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Heart Failure, a more comprehensive tx plan = less HF + CV death (so we…
Heart Failure
8. Pharm Management
beta blockers
start low, go slow
improves LVEF, decreases mortality; but a/e of fatigue (usually improves over time)
bisoprolol, carvedilol
, metoprolol succinate (first two are preferred)
c/I: cariogenic shock, decompensated heart failure
do not stop BB abruptly, due to risk of rebound HTN and arrythmia
monitor: lightheadedness, fatigue, HF sx, claudication, sexual dysfunction, BP and HR, fluid assessment
MRAs
decreases mortality and hospitalizations (RALES, EMPHASIS-HF)
gynecomastia a/e as well as ED and menstrual irregularities (
spironolactone
)
spironolactone 50mg qd, eplerenone 50mg qd
acts on brain, blood vessels, heart and kidneys
decreases SNS, helps with endothelial dysfunction, decreases inflammation in the heart, helps with electrolyte imbalances in kidneys
c/I: hyperkalemia, eGFR <30, major liver dysfunction
monitor: lightheadedness, K, eGFR, BP (minimal impact)
NOT BEING USED AS A DIURETIC: IT IS BEING USED FOR ITS MULTI-ORGAN EFFECTS
RAAS inhibition (ACEi/ARB/ARNI)
HFrEF
c/I: angioedema, pregnancy, renal artery stenosis, systole < 90
monitor: BP, K, SCr, cough (is it due to the ACEi/ARNI or was it there before?); fluid status with ARNI, lightheadedness
ARNI > ACEi
ARNI
= sacubitril/valsartan;
target dose of 200mg BID
converting from ACEi to ARNI:
stop ACEi for 36h
, then start ARNI
converting from ARB to ARNI: stop ARB, start ARNI when next dose is supposed to be due
even tho these are BP lowering drugs, BP is NOT the target here, HF is. dizziness is common in first 2 weeks; switch to ARB if ACEi is causing bothersome cough
SGLT2i
lowers hospitalizations and CV Death (actually adds up to 2 years to your lifespan)
monitor: volume status, genital infections (tx with anti fungal; prevented by having good hygiene and glycemic control), BP, fluid assessment, eGFR
works regardless of diabetes status
lowers preload/afterload and hypertrophy and fibrosis in the heart
c/I: T1DM, ketoacidosis, eGFR <20, be careful if you're also using insulin
dapagliflozin 10mg qd, empagliflozin 10mg qd (NO TITRATION NECESSARY) ✅
diuretics (not specific to one type of HF)
loop
: furosemide, bumetanide
metolazone (used in diuretic resistance); sometimes works a bit too good and can lead to volume depletion
for rapid sx relief of fluid retention
only
monitor: sx of hypo/hypervolemia, BP, electrolytes, SCr,
weight
, d/I with digoxin and lithium
decrease preload by decreasing Na and water retention, thereby decreasing peripheral and pulmonary edema
in acute decompensated HF, the dose-response curve of loop diuretics shifts down and to the right, meaning we have to dose these diuretics
at a higher dose
than normal to have the desired effect
caution with over-diuresis as it can lead to a low Cardiac output and hypotension; as cardiac output decreases, SCr increases so be careful
sx improvement in 1-2 hours; pedal edema (ankles) takes longer to resolve
others
ivabradine
if HR > 70, and maxed on beta blockers
hydralazine + nitrates
for Black pts or ACEi intolerance
iron therapy if deficient
digoxin
for A-Fib or sx control if maxed on other meds, also indicated for HFrEF in sinus rhythm despite max doses of other meds
c/I: Wolff-Parkinson-White syndrome, AV block
monitor: bradycardia, toxicity (can lead to hyperkalemia), hypokalemia (can lead to toxicity), SCr
7. Non-Pharm Management
daily weighing to see if fluid retention is going away
more than 2lbs in 24hrs or 5lbs in 1 week = fluid retention
exercise
fluid restriction (2L/d)
vaccines: flu, pneumonia, COVID, RSV
sodium restriction (2-3g/d)
smoking/alcohol cessation
6. Treatment Goals
decrease hospitalizations
improve QofL and sx
reduce mortality
reduce morbidity
general approach: fluid assessment ➡️ disease modification (depends on type of HF) ➡️ risk reduction nonpharm
4. Diagnosis
signs: crackles, high JVP, S3
investigations to identify what type of HF it is
BNP/NT-proBNP
elevated plasma concentrations of these (>500) can be used in diagnosis and monitoring
they are naturally produced by the heart as a way to regulate BP, so in heart failure they will be elevated bc the body is trying to help you out
good for ruling out HF, but should not be used alone to diagnose it (need signs/sx and echo as well)
echo
tells you size/shape of heart, how well it can pump; the structure of the heart (helps with causes of HF)
sx: dyspnea, orthopnea, fatigue
rule out non-HF causes
is it HF? what type of HF is it? what is the underlying cause? how can we tx it?
11. Monitoring and Titration
BP, HR, weight, sx
start with low dose, titrate every 2-4 wks to max dose usually (reached in 3-6 months)
labs: K, SCr, eGFR
sick day protocol for RAASi and SGLT2i (SADMANS)
when SGLT2i and ACEi/ARB/ARNI are combined, there is risk of low kidney perfusion as they both dilate efferent arteriole but SGLT2i can constrict afferent arteriole
if SCr goes up too high or eGFR drops below 30, stop using any NSAIDs, and decrease SGLT2i/ACEi/ARB/ARNI dose; might also need to decrease diuretic dose or increase fluid intake
Classification
by EF
HFmrEF: LVEF 41-49%
HFpEF: LVEF >50
usually an older female
usually results in non-CV death
HFrEF: LVEF <40%
usually a younger male after having a heart attack
usually results in CV death
keep in mind you need both LVEF AND sx/signs to classify it as HF for sure
we usually ADD medications if classification of LVEF changes; but we usually don't REMOVE medications as the classification changes
by duration
chronic
acute on chronic (decompensation)
acute
output
low out put: metabolic demands are normal, but the heart can't meet them
high out put: metabolic demands are high, and heart can't meet them
anatomy
right sided HF: blood is not properly pumped from right ventricle
biventricular: both ventricles can't pump blood properly
left sided HF: blood is not properly pumped from left ventricle
1. Definition of HF
ventricular filling (diastole) or ejection (systolic) dysfunction
types: HFrEF, HFpEF, HFmrEF
clinical syndrome of low cardiac output
9. Device Therapy
CRT indications: EF < 35%, QRS > 130, LBBB
LVAD/transplant: advanced HF
ICD: primary prevention in HFrEF
monitors rhythm, and delivers electrical shock
5. Risk and Exacerbating Factors
drugs: NSAIDs, CCBs, steroids, alcohol
infections, anemia, thyroid disorders
age, HTN, MI, angina, DM, A-Fib, valvular disease, FHx, hyperlipids, LVH, COPD
10. HFpEF/HFmrEF tx
HFmrEF: consider HFrEF meds
ACEi/ARB/ARNi, BB,
MRA, SGLT2i
(for sure this one)
role of ARNI and BB is unclear
in Canada, there's no evidence for anything yet except SGLT2i
HFpEF:
SGLT2i
, sx management with diuretics, manage comorbidities
ARB, MRA, GLP1, SGLT2i (for sure)
in these types of HF, nothing reduces death
2. Pathophysiology
Frank-Starling Curve
ability of the heart to alter force of contraction based on changes in preload (stretching)
a
high
ventricular volume =
high
contractility =
high
stroke volume
chronic maladaptive responses (fluid retention, hypertrophy)
low cardiac output (low BP) --> compensatory mechanisms are:
SNS (sympathetic nervous system) activation
ventricular remodelling
RAAS activation
a more comprehensive tx plan = less HF + CV death (so we want to actually be giving as many drugs as we can, and keep them lifelong)