Cardiovascular: Pharmacology

Groupings:
1. Hypertension
2. Antianginal Therapy
3. Lipid-Lowing Agents
4. Cardiac Glycosides
5. Antiarrythmics

Anti-Hypertensive Drugs

Primary (Essential) Hypertension: (4)
1. Thiazide Diuretics
2. ACE Inhibitors
3. Angiotensin II Receptor Blockers (ARBs)
4. Dihydropyridine Ca Channel Blockers

Hypertension with Heart Failure: (4)
1. Diuretics
2. ACE Inhibitors/ARBs
3. Beta Blockers (compensated heart failure)
4. Aldosterone Antagonists

Hypertension with Heart Failure: therapeutic considerations –> ________________ must be used cautiously in decompensated HF.
Beta Blockers

Hypertension with Heart Failure: therapeutic considerations –> Beta Blockers are contraindicated in ________________.
cardiogenic shock

Hypertension with Diabetes Mellitus: (4)
1. ACE Inhibitors/ARBs
2. CCBs
3. Thiazide diuretics
4. Beta blockers

Hypertension with Diabetes Mellitus: therapeutic considerations –> ________________ are protective against diabetic neuropathy.
ACE Inhibitors/ARBs

Hypertension in Pregnancy: (4)
1. Hydralazine
2. Labetalol
3. Methyldopa
4. Nifedipine

HTN: calcium channel blockers –> dihydropyridines (5)
1. Amlodipine
2. Clevidipine
3. Nicardipine
4. Nifedipine
5. Nimodipine

HTN: calcium channel blockers –> dihydropyridines
-Site of action?
Vascular Smooth Muscle

HTN: calcium channel blockers –>non-dihydropyridines
1. Diltiazem
2. Verapamil

HTN: calcium channel blockers –>non-dihydropyridines
-Site of action?
Act on the heart

CCBs: mechanism
Block voltage-dependent L type calcium channels of cardiac and smooth muscle –> decrease muscle contractility

CCBs: mechanism –> relative effect on vascular smooth muscle (strongest –> weakest)
Amlodipine = Nifedipine > Diltiazem > Verapamil

CCBs: mechanism –> relative effect on heart
Verapamil > Diltiazem > Amlodipine = Nifediine
**Verapamil = Ventricle**

CCBs: clinical use –> Dihydropyridines (except Nimodipine)
1. HTN
2. Angina (including prinzmetal)
3. Raynaud phenomenon

CCBs: clinical use –> Nimodipine (1)
1. Subarachnoid Hemorrhage (prevents cerebral vasospasm)

CCBs: clinical use –> Clevidipine (1)
1. Hypertensive urgency or emergency

CCBs: clinical use –> Non-dihydropyridines (3)
1. HTN
2. Angina
3. Atrial Fibrillation/Flutter

CCBs: adverse effects –> Non-dihydropyridines (4)
1. Cardiac Depression
2. AV block
3. Hyperprolactinemia
4. Constipation

CCBs: adverse effects –> Dihydropyridines (4)
1. Peripheral edema
2. Flushing
3. Dizziness
4. Gingival hyperplasia

Hydralazine

Hydralazine: mechanism
1. Increase in cGMP
2. Smooth muscle relaxation
3. Vasodilation of arterioles > veins
4. Reduced afterload

Hydralazine: clinical use (2)
1. Sever HTN (particularly acute)
2. HF (organic nitrate)

Hydralazine: indication
safe to use during pregnancy

Hydralazine is co-administered with _______________.
Beta Blocker –> prevent reflex tachycardia

Hydralazine: adverse effects (5)
1. Compensatory tachycardia (contraindicated in angina/CAD)
2. Fluid retention
3. Headache
4. Angina
5. Lupus-like syndrome

Hypertensive Emergency: drugs used (2)
1. Nitroprusside
2. Fenoldopam

Hypertensive Emergency: Nitroprusside –> mechanism
Short Acting: increase in cGMP via direct release of NO

Hypertensive Emergency: Nitroprusside –> adverse effects
Cyanide toxicity (releases cyanide)

Hypertensive Emergency: Fenoldopan –> mechanism
Dopamine D1 Receptor Agonists: coronary, peripheral, renal, and splanchnic vasodilation
-Decrease in BP
-Increase in natriuresis

Fenoldopan: clinical use other than in a hypetensive emergency?
Post-op anti-hypertensive

Hypertensive Emergency: Fenoldopan –> adverse effects (2)
1. Hypotension
2. Tachycardia

Nitrates

Nitrates: (3)
1. Nitroglycerin
2. Isosorbide dinitrate
3. Isosorbide mononitrate

Nitrates: mechanism
1. Vasodilation: increase in NO in vascular smooth muscle
2. Smooth Muscle Relaxation: increase in cGMP

Nitrates: vessels affected
Veins > Arteries –> decreases preload

Nitrates: adverse effects
1. Reflex tachycardia
2. Hypotension
3. Flushing
4. Headache

Nitrates: an adverse effect from industrial exposure is known as “Monday Disease,” results in development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend –> what does this lead to?
1. Tachycardia
2. Dizziness
3. Headache upon exposure

Antianginal Therapy

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