Treatment of CHF Flashcards Preview

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Flashcards in Treatment of CHF Deck (31):
1

4 Major determinants of CO

Preload
Afterload
HR
Contractility

2

List some common causes of Acute CHF

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

3

Common causes of Chronic CHF

Ischemic Cardiomyopathy
Hypertrophic Cardiomyopathy
Dilated Cardiomyopathy

4

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

-Infarct
-High Na+ Intake
-Arrhythmia
-PE

5

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

Diuretics
Loop diuretics (furosemide) or thiazides

6

Adverse Effects of Loop Diuretics

Hypokalemia
Hyponatremia
Hypomagnesemia
Metabolic alkalosis
Ototoxicity
Hyperuricemia
Allerigies
Diuretic Resistance

7

What are potent vasodilators useful in acute CHF?

Nitrates and Nitroglycerin

8

What is niseritide?

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

Activates vasodilation and blocks Na+ reabsorption (causes diuresis)

9

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

Beta Adrenergic Agonists

Phosphodiesterase Inhibitors

10

Generally, how do Beta adrenergic agonists increase contractility?

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

11

What receptors does isoproterenol work on?

Nonselective B1/B2 agonist

12

What receptors does dopamine work on?

Low dose- B1 only
High dose A1

13

What receptors does dobutamine work on?

B1 selective

14

What receptors does norepinephrine work on?

Nonselective
Only used in pts with extremely reduced CO

15

List the two phosphodiesterase inhibitors

Inamrinone
Milrinone

16

What is the general MOA of phosphodiesterase inhibitors?

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

17

How do nitroprusside and nitroglycerin treat HF?

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

18

What are general treatment objectives in chronic CHF?

Early recognition of ventricular dysfunction (without symptoms)

Prevent ventricular remodeling

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

19

What is the general mechanism of digitalis (digoxin)?

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

20

How is digoxin eliminated?

Renally, which complicates the dosing in patients undergoing renal failure

21

What is the primary clinical use of digitalis?

Patients with CHF and atrial fibrillation with rapid ventricular response

22

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

1-2ng/mL is the therapeutic window.

Above 2.5ng/mL is toxic.

23

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

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

24

What drugs are contraindicated in Acute CHF?

Ca2+ channel blockers
They are vasodilators, but they have negative inotropic effects

25

What vasodilator classes are used in chronic CHF?

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

26

How are ACE Inhibitors useful in chronic CHF?

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

27

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

Valsartan + Sacubitril

Valsartan is an angiotensin II receptor inhibitor.

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

28

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

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

29

What are some "nonpharmacological" therapies for chronic CHF?

Surgery
-Revascularization for ischemic disease
-Valve repairs/replacements
-Aneurysmectomy

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

Cardiac resynchronization therapy

Cardiac Transplant

30

What is the very basic mechanism of an LVAD?

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

31

What is the goal of cardiac resynchronization therapy?

Used in pts with abnormal conduction

Goal: resynchronize the conduction so contraction will occur normally

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