The Scope of ECG in Heart Disease

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Dr. Kader provides a detailed analysis of the ECG over a wide range of conditions.

Introduction

Myocardial infarction is the most common cause of sudden death in tropical countries. It could be the first event in an asymptomatic person or could be the end of a spectrum commencing from angina. Premonitory subjective symptoms are usually absent in most individuals. It occur more in drivers than conductors, and in sitting post office clerks than postmen. Hypertension, hyperlipidemia, diabetes, obesity, smoking and physical inactivity are the major risk factors.

Predisposing factors

Family history of premature myocardial infarction, advancing age, heavy consumption of alcohol, type A personality, abundance, life style with ambition, unnecessary emotion, hurry, anger, fear, stress, depression, lack of smile, negative mood, negative partner, lack of rest, insufficient sleep, persistent use of sympathomimetics, excess of salt, sucrose and coffee; nasal block, COPD (hypoxia), renal insufficiency, hepatic insufficiency, male sex, excess of testosterone, menopausal women, oral contraceptive pills, metabolic disorder, hyperuricemia, hyper triglyceremia, hypothyroidism, hyperthyroidism; recurrent infectious myocarditis, syphilis; Asians (small sized vessels, thin and irritable pericardium), hereditary aortic aneurism; congenital heart diseases; hereditary short refractory period of myocardium, hypercalcaemia, consumption of prawn, sea fishes, shell fish, osteoporosis, tropical climate, cardiac overwork with rapid rate, CO2 excess, lack of sufficient water intake, high Mg++ (consuming excess of green vegetable, hard water, or water near sea coast), food or air contaminated with heavy metals like lead, presence of old iron particles in blood, etc. have a major role in development of sclerosis and infarction. Unstable angina is a precursor of myocardial infarction. Coronary artery diseases constitutes only 35 % of all myocardial diseases

Angina pectoris

Precordial pain may spread centrifugally in any direction, or it may occur as choking sensation in throat or chest. It may be felt as numbness on inner fingers as occurs in cervical mono neuritis or carpel tunnel syndrome.

There are often multiple predisposing factors such as anemia, arterial spasm, thrombosis, atheroma, stasis of blood in great cardiac vein, aortic stenosis, mitral stenosis, mitral incompetence, COPD, LVH with small cavity size, slow rate with low output, failure with peripheral capillary dilatation, chronic rheumatism, haemostasis of blood due to central hypertension, conditions with increased viscosity like polycythaemia, and coronary sclerosis. Thebesian veins can supply to cardiac muscle when collateral circulation is reduced. Incidence of arterial thrombosis is more in unsupported vessels like coronary, carotid or radial arteries. Thrombosis is common in veins due to low vascular pressure. Normal coronary flow is about 20% of stroke volume.

ELECTROCARDIOGRAM

Even though many novel and sophisticated instruments have been discovered in the last 100 years, physical examinations and ECG remain the most important diagnostic procedures for the general practitioner.

The Electrocardiogram is a graphic representation of the electrical potential associated with the heart beat. It is a lab test only.

Scope of ECG

It is helpful to estimate fitness of sportsman, drivers, sailors and pilots;to detect atrial and ventricular hypertrophy, myocardial ischemia, injury and infarction; to find out the old infarction, the progress of treatment in infarction; to evaluate cardiac muscle properties, cardiac rate, arrhythmia, atrial fibrillation, AV block, bundle branch block; to detect cardiac position; and to evaluate effects of drugs, hormonal & electrolyte imbalance.

History

Galvani Luigi (Italy) first described animal electricity in 1786. Marey invented the electrometer in 1876; Augustus D.Waller traced human electricity experimentally first, in St. Mary hospital London in 1887. Willem Einthoven had attended Waller’s demonstration in 1889. Einthoven invented the ECG machine in 1901 and put forward a hypothesis that the potential in lead II is equal to the sum of potentials of lead I and lead III based on the dipole theory. He was awarded the Nobel Prize in 1924. FrankWilson introduced unipolar leads in 1934. Emanuel Goldberger introduced the augmented unipolar limb lead in 1942.

Anatomy

The human body is like a community of cells. The heart helps to supply food as a civil supply department and removes wastes as a sanitary department, being the central organ of the cardiovascular system.The ventricle is chamber, the atrium, ante chamber. Normal thickness of the left atrium, right atrium, right ventricle and left ventricle are about 3mm;4mm, 5mm, 15mm respectively.

Properties of cardiac muscles

Automaticity, rhythmcity, conductivity, excitability, refractoriness, one or none law, aberrant conduction, contractility (can be detected partly by ECG), tonicity (cannot be detected by ECG),

Normal ECG waves

The ECG can be divided into atrial, septal and ventricular waves. P (p, p1, PT) wave; q, r (qT, rT) wave; R, S, (r, R1, S1) waves; T, and U waves. The Intervals are P-R, QRS, Q-T interval; Segments are PR segment, ST segment and TP segment.

Normal ECG wave Lead I

ECG paper

Paper speed is usually set at 1500mm/minute. Small size blocks represents1mm height x 1mm (0.04 second- horizontally); large size blocks represents 5mm height x5mm (0.2 second – horizontally). The machine is usually standardized with a signal of 1mm producing a wave 10 mm vertically.

LEAD

The lead axis is the imaginary line between two opposite points (poles).

ECG leads are standard leads (LI, LII, LIII),unipolar limb leads (aVR, aVL, aVF), and unipolar chest leads(V1, V2, V3, V4, V5, V6, V7). The Bipolar lead records the potential difference of two poles simultaneously. Unipolar lead records electric potential from one pole only through exploring electrode.

ECG lead position

ECG vector should be analyzed with all three leads-STD, unipolar limb, and chest leads. Electrographically, the heart can be divided to three portions- the anterior, posterior, and cavity.

Normal 12 lead ECG

Representation of right or left ventricle in leads may vary in accordance with alternations in cardiac position. TheR wave in LIII represents to right ventricle in the horizontal position, but to the left ventricle in extreme vertical position.

Electric field

Electrical potentials are due to exchange of K+ out and Na+ in. K ion is about 150 Meq/L inside and 10 Meq/L outside the cell. Na + is 5 Meq/L inside and 142 Meq/L outside the cell. The intercellular potential is about less than -90mv normally. Cell membranes act as resistance {5000 ohm}. Cell cannot be excited if potential is increased more than about -60mv.

Normally the electro motive force (EMF) is transmitted in waves in 7 directions with depolarization following SA node stimulation. 80% of electric potentials are lost during transition to the body surface (surface ECG).

Negative charge at right shoulder and positive charge at left hip are developed in normal condition in each SA node excitation. (Dipole theory-Maximum potentials are near zero line. Electrical charges interact according to Coulombs law: the force of interaction is directly proportional to the magnitude of charges and indirectly proportional to the square of the distance between them)

BASIC PRINCIPLE

Positive waves are registered when current of electricity flows towards the exploring electrode and negative waves are registered when current flows away from electrode.

Depolarization time of ventricle, i.e ventricular activation time (VAT) is short both on strong stimulation and in thin fiber.

When two excitations occur through two fibers to the same direction and depolarize simultaneously, net potentials are developed (fusion-tall and wide wave).

If current of excitations occur towards two opposite directions simultaneously through two fibers, biphasic waves occur in exploring electrode. When it occurs in different masses, the large mass or the strong stimuli can make waves first. If currents flow towards 90 degree to electrode, waves can’t be seen.

ISCHEMIA, INJURY AND INFARCTION

 

Ischemia

Normally repolarization starts from the opposite end to the stimulation within1/100 seconds after depolarization. Depolarization takes a longer time than usual to complete in chronic ischemia, degeneration, thick fiber, and in slow inter ventricular conduction. Repolarisation begins from the stimulated end itself. So T wave is seen as inverted in the nearby lead.

Ischemia epicardial portion only:

Wide or flat T wave

Transmural Ischemia:

Deep symmetrical inverted T wave

Sub endocardial Ischemia:

Tall and wide T wave because of late repolarisation from inner end without opposing force from opposite wall

Sub endocardial Ischemia at opposite wall:

T wave has become low or depressed due to late repolarisation of sub endocardium to opposite direction

Transmural Ischemia at opposite wall:

Tall R wave and tall T wave.

Chronic ischemia

Signs are persistent T wave inversion, wide QRS interval, wide QT interval, and inverted u wave at V6. Ischemic or injury changes at posterior wall are reversible. Chronic myocarditis, coronary thrombosis, digitalis toxicity, cardiac depressants and hypokalemia have similar ECG pattern.

Prinzemetal angina

Pain persists even at rest and expresses high ST segment elevation (hyperkalemia). Reciprocal ST segment & T wave changes are absent. It is due to coronary spasm. Pain may persist even at rest and is better by vasodilators.

Acute coronary insufficiency

Unstable angina is used to denote the recurrent pain lasting more than 5 -15 minutes with ECG changes like sub endocardial infarction. ECG signs are ST segment depression, symmetrical T wave inversion, absence of Q wave, poor R wave progression, and U wave inversion. The reciprocal ST segment elevation in aVR is absent.

Ischemia, injury and infarction primarily develop at deeper parts than superficial, due to less blood supply.

Exercise ECG test:

Take exercise that increases heart rate more than 140/minute for 1.5 minutes or 3 minutes. Take ECG immediately, and after 6 minutes. Avoid exercises that induce cardiac rate >140/minute in adult. ECG also can be traced with pace maker which induces cardiac rate 220-age/minute. Positive indication is ST depression. Other indications are elevation of ST segment, increase in voltage of R wave or T wave, increase in R height / increase in depth of ST segment >1; emerging of PVEB, pain, syncope etc.

Myocardial injury

It may occur at epicardial, transmural or subendocardial portion. Main causes are infections, toxins, metabolic or neoplasm infiltration, fatty degeneration of muscles and ischemia.

Epicardial injury

Depolarization begins from stimulated inner end but it completes slowly in stage by stage. The epicardial end becomes negative from injury, but it is comparatively more positive to already depolarized (negative) inner portion. The further depolarization (flow of current) is developed slowly (when ion exchange occur through the injured portion). The second limb of R wave now seems as ST segment elevation. The least peripheral injury is marked as concave elevation, and transmural injury is seen as convex ST elevation.

Sub endocardial injury

When the injury occurs at sub endocardial portion (opposite to electrode and at the same portion of stimulation), the depolarization begins as usual to electrode direction. But depolarized outer portion now becomes comparatively more negative than injured (non depolarized) sub endocardial end. So current goes slowly far away from electrode direction, after initial positive wave. ST segment shifts below to the baseline and seems as depressed.

Infarction

Changes occurring in infarction are like a train accident. Some fibers are dead, more are injured and others are normal. Myocardial infarction can be categorized as atrial, septal, or ventricular; anterior or posterior; acute, recent, sub acute or old; multi focal, recurrent; epicardial, sub endocardial, transmural or reciprocal infarctions.

Lead representations of heart surface are LI, V1, V2, V3, and V4: anterior surface;

aVL, V5, and V6 : lateral surface;

LII, LIII, and aVF: posterior-inferior surface;

V1 and V2: reciprocal lead of posterior surface; and .aVR or aVL: cardiac cavity.

Healthy opposite wall is depolarized first in infarction. Thus negative depolarization wave manifests in electrode near the injured part and tall R waves occur in lead at opposite healthy wall.

Epicardial infarction:

Q wave with small R wave.

Transmural infarction:

Deep Q wave, absence of R wave, deep T wave (tall T wave may occur in early stage due local hyperkalemia)

Sub endocardial infarction:

Q wave may be absent, ST depression occurs as in injury; wide S wave may develop; ST segment elevation may manifest in cavity lead either aVR or aVL

Transmural infarction at opposite wall:

Tall R wave and tall T wave

Epicardial infarction at opposite wall:

ST segment depression as injury sign

Infarction with little healthy tissue:

Deep Q wave like letter W

Infarction with more healthy tissue:

QR or RS wave pattern.

Electrode at junction of infarction and healthy portion:

Wide R wave or q with R wave.

ECG usually shows combined pattern of ischemia, injury and infarction in the first few weeks of infarction.

Symptoms

Persistent precordial pain or choking sensation with symptoms of shock are the common symptoms. Other features are fever, SGOT>40 units, high ESR, and leucocytosis (all these sign may be absent in sub endocardial infarction).

Similar pain is occurs in other conditions like pericarditis, pulmonary embolism, peptic ulcer perforation, thoracic radiculitis, reflux eosophagitis, gall bladder disorder, acute myocardial ischaemia, or pancreatic disorder.

Acute infarction (3 days)

Common early signs are sudden giant transient T wave elevation (rare), ST segment convex elevation with reciprocal depression.

Recent infarction, ST segment elevation

Sub acute infarction (3 weeks)

Deep Q wave, T wave inversion, and low R wave ST segment set at on isoelectric level. Atrial fibrillation, ventricular tachycardia and AV block may develop with pain or shock. Q wave is sometimes absent in anterior infarction.

Sub endocardial infarction

Silent infarction may occur in diabetic peripheral neuropathy, or in anterior wall sub endocardial infarction. Frozen shoulder on left side usually develops in posterior infarction. Post infarction failure manifests as rapid rate, low pulse volume, low pulse rate, low BP and ventricular tachycardia. Shock is commonly due to acidosis.

ECG changes in other cardiac diseases

Pericarditis

It usually lasts for 4 weeks. The main causes are viral infection, hyperuraemia, rheumatism and tuberculosis. ECG changes are concave ST segment elevation in all leads, low voltage, electric alternans, and tachycardia. ST segment may be depressed in aVR. (Low pulse pressure, soft 1st sound and pericardial rub are other features).

Myocarditis

It usually lasts for 6 weeks. The predisposing factors are toxins, infections including secondary bacterial infections or water borne viral infections. Features are ST segment depression, T wave inversion, low voltage, and prolonged QT interval.

Chronic myocardial disease-ST depression for deep injury

Atrial disorders

P wave is the compound atrial wave. Atrial activation time is increased more than 0.04 sec in right atrial enlargement, or is increased more than 0 .06 second in left atrial enlargement. If P wave duration / P-R interval is more than 1.6 (giant P wave), it indicates atrial hypertrophy.

Right atrial enlargement

Retrograde conduction is seen as upright P wave in aVR or as inverted P wave in lead II. It occurs from lower strong ectopic stimulus, lower escape beat or in idio-junctional rhythm. PR interval is short in retrograde atrial (injury or sympathetic stimulation) and ventricular conduction; and in SA node beat following aberrant conduction, due to early recovery from refractive period of ventricle (Chung phenomena). Early transient acceleration of rate by escape foci can be seen also in ECG in case of slow sinus rhythm (treppe phenomenon). P-R interval is prolonged in long refractive period of ventricle, AV block (including vagus irritation) and atrial septal defects.

Congenital heart

ASD right to left shunt:

ECG signs are wide P wave in L1, LII, and aVL; P wave inversion in V1, P-R interval prolonged and atrial ectopic left side origin (reactive hyperemia, central cyanosis, and flow murmur at aortic area).

ASD left to right shunt:

ECG signs are all P wave in V1, LII, L III, aVR, P wave inversion in aVL, LI and V5; prolonged P-R interval; atrial ectopic right side origin, right axis deviation, tall R wave in V1, and right bundle branch block pattern (letter M like waves in V1). (Other signs are retrograde venous pulse, excess of bronchial secretion due to pulmonary congestion, etc).

Mitral stenosis

ECG signs are wide or bifid P wave in aVL, LI and LII; inverted P wave in VI, left atrial ectopic, atrial flutter, paroxysmal atiral tachycardia, and prolonged P-R interval. (other features are hypotension, weak pulse, low pulse pressure, loud 1st sound, diastolic murmur, red face, effort dyspnoea, productive cough (pulmonary congestion) and sometimes raised ESR. Tall T wave and sign of LVH are marked in mitral incompetence).

Heart rate50/minute, mitral stenosis, P wave bifid

Rheumatic heart

Low R wave, prolonged P-R interval, wide QRS interval, raised ST segment, tachycardia, ectopic beat, and signs of conductive block are seen.

Cardiac fibrosis

Etiology: Malnutrition, anemia, rheumatism, hypertension, metabolic degeneration, and diabetes mellitus etc. Common features are low voltage, ST segment depression and deep T wave inversion. Conditions following atrial fibrosis with dilatation can promote ADH secretion, Na retention, and venous stasis, paroxysmal atrial tachycardia and pain. Clot or vascular polyp formed following the stasis, can lead to embolic phenomena either in pulmonary or in cerebral vessels.

Low voltage

Etiology: weak stimulation, thick chest wall, presence of air or fluid, emphysema, pericardial effusion; parasympathomimetic (it can depress SA node and AV node, while sympathomimetic can stimulate atrium and ventricles), hypothyroidism, hyperkalemia, equal force from reciprocal area, diffuse old infarction etc.

Systemic hypertension

Features are tall R wave, left axis deviation, VAT> 0.04 in V5 presence of ventricular ectopic, and signs of cardiac rotation.

High voltages

Etiology: strong stimulation, sinus node stimulation, absence of opposing force, thin fibre, thin chest wall, electrode close to heart, early period of ventricular hypertrophy; beat after long refractive period like post aberrant conduction, post ectopic beat, post SA block and AV block etc.

Ventricular hypertrophy

Common causes are aortic hypertension and chronic ischemia.

Normal VAT is less than 0.02seconds in VI, {q+1/2r wave}, and less than 0.05 in V5

Stage A:

Tall R wave (reactive hyperemia induced by ischemia)

Stage B:

Tall R wave with wide QRS interval (thick fibre)

Stage C:

Tall R wave, wide QRS, and inverted T wave, (prolonged depolarization)

Stage D:

Low voltage of R wave.

Stage E:

Q wave with inverted T wave

Right ventricular hypertrophy

Shows tall R wave V1-V2 with ST depression wave with raised ST segment in V1 and V2 are due to right ventricular infarction.

Hypertension with systolic strain

Tall R wave, ST segment depression, T wave inversion, U inversion (V6) and LBBB pattern.

Hypertension with diastolic strain

Tall R wave and tall T wave

Hypertension with fibrosis

Low R wave, ST segment depression, T wave inversion, wide QRS interval, prolonged Q-T interval and tachycardia.

Hypotension

Lower aortic pressure causes stimulation of the vasomotor centre at medulla. This secondarily results in sinus tachycardia, parasympathetic splanchnic vasodilatation and sympathetic peripheral constriction reflexively. Occasionally this can record increases in blood pressure.

Ectopic wave

Ectopic beats are triggered due to decreased refractory period of muscles caused by ischemia, injury and fibrosis; toxins like digitalis, rauwolfia, aconitum, tobacco; or hypercalcaemia.

Paroxysmal atrial tachycardia

It may last up to 4 days. Atrial rate is paroxysmal, rapid and painful (Blocked PAT or blocked flutter is painless). It mostly occurs due to atrial ischemia.

Atrial flutter originates from lower atrial multiple foci and is seen as up and down multiple P waves. Ectopics from lower atrial origin can show upright P wave in avR and inverted P wave in LII. Pulse deficit can be felt in atrial fibrillation, failure and weak extra systole.

Most of ventricular ectopics are developed from ventricular ischemia or gastric causes (sympathetic irritation). Ectopics originated from left ventricle are seen as upright waves in right side leads and as inverted waves in left side leads.

Ventricular tachycardia

AV Block

Vertigo or syncope may develop in AV block, sinus arrest, slow ventricular rhythm, vagal irritation, hypotension, asystole and in acute aortic or mitral stenosis (brain death occurs if cerebral insufficiency last more than 6-8 minutes). Escape beats originate from either his bundles or distally from right or left bundle branches, or from ventricular muscle itself in complete AV block. Impulses may travel through accessory pathways like James fibers in some individuals.

Left bundle branch block

Bundle branch block

Normally simultaneous conduction occurs through the right bundle branch and left anterior bundle branch. Then conduction occurs through left posterior branch. This fails in bundle branch block. Ventricles take a long time to complete depolarization in bundle branch block. The repolarization begins from healthy portion. T wave is becomes opposite to terminal portion of depolarization (wide) wave and is seen as inverted in electrode at blocked part. Either right or left bundle branch block may be developed in septal infarction. Bundle branch block occurs in chronic ischemia, fibrosis, old age, septal infarction, and anterior infarction. Left anterior hemi block is marked as deep q wave, left axis deviation, tall and wide R wave in LI & V5. Isolated distal bundle branch block pattern can be considered a sign of old infarction. ECG changes are deep Q wave or wide QRS interval in V3.

PROGNOSIS

It is good in SA block, 1st degree AV Block, paroxysmal AV block, RBBB, posterior wall injury and preliminary epicardial injury of healthy individual. Changes in inferior infarction are reversible.

Bad prognosis

This includes multiple andmassive infarction; old infarction with left bundle branch block, infarction with left and right bundle branch block, infarction with left anterior hemi block (deep Q wave and wide tall R wave in V5), 3rd AV block, left side distal block, slow ventricular rhythm, ventricular tachycardia, atrial fibrillation with clot embolism, aortic or ventricular aneurysm, and ball valve thrombosis.Injury changes of anterior surface are mostly irreversible. Ventricular ectopic beat of multi foci origin or continuous ectopic more than five have bad prognosis.

Sudden death may occur in left ventricular failure, complete AV block, and ventricular fibrillation by infarction, mitral ball valve like stasis clot with left atrial fibrillation, emboli from right ventricle with pulmonary infarction or emboli from left ventricle with cerebral infarction. Bilateral bundle branch block or tri facicular block with absence of escape beat also can induce sudden death.

ECG changes in other common conditions

Psychoneurosis & anxiety

The autonomic nervous system controls internal organs, lungs and heart through endocrine system. Signs are atrial tachycardia, prolonged P-R interval, ST segment depression, flat T wave and prolonged QT interval.

Tobacco heart

ECG signs are premature ventricular ectopic complex, atrial tachycardia, (sympathetomimic), ST segment depression and flat T wave

Hypothyroid

ECG signs are sinus bradycardia, low R wave, prolonged P-R interval, T wave inversion or flat T wave.

Hyperthyroid

Paroxysmal atrial tachycardia, atrial fibrillation, tall R wave, ST segment depression, and signs of failure (low R wave).

Hyper parathyroid

ECG signs are tall P wave, tall R wave, prolonged P-R interval, and short Q-T interval. (PTH may be formed from damaged kidney).

Addison’s disease

Signs are tall T wave (hyperkalemia), ST segment elevation, low P and R waves or absent P wave. Normally renal tubules excrete H+ and K+ with re absorption of H2O and Na+. When these are disturbed hyperkalemic alkalosis (SA block, clotting) or hypokalemic acidosis (ventricular tachycardia, bleeding) develop.

Hyperkalaemia signs can be seen best in precordial lead. Tall T wave, absent P wave, wide QRS interval are the ECG features of hyperkalemia alkalosis.

Renal insufficiency

Signs of hypokalaemia like prolonged Q-T interval, tall R wave, prolonged P-R interval, atrial tachycardia, ST segment depression, and flat T wave may occur. ST segment is prolonged if Ca ++ is decreased in blood.

Cushing’s syndrome

Features of hypokalaemia may appear.

Uraemia

Tall T wave, wide QRS interval, SA block 2:1 or atrial arrest, raised ST segment, low R wave, and acidosis.

Micro albuminuria (Insulinuria)

It develops with excess of renal K+ excretion. ECG changes are prolonged P-R interval, Prolonged Q-T interval, tall R wave, and ST –T depression.

Hyper insulinism

It is characterized by high K+ requirement, high hydrogen excretion and lower oxygen consumption. Signs of hypokalaemia develop.

Hepatic insufficiency

ECG signs are ST segment prolongation more than 0.12second and sinus bradycardia

Beriberi

ECG signs are sinus tachycardia, low R wave voltage, electric alternans, ST segment depression and flat T wave. First heart sound becomes soft.

Asthma & COPD

ECG signs are tall R wave in right sided leads, right axis deviation, deep and wide S wave in L1&V5, clock wise rotation and tall R wave in aVR. VAT may increase more than 0.02 second in V 1.

ECG characteristics

Summary

Rate

atrial rate

1500/number of small blocks in between two P waves

Sinus bradycardia: < 60/minute, sinus tachycardia: > 100/minute, SA block 2:1

Rate

ventricular rate

1500/number of small blocks in between two R waves or two S waves

Tachycardia: Atrial & ventricular irritation, sympathetomimetics

Slow rate: SA block, Sinus arrest, AV. block, Idio ventricular rhythm

Rhythm

Sinus regular rhythm: relation between P wave and R wave are fixed.

Regular rhythm: Normal SA node automaticity, S A block 2:1, paroxysmal atrial tachycardia with AV block 2:1;

Arrhythmias: SA block 3:1 or 3:2, Sinus arrest, AV Block 3:1, bradycardia with escape beat or with ectopic beat,

paroxysmal tachycardia, and fibrillation

P waves

Height < 2.5 mm (2.5 blocks), Duration < 0.10 seconds (2.5 blocks).

Absent P wave: SA block, Junctional beat;

Small P wave: Atrial rhythm;

Tall P wave: Atrial hypertrophy; wide or bifid P wave: left atrial hypertrophy, inter atrial block;

Inverted P wave: Normal in aVR, hypertrophy of opposite atrium

q waves

Normal depth of q wave is 1/4 of following R wave, < 0.04 sec (1 block)

Deep Q wave: Dominance of opposite wall potential

Wide Q wave: Infarction of same wall at electrode

R waves Voltage

Normal R voltage in lead LI, LII and LIII: > 5 mm and < 16mm;

aVL or LI: < 13 mm; aVF : < 20 mm;

LI R +L III S: < 21 mm; v5: < 25 mm; v1: < 5 mm; V1 S+ V5 R: < 36 mm; V2 S+V6 R: < 40mm;

R wave size is progressive from V1 to V5

ventricular activation time:V1 = < 0.2 sec(1/2 block);

V5 = < 0.4 sec (1 block)

P-R interval

0.12 seconds (3 blocks) to 0.22 seconds (5 blocks)

Prolonged P-R interval: AV block;

Short P-R interval: WPWS, accessory atrio-ventricular conduction

S waves

S wave size regression from V1 to V5

Deep S wave: Increased potential of opposite wall;

Wide S wave : Slow potential of opposite wall by hypertrophy or block or infarction

QRS interval


0.04 seconds (1 block) to 0.08 seconds (2 blocks).

Short QRS interval: Hypercalcaemia

Prolonged QRS interval: Bundle branch block, hyperkalemia, inter-ventricular block, aberrant ventricular conduction

ST segment

Normally at iso electrical level

ST segment elevation: Injury at epicardium, hyperkalemia, slow depolarization at epicardium;

ST depression: Injury at sub endocardium, opposite wall acute infarction;

ST segment prolongation: Hypocalcaemia

T waves

Upright and asymmetrical T wave more than 1/10 of preceding R wave

Tall T wave: Hyperkaemia, Flat T wave: ischemia

Symmetrically T wave inversion: Mono fascicular repolarisation, ischemia

Q-T interval

0. 28 (7 blocks) to 0.42 second (10 blocks).

Q-Tc interval: Estimated Q-T interval / square root of R-R interval

Short QT interval: Stimulators, hypercalcaemia, digitalis, and short fiber

Prolonged QT interval: Depressants, china, low nor adrenaline or dopamine.

U waves

Same direction of T wave.

Prominent U wave: Late repolarisation by strong stimuli (V6).

U wave inversion: Ischemia at posterior wall V6, posterior LVH inV3

Position

Normal position is intermediate; equal upright R wave in aVL and aVF.

Vertical position: Inverted R wave in aVL;

Horizontal position: Inverted R wave in aVF

Rotation

Equal size of R and S wave at V3 normally

Clockwise: Equal size of R wave& S wave at V5

Anti clockwise: Equal size of R wave & S wave at V1

Mean

electric axis

Normal axis is in between 0 to + 90 degree:

Upright R waves in LI and LIII

Left axis deviation: Tall R wave at LI and deep S wave LIII

Right axis deviation: Deep S wave in LI and Tall R wave in LIII

Physical constitution

Thick built (High diaphragm): Horizontal position and low R wave voltage.

Thin built (Asthenia, children): Vertical position and tall R wave.

Female (central obesity, horizontal position): Low or flat T wave.

Race: Asians & black: ST segment concave elevation.

Clinical examination

Physical examination: Eyes first and much, hand next and least, tongue not at all.

Signs of heart disease

Common signs are fatigue, palpitation, exertional dyspnoea, stasis oedema, piles, cough, angina and pain even on calves. Frontal baldness, horizontal line at mount Venus and multiple deep craters on heart line in palm were considered as signs of heart disease in gypsy civilization.

About the author

P.B. Kader

Dr. P.B. Kader D.H.M.S, Dc.M.N - born 17.4.1959, studied homeopathy and received his degree from Dr. Padiyar Memorial Medical College, Chottanikara , in 1981. He has published four medical books- three in Malayalam: *Arinjirekenta Rogangal (essays about 28 diseases for public awareness) *E.C.G. Apagradhanum (interpretation of E.C.G. waves) * Premaham -A complete book about diabetes written for lay people
*The keynotes to the Holistic Therapeutics. (English-208 pages) Dr. Kader has also published more than 40 articles in various journals and Malayalam magazines and has conducted over 50 medical camps. He is currently available for consultations at the Homoeopathic Research Centre in Kerala, India.

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