The document discusses several classes of drugs used to treat cardiovascular conditions. It describes the mechanisms of calcium channel blockers, diuretics, vasodilators, cardiac glycosides, alpha blockers, beta blockers, ACE inhibitors, and ARBs. Calcium channel blockers work by blocking calcium entry into cells to decrease contraction. Diuretics reduce fluid volume to decrease preload and workload on the heart. ACE inhibitors block angiotensin conversion to lower blood pressure.

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.  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. 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. 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. 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. 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. 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. 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. 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. 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