Treatment of CHF

Question 1

4 Major determinants of CO

Answer 1

Preload
Afterload
HR
Contractility

Question 2

List some common causes of Acute CHF

Answer 2

Acute MI
Global Myocardial ischemia
Acute Viral Myocarditis
Acute Valvular Regurgitation
Arrhythmias
Acute Pericardial Tamponade
Massive PE

Question 3

Common causes of Chronic CHF

Answer 3

Ischemic Cardiomyopathy
Hypertrophic Cardiomyopathy
Dilated Cardiomyopathy

Question 4

What are some events that could cause acute CHF in the setting of preexisting chronic CHF?

Answer 4

• Infarct
• High Na+ Intake
• Arrhythmia
• PE

Question 5

What drug class helps to relieve pulmonary congestion in acute CHF? What is most commonly used?

Answer 5

Diuretics
Loop diuretics (furosemide) or thiazides

Question 6

Adverse Effects of Loop Diuretics

Answer 6

Hypokalemia
Hyponatremia
Hypomagnesemia
Metabolic alkalosis
Ototoxicity
Hyperuricemia
Allerigies
Diuretic Resistance

Question 7

What are potent vasodilators useful in acute CHF?

Answer 7

Nitrates and Nitroglycerin

Question 8

What is niseritide?

Answer 8

Human Recombinant BNP
Used for ACUTE CHF
Normally made by stretched ventricles

Activates vasodilation and blocks Na+ reabsorption (causes diuresis)

Question 9

What drug classes could you give to increase contractility in patients in acute CHF?

Answer 9

Beta Adrenergic Agonists

Phosphodiesterase Inhibitors

Question 10

Generally, how do Beta adrenergic agonists increase contractility?

Answer 10

Increase intracellular cAMP levels, increasing inotropy (contraction), lusitropy (relaxation), chronotropy (HR inc), and rate of conduction

Question 11

What receptors does isoproterenol work on?

Answer 11

Nonselective B1/B2 agonist

Question 12

What receptors does dopamine work on?

Answer 12

Low dose- B1 only

High dose A1

Question 13

What receptors does dobutamine work on?

Answer 13

B1 selective

Question 14

What receptors does norepinephrine work on?

Answer 14

Nonselective

Only used in pts with extremely reduced CO

Question 15

List the two phosphodiesterase inhibitors

Answer 15

Inamrinone

Milrinone

Question 16

What is the general MOA of phosphodiesterase inhibitors?

Answer 16

Inhibit degradation of cAMP, thus increasing inotropy (contraction), lusitropy (relaxation), chronotropy (HR inc), and rate of conduction

Question 17

How do nitroprusside and nitroglycerin treat HF?

Answer 17

Reduction of afterload (lower systemic vascular resistance), thus increasing SV and CO

Question 18

What are general treatment objectives in chronic CHF?

Answer 18

Early recognition of ventricular dysfunction (without symptoms)

Prevent ventricular remodeling

Decrease symptoms (pulm congestion, edema)
Increase CO
Prolong survival

Question 19

What is the general mechanism of digitalis (digoxin)?

Answer 19

Block the Na+/K+ ATPase, thus increasing Na+ inside the cardiac myocytes. This inhibits the drive for Na+ to enter cell via the Na+/Ca2+ antiporter, so more Ca2+ stays inside the cell and gets stored in the SR. Thus, more Ca2+ is released from the SR with each contraction

Question 20

How is digoxin eliminated?

Answer 20

Renally, which complicates the dosing in patients undergoing renal failure

Question 21

What is the primary clinical use of digitalis?

Answer 21

Patients with CHF and atrial fibrillation with rapid ventricular response

Question 22

What is the therapeutic window of digitalis? What are toxic levels

Answer 22

1-2ng/mL is the therapeutic window.

Above 2.5ng/mL is toxic.

Question 23

In digitalis toxicity, what drug can be given to rid the blood of digitalis?

Answer 23

Digibind (Monoclonal antibodies used to treat life threatening digitalis toxicity)

Question 24

What drugs are contraindicated in Acute CHF?

Answer 24

Ca2+ channel blockers

They are vasodilators, but they have negative inotropic effects

Question 25

What vasodilator classes are used in chronic CHF?

Answer 25

ACE Inhibitors
Angiotensin Receptor Blockers
Hydralazine
Minoxidil
Prazocin
LCZ696 (Valsartan + sacubritil)

Question 26

How are ACE Inhibitors useful in chronic CHF?

Answer 26

Prevent ventricular remodeling, slow chronic CHF progression, reduce mortality.

Question 27

What is LCZ696 a combination of? What are their functions?

Answer 27

Valsartan + Sacubitril

Valsartan is an angiotensin II receptor inhibitor.

Sacubitril is a neprilysin inhibitor (prevents bradykinin, natiuretic peptide, and adrenomedullin degradation).

Question 28

Given in addition to digoxin, ACE inhibitors, and diuretics, beta blockers help improve survival in chronic CHF. How?

Answer 28

Reduce HR and chronic sympathetic activation
Reduce fetal gene activation
Prevent SR Ca2+ leak
Prevent myocardial apoptosis
Decrease LV remodeling

Question 29

What are some “nonpharmacological” therapies for chronic CHF?

Answer 29

Surgery

• Revascularization for ischemic disease
• Valve repairs/replacements
• Aneurysmectomy

Left Ventricular Assist Devices (LVADs) as a “Bridge to transplant”

Cardiac resynchronization therapy

Cardiac Transplant

Question 30

What is the very basic mechanism of an LVAD?

Answer 30

Removes blood fro the LV and pumps it into the aorta continuously.

Question 31

What is the goal of cardiac resynchronization therapy?

Answer 31

Used in pts with abnormal conduction

Goal: resynchronize the conduction so contraction will occur normally