ECG diagnoses Flashcards
P wave duration, amplitude & Characteristics
P duration < 0.12 sec = 3 small squares
P amplitude < 2.5 mm
Notched P waves “P mitrale” = Left atrial enlargement. Normal amplitude but increased duration (> 3 small squares )
If the P is not seen in LII, look for it in V1
FREQUENCY CALCULATION
Vertical bar every 15 big squares
30 bigs squares = 6 sec
Number of Rs x 10 in 6 sec = Heart frequency
300, 150, 100, 75, 60, 50, 40
PR interval duration
0.12 - 0.20 sec
3 - 5 small squares
1 big square = 0.20 seg = 200 ms
Prolong PR interval cause
> 1 big square or > 220 ms
1st degree AV Block
Short PR interval cause
< 0.12 sec or < 3 small squares
Presence of an accessory pathway
Asocc with delta wave = WPW
ECG Normal Axis
Lead I: QRS (+)
AVF: QRS (+)
(0 to +90)
ECG Left deviated Axis
Lead I: QRS (+)
AVF: QRS (-)
(0 to +90)
CAUSES OF LEFT AXIS DEVIATION
Left ventricular hypertrophy
Left bundle branch block
Wolff-Parkinson-White Syndrome
Horizontally orientated heart: Short patient, pregnant or ascites
ECG Rigth deviated Axis
Lead I: QRS (-)
AVF: QRS (+)
(+90 to +180)
CAUSES OF RIGHT AXIS DEVIATION
Right ventricular hypertrophy
Pulmonary embolism
Lateral/posterior wall STEMI
Chronic lung disease: COPD
Sodium-channel blockade: TCA poisoning
Wolff-Parkinson-White syndrome
Dextrocardia
Normal paediatric ECG <2yo
Left Ventricle Hypertrophy (LVH) in the ECG
Left deviated Axis
V6: QRS (+) & T (-)
V1: QRS (-) & T (+)
Left Ventricle Hypertrophy (LVH) CAUSES
- Essential hypertension
- Hypertrophic Obstructive Myocardiopathy (HCOM)
- Subaortic and Aortic stenosis
- Aortic regurgitation
- Mitral regurgitation
- Coarctation of the aorta
- Ventricular septal defect (VSD)
- Infiltrative cardiac processes: Amyloidosis, Fabry disease, Danon disease
HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY (HCOM) in the ECG
Classic dagger Q waves on the left precordial leads
Right Ventricle Hypertrophy (LVH) in the ECG
Right deviated Axis:
V6: QRS (-) & T (+)
V1: QRS (+) & T (-)
Normal QRS duration
Right Ventricle Hypertrophy (LVH) causes
- Acyanotic Congenital Heart Diseases: ASD & VSD
- Pulmonary valve stenosis (Amiodarone)
- Tricuspid valve regurgitation
- Tetralogy of Fallot
- Lung diseases: Pulmonary fibrosis, chronic obstructive pulmonary disease, and sleep apnoea.
Lead II Isoelectric meanings
- Right Ventricle Hypertrophy (RVH)
- Mechanical: Right deviated Axis
- Electrical Conduction impaired: Normal Axis
- Left Branch Bundle Block (LBBB)
Left Branch Bundle Block (LBBB) in the ECG
Lead II : P wave wide & prolong PR interval
Axis will be normal or Left deviated
V6: QRS (+) usually notched & T (-) with ST depression
V1: QRS (-)
Rigth Branch Bundle Block (RBBB) in the ECG
V1: QRS (+) Wide-notched and T (-) with ST depression
V6: Prominent S
- RsR’ on V1 –V2
Axis will be normal or Right deviated
QRS Duration
0.06 - 0.10 sec
1.5 - 2.5 small squares
> 2.5 small squares = Wide QRS
Wide QRS causes
- Hyperkalemia.
- Hyper- or hypo-magnesemia.
- Supraventricular tachycardia (SVT) + bundle branch block (BBB)
- SVT with aberrant conduction.
- Atrial fibrillation (Afib) + Wolff-Parkinson-White syndrome (WPWS)
- Mono-morphic ventricular tachycardia (VT)
- Sodium Channel Blockers: Phenytoin, Lidocaine, Triamterene, Lamotrigine, Oxcarbazepine, and Amiloride
- Drug overdose and toxicities: TCA’s, digoxin, cocaine, lithium, diphenhydramine
Q wave present indicates
- Post STEMI
- Pulmonary Embolism: S1Q3T3
- HCOM: Dagger Q waves in left leads
S waves meaning
Final DEPOLARIZATION of the ventricles (Purkinje fibers)
Mirror effect, shows the opposite side
U waves meaning
Represent REPOLARIZATION of the ventricles (Purkinje fibers).
Best seen in the right precordial leads. Usually not seen.
Amplitude is usually < 1/3 T wave amplitude in the same lead.
Increment in U wave amplitude = Premature ventricular complexes (PVC)
QT segment Duration
- Normal = 0.4 to 0.44 sec
(2 big squares) - Short QT < 0.35 sec
- Prolong QT > 0.44 sec Predecessor of Torsade pointes(PVT) then VF
Prolong QT Causes
- HYPOS:
- Hypokalaemia
- Hypomagnesaemia
- Hypocalcaemia
- Hypothermia - Raised intracranial pressure
- Drugs
- Congenital:
- Romano Ward syndrome (AD)
- Jervell and Lange Nielsen syndrome (AR) - bilateral sensorineural hearing loss -
Prolong QT Causes: Drugs
- Antipsychotics
- TCAs
- SSRIs: Citalopram, Escitalopram
- SNRIs: Venlafaxine
- Apitypical Antidep: Bupropion
- MAOIs: Moclobemide
- Antihistamines
- Antiarrhythmics: Quinidine, procainamide, flecainide, sotalol,
and Amiodarone. - Antimalarial: Chloroquine, Hydroxychloroquine, and quinine
- Macrolides: Erythromycin, and Clarithromycin
Digoxin
TCA Intoxication ECG
Prolong QT Symptom
Syncope
Prolong QT Management
- Correct underline causes
- B-Blockers
- Implantable cardioverter-defibrillator (ICD)
UNSTABLE: Torsade de Pointes Treatment
Raised Intracranial Pressure ECG changes
Widespread giant T-wave inversions (“cerebral T waves”)
QT prolongation
Bradycardia
Short QT Causes
HYPERS:
Hypercalcemia
Hyperkalemia
Hyperthermia
Digoxin: Salvador Dali Sign
PULMONARY EMBOLISM IN ECG
S1 Q3 T3 : Cor Pulmonale
- Deep S in Lead I
- Q in Lead III
- T inverted In Lead III
✓ SINUSAL TACHICARDIA
✓ RBBB can be associated
Causes of ST-Segment Elevation
- Being an MI until proven otherwise
- Pericarditis
- Ventricular aneurysm
Causes Of ST-segment Depression
- Myocardium Ischaemia – Non-Stemi
- Unstable Angina
ACUTE PERICARDITIS ECG CHANGES
ST-segment elevation with reciprocal PR-segment depression in all leads except V1 and AVR
Aneurism ECG changes
V1 - V3 ST elevation with concave morphology
Deep Q waves
Brugada syndrome ECG changes
ST-segment elevation V1-V3 followed by a negative T wave.
Association with clinical criteria:
- Family history of sudden cardiac death at <45 years old .
- Young, Male, Southeast Asian patient
- Syncope
Takotsubo Cardiomyopathy (Broken Heart) ECG changes
Same ECG that STEMI: T wave inversion leads II, III, aVF, V3-6
In the context of:
- Pregnancy with CHF
- Sepsis with CHF
- Alcohol Cardiomyopathy
ECG MI: Anterior wall
Leads Affected: V2 to V4
Vessel Involved: Left Anterior Descending artery (LAD) – Diagonal branch
ECG MI: Septal wall
Leads Affected: V1 and V2
Vessel Involved: Left Anterior Descending artery (LAD) – Septal branch
ECG MI: Lateral wall
Leads Affected: I, aVL, V5, V6
Vessel Involved: Left Coronary Artery (LCA) – Circumflex branch
ECG MI: Inferior wall
Leads Affected: II, III, aVF
Vessel Involved: Right Coronary Artery (RCA) – Posterior descending branch
ECG MI: Posterior wall
Leads Affected:
V1 to V4 Mirror image ST depression
V7-V9
Vessel Involved:
*Left Coronary Artery (LCA) – Circumflex branch
*Right Coronary Artery (RCA) – Posterior descending branch
Hyperkalemia ECG changes
5.5 - 6.5 *Peaked T waves
6.5 - 7 *P waves widening,
flattening or absent
*Prolong PR interval
7 - 9 *Bradyarrhythmias
*Prolonged QRS
> 9 *Asystole
*Ventricular fibrillation
*PEA
Hypokalemia ECG changes
K < 2.7 mmol/L
- Increased P wave amplitude (>2,5 mm)
- Prolongation of PR interval (> 1 big square)
- Widespread ST depression and T wave flattening/inversion
- Prominent U waves - PVC (best seen in V2-V3)
- Apparent long QT interval due to fusion of T and U waves (= long QU interval)
Digitalis toxicity in ECG
- ST depression and T wave inversion in V5-6 in a reversed tick pattern.
- Bradycardia
- Prolonged PR
- Shortened QT
- Arrhythmias, especially heart block or bigeminy
Amiodarone overdose ECG Changes
Widening of QRS complex
Prolongation of the PR and QT intervals
Ventricular tachycardia and ventricular fibrillation
Amiodarone overdose ECG Changes
Widening of QRS complex
Prolongation of the PR and QT intervals
Ventricular tachycardia and ventricular fibrillation
List: Narrow Complex (Supraventricular) Tachycardia: ATRIAL – REGULAR
- Sinus tachycardia (ST)
- Atrial tachycardia (AT)
- Atrial flutter
List: Narrow Complex (Supraventricular) Tachycardia: ATRIAL – IRREGULAR
- Atrial fibrillation (AF)
- Atrial flutter with variable block
- Multifocal atrial tachycardia (MAT)
ATRIAL TACHYCARDIA (AT) & PAROXYSMAL AT: Clinical features
A rapid atrial rate overrides the SA Node and becomes the dominant pacemaker
Rhythm arround 150 bpm
In a px that has Hx of Heart disease (long standing AHT, valvar deseas, etc) or cocaine use
Paroxysmal: SVT and then stop
FA important facts
Prevalence:
< 55 yo = 0.1%
> 80 yo = 10%
Risk Factors:
- HTA (Most important 20%)
- Ischaemic heart disease
- Tirotoxicosis
- Reumatic fever (aboriginal and in developing countries)
Complications:
1) Stroke - Risk:
< 65 yo 2.5 - 3%
> 65 yo 10%
2) Femoral artery embolism
Paroxysmal AF Clinical Features
Spontaneous ends in less than 7 days (usually in 24 h)
After heavy alcohol, drugs
Paroxysmal AF Management
Rapid = Convert
No rapid = No convert
NEEDS BETTER EXPLANATION
Persistent AF Management
Fails to revert within 7 days
Usually converts with syncronized cardioversion
Elderly with previous heart conditions, just rate control and anticoagulants.
Definitive treatment: AV node ablation + permanent pacemaker
Atrial fibrillation (AF): STABLE < 48H Management
- Rate control (Aim < 110 bpm):
A) B-Blockers or CCB (Verapamil. Contraindicated EF<40)
B) EF<40 = Amiodarone
C) If the previous didn’t work or contraindications: Add Digoxin
If pharmacological failure WITHOUT left Ventricle systolic dysfunction: Pharmacological cardioversion with Flecainide (EF<40)/Amiodarone or Synchronized CV
- CHA2DS2VaSc
- Definitive treatment: AV ablation + permanent pacing (pacemaker)
Atrial fibrillation (AF): STABLE > 48H Management
- Rate control (Aim < 110 bpm):
A) B-Blockers or CCB (Verapamil. Contraindicated EF<40)
B) EF<40 = Amiodarone
C) If the previous didn’t work or contraindications: Add Digoxin - Anticoagulation: LMWH x 5 days. Add Warfarine (INR 2-3) FOR 1 MONTH
- Synchronized Cardioversion
Atrial fibrillation (AF): UNSTABLE
Synchronized Cardioversion
CHA2DS2VaSc
CHF (EF<40%)
Hypertension
Age > 65 yo /// Age > 75 yo = 2
Diabetes mellitus
Stroke (no hemorrhagic) or TIA = 2
Vascular disease (PVD)
Female
CHA2DS2VaSc score
0: No anticoagulation or aspirin
1: Antiplatelets
2 or more: Anticoagulation is recommended if not at high risk of bleeding.
Atrial flutter: Clinical Features
AV Node conducts impulses to the Ventricle at a 2:1, 3:1, 4:1 or more.
- Degree may be consistent or variable
- The foci do not have enough electricity to conduct and produce a Ventricular contraction.
- Ps of the foci and the P of SA node that is conducted.
- Can be quick rate or normal rate
Atrial flutter: ECG Characteristics
Rhythm= Regular
P= 4:1 – only P conducted from SA node (Saw-tooth)
PR = short
QRS= width normal
Atrial flutter: Management
Same as AF STABLE < 48H
Permanent:
- Radiofrequency ablation
- Medical: Sotalol, amiodarone
Multifocal atrial tachycardia (MAT): ECG Characteristics
Rhythm= Irregular
P= DIFFERENTS but all conducted
PR= normal
QRS= width normal
3 or more P waves, each different in the same ECG
Narrow Complex Supraventricular Tachycardia (SVT) : ATRIOVENTRICULAR – REGULAR
- Atrioventricular re-entry tachycardia (AVRT WPW)
- AV nodal re-entry tachycardia (AVNRT)
Wolf Parkinson White (WPW): ECG Characteristics
- Rhythm: Regular
- P: PR is short
- W: wide QRS
- S: slurring of upstroke (delta wave)
(+ FA Irregular rhythm)
How to differentiate AVRT of AVNRT
Valsava maneuver are effective in the termination of AVRT
NOT to AVNRT
REVIEW!!!!!!
WPW Management
Refer to cardiologist.
Definitive Therapy: Ablation of the accessory pathway.
AVOID:
- Adenosine
- CCB
SVT: ECG Characteristics
AVNRT More common (> 60%) than AVRT
Heart rate: Regular 150-160 bpm.
P waves hidden in T waves
QRS: Narrow complex
SVT STABLE Management
Step 1: Carotid massage/Valsalva manoeuvre
Step 2: Adenosine x 2 (2min)
Step 3: Verapamile x 2 (30 min)
Step 3: Direct current (DC) cardioversion or pharmacological cardioversion (amiodarone or overdrive pacing may be required.
Recurrent: Ablation or amiodarone
AF + WPW ECG
Irregular and wide complex tachi with delta wavw
SVT + WPW ECG
Regular and narrow but abnormal QRS
Wide Complex Tachycardia: REGULAR
- Ventricular tachycardia (VT)
- Regular SVT with bundle branch block or aberrant.
Wide Complex Tachycardia: IRREGULAR
- Ventricular fibrillation (VF)
- Polymorphic VT (PVT)
- Torsade de Pointes
- AF with Wolff-Parkinson-White syndrome
- Irregular SVT with bundle branch block.
Ventricular arrhythmias (WIDE complex) list
- Premature ventricular contractions(PVCs)
- Accelerated idioventricular rhythm
- Monomorphic ventricular tachycardia
- Polymorphic ventricular tachycardia
- Ventricular fibrillation
- Torsades de pointes
- Arrhythmogenic right ventricular dysplasia
- Re-entry ventricular arrhythmia
Premature ventricular contractions(PVCs): Clinical Features
- PVC or Ventricular extrasystoles (95% benign)
- Patient feels like he skipped a beat.
- The PVC does not generate a beat, because the ventricles are half-filed.
Premature ventricular contractions(PVCs): ECG Characteristics
P= normal P conducted
PR = normal
QRS= normal and a PVC following a T, Then a compensatory pause (always)
PVCs in bigeminy
Premature ventricular beats occurring after every normal beat are termed(1:1)
1 Normal QRS 1 PVC (repeat)
PVCs in trigeminy
PVCs that occur at intervals of 2 normal beats to 1 PVC (1:2)
PVCs in couplet
Normal QRS + PCV + PVC (repeat)
PVCs in triplet
Normal QRS + PVC + PVC + PVC (Repeat)
Non-sustained ventricular tachycardia(NSVT) Definition
Groups of three PVCs (Couplets or Paired PVCs) and last less than 30 seconds
(> 30 sec = VT)
Non-sustained ventricular tachycardia(NSVT) STABLE: Management
◦ First line: metoprolol (BB)
◦ Second line: Verapamil (CCB) or flecainide if BB are Contraindicated. NO OPTION FOR EF <40
◦ If symptoms persist: amiodarone.
◦ Last option: catheter ablation.
MONOMORPHIC VT: Characteristics
QRS = Same shape and amplitude
T = WIDE COMPLEX
- Pulseless or perfusing
- Can deteriorate into VF or unstable VT if sustained and not treated.
Mechanism: Re-entry loop from one ectopic area so all the QRS look the same.
Usually cause of MONOMORPHIC VT
MI (ischaemia) in 1 area
SUSTAINED VT STABLE: Management
Sustained VT w/ no structural heart disease:
- First Line: beta-blockers (never a BB is acute left heart failure) (eg: atenolol, metoprolol tartrate/IV)
- Second Line or if CI to BB: flecainide or verapamil.
◦ Sustained VT w/ structural heart disease
- First line: Amiodarone or sotalol.
POLYMORPHISM VT: Characteristics
QRS = Different shape and amplitude
- Can be non-perfusing or perfusing
- Consider electrolyte abnormalities or drugs toxicity as the possible etiology
- Re-entry loop from multiple ectopic areas, different areas with different morphology on ECG.
TORSADE DE POINTES: Characteristics
- QRS reverses polarity and the strips shows a spindle effect.
- It is a variant of polymorphic VT with normal or long QT intervals
- Can deteriorate to VT or VF
- Drugs that causes prolonged QT and electrolyte abnormalities like hypomagnesemia can cause Torsade de points.
STABLE TORSADE DE POINTES: Management
Magnessium Sulphate 10 mmol in slow IV bolus
NEVER Sodium Bicarbonate!!!
UNSTABLE TORSADE DE POINTES: Management
UNSYNCRONIZED (DC) CARDIOVERSION
TORSADE DE POINTES: Most common cause
Drugs toxicity (QT prolonging medications)
VENTRICULAR FIBRILLATION (VF): Characteristics
- Chaotic electrical activity with no ventricular depolarization or contraction.
- There is no pulse or cardiac output.
- Small amplitude – no pulse is possible or rhythm
Unstable Tachys and VF - SHOCKABLE -Management
UNSYNCRONIZED CARDIOVERSION
Adrenaline 1 mg after 2nd shock
Amiodarone 300 mg after 3rd shock
Note: CPR X 2 min between shocks
PULSELESS ELECTRICAL ACTIVITY (PEA)
- Electrical rhythm, with no pulse detected.
- PEA can be called electromechanical dissociation
- CONSIDER AND CORRECT:
“4H and 4T”
Non-Shockable Rhythms
PEA
Asystole
SINUS BRADY + NO PULSE
Non-Shockable Rhythms Management
Adenaline 1 mg inmediatly
Then every 2 CPR (X 2 min) Adrenaline again.
UnstableList of Bradyarrhythmias with P WAVES PRESENT
- Sinus bradycardia
- Sinus node dysfunction
a) Sinus Pause.
b) Sinus Arrest.
c) SA Nodal Exit Block. - AV Blocks (I, II, III)
SINUS Bradyarrhythmia causes
Normal in athletes and during sleep.
In acute MI it may be protective and beneficial.
B-blockers can cause sinus bradycardia
Bradyarrhythmia: SINUS NODE DYSFUNCTION ECG Characteristics
Rhythm= Irregular
P= all same
PR= constant - Normal
QRS= width normal
Mechanism: SA node discharges irregularly
- The pacing rate of SA node varies with respiration, specially in children and elderly
SINUS BRADY + NO PULSE Causes
Tension Pneumothorax
Cardiac Tamponade
NO SHOCKABLE!!!!
Bradyarrhythmia: SINUS ARREST – DROPPED BEAT ECG Characteristics
Rhythm= irregular
P= all same - dropped beat
PR= Normal
QRS= width normal. After the dropped beat, cycles continue on time.
- Cardiac output may decrease causing syncope or dizziness.
Sinus arrest Investigation
Holter
Bradyarrhythmias Emergency Management
People with asymptomatic bradycardia usually need no treatment
A) Correction of the cause (cardiac infections, Ischaemia, hypos, drugs: digoxin, beta-blockers, CCB, amiodarone)
B) Pharmacological:
1. Atropine 0.5 mg bolus IV (Repeat every 3-5 min - MAX 3 mg)
2. Isoprenaline
3. Adrenaline / Epinephrine (Hypotension)
4. Dobutamine (CHF)
C) Transcutaneous Pacemaker (If ineffective pharmacological or MOBITZ 2 / 3rd degree AV Block)
Combinations of drugs that block the atrioventricular (AV) node
Verapamil + Beta-blocker
Bradycardia due to drug toxicity MANAGEMENT: B-Blockers
First-line antidote: Glucagon
Second-line: Inotropes (adrenaline, dobutamine, isoprenaline)
Bradycardia due to drug toxicity MANAGEMENT: Calcium channel blockers
First-line antidote: Calcium gluconate
Second-line: Glucagon
Bradycardia due to drug toxicity MANAGEMENT: Digoxin
Digoxin-specific antibodies (Fab fragments)
Allergenic and expensive.
Only to be used in life-threatening arrhythmias attributed to digoxin.
Bradyarrhythmias: AV Blocks List
The most common cause of bradycardia.
Mechanism: AV node dysfunction
- First-degree heart block, which manifests as PR prolongation
- Second-degree heart block
- Type 1 Second-degree heart block, also known asMobitz IorWenckebach
- Type 2 Second-degree heart block, also known asMobitz II or Hay
- Third-degree heart block, also known ascomplete heart block
Bradyarrhythmias: 1ST DEGREE AV BLOCK ECG Characteristics
Rhythm= Regular
P= Normal - all conducted
PR= PROLONGED
QRS= width normal
- Benign
- If associated with MI, it can lead to AV defects.
- Usually caused by drugs.
Drugs that cause 1st degree AV Block
Antiarrhythmics:
Quinidine, procainamide, disopyramide, flecainide, encainide, propafenone, beta-blockers, amiodarone, sotalol, calcium channel blockers
Digoxin
Magnesium
ECG Characteristics: 2ND DEGREE TYPE 1 / MOBITZ I / WENCKEBACH
Rhythm= Irregular
P= normal – a P is blocked
PR = Progressively longer until one P wave is totally blocked and produces no QRS.
QRS= width normal
Causes: 2ND DEGREE TYPE 1 / MOBITZ I / WENCKEBACH
- B-blockers
- Digoxin
- Calcium channel blockers
- Ischaemia involving the right coronary artery.
ECG Characteristics: 2ND DEGREE TYPE 2 / MOBITZ II / HAY.
Rhythm= Regular
P = Look normal at the same pace, all regular. Some P’s are blocked (Eg 3:1)
PR = Normal in the conducted P
QRS= Width normal
Mechanism: Conduction error in the bubble of His.
Clinical features: 2ND DEGREE TYPE 2 / MOBITZ II / HAY
ALWAYS SYMPTOMATIC: Dizziness, palpitations, weakness, and syncope.
ALWAYS URGENT REFER AND PACEMAKER
ECG Characteristics: 3RD DEGREE AV BLOC
Rhythm= Regular 25 - 50 rpm
P= look normal at a regular pace – none conducted
PR = Absent
QRS= abnormal
Clinical Features: 3RD DEGREE AV BLOCK
Mechanism: Lack of conduction of atrial impulse to ventricle leading to independent contractions.
Signs & Symptoms:
- Hypotension
- Large volume pulse
- Increased JPV (CANNON WAVE)
- Systolic murmur
Can lead to asystole and cardiac arrest.
ALWAYS PACEMAKER
Pacemaker in the ECG
Spike + QRS + T
No p wave
The Reversible Causes of Cardiac Arrest: 4 Hs, 4 Ts
Hypoxia
Hypokalaemia/hyperkalaemia
Hypothermia/hyperthermia
Hypovolaemia
Tension pneumothorax
Tamponade
Thrombosis
Toxins
