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