrial rate is 150SVT with a 2:1 block. P waves are inverted in the inferior limb leadsThis points towards a low atrial location as the site of the ectopy. This is most likely a paroxysmal atrial tachycardia with block

Right bundle branch block & left anterior hemiblock

Wide QRS complex tachycardia. ventricular tachycardia

The QRS complex is wider than 140 ms. The R:S ratio in lead V6 is less than 1.

77 y o m with palpitation history of MI 3 years ago

Nodal idiojunctional

30 year old male sudden loc No PMHHis brother died at age of 39

Brugada

down-sloping Coved type or less commonly saddle-back type ST segment elevation followed by inverted T waves

Second-degree AV block

Mobitz type I AV block

Ventricular fibrillation

Multifocal atrial tachycardia

different P wave morphologies

45 y. o. m. heavy smoker with worsening SOB

Atrial flutter with 2:1 AV conduction.

Atrial flutter with 4:1 AV conduction.

Atrial fibrillation with ventricular preexcitation

S. rhythm with ventricular preexcitation.

17 year old with sudden palpitation

Sinus arrhythmia.

Multifocal atrial tachycardia.

The presence of at least three distinct P-wave morphologies and varying P-P, R-R, and PR intervals

MAT

7 year old with diarrhea and BP of 50/29

65 YEAR OLD WITH SYNCOPE AND HYPOTENSION

WPW Type Preexcitation

19 year old with on/off palpitation

There are ectopic P wave before them; therefore these are PAC's with RBBB aberration

LBBB and 2nd degree AV Block, Mobitz Type II

RBBB + LAFB = Bifascicular block-KH

The LAFB is recognized by the marked left axis deviation (-75 degrees) in the frontal plane, rS complexes in II, III, aVF, and the tiny q-wave in aVL.

RBBB plus Mobitz II 2nd Degree AV Block

In this rhythm strip of sinus arrhythmia, the faster rates have a LBBB morphology. In some patients with a diseased left bundle branch, the onset of LBBB usually occurs initially as a rate-dependent block; i.e., the left bundle fails to conduct at the faster rate because of prolonged refractoriness

Marked widenening of the QRS duration combined with tall, peaked T waves are suggestive of advanced hyperkalemia. Note the absence of P waves, suggesting a junctional rhythm, but in hyperkalemia the atrial muscle may be paralyzed while still in sinus rhythm. The sinus impulse conducts to the AV node through internodal tracts without activating the atrial muscle

Advanced Hyperkalemia

50 year old with pulmonary edema

Lateral Myocardial Infarction

•A23-year-old female was brought to the emergency department by ambulance after a "fainting spell."

•She felt acutely light-headed, weak and thought she was "going to pass out."

•She felt better approximately 5 minutes later, after lying down.

•There was no loss of consciousness and no evidence of seizure activity.

•She thought her heart might have been racing during the episode.

•She had never experienced any similar episodes in the past.

Case

PMH revealed a 3-year history of anorexia nervosa.

Over the past 4 weeks she had significantly reduced her oral intake and had lost approximately 20 lbs. Her present weight was 90 lbs.

She smoked half a pack of cigarettes a day and denied recent alcohol intake.

Case

Examination revealed a thin, pale woman in minimal distress.

Lying HR 86 beats/min BP 102/60 mm Hg.Standing HR 95 beats/min BP 90/58 mm Hg.

She was quite thin and had decreased muscle mass, No other pertinent physical findings were noted.

Case

BUN 9.8 mmol/LCr 110 µmol/LCa 0.7 mmol/LMg 2.09 mmol/Lphosphate 1.8 mmol/L.

LabHGB of 110 g/L Na130 mmol/LCl 91 mmol/LHCO3 28 mmol/LK 3.0 mmol/L

Case

During her ED stay the patient experienced another brief episode of "light-headedness" with palpitations. A rhythm strip was obtained

Case

The most likely cause of the patient's symptoms is:

1. Orthostatic hypotension 2. Wolff-Parkinson-White syndrome 3. Sinus bradycardia 4. Ventricular arrhythmia secondary to prolonged QT

syndrome

Case

Prolonged QT syndromeProlonged QT syndrome

60 year old female presented with sever dizziness and sweating started 2 hours ago

20 minute later C/O C_P

65 y. o. m. p. with typical CP.

(TCA ingestionsinus tachycardia widened QRS complex, deep S wave in lead I,and prominent R wave in lead aVR.

Ventricular paced rhythm with underlying complete heart block

infero-postero-lateral MI.

A 68-year-old man presented with chest pain radiating to the left arm of 3 hours’ duration .

He was diaphoretic and pale.

ST-segment depression, prominent R wave, and upright T waves in leads V1 to V3 in addition, ST-segment depression was seen in the inferior and lateral leads

V7, posterior axillary line;

V8, posterior scapular line;

V9, left border of spine.

Posterior Leads

All in the same horizontal plane of V4

to V6

ST-segment elevation in leads V8 and V9 minimal ST-segment depression with large R waves in the right

precordial leads (V1 to V3), confirming posterior wall AMI .

•Inferior STE & reciprocal STD •STE in lead V1 is typical for RV AMI • widespread STE

Inferior & RV MI

V1R is same as standard V2,

V2R is the same as standard V1,

V3R is halfway between V2R

V4R, V4R is fifth intercostals space at right midclavicular line, V5R is same level as V4R in right anterior axillary line

V6R is same level in right midaxillary line

• A. fib with subtle signs of acute inferior (MI) with ST elevations intermittently apparent in leads II, II and aVF.

• The right-sided chest leads show evidence of concomitant (RV) MI with slight ST elevations in leads V4R to V6R.

70-yr-old man presents with severe chest pain, nausea, vomiting and diaphoresis. Right-sided chest leads are shown (i.e., V1R to V6R).

SVT

Multifocal atrial tachycardia.

Wide complex tachycardia: rate-related BBB.

After adenosine became

VT

Ventricular Tachycardia.

Ventricular tachycardia with AV dissociation. (arrows denote regular P waves, although some are lost in the intervening complexes).

Wide complex tachycardia. A fusion beat (arrow) is seen in the rhythm strip;

its presence confirms VT.

Accelerated idioventricular rhythm.

Wolff Parkinson White syndrome and atrial fibrillation.

(A) Hypercalcemia shortened QT interval.prominent U waves (arrows) (B) Normocalcemia. This is baseline ECG from the same patient as in (A) when her

serum calcium level was normalized (7.8 mg/dL).

Hypocalcemia. prolonged QT interval. The deeply inverted T waves were present on the baseline ECG.

(A) Hyperkalemia. B) Resolving hyperkalemia..

Sine wave rhythm of hyperkalemia. The patient was administered IV calcium gluconate, causing an immediate narrowing of the QRS complex.

Hyperkalemia. minimal narrowed peaking of the T waves.

Hypokalemia. demonstrating T-wave flattening and prominent U waves (arrows)

Thank You