Pharmacology of Drugs Acting on Cardio Vascular System
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CONTAINTS
- Introduction to hemodynamic and electrophysiology of heart.
- Drugs used in congestive heart failure.
- Anti-hypertensive drugs.
- Anti-anginal drugs.
- Anti-arrhythmic drugs.
- Anti-hyperlipidemic drugs.
HEART
Hemodynamics is a physical and physiological principle of blood flow (circulatory system) in the body.
The main functions of blood are:
- Transportation of blood gases, nutrients, wastes
- Homeostasis (regulation) of pH, body temperature, water content
- Protection
The Forces Involved with the Movement of Blood Throughout The Human Circulatory System Include:
- Kinetic and potential energy provided by the cardiac pump
- Gravity
- Hydrostatic Pressure (weight of the liquid acting on a unit area at that depth plus any pressure acting on the surface of the liquid)
- Pressure gradients or differences between two any points
Properties of Blood Itself That Affect Its Flow:
- Viscosity
- Inertial mass (mass of an object measured by its resistance to acceleration)
- Volume of blood to be moved
Factors that affect the motion of blood through the vascular channels include:
- Size of the blood vessel.
- Condition of blood vessel.
- Smoothness of lumen.
- Elasticity of muscular layer (tunica media).
- Destination of blood (vascular bed).
Pressure: Force per unit area (Unit- Newtons/m2, Pascal(Pa), mmHg)
Flow rate: Amount of fluid passing a given point over a given period of time
Viscosity: The internal friction between adjacent layers of fluid. Blood is 1.5 times as viscous as water and its viscosity.
Kinetic Energy: Active energy, the energy of motion as forward movement of blood. It is transformed in to potential energy when it produces a lateral pressure or stretching of vessel walls during systole.
Potential energy: Stored energy, it is converted back in to kinetic energy when the arterial walls rebound during diastole.
Cardiac Output:
Cardiac output is defined as the amount of blood flowing from the heart (from the left
ventricle in to aorta) over a given period of time (or in one heart beat).
Cardiac Output = Stroke volume x Heart rate
= 70 ml x 72/min
= 5040 ml/min = About 5 litre /min
Where Stroke volume = Volume of blood pumped by heart/heart beat
Heart rate = Ventricular systole/min
Nonautomatic fibres:
These are the ordinary working myocardial fibres; cannot generate an impulse of their own. During diastole, the resting membrane potential remains stable (approximately 90 mv negative inside). When stimulated, they depolarize very rapidly (fast 0 phase) with considerable overshoot (+30 mv) >> rapid return to near isoelectric level (phase1) >> maintenance of membrane potential at this level for a considerable period (phase-2, plateau phase) during which Ca2+ ions flow in and bring about contraction >> relatively rapid repolarization (phase- 3) during which membrane Na+K+ pump gets activated and tends to restore ionic distribution to the resting pattern. Resting membrane potential, once attained, does not decay (stable phase-4).
II. Automatic fibres:
These are present in the sinoatrial (SA) and atrioventricular (A-V) nodes, and in the His-Purkinje system, i.e. specialized conducting tissue. In addition, patches of automatic tissue are present in the interatrial septum, A-V ring and around openings of the great veins. The most characteristic feature of these fibres is phase-4 or slow diastolic depolarization, i.e. after repolarizing to the maximum value, the membrane potential decays spontaneously. When it reaches a critical threshold value—sudden depolarization occurs automatically. Thus, they are capable of generating their own impulse. The rate of impulse generation by a particular fibre depends on the value of maximal diastolic potential, the slope of phase-4 depolarization and the value of threshold potential.
Complications of high ceiling and thiazide type diuretic therapy:
1. Hypokalaemia:
This is the most significant problem. It is rare at low doses, but may be of grave consequence when brisk diuresis is induced or on prolonged therapy, especially if dietary K+ intake is low. Degree of hypokalaemia appears to be related to the duration of action of the diuretic; longer acting drugs cause more K+ loss. The usual manifestations are weakness, fatigue, muscle cramps; cardiac arrhythmias are the serious complications. Hypokalaemia is less common with standard doses of high ceiling diuretics than with thiazides, possibly because of shorter duration of action of the former which permits intermittent operation of compensatory repletion mechanisms.
Hypokalaemia can be prevented and treated by:
(a) High dietary K+ intake or
(b) Supplements of KCl (24–72 mEq/day) or
(c) Concurrent use of K+ sparing diuretics.
2. Acute saline depletion:
Over enthusiastic use of diuretics, particularly high ceiling ones, may cause dehydration and marked fall in BP (especially in erect posture). Haemoconcentration increases risk of peripheral venous thrombosis. Serum Na+ and Cl¯ levels remain normal because isotonic saline is lost. It should be treated by saline infusion.
3. Dilutional hyponatraemia:
Occurs in CHF patients when vigorous diuresis is induced with high ceiling agents, rarely with thiazides. Kidney tends to retain water, though it is unable to retain salt due to the diuretic; e.c.f. gets diluted, hyponatraemia occurs and edema persists despite natriuresis. Patients feel very thirsty. Treatment of this distortion of fluid-electrolyte balance is difficult: withhold diuretics, restrict water intake and give glucocorticoid which enhances excretion of water load. If hypokalaemia is present, its correction helps.
4. GIT and CNS disturbances:
Nausea, vomiting and diarrhoea may occur with any diuretic Headache, giddiness, weakness, paresthesias, impotence are occasional complaints with thiazides as well as loop diuretics.
5. Hearing loss:
Occurs rarely, only with high ceiling diuretics and when these drugs are used in the presence of renal insufficiency. Increased salt content of endolymph and direct toxic action on the hair cells in internal ear appear to be causative.
6. Allergic manifestations:
Rashes, photosensitivity occurs, especially in patients hypersensitive to sulfonamides. Blood dyscrasias are rare; any diuretic may be causative.
7. Hyperuricaemia:
Long-term use of higherdose thiazides in hypertension has caused rise inblood urate level. This is uncommon now due touse of lower doses. Furosemide produces a lower incidence of hyperuricaemia. This effect can be counteracted by allopurinol. Probenecid is better avoided, because it may interfere with the diuretic response, particularly of loop diuretics.
8. Hyperglycaemia and hyperlipidemia:
These are occurred in the use of diuretics as antihypertensive. These metabolic changes are minimal with low dose thiazides now recommended.
9. Hypocalcaemia may occur with high ceiling diuretics when these are administered chronically. Thiazides, on the other hand, tend to raise serum Ca2+; may aggravate hypercalcaemia due to other causes.
10. Magnesium depletion:
It may develop after prolonged use of thiazides as well as loop diuretics, and may increase the risk of ventricular arrhythmias, especially after MI or when patients are digitalized. K+ sparing diuretics given concurrently minimise Mg2+ loss.
11. Thiazides have sometimes aggravated renalin sufficiency, probably by reducing g.f.r.
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