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