ECG

Conductive system of the heart:

1. SA node

2. AV node

3. Bundle of His

4. Left bundle branch (LBB) and right bundle branch (RBB)

5. Purkinje fibers.

Depolarization: This means the initial spread of stimulus through the muscle, causing activation or contraction.

Repolarization: This means the return of stimulated muscle to the resting state (recovery from activation or contraction).

Normal spread of electrical activity in the heart:

1. Depolarisation starts in the sinoatrial node and spreads through the atria

2. Then through the atrioventricular node

3. Depolarisation then spreads through the bundle of His and the bundle branches to reach the ventricular muscle

4. Repolarisation spreads from epicardium to endocardium

The dominant pacemaker is the SA node. When the SA node fails, other pacemaker sites can initiate impulses at a slow rate.

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Rates of pacemakers:

1. SA node: 60-100 bpm.

2 Atrial cells: 55-60 bpm

3. AV node: 45-50 bpm

4. Bundle of His: 40-45 bpm

5. Bundle branch: 40-45 bpm

6. Purkinje cells: 35-40 bpm

7. Myocardial cells: 30-35 bpm

There is no difference between an ECG and an EKG.

Both refer to the same procedure, however one is in English (electrocardiogram – ECG) and the other is based on the German spelling (elektrokardiogramm – EKG).

1. The physiological basis of an ECG: Electrical depolarization of myocardial tissue produces a small dipole current, which can be detected by electrode pairs on the body surface.

2. These signals are amplified and either printed or displayed on a monitor

3. During sinus rhythm, the SA node triggers atrial depolarisation, producing a P wave. Depolarisation proceeds slowly through the AV node, which is too small to produce a depolarization wave detectable from the body surface.

4. The bundle His, bundle branches, and Purkinje system are then activated, initiating ventricular myocardial repolarization, which produces the QRS complex.

5. The muscle mass of the ventricles is much larger than that of the atria, so the QRS complex is larger than the P wave.

6. The interval between the onset of the P wave and the onset of the QRS complex is termed the 'PR interval' and largely reflects the duration of AV nodal conduction.

7. Injury to the left or right bundle branch delays ventricular depolarisation, widening the QRS complex.

8. Selective injury of one of the left fascicles affects the electrical axis.

9. Repolarisation is slower and spreads from the epicardium to the endocardium.

10. Atrial repolarization does not cause a detectable signal but ventricular repolarization produces the T wave.

11. The QT interval represents the total duration of ventricular depolarization and repolarization.

P wave: atrial depolarisation, (0.12 sec)

QRS complex: ventricular depolarisation, (0.10 sec)

T wave: ventricular repolarization

PR interval (0.20 sec)

QT interval (0.42 sec at a rate of 60/min)

Vector of ECG:

The vector is a diagrammatic way to show the strength and the direction of the electrical impulse.

1. Direction of a Vector is denoted in Terms of degree

2. When a vector is exactly horizontal and directed toward the person's left side, the vector is said to extend in the direction of 0 degrees.

3. From this zero reference point, the scale of vectors rotates clockwise:

✓ When the vector extends from above and straight downward: +90 degrees

✓When it extends from the person's left to right: +180 degrees

✓ When it extends straight upward: -90 (or +270) degrees.

4. In a normal heart: Average direction of the vector during the spread of the depolarization wave through the ventricles, called the mean QRS vector, is about +59 degrees.

General principles of vector:

1. The vectors add up when they are going in the same direction and they get canceled if they point in the opposite directions.

2. But in case if they are at an angle to each other, they add or subtract energy and change their resultant direction of flow.

3. Millions of cells in the heart produce millions of vectors. When these millions of vectors add up, subtract or change direction, we finally get a resultant vector. This resultant vector is known as the electrical axis of the ventricle.

Electrodes and vector:

Electrodes are the sensing devices that pick up the electrical activity occurring under it.

1. When a positive impulse (Depolarization) is moving away from the electrode: Negative wave.

2. When a positive impulse (Depolarization) is moving towards the electrode: Positive wave.

3. When the electrode is in the middle of the vector: Positive deflection for the amount of energy that is coming towards the electrode and the negative wave for the amount of energy that is going away from the electrode.

Each lead is actually a pair of electrodes connected to the body on opposite sides of the heart, and the direction from the negative electrode to the positive electrode is called the "axis" of the lead.

The 12 'leads' of the ECG:

1. Six limb leads:

Bipolar: I, II, and III

In these leads, one limb carries a positive electrode and the other limb carries a negative electrode

Augmented: aVR, aVL, and aVF

In these leads, one limb carries a positive electrode, while the central terminal provides the negative pole, which is measured as 'zero'.

2. Six unipolar chest leads: VI-V6

Chest leads are placed in such a way that they bisect the heart in the horizontal plane.

Signal recording by leads:

1. Lead I: Signal between the right (negative) and left (positive) arms.

2. Lead II: Signal between the right arm (negative) and left leg (positive).

3. Lead III: Signal between the left arm (negative) and left leg (positive).

4. Leads aVR, aVL, and aVF: Electrical activity between a limb electrode and a modified central terminal, e.g.

Lead aVL: Signal between the left arm (positive) and a central (negative) terminal

Lead aVR: Signal from the right arm (positive) and a central (negative) terminal

Lead aVF: Signal left leg (positive) and a central (negative) terminal

5. Leads VI-V6: Records the signal between the corresponding chest electrode (positive) and the central terminal (negative).

Must remember:

1. Depolarisation towards electrode: +ve deflection

2. Depolarisation away from electrode: -ve deflection

3. When the vector is at right angles to a lead: Depolarisation in that lead is equally negative and positive (isoelectric),

The average vector of ventricular repolarization is known as the frontal cardiac axis.

The LV has the greater muscle mass and contributes the major component of the QRS complex.

Relationship of Leads to Heart:

1. VI-V2: Right ventricle

2 V3-V4: Ventricular septum

3. 1, aVL V5-V6: Lateral wall

4. II, III, aVF: Inferior wall

5. VI to V6: Anterior aspect of the heart.

6. 1, aVL, VI to V6: The extensive anterior aspect of the heart or anterolateral.

7. I and aVL: High lateral.

8. II, LIII, aVF, I, aVL, V5 and V6: Inferolateral.

Let's imagine that leads are cameras, which are kept at different angles from the heart. These cameras will take pictures of the heart in those angles in which they have been placed. When we arrange all the photographs which are taken at different angles from the heart, we get a 3D (3-dimensional) picture of the heart.

1. Placement of limb leads:

Right arm (RA)

Left-arm (LA)

Right leg (RL)

Left leg (LL)

2. Placement of Chest Leads:

V1: 4th intercostal space at the right sternal border

V2: 4th intercostal space at the left sternal border

V4: 5th intercostal space at mid clavicular line

V3: Midway between V2 and V4

V5: At the same horizontal level as V4 in the anterior axillary line

V6: At the same horizontal level as V4 in the midaxillary line.

Paper speed:

25 mm per sec (i.e. 1500 mm/min)

✓ Each large (5 mm) square= 0.2 sec

✓ Each small (1 mm) square= 0.04 sec

How to Name the QRS Complex?

1. The first negative deflection (below the baseline) is called Q wave.

2. The first positive deflection is called the R wave. If there is a second positive complex, it is called R' (R prime).

3. The negative deflection following the R wave is the S wave.

4. These three rules are applicable to all leads except for aVR.

The shape of the QRS complex varies across the chest leads:

1. Depolarisation of the interventricular septum occurs first and moves from left to right; this generates a small initial negative deflection in lead V6 (Q wave) and an initial positive deflection in lead V1 (R wave).

2. The second phase of depolarisation is the activation of the body of the LV, which creates a large positive deflection or R wave in V6 (with reciprocal changes in V1).

3. The third and final phase involves the RV and produces a small negative deflection or S wave in V6.

Normal R wave progression in chest leads:

1. As we move in the direction of the electrically predominant left ventricle, the R wave tends to become relatively larger and the S wave relatively smaller.

2. Generally, in V3 or V4 the ratio of R wave to S wave becomes 1. This is called the transition zone.

3. If the transition occurs as early as V2, then it is called early transition and if the transition occurs as late as V5, it is called late transition.

1.Look for standardization and lead aVR: calibration

At the end of the ECG strip, a standardization box is present which should be 10mm in height and 5mm wide (0.20s).

All waves in aVR will be inverted unless leads are wrongly placed or dextrocardia present.

2. Rate:

Look at the Rhythm strip (lead II) to determine heart rate and rhythm.

If RR interval is regular:

Heart rate= 1500/RR interval (mm)

or, Heart rate= 300÷ number of large squares between beats.

e.g. R-R interval is 20 small squares, Heart rate is= 1500/20-75/min

If RR interval is not regular:

That means the R-R interval is variable.

Heart rate= Number of R in 30 large squares (6 seconds) X 10

e.g. 8 QRS complexes in 30 large squares (6 S). So, HR-8X10-80 beats/min

3. Rhythm:

See if sinus rhythm presents or not.

Regular: RR interval is regular

Irregular: RR interval is irregular.

Causes

✓Physiological: .Sinus arrhythmia

✓ Pathological:

Atrial fibrillation

Atrial flutter with variable block

Ectopic beat

SA block or sinus arrest

Atrial tachycardia with block

Second degree heart block

Ventricular fibrillation.

Features of sinus rhythm:

a. Each P wave should be followed by QRS complex

b. Normal P-R interval

c. Normal P wave morphology

d. The R-R interval should be equal.

4. Cardiac axis:

Normal: If QRS complexes +ve in leads I and II

Left axis deviation: If QRS complexes +ve in leads I and -ve in lead II (Left leaves)

Right axis deviation: If QRS complexes -ve in leads I and +ve in lead II (Right reaches)

Extreme RAD: : If QRS complexes -ve in leads I and aVF

Cause of left axis deviation:

1. LVH

2. LBBB

3. Left anterior hemiblock

4. WPW syndrome

5. Hypertrophic cardiomyopathy

Causes of right axis deviation:

1. RVH

2. RBBB

3. Left posterior hemiblock

4. COPD with cor pulmonale

5. Fallot's tetralogy

5. P wave:

Represents atrial depolarization

Normal Height X Width- 2.5mm X 2.5mm.

Best seen in lead II.

Positive in all leads except aVR.

The SA node starts depolarization at the right atrium.

So, the 1st part represents the right atrium and the latter part represents the left atrium.

Different morphology of P waves depends on various locations of the pacemaker.

P mitrale: (left atrial enlargement)

Width> 2.5 small squares

Mechanism: If the left atrium is enlarged, it will take more time to be depolarized than the right atrium.

So, a wide and notched P wave is formed.

P pulmonale: (right atrial enlargement)

Height > 2.5 small squares

Inverted P Wave:

✓ Occurs when impulse in generated at or below AV node

✓ Spreading the impulse in the retrograde direction will produce an inverted P wave.

6. PR interval:

Is the distance between the onset of the P wave to the beginning of the QRS complex.

✓ Normal = 0.12-0.20 sec i.e. 3-5 small squares. ✓Prolongation denotes impaired AV nodal conduction.

Short PR interval:

If <3 small squares. Occurs in

Wolff-Parkinson- White syndrome, Lown-Ganong-Levine syndrome, Nodal ectopic

WPW syndrome ( W> wave: delta wave, P> PR interval short, W> Wide: wide QRS)

Prolonged PR interval:

If>5 small squares. Occurs in

a) First-degree heart block:

PR is prolonged >5 small squares and remains constant beat to beat.

b) Second-degree heart block:

Mobitz type I: Progressive lengthening of the PR interval followed by drop beat.

Mobitz type II: PR interval of the conducted impulses remains constant but some P waves are not conducted.

c) Third-degree atrioventricular block:

Conduction fails completely and the atria and ventricles beat independently. It always has more P waves than the QRS complex.

Long PR interval causes:

1. 1° Heart block: Aortic Root Dilatation, infective endocarditis

2. B> Beta blockers

C> CCBs

D> Digoxin

3. B> Borreliosis/Lyme Disease

D> DM: Dystrophia myotonica

S> sarcoidosis

7. Q Wave:

This is due to septal depolarization.

Normal Q Wave:

a) Usually absent in most of the leads. But small q waves may be present in I, II, III, aVL, V5 and V6. b) Depth< 2 small squares, width <1 small squares, ¼th or 25% or less in amplitude of the following R wave in the same lead.

Pathological Q Wave:

a) Deep>2 small squares &> ¼th or 25% of R wave of the same lead.

b) Wide > 1 small square

c) Present in more than one lead

d) Associated with loss of height of R wave.

Causes:

a. Old MI

b. Ventricular hypertrophy

c. LBBB

d. Cardiomyopathy

e. Emphysema (due to axis change or cardiac rotation).

f. Q only in LIII is associated with pulmonary embolism (SI, QIII and TIII pattern).

8. R wave:

Normal R Wave: Due to ventricular depolarization.

a.Duration<0.01 sec.

b. R wave usually small (< 1 mm) in VI and V2

c. Increases progressively in height in V3 to V6 (tall in V5 and V6), i.e. R is small in V1 and V2, tall in V5 and V6.

d. Height: aVL < 13 mm, aVF <20 mm, V5 and V6 <25 mm.

Abnormalities: of R Wave: Tall, Small and Poor progression.

Causes of tall R wave:

a. Left ventricular hypertrophy: In V5/V6> 25 mm, aVL >13 mm, aVF > 20 mm

b. In V1, tall R may be due to:

Normal variant

RVH

True posterior MI

Dextrocardia

RBBB

WPW syndrome (type A)

Causes of small R wave:

Looks like low voltage tracing.

a. Incorrect ECG calibration (standardization)

b. Obesity

c. Emphysema

d. Pericardial effusion

e. Hypothyroidism

f. Hypothermia.

Poor progression of R wave:

Amplitude of R wave is progressively reduced in V5 and V6.

Causes:

a. Anterior or anteroseptal myocardial infarction

b. LBBB c. Dextrocardia

d. Cardiomyopathy

c. COPD

f. Left sided pneumothorax

g. Left sided pleural effusion (massive)

h. Marked clockwise rotation

i. Chest electrodes placed incorrectly

j. Deformity of the chest wall k. Normal variation.

l. LVH (though R is tall in most cases)

9. S wave:

Negative deflection after R wave (1/3 of R wave).

Normally, deep in V1 and V2: An impulse is going to the muscles of the left ventricle then to the right ventricle

Progressively diminished from V1 to V6 (small S wave may be present in V5 and V6)

In V3, R and S waves are almost equal (corresponds with interventricular septum).

10. QRS complex:

Represents ventricular depolarization

Normal duration <0.12 sec or <3 small squares. Duration If >0.12 sec, ventricular conduction is abnormal (left or right bundle branch block)

Causes of high voltage QRS:

a.Incorrect calibration.

b. Thin chest wall.

c. Ventricular hypertrophy (right or left or both).

d. WPW syndrome.

e. True posterior myocardial infarction (in V1 and V2).

Low voltage QRS:

<5 mm in I, II, III and < 10 mm in the chest leads.

Causes

a. Incorrect calibration

b. Thick chest wall or obesity

c. Hypothyroidism

d. Pericardial effusion

e. Emphysema

f. Chronic constrictive pericarditis

g. Hypothermia.

Wide QRS:

>0.12 seconds, 3 small squares.

Causes

a. LBBB or RBBB

b. Ventricular ectopics.

c. Ventricular tachycardia

d. Idioventricular rhythm

e. Ventricular hypertrophy

f. Hyperkalemia

g. WPW syndrome

h. Pacemaker (looks like LBBB with spike)

Drugs:

TCA

Quinidine

Procainamide

Phenothiazine

Variable QRS:

Causes

a. Ventricular fibrillation

b. Multifocal ventricular ectopics

c. Torsades de pointes

11. ST segment:

Measured from the end of S to the beginning of T wave.

Represents beginning of ventricular repolarization.

Normal:

In isoelectric line or,

Elevation is up to 1 mm in limb leads and 2 mm in chest leads or,

Depression < 1 mm.

ST elevation: > 2 mm

a. Recent MI (Convexity upward)

b. Acute Pericarditis (Concavity upwards, chair shaped or saddle shaped)

c. Left ventricular aneurysm (Persistent ST elevation)

d. Prinzmetal's angina (ST elevation with tall T)

e. Hyperkalemia

E> ERS

L> LBBB

E> Electrolytes: hyperkalemia

V> Ventricular Hypertrophy

A> Aneurysm

T> Thrombotic occlusion, pericardiocentesis

I> Infarction: MI, inflammation: pericarditis

O> Osborn wave in hypothermia

N> Neurogenic, non occlusive vasospasm, normal variant: Caucasian: African- Asian

ST depression: >1mm

a. Acute Myocardial ischaemia

b. Acute posterior Myocardial infarction: In V1, V2

c. Ventricular hypertrophy with strain

Nod. Digoxin toxicity (reverse tick pattern), Hypokalemia

12. T waves:

Follows S wave and ST segment.

Indicates ventricular repolarization

Size and shape:

Upright in all leads, except aVR. But May be normally inverted in V1 and V2.

Tip of the T is smooth (rounded).

Not more than 5 mm in standard leads and 10 mm in chest leads.

Minimum ¼th of R wave of the same lead.

Causes of T inversion:

a. Myocardial ischemia and infarction

b. Subendocardial myocardial infarction (non-Q wave myocardial infarction)

c. Ventricular ectopics

d Ventricular hypertrophy with strain

e. Acute pericarditis

f. Cardiomyopathy

g. Myxoedema

h. Bundle branch block

i. Drugs (digitalis, emetine, phenothiazine)

j. Physiological (smoking, anxiety, anorexia, exercise, after meal or glucose)

Causes of tall peaked T wave:

a. Hyperkalemia (tall, tented or peaked))

b. Hyperacute myocardial infarction (tall T wave)

c. Acute true posterior myocardial infarction (tall T in VI to V2)

d. Maybe normal in some Africans and Asians.

Causes of small T wave:

a. Hypokalemia

b. Hypothyroidism

c. Pericardial effusion

13. QT interval

Distance from the beginning of Q wave (or R wave, if there is no Q wave) to the end of T wave.

Represents the total time required for both depolarization and repolarization of the ventricles.

Better seen in aVL

Normal <0.42 sec

Varies with heart rate, becoming shorter as the heart rate increases and longer as the heart rate decreases.

QT prolongation:

a) Bradycardia

b) Congenital long QT syndrome

c) Low K+, Mg2+ or Ca2+

d) Drugs

Disopyramide, flecainide and other class la, lc anti-arrhythmic drugs

Sotalol, amiodarone and other class III antiarrhythmic drugs

Amitriptyline and other TCAS

Chlorpromazine and other phenothiazines

Erythromycin and other macrolides

Causes of short QT interval:

Digoxin effect.

Hypercalcemia

Hyperthermia

Tachycardia

14. U Waves:

Look for prominent U waves.

Usually most apparent in chest leads V2-V4

May be a sign of hypokalemia or drug effect or toxicity (e.g., amiodarone, dofetilide, quinidine, or sotalol).

15. Hypertrophy:

Left ventricular hypertrophy:

S in VI R in V5 or V6 >35mm

or R in V5 or V6>26mm

Mechanism:

LVH indicates large or hypertrophied left ventricle suggesting more mass and cell presence in the left ventricle. So, more action potential is generated causing a large vector and increased amplitude on ECG. They are best seen in chest leads.

LVH with Strain:

Findings of LVH

ST depression and T inversion (in I, aVL, V4 to V6)

RVH with Strain:

Features of RVH

ST depression and T inversion (in V1 and V2)

16. Bundle branch block:

Right bundle branch block (RBBB):

Criteria:

a. Broad QRS >3mm

b. M (RSR') pattern in V1 and V2

c. Broad deep S in V5 and V6

d. Right axis deviation may be present

Mechanism:

When there is RBBB, impulses are not transmitted through normal pathways, transmitted through cell to cell depolarization in part of the interventricular septum and RV. This slow impulse causes slower depolarization time causing prolongation of the QRS complex on ECG.

RBBB: MARROW

M pattern in V1, V2 with wide QRS

W pattern in V5, V6

Left bundle branch block (LBBB):

Criteria:

a. Broad QRS >3mm

b. M (RSR') pattern in VS and V6, also Lead 1 and aVL

Mechanism:

The block in the left bundle branch causes an electrical potential to travel down first in the right bundle. So, ventricular depolarization occurs from right to left by cell to cell transmission Because the vector from right to left, the QRS complex will be negative V1-V2 and positive V5, V6 & lead I.

LBBB: WILLIAM

W pattern in V1,V2

M pattern in V5, V6 with wide QRS

Determination of sites of MI:

1. I, aVL V5-V6: Lateral MI

2. I, aVL: High lateral MI

3. II, III, aVF: Inferior MI

4. VI to V6: Extensive Anterior MI

5. Anteroseptal MI: VI to V4

6. II, III, aVF, I, aVL, V5 and V6: Inferolateral MI

7. VI-V2: Posterior MI

8. VI-V6, I, aVL: Anterolateral MI

9. Symmetrical T inversion in all chest leads: Subendocardial MI

Acute inferolateral MI

(ST elevation in II, III, aVF, V5, V6. Reciprocal ST depression in I, aVL, VI and V2)

Old inferior MI

(Pathological Q wave II, III, aVF)

Acute inferior MI

(ST elevation in II, III, aVF and reciprocal ST depression in I, aVL, V5, V6)

Posterior MI

Tall R waves and ST depressions in leads VI and V2

Acute posterior MI

(Tall R wave in V1 and V2)

Recent anterior non-ST elevation (subendocardial) MI

(Deep symmetrical T-wave inversion, together with a reduction in the height of the R wave in leads V1, V2, V3 and V4)

Acute anterolateral MI

(ST elevation in leads 1, aVL, V2, V3, V4, V5 and V6, and Q waves in leads V3, V4 and V5).

Acute inferolateral MI

(ST elevation in II, III and aVF and lateral leads V4, V5 and V6 and reciprocal" ST depression in leads aVL and V2)

MYOCARDIAL ISCHEMIA

Criteria:

1. ST depolarization (Horizontal or downsloping)

[Up sloping ST depolarization normal]

2. T inversion or both

LEFT VENTRICULAR HYPERTROPHY

Left ventricular hypertrophy:

Criteria: S in VI+ R in V5 or V6 >35mm or R in VS or V6> 26mm

Mechanism: LVH indicates large or hypertrophied left ventricle suggesting more mass and cell present in the left ventricle. So, more action potential is generated causing a large vector and increased amplitude on ECG. They are best seen in chest leads.

LVH with Strain:

✓ Findings of LV

✓ST depression and T inversion (in L1, aVL, V4 to V6)

RIGHT VENTRICULAR HYPERTROPHY

Criteria: R wave in VI > 7 mm

RVH with Strain:

✔Features of RVH

✓ST depression and T inversion (in V1 and V2)