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:
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Wide or flat T wave |
Transmural Ischemia:
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Deep symmetrical inverted T wave |
Sub endocardial Ischemia:
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Tall and wide T wave because of late repolarisation from inner end without opposing force from opposite wall
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Sub endocardial Ischemia at opposite wall:
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T wave has become low or depressed due to late repolarisation of sub endocardium to opposite direction
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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:
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Tall R wave and tall T wave |
Epicardial infarction at opposite wall:
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ST segment depression as injury sign |
Infarction with little healthy tissue: |
Deep Q wave like letter W |
Infarction with more healthy tissue:
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QR or RS wave pattern. |
Electrode at junction of infarction and healthy portion:
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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:
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Tall R wave (reactive hyperemia induced by ischemia) |
Stage B:
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Tall R wave with wide QRS interval (thick fibre) |
Stage C:
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Tall R wave, wide QRS, and inverted T wave, (prolonged depolarization) |
Stage D:
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Low voltage of R wave. |
Stage E:
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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
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|
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
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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.
Right ventricular failure:
|
Stasis oedema |
Mitral stenosis:
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Red face |
ASD:
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Blue lip and scoliosis |
Dizziness of cardiac origin:
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It occurs even at rest. |
Right atrial fibrillation:
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Congestive headache |
Left atrial fibrillation:
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Cough, thrombus formation |
Endocarditis:
|
Black face |
Heart sounds
Heart sounds are best audible at centre of chest on lying supine, at lateral to nipple on lying left lateral position, and at right to sternum on lying in right lateral position.
First heart sound loud:
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Expiration, hyperthyroidism, Mitral stenosis, Left ventricular hypertrophy. |
First heart sound soft:
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Presence of air, fluids, old age, beriberi, thick chest and infarction. |
2nd heart soundloud:
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Hypertension, pulmonary hypertension, aortic incompetence, and pulmonary incompetence. |
Second heart sound soft:
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Aortic stenosis, pulmonary stenosis, aortic incompetence, failure and shock. |
Second heart sound split:
|
Left bundle branch block at aortic area |
Pulse
Prefer radial artery of right arm of female and left arm of male and examine with middle three fingers on slightly flexed wrist for 30 seconds. Keep the examiner’s thumb at back of wrist.
Completely irregular: |
Atrial fibrillation
|
occasionally irregular: |
Extra systole
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High pulse volume: |
Hyperthyroidism, hypokalemia, left ventricular hypertrophy, aortic incompetence,mitral incompetence, and post ectopic beat
|
Low pulse volume: |
Aortic stenosis, Mitral stenosis, and shock
|
Strong and weak pulse: |
Failure
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Strong pulse: |
Inspiration, jaundice, typhoid fever.
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Pulse deficit: |
Atrial fibrillation, shock, and extra systole
|
Slow pulse rate: |
Inspiration, pericardial effusion, A V block, atrial fibrillation, and brain disorder |
Blood pressure
Wide pulse pressure: Aortic atherosclerosis
Short pulse pressure: Mitral stenosis (low blood volume) and pericarditis
CARDIAC TREATMENT
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Prophylactic treatment |
Avoid all predisposing factors
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Strong individual |
Cure (Elimination of toxins (miasm) and re establishment of homoeostasis. |
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Weak individual |
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Conditions |
Acute (medicines with primary action) |
Chronic (medicine with secondary action or medicine with primary action in non susceptible )
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Hypertension |
Rauwolfia, veratrum, sympatholytics |
Belladonna, ephedra, lobelia, tabacum |
|
Hypotension |
Ephedra, thuja |
Aconitum, china, nux.v, secale, veratrum, viscum alb, snake root |
|
Fatty heart |
Kalmegh |
Phosphoric acid |
|
Tachycardia |
Aconitum, aristolochia, china, digitalis, nux vomica, oleander, secale, squilla, strophanthus, valariana, veratrum, viscum alb, yohimbinum |
Belladonna, ephedra, Sympathatomimics |
|
Paroxysmal atrial tachycardia |
Aconitum, china, nux vomica, secale cor, veratrum |
Calc phos, Digitalis |
|
Ectopics |
Kali mur, aconitum, china, nux vomica, secale cor, veratrum |
Calc phos, digitalis, ricinus com |
|
Rheumatism |
Digitalis, sulphuric acid |
Bryonia, kalmia |
|
Bradycardia |
Belladonna, hyoscyamus stramonium |
Aconitum, china, nux vomica, secale cor, veratrum |
|
SA. block |
Belladonna, ephedra |
China, digitalis, physostigma |
|
Failure |
Calc phos, ephedra, tabacum |
Arsenic alb, china, kali mur, rauwolfia, sulphur |
|
Thrombosis varicose vein |
Sulphuric acid,china, melilotus, salix nigra, sulphur |
Alfalfa, calc phos, china, gelsemium, aloes.s, mag phos |
|
LVF |
Calcium phos, opium, rauwolfia |
Arsenic alb, nux vomica |
|
Beriberi |
Allium cepa, arsenic alb, china opium, sulphur |
Sulphuric acid |
|
Hyper cholestremia |
Allium sativa, embelica ribes, sulphuric acid, terminalia chebula, podophyllum |
Oleum jecoris, ricinus communis |
|
Congenital ASD |
Calcarea phosphate |
||
Over active state congenital |
Alfalfa, china, Secale cor, Viscum album |
||
Recurrent angina |
Cactus.g, aconitum, mag phos, alcohol |
||
Effort syndrome |
Aconitum, arsenic alb |
||
Atrial fibrillation |
Digitalis |
||
Phlebitis |
Aloes.s, hamamelis |
||
Pericarditis |
Bryonia, spigelia |
||
RVF |
Arsenic alb, digitalis |
||
Syphilitic heart |
Cactus.g, aurum met, mercury, podophyllum |
||
Aneurysm |
Abrotanum, secale cor |
“Anybody can be a heart specialist. The only requirement is loving somebody”
References
1. V.N Orlov, Electrocardiography for practicing physician, Mir publishers, Moscow
2. Michael L Armstrong, Electrocardiograms, a systemic method of reading them, John Wright & son Ltd, Techno house, England
3. Mevin J. Goldman, Principles of clinical electrocardiography, Maruzen, Company Ltd
4. C.R. Maiti and N. Goswami, Practical hints to clinical electrocardiography, New Central book agency, Calcutta-India
5. A.F Golwala, Electrocardiography for students and practitioners, India printing works, Bombay-India
A very useful article for proper understanding of heart and role of ECG as a diagnostic toolS8Bk
a must read article to understand ECG better
Very Nice Article. Thankyou Dr. Kader
very good article nice one. But my view is we should not try homoeopathy medicine in any acute cardiac illnessess. In chronic diseases yes