11 18 2014 Heart Failure Drugs

Question 1

Acute vs. Chronic Heart Failure - what is that is happening and what is the goal of the treatment?

Answer 1

Acute – occuring after myocardial infarct or cardiogenic shock

Goal: maintain blood pressure and increase cardiac output

Chronic – congestive heart failure from cumulative damage

Goal: increase CO, decrease PVR (peripheral vascular resistance)

Control symptoms and increase exercsie tolerance and prevent cardiac hypertrophy and remodeling.

Question 2

toresmide, bumetanide, ethacrycin acid, furosemide

1. what type of drug?
2. Mechanism
3. Benefits
4. Adverse effects?

Answer 2

Loop Diuretic

Block cotransporter NKCC2 on thick ascending limb * Decrease reabsorption of Na+ but promotes excretion of K+

Induce prostaglandin and NO and reduce VR and pulmonary congestion,

Ethacrynic acid is used for patients allergic to sulfonamides

Adverse effects:

Hypokalemia, metabolic alkalosis, hypomagnesium, hypovolemia

Question 3

metolazone, indapamidem, chlorothiazide, Hydrochlorothiazide, Chlorthalidone

1. what type of drug?
2. Mechanism
3. Benefits
4. Adverse effects?

Answer 3

1. Thiazide diuretic
2. Blocks NCC symporter ( Na+, Cl-) in distal convoluted tubule
3. Orally availble. Decrease the absorption of Na+ – decrease BP in HTN pts.
4. Hypokalemia, metabolic alkalosis, hyponatremia, hypercalcemia, hyperglycemia, hyperuricemia

Question 4

Triamterene, Amiloride, Spironolactone

1. what type of drug?
2. Mechanism
3. Benefits
4. Adverse effects?

Answer 4

1. K+ Sparing
2. Triamterene, amiloride = block ENAC (Na+) channel
   - channel can be further activated in presence of aldosterone

Spironolactone = directly aldosterone antagonist.

ALL OPPOSE ALDOSTERONE ACTION IN LATE DISTAL TUBULE AND COLLECTING DUCT

3. Prevent myocardial and vascular fibrosis. Decreases Na+ absorption = diuresis = decrease afterload.
4. Hyperkalemia, hyperchloremic metabolic acidosis, gynecomastia (spironolactone)

Question 5

Captopril, Enalopril, Lisinopril, Quinapril, Ramipril

1. what type of drug?
2. Mechanism
3. Benefits
4. Adverse effects?

Answer 5

1. Vasodilator – ACE INHIBITOR
2. Target ACE enzyme and decrease production of AII.

Also inhibits degradation of bradykinin – produces prostaglandins and NO

3. Lower PVR = reduce preload by decreasing aldosterone sysnthesis

Decreases long term remodeling of heart

Decreases SNS activity by reducing NE release

4. Cough and angioneurotic edema ( swelling of nose, thorat, glottis, tongue)
   - risk of hypotension on onset of therapy due to decrease PVR

Question 6

Valsartan, Losartan, Candesartan, Valsartan

* artans

1. what type of drug?
2. Mechanism
3. Benefits
4. Adverse effects?

Answer 6

1. Vasodilators : ARBs : Angiotensin II receptor Blockers
2. Blocks AT1 and decreases pVR

* does not affect Bradykinin and therefore will not cause the cough that one sees with ACE inhibitors

3. More selective inhibiot of AII since there are other enzymes that can convert AI to AII
4. Hypotension

Question 7

1. Which are the two Beta- blockers that can be used to treat heart failure?
2. Mechanism
3. Benefits
4. Adverse effects?

Answer 7

1. Carvedilol and metoprolol succinate
2. Negative ionotropes – block Beta- receptors
3. Decrease remodeling, hypertrophy, and cell death.

They decrease morbidity and mortality

Decrease HR to keep heart from working to hard and also attenuate response to increased catecholamines seen in HF.

4. Bradycardia/ heart block

DO NOT USE IN PATIENTS WITH ASTHMA

Question 8

Digitalis, digoxin, ouabain

1. what type of drug?
2. Mechanism
3. Benefits
4. Adverse effects?

Answer 8

1. Positive inotropic agents – cardiac glycosides
2. Block Na+/K+ ATPase in order to increase intracellular levels of Ca2+.
3. Increase cardiac contractility! Increase Co, decrease size of heart, decrease venous pressure, increase diuresis ( blocking channel in kidneys = block Na+ absorption = promote peeing)

Digitalis enhances vagal tone.

4. Digitalis: AV block, nausea, vomiting, visual distrubances

All: increase chance of delayed afterdepolarizations!!

Question 9

Dobutamine, NE, and Epi

1. what type of drug?
2. Mechanism
3. Benefits

Answer 9

1. Beta 1 agonists – inotropic drug
2. and3.

Dobutamine is used for treatment of heart failure NOT accompanied by hypotension

Increase contractility via beta-agonist but does not decrease PVR

NE: beta 1 and peripheral alpha receptor agonist * used for WARM septic shock

Epi: increase contraction and HR – used for CARDIAC ARREST

Question 10

Milrinone, Inamrinone (amrinone)

1. what type of drug?
2. Mechanism
3. Benefits
4. Adverse effects?

Answer 10

1. Bipyridine – inotropic drug
2. Block PDE3 ( which usually would degrad cAMP).

Incrase in cAMP = increase in activation of L-type Ca2+ channel

3. Increases myocardial contractility

Safe only in SHORT TERM TREATMENT : < 24hrs of use

4. fatal arrhythmias; bone marrow and liver toxicity

* Milrinone is used preferentially

THIS IS A LAST RESORT!!