ECGs

Anatomical locations for V1-V6

V1 4th Intercostal space, right of the sternum

V2 4th Intercostal space, left of the sternum

V4 5th Intercostal space, on left midclavicular line

V6 On the left mid-axillary line, level with V4

V3 Midway between V2 and V4

V5 Midway between V4 and V6

V4R 5th Intercostal space, on the right midclavicular line

Which are the Lateral Leads and what part of the heart does each lead look at and what arteries supply the blood.

• Left Circumflex (LCx) or LAD

• Lead I (Superior part of the left ventricle) LCx

• aVL (Superior part of the left ventricle) LCx

• V5 (Lateral wall of the left ventricle)  (LCx) and the diagonal branches of the (LAD)         

• V6 (Lateral wall of the left ventricle) (LCx) and the diagonal branches of the (LAD)       

Which are the Inferior Leads and what part of the heart does each lead look at and what arteries supply the blood.

• Right Coronary Artery (RCA) or sometimes Left Circumflex Artery (LCx) (in left dominant hearts)

• Lead II: Inferior wall of the left ventricle

• Lead III: Inferior wall of the left ventricle

• aVF: Inferior wall of the left ventricle

Which are the Septal & Anterior Leads and what part of the heart does each lead look at and what arteries supply the blood.

• Left Anterior Descending Artery (LAD)

• V1: septum

• V2: septum

• V3: Anterior wall of the left ventricle

• V4: Anterior wall of the left ventricle

Which are the Non localizing leads and what part of the heart does each lead look at and what arteries supply the blood.

• aVR

• No direct artery; reflects global ischemia or reciprocal changes

Which are the Right Leads and what part of the heart does each lead look at and what arteries supply the blood.

• Right Coronary Artery (RCA)

• V4R (Anterior Wall Right Ventricle)

Normal Axis angle

Left Axis angle

Right Axis angle

Extreme Axis angle

-30° to +90°

-90° to -30°

+90° to 180°

180° to -90°

What lead findings indicate normal axis

lead I and aVF are both positive OR

Lead I is Positive and aVF is negative and lead II is positive

lead I and aVF are positive, what is the axis

normal

What lead findings indicate right axis

Lead I in negative and aVF is positive

Lead I is negative and aVF is positive, what is the axis

Right

What lead findings indicate extreme axis

lead I and aVF are both negative

lead I and aVF are both negative, what is the axis

Extreme

What lead findings indicate left axis

Lead I is Positive and aVF is negative and lead II is negative

what’s the time period of the following

• one small square

• one large square

• 5 large squares

• 40 milliseconds/0.04 seconds

• 200 milliseconds/ 0.2 seconds

• 1 second

Calculating Rate, 300 ÷ the number of large square between each QRS

1

2

3

4

5

6

50

60

75

100

150

300

Irregularly irregular heart rhythms are most commonly associated with?

1. Atrial Fibrillation (AF)

2. Atrial Flutter with Variable Conduction

3. Multifocal Atrial Tachycardia (MAT)

4. Ventricular Fibrillation (VF)

An irregularly regular heart rhythm is associated with what rhythms?

• Second-Degree AV Block (Type I - Wenckebach) Progressive lengthening of the PR interval until a beat is dropped

• Second-Degree AV Block (Type II - Mobitz II) Sudden failure of a P wave to conduct to the ventricles

• Bigeminy or Trigeminy (PACs or PVCs)

During deep inspiration _______ waves and __________waves disappear in lead ___________

small Q waves

inverted T waves

III

P wave criteria

Positive in lead II

duration less that 120ms (3 small squares)

Amplitude of less that 2.5 mm (2.5 small squares) in limb leads

Amplitude of less that 2.5 mm (2.5 small squares) in precordial leads

Abnormal P Wave Features

• P wave > 120 ms → Suggests left atrial enlargement (P mitrale).

• P wave > 2.5 mm → Suggests right atrial enlargement (P pulmonale).

• Biphasic P wave in V1 → Can indicate atrial enlargement (left or right).

• Inverted P wave in lead II → May suggest an ectopic atrial rhythm or junctional rhythm.

what can U waves indicate

hypokalemic patients or normal finding

Criteria for a Normal P-R Interval

Normal range: 120–200 ms (3–5 small squares)

Even duration every time

Abnormal P-R Intervals

1. short?

2. Long?

3. Varying?

1. Pre-excitation syndromes (e.g., Wolff-Parkinson-White Syndrome - WPW)

2. First-degree AV block if consistent

Second-Degree AV Block (Mobitz Type I – Wenckebach)

Electrolyte disturbances (e.g., hyperkalemia).

3. Second-Degree AV Block (Mobitz Type I – Wenckebach)

Second-Degree AV Block (Mobitz Type II)

Complete (Third-Degree) AV Block

Multifocal Atrial Tachycardia (MAT)

Criteria for a Normal QRS Complex

• Normal: < 120 ms (< 3 small squares)

• Should have a normal progression across precordial (chest) leads:

  • V1-V2: Small R wave, deep S wave.

  • V3-V4: Transition zone (R and S waves approximately equal).

  • V5-V6: Large R wave, small S wave.

QRS Abnormalities

1. Criteria for a Normal Q Wave

1. Bundle branch block (BBB), ventricular rhythms, WPW

2. LVH, RVH, hypertrophic cardiomyopathy

3. Pericardial effusion, obesity, hypothyroidism, COPD

Criteria for a Normal Q Wave

< 40 ms (0.04 sec, 1 small square)

< 25% of the R wave height in the same lead

Abnormal Q Waves

1. Wide (> 1 small square)

2. ≥ (25%) of the R wave height

1. Seen in prior myocardial infarction (MI) if present in infarcted leads

2. Can suggest previous MI, hypertrophic cardiomyopathy, or conduction abnormalities

Normal ST Segment criteria

Should be isoelectric (baseline) or show only slight deviations.

Normal: < 0.20 sec (5 small squares)

ST Elevation (Normal)

• Normal: ≤ 1 mm (1 small square) in limb leads (I, II, III, aVL, aVF)

• Normal: ≤ 2 mm (2 small squares) in precordial leads (V1-V6)

ST Segment criteria for MI

Elevation > 1 mm (limb) or > 2 mm (precordial) → STEMI

Depression > 0.5 mm in contiguous leads → Ischemia/NSTEMI

Concave (pericarditis or early repolarization (Mabey))

convex (STEMI), down sloping (ischemia)

reciprocal depression → STEMI

Normal criteria for T waves

Criteria for Limb leads (I, II, III, aVL, aVF): ≤ 5 mm (0.5 mV)

Precordial leads (V1-V6): ≤ 10 mm (1.0 mV)

Abnormal T waves

• Tall, peaked T waves (> 10 mm in precordial leads, > 5 mm in limb leads)

• Low amplitude T waves (< 1 mm)

• Flattened or biphasic

• Hyperkalemia

• Hypokalemia, pericardial effusion, hypothyroidism

• Hypokalemia, ischemia

Criteria for Normal Q-T interval

less than half the preceding R-R interval

Abnormal Q-T interval

less than half the preceding R-R interval

> 440 ms in men (11.75 small squares) LQTS, meds, hypokalemia

> 460 ms in women (12 small squares) LQTS, meds, hypokalemia

<350 ms in either (8.75 small squares) Hypercalcemia, digoxin

Long PR interval criteria and causes

A distance of more than five small squares from the start of the P wave to the start of the R wave (or Q wave if there is one)

First-Degree AV Block (most common)

Second-Degree AV Block (Type I - Mobitz I/Wenckebach)

It rarely requires action, but in the presence of other abnormalities might be a sign of hyperkalemia, digoxin toxicity, or cardiomyopathy.

why is the Q wave negative and which leads should we see it?

The Q wave depolarizes the left ventricle first so the overall direction is left to right, away from so they can be seen in the lateral/ left leads, I, aVL, V5, V6

Q waves should not be seen in Right sided/ anterior leads leads, V1-V3 this could indicate anterior myocardial infarction (MI), structural heart disease, or conduction abnormalities.

Pathological Q waves

> 40ms (1mm wide)

2mm deep

more that 25% of QRS complex

seen in V1, V2, V3

can indicate current it past anterior MI

prolonged Q-T

what is it for men a women?

what can it indicate?

• Prolonged if >440ms in men, >460ms in women

• Normal QT is less than half the preceding RR interval

Causes:

• Hypokalaemia

• Hypomagnesaemia

• Hypocalcaemia

• Hypothermia

• Myocardial ischaemia

• ROSC (Return of Spontaneous Circulation)

• Raised ICP (Intracranial Pressure)

• Congenital long QT syndrome

• Medications / drugs

what are the 3 common R wave abnormalities

• Dominant R wave in V1

• Dominant R wave in aVR

• Poor R wave progression

what can Dominant R wave in V1 indicate

• Normal in children and young adults

• Right ventricular hypertrophy → Pulmonary embolism, left-to-right shunt

• Right Bundle Branch Block

• Posterior Myocardial Infarction

what can Dominant R wave in aVR indicate

sodium channel blocking dugs poisoning

what can Poor R wave progression indicate

• Prior anteroseptal MI

• LVH (Left Ventricular Hypertrophy)

• Inaccurate lead placement

What is J point

the junction between the termination of the QRS and the beginning of the S-T

Normal T waves criteria

Upright in all leads except aVR and V1

Amplitude <5mm in limb leads, 10mm in precordial leads

Draw as many T wave patters as you can and label what they indicate

what is that and what can it indicate

Hyperacute T waves, can be first sign of MI

What is a U wave?

When will you see it?

What can it indicate?

The U wave follows the T wave and represents delayed repolarisation of the Purkinje Fibers.

U wave becomes visible when the heart rate slows below <60 bpm

Abnormalities of U waves:

• Prominent U waves: Bradycardia, severe hypokalaemia, digoxin

• Inverted U waves: Coronary artery disease, hypertension, valvular heart disease, cardiomyopathy

what is a delta wave

what does it look like

what does it indicate

• pre-excitation of the ventricles

• The Delta wave is a slurred upstroke in the QRS complex

• Often associated with shortening of the PR interval
  Most associated with pre-excitation syndromes such as Wolff-Parkinson-White

Left ventricular hypertrophy can be identified with the Sokolow–Lyon index explain it

Does the sum of the S wave in lead V1 and the R wave in V6 add up to more than 3.5 mV, ie, 35 small or seven big squares?

A wide QRS complex despite sinus rhythm is the hallmark of bundle branch block. Left bundle branch block (LBBB) can cause the ECG to look extremely abnormal

Both LBBB and RBBB cause a wide QRS complex due to delayed conduction.

what changes are you looking for in what leads to differentiate L from R BBB

Look at Leads V1 & V6

• V1 is a right-sided chest lead.

• V6 is a left-sided chest lead.

• The bundle branch that is blocked will cause a delayed activation of that ventricle, producing characteristic patterns.

Lead	LBBB	RBBB
V1	Deep S wave ("W" pattern)	R-S-R' ("M" pattern, "Rabbit ears")
V6	Broad, notched ("M" pattern) R wave	Broad R wave with slurred S wave

• LBBB: V1 shows a deep wide S wave, V6 shows a broad notched R wave.

• RBBB: V1 shows an R-S-R' (M pattern or "Rabbit ears"), V6 shows a wide slurred S wave.

AV Node

1. where is it located ?

2. What artery supplies it?

3. What’s is its inherent rate?

4. what id its function

1. inferior portion of the right atrium within atrioventricular septum

2. RCA

3. 40-60

4. connects electrical structure of atrial to the ventricles and acts to delay impulses to the ventricles to allow them to fill with blood.

Bundle if Hiss

1. where is it located ?

2. What artery supplies it?

3. What’s is its inherent rate?

4. what id its function

• Location: Originates at the AV node (inferior part of Right atrium) and moved down the introventricular septum.

• Artery Supply: Right coronary artery (in most people)

• Inherent Rate: 30-45 beats per minute

• Function: Conducts electrical impulses from the AV node to the L & R BB

Bundle branches

1. What artery supplies them?

2. What’s is its inherent rate?

3. what id its function

• Artery Supply: Left anterior descending (LAD) artery and right coronary artery (RCA)

• Inherent Rate: 20-40 beats per minute

• Function: Transmit electrical impulses from the Bundle of His to the Purkinje fibers for ventricular contraction

Purkinje fivers

1. where is it located ?

2. What’s is its inherent rate?

3. what id its function

Myocardium muscle

1. What’s is its inherent rate?

• Purkinje Fibers Location: Inner ventricular walls (subendocardial layer)

• Inherent Rate: 20-40 beats per minute

• Function: Rapidly conduct electrical impulses to the ventricles, ensuring coordinated contraction

What are the pacemaker sites of the heart and what are the rates?

• sinoatrial (SA) Node: 60-100 beats per minute (primary pacemaker)

• Atrioventricular (AV) Node: 40-60 beats per minute (backup pacemaker)

• Bundle of His: 30-45 beats per minute

• Bundle Branches: 20-40 beats per minute

• Purkinje Fibers: 20-40 beats per minute

Respiratory Sinus arrythmia RSA

1. Who gets it

2. What causes it

3. Describe the mechanism

1. Young healthy people

2. Breathing causes reflex changes in vagal tone

3. Inspiration > negative pressure > reduces vagal tone > faster HR

   Exhalation > thoracic cavity pressure increases > increases vagal tone > slower HR

The five steps of the cardiac electrical cycle are

1. Sinoatrial (SA) Node Activation – The pacemaker generates an impulse, causing atrial depolarization (P wave).

2. Atrioventricular (AV) Node Delay – The impulse slows to allow ventricular filling (PR interval).

3. Ventricular Depolarization – The impulse rapidly travels down the Bundle of His and Purkinje fibers, triggering ventricular contraction (seen as the QRS complex on an ECG).

4. Ventricular Repolarization – The ventricles recover and relax (T wave).

5. Diastolic Resting Phase – The heart resets electrically, preparing for the next cycle (TP segment).

 

 

Sick sinus syndrome caused by 3 key arrhythmias

Sinus arrest or pause, pause of 3 seconds or more without atrial activity

Sinoatrial exit block, interruption of signal from SA node to atria

Tachy-brady syndrome, bradycardia alternating with SVT

What are the four types of Rhythms and where they originate

1. Sinus Rhythms . SA Node

2. Atrial Rhythms. Atria

3. Junctional Rhythms AV Node or hiss bundle

4. Ventricular Rhythms Ventricles

Sinus Rhythms

types and characteristics

• Normal Sinus Rhythm (NSR): 60–100 bpm, regular, normal P waves before each QRS.

• Sinus Bradycardia: <60 bpm, regular rhythm.

• Sinus Tachycardia: >100 bpm, regular rhythm.

• Sinus Arrhythmia: Irregular rhythm, varies with respiration.

• Sinus Pause/Arrest: Sudden failure of SA node to fire, causing missed beats.

• Sinoatrial Exit Block: SA node fires but impulse fails to exit, causing dropped beats.

Atrial Rhythms

types and characteristics

• Premature Atrial Complexes (PACs): Early P waves with abnormal morphology.

• Atrial Tachycardia: 150–250 bpm, abnormal P waves.

• Multifocal Atrial Tachycardia (MAT): Irregular rhythm, multiple P wave morphologies, often in COPD.

• Atrial Flutter: Sawtooth P waves (F waves), atrial rate ~250–350 bpm, typically 2:1 conduction.

• Atrial Fibrillation (AFib): Irregularly irregular rhythm, no distinct P waves, atrial rate >350 bpm.

• Supraventricular Tachycardia (SVT): Narrow complex tachycardia >150 bpm, often sudden onset/termination.

• Wolff-Parkinson-White Syndrome (WPW): Pre-excitation syndrome with short PR interval, delta wave, and wide QRS, can trigger SVT or AFib.

Junctional Rhythms

types and characteristics

• Premature Junctional Complexes (PJCs): Early beats, no or inverted P wave.

• Junctional Escape Rhythm: 40–60 bpm, narrow QRS, absent or inverted P waves.

• Accelerated Junctional Rhythm: 60–100 bpm, same characteristics as junctional escape rhythm.

• Junctional Tachycardia: >100 bpm, absent or inverted P waves, narrow QRS

• Atrioventricular Nodal Reentrant Tachycardia (AVNRT): Most common type of SVT, caused by a reentry circuit within the AV node, producing a regular, narrow-complex tachycardia (140–250 bpm).

• Atrioventricular Reciprocating Tachycardia (AVRT): A reentrant tachycardia involving an accessory pathway (e.g., WPW Syndrome), leading to narrow or wide QRS tachycardia depending on conduction direction.

Ventricular Rhythms

types and characteristics

• Premature Ventricular Complexes (PVCs): Early, wide QRS, no preceding P wave.

• Idioventricular Rhythm: 20–40 bpm, wide QRS, no P waves.

• Accelerated Idioventricular Rhythm (AIVR): 40–100 bpm, wide QRS, no P waves.

• Ventricular Tachycardia (VT): >100 bpm, wide QRS, no P waves.

• Torsades de Pointes: Polymorphic VT with prolonged QT, twisting QRS.

• Ventricular Fibrillation (VF): Chaotic electrical activity, no cardiac output.

what’s the rhythm

what’s the cause/mechanism

Atrial fibrillation

Multiple chaotic electrical impulses in the atria

what causes AF

Instead of a single signal from the SA node, multiple random signals fire across the atria, making them quiver instead of pumping properly.

Conditions that enlarge or strain the atria can trigger AF.

hings like heart disease, high blood pressure, alcohol, or thyroid issues can disrupt normal heart rhythms.

what’s the rhythm

what’s the cause/mechanism

Atrial Flutter with 4:1 conduction ( rate aproxx 75)

Reentrant circuit in the atria

Top first then bottom

what’s the rhythm

what’s the cause/mechanism

Atrial Flutter

Reentrant circuit in the atria

Atrial fibrillation

Multiple chaotic electrical impulses in the atria

mechanism for Premature Atrial Complex (PAC)

Area of the atria has increased automaticity and fires an early electrical impulse before the SA node has a chance to fire.

 

what are some characteristics of junctional rhythms

what are some ECG characteristics/appearances

Normally 40-60 BPM

Junctional rhythms that are over 60 are accelerated rhythms

There are normally no p wavers

QRS should be normal

Appearance on an ECG

·       No P waves

·       Inverted P waves

·       P waves after the QRS

What are the 4 valves in the heart?

• Tricuspid Valve – Between the right atrium and right ventricle

• Pulmonary Valve – Between the right ventricle and pulmonary arteries

• Aortic Valve – Between the left ventricle and aorta

• Mitral (Bicuspid) Valve – Between the left atrium and left ventricle

How to tell PAC and PJC apart

• PAC: Has a visible, abnormal P wave before the QRS.

• PJC: Either has no visible P wave, an inverted P wave, or a P wave buried in the QRS due to the impulse coming from the AV node.

• The QRS from the PJS will often be lower in amplitude than the other QRSs

What is this? Top and bottom

Top Capture beat

A occasional atrial beat has reached the ventricles in between the ventricular beats in VT

Bottom Fusion beat

A occasional atrial beat has reached the ventricles in between the ventricular beats in VT but the atrial beat and ventricular beat happen at the same time.

What’s the rhythm?

what’s the mechanism?

How is it managed,

Torsades de Pointes ("Tor-SAHD duh PWAHNT) a form of VT

Inhibition of potassium current causing prolonged repolarisation, then a ectopic (early or extra heartbeat) occurs this causes Torsades de Pointes.

If pulseless or severe hypotension defibrillation and ACLS, then potassium or magnesium supplementation (IV potassium or magnesium sulfate)

From top to bottom name these rhythms

1. Trigemini, Unifocal PVC

2. Bigeminy,  Unifocal PVC

3. Trigemini , Multifocal PVC

4. Trigemini , Unifocal PVC

what are the three mechanism for SVT

Re-entrant (Most Common - ~90%)

Automaticity (Ectopic Focus - ~10%)

Triggered Activity (Rare)

what effect does calcium, magnesium and potassium have on heart automaticity

Calcium (Ca²⁺)

·       Hypercalcemia: Can increase excitability and shorten repolarization

·       Hypocalcemia: Reduces automaticity, slowing conduction

Potassium (K⁺)

·       Hyperkalemia: Depresses automaticity

·       Hypokalemia: Increases automaticity

Magnesium (Mg²⁺)

·       Hypomagnesemia: Increases excitability and risk of torsades de pointes

·       Hypermagnesemia: Decreases automaticity, leading to bradycardia

BBB causes L and R

• LBBB is more often linked to left-sided heart conditions, such as hypertension, cardiomyopathy, ischemic heart disease, and aortic valve disease.

• RBBB is commonly associated with right heart strain, pulmonary diseases, congenital heart disease, and ischemic events affecting the right coronary artery.

RBBB criteria

QRS > 120ms

rSR pattern in V1-V3  occurs because the right ventricle depolarizes late due to delayed conduction through the right bundle, causing a second R wave (R') as the right ventricle is activated after the left ventricle

Wide slurred S wave  in lateral leads delayed right ventricular activation creates an electrical vector directed away from the lateral leads, resulting in a prolonged and widened S

ST depression & T wave inversion in right sided chest leads (maybe) from abnormal repolarisation of the R venticle.

LBBB criteria

QRS > 120ms

No Q waves in lateral leads  Normally, small Q waves appear in the lateral leads due to early left-to-right depolarization of the interventricular septum. In LBBB, the normal conduction through the left bundle is blocked, so the septum is depolarized abnormally from right to left via the right bundle branch.

Wide, broad, monophasic, notched R waves in lateral leads

Deep, broad S waves in leads (V1-V3)

Poor r wave progression

ST elevation in V1-V3 because of abnormal repolarization

ST depression in lateral leads because of abnormal repolarization

non concordant T waves in all leads because of abnormal repolarization

Pacemakers

1. Two types

2. explain different chambering

3. What do ventricular paced rhythms look like

4. what the the best leads to see the pacing spikes

5. what is occurring in the image

Fixed, always fires

Demand sensing, kick in when the heart rate drops below 60-70

Pacemakers can chamber just the atria the ventricles or the atria and ventricles

LBBB

V3-V6

Failure to capture of a ventricular chambered pacemaker

STEMI Characteristics

T Waves:

• Hyperacute T waves (early stage) – taller than 50% of the QRS complex.

• Inverted T waves (later stage) – occur as the infarct evolves.

ST-Segment:

• ST elevation in at least two contiguous leads indicates transmural ischemia.

• Reciprocal ST depression supports STEMI diagnosis (except in wide QRS, where LBBB must be ruled out).

• ST-elevation thresholds:

  • ≥1 mm in at least two contiguous limb leads.

  • ≥2 mm in at least two contiguous precordial leads.

  • ≥1.5 mm in V2-V3 (women).

  • ≥2 mm in V2-V3 (men ≥40 years old).

  • ≥2.5 mm in V2-V3 (men <40 years old).

• ST depression ≥0.5 mm in two contiguous leads suggests myocardial ischemia.

Q Waves:

• Pathological Q waves (≥25% of the R wave height or ≥1 small square wide) indicate late-stage infarction.

STEMI Criteria

• ST-elevation thresholds:

  • ≥1 mm in at least two contiguous limb leads.

  • ≥2 mm in at least two contiguous precordial leads.

  • ≥1.5 mm in V2-V3 (women).

  • ≥2 mm in V2-V3 (men ≥40 years old).

  • ≥2.5 mm in V2-V3 (men <40 years old).

  • the absence of wide QRS

4 stages of STEMI evolution

1. Hyperacute T waves (minuets to hours)

2. S-T elevation (0-12 hours)

3. Pathological Q waves (1-12 hours)

4. S-T elevation with T wave inversions (2-5 days)

What is occurring here, what ae the stages>?

Progression of STEMI

1. Hyperacute T waves (minuets to hours)

2. S-T elevation (0-12 hours form) (fully establisher 12-24 hours)

3. Pathological Q waves (1-12 hours)

4. S-T elevation with T wave inversions (2-5 days)

what is the significance of each of these 3 findings

Upsloping ST depression → Less specific for ischemia, can be normal.

Down sloping ST depression → Strongly suggests ischemia, high-risk finding.

Horizontal ST depression → Likely ischemic, seen in ACS and NSTEMI.

1. What is ischemia, and which part of the heart muscle does it affect first?

2. What is transmural ischemia, and how does it differ from regular ischemia?

3. What is infarction, and what causes it?

4. How does ATP depletion affect potassium ion movement in cardiomyocytes?

5. What causes ST elevation on an ECG, and what does it indicate?

6. What ECG change is seen in subendocardial ischemia, and why does it occur?

1. Ischemia is a reduction in blood flow leading to oxygen deprivation, primarily affecting the subendocardium first. the cells cant product enough ATP.

2. Transmural ischemia is a complete loss of blood supply affecting the entire thickness of the myocardium.

3. Infarction is the irreversible cell death of heart tissue due to prolonged ischemia.

4. The leakage of potassium ions due to ATP depletion leads to early depolarization of cardiomyocytes and an increase in baseline potential.

5. ST elevation occurs if transmural ischemia (full thickness of the myocardium) is present, as injured cells remain partially depolarized at rest, shifting baseline potentials and leading to ST elevation in affected leads.

6. ST depression occurs in subendocardial ischemia (inner layer affected but not full thickness) due to repolarization changes that shift the ST segment downward.

Causes of S-T elevation (ELEVATION)

• Electrolytes: hyperkalaemia

• Left Bundle Branch Block

• Early Repolarisation

• Ventricular Hypertrophy (left)

• Aneurysm (ventricular)

• Thailand (Brugada Syndrome)

• Inflammation (Pericarditis)

• Osborn J waves (hypothermia)

• Non-ischemic Vasospasm