Heart Failure Flashcards
Primary signs/sxs of HF
tachycardia, decreased exercise tolerance, SOB, cardiomegaly, peripheral/pulmonary edema
Compensatory responses in HF
increased SNS activity, increased preload, vasoconstriction, ventricular hypertrophy/remodeling
What are the 2 goals of treatment of HF
- reduce sxs and slow progression as much as possible
- manage acute episodes of decompensated failure
Pharmacological tx for stage C HF with reduced EF?
Renin-Angiotension System Inhibition with ACE-I or ARB or ARNI
ARNIs should not be given to pts who…
are taking an ACE-I
those with hx of angioedema
Ivabradine can be beneficial to which pts?
Can reduce HF hospitalizations for pts with symptomatic stable chronic HFrEF who are receiving max dose of BB and are in NSR
What is recommended in additional to standard HF therapy in African American pts?
venodilator: hydralazine Isosorbide Dinitrate
MOA of Ivabradine
prolongs diastolic time by selectively and specifically inhibiting the Icurrent within the HCN channel, reducing HR
Side effects of Ivabradine
dizziness, fatigue
less common: increase BP, visual light disturbances, Afib
contraindications for Ivabradine
acute decompensated HF, BO <90/50, sick sinus syndrome, AA block, severe hepatic impairment, PPM dependent
Avoid use of Ivabradine with…
strong CYP3A4 inhibitors
Define systolic dysfunction
reduced mechanical pumping action and reduced EF
Define diastolic dysfunction
stiffening and loss of adequate relaxation —> reduction in filling and CO (EF may be norm)
What are the 4 stages in the ACC/AHA heart failure staging system?
Stage A: Pt at high risk for developing HF
Stage B: Pt with structural heart disease but no HF
Stage C: Pt with structural heart disease + current or hx of HF sxs
Stage D: refractory HF requiring specialized interventions
Therapies used in chronic systolic HF
diuretics, aldosterone antagonist, ACE-I, ARBs, BB, cardiac glycosides, vasodilators, resynchronization/CCV
Therapies used in acute HF
diuretics, vasodilators, beta agonists, bipyridines, natriuretic peptide, LVAD
What lab marker can be used to predict the prognosis and classification of HF?
BNP
Na/K ATPase inhibitors- example? MOA?
Digoxin
increases Ca, increase cardiac contractility (Chronic HF)
Renal sodium transporter inhibitor- example? MOA?
Furosemide, Spironolactone, other diuretics
reduce preload and afterload (acute and chronic HF)
ACE-I: example? MOA?
Lisinopril
reduce preload and afterload, reduce remodeling
Vasodilators: example? MOA?
Nitroprusside, Nitroglycerine
reduce preload and afterload
acute HF
Phosphodiesterase inhibitors: example? MOA?
Milrinone
vasodilation, increase contractility (acute HF)
Natriuretic peptide: example? MOA?
Nesiritide
vasodilation reduces preload and afterload; some diuretic effect (acute HF)
HCN:example? MOA?
Ivabradine
slows HR
(chronic stable worsening HF)
Where in the nephron does Furosemide act?
loop diuretic
decreases NaCl and KCl reabsorption in the thick ascending loop of henle
Loop diuretic (Furosemide) toxicities?
hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity
avoid in those with sulfa allergy
What will happen if you give a higher dose of Furosemide than what is included in the usual range (20-160mg)?
it is not likely that there will be an additional response.
HCTZ MOA?
decreases NaCL reabsorption in the distal convoluted tubule
same effect Furosemide but not as strong
When should you prescribe HCTZ?
in mild chronic HF, mild-mod HTN, hypercalciuria
HCTZ toxicities? contraindications?
hyponatremia, hypokalemia, hyperglycemia, hyperurecemia, hyperlipidemia
sulfa allergy
What should you monitor in patients on HCTZ?
glucose, uric acid, electrolytes
Name an Aldosterone Antagonist. MOA?
Spironolactone
blocks aldosterone receptors in collecting tubules of nephron -> increases Na and water excretion, reduces remodeling, reduces mortality
When should you use an Aldosterone antagonist (Spironolactone)?
in chronic HF
also: aldosteronism, HTN
Really good bc it reduces remodeling
Aldosterone Antagonist toxicities?
hyperkalemia, antiandrogen actions (i.e gynecomastia), renal toxicity
How can you reduce the risk for hyperkalemia with Aldosterone Antagonists?
Start slow and make sure they have a Cr clearance so that the drug can be cleared
Avoid K+ supplements, avoid foods high in K+, avoid NSAIDS
monitor Cr
~need to give this drug carefully but can be very beneficial
Effects of ACE-I
arteriolar and venous dilation, reduces aldosterone secretion, reduces cardiac remodeling
Clinical applications for ACE-I?
Chronic HF, HTN, diabetic renal disease
ACE-I side effects?
cough, hyperkalemia, angioedema
Avoid use with: other angiotensin antagonist
When should you use an ARB? side effects?
When pt can’t tolerate ACE-I
hyperkalemia, angioedema
Name a ANRi (Angiotensin Receptor Naprilosin Inhibitor)
Savubitril/valsartan (Entresto)
What should you discontinue before starting pt on ANRi?
ACE-I (at least 36 hrs before starting)
BB example? MOA?
Carvedilol
blocks B1 receptors and alpha1 receptors –> slows HR, reduces BP
When should you use a BB?
in chronic HF, slows progression
BB side effects?
bronchospasm, bradycardia, AV block, acute cardiac decompensation
Name 3 Vasodilators
Veno: Isosorbide Dintrate, Hydralazine Isosorbide Dinitrate,
Arterial: Hydralazine
Isosorbide dinitrate MOA?
releases nitric oxide- activates guanylyl cyclase -> venodilation: reduces preload and ventricular stretch
Side effects of isosorbide dinitrate?
postural hypotension, tachycardia, HA
Effect of Hydralazine?
reduces BP and afterload: results in increased CO
Side effects of Hydralazine?
tachycardia, fluid retention, lupus like syndrome
What class of drug is Nitroprusside in? MOA?
Vasodilator
rapid powerful vasodilation reduces preload and afterload
When should you use Nitroprusside?
acute severe decompensated failure
Nitroprusside toxicities?
excessive hypotension, thiocyanate and cyanide toxicity
Can you give Nitroprusside over several days?
NO! Its metabolism causes cyanide
Name a cardiac glycoside, MOA?
Digoxin
Na/KATPase inhibition results in reduced Ca expulsion and increased Ca stored in SR –>
increases cardiac contractility, cardiac parasympathomimetic effect??
When can you use Digoxin?
chronic sxs HF
rapid ventricular rate in AFib
Side effects of Digoxin?
N/V/D
cardiac arrhythmias
Digoxin dose should be lowered in which pts?
elderly, those with low lean body mass, impaired renal func.
Effects of Digoxin on ECG: therapeutic dose, toxic dose?
increases PR interval, decreased QT interval
tachycardia, fibrillation, arrest at really high dose
Name 2 Beta Adrenoceptor Agonists
Dobutamine, Dopamine
Dobutamine MOA?
beta1 selective agonist–> increases cardiac contractility
only use in acute HF
Dobutamine toxicities?
arrhythmias
Dopamine MOA?
dopamine receptor agonist –> increased renal blood flow, higher doses increase cardiac force and BP
When can you use Dopamine?
Acute decompensated HF and shock
Dopamine toxicities?
arrhythmias
additive effect with sympathomimetics
Name a bipyridine, MOA?
inamrinon, milrinone
phosophodiesterase type 3 inhibitors- decreased cAMP breakdown—> vasodilators, lower PVR and increased cardiac contractility
When can you use bipyridines? toxicities?
acute decompensated HF
( increases mortality in chronic HF)
arrhythmia
Name a natriuretic peptide, MOA?
Nesiritide
activates BNP receptors, increases cZGMP–> vasofilation and diuresis
When can use a natriuretic peptide? toxicities?
acute decompensated failure
renal damage, hypotension, may increase mortality
Ivabradine is a…
HCN I-f inhibitor
When can you use Ivabradine?
when pt has sxs of HF that are stable
normal HR, taking a BB at highest dose tolerated
How should you treat class A HF?
No sxs but risk factors:
Treat obesity, HTN, DM, hyperlipidemia, etc.
How should you treat class B HF?
sxs with severe exercise:
diuretic, ACEI/ARB, BB
How should you treat class C HF?
sxs with marked or mild exercise:
diuretic, ACEI/ARB/BB +
aldosterone antagonist, Digoxin, CRT, hydralazine/nitrate
How should you treat class D HF?
drugs from class A-C
transplant, LVAD
