CHF

Question 1

Bidil

Answer 1

hydralazine + isosorbide dinitrate - only drug the FDA ever approved for a specific ethnic [african americans]
Hydralazine - direct vasodilation of arterioles, increased bioavailability with food
Isosorbide Dinitrate - stimulation of intracellular cGMP –> smooth muscle relaxation (veins). decreases O2 demand by decreasing preload

Question 2

Spironolactone

Answer 2

Competes with aldosterone for receptor sites in the distal renal tubules, increasing sodium chloride and water excretion while conserving potassium and hydrogen ions; may block the effect of aldosterone on arteriolar smooth muscle as well

Question 3

Enalapril

Answer 3

Competitive inhibitor of angiotensin-converting enzyme (ACE); prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor; results in lower levels of angiotensin II which causes an increase in plasma renin activity and a reduction in aldosterone secretion

Question 4

Angiotensin Pathway

Answer 4

angiotensinogen*→ angiotensin I** → angioensin II [VASOCONSTRICTION]→ increased aldosterone → Na+ retention→ fluid retention

• decreased BP→ renin converts angiotensinogen→ angiotensin I
• *angiotensin converting enzyme (ACE) converts Ang I→ Ang II

Question 5

Loop Diuretics

Answer 5

• inhibit Na/K/2 CL symporter, prevent Na and Cl reabsorption –> less water reabsorbed –> more urine output and less edema

Question 6

Beta-blockers (Metoprolol)

Answer 6

Beta blockers, in addition to their sympatholytic B1 activity in the heart, influence the renin/angiotensin system at the kidneys. Beta blockers cause a decrease in renin secretion, which in turn reduces the heart oxygen demand by lowering extracellular volume and increasing the oxygen-carrying capacity of blood. Beta blockers’ sympatholytic activities reduce heart rate, thereby increasing the ejection fraction of the heart despite an initial reduction in ejection fraction.

Question 7

Angiotensin Receptor Blockers (-artans)

Answer 7

AT1-receptor antagonists; that is, they block the activation of angiotensin II AT1 receptors. Blockage of AT1receptors directly causes vasodilation, reduces secretion of vasopressin, and reduces production and secretion of aldosterone, among other actions. The combined effect reduces blood pressure.

Question 8

Aldosterone

Answer 8

stimulated by angiotensin II in response to low blood volume –> increases reabsorption of Na and water in kidneys

Question 9

Eplerenone

Answer 9

Aldosterone Antagonist
- Eplerenone selectively blocks mineralocorticoid receptors reducing blood pressure in a dose-dependent manner and appears to prevent myocardial and vascular fibrosis.

Question 10

Dyspnea

Answer 10

sensation of difficult or uncomfortable breathing

Question 11

Orthopnea

Answer 11

sensation of breathlessness in recumbant position relieved by sitting or standing

Question 12

Paroxysmal Nocturnal Dyspnea

Answer 12

sensation of shortness of breath that awakens the patient, relieved by sitting up or sleeping upright

Question 13

Treatment of CHF

Answer 13

ACE inhibitor (enalapril)
Beta-blocker
Loop diuretic
Thiazides
Bidil for african americans who are symptomatic
Aldosterone antagonists
DON’T USE STATINS FOR CHF UNLESS PATIENT HAS INDICATION

Question 14

Left sided heart failure

Answer 14

Congestion into the pulmonary beds (pulmonary effusion), as well as hypo-perfusion of systemic organs
- dyspnea, orthopnea, edema, “perceived” hypotension

Question 15

Right sided heart failure

Answer 15

Caused by Left sided heart failure

- renal congestion –> greater fluid retention –> edema