Cardiovascular Pharmacology

Front 1

Hypertension

Back 1

-Diagnosed by serial readings (Average of 2)
-Categorize stage by highest reading
-Increased BP can result from either increase in CO or increase in PVR
-Controlled by sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS)

Front 2

Classification of Blood Pressure

Back 2

Stage I - Drug Therapy
Stage II - 2 Drug Combination Therapy

Front 3

Blood Pressure Goals

Back 3

Associated with mortality and outcomes

Different goal for each disease state

Front 4

Hypertension Mathematical Equation

Back 4

BP = Cardiac Output (CO) x Peripheral Vascular Resistance (PVR)

Front 5

Sympathetic Nervous System Regulation of Hypertension

Back 5

Activation of Beta receptors on the heart --> CO

Activation of alpha1 receptors on the heart --> PVR

Front 6

RAAS Regulation of Hypertension

Back 6

Angiotensin II causes

1. Sodium and Water Retention --> CO
2. Vasoconstriction --> PVR

Front 7

Causes of Increased CO

Back 7

-Increased fluid volume (excess sodium and water)
-Excess stimulation of the RAAS
-Sympathetic nervous system overactivity

Front 8

Causes of Increased PVR

Back 8

-Excess stimulation of RAAS
-Sympathetic nervous system overactivity

Front 9

Medications Used to Treat Hypertension

Back 9

1. Diuretics
2. Beta Blockers
3. Angiotensin Converting Enzyme Inhibitors (ACEI)
4. Angiotension receptor blockers (ARB)
5. Direct Renin Inhibitor
6. Calcium Channel Blockers (CCB)
7. Alpha 1 Receptor Antagonists
8. Alpha 2 Receptor agonists
9. Vasodilators

Front 10

Diuretics

Back 10

Initial blood pressure decrease:
- Decrease blood volume --> decrease CO
- Compensatory increase in PVR -- not sustained, the body compensates

Sustained blood pressure decrease:
-decreases PVR --> decrease in sodium content of smooth muscle cells (gradual effect - over 2-4 weeks)
- long term reduction in BP

Front 11

Classifications of Diuretics

Back 11

1. Carbonic Anhydrase Inhibitors
2. Loop diuretics
3. Thiazide diuretics
4. Potassium sparing diuretics

Each with different potencies and work in different parts of nephron

Front 12

Carbonic Anhydrase Inhibitors

Back 12

MOA - Block NaHCO3 reabsorption and cause diuresis predominately in the proximal tubule

Least potent - even though it is in the proximal tubule it works on NaHCO3 channels

Not an effective class to use for diuresis and therefore not routinely used to treat hypertension - tx specific disease states

Front 13

Acetazolamide (Diamox)

Back 13

Carbonic Anhydrase Inhibitors

Therapeutic uses
-Glaucoma
-Urinary alkalinization - b/c NaHCO3
-Metabolic acidosis
-Acute mountain sickness

Adverse effects
- hyperchloremic metabolic acidosis - w/ elimination of NaHCO3 & not chloride
-Renal stones - dysregulation of phosphate and Ca2+
-Drowsiness
-Paresthesias
-Hypersensitivity reactions