PHARMACOTHERAPY IN CADIOVASCULAR DISEASE

DEPT.PHARMACOLOGY & TOXICOLOGY FACULTY OF MEDICINE G M U

CARDIOVASCULAR DISTURBANCES
SHOCK CHRONIC ORTHOSTATIC HYPOTENSION HYPERTENSION ANGINA PECTORIS CARDIAC DYSRHYTHMIA CARDIAC FAILURE HYPERLIPIDAEMIA

SHOCK
Is a state of inadequate capillary perfusion (oxygen deficiency) of vital tissues to an extent that adversely affects cellular metabolism (capillary endothelium and organs) causing malfunction, including release of enzymes and vasoactive substance ( low flow or hypoperfusion state) The cardiac output and blood pressure are low The essential element, pump failure (myocard infarct), maldistribution (septic shock), or loss of total intravascular volume ( bleeding, burned, anoxia).

SHOCK TREATMENT
Treatment of the cause : pain, wounds, bleeding, infections, adrenocortical deficiency Replacement of any fluid loss from the circulation Maintenance of diastolic blood pressure and perfusion of vital organs (brain, heart, kidneys)

CHRONIC ORTHOSTATIC HYPOTENSION

Occur s with age, in primary progressive autonomic failure Initial treatment is by expansion of blood volume using a sodium retaining adrenocortical steroid plus elastic support stocking to reduce venous pooling of blood Postprandial due to redistribution of blood to the splanchnic area

HYPERTENSION
Is the most common CV disease, 20-30% adult population In fact, hypertension usually asymptomatic Etiology of hypertension only 10-15% can be established (renal artery constriction, coartation of the aorta, pheochromocytoma, cushings disease, primary aldosteronism)

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Essential hypertension, patient in whom no specific cause of hypertension can be found Autonomic nervous system function Baroreceptor reflexes The RAA system The kidney failure Is usually caused by a combination of several abnormalities (multifactorial)

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Epidemiologic evidence point to: >genetic inheritance >psychological stress >environmental and >dietary factors

BP= CO X PVR
BP: blood pressure, CO: cardiac output, PVR : peripheral vascular resisteance BP is maintained by: arteioles, post capillary venules (capasitance vessels), heart, kidney, local release of hormones from vascular endothelium (nitric oxide-dilate; endothelin 1, vaso active peptide- contricts blood vessels)

BASIC PHARMACOLOGY OF ANTIHYPERTENSIVE AGENT

Act at one or more of anatomic controle site DIURETIC: by depleting the body of sodium; by reducing blood volume; by other mechanism. SYMPATHOPLEGIG AGENT : by reducing peripheral vascular resistance; by inhibiting cardiac function; by increasing venous pooling in capasitance vessels

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DIRECT VASODILATORS: by relaxing vascular smooth muscle--- dilating resistance vessels AGENT that block production or action of angiotensin

ACTION OF ANTIHYPERTENSIVE DRUG

DIURETIC
Lower BP primarily by depleting body sodium stores Sodium contribute to vascular resistance by increasing vessel stiffness and neural activity Some diuretics have direct vasodilating effect (1.e. Indapamide); inhibit smooth muscle responses to contractile stimuli (i.e. Amiloride)

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Are effective in lowering BP by 10-15mmHg In single (alone) { for mild and moderate essensial hypertension Are used in combination with sympathoplegig and vasodilator drugs in more severe hypertension Potassium-sparing diuretics are useful to avoid exessive potassium depletion particularly in patients taking digitalis

DIURETIC

ANGINA PECTORIS
THE PRINCIPAL MANAGEMENT
INCREASE OXYGEN SUPPLY DECREASE OXYGEN DEMAND

CARDIAC ARRYTHMIA
ARRYTHMOGENIC DRUG:

digitalis, verapamil,diltiazem, betablockers, clonidine, methyldopa, quinidine,flecainide, propafenone, theophylline, sotalol, amiodarone CONDITIONS: physical: angina pectoris, myocard infarct, nodefiber;metabolism: electrolite, hormonal; psychological : depression

CARDIAC DYSRYTHMIA

CARDIAC FAILURE
Heart may fail from disease of myocard itself or from an excessive workload imposed on it by arterial hypertension, valvular disease or an arteriovenous shunt. Drug used to treat cardiac failure, produces reduction preload or/and afterload

DIGITALIS

ANGIOTENSIN II
Altered Pheripheral Resistance: 1. Direct vasoconstriction 2. Enhancement of noradrenergic neurotransmission: A. NE release > B. NE reuptake < C.Vascular respons > 3. Increase Sympathetic Discharge (CNS) 4.Realease catecholamines from adrenal medulla Altered Renal Function: 1.Direct effect to increase Na reabsorption in proximal tubule. 2. Release aldosterone from adrenal cortex(Na reabsorption >;K secretion> in distal nephron) 3. Altered Renal Hemodynamics: A.Renal vasoconstrict B.Noradrenergic trans > C.Renal sympathetic tone (CNS) >

HYPERLIPIDAEMIA

METABOLISM OF LIPOPROTEIN