Review on ECG Diagnosis and Cardiac Treatment



Hpathy Ezine, February, 2011 | Print This Post Print This Post |

The author provides detailed information about the role of ECG in cardiac diagnosis and gives a summary of some relevant homeopathic remedies.

Cardiology deals with the heart, aorta, peripheral vessels and blood. Ventricle is the main chamber, atrium is the antechamber. Left atrial wall thickness is 3mm, right atrium is 4mm, RV is 5mm, and LV is 15mm.

Properties of cardiac muscles: Automacity, rhythmicity, conductivity, excitability, refractioneries, tonicity, all or none law, contractility, aberrant conduction.

Coronary artery and its branches

Left CA supplies to left and right ventricles but Right CA supplies mostly to left ventricle posterior surface. Length of coronary trunk is 4 cm and diameter of coronary artery is about 1cm. Length of a capillary is about 1cm, one capillary supplies for each muscle fiber. Capillary pressure at artery end is 32mm and 20 mm at venal end. (Total lengths of blood vessels are about 1,00,000 km)

Stroke Volume x Rate = Output. Coronary circulation takes about 5%-20% of cardiac output i.e., 200ml-800ml. Output x Mean Pressure= Work. Peripheral vasoconstriction causes sufficient rise in SBP which promotes optimum blood supply to coronary as well as to central organs.

Cardiac pains

Etiology: paroxysmal atrial tachycardia-overwork, coronary insufficiency-osseous obstruction, polyp thrombosis, spasm, ischemic anoxia, aortic aneurysms, low output by LVH, failure (peripheral capillary dilatation with low volume, parasympathetic irritation, MS, AS, LVH, etc. All poisons, CO2, H+, urea, excess of bitter, cold, etc.

Coronary ischemia

Etiology: atheroma, spasm, coronary osteal plaque obstruction, low flow due to failure, low stroke volume <40ml/beat, low minute volume, reactive venous stasis-thrombosis, LVH, less size of cardiac cavity, low output with low rate (parasympathetic, sympatholytics, hypothyroid, anemia), AS, MS, verrucous endocarditis (infection, rheumatism, failure, peripheral capillary dilatation). Coronary artery stasis and clot formation may be developed secondary to the damage of coronary vein & capillaries.

Ventricular Hypertrophy

Common causes are aortic hypertension and myocardial ischemia. Ischemia later may result in VH, work failure, finally local injury itself or infarction. The extra systole waves are developed from injured or infracted fibrosis scar. Atrial fibrosis and resultant dilatation increase the atrial rate, pain, ADH secretion, Na+ retention, venous stasis. It later causes PAT, clot formation, polyp and finally results in embolic phenomena in lungs or brain. Aortic low BP stimulates the VMC at medulla and causes sinus tachycardia, sympathetic peripheral constriction, para sympatholytic splanchnic vasoconstriction and thus increases blood pressure reflexively. Vagal excitation may manifest as aphonia, bronchospasm, low pulse or low BP also.

Efferent sympathetic (cervical) to medulla may cause (parasympathetically) bradycardia. Parasympathetic from front of neck to medulla may cause sympathetic tachycardia. Fibrosis develops early on hypertrophied fiber.

Injury

Myocardial injury occurs spreading from pericardium or endocardium. It may be due to toxins, neoplasm, urea infiltrations, fatty degeneration deposit on muscles, ischemic anoxia. It occurs at epicardial or subendocardial or transmural portion itself. Injury signs are ST elevation for superficial injury or ST depression for deep injury.

Myocardial infarction

It is the most common cause of sudden death in many countries; about 30%. Coronary arterial diseases constitute only 35% of all myocardial diseases. Infarction is more often seen in people with high-stress jobs and less in people who have a relaxed work environment, are vegetarians or live in a cooperative culture.

Premonitory subjective symptoms for infarction are usually absent in many patients. (Latent signs are seen as horizontal line at the mount of Venus in the palm, and deep crater on heart line).

Differential diagnosis

Gall bladder disorder, esophageal spasm, parasympathetic irritation (aphonia and bronchospasm, peptic ulcer), pleurisy, osteochondritis, cervical radiculopathy, etc.

Etiology

Heredity, Asians (small sized vessels, thin and inflammatory pericardium) Hereditary-aortic aneurism, syphilis, congenital heart diseases, High Mg (hard water -sea coast), excess of salt, high cholesterol, hypothyroidism-lipid pericardial effusion, hyperthyroid, overwork, hypercalcaemia (prawn, sea fish, shell fish), high BP, smoking, ambition, overwork with rapid rate, lead contamination-petrol & paints, old hemoglobin particle, O2 lack, CO2 excess, lack of water intake, lack of rest, excess of heat, stress, anger, lack of smile, fear, depression, negative personality.

Summary of ECG

The Electrocardiogram is a graphic representation of the electrical potential produced in association with the heart beat.

Scope of ECG

To estimate fitness of sportsman, drivers, sailors, and pilots; to detect hypertrophy, injury, hormonal & electrolyte imbalance, arrhythmia- atrial fibrillation, AV block; LBBB, wall disorder, position of heart, drug effects, progress of treatment, old infarction, etc.

BASIC PRINCIPLE

Potentials are due to exchange of K+ outside and Na+ into the cell.

The electromotive force is transmitted to 7 different directions in each beat. 80% of electric potential is lost during transition. Positive waves occur when current flows toward exploring electrode and negative waves occur when current of electricity flows away from the electrode as result of excitation. Activation time is short on strong stimulation and in thin fiber.

ECG WAVES

ECG can be divided into atrial P and ventricular q R S T U waves units. P-R, qRS, Q-T interval; Segment are PR, ST, TP segments.

P wave is a compound atrial wave. P wave duration / P-R interval if > 1.6 (giant P) indicates atrial hypertrophy. Atrial activation time > 0.02 seconds indicates right atrial enlargement > 0 .03 seconds indicates left atrial enlargement, P-R interval is increased in long refractive period of ventricle or AV block by vagus irritation.

LEAD

Lead axis is the imaginary line between two points of opposite poles. ECG leads are standard lead, unipolar limb lead, and unipolar chest lead.

Heart has three portions – anterior surface, posterior surface, and cavity. Representation of right & left ventricles may vary in LII, avL, avF with changes in position.

The LIII R represents the Lt ventricle in vertical position and the Lt ventricle in horizontal position.

Summary of ECG diagnosis

1. HEART RATE:

Normal heart rate is 60 -100/ minute. Atrial rate = 60 / P-P interval, i.e., 300 / number of 0.2 seconds (large box) or 1500 / number of 0.04 seconds (small box) in between P-P interval. Ventricular rate = 60 / R-R interval i.e., 300 / number of 0.2 seconds (large box) or 1500 / number of 0.04 seconds (small box) in between R-R interval. (Speed of machine is 1500 cm/minute.)

RATE RAPID- regular:

Sinus tachycardia: rate more than 100/minute. Cycle duration < 0.60 seconds: (causes: fever, thyrotoxicosis, emotion, anemia, beriberi, belladonna, liver disorder, pericarditis, carditis, cardiac failure, low vitamin B1, COPD, and child),

Paroxysmal atrial tachycardia

RATE RAPID irregular: Idio atrial, idio nodal, idio ventricular tachycardia; paroxysmal nodal tachycardia: paroxysmal ventricular tachycardia, atrial flutter, atrial fibrillation.

Supra Ventricular tachycardia: (causes: mitral stenosis, hyperthyroidism, ASD, WPWS, emotion, tea, menses, and drugs- Ephedrine like sympathomimetics)

RATE SLOW regular:

Sinus bradycardia: Rate less than 60/minute, cycle duration >1.00 seconds (causes: parasympathomimetic, vagotonic effect, sympathetic inhibition, beta blockers, increased intracranial tension, athletes, old age, hypothermia, hypothyroidism, sino-atrial node disease, uraemia, jaundice, convalescence.)

RATE SLOW irregular:

S.A block 2:1, sinus arrest, wandering (SA node and atrial ) pacemaker, idio ventricular rhythm, complete A.V block, ventricular standstill.

2. RHYTHM: Normal is a regular sino-atrial node rhythm.

SINUS ARRHYTHMIA: Cerebrovascular accident, atrial ischaemia, hyperkalaemia:3.5-4.5meq/l (causes are diabetes mellitus, infections, Addison’s disease, burns, ADH and H2O retention.)

ECG changes are: SA block, sinus arrest, atrial arrest, absence of P wave, low P wave & low R wave, ST segment slight elevation, tall giant T wave, wide QRS interval)

ARRHYTMIA: Sinus Rhythm with SA block, Sick sinus syndrome, Wandering pacemaker, Supra ventricular rhythm with AV block, Atrial Flutter, Ventricular Flutter, or fibrillation

ECTOPIC WAVES

Premature ectopic wave: seen at early part of cycle. (Causes are: carditis, toxins, infiltration, drugs, sympathatomimetics, hyperkalaemia, tea, coffee, meals, flatulence, hyperthyroidism, carcinoma, ischaemia, fatigue, hypokalemia, old scar irritation.)

ESCAPE BEAT: -

(Physiological and beat at late part of cycle);

Ectopic sinus beat, atrial escape beat; junctional escape beat, ventricular escape beat.

3. POSITION

Normal position in frontal plane is intermediate. Upright waves are in avL & avF.

Abnormal position:-

HORIZONTAL POSITION: 0 degree to – 30 degree: Upright qRS waves in avL and inverted qRS wave complex in avF (central obesity, flatulence, ascitis, left ventricular hypertrophy, left anterior hemi-block, left anterior myocardial infarction, aortic incompetence, old age).

VERTICAL POSITION: + 75 degree to +110 degree: Upright waves in avF and inverted qRS wave complex in avL. (thin chest, emphysema, rt ventricular hypertrophy, ASD lt to rt)

4. ROTATION: position in horizontal plane normally lies transitionally at V3

Abnormal: -

CLOCKWISE ROTATION:

RVH (deep S wave in v5), LVH (tall R in aVR), anterior infarction. Rt ventricle rotates anteriorly to left.

ANTI CLOCKWISE ROTATION:

RVH (tall R in V1), Posterior myocardial infarction, bilateral hypertrophy. Lt Ventricle rotates anteriorly to right.

5. MEAN ELECTRIC AXIS

Vector normally lies in between 0 to + 90 Degree.

Upright qRS wave complex both in LI and LIII

LEFT AXIS DEVIATION: Inverted qRS wave complex in LIII only, negative >30 degree (Normally in 10%, left bundle branch block, left anterior hemi-block, LVH, WPWS, ectopic beat originating from rt ventricle)

RIGHT AXIS DEVIATION:

Inverted QRS wave complex in LI only > + 110 degree (children, left posterior hemi branch block, RVH, LVEB, dextrocardia, inferior M infarction)

6. P WAVE

Height: 1 to 2 mm; Duration: 0.10 seconds, Top of P wave is rounded.

ABSENT P wave: SA block 2:1, Hyper K+, AF, junctional rhythm, ventricular rhythm.

DISTORTED P wave:

P pulmonale (Tall P):

Right atrial enlargement seen in L II, and VI; ASD left to right shunt, tricuspid incompetence, RVH, pulmonary hypertension)

P Mitrale (P wide):

Left atrial enlargement seen in LI, aVL, mitral stenosis, mitral incompetence, ASD (right to left shunt), wandering pacemaker, inter atrial block, aberrant atrial conduction, respiration movement.

NOTCHED P wave: Mitral stenosis, inter atrial block

INVERTED P wave: Dextrocardia, left atrial ectopic beat (avL), retrograde conduction (P wave upright in avR) (LII), left atrial enlargement (V1)

WANDERING P wave:

Sick sinus syndrome, mitral stenosis, hyperkalaemia.

BIPHASIC P wave: Atrial hypertrophy (V1)

MULTIPLE P wave: Blocked atrial premature beat, 3rd degree AV block, atrial flutter with AV block, carcinoma of chest, recent myocardial infarction, thyrotoxicosis, rheumatism, 2nd degree AV block (Causes of AV block are atrial flutter, rheumatism, beta blockers, coronary thrombosis, septal infarction).

7. P-R INTERVAL:

Normal period is between.10 to 0.22 seconds.

P-R Interval prolonged:

Parasympathetic over activity of left vagus, digitalis effect, 1st degree A.V. block, ASD, hypothyroidism, mitral stenosis, hypokalaemia, hypercalcaemia, hyper magnesimia, china toxicity, post ventricular ectopic beat(early P wave), post prolonged Q-T interval beat, (late R wave ) rheumatism, acute infection, beta blockers, atrial ischaemia, anxiety (1st sound may be soft in this condition as in pericardial effusion or emphysema).

P-R interval short: Wolf Parkinson White Syndrome (W P W S), low Mg++, post aberrant beat (early R wave), lack of delay at AV node, AV node bypass conduction beat.

8. q WAVE:

Normally < 1/4 of following R wave, Duration < 0.04 seconds; represents inter ventricular septum depolarization.

Q WAVES:

Old myocardial infarction, left ventricular septal hypertrophy (V5), LAHB (V5), pulmonary emboli (anterior infarction), cardiomyopathy, recent myocardial infarction, expiration(L III), RVH (V1), LBBB (V1), Pulmonary hypertension (LII), PDA, amyloidosis, familial cardiomyopathy.

q ABSENT: normally at v3 (perpendicular to electrode), LBBB (V5), septal infarction (V5).

9. R WAVES:

VOLTAGE:

Normal height in bipolar leads > 5mm, < 16 mm, in avL < 12 mm, in avF < 20 mm, in V1 < 5 mm. in V5 < 25 mm, LIR+LIIIQ= 21mm, V1Q+V5R= 36mm, V2Q+V6R = 42 mm. R wave size is progressive from V1 to V5.

HIGH VOLTAGE:

Ventricular hypertrophy (thick fibre), BBB (absence of opposing depolarization wave), WPWS, SLE, acromegaly, cardiomyopathy, thyrotoxicosis (high stimulation), nephritis (K+ loss) hypokalaemia (causes are tumors, Cushing’s syndrome, aldosteronism, hyperinsulinism (without K diet), colitis), thin chest (near to electrode), RVH, fever, anemia and on expiration (near to electrode).

LOW VOLTAGE:

Para sympathetic over activity(weak stimulation), hyper kalaemia, hypothyroidism, pericardial effusion (defect in conduction media), pericarditis, thick chest, emphysema, diffuse coronary disease (thin fibre), myocardial infarction, fibrosis (ischaemia, rheumatism, Addison’s disease).

10. S WAVE

Size of S wave is regressed from V1 to V5.

DEEP S:

RVH (LI, V5), LVH (V1, V2) Left axis deviation (L III), Horizontal (avF) vertical (avL).

WIDE S:

RBBB (LI, V5).

11. QRS INTERVAL:

Normal period is 0.04 seconds to 0.08 seconds.

Ventricular activation time: < 0.02 seconds in V1(r wave), < 0.04 seconds in V5 (qRwave).

WIDE QRS INTERVAL:

Old age (slow depolarization), bradycardia (weak stimulation), hyperkalaemia, hypocalcaemia, BBB, aberrant conduction, VH with fibrosis, WPWS and cardiac depressant like Aconitum, Cinchona,. PVE waves (causes are tobacco, flatulence, thyroid hormone, toxins, ventricular ischaemia, hypokalaemia).

Hyper magnesemia. (ECG changes of low Mg: Prolonged P-R interval, wide QRS, Tall T waves); (High Mg++ (coastal land water) will induce coronary ischaemia, sleepiness, diaphragmatic paralysis and low BP. (ACh &Ca++ are antidotes of Mg++).

SHORT QRS:

Tachycardia, hypercalcaemia, children.

CHANGE IN SHAPE QRS:

BBB, aberrant conduction, ventricular ectopic, myocardial infarction, hyperkalaemia, electric alternans (pericardial effusion, hyperventilation, post prandial state, anxiety).

12. ST SEGMENT

Normally lies at iso-electrical level.

ST SEGMENT ELEVATION (slow depolarisation near electrode, or early repolarisation at opposite end.)

> 2 mm:.ST convex elevation: acute myocardial infarction; concave elevation: > 2 mm aneurism, epicarditis, chronic rheumatism, thyrotoxicosis, hyperkalaemia, leukemia, recent epicardial infarction, sub-endocardial infarction (avR).

< 2mm = Asian (irritable epicardium), pericarditis.

ST SEGMENT DEPRESSION:

Late depolarisation (at opposite end to electrode) more than 0.5mm: Hypokalaemia (slow repolarisation begin from opposite end), diabetes mellitus, bundle branch block, sub-endocardial infarction, hypo feraemia, ischemia, LVH with strain, coronary thrombosis, supraventricular tachycardia, CVA weak sympathetic-slow depolarisation with beginning of repolarisation on opposite end, ectopic beats, cardio myopathy. pericarditis (in aVR).

ST SEGMENT PROLONGATION > 0.12 seconds:

Hypocalcaemia, hypo-albuminaemia, liver disorders, children. Bilateral hypertrophy.

11. T WAVES

Normally upright in all leads except in avR & V1 or LIII. Its limbs are asymmetrical, more than 1/10 of preceding R wave. Normally tall at V3 due to repolarisation from both sides of electrode.

TALL T WAVE: Asians (thin chest), hyperkalaemia, renal failure, Addison’s disease, right ventricular diastolic overload (thin cardiac wall – V1), Left ventricular diastolic overload (thin cardiac wall V5), LVH, ectopic wave left side origin (V5, LI), posterior or inferior myocardial infarction (V1), in leads reciprocal to infarction, early acute infarction ( K+ release).

FLAT T WAVE: after glucose drinks, after food (low K+ due to insulin with subsequent entry of K+ into cell), after cold bath, after cool drinks, (vasoconstriction) following low R wave, emphysema, ischaemia, pericarditis (low voltage R wave), cardiomyopathies, hypothyroid (weak stimulation).

INVERTED T WAVES: Hyperventilation, atrial tachycardia, after cool drinks, after glucose drinks, hypoferaemia, anxiety, childhood, SVT, horizontal position (LIII ), CVA (Autonomic nervous system – dysfunction of higher centre causes vagus irritation leading to parasympathetic activity-inhibition to SA node. or sympathetic stimulation causes atrial ectopic so weak stimulation), hypokalaemia, VH, cardiomyopathies, pericarditis, ischaemia, subendocardial infarction (Symmetrical T wave pattern) ectopic wave right side origin (V5), LBBB, strain (V5).

14. Q-T INTERVAL:

It is normally between 0. 28 to 0.42 seconds. Corrected Q-T interval (Q-Tc) =estimated Q-T Interval / square root of R-R Interval.

PROLONGED Q-T interval: Hypo Ca++ (causes: low parathyroid hormone, low albumin, liver & renal disorder. Symptoms are – Stridor at throat and spasm. ECG Changes are: Prolonged ST segment, Prolonged QT interval)

Hypo Na+(Symptoms are water retention induced headache, nausea). ECG changes same as hypocalcaemia, hypo albuminemia, hyper K+), carditis, ventricular hypertrophy, valvulitis, hypo K+, hypo Mg++ {symptoms are tremor, vasomotor changes, migraine (high serotonine), hypertension. short P-R & prolonged QT interval}, congenital prolongation, central nervous system lesion, cerebrovascular accidents (sympathetic overactivity), head trauma, brain tumors, old age, bradycardia, ischemia, autonomous neuropathy (parasympathetic over activity with weak SA node stimulation – reactive atrial tissue excitability or sympathetic overactivity with rapid atrial rate).

SHORT Q-T INTERVAL: Post exercise, hypercalcaemia, digitalis overdose, adrenaline toxicity, tachycardia, hyperkalemia.

15. U WAVE

Normally seen in same direction of T wave in V5 due to repolarisation of basal part of heart, posterior upper part of RT ventricle and septum by strong stimulation.

U WAVE PROMINENT: Bradycardia, hyperthyroid, digitalis, hypokalemia (slow and late repolarisation of basal portion, conus, upper part of septum by strong stimulus) LVH.

Ischemia-Compensatory Hypertrophy-Fibrosis; Injury, Infarction. Failure

Ischemia, injury and infarction usually first begin at a superficial part then proceed to the deep part.

Ischemia: normally repolarisation starts at opposite end of stimulation after 1/100 seconds. Repolarisation wave unusually begins from stimulated end itself in case of ischemia, with thick fiber or weak stimulation. So T wave is seen as inverted on electrode placed at opposite end.

Injury: The superficial end becomes primarily negative on superficial injury, but it is comparatively more positive to the already depolarized negative inner surface portion, thus depolarization becomes slow at the injured portion. So this part of the wave appears as ST segment elevation. If the injury is at inner end opposite to electrode and at the same end of stimulation- the depolarization begins usually, but depolarized outer portion becomes negative compared to the injured non depolarized inner end, so current goes slowly far away from electrode. So ST segment appears depressed.

Infarction: Damage of myocardium in infarction is like in train accident some fibers are dead, more are injured, some are normal.

Non injured wall will depolarize first in infarction. So negative wave occurs in electrode at injured and taller wave may occur on reciprocal lead at non injured wall.

Normally conduction occurs through RBB and LAHB branches simultaneously and LPHB conduction occurs slightly later. This sequence is altered on deep injury and in conductive block. So depolarization takes long time to complete on affected fascicle portion. Repolarization begins at non blocked area, then proceeds to blocked site so inverted T will develop at electrode placed at affected portion.

Ischemia signs are T wave inversion, depressed ST Segment., wide QRS, wide QT interval, inverted U wave at V6. Posterior wall ischemia is reversible.

Paroxysmal Atrial Tachycardia: rate is paroxysmal and rapid – not continuous, lasts <4 days. It is irregular and painful (Blocked PAT or blocked flutter is painless). Flutter is originated from the focus at lower atrial site, makes up-down multiple P waves. Pulse deficit can be felt in atrial fibrillation and failure or weak extra systole. PAT later results in venacaval dilatation and secretion of ADH and finally causes water retention.

Embolism is developed in post mitral stenosis ( atrial fibrosis and dilatation with clot formation).

Hypertrophy: early ECG signs are

1. Tall R wave -ischemia-induced reactive hyperemia

2. Tall R with wide QRS thick fiber

3. Tall R, wide QRS, and inverted T, long depolarization

4. low R wave

5. Q wave with inverted T wave.

RV hypertrophy shows tall R wave V1-V2 with ST depression. Q wave with raised ST in V1, V2 is due to RV infarction.

Criteria of LVH: Sum of voltage of R and S wave in reciprocal leads i.e. LI R+LIII S=>21mm.V5 R+V1 S=>35mm, avL > 12mm, avF > 20 mm. Low voltage may be seen in bilateral hypertrophy. Amplitude of Q wave should be >4mm depth but duration < 0.04 second in all non-infarction conditions. Q wave also may be seen in septal LVH in V5, LPHB in avF.

Ventricular Ectopic: Ectopics are due to decreased refractory period of muscles occurring due to ischemia, digitalis, hypercalcaemia, from post MI fibrosis or by WPWS, aberrant excitation. Low atrial origin ectopic will show upright P wave in avR and Inverted P in LII. Ventricular ectopic beat of multi foci (bad prognosis) of left v. origin will show upright wave in rt side leads.

Ventricular ectopics are mostly by gastric sympathetic irritation reflex origin.

Infarction: High ESR, raised SGOT > 40 I.U., raised WBC are the lab sign of MI. Heart surface leads are anterior – LI, avL, V1, V2, V3, V4, posterior-inferior – LI, LIII, avF, reciprocally in V1, V2 and cavity avR or avL. Changes may be irreversible (at anterior) or reversible. It is more painful at muscular part – both anterior and posterior. Infarction can be atrial, ventricular, anterior, posterior, septal, acute, recent, old, multiple, recurrent, epicardial, subendocardial, transmural, or multi focal etc.

ECG changes are R wave without Q at neighboring normal area, Q & R pattern near junction and Q wave only at infarcted area. Wave like Q wave occurs if healthy tissue is slightly present in centre of infarction area. Q&R wave pattern are seen if more healthy tissue present at periphery. Wide R or R with S wave pattern is seen if much healthy tissue is present.

Septal MI may cause ECG as BBB pattern mostly seen in V3. ECG changes may be seen in combined pattern of ischemia, injury and infarction in later period .Sign of intramural infarction (i.e., Q wave and deep symmetrical T wave) may be seen combined with sign of subendocardial infarction ( or LBBB pattern – wide QRS, T wave opposite to QRS wave terminal according to affected bundle branch and lead position.)

Frozen shoulder is seen in posterior MI.

Failure: causes are low thiamine (others are Hb, insulin, renin), low BP, low Ca++, sympathetic weakness due to early sympathetic overactive, low adrenaline (low stimulation), overwork, hyperthyroidism, hyper K+ etc. Failure may occur due to low minute volume by low rate or rapid rate with low stroke volume. RVF (stasis oedema) usually occurs secondary to LVF (pulmonary oedema).

Sinus arrest may be developed by high vagal irritation- ACh, high O2, hypothermia or hyperkalemia. Vagal effect is seen as prolonged T-P or PR interval as seen in hyper K+ effect. High K+ induced changes may be similar to ACh effect.

Prognosis good: in 1st degree AV block and SA block. RBBB, posterior wall changes, outer wall changes in previously healthy heart.

Bad prognosis: massive infarction; LBBB + RBBB, old MI + LBBB, LAHB-deep Q wave and wide tall R wave in V5(-lead near to posterior branch), 3rd AV block, left distal block, low ventricular rhythm, VT, atrial fibrillation with clot embolism, aortic and ventricular aneurysm, ball valve thrombosis, etc.

Sudden death may occur in LV failure, MI induced paroxysmal tachycardia, AV block, MI induced fibrillation, failure. Atrial fibrillation induced stasis clot, ball valve thrombus or embolism, bilateral BBB or trifacicular block with absence of escape beat may induce sudden death.

Heart and nerve control

Heart, mainly ventricles, are under sympathetic control. Sympathetic stimulation can also cause rapid pulse, high BP, and short P-R etc. It increases stroke volume but it increase work through increasing rate and peripheral resistance. Heart, vena cava, aorta and bronchi are mainly under sympathetic control while lungs are under para sympathetic control. Pulmonary high secretion is due to excess of parasympathetic activity. Prostatism (leucorrhoea, asthma, palmar sweating-smooth hand) is due to sympathetic weakness. No sympathetic supply to esophagus. Sympathomimetics can cause brochodilatation, pulmonary constriction, arterial hypertension and erection. Prostatic congestion in old age is due to sympathetic weakness.

Sympathetic system may become weak before middle age due to over-performance.

Ventricular stimulators {rate and force} are sympathomimetics like adrenaline, ephedrine, thuja, coffea. Atrial stimulators are parasympathomimetics -Urginea -the Indian onion, convaleria, oleander, digitalis, low potassium. Stramonium; black hellebore, vit D, calcium, reabsorbed renal sodium carbonate, sodium lactate cold water (externally) etc., are other stimulators. Sympathetic stimulators like cold water on skin, NH4, alcohol, tobacco, cocculus, CO2, acidosis, skin and venous puncture, may precipitate hypertension through vasomotor centre.

Cardiac inhibitors: Nux vom, secale cor, intake of cold water (parasympathomimetic) etc., reduce heart rate. Other depressants are china, aconitum, high potassium, veratrum, viscum album, valariana, aristolochia and rauwolfia. Cardiac depressant like china, aconite are preferable for acute ventricular tachycardia or tachycardia like condition. In congenital disorders prefer potassium rich food in early stage of ventricular extra systole.

Tobacco, alcohol, belladonna, nitrates, etc may act as central vessel dilators for short duration.

Peripheral vasoconstrictors are ephedra, coffee, aspirin, belladonna, tabacum can also act as transient vasodilators by blocking sympathetic ganglion(sympatholytic action). Thus its rebound action is hypertension.

Peripheral arteriolar dilators are sympatholytics thus they can reduce aortic hypertension.

Digitalis like (parasympathetic) atrial stimulator is better for atrial tachycardia and not the depressant practically. It is a homeopathic proof. Digitalis is vagolytic in action, thus it is an SA node and AV node depressant. Secondary action is SA stimulation.

Digitalis can induce ectopic beats in toxic dose in health while it corrects ectopics in disease. The medicine for fatty heart or alcoholic heart is phosphoric acid.

Prophylaxis

Begin a prophylactic life style early. Keep homoeostasis of all ‘dhathu’ with season, place and people always. Remove the miasma-toxins: hereditary, congenital, growth, season, place, education, mind, special sense, life style, food, air; water (Coxsackie virus) etc. Drink sufficient water. Skin massage is better for hypertension. Close the eyes and hand on acute infarction, take a deep breath. Avoid foods having high residue in the first few weeks.

Homoeopathic medical treatment- Summary

Conditions

Strong individual

Expulsion of miasma; Homoeostasis

Weak individual

Too weak ( lowest effective dose)

WEAK( lowest effective dose)

ASD

Calc Phos

Calc phos

Congenital over active

China

Syphilitic heart endocarditis

Cactus, Aurum met, Mercury

Angina

Cactus.g,-nitrates

Mag phos, (Placebo)

Effort syndrone

Expiration, Acon, exercise

Sweet, Sugar of milk

Hypertension

Sympatholytics , Bitter Astringent, pungent

Bell, Ephedra, Tabacum Lobelia, Alcohol

Hypotension

Ephedra, Thuja

Aconitum, Veratrum, Secale, Nux.v, China, viscum, snake root

Fatty Heart

Kalmegh

Phosphoric acid

Tachycardia

Digitalis group, Aconitum Veratrum , Secale, valariana, Yohimbinum, Aristolochia, Viscum alb, Nux.v, China, cold intake

Bell, Ephedra, Heat ext

Paroxysmal atrial tachycardia

Aconitum, Veratrum, Secale, Nux.v, China

Atrial fibrillation

Digitalis

Ectopics

Kali mur, Aconitum, China, Veratrum, Secale, Nux.v

Calc Phos, Digitalis, Ricinus com.

Rheumatism

Digitalis

Kalmia, Bryonia

Pericarditis

Spigelia, Bryonia

Bradycardia

Belladonna groups

Aconitum, Veratrum, Secale, Nux.v, China

SA. block

Bell, Ephedra

Digitalis, China

Failure

Calc phos, Ephedra, Tabacum Sweet, Sour, salt, B1-thiamine

Kali mur, China, Rauwolfia, Ars Alb

Aortic aneurysm

Secale

Thrombosis

Sulphur, Melilotus, H2SO4, China, Salix nigra, Acids

Alfalfa, Calc Phos

Periniosis

Aconitum, Veratrum, Secale, Valariana, Yohimbinum, Aristolochia, Viscum alb, Nux.v, China, external oils

Bell, Ephedra, Tabacum, Lobelia, Alcohol

Phlebitis

Aloes.s

Hamamelis

Fatty degeneration

Phosphoric acid

P.B. Kader

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

Comments

  1. Janaki Subramaniam

    Janaki Subramaniam

    February 17, 2011

    Very good & informative article. It would have been better if ECG samples had also been given alongside.
    Dr. Janaki

  2. S.N.Ojha

    February 18, 2011

    Dear Sir,

    This article by Dr. Kader is very impressive , elaborated detail on ECG. It could have been more attractive and impressive if some of the scanned copy of ECG were attached.

    Has Dr. Kader written a book in English on interpretation of E.C.G. waves? If yes , how can one obtain. it. Please email to me.

    with regards,

    S.N.Ojha

  3. Dr.K.K.Nassir

    February 19, 2011

    Very nice work & useful & informative ,Congratulations………….

  4. H.Dr Muhammad Ayub Khan

    February 20, 2011

    Dear Sir,
    With great respect to your dignity. I have learnt much from your article. It is a best way to show the work for the followers, Sir.

  5. mehra

    Dr Mehra

    February 20, 2011

    Very useful and informative article. It would have been much better if details of the ECG graph with their interpretations and some case reports, were added. Also throw some light on Homeopathic potencies which are to be employed in such cases. Generally we are advised to give mother tinctures (cactus etc.) in cardiac troubles. In your opinion what do you suggest. You have not discussed anything about the systolic hypertension due to aging. Is it be ignored, or you can suggest some medicines?

    • Dr.P.B. kader

      DR..P.B.KADER

      March 4, 2011

      thanks for your information.

      sympathatolytic like Nux omica Veratrun viride,Secale cor,Rauwolfia are

      some drugs for systolic hypertension.Zingiber,Boerhavia difusa also

      effective.

  6. george vallikappil

    george

    February 24, 2011

    Sir,
    I want to contact Dr.Kader.
    So please let me know where the Homoeopathic Research Centre in Kerala, India is situated.
    My mail id is gorgvc@gmail.com
    .Thanking you
    george

  7. drcsgupta

    DR C S GUPTA

    February 25, 2011

    DEAR DR KADER,

    YOUR ARTICLE ON HEART DISEASES ARE V V EXHAUSTIVE AND GIVE FULL DETAILS OF HOMEO REMEDIES IN VARIOUS CONDITIONS AND I THINK THERE IS NO NEED TO CONSULT ANY OTHER REPERTORY.
    THANKS
    DR SHEKHAR

  8. Adv.K.N.Prathapan

    March 3, 2011

    You have done a great work. It seems that you really have profound knowledge on ECG. Even though it is little difficult to understand for an ordinary person,it is an asset to cardiologists as well as all the doctors.

  9. BHUVANESWARI

    sanker

    March 6, 2011

    Sir,
    I want to contact Dr.Kader.
    So please let me know where the Homoeopathic Research Centre in Kerala, India is situated.
    My mail id is utterker@gmail.com
    .Thanking you

    • Dr.P.B. kader

      Dr.P.B.Kader

      March 6, 2011

      Thanks,
      Homoeopathic research centre is situiated at kochangadi,west cochin,kerela,india.

  10. jsdrjohnsamuel

    S.JOHNSAMUEL

    August 25, 2012

    I learn more about heart troubles &remdies INDETAIL.THANK YOU

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