Treatment of CHF Flashcards
4 Major determinants of CO
Preload
Afterload
HR
Contractility
List some common causes of Acute CHF
Acute MI Global Myocardial ischemia Acute Viral Myocarditis Acute Valvular Regurgitation Arrhythmias Acute Pericardial Tamponade Massive PE
Common causes of Chronic CHF
Ischemic Cardiomyopathy
Hypertrophic Cardiomyopathy
Dilated Cardiomyopathy
What are some events that could cause acute CHF in the setting of preexisting chronic CHF?
- Infarct
- High Na+ Intake
- Arrhythmia
- PE
What drug class helps to relieve pulmonary congestion in acute CHF? What is most commonly used?
Diuretics Loop diuretics (furosemide) or thiazides
Adverse Effects of Loop Diuretics
Hypokalemia Hyponatremia Hypomagnesemia Metabolic alkalosis Ototoxicity Hyperuricemia Allerigies Diuretic Resistance
What are potent vasodilators useful in acute CHF?
Nitrates and Nitroglycerin
What is niseritide?
Human Recombinant BNP
Used for ACUTE CHF
Normally made by stretched ventricles
Activates vasodilation and blocks Na+ reabsorption (causes diuresis)
What drug classes could you give to increase contractility in patients in acute CHF?
Beta Adrenergic Agonists
Phosphodiesterase Inhibitors
Generally, how do Beta adrenergic agonists increase contractility?
Increase intracellular cAMP levels, increasing inotropy (contraction), lusitropy (relaxation), chronotropy (HR inc), and rate of conduction
What receptors does isoproterenol work on?
Nonselective B1/B2 agonist
What receptors does dopamine work on?
Low dose- B1 only
High dose A1
What receptors does dobutamine work on?
B1 selective
What receptors does norepinephrine work on?
Nonselective
Only used in pts with extremely reduced CO
List the two phosphodiesterase inhibitors
Inamrinone
Milrinone
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
How do nitroprusside and nitroglycerin treat HF?
Reduction of afterload (lower systemic vascular resistance), thus increasing SV and CO
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
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
How is digoxin eliminated?
Renally, which complicates the dosing in patients undergoing renal failure
What is the primary clinical use of digitalis?
Patients with CHF and atrial fibrillation with rapid ventricular response
What is the therapeutic window of digitalis? What are toxic levels
1-2ng/mL is the therapeutic window.
Above 2.5ng/mL is toxic.
In digitalis toxicity, what drug can be given to rid the blood of digitalis?
Digibind (Monoclonal antibodies used to treat life threatening digitalis toxicity)
What drugs are contraindicated in Acute CHF?
Ca2+ channel blockers
They are vasodilators, but they have negative inotropic effects
