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Scalar 12 lead surface electrocardiogram
Characteristics of heart muscles
Automaticity.
Excitability.
Contractibility.
Rhythmicity.
Refractory period.
Tonicity on relaxation.
All or none law.
ECG units
Atrial unit. Action potential.
Ventricular unit. Action potential.
Resting potential (- 20 mv).
Potassium ion inside the cell,Sodium ions outside the cell.
Stimulation from Sino atrial node.
Action potential.
Sequence of excitation.
Action potential from different sized muscle cells.
Mean electric energy.
Electric current.
Different wave patterns on around the heart and at skin (Aura is absent as the surrounding air is bad conductor of electricity).
Depolarization, Repolarization.
Waves.
Positive waves.
Negative waves.
Depolarization and repolarization waves of right atrium, left atrium, interventricular septum, right ventricle, and left ventricle.
Exchange of Intracellular potassium ions (magnesium ions) and outer cellular sodium ions (calcium cations).
ECG Paper
Horizontally 1 mm small square represents 0.04 second, large square represents 0.2 second.
Vertically 1mm represents 0.1mv.
Name of waves
Middle of the alphabet PQRSTU.
Small letters represent low waves.
Capital letters represent large waves.
12 Leads
3 Bipolar limb leads.
3 Unipolar limb leads.
6 unipolar chest leads.
L1, L2, L3.
avR, avL, avF.
V1, V2, V3, V4, V5, V6.
Long lead LII is traced for rhythm evaluation (Diagonal lead axis).
Heart surface & Leads
Anterior leads.
Lateral leads.
Posterior leads.
Inferior leads.
Heart cavity lead: avR.
Evaluation of ECG
Configuration of each wave (P, qRS, T, U).
Sharp single wave.
Compound wave.
Complex waves.
Split wave.
Changes in configuration of waves are depend on strength of stimulation, velocity through conduction tissue, thickness of muscle fibre, relation of the position of electrode to path of excitation, and action potential.
Changes in intervals (PR interval, QRS interval, QT interval, Qu interval, PP interval, RR interval, SS interval).
Shifts in segments (Pt segment, ST segment, TP segment).
Changes in T wave.
Normal configuration of the T (primary) wave is the opposite to the qS wave or R wave direction. Limbs are symmetrical. Configuration of compound T (Anterior lead) wave is seen as the same as the direction of the QRS complex with asymmetrical limbs normally. Changes in rhythm. Variations in the interval between two P waves.
Variations in the interval between two QRS complexes. Variation in the interval P wave and QRS complex.
Changes in voltage of atria. Variation in amplitude of P waves.
Changes in voltage of the ventricle. Variation in amplitude of R waves and S waves.
Changes in normal mean electrical axis.
Changes in mechanical position (unipolar limb lead).
Intermediate position.
Vertical position.
Horizontal position.
Rotation (Chest leads)
Clockwise rotation.
Anticlockwise rotation (RVH).
Tall R wave in V1 represents anticlockwise rotation (RVH, PMI), Deep sharp S wave in V5 represents clockwise rotation due to LVH (posterior wall hypertrophy, Anterior wall degeneration).
Determination of electric mean axis deviations.
Deviations of mean axis electrical potential may be taking place by weakness of one ventricle, hypertrophy of one ventricle, and block in one of the conduction branch pathways.
R wave progression
The R wave is progressive from V1 to V5 normally.
Ventricular activation time.
Right ventricle < 0.02 second Left ventricle < 0.04 second.
Duration of atrial electric systole (P wave, merging of atrial repolarization wave).
Duration of ventricular electric systole (qRSTU interval).
Duration of atrial electric diastole?
Duration of ventricular electric diastole (uq).
Changes in electrolytes (Calcium and sodium, Potassium and magnesium).
Variations in amplitude (High - calcium).
Variations in QRS interval (wide - potassium excess).
Slurring of R wave (pre -excitation, Calcium excess, ischemia, early repolarization).
Shift of ST segment (elevation. excess of potassium).
Amplitude of T wave (elevation - hyperkalemia).
Dominance of U wave (hypokalemia).
Changes in endocrine system (hyperthyroid tachycardia, ST segment elevation in hypoinsulin, Hyperglycemia, hyper adrenalism).
Autonomic nerve system (sympathomimetic tachycardia, ventricular ectopic).
Bradycardia due to vagal stimulation.
ST elevation in excess of adrenaline, stress hormones).
ECG and Organs
ST segment duration: prolongation in hypoalbuminemia in liver insufficiency.
QT prolongation and bradycardia in head injury.
Sinus atrial block on right vagus injury.
AV block in left brain and medulla injury.
Rate of atrium and ventricles /minute.
Estimation of atrial rate/minute.
1500/ numbers of small squares between two P waves.
Estimation of ventricular rate /minute.
1500/ numbers of total small squares between two R waves.
Rapid rate.
Sinus tachycardia.
Paroxysmal atrial tachycardia.
Paroxysmal ventricular tachycardia.
Ventricular fibrillation.
Slow rate.
Sinus bradycardia.
Atrial flutter with AV block.
Atrial fibrillation with AV block.
AV block with conduction through aberrant pathways.
Inter atrial conduction block.
Intraventricular conduction block.
SA block 2:1.
First degree AV block.
Second degree AV block.
Complete AV block.
Ventricular arrest.
Rhythm
Rhythm of atria and ventricles.
Ratio of rhythm atrial and ventricles.
Conduction defects may be developed in SA node, AV node, interatrial conduction pathways, Atrioventricular conduction pathway, His bundle, Septal branch, three bundle branches and in aberrant pathways.
Escape beat
Physiologically originates from rt atria, left atria; junctional tissue; bundle branch, Purkinje fibre, rt ventricle or left ventricle. It may have originated from single focus, or multiple foci.
Ectopic beat, Extra electric systole
Pathologically originates from right atria, left atria, junctional tissue, AV node, right ventricle, left ventricle, His bundle, triple bundle branches. It may have originated from single or multiple foci.
Amplitude and hypertrophy.
High amplitude of R wave in limb leads. (LIR + LIII S), R wave in v5, R wave in v5 +S wave in v1).
Conduction
Excitation of action potentials in conductive tissue are conducted from SA node to AV node, SA node to atria, AV node to His bundle, septal branch, triple bundle branches to Purkinje fibers, Purkinje to sub endocardium, to myocardium, and finally the action potentials from epicardium to skin.
Conduction media
Pericardial fluid, fibrous pericardium, emphysema, thick chest bone, organs and thickness of fat skin.
ECG pattern in different cardiac disease conditions.
Rest ECG.
Random ECG.
T wave low after food,cool drinks.ST elevation from sunheat, Sinus tachycardia from anxiety, Deep q wave and left axis deviation from flatulence. low voltage due to inspiration.
Post exercise ECG.
ST segment depression.
Ratio of increase in amplitude in R wave and increase in depth of ST segment more than 1.
Extrasystole.
PVEB.
Increase the amplitude of the R wave.
Increase the amplitude of the T wave.
Decrease amplitude of T wave.
symmetrically inverted T waves.Inverted U wave.
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Heart rate variability (HRV). SDNN (30 -100). More than 100 indicate parasympathetic dominance - good digestion, and slow breathing rate. Less than 30 indicate sympathetic overactivity.
Interpretation.
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Remedies.
Homeopathicity is beneficial in chronic cardiac dysfunctions. Cardiac depressants (Remedies) are good for the rejuvenation of properties of cardiac tissues. Cardiac diseases (70%) are muscular, conductive and connective type tissue origin. 30% of cardiac diseases are coronary vascular related.
