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Myocardial infarction is the most common cause of premature death (30%) in south India since many decades. It could be the first event in an asymptomatic person or could be the end of a spectrum commencing from solitary angina. It is occurred more in drivers than conductors, in sitting post office clerks than postman, and it was more in Finland than Indian sikku, more in Yemeni Jews than colony Jews, and least in Bantu. Coronary artery diseases constitute 35 % of all heart diseases.
Heart diseases. The major risk factors
Congenital heart diseases.
Hypertension.
Hyperlipidemia.
Sucrose consumption.
Obesity.
Smoking.
Physical inactivity.
Dehydration & malnutrition.
Excess of homocysteine.
Predisposing factors
Advancing age.
Family history of premature myocardial infarction.
Habit of heavy alcohol consumption.
Type A personality.
Abundance.
Persistent sympathetic overactivity.
Life style with over ambition.
Greed.
Unnecessary emotion (Hurry, anger, fear, stress, depression, lack of smile).
Negative mood.
Selfishness.
Negative partner
Lack of rest
Sleep insufficiency.
Persistent use of sympathomimetic.
Hyperthyroidism.
Excess of salt, sucrose and coffee, heavy metals (Lead), high Mg (Hard water, or well water near sea).
Nasal block
Chronic obstructive pulmonary diseases (Hypoxia).
Renal insufficiency.
Hyperuricemia .
Hepatic insufficiency.
Hypertriglyceridemia.
Male sex, excess of testosterone.
Menopause.
Oral contraceptive pills.
Metabolic disorder.
Hypothyroidism.
Recurrent autoimmune myocarditis.
Syphilis diathesis.
Asians (Small size of blood vessels, thin and irritable pericardium).
Hereditary aortic aneurysm.
Congenital heart diseases.
Hereditary short refractory period of myocardium (< 0.22 second).
Calcification, Hypercalcaemia- mineral (Consumption prawn, sea fishes, shellfish, high PTH, osteoporosis, tropical climate).
Cardiac overwork with rapid rate (Sympathetic over activity).
O2 lack.
Co2 excess.
Lack of sufficient water intake (cirrhosis).
Food or air contaminated with heavy metal like Lead.
Lead toxicity.
Vascular infiltration of old blood cells (WBC & platelets, Iron particles). Multiple Coxsackies viral infections.
ELECTROCARDIOGRAM
Even though many novel and sophisticate instruments have been discovered in last 100 years, physical examinations and ECG are remaining the best diagnostic procedures for general practitioners.
Electrocardiogram is a graphic representation of the electrical potential produced in associated with the heartbeat. It is only a lab test.
Scope of ECG
Estimate fitness of V.V.I.P, Doctors, drivers, sailors, pilots, sportsmen.
Evaluate the properties of cardiac muscles.
Detect atrial and ventricular hypertrophy.
Detect focal Ischemia, Injury and Infarction.
Detect pulmonary dysfunctions.
Find out old infarctions.
Determine cardiac rate, arrhythmia, atrial fibrillation, paroxysmal atrial tachycardia, and paroxysmal ventricular tachycardia.
Determine SA block, sinus arrest, A.V block, bundle branch block, and cardiac arrest.
Detect cardiac position, electric axis and rotation.
Evaluate hormonal & electrolyte imbalance.
Find out the progress in treatment.
Evaluate effects of drug and toxins.
History
Galvani luigi (Italy) first described about animal electricity in 1776 (published-1791).
Marey invented electrometer in 1876.
Augustus. D. Waller traced human electricity experimentally first in St: Marey hospital London in 1887.
Willem Einthoven had attended Waller’s demonstration in 1889. Einthoven invented ECG machine in 1901 and put forward a hypothesis that potential in lead II is equal to sum of potentials of lead I and lead III based on the dipole theory. He was awarded Nobel Prize in 1924.
Frank Wilson introduced unipolar lead in 1934.
Emanuel Goldberger introduced augmented unipolar limb lead in 1942.
Properties of cardiac muscles
Automaticity
Rhythmicity
Conductivity
Excitability
Refractoriness
One or none law
Aberrant conduction
Contractility (can be detected partly by ECG)
Tonicity (cannot be detected by ECG)
Evaluation of ECG (Methodical approach) Summary
RATE
Atrial rate300 divided by number of large blocks in between two P waves.
1500 divided by number of small blocks in between two P waves.
Sinus bradycardia: Rate < 60/minute.Sinus tachycardia: Rate > 100/minute.
Ventricular rate300 divided by number of large blocks in between two R waves.
1500 divided by number of small blocks in between two R waves or two S waves.
RHYTHM
RegularRegular rhythm:S.A node rhythm (Normal rhythm). S A block 2:1. Paroxysmal atrial tachycardia with A.V block 2:1.
Sinus node rhythmP waves and R waves are regular, normal configuration of P, Q, R, S, T, u waves, with normal P-R interval.
Irregular rhythm
Slow rate with irregular rhythm Sinus arrest.SA block 3:1 or 3:2.AV Block 3:1. Bradycardia with escape beat or ectopic beat.
Rapid rate with irregular rhythm Paroxysmal atrial tachycardia. Paroxysmal ventricular tachycardia. Atrial flutter. Atrial fibrillation. Ventricular fibrillation.
P wave
Height Normally < 2.5 mm (2.5 blocks).Duration Normally < 0.10 second (2.5 blocks).
Absent P wave SA block, Junctional beat, atrial fibrillations. Small P wave Atrial rhythm, atrial ectopic.
Tall P wave Right atrial hypertrophy.
Wide or bifid P waveLeft atrial hypertrophy, interatrial block.
Inverted P wave Normally in aVR lead, hypertrophy of atrium at opposite side of tracing leads, retrograde conduction(LII).
q wave
Normally the depth of q wave <1/4 of succeeding R wave.Duration normally < 0.04 second (< 1 block).
Deep Q wave Potential (primary) dominance of opposite wall (Ventricular hypertrophy).
Deep & wide Q wavePotential (primary) dominance of opposite wall to the exploring electrode (Infarction).
P-R interval
DurationNormally in between 0.12 second (3 blocks) and 0.22 second (5.5 blocks).
Prolonged P-R interval 1 st degree AV block; Atrial septal defect, Mitral stenosis.
Short P-R interval WPWS, Accessory atrio-ventricular conduction, Junctional beat, Low atrial origin beat.
R wave
VoltageNormal R voltage in lead LI, LII and LIII:Height > 5 mm and < 16 mm.
R wave height is progressive from V1 to V5.
Voltage high
Height in aVL or LI: > 13 mm. Height in aVF: > 20 mm Height in V1: > 5 mm
Height in V5: > 25 mm
Sum in LI R + LIII S: > 21 mm
Sum in V1 S + V5 R: > 36 mm
Sum in V2 S + V6 R: > 40mm.
S wave
Depth of S wave takes regression from V1 to V5.
Deep S wave Reflection of Increased vector at opposite wall.
Wide S wave Slowness of vector due to thickness at opposite wall by hypertrophy, or one way travel of potential away from block; Infarction at wall of same side (QS).
QRS interval
DurationNormal duration between 0.04 second (1 block) and 0.08 second (2 blocks).
Short QRS interval Hypercalcaemia
Prolonged QRS intervalBundle branch block, hyperkalemia, inter ventricular block, aberrant ventricular conduction
Activation time of right ventricle At V1 = Normally < 0.02 second (1/2 block).
Activation time of left ventricle V5 = < 0.04 second (1 block)
Increase in VAT (Ventricular activation time) Thick fibre, hypertrophy, slow inter ventricular conduction.
ST Segment position
Segment normally lies at Iso electrical level.
ST segment elevation Injury at epicardium, hyperkalemia, slowness of depolarization at epicardium of same side, aneurysm.
ST depression Recent injury at sub endocardium of same side, Recent infarction at opposite wall, Chronic transmural ischemia of same side.
ST segment prolongationHypocalcaemia and hypoalbuminemia due to liver weakness.
T wave configuration
Normally upright and asymmetrical. Height of T wave is more than 1/10 of preceding R wave.
Tall T wave Hyperkalemia (in chest leads -Focal injury or renal disease).
Flat T wave Ischemia, low height of R wave (Weakness, hypothyroid).
Symmetrically T wave inversionSub endocardial infarction, unstable angina, ventricular hypertrophy with strain, Aberrant conduction, right bundle branch block.
U wave
Normal configuration of U wave is as the same direction of T wave.
Prominent U waveLate or prolonged repolarisation at infro-posterior wall by strong stimuli -Hypokalemia, LVH (V6).
U wave inversion Ischemia at posterior wall (at V6), Posterior LVH (at V3).
Q-T interval
DurationBetween 0. 28 second (7 blocks) and 0.42 second (10 blocks).
Q-Tc (corrected) interval Estimated Q-T interval / square root of R-R interval.
Short QT interval Stimulators, hypercalcaemia, digitalis, sympathomimetic, and short fiber.
Prolonged QT intervalDepressants, sympatholytic, cinchona toxicity, hypocalcaemia, hyperkalemia, hypomagnesemia, Ischemia, and cardiomyopathy.
Cardiac position
Normal position is intermediate-Apex vector facing to left hip. R waves are upright both in aVL and aVF. Horizontal position R waves are upright in aVL, and S waves in aVF.
Vertical position S waves are in aVL, and R waves in aVF.
Cardiac rotation
Apex of heart is facing forward and downwards normally when looking from below. Equal size of R and S waves are seen at V3. It is rotated in hypertrophy.
Clockwise Size of R wave & S wave are seen as equal at V5 (RVH).
Anti-clockwise size of R wave & S wave are seen as equal at V1(RVH or LVH anterior wall).
Cardiac mean electric axis
Cardiac muscles depolarize totally in 7 directions with different electrical potential in each cycle. So different vectors, and resultant waves are developed in surface ECG. Mean electro motive force -vector axis normally lies in between -15 degree and + 90 degree:
Normal axisECG in standard leads shows upright R waves in LI, (LII), and LIII.
Left axis deviation Tall R waves at LI, and deep qRS (S) waves in LIII.
Left axis deviation LAHB, LVH, AMI (Left ventricular potential is weaker at anterior wall & Stronger at posterior wall).
Right axis deviationDeep S waves in LI, and Tall qRS (R) waves in LIII.
Right axis deviationLPHB, RVH, PMI (Left ventricular potential is stronger at anterior wall & weaker at posterior wall).
Normal ECG waves
ECG vectors can be divided into Atrial, Septal and Ventricular units.
Atrial unitsP (P, p1, PR segment-pT wave) wave.
Septal unitsq, Q, r (qT, rT) wave.
Ventricular unitsR, S, (r, R1, S1) waves.
Intervals
P-P interval
R-R interval
P-R interval
QRS interval
Q-T interval.
Segments
PR segment
ST segment.
ECG paper
Machine is usually set at speed of 1500 mm/minute (25 mm/second).
One small square box represents 1mm in height vertically for voltage, and 1mm length horizontally represents for duration (1 mm is equal to 0.04 second).
Large box represents 5 mm in height vertically, and 5 mm in duration horizontally (Duration: 5 mm is equal to 0.2 second).The machine is usually standardized with potential of 1milli volt can produce height 10 mm.
Lead
Lead axis is the imaginary line between two opposite poles.
Bipolar lead or standard lead records potential difference of two poles simultaneously.
Unipolar lead records electric potential through one exploring electrode (Other electrode-indifferent electrode is arranged in zero potential by connecting wires from three limbs).
Standard leads
LI, LII, LIII.
Unipolar augmented limb leads
aVR, aVL, aVF.
Unipolar chest leads
V1, V2, V3, V4, V5, V6, V7. Conventional ECG tracing include totally waves of 12 leads- 3 standard leads, 3 unipolar limb leads, and 6 chest leads. Each leads should be analyzed separately. Electrographically heart can be divided to three portions- the anterior surface, posterior surface, and cavity.
Heart contains three types of tissues- Muscular tissue, Conductive tissue (1%) and Connective tissue.
Normally the vector in some leads may vary in accordance with alternations in cardiac position.The R waves in LIII represents to the right ventricle in intermediate and horizontal position.The R waves in LIII represents to the left ventricle in extreme vertical position.
Electric field
Electrical potential in cells are produced due to rapid entry of sodium ion and slowly going out K+. It is the depolarization. Ca++ go in during early part of repolarization. K+ go out quickly during repolarization. Then some sodium go out and K+ enter inside. Some sodium ions enter to cell with exchange of calcium ions.
K ion is about 150 Meq/L inside the cell and 5 Meq/L outside the cell. Na+ is 5 Meq/L inside the cell and 142 Meq/L outside the cell. Membrane potential of cell is about less than -90mv during resting normally. Cell membrane act as resistance {5000 ohm}. Cell cannot be excited if resistance (membrane- cholesterol, or excess of cat-ion inside the cell) is increased more than about -60mv. Cell be stimulated easily when membrane potentials are less than -110 mv (Hypokalemia).
The electro motive force (Action potential) generated in pacemaker cell in sino arial node are conveyed through conductive system fibres end cause excitation of atrial and ventricular contractile muscle tissues (different 7 directions) and finally end in skin surface. Normally. 80% of electric potentials are lost during the transit to body surface.
Negative electric charges at direction of right shoulder and positive charges at direction of left hip are developed automatically following each SA node excitation. (Dipole Theory-Maximum potentials are near zero line. Electrical charges interact according to Coulomb's law: -the force of interaction is directly proportional to magnitude of charges and indirectly proportional to square of distance between them)
Basic principle
Positive waves are registered when current of electricity flows towards the positive electrode. Negative waves are registered in positive electrode when current flows away from positive electrode.
Depolarization time become short on strong stimulation, tissue with longitudinal cells, tissue with increased cell gap, tissue with less number of cells, and in thin cardiac wall.
When depolarization is occurred through multiple fibres to same direction and simultaneously, net vector is marked increasingly (Fusion wave-tall wave or deep wave).
Positive electrode is placed at middle of fibre, and if depolarization starts from one end, biphasic waves will be appeared.
When depolarization begins from one point and travels towards two opposite direction simultaneously through multiple and different myocardial fibres, fibres with large mass will make tall upward wave with or without small downward wave. If the current of electricity flow towards 90 degree to electrode, waves can’t be appeared.
Ischemia (Repolarization changes)
Normally repolarization changes start from the opposite end towards the stimulated end within 1/100 second after depolarization (single fiber). If iit true T wave will be appeared as negative (in single fibre potential). If depolarization takes long time to complete the process than usual (in chronic ischemia, degeneration, thick fibre, and in slow ventricular conduction), the repolarization will begin from the stimulated end itself and current will flow towards the opposite negative terminal or away from the exploring electrode. So T wave is seen as inverted in leads near positive electrode.
Ischemia epicardial portion only Low height of T wave Transmural ischemia Symmetrical inverted T wave
Sub endocardial ischemia T wave changes are absent
Transmural ischemia at opposite wall Tall T wave due to lack of opposing repolarisation potential.
Chronic transmural ischemia
Major signs are persistent T wave inversion (Repolerisation changes-primary), wide QRS interval (Slow depolarization), wide QT interval (slowness of total duration of electrical systole), and inverted u wave at V6 (posterior wall ischemia-Coronary thrombosis). Changes due to ischemic or injury at posterior wall are reversible because of high collateral circulation. Quantity of blood supply and quantity of muscular fibers are less at subendocardial region. Injury or ischemia are usually developed from outer side to inwards. Subendocardial lesion are painless than epicardial lesion, but it has more prognostic value. Myocardial ischemia, hypokalemia, coronary thrombosis, chronic myocarditis, digitalis toxicity, cardiac depressants (sympatholytics-Cinchona) all may exhibit similar ECG patterns.
Prinzemetal angina
It is due to coronary spasm. Pain may persist even at rest, and it is relieved by vasodilators (Nitrates). ECG expresses as high ST segment elevation (Anoxic -very slow depolarization-excess of Na+ and Ca++ entry). Reciprocal ST Segment depression & T wave changes are absent. Fever, high SGOT, high ESR, leucocytosis, Troponin H, LDH, are absent.
Acute coronary insufficiency (Unstable angina)
The term unstable angina is used to denote the recurrent pain lasting more than 5 -15 minutes with ECG changes like subendocardial infarction (painless).
ECG shows deep ST segment depression, symmetrical T wave inversion, absence of Q wave, poor R wave progression, and U wave inversion (v6). The reciprocal ST segment elevation in aVR is absent.
Ischemia, injury and infarction primarily develop at deeper part of left ventricle than right ventricle due to less thebesian blood supply.
Ischemia, Injury and Infarction
Normal ↓ Normal ↑ Ischemia → ↑ Chronic Ischemia → ↑ ↓
Ectopic →
Failure
30% ischemia & 70% others →Degeneration ↑Compensatory Hypertrophy & Hypertension → ↓ ↑
Injury → ↑ ↓ Aneurysm ↑Infarction → ↓ Ectopic.Bundle branch block . Fibrosis. → Scar →
Exercise ECG test
Take exercises (hoping 20 times) for 1.5minutes or 3 minutes .It can increase heart rate more than 140/minute (220-age). Take ECG immediately, and after 6 minutes. ECG also can be traced with placing pacemaker which inducing cardiac rate 220-age/minute.
Positive indication
ST depression > 0.5mm.
Other indication
Elevation of ST segment.Increase in voltage of R wave or T wave.Increases in ratio of R height / increases in depth of ST segment >1.Emerging of PVEB.Emerging of pain.Emerging of syncope.
Myocardial injury
It may be occurred at epicardial, transmural or subendocardial portion.Main causes of injury are severe ischemia, infections, toxins, metabolic or neoplasm infiltration (WBC, calcium, uric acid), and fatty degeneration of muscles.
Epicardial injury
Depolarization begins from stimulated (inner side) end but it completes slowly in stage by stage. The epicardial end is also becomes more negative at same time due to injury, but it is comparatively more positive even to already depolarized (negative) inner portion. So subsequent depolarization (flow of current) is developed slowly (Some K ions have exchanged early through the injured wall. So epicardial end became –ve; more Na ions are entered into the cells). So second limb of R is seen as raised, and thus it seems asif the ST segment is elevated. The ST segment elevation is appeared as concave elevation in least peripheral injury, but in transmural injury it is seen as convex ST elevation. The height of depolarization potential is increased at electrode of opposite wall in in transmural injury.
Subendocardial injury
When the injury occurs at subendocardial portion (opposite to exploring electrode and at the same portion of stimulation), the depolarization begins as usual to electrode direction. Depolarized outer portion is now become comparatively more negative than injured (not depolarized) subendocardial end. Depolarization of opposite wall makes negative potential before subendocardial depolarization is completed. Then current goes slowly far away from electrode after initial positive and or negative wave. So the second limb of S wave is seen wide and is appeared as ST segment depressed. Upward potential is marked in cavity lead-aVR or aVL).
INFARCTION
Myocardial infarction can be categorized into as follows
Atrial Anterior surface Early Epicardial Septal Posterior surface Acute Transmural Ventricular Postero-Inferior infarction of some duration Subendocardial Focal Anterio- lateral Sub-acute Reciprocal Diffuse Anterio-septal Old Multiple
Changes that are occurred in infarction are similar as train accident. Few fibers are dead, some are injured, some more are ischemic and others are normal. So ECG configuration usually shows combined pattern of ischemia, injury and infarction for first few weeks.
Lead & Heart surface
Anterior surface LI, V1, V2, V3, and V4. Lateral surface aVL, V5, and V6. Posterior-inferior surface LII, LIII, and Avf. Cardiac cavity aVR or aVL. Reciprocal lead of posterior surface LI, V1 and V2.
Depolarization vector of opposite healthy wall is developed first in infarction. Thus negative depolarization wave is manifested in exploring electrode near the injured part, and tall R wave is formed in exploring electrode near healthy wall.
ECG changes
Epicardial infarction ST convex elevation. Q wave with small R wave. (Tall T wave may occur in early stage due local hyperkalemia)
Transmural infarction Infarction of some duration Deep Q wave, absence of R wave, deep T wave.
Subendocardial infarction Q wave may absent, deep ST depression. wide S wave may develop; ST segment elevation may manifest in cavity lead either aVR or Avl
Epicardial infarction at opposite wall
Reciprocal ST segment depression Transmural infarction at opposite wall
Reciprocal tall R wave and tall T wave Infarction with a little healthy tissue Deep Q wave with small r wave in middle of QS as letter W Infarction with more healthy tissue
QR pattern or R wave with wide S pattern. When electrode placed at junction of infarction and healthy portion
Q wave with R wave or Wide R wave only.
Signs of infarction
Early infarction (1-3 days)
Common early signs are sudden giant transient T wave elevation (rare), ST segment convex elevation with reciprocal depression.
Acute infarction
Common signs are huge ST segment convex elevation with raised T wave, and reciprocal ST depression. Development of deep Q wave.
Recent infarction (1-6 days)
Q wave, T wave inversion, low R wave, and regression of ST segment.
Infarction of some duration (1-3 weeks)
Deep Q wave, T wave inversion, low R(r) wave, ST segment sets at on isoelectric level. Atrial fibrillation, ventricular tachycardia or AV block may develop with pain or shock at any time. Q wave sometime absent in right ventricular infarction due to less muscular tissue and much of conductive tissue in right ventricle. Infarction may silent in individual with diabetic peripheral neuropathy, and in some anterior wall (non muscular part) or subendocardial infarction.
Frozen shoulder syndrome on left side may develop in posterior wall infarction. Cardiac failure following infarction manifested as rapid rate, low pulse volume, low BP and ventricular tachycardia. Shock may develop due to acidosis (co2, Hyperkalemia) commonly.
ECG CHANGES IN OTHER CARDIAC DISEASE
Pericarditis
It usually lasts for 4 weeks. The main causes are viral infections, uremia, rheumatic fever, post infarction aneurysm and tuberculosis. ECG changes are concave ST segment elevation in multiple leads, low R wave voltage, electric alternans, and tachycardia. ST segment may be depressed in aVR. (Low pulse pressure, soft 1stsound and pericardial rub are other features).
Myocarditis
It usually lasts for 4-6 weeks. The predisposing factors are toxins, infections including secondary bacterial infections or water borne (Coxsackies) viral infections, HIV, syphilis. Features are ST segment depression, T wave inversion, low R wave voltage, and prolonged QT interval.
Atrial disorders
P wave is a compound (atrial) wave normally. Atrial activation time is increased > 0.04 second in right atrial enlargement (Tall P wave), or > 0 .06 second in left atrial enlargement. If P wave duration / P-R interval is more than 1.6 (giant P wave), it indicates bilateral hypertrophy.
Retrograde conduction is seen as upright P wave in aVR or as inverted P wave in lead II. It is occurred by strong stimulus from lower ectopic foci or lower escape foci. P-R interval is short in retrograde ventricular conduction (Injury or sympathetic stimulation); WPWS, and in strong SA node cycle following aberrant conduction (due to early recovery from refractive period of ventricle -Chung phenomena). Early transient acceleration of rate by atrial escape foci can be seen also in ECG in case of sudden slow sinus rhythm (treppe phenomenon).
P-R interval is prolonged in long refractive period of ventricle, A.V block (including left vagus stimulation) and atrial septal defects.
Congenital ASD right to left shunt (Left atrial enlargement)
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 (Central cyanosis, reactive hyperemia, and flow murmur at aortic area).
ASD left to right shunt (Right atrial enlargement)
ECG signs are tall P wave in V1, LII, LIII, aVR; P wave is inverted 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 clinical signs are retrograde venous pulse, excess of bronchial secretion due to pulmonary congestion etc (Treatment in childhood = Calcium supplements for rapid septal development).
Mitral stenosis (Left atrial enlargement)
ECG signs are wide or bifid P wave in aVL, LI and LII; inverted P wave in VI; left atrial ectopic, paroxysmal atrial tachycardia, atrial flutter, fibrillation (clot formation), and prolonged P-R interval. Other clinical features are hypotension, weak pulse, low pulse pressure, loud Ist sound, diastolic murmur, red face, effort dyspnoea, productive cough (pulmonary congestion) and rarely raised ESR. Tall T wave and signs of LVH are marked in mitral incompetence. Atrial thrombi are formed following the stasis (70 ml stroke volume and more in left atrium) may lead embolic phenomena in coronary, renal, hepatic or cerebral vessels branches (Treatment = Sulphur or Salicylic acid contain herbs).
Rheumatic heart (Cardiac fibrositis)
Signs are prolonged P-R interval, wide QRS interval, raised ST segment, low R wave tachycardia, and ectopic beat.
Chronic cardiac fibrosis
Common features are low R voltage, ST segment depression and T wave inversion. Condition following atrial fibrosis with dilatation may promote ADH secretion (Fluid retention- Na retention, and venous stasis, paroxysmal atrial tachycardia and pain). Venous clot or polyp is formed following the stasis which may lead to embolic phenomena in pulmonary or remote vessels.
AetiologyMalnutrition (Deficiency of O2, vitamin B1-sulphur; globulin, calcium, water, niacin, ascorbic acid, vitamin E, lactate, and arsenic) anemia, rheumatism, hypertension, metabolic degeneration, and diabetes mellitus etc.
Low voltage (R wave)
Etiology: weak stimulation, para sympathetomimic – vagus stimulation (It can depress SA node and AV node, while sympathetomimic (as Calcium) can stimulate atrium and ventricles), hypothyroidism, hyperkalemia, thick chest wall, presence of air or fluid in between heart and electrode, emphysema, pericardial effusion; multiple equal vectors at same time or strong potential from the reciprocal wall, diffuse old infarction, and cardiac fibrosis (Homoeopathicity for low voltage fibrosis chronica = sympatholytic remedies).
High voltage (R wave)
Etiology: Strong sinus node stimulation, hypokalemia, low digitalis; excess of adrenaline, excess of calcium; absence of opposing potential, thickness of longitudinal cardiac cells, increased gap between cardiac cells, early period of ventricular hypertrophy, thin chest wall, exploring electrode close to heart; The beat following the long refractive period- beat after aberrant conduction, post ectopic beat, SA block and AV block; BBB,WPWS (lack of opposing force) etc.
Systemic hypertension
Features are tall R wave (LI, aVL), Left (north) axis deviation, VAT > 0.04 in V5, presence of ventricular ectopic, and signs of cardiac rotation mostly to anticlockwise.
Systemic hypertension with systolic strain
Tall R wave, ST segment depression, T wave inversion, U inversion (V6) and wide QRS pattern.
Hypertension with diastolic strain
(Lack of tonicity, one side potential-T wave) Tall R wave, wide QRS, and tall T wave
Hypertension with fibrosis (dryness, less water)
Low R wave, ST segment depression, T wave inversion, wide QRS interval, prolonged Q-T interval, and tachycardia.
Ventricular hypertrophy
Common causes are pulmonary artery stenosis (RVH); Aortic stenosis, systemic hypertension (LVH) and chronic ischemia.
Normal VAT is less than 0.02 second in VI (1/2 r-septum) and less than 0.05 second in V5 (q+1/2 R wave)
Stage A Tall R wave (Thick fiber).
Stage B Tall R wave, and inverted T wave (slow depolarization with posterior wall repolarization dominance); Low voltage of R wave or deep Qs wave with opposite T wave (on reciprocal lead).
Stage C Tall R wave, inverted T wave with wide QRS interval (too slow depolarization).
Stage D T wave inverted with wide QRS interval; ST segment depressed (opposite wall depolarization dominance).
Right ventricular hypertrophy
ECG shows tall R wave V1-V2, ST-T depression. R wave with raised ST segment in V1 and V2 are due to right ventricular infarction.
Hypotension
Low aortic pressure can cause stimulation on the vasomotor center at medulla. This reflexively result atrial tachycardia, sympathetic peripheral constriction (Reynaud’s), and parasympathetic splanchnic venacaval dilatation. This help to increase cardiac output. (This may result to low reserve of sympathetic group hormone effect finally - bradykinesia.)
Ectopic wave
Ectopic beats are originated due to decreased refractory period of myocardial cells. Its causes are ischemia, injury, fibrosis; toxins, infiltrations, digitalis, rauwolfia, aconitum, tobacco, belladonna, thyroid hormones, adrenaline, and calcium excess.
Paroxysmal atrial tachycardia
It may last up to 4 days. Atrial rhythm is paroxysmal, rapid and painful (Blocked PAT or blocked flutter are painless because of the normal ventricular rate). It mostly occurs due to atrial ischemia, hyperthyroid, and sympathetic vasomotor effects.
Atrial flutter originated from lower atrial multiple foci can produce up & down multiple P waves in aVR and inverted P waves in LII. Irregular pulse can be felt in atrial fibrillation, failure and weak ventricular extra systole.
Ventricular ectopic
Most of ventricular ectopic are developed by ventricular ischemia or gastric causes (Spinal T1-T4 sympathetic nerve irritations). Ectopic originated from left ventricle are seen as upright waves in right side leads and as inverted waves in left side leads. A.V block
Vertigo or syncope may develop in complete AV block, sinus arrest, very slow ventricular rhythm, vagal irritation, cerebral hypotension, acute aortic or mitral stenosis and ventricular arrest (Brain death may occur if cerebrovascular insufficiency last more than 6-8 minutes).
Escape beats be originated from either his bundles or distally from right or left bundle branches or from ventricular muscles itself in complete AV block. Impulses may travel through accessory path ways like Kent bundles, James fibers to either direction. (WPWS in AV block, or Paroxysmal atria tachycardia from retrograde impulses from ventricles in complete AV block).
Bundle branch block
Normally simultaneous conduction are occurred through right bundle branch and left anterior bundle branch. Then it passes through left posterior branch. This trifascicular system fails in bundle branch block. Affected ventricular portion takes long time to complete depolarization. So the repolarization begins first from myocardium near unaffected branch. So T wave appear opposite to terminal portion of depolarization (tall & wide) wave. So R or S wave with opposite T wave is seen in electrode at affected side.
Either right or left bundle branch block may be developed in septal infarction. Left bundle branch block is occurred in chronic ischemia, cardiac fibrosis, old age, septal infarction, and anterior infarction (Left coronary). Left anterior hemi block is marked as deep q wave, left (north) axis deviation, tall and wide R wave in LI & V5. Isolated bundle branch block pattern at v3 (wide QrS) can be considered a sign of old septal infarction (Beware about strict preventive treatment).
PROGNOSIS
It is not bad in isolated SA block, 1st degree AV Block, paroxysmal AV block, RBBB, and minimum epicardial injury in posterior wall of healthy individual.
ECG changes developed in inferior infarction are reversible.
Prognosis are bad in multiple and diffuse 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, very slow ventricular rhythm, ventricular tachycardia, atrial fibrillation following with clot or embolism, mitral stenosis and ball valve thrombus; aortic stenosis and ventricular aneurysm.
Injury changes in anterior surface are mostly irreversible. Ventricular ectopic beat of multi foci origin or ectopic more than five/minute have bad prognosis.
Sudden death may occur in left ventricular failure, complete AV block, ventricular fibrillation by infarction, left atrial fibrillation with mitral ball valve thrombus, pulmonary emboli developed from large veins or from right sided heart with pulmonary infarction, and aortic emboli from left atrium with cerebral infarction. Bilateral bundle branch block or tri fascicular block with absence of escape beat also can induce sudden death.
ECG changes in other common conditions
Psychoneurosis & anxiety
The autonomous nerve system controls internal organs, lungs and heart through endocrine system. Sympathetic signs are atrial tachycardia, short P-R interval, flat T wave and prolonged QT interval with or without hypotension. Parasympathetic signs are bradycardia and sinus arrhythmia.
Tobacco heart
ECG shows signs of premature ventricular ectopic complex, atrial tachycardia, (sympathetomimic), ST segment depression and flat T wave.
Hyperthyroid
ECG shows sympathetic signs, paroxysmal atrial tachycardia, atrial fibrillation, tall R wave, ST segment depression, or signs of failure (low R wave).
Hypothyroid
ECG shows sinus bradycardia, low R wave, prolonged P-R interval, and flat T wave.
Hyper parathyroid
ECG shows tall P wave, tall R wave, and short Q-T interval. (Hyper calcium-PTH may be formed from damaged kidney).
Addison’s disease
ECG shows signs include tall T wave (hyperkalemia), ST segment elevation, low P and R waves or absent P wave.Normally renal tubules excrete H+ and K+ with reabsorption of H2O, Ca++ and Na+. When these are disturbed -first hypokalemic alkalosis ( tachycardia, hypertension), hyperkalemic alkalosis (SA block, bradycardia, clotting), then hyperkalemic acidosis (ventricular tachycardia, bleeding, shock) are developed.
Hyperkalaemia signs can be seen best in precordial lead. Tall T wave, absent P wave, wide QRS interval are the ECG features.
Renal insufficiency & Cushing’s syndrome
ECG shows signs of hypokalemia: Prolonged Q-T interval, tall R wave, prolonged P-R interval, sinus tachycardia, ST segment depression, and flat T wave, prominent U wave (v6) may occur. ST segment is prolonged if Ca ++ is decreased in blood.
Uraemia
Tall T wave, wide QRS interval, SA block 2:1 or sino-atrial arrest, raised ST segment, low R wave, and acidosis.
Micro albuminuria (Insulinuria-Anion protein loss)
It develops with excess of renal K+ excretion. ECG changes are similar to signs of hypokalemia: prolonged Q-T interval, tall R wave, and ST –T depression.
Hyper insulinism
It is characterized by hypoglycemia, signs of hypokalemia, high hydrogen excretion (alkalosis, thrombosis) and increased oxygen reserve.
Hepatic insufficiency
ECG signs are ST segment prolongation more than 0.12 second and sinus bradycardia.
Beriberi (Sulphur)
ECG signs are bradycardia if failure is not developed, low voltage of R wave, electric alternans, ST segment depression and flat T wave. First heart sound becomes soft (pericarditis).
Asthma, Emphysema,& COPD
ECG signs are tall R wave in right sided leads, right axis deviation, deep and wide S wave in L1&V5, clockwise rotation, and tall R wave in aVR. V.A.T may increase more than 0.02 second in V1.
Cardiac medicines
Cardiac stimulant medicinesSinapis, Spartium, Capsicum, Camphor, Coffee, Sulphur, Ginkgo, Granatum, Aspidosperma, Kola, Zingiber, Lobelia, Myrrha, Nux vomica, Allium sativa, Arsenic album, Adonis, Cactus.
Stimulants remediesSympathomimetic, low dose of sympatholytic, low dose of digitalis, calcium, high dose of belladonna (AV node), low dose of potassium, Cinchona, Aconitum, Colchicum, Pilocarpus, Crataegus, Digitalis, Helleborus, Gelsemium, Nux vomica.
DepressantsHigh dose of sympatholytic, Crataegus, Digitalis, Cinchona, Magnesium, Potassium, Ipecac.
Central vasodilatorsSympathomimetic, Nitrates, Ammi visnaga.
Peripheral vasodilatorsSympatholytic
DiureticsStrophanthus, Adonis,Tabacum, Boerhavia diffusa
Laxatives Ricinus communis, Cascara Sagrada.
Hemostatic-anticoagulantsSalix nigra, Melilotus, Sulphuric acid.
CoagulantsAlfalfa, Calcium.
Micro vascular circulatory promotersArsenic alb, Ginkgo biloba, Taraxacum.
NutrientsLecithin (Trigonella), Lactate, Globulin, B1, Vitamin E, Vitamin C, Electrolytes.
Heart diseases. The major risk factors
Congenital heart diseases.
Hypertension.
Hyperlipidemia.
Sucrose consumption.
Obesity.
Smoking.
Physical inactivity.
Dehydration & malnutrition.
Excess of homocysteine.
Predisposing factors
Advancing age.
Family history of premature myocardial infarction.
Habit of heavy alcohol consumption.
Type A personality.
Abundance.
Persistent sympathetic overactivity.
Life style with over ambition.
Greed.
Unnecessary emotion (Hurry, anger, fear, stress, depression, lack of smile).
Negative mood.
Selfishness.
Negative partner
Lack of rest
Sleep insufficiency.
Persistent use of sympathomimetic.
Hyperthyroidism.
Excess of salt, sucrose and coffee, heavy metals (Lead), high Mg (Hard water, or well water near sea).
Nasal block
Chronic obstructive pulmonary diseases (Hypoxia).
Renal insufficiency.
Hyperuricemia .
Hepatic insufficiency.
Hypertriglyceridemia.
Male sex, excess of testosterone.
Menopause.
Oral contraceptive pills.
Metabolic disorder.
Hypothyroidism.
Recurrent autoimmune myocarditis.
Syphilis diathesis.
Asians (Small size of blood vessels, thin and irritable pericardium).
Hereditary aortic aneurysm.
Congenital heart diseases.
Hereditary short refractory period of myocardium (< 0.22 second).
Calcification, Hypercalcaemia- mineral (Consumption prawn, sea fishes, shellfish, high PTH, osteoporosis, tropical climate).
Cardiac overwork with rapid rate (Sympathetic over activity).
O2 lack.
Co2 excess.
Lack of sufficient water intake (cirrhosis).
Food or air contaminated with heavy metal like Lead.
Lead toxicity.
Vascular infiltration of old blood cells (WBC & platelets, Iron particles).
Multiple Coxsackies viral infections.
ELECTROCARDIOGRAM
Even though many novel and sophisticate instruments have been discovered in last 100 years, physical examinations and ECG are remaining the best diagnostic procedures for general practitioners.
Electrocardiogram is a graphic representation of the electrical potential produced in associated with the heartbeat. It is only a lab test.
Scope of ECG
Estimate fitness of V.V.I.P, Doctors, drivers, sailors, pilots, sportsmen.
Evaluate the properties of cardiac muscles.
Detect atrial and ventricular hypertrophy.
Detect focal Ischemia, Injury and Infarction.
Detect pulmonary dysfunctions.
Find out old infarctions.
Determine cardiac rate, arrhythmia, atrial fibrillation, paroxysmal atrial tachycardia, and paroxysmal ventricular tachycardia.
Determine SA block, sinus arrest, A.V block, bundle branch block, and cardiac arrest.
Detect cardiac position, electric axis and rotation.
Evaluate hormonal & electrolyte imbalance.
Find out the progress in treatment.
Evaluate effects of drug and toxins.
History
Galvani luigi (Italy) first described about animal electricity in 1776 (published-1791).
Marey invented electrometer in 1876.
Augustus. D. Waller traced human electricity experimentally first in St: Marey hospital London in 1887.
Willem Einthoven had attended Waller’s demonstration in 1889. Einthoven invented ECG machine in 1901 and put forward a hypothesis that potential in lead II is equal to sum of potentials of lead I and lead III based on the dipole theory. He was awarded Nobel Prize in 1924.
Frank Wilson introduced unipolar lead in 1934.
Emanuel Goldberger introduced augmented unipolar limb lead in 1942.
Properties of cardiac muscles
Automaticity
Rhythmicity
Conductivity
Excitability
Refractoriness
One or none law
Aberrant conduction
Contractility (can be detected partly by ECG)
Tonicity (cannot be detected by ECG)
Evaluation of ECG (Methodical approach) Summary
RATE
Atrial rate
300 divided by number of large blocks in between two P waves.
1500 divided by number of small blocks in between two P waves.
Sinus bradycardia: Rate < 60/minute.
Sinus tachycardia: Rate > 100/minute.
Ventricular rate
300 divided by number of large blocks in between two R waves.
1500 divided by number of small blocks in between two R waves or two S waves.
RHYTHM
Regular
Regular rhythm:
S.A node rhythm (Normal rhythm).
S A block 2:1.
Paroxysmal atrial tachycardia with A.V block 2:1.
Sinus node rhythm
P waves and R waves are regular, normal configuration of P, Q, R, S, T, u waves, with normal P-R interval.
Irregular rhythm
Slow rate with irregular rhythm
Sinus arrest.
SA block 3:1 or 3:2.
AV Block 3:1.
Bradycardia with escape beat or ectopic beat.
Rapid rate with irregular rhythm
Paroxysmal atrial tachycardia.
Paroxysmal ventricular tachycardia.
Atrial flutter.
Atrial fibrillation.
Ventricular fibrillation.
P wave
Height Normally < 2.5 mm (2.5 blocks).
Duration Normally < 0.10 second (2.5 blocks).
Absent P wave
SA block, Junctional beat, atrial fibrillations.
Small P wave
Atrial rhythm, atrial ectopic.
Tall P wave
Right atrial hypertrophy.
Wide or bifid P wave
Left atrial hypertrophy, interatrial block.
Inverted P wave
Normally in aVR lead, hypertrophy of atrium at opposite side of tracing leads, retrograde conduction(LII).
q wave
Normally the depth of q wave <1/4 of succeeding R wave.
Duration normally < 0.04 second (< 1 block).
Deep Q wave
Potential (primary) dominance of opposite wall (Ventricular hypertrophy).
Deep & wide Q wave
Potential (primary) dominance of opposite wall to the exploring electrode (Infarction).
P-R interval
Duration
Normally in between 0.12 second (3 blocks) and 0.22 second (5.5 blocks).
Prolonged P-R interval
1 st degree AV block; Atrial septal defect, Mitral stenosis.
Short P-R interval
WPWS, Accessory atrio-ventricular conduction, Junctional beat, Low atrial origin beat.
R wave
Voltage
Normal R voltage in lead LI, LII and LIII:
Height > 5 mm and < 16 mm.
R wave height is progressive from V1 to V5.
Voltage high
Height in aVL or LI: > 13 mm.
Height in aVF: > 20 mm
Height in V1: > 5 mm
Height in V5: > 25 mm
Sum in LI R + LIII S: > 21 mm
Sum in V1 S + V5 R: > 36 mm
Sum in V2 S + V6 R: > 40mm.
S wave
Depth of S wave takes regression from V1 to V5.
Deep S wave
Reflection of Increased vector at opposite wall.
Wide S wave
Slowness of vector due to thickness at opposite wall by hypertrophy, or one way travel of potential away from block; Infarction at wall of same side (QS).
QRS interval
Duration
Normal duration between 0.04 second (1 block) and 0.08 second (2 blocks).
Short QRS interval
Hypercalcaemia
Prolonged QRS interval
Bundle branch block, hyperkalemia, inter ventricular block, aberrant ventricular conduction
Activation time of right ventricle
At V1 = Normally < 0.02 second (1/2 block).
Activation time of left ventricle
V5 = < 0.04 second (1 block)
Increase in VAT (Ventricular activation time)
Thick fibre, hypertrophy, slow inter ventricular conduction.
ST Segment position
Segment normally lies at Iso electrical level.
ST segment elevation
Injury at epicardium, hyperkalemia, slowness of depolarization at epicardium of same side, aneurysm.
ST depression
Recent injury at sub endocardium of same side, Recent infarction at opposite wall, Chronic transmural ischemia of same side.
ST segment prolongation
Hypocalcaemia and hypoalbuminemia due to liver weakness.
T wave configuration
Normally upright and asymmetrical. Height of T wave is more than 1/10 of preceding R wave.
Tall T wave
Hyperkalemia (in chest leads -Focal injury or renal disease).
Flat T wave
Ischemia, low height of R wave (Weakness, hypothyroid).
Symmetrically T wave inversion
Sub endocardial infarction, unstable angina, ventricular hypertrophy with strain, Aberrant conduction, right bundle branch block.
U wave
Normal configuration of U wave is as the same direction of T wave.
Prominent U wave
Late or prolonged repolarisation at infro-posterior wall by strong stimuli -Hypokalemia, LVH (V6).
U wave inversion
Ischemia at posterior wall (at V6), Posterior LVH (at V3).
Q-T interval
Duration
Between 0. 28 second (7 blocks) and 0.42 second (10 blocks).
Q-Tc (corrected) interval
Estimated Q-T interval / square root of R-R interval.
Short QT interval
Stimulators, hypercalcaemia, digitalis, sympathomimetic, and short fiber.
Prolonged QT interval
Depressants, sympatholytic, cinchona toxicity, hypocalcaemia, hyperkalemia, hypomagnesemia, Ischemia, and cardiomyopathy.
Cardiac position
Normal position is intermediate-Apex vector facing to left hip. R waves are upright both in aVL and aVF.
Horizontal position
R waves are upright in aVL, and S waves in aVF.
Vertical position
S waves are in aVL, and R waves in aVF.
Cardiac rotation
Apex of heart is facing forward and downwards normally when looking from below. Equal size of R and S waves are seen at V3. It is rotated in hypertrophy.
Clockwise
Size of R wave & S wave are seen as equal at V5 (RVH).
Anti-clockwise
size of R wave & S wave are seen as equal at V1(RVH or LVH anterior wall).
Cardiac mean electric axis
Cardiac muscles depolarize totally in 7 directions with different electrical potential in each cycle. So different vectors, and resultant waves are developed in surface ECG. Mean electro motive force -vector axis normally lies in between -15 degree and + 90 degree:
Normal axis
ECG in standard leads shows upright R waves in LI, (LII), and LIII.
Left axis deviation
Tall R waves at LI, and deep qRS (S) waves in LIII.
Left axis deviation
LAHB, LVH, AMI (Left ventricular potential is weaker at anterior wall & Stronger at posterior wall).
Right axis deviation
Deep S waves in LI, and Tall qRS (R) waves in LIII.
Right axis deviation
LPHB, RVH, PMI (Left ventricular potential is stronger at anterior wall & weaker at posterior wall).
Normal ECG waves
ECG vectors can be divided into Atrial, Septal and Ventricular units.
Atrial units
P (P, p1, PR segment-pT wave) wave.
Septal units
q, Q, r (qT, rT) wave.
Ventricular units
R, S, (r, R1, S1) waves.
Intervals
P-P interval
R-R interval
P-R interval
QRS interval
Q-T interval.
Segments
PR segment
ST segment.
ECG paper
Machine is usually set at speed of 1500 mm/minute (25 mm/second).
One small square box represents 1mm in height vertically for voltage, and 1mm length horizontally represents for duration (1 mm is equal to 0.04 second).
Large box represents 5 mm in height vertically, and 5 mm in duration horizontally (Duration: 5 mm is equal to 0.2 second).
The machine is usually standardized with potential of 1milli volt can produce height 10 mm.
Lead
Lead axis is the imaginary line between two opposite poles.
Bipolar lead or standard lead records potential difference of two poles simultaneously.
Unipolar lead records electric potential through one exploring electrode (Other electrode-indifferent electrode is arranged in zero potential by connecting wires from three limbs).
Standard leads
LI, LII, LIII.
Unipolar augmented limb leads
aVR, aVL, aVF.
Unipolar chest leads
V1, V2, V3, V4, V5, V6, V7.
Conventional ECG tracing include totally waves of 12 leads- 3 standard leads, 3 unipolar limb leads, and 6 chest leads. Each leads should be analyzed separately. Electrographically heart can be divided to three portions- the anterior surface, posterior surface, and cavity.
Heart contains three types of tissues- Muscular tissue, Conductive tissue (1%) and Connective tissue.
Normally the vector in some leads may vary in accordance with alternations in cardiac position.
The R waves in LIII represents to the right ventricle in intermediate and horizontal position.
The R waves in LIII represents to the left ventricle in extreme vertical position.
Electric field
Electrical potential in cells are produced due to rapid entry of sodium ion and slowly going out K+. It is the depolarization. Ca++ go in during early part of repolarization. K+ go out quickly during repolarization. Then some sodium go out and K+ enter inside. Some sodium ions enter to cell with exchange of calcium ions.
K ion is about 150 Meq/L inside the cell and 5 Meq/L outside the cell. Na+ is 5 Meq/L inside the cell and 142 Meq/L outside the cell. Membrane potential of cell is about less than -90mv during resting normally. Cell membrane act as resistance {5000 ohm}. Cell cannot be excited if resistance (membrane- cholesterol, or excess of cat-ion inside the cell) is increased more than about -60mv. Cell be stimulated easily when membrane potentials are less than -110 mv (Hypokalemia).
The electro motive force (Action potential) generated in pacemaker cell in sino arial node are conveyed through conductive system fibres end cause excitation of atrial and ventricular contractile muscle tissues (different 7 directions) and finally end in skin surface. Normally. 80% of electric potentials are lost during the transit to body surface.
Negative electric charges at direction of right shoulder and positive charges at direction of left hip are developed automatically following each SA node excitation. (Dipole Theory-Maximum potentials are near zero line. Electrical charges interact according to Coulomb's law: -the force of interaction is directly proportional to magnitude of charges and indirectly proportional to square of distance between them)
Basic principle
Positive waves are registered when current of electricity flows towards the positive electrode. Negative waves are registered in positive electrode when current flows away from positive electrode.
Depolarization time become short on strong stimulation, tissue with longitudinal cells, tissue with increased cell gap, tissue with less number of cells, and in thin cardiac wall.
When depolarization is occurred through multiple fibres to same direction and simultaneously, net vector is marked increasingly (Fusion wave-tall wave or deep wave).
Positive electrode is placed at middle of fibre, and if depolarization starts from one end, biphasic waves will be appeared.
When depolarization begins from one point and travels towards two opposite direction simultaneously through multiple and different myocardial fibres, fibres with large mass will make tall upward wave with or without small downward wave. If the current of electricity flow towards 90 degree to electrode, waves can’t be appeared.
Ischemia (Repolarization changes)
Normally repolarization changes start from the opposite end towards the stimulated end within 1/100 second after depolarization (single fiber). If iit true T wave will be appeared as negative (in single fibre potential). If depolarization takes long time to complete the process than usual (in chronic ischemia, degeneration, thick fibre, and in slow ventricular conduction), the repolarization will begin from the stimulated end itself and current will flow towards the opposite negative terminal or away from the exploring electrode. So T wave is seen as inverted in leads near positive electrode.
Ischemia epicardial portion only | Low height of T wave |
Transmural ischemia | Symmetrical inverted T wave |
Sub endocardial ischemia | T wave changes are absent |
Transmural ischemia at opposite wall | Tall T wave due to lack of opposing repolarisation potential. |
Chronic transmural ischemia
Major signs are persistent T wave inversion (Repolerisation changes-primary), wide QRS interval (Slow depolarization), wide QT interval (slowness of total duration of electrical systole), and inverted u wave at V6 (posterior wall ischemia-Coronary thrombosis). Changes due to ischemic or injury at posterior wall are reversible because of high collateral circulation. Quantity of blood supply and quantity of muscular fibers are less at subendocardial region. Injury or ischemia are usually developed from outer side to inwards. Subendocardial lesion are painless than epicardial lesion, but it has more prognostic value. Myocardial ischemia, hypokalemia, coronary thrombosis, chronic myocarditis, digitalis toxicity, cardiac depressants (sympatholytics-Cinchona) all may exhibit similar ECG patterns.
Prinzemetal angina
It is due to coronary spasm. Pain may persist even at rest, and it is relieved by vasodilators (Nitrates). ECG expresses as high ST segment elevation (Anoxic -very slow depolarization-excess of Na+ and Ca++ entry). Reciprocal ST Segment depression & T wave changes are absent. Fever, high SGOT, high ESR, leucocytosis, Troponin H, LDH, are absent.
Acute coronary insufficiency (Unstable angina)
The term unstable angina is used to denote the recurrent pain lasting more than 5 -15 minutes with ECG changes like subendocardial infarction (painless).
ECG shows deep ST segment depression, symmetrical T wave inversion, absence of Q wave, poor R wave progression, and U wave inversion (v6). The reciprocal ST segment elevation in aVR is absent.
Ischemia, injury and infarction primarily develop at deeper part of left ventricle than right ventricle due to less thebesian blood supply.
Ischemia, Injury and Infarction
Normal ↓ | Normal ↑ Ischemia → ↑ | Chronic Ischemia → ↑ ↓ | Ectopic → | Failure |
30% ischemia & 70% others → Degeneration | ↑ Compensatory Hypertrophy & Hypertension → ↓ | ↑ Injury → ↑ ↓ | Aneurysm ↑ Infarction → ↓ | |
Ectopic. Bundle branch block . Fibrosis. → | Scar → | |||
Exercise ECG test
Take exercises (hoping 20 times) for 1.5minutes or 3 minutes .It can increase heart rate more than 140/minute (220-age). Take ECG immediately, and after 6 minutes. ECG also can be traced with placing pacemaker which inducing cardiac rate 220-age/minute.
Positive indication
ST depression > 0.5mm.
Other indication
Elevation of ST segment.
Increase in voltage of R wave or T wave.
Increases in ratio of R height / increases in depth of ST segment >1.
Emerging of PVEB.
Emerging of pain.
Emerging of syncope.
Myocardial injury
It may be occurred at epicardial, transmural or subendocardial portion.
Main causes of injury are severe ischemia, infections, toxins, metabolic or neoplasm infiltration (WBC, calcium, uric acid), and fatty degeneration of muscles.
Epicardial injury
Depolarization begins from stimulated (inner side) end but it completes slowly in stage by stage. The epicardial end is also becomes more negative at same time due to injury, but it is comparatively more positive even to already depolarized (negative) inner portion. So subsequent depolarization (flow of current) is developed slowly (Some K ions have exchanged early through the injured wall. So epicardial end became –ve; more Na ions are entered into the cells). So second limb of R is seen as raised, and thus it seems asif the ST segment is elevated. The ST segment elevation is appeared as concave elevation in least peripheral injury, but in transmural injury it is seen as convex ST elevation. The height of depolarization potential is increased at electrode of opposite wall in in transmural injury.
Subendocardial injury
When the injury occurs at subendocardial portion (opposite to exploring electrode and at the same portion of stimulation), the depolarization begins as usual to electrode direction. Depolarized outer portion is now become comparatively more negative than injured (not depolarized) subendocardial end. Depolarization of opposite wall makes negative potential before subendocardial depolarization is completed. Then current goes slowly far away from electrode after initial positive and or negative wave. So the second limb of S wave is seen wide and is appeared as ST segment depressed. Upward potential is marked in cavity lead-aVR or aVL).
INFARCTION
Myocardial infarction can be categorized into as follows
Atrial | Anterior surface | Early | Epicardial |
Septal | Posterior surface | Acute | Transmural |
Ventricular | Postero-Inferior | infarction of some duration | Subendocardial |
Focal | Anterio- lateral | Sub-acute | Reciprocal |
Diffuse | Anterio-septal | Old | Multiple |
Changes that are occurred in infarction are similar as train accident. Few fibers are dead, some are injured, some more are ischemic and others are normal. So ECG configuration usually shows combined pattern of ischemia, injury and infarction for first few weeks.
Lead & Heart surface
Anterior surface | LI, V1, V2, V3, and V4. |
Lateral surface | aVL, V5, and V6. |
Posterior-inferior surface | LII, LIII, and Avf. |
Cardiac cavity | aVR or aVL. |
Reciprocal lead of posterior surface | LI, V1 and V2. |
Depolarization vector of opposite healthy wall is developed first in infarction. Thus negative depolarization wave is manifested in exploring electrode near the injured part, and tall R wave is formed in exploring electrode near healthy wall.
ECG changes
Epicardial infarction | ST convex elevation. Q wave with small R wave. (Tall T wave may occur in early stage due local hyperkalemia) |
Transmural infarction Infarction of some duration | Deep Q wave, absence of R wave, deep T wave. |
Subendocardial infarction | Q wave may absent, deep ST depression. wide S wave may develop; ST segment elevation may manifest in cavity lead either aVR or Avl |
Epicardial infarction at opposite wall | Reciprocal ST segment depression |
Transmural infarction at opposite wall | Reciprocal tall R wave and tall T wave |
Infarction with a little healthy tissue | Deep Q wave with small r wave in middle of QS as letter W |
Infarction with more healthy tissue | QR pattern or R wave with wide S pattern. |
When electrode placed at junction of infarction and healthy portion | Q wave with R wave or Wide R wave only. |
Signs of infarction
Early infarction (1-3 days)
Common early signs are sudden giant transient T wave elevation (rare), ST segment convex elevation with reciprocal depression.
Acute infarction
Common signs are huge ST segment convex elevation with raised T wave, and reciprocal ST depression. Development of deep Q wave.
Recent infarction (1-6 days)
Q wave, T wave inversion, low R wave, and regression of ST segment.
Infarction of some duration (1-3 weeks)
Deep Q wave, T wave inversion, low R(r) wave, ST segment sets at on isoelectric level. Atrial fibrillation, ventricular tachycardia or AV block may develop with pain or shock at any time. Q wave sometime absent in right ventricular infarction due to less muscular tissue and much of conductive tissue in right ventricle.
Infarction may silent in individual with diabetic peripheral neuropathy, and in some anterior wall (non muscular part) or subendocardial infarction.
Frozen shoulder syndrome on left side may develop in posterior wall infarction.
Cardiac failure following infarction manifested as rapid rate, low pulse volume, low BP and ventricular tachycardia. Shock may develop due to acidosis (co2, Hyperkalemia) commonly.
ECG CHANGES IN OTHER CARDIAC DISEASE
Pericarditis
It usually lasts for 4 weeks. The main causes are viral infections, uremia, rheumatic fever, post infarction aneurysm and tuberculosis. ECG changes are concave ST segment elevation in multiple leads, low R wave voltage, electric alternans, and tachycardia. ST segment may be depressed in aVR. (Low pulse pressure, soft 1stsound and pericardial rub are other features).
Myocarditis
It usually lasts for 4-6 weeks. The predisposing factors are toxins, infections including secondary bacterial infections or water borne (Coxsackies) viral infections, HIV, syphilis. Features are ST segment depression, T wave inversion, low R wave voltage, and prolonged QT interval.
Atrial disorders
P wave is a compound (atrial) wave normally. Atrial activation time is increased > 0.04 second in right atrial enlargement (Tall P wave), or > 0 .06 second in left atrial enlargement. If P wave duration / P-R interval is more than 1.6 (giant P wave), it indicates bilateral hypertrophy.
Retrograde conduction is seen as upright P wave in aVR or as inverted P wave in lead II. It is occurred by strong stimulus from lower ectopic foci or lower escape foci. P-R interval is short in retrograde ventricular conduction (Injury or sympathetic stimulation); WPWS, and in strong SA node cycle following aberrant conduction (due to early recovery from refractive period of ventricle -Chung phenomena). Early transient acceleration of rate by atrial escape foci can be seen also in ECG in case of sudden slow sinus rhythm (treppe phenomenon).
P-R interval is prolonged in long refractive period of ventricle, A.V block (including left vagus stimulation) and atrial septal defects.
Congenital ASD right to left shunt (Left atrial enlargement)
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 (Central cyanosis, reactive hyperemia, and flow murmur at aortic area).
ASD left to right shunt (Right atrial enlargement)
ECG signs are tall P wave in V1, LII, LIII, aVR; P wave is inverted 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 clinical signs are retrograde venous pulse, excess of bronchial secretion due to pulmonary congestion etc (Treatment in childhood = Calcium supplements for rapid septal development).
Mitral stenosis (Left atrial enlargement)
ECG signs are wide or bifid P wave in aVL, LI and LII; inverted P wave in VI; left atrial ectopic, paroxysmal atrial tachycardia, atrial flutter, fibrillation (clot formation), and prolonged P-R interval.
Other clinical features are hypotension, weak pulse, low pulse pressure, loud Ist sound, diastolic murmur, red face, effort dyspnoea, productive cough (pulmonary congestion) and rarely raised ESR.
Tall T wave and signs of LVH are marked in mitral incompetence. Atrial thrombi are formed following the stasis (70 ml stroke volume and more in left atrium) may lead embolic phenomena in coronary, renal, hepatic or cerebral vessels branches (Treatment = Sulphur or Salicylic acid contain herbs).
Rheumatic heart (Cardiac fibrositis)
Signs are prolonged P-R interval, wide QRS interval, raised ST segment, low R wave tachycardia, and ectopic beat.
Chronic cardiac fibrosis
Common features are low R voltage, ST segment depression and T wave inversion. Condition following atrial fibrosis with dilatation may promote ADH secretion (Fluid retention- Na retention, and venous stasis, paroxysmal atrial tachycardia and pain). Venous clot or polyp is formed following the stasis which may lead to embolic phenomena in pulmonary or remote vessels.
Aetiology
Malnutrition (Deficiency of O2, vitamin B1-sulphur; globulin, calcium, water, niacin, ascorbic acid, vitamin E, lactate, and arsenic) anemia, rheumatism, hypertension, metabolic degeneration, and diabetes mellitus etc.
Low voltage (R wave)
Etiology: weak stimulation, para sympathetomimic – vagus stimulation (It can depress SA node and AV node, while sympathetomimic (as Calcium) can stimulate atrium and ventricles), hypothyroidism, hyperkalemia, thick chest wall, presence of air or fluid in between heart and electrode, emphysema, pericardial effusion; multiple equal vectors at same time or strong potential from the reciprocal wall, diffuse old infarction, and cardiac fibrosis (Homoeopathicity for low voltage fibrosis chronica = sympatholytic remedies).
High voltage (R wave)
Etiology: Strong sinus node stimulation, hypokalemia, low digitalis; excess of adrenaline, excess of calcium; absence of opposing potential, thickness of longitudinal cardiac cells, increased gap between cardiac cells, early period of ventricular hypertrophy, thin chest wall, exploring electrode close to heart; The beat following the long refractive period- beat after aberrant conduction, post ectopic beat, SA block and AV block; BBB,WPWS (lack of opposing force) etc.
Systemic hypertension
Features are tall R wave (LI, aVL), Left (north) axis deviation, VAT > 0.04 in V5, presence of ventricular ectopic, and signs of cardiac rotation mostly to anticlockwise.
Systemic hypertension with systolic strain
Tall R wave, ST segment depression, T wave inversion, U inversion (V6) and wide QRS pattern.
Hypertension with diastolic strain
(Lack of tonicity, one side potential-T wave) Tall R wave, wide QRS, and tall T wave
Hypertension with fibrosis (dryness, less water)
Low R wave, ST segment depression, T wave inversion, wide QRS interval, prolonged Q-T interval, and tachycardia.
Ventricular hypertrophy
Common causes are pulmonary artery stenosis (RVH); Aortic stenosis, systemic hypertension (LVH) and chronic ischemia.
Normal VAT is less than 0.02 second in VI (1/2 r-septum) and less than 0.05 second in V5 (q+1/2 R wave)
Stage A | Tall R wave (Thick fiber). |
Stage B | Tall R wave, and inverted T wave (slow depolarization with posterior wall repolarization dominance); Low voltage of R wave or deep Qs wave with opposite T wave (on reciprocal lead). |
Stage C | Tall R wave, inverted T wave with wide QRS interval (too slow depolarization). |
Stage D | T wave inverted with wide QRS interval; ST segment depressed (opposite wall depolarization dominance). |
Right ventricular hypertrophy
ECG shows tall R wave V1-V2, ST-T depression.
R wave with raised ST segment in V1 and V2 are due to right ventricular infarction.
Hypotension
Low aortic pressure can cause stimulation on the vasomotor center at medulla. This reflexively result atrial tachycardia, sympathetic peripheral constriction (Reynaud’s), and parasympathetic splanchnic venacaval dilatation. This help to increase cardiac output. (This may result to low reserve of sympathetic group hormone effect finally - bradykinesia.)
Ectopic wave
Ectopic beats are originated due to decreased refractory period of myocardial cells. Its causes are ischemia, injury, fibrosis; toxins, infiltrations, digitalis, rauwolfia, aconitum, tobacco, belladonna, thyroid hormones, adrenaline, and calcium excess.
Paroxysmal atrial tachycardia
It may last up to 4 days. Atrial rhythm is paroxysmal, rapid and painful (Blocked PAT or blocked flutter are painless because of the normal ventricular rate). It mostly occurs due to atrial ischemia, hyperthyroid, and sympathetic vasomotor effects.
Atrial flutter originated from lower atrial multiple foci can produce up & down multiple P waves in aVR and inverted P waves in LII. Irregular pulse can be felt in atrial fibrillation, failure and weak ventricular extra systole.
Ventricular ectopic
Most of ventricular ectopic are developed by ventricular ischemia or gastric causes (Spinal T1-T4 sympathetic nerve irritations). Ectopic originated from left ventricle are seen as upright waves in right side leads and as inverted waves in left side leads.
A.V block
Vertigo or syncope may develop in complete AV block, sinus arrest, very slow ventricular rhythm, vagal irritation, cerebral hypotension, acute aortic or mitral stenosis and ventricular arrest (Brain death may occur if cerebrovascular insufficiency last more than 6-8 minutes).
Escape beats be originated from either his bundles or distally from right or left bundle branches or from ventricular muscles itself in complete AV block. Impulses may travel through accessory path ways like Kent bundles, James fibers to either direction. (WPWS in AV block, or Paroxysmal atria tachycardia from retrograde impulses from ventricles in complete AV block).
Bundle branch block
Normally simultaneous conduction are occurred through right bundle branch and left anterior bundle branch. Then it passes through left posterior branch. This trifascicular system fails in bundle branch block. Affected ventricular portion takes long time to complete depolarization. So the repolarization begins first from myocardium near unaffected branch. So T wave appear opposite to terminal portion of depolarization (tall & wide) wave. So R or S wave with opposite T wave is seen in electrode at affected side.
Either right or left bundle branch block may be developed in septal infarction. Left bundle branch block is occurred in chronic ischemia, cardiac fibrosis, old age, septal infarction, and anterior infarction (Left coronary). Left anterior hemi block is marked as deep q wave, left (north) axis deviation, tall and wide R wave in LI & V5. Isolated bundle branch block pattern at v3 (wide QrS) can be considered a sign of old septal infarction (Beware about strict preventive treatment).
PROGNOSIS
It is not bad in isolated SA block, 1st degree AV Block, paroxysmal AV block, RBBB, and minimum epicardial injury in posterior wall of healthy individual.
ECG changes developed in inferior infarction are reversible.
Prognosis are bad in multiple and diffuse 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, very slow ventricular rhythm, ventricular tachycardia, atrial fibrillation following with clot or embolism, mitral stenosis and ball valve thrombus; aortic stenosis and ventricular aneurysm.
Injury changes in anterior surface are mostly irreversible. Ventricular ectopic beat of multi foci origin or ectopic more than five/minute have bad prognosis.
Sudden death may occur in left ventricular failure, complete AV block, ventricular fibrillation by infarction, left atrial fibrillation with mitral ball valve thrombus, pulmonary emboli developed from large veins or from right sided heart with pulmonary infarction, and aortic emboli from left atrium with cerebral infarction. Bilateral bundle branch block or tri fascicular block with absence of escape beat also can induce sudden death.
ECG changes in other common conditions
Psychoneurosis & anxiety
The autonomous nerve system controls internal organs, lungs and heart through endocrine system. Sympathetic signs are atrial tachycardia, short P-R interval, flat T wave and prolonged QT interval with or without hypotension. Parasympathetic signs are bradycardia and sinus arrhythmia.
Tobacco heart
ECG shows signs of premature ventricular ectopic complex, atrial tachycardia, (sympathetomimic), ST segment depression and flat T wave.
Hyperthyroid
ECG shows sympathetic signs, paroxysmal atrial tachycardia, atrial fibrillation, tall R wave, ST segment depression, or signs of failure (low R wave).
Hypothyroid
ECG shows sinus bradycardia, low R wave, prolonged P-R interval, and flat T wave.
Hyper parathyroid
ECG shows tall P wave, tall R wave, and short Q-T interval. (Hyper calcium-PTH may be formed from damaged kidney).
Addison’s disease
ECG shows signs include tall T wave (hyperkalemia), ST segment elevation, low P and R waves or absent P wave.
Normally renal tubules excrete H+ and K+ with reabsorption of H2O, Ca++ and Na+. When these are disturbed -first hypokalemic alkalosis ( tachycardia, hypertension), hyperkalemic alkalosis (SA block, bradycardia, clotting), then hyperkalemic acidosis (ventricular tachycardia, bleeding, shock) are developed.
Hyperkalaemia signs can be seen best in precordial lead. Tall T wave, absent P wave, wide QRS interval are the ECG features.
Renal insufficiency & Cushing’s syndrome
ECG shows signs of hypokalemia: Prolonged Q-T interval, tall R wave, prolonged P-R interval, sinus tachycardia, ST segment depression, and flat T wave, prominent U wave (v6) may occur. ST segment is prolonged if Ca ++ is decreased in blood.
Uraemia
Tall T wave, wide QRS interval, SA block 2:1 or sino-atrial arrest, raised ST segment, low R wave, and acidosis.
Micro albuminuria (Insulinuria-Anion protein loss)
It develops with excess of renal K+ excretion. ECG changes are similar to signs of hypokalemia: prolonged Q-T interval, tall R wave, and ST –T depression.
Hyper insulinism
It is characterized by hypoglycemia, signs of hypokalemia, high hydrogen excretion (alkalosis, thrombosis) and increased oxygen reserve.
Hepatic insufficiency
ECG signs are ST segment prolongation more than 0.12 second and sinus bradycardia.
Beriberi (Sulphur)
ECG signs are bradycardia if failure is not developed, low voltage of R wave, electric alternans, ST segment depression and flat T wave. First heart sound becomes soft (pericarditis).
Asthma, Emphysema,& COPD
ECG signs are tall R wave in right sided leads, right axis deviation, deep and wide S wave in L1&V5, clockwise rotation, and tall R wave in aVR. V.A.T may increase more than 0.02 second in V1.
Cardiac medicines
Cardiac stimulant medicines
Sinapis, Spartium, Capsicum, Camphor, Coffee, Sulphur, Ginkgo, Granatum, Aspidosperma, Kola, Zingiber, Lobelia, Myrrha, Nux vomica, Allium sativa, Arsenic album, Adonis, Cactus.
Stimulants remedies
Sympathomimetic, low dose of sympatholytic, low dose of digitalis, calcium, high dose of belladonna (AV node), low dose of potassium, Cinchona, Aconitum, Colchicum, Pilocarpus, Crataegus, Digitalis, Helleborus, Gelsemium, Nux vomica.Depressants
High dose of sympatholytic, Crataegus, Digitalis, Cinchona, Magnesium, Potassium, Ipecac.
Central vasodilators
Sympathomimetic, Nitrates, Ammi visnaga.
Peripheral vasodilators
Sympatholytic
Diuretics
Strophanthus, Adonis,Tabacum, Boerhavia diffusa
Laxatives
Ricinus communis, Cascara Sagrada.
Hemostatic-anticoagulants
Salix nigra, Melilotus, Sulphuric acid.
Coagulants
Alfalfa, Calcium.
Micro vascular circulatory promoters
Arsenic alb, Ginkgo biloba, Taraxacum.
Nutrients
Lecithin (Trigonella), Lactate, Globulin, B1, Vitamin E, Vitamin C, Electrolytes.
HOMEOPATHIC MEDICINAL TREATMENT
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Prophylactic treatment
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Avoid all predisposing factors.
Avoid all risk factors.
Saturated fat, Trans fat, Coffee, Sugar, Acidosis, Hypoxia, Sodium
excess, Adrenaline exhaustion, Malnutrition.
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Strong individual
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Cure (word means clean. Elimination of toxins (miasm)
Re establishment of homoeostasis (mental and physical) |
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Weak individual
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Healing with natural medicinal treatment |
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Conditions |
Acute & severe Medicines with primary action.
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Chronic & mild
A Medicine (remedy) with reflex action or with secondary action.
B Medicine with primary action in non-susceptible stage. |
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Hypertension
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Rauwolfia, Veratrum, Cinchona, Sympatholytics, (Secale (large dose).
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Belladonna, Ephedra, Lobelia, Tabacum, Secale (low).
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Hypotension
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Ephedra, Thuja.
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Aconitum, China, Nux vomica, Secale, Veratrum, Viscum alb.
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Tachycardia
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Aconitum, Aristolochia, Cinchona (large single dose), Digitalis, Nux vomica, Oleander, Secale, Squilla, Strophanthus, Valariana, Veratrum, Viscum
alb, Yohimbinum.
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Belladonna, Ephedra, Sympathetomimic.
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Paroxysmal atrial tachycardia
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Aconitum, China, Nux vomica, Secale cor, Veratrum, Digitalis (large
single dose-Depressant), Strophanthus.
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Calc phos, Digitalis.
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Ectopic
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Kali mur, Aconitum, China, Nux vomica, Secale cor, Veratrum.
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Calc phos, Digitalis, Ricinus com, cold water (Oral).
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Rheumatism
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Digitalis, Sulphuric acid.
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Bryonia, Kalmia, Viscum alb.
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Bradycardia
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Belladonna, Hyoscyamus, Stramonium, Ephedra, Lobelia.
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Aconitum, China, Nux vomica, Secale cor, Veratrum, Digitalis, Kali.
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S A block
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Belladonna, Ephedra.
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China, Digitalis, Strophanthus, Oleander, Physostigma, Kali, Cold, O2, Acetic acid, Para sympathomimetic.
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Failure
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Calc phos, Ephedra, Tabacum, Adonis.
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Arsenic alb, China, Nux vomica, Gelsemium, Helleborus, Colchicum, Aconitum, Pilocarpus. Kali mur, Rauwolfia, Sulphur (B1),Crataegus.
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Beriberi
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Allium cepa, Arsenic alb, China, Opium, Sulphur.
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Sulphuric acid, Allium sativa, Urginea, Allium cepa.
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Thrombosis
varicose vein
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Sulphuric acid, China, Melilotus, Salix nigra, Sulphur.
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Alfalfa, Calc phos, China, Gelsemium, Aloe.s, Mag phos.Juglans regia, Calcaeria fluor, Gun powder, Terminalia chebua,Accasia.
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Phlebitis
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Aloe.socotrina, Hamamelis, Sulphur, Salix nigra.
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Calc phos.
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Hyper
cholestremia
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Allium sativa, Emblica ribes, Sulphuric acid, Terminalia chebula, Podophyllum.
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Oleum jecoris, Ricinus communis, Aloe. s, Kalmegh, Citric acid.
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Fatty heart
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Kalmegh.
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Phosphoric acid, Curcuma, Allium cepa.
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Congenital ASD
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Calcarea phos.
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Overactive state congenital
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Alfalfa, China, Aconitum, Secale
cor.
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Viscum album, Sulphur, Salix nigra, Aloe socotrina
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Recurrent angina
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Cactus grandiflora, Aconitum, Cocculus, Mag phos. Alcohol, Tabacum.
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Effort syndrome
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Nux vomica, China, Cold drinks. |
Aconitum, Arsenic alb.
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Atrial fibrillation
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Digitalis.
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Calcarea phos.
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Pulmonary congestion
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Belladonna, Stramonium, Hyoscyamus.
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Ipecac, Physostigma.
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Pericarditis
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Bryonia, Spigelia.
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Right VF
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Digitalis.
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Arsenic alb, Digitalis, Aconitum, Sulphur, Salix nigra.
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Left VF
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Calc phos.
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Arsenic alb, Rauwolfia, Sulphur, Salix nigra, Nux vomica, Kali mur, Opium, Gelsemium.
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Cardiac cirrhosis
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Cactus, Podophyllum, Curcuma long, Arsenic alb, Nux vomica.
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Aneurysm
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Secale cor.
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Vascular thrombosis, polyp |
Cinchona, Lobelia, Arsenic alb, Sinapis, Nux vomica, Thuja, Podophyllum, Sulphuric acid.
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Arteriosclerosis
Herbal chelation
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Silicea < Iron containing herbs.
Iron < Lead containing herbs. Lead < Copper containing herbs. Copper < Mercury containing herbs. Mercury < Arsenic containing herbs. Arsenic < Sulphur containing herbs. Sulphur < phosphorus containing herbs.
Phosphorus < Aurum containing herbs. < Magnesium containing herbs. |
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Crocus sativa (Hypercholerstremia, Mn, Anti inflammatory).
Syzigum aromaticus (Mn, Anti inflammatory).
Zingiberis. (S, Blood thinning).
Allium sativa (S, Blood thinning, Hypercholerstremia, Anti inflammatory).
Cardamom (Mn).
Crataegus (Plaque inhibition).
Curcuma long (Blood thinning).
Piper nigrum (P, Blood thinning, Hypercholerstremia).
Citrus medica (Blood thinning).
Terminalia arjuna (Cardiomyopathy).
Terminalia chebula (Hypercholerstremia, Laxative).
Gulgul mukul (Hypercholerstremia).
Gingko biloba (Blood thinning).
Cinnamon (Mn, Blood thinning).
Hypericum (Blood thinning).
Aeseculus hip (varicosity).
Juglan regia (Varicosity).
Thea sinensis (Blood clotting).
