20 IMPORTANT ECGs

NOOR ATIKAH SAINI080201033

Ecg 1

h/o: 60 years old man with 4 hours crushing chest pain

This ECG shows :• Rate = 60/min• Rhythm = sinus rhythm• Axis = normal• P wave = normal• QRS complex = normal• T wave = normal• ST segment = elevated in the anterior leads V1-V6, I and aVL = reciprocal ST depression in the inferior leads ( leads II,III, aVF)• PR interval = normal• QT interval = normal

Diagnosis = Acute Anterolateral Myocardial Infarction

Ecg 2 :

H/o: A 56 years old man with chest pain and vomiting for 90 minutes

This ECG shows :• Rate = 50/min• Rhythm = sinus• Axis = normal• P wave = normal• QRS complex = normal• T wave = normal• ST segment = elevated in the inferior leads II, III, aVF. reciprocal ST depression in the anterior leads ( V1-V4).• PR interval = normal• QT interval = normal

Diagnosis = Acute Inferior Myocardial Infarction

Ecg 3 :

H/o: A 78 years old lady with chest pain and collapse, BP 60/40

This ECG shows :• Rate = 50/min• Rhythm = sinus• Axis = normal• P wave = normal• QRS complex = tall R wave in leads V1-V3• T wave = tall upwright T wave in leads V1-V3• ST segment = depression in anterior leads V1- V3• PR interval = normal• QT interval = normal

Diagnosis = Acute Posterior Myocardial Infarction

Summary :1. Features of MI based on its site of infarction:

Changes of ECG

Anterolateral MI

Inferior MI Posterior MI

ST segment

•ST elevetion in leads V1-6, I and aVL

•With ST depression in leads II,III,aVF

•ST elevation in the leads II, III and aVF

•With ST depression in leads V1-V4

ST elevation in leads V1-3

R wave - - Tall R wave in leads V1-V3

T wave - - Tall T wave in leads V1-3

Progression of Ischaemia to Injury to Infarction

ECG changes:• Ischaemia = only T wave abnormalities • Injury = T waves + ST segments abnormalities • Infarction = T waves + ST segments + QRS complexes abnormalities

Ecg 4 :

H/o: A 64 years old man with breathlessness and a raised JVP

This ECG shows:• Rate = 120 beats/min• Rhythm = sinus• Axis = normal• P wave = normal • QRS complex = normal• T wave = small or inverted• ST segment = widespread • PR interval = normal• QT interval = normalOther features = alternating high and low voltages of all the ECG waveforms Diagnosis = Electrical alternans of pericardial effusionThe classic example is a pericardial effusion with the heart "swinging" in it

and changing its location and proximity to the chest wall (where the electrodes are) from beat to beat.

electrical alternans/low voltage alternans:=>alternate-beat variation in the direction, amplitude, and duration of any

component of the ECG waveform (ie, P, PR, QRS, R-R, ST, T, U).

Causes :1. Physical : hypothermia2. Infections : myocarditis, pericardial TB3. Neoplasm : pericardial mesothelioma4. Metabolic disorders : obesity, heart amyloidosis,haemochromatosis

cardiomyopathy5. Structural disorders : pericardial effusion, cardiac temponade,

hydro/hemopericardium,pneumothorax6. Poisoning : chronic alchoholism

60 year old male with chronic kidney disease on mantainance hemodialysis is brought to emergency with breathlessness and volume overload

Findings:-sinus rhythm-small or absent P wave-long PR interval-shortened ST segment -normal axis-broad QRS complexes-tall tented T waves

Hyperkalemia Definition:plasma potassium level of

5.5mM Changes in hyperkalemia:1.mild-prolongation of PR and QRS interval.2.moderate-loss of Pwave and progressive

widening of QRS complex3.severe-sine wave sinoaventricular rhythm

Management:-IV administration of glucose along with

insulin to encourage shift of potasium from EC to IC compartment

-50ml of 50% glucose plus 10 unit of soluble insulin as bolus

-500ml 20% glucose plus 10 unit of soluble insulin as infusion over 6 – 12 hours

-10ml of 10% calcium gluconate IV slowly over 2-5 min to stabilise myocardial cell

-50 – 100ml of 8.4% sodium bicarbonate IV-nebulisation of beta agonist( salbutamol)-if these measure fail hemodialysis is

indicated

Case 2A 22 year old lady with prolonged vomitting

Findings:-sinus bradycardia-long PR interval-normal axis-small T wave-Presence of U wave (repolarization of

papillary muscles or purkinje fibres) -ST segment deviation-prolonged QT interval

ECG changes of hypokalemia-increased amplitude and width of Pwave-prolongation of PR interval-T wave flattening and inversion-ST depression-prominent U wave-apparent long QT interval due to fusion of T

and U waves

Hypokalemia-causes:1.Low PTH level:parathyroid agenesis,

destruction, reduced function2.High PTH level:vit D deficiency, drugs, PTH

resistance syndrome, acute pancreatitis-features1.Asymptomatic2.Paresthesia of fingers ,toes,circumoral

regions3.severe:seizure, carpopedal spasm,

bronchospasm, laryngospasm

Case 3A 65 year old women with congestive cardiac failure and on treatment come with the ECG.

Findings:-Abnormal rhythm-inverted T wave-downward sloping ST segment- reversed tick

sign -depressed ST – J point-shortened QT interval

Digitalis effects-digitalis is a drug used in CCF and to slow

the ventricular rate in atrial tachyarrhythmias

-digitalis effects is due to early recovery and repolarisation of myocardial cells.

1.coved ST segment depression 2.flattened T wave 3.decreased QT interval

Digitalis toxicity-due to excessive amount of digitalis >2ng/ml-features: 1.general symptoms-weakness, anorexia,

nausea, vomitting, visual effects and mental changes.

2.arrhythmias and conduction disturbance-ventricular arrhythmia,bidirectional ventricular tachycardia,AV junctional rhythm,sinus bradycardia

-treatment: 1.prevention-baseline ECG, serum electrolyte,

BUN and creatinine. 2.definitive treatment depend on arrhythmia minor-discontinuation of digitalis and

careful observation serious-suppression with IV drugs lidocaine -pacemaker in patient with

complete heart block -digitalis binding antibody IV

(digoxin immune Fab)-lethal dose

Case 4A 40 year old male, asymptomatic came with the ECG

Findings :-sinus rhythm-inverted P wave in lead I-increased PR interval-right axis deviation-QRS complexes get progressively smaller

from V1 to V6 with small R wave

Dextrocardia It is the condition in which the cardiac

apex is in the right side of the chest D/D-accidental reversal of the left and right arm

electrodes-situs inversus : congenital condition in

which major visceral organs are reversed from their normal position

CASE #1• A 27 year old female, Mrs. Terry,

a known case of α₁-antitrypsin deficiency, complained of fever, increased breathlessness and wheezing since 3 days.

COPD

• Rhythm : sinus rhythm• Axis : right axis deviation• P wave : P pulmonale ( >2.5mm in lead II)

D/D for P pulmonaleValvular disease

• Tricuspid stenosis

• Tricuspid regurgitation

Pulmonary hypertension

• COPD• Pulmonary

embolism• ILD• Sleep apnoea• LV systolic

dysfunction

Congenital heart disease

• Ebstein’s anomaly

EBSTEIN’S ANOMALY-congenital condition often associated with WPW syndrome

ECG findings- ‘Himalayan’ P wave- prolong PR interval

ECG 240 year old female with history of chronic breathlessness

• Rhythm : irregularly irregular• Axis : right axis deviation• P wave : diminished

MITRAL STENOSIS

LA enlargement???

CASE #3• An 83-year-old man who is

apparently asymptomatic came to OPD.He is regularly seen by your colleague. Since your colleague is on leave,this patient asked your review on his current heart condition.

ECG #3

• Rhythm : sinus rhythm• Axis : left axis deviation• P wave : biphasic (2nd half of wave is –ve)• QRS complex : deep S wave, tall R wave

DIAGNOSING LVH ON ECG• Limb Leads (Low sensitivity, high specificity)

– R wave lead I + S wave lead III > 25 mm– R wave aVL > 11mm– R wave aVF > 20mm– S wave in aVR > 14mm

......

• Precordial Leads (High sensitivity, low specificity)

– R wave V5 or V6 > 26mm– R wave V5 or V6 + S wave in V1 > 35mm– Largest R wave + largest S wave in precordial leads

> 45mm

........

• The Sokolow-Lyon criteriumR in V5 / V6 + S in V1 > 35mm

• The Cornell criteriumR in aVL and S in V3 >28 mm in menR in aVL and S in V3 >20 mm in women

ECG #4

CASE #4• A 60-year-old female, known

case of IHD, presented with palpitations in the OPD. On examination, her measured systolic BP is 80.

Torsades de Pointes

TORSADES DE POINTES(Polymorphic ventricular tachycardia)

• Acute management1)Electrolyte2)Drugs3)Heart rate4)MgSo₄5)IV isoprenaline

• Long-term management1)β-blockers2)Left cardiac sympathetic

denervation3)Pacemaker

ECGNUR SHUHAIZA BINTI SUPIAN

080201039

CASE 1A 23 years old male with h/o episodes of palpitation

ECG FINDINGS: Normal rate Sinus rhythm Normal axis Short PR interval Slurred upstroke of QRS complex, best seen

in I, V4, V5 Widened QRS complex due to ‘delta’ wave

WPW SYNDROME

WOLFF-PARKINSON-WHITE SYNDROME

one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes.

majority of individuals with WPW remain asymptomatic throughout their entire lives

risk of sudden cardiac death associated with the syndrome.

caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles

Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.

CASE 2A 50 years old male with h/o chest pain for 24 hours

Sinus rhythm with ventricular bigeminy Normal rate and axis Bigeminy : every sinus beat is followed by a

ventricular premature beat No preceding P wave The coupling interval is usually constant Usually followed by compensatory pause

VENTRICULAR BIGEMINY

Compensatory pause:The R-R interval between the beats directly preceding and following the VPB is exactly twice that of regular R-R interval

Common cause for ventricular bigeminy: May occur in normal individual Ischemic heart disease Digoxin toxicity Left ventricular dysfunction

CASE 3A 40 years old female, bedridden for 48 hours, come with c/o breathlessness

Sinus tachycardia Normal rate Normal axis Prominent S wave in Lead I Small Q wave, inverted T wave in Lead III

S1 Q3 T3 PATTERN

ACUTE PULMONARY EMBOLISM

CASE 4A 60 years old male, recently diagnosed with myocardial infarction

Rate increased (>100/min) Sinus rhythm Independent P wave Broad QRS complexes (>0.16s) beat to beat variability of the QRS

morphology

VENTRICULAR TACHYCARDIA

Fusion beat:When one impulse originating from ventricle and a second supraventricular impulse simultaneously activate the ventricular myocardium

Capture beat:Normal conduction momentarily “captured” control of ventricular activation from VT focus

Brugada Criteria: Lack of an RS complex in the precordial leads

Whether the longest interval in any precordial lead from the beginning of the R wave to the deepest part of the S wave when an RS complex is present is greater than 100 ms

Whether atrioventricular dissociation is present

Whether both leads V1 and V6 fulfilled classic criteria for ventricular tachycardia.

Immediate cardioversion in synchronised mode

IV Amiodarone : given as bolus followed by continuous infusion

IV Lidocaine

TREATMENT OF VT:

AV BLOCKS

• FIRST DEGREE- All impulses conducted, but delay present

(prolonged PR interval)In coronary artery disease, drug toxicity(digoxin, CCB’s, β blockers) electrolyte disturbances(hyperkalemia) acute rheumatic carditis, congenital heart diseases(ASD, Ebstein’s anomaly)

• SECOND DEGREE- Impulse completely fails to pass through the AV

node Mobitz type ll Wenkebach phenomenon/Mobitz type l Causes- o Physiological- atheletes, vagotonic individualso Acute rheumatic carditiso MI (eg inf wall, right ventricular)o Acute diphtheric myocarditiso Drugs- digitaliso Idiopathic fibrosis of the conduction system

(Lenegre’s disease)

• THIRD DEGREE- Atrial contraction is normal, but no beats are

conducted to the ventricles Causes- o Drugs-o Acute MIo Acute rheumatic carditiso Congenital heart disease(ASD, VSD)

HOW TO DIAGNOSE

• LOOK FOR-R-R INTERVAL

P WAVES

P-R INTERVAL

R-R INTERVAL

REGULAR IRREGULARP-R INTERVAL 2ND DEGREE

SAME VARIABLE P-R INTERVAL

1ST DEGREE 3RD DEGREE CHANGES FIXED MOBITZ TYPE I TYPE II

CASE I

• 70 year old male, complains of exercise intolerance

• RATE- normal• RHYTHM- regular( dual rhythm)• AXIS- normal• P WAVE• QRS COMPLEX• T WAVE• PR INTERVAL• QRS INTERVAL

CASE II

• 90 year old male, presented with syncope

Rhythm : sinus rhythmAxis : normalP wave : QRS complex : widersR’ pattern (M shaped) in V1, V2

•T wave : inversion in V1, V2 •wide, slurred S wave in L I and V5, V6 ST segment : depression in V1, V2PR interval :QT interval :

CAUSES

• acute myocardial infarction,• acute pulmonary embolism,• chronic cor pulmonale• Congenital heart disease(ASD, VSD, Ebstein’s

anomaly)• Myocarditis• Cardiac contusion

CASE III

• 90 year old male presented with sudden onset of chest pain and was diagnosed to have myocardial infarction

•Rhythm : sinus rhythm•Axis : normal•P wave : •QRS complex :wide small r waves followed by deep, wide and slurred S waves in V1, V3;•broad, notched or slurred (M shaped) R wave in L I, aVL, V5, V6;absence of q waves in L I, aVL, V5, V6;•T wave : inversion•ST segment :depression in L I, aVL, V5, V6 •PR interval :•QT interval :

CAUSES

• Always pathological• acute myocardial infarction,• hypertensive heart disease • dilated cardiomyopathy• Aortic valve disease• Drugs (quinidine).

CASE IV

• 90 year old male with a past history of MI, which was complicated by LBBB. He is currently asymptomatic

WHERE IS THE PACEMAKER ?• Atrial pacing spikes- short vertical lines

preceding the P waves and best seen in lead III• Ventricular pacing spikes- precede the QRS

complex and best seen in lead V2 , V3, V4 & V5