Heart Failure

all HFrEF

BP, renal function and potassium 1-2 weeks after initiation or dose change

hyperkalemia, hypotension, renal impairement, angioedema and cough

once pattient is stable on ACEI

monitor BP, HR, sx for HoTM, bradycardia and dizziness

stage C

blocks the effects of aldosterone in the kidneys, heart and vasculature

spironolactone and eplerenone

hypokalemia

mental confusion, diarrhea, cramping, gynecomastia, ED

reduce salt and water retention
inhibits Na+ reabsorption in the ascending loop of henle

furosemide bumetanide, torsemide

ototoxicity, electrolyte imbalance (Na, K), glucose control, urinary retention

HCTZ, chlorthalidone and metolazone

electrolytes (Na, K)

stage C heart failure

arterial vasodilator --> decreases afterload
increase effect of nitrates through antioxidant mechanism

stimulates norepinephrine signaling endothelium
venous vasodilator --> decreases preload

patients who cannot tolerate ACEI or ARBs
african americans in class III or IV

volume depletion and hypotension

h/a and hypotension

HFrEF and perisstent or worsening symptoms despite adequiate treatment regimen with first line drugs

prodrug metabolized to an active metabolite that inhibits neprilysin, increase natriuretic peptide concentration

all HFrEF

all HFrEF

monitor for hypotension, dizziness or cough
lab studies for hyperkalemia

MOA: reversible inhibition of SGLT-2 in the proximal tubule of the kidney which decreases reabsorption in the proximal convoluted tubule of the kidney causing glycosuria and polyuria

HFrEF in class II-IV

dapagliflozin
empagliflozin

dehydration
weight loss
hypotension
GFR

UTI
genital infection
dehydration
weight loss
DKA

CKD
recurrent UTIs

continuous IV ionotropic support as a bridge to transplant or mechanical circulatory support

digoxin
diuretics

HFrEF with perisistent symptoms despite treatment with first line meds

positive inotropic and negative chronotropic effects
increase of intracellular sodium concentrations because of Na+/K+-ATPas inhibition
increases force of myocardial contractions

renal impairement
potassium
magnesium
serum creatinine
calcium

GI anorexia
d/n/v
CNS and other apathy
confusion
diziness
h/d
mental disturbances
visual disturbance
gynecomastia

ivabradine

slows the firing of the SA node which reduces HR

If all are present:
class II-III
stable HFrEF less than or equal to 35%
sinus rhythm with HR of greater than or equal to 70 at rest on maximum tolerated bb dose

atrial fibrillation
bradycardia
strong CYP3A4 interactions

nausea
vomiting
abdominal pain

weakness
confusion

hyperkalemia

bradycardia
heart block
arrhythmias

blurred vision
photophobia
yellow hallows around light

no

no change in BP
raises HR and cardiac output

HF
cardiogenic shock
cardiac stress testing

tachycardia and arrhythmias

chronotropic effects at lower doses
vasoconstriction at higher doses

tachycardia

nitric oxide induced stimulation of GC to convert GTP to cGMP

warm and wet ADHF
alternative to inotropes in cold and wet ADHF
hypertensive crisit

hepatically metabolized
renally excreted

hypotension
thiocyanate and cyanide toxicity

Recombinant B type natriuretic peptide binds to natriuretic peptide receptor A to stimulate guanylate cyclase and production of cGMP

warm and wet ADH
alternative to inotropes in cold and wet ADHF

natriuretic peptide receptor C

hypotension and tachycardia

combines with sufhydryl groups in vascular endothelium to create S-nitrosothiol compounds that mimic nitric oxide's stimulation of guanylate cyclase and productions of cGMP

wet and warm ADH
ACS
hypertensive crises

renally

hypotension
reflex tachy
h/a
tachyphylaxis

inhibits phosphodiesterase 3 intracellular enzyme

acute heart failur or chronic heart failure

arrhthmias
thrombocytopenia
liver enzyme changes
tachycardia
ventricular arrhythmias

severe obstructive cardiomyopathy
ventricular aneurysm
hypovolemia
tachycardia

selective vasopressin 2 receptor antagonist

no