Cardiovascular system Pharmacology

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This presentation briefly describes the pharmacology of cardiovascular system

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Cardiovascular system Pharmacology

  1. 1. Drugs Acting on Heart &Drugs Acting on Heart & Cardiovascular SystemCardiovascular System Drugs Acting on Heart &Drugs Acting on Heart & Cardiovascular SystemCardiovascular System Antihypertensive Agents- •Calcium channel blocker •Adrenergic agents •Diuretics •Vasodilators •Angiotensin converting enzyme inhibitors •Angiotensin II receptor blockers  Drug of Cardiac Failure- •Digoxin and Digitoxin -Cardiac Glycosides •Bipyridine Derivatives -Milrinone and Inamrinone Antihypertensive Agents- •Calcium channel blocker •Adrenergic agents •Diuretics •Vasodilators •Angiotensin converting enzyme inhibitors •Angiotensin II receptor blockers  Drug of Cardiac Failure- •Digoxin and Digitoxin -Cardiac Glycosides •Bipyridine Derivatives -Milrinone and Inamrinone
  2. 2.  Anti-arrhythmic Drugs- •Sodium channel blockers •Beta Adrenergic Blockers •Potassium channel blockers •Calcium channel blockers  Drug of Ischemic Heart Disease- •Organic Nitrates •Calcium Channel Blockers in Ischemic Heart Disease •Potassium Channel Openers  Anti-arrhythmic Drugs- •Sodium channel blockers •Beta Adrenergic Blockers •Potassium channel blockers •Calcium channel blockers  Drug of Ischemic Heart Disease- •Organic Nitrates •Calcium Channel Blockers in Ischemic Heart Disease •Potassium Channel Openers
  3. 3. Calcium Channel BlockersCalcium Channel BlockersCalcium Channel BlockersCalcium Channel Blockers  Mechanism:  blocking the binding of calcium to its receptors  preventing muscle contraction  decreased peripheral smooth muscle tone  decreased systemic vascular resistance  Resulting decreased blood pressure  Mechanism:  blocking the binding of calcium to its receptors  preventing muscle contraction  decreased peripheral smooth muscle tone  decreased systemic vascular resistance  Resulting decreased blood pressure
  4. 4. Diuretics & VasodilatorsDiuretics & VasodilatorsDiuretics & VasodilatorsDiuretics & Vasodilators Mechanism of Diuretics-  Decrease the plasma and extracellular fluid volumes  Resulting decreased preload  decreased cardiac output,  decreased total peripheral resistance  Overall effect: decreased workload of the heart, and decreased blood pressure Mechanism of Diuretics-  Decrease the plasma and extracellular fluid volumes  Resulting decreased preload  decreased cardiac output,  decreased total peripheral resistance  Overall effect: decreased workload of the heart, and decreased blood pressure Mechanism of Vasodilators-  Directly relaxes arteriolar smooth muscle  Resulting decreased systemic vascular response  decreased after load & peripheral vasodilatation Mechanism of Vasodilators-  Directly relaxes arteriolar smooth muscle  Resulting decreased systemic vascular response  decreased after load & peripheral vasodilatation
  5. 5. Cardiac GlycosideCardiac GlycosideCardiac GlycosideCardiac Glycoside  Cardiac glycosides are naturally occurring plant substances that have characteristic effects on the cardiac muscle. These specific compounds contain a carbohydrate molecule.  CHO molecule combined with water,  converted into a simple sugar plus 1 or more active substances.  Glycosides may actually work by blocking certain ionic pumps in the cellular membrane.  This action, indirectly increases the calcium concentration reaching the contractile proteins.  e.g digoxin (Lanoxin); it is used to treat heart failure and to treat certain types of tachycardias.  Cardiac glycosides are naturally occurring plant substances that have characteristic effects on the cardiac muscle. These specific compounds contain a carbohydrate molecule.  CHO molecule combined with water,  converted into a simple sugar plus 1 or more active substances.  Glycosides may actually work by blocking certain ionic pumps in the cellular membrane.  This action, indirectly increases the calcium concentration reaching the contractile proteins.  e.g digoxin (Lanoxin); it is used to treat heart failure and to treat certain types of tachycardias.
  6. 6. Alpha1 BlockersAlpha1 BlockersAlpha1 BlockersAlpha1 Blockers Mechanism of Action  Block the alpha1-adrenergic receptors  SNS is not stimulated  Resulting decreased blood pressure Mechanism of Action  Block the alpha1-adrenergic receptors  SNS is not stimulated  Resulting decreased blood pressure
  7. 7. Beta BlockerBeta BlockerBeta BlockerBeta Blocker Block beta adrenergic receptors in the sympathetic nervous system Very beneficial in people who have had myocardial infarctions, especially those with low ejection fraction Reduce workload of heart Increase survival rates, decrease hospitalizations. Block beta adrenergic receptors in the sympathetic nervous system Very beneficial in people who have had myocardial infarctions, especially those with low ejection fraction Reduce workload of heart Increase survival rates, decrease hospitalizations.
  8. 8. Angiotensin-converting Enzyme InhibitorsAngiotensin-converting Enzyme InhibitorsAngiotensin-converting Enzyme InhibitorsAngiotensin-converting Enzyme Inhibitors  Large group of safe and effective drugs  Often used as first-line agents for CHF and hypertension  May be combined with a thiazide diuretic or calcium channel blocker  Large group of safe and effective drugs  Often used as first-line agents for CHF and hypertension  May be combined with a thiazide diuretic or calcium channel blocker Mechanism -RAAS: Renin Angiotensin-Aldosterone System  When the enzyme angiotensin I is converted to angiotensin II, the result is potent vasoconstriction and stimulation of aldosterone  Result of vasoconstriction: increased systemic vascular resistance and increased after load  Therefore, increased BP Mechanism -RAAS: Renin Angiotensin-Aldosterone System  When the enzyme angiotensin I is converted to angiotensin II, the result is potent vasoconstriction and stimulation of aldosterone  Result of vasoconstriction: increased systemic vascular resistance and increased after load  Therefore, increased BP
  9. 9. Mechanism-ACE Inhibitors Aldosterone stimulates water and sodium resorption. Resulting increased blood volume ACE Inhibitors block the angiotensin-converting enzyme, thus preventing the formation of angiotensin II. Also prevent the breakdown of the vasodilating substance, bradykinin Resulting decreased systemic vascular resistance (afterload), vasodilation and therefore, decreased blood pressure Mechanism-ACE Inhibitors Aldosterone stimulates water and sodium resorption. Resulting increased blood volume ACE Inhibitors block the angiotensin-converting enzyme, thus preventing the formation of angiotensin II. Also prevent the breakdown of the vasodilating substance, bradykinin Resulting decreased systemic vascular resistance (afterload), vasodilation and therefore, decreased blood pressure
  10. 10. Angiotensin II Receptor BlockersAngiotensin II Receptor Blockers                                 Angiotensin II Receptor BlockersAngiotensin II Receptor Blockers                                  Mechanism of Action Allow angiotensin I to be converted to angiotensin II, but  block the receptors that receive angiotensin II  Block vasoconstriction and release of aldosterone  Mechanism of Action Allow angiotensin I to be converted to angiotensin II, but  block the receptors that receive angiotensin II  Block vasoconstriction and release of aldosterone 

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