heart failure with reduced ejection fraction HFrEF

what is ejection fraction

stroke vol / end-diastiolic volume *100

• so like left vent fills up with a 100 mLs, but can only pump out 60 mL, would be 60%

what is gdmt

guideline directed medical therapy

what is stage a and stage B

stage A— describes risk

stage B— pre-HF without HF symptoms

what can make prognosis worse for mortality in HFF (rEF)

• greater symptom burden

• recent or recurrent HF hospitalizations

• renal dysfunction

• higher or persistently elevated BNP

  • comordbities like CAD or DM

in HFrEF which side of heart is enlarged

left ventricle

• systolic heart failure

  • a pumping/getting things out probelm

which one is systolic heart failure

HFrEF

• bc its a contraction problem (when ventricle contracts and ejects blood)

valve from right atria to ventricle called?

tricuspid

valve from right ventricle to lungs

pulmonary valve

valve from left ventricle out called?

aortic

valve from right atria to ventricle called?

mitral

what is stenosis ? how does this effect ventricle function?

narrowed valve opening

• forces ventricle to generate higher pressure to force blood through a smaller space

• this means ventricle becomes overgrown with thick walls

what is regurgitation ? how does this effect the ventricle?

when a valve lets some blood leak backwards

• increases the volume that gets stuck in teh ventricle

• causes ventricle to get overgrown also

track blood flow!

vena cava— right atria— r vent—lungs (get oxigenatized)— left atria— left vent— through aorta— to the body

which side is oxygenated

left side!

which node causes atria to contract into ventricle

SA node

what does concentric vs eccentric hypertrophy mean

concentric— muscle does thicker, making pumping chamber smaller (pressure overload)

• eccentric — (volume overload)— ventricle is overstretched, like over filled balloon

what does diastolic dysfunction mean

preserved ejection fraction

• ventricle is stiff

why does CAD/CHD cause HFrEF

arteries to the heart are narrowed, so muscle is weaker

• cannot pump as much

why do MIs or ACS cause HFrEF

bc lack of perfusion means heart does not get enough perfusion so muscle dies and cannot pump out more

describe what besides ischemia can cause HFrEF

• viral myocarditis — killing heart

• drug-induced— elicit drug use, alcohol, chemo — all toxic to heart muscle

• postpartum cardiomypotathy

what causes pressure overload that leads to HFrEF

HTN esp in lungs

• stenosis in aortic valve (left side out to body) or pulmonic

what causes voluemen overload

• shunts— rando vessels that lead into heart

• valvular regurgitation

what are causes of HFpEF

anything causing muscle hypertrophy

• HTN— so much pressure ot overcome

• hypertrophic cardiomyopathy— genetic disease— massively thick ventricular wall— heart just doesn’t stop growing

  • could be from valve

what is pericardial dsiease

disease sthat interfere with teh sac around the heart

what side of heart failure is normally treated

left-sided

what is most common cuase of RIGHT sided heart failure

LEFT sided heart failure lol

what effects preload (which bigger prelaod means bigger SV)

• venous return

  • filling time

what effects contractility (which bigger means bigger stroke volume)

SNS innervation

horomones

what effects afterload (which if bigger means smaller stroke volume )

vasodilation or contriction

how is contracility related to ESV (end of systolic volume )

the more you contract th emore you get out so ESV will be smaller

what is storke volume equation

end diastoilc volume (how much you took in) MINUS end systolic volume

what is units of cardiac output

volume of blood eeject per unit time (L/min)

• Co= HR*SV

equation for ejection fraction

SV / EDV *100%

(recall sv= edv-esv)

factors taht affect heart rate

1. PNS — vagus nerve hits sa/av to release Acetylcholine and decreases heart rate

2. SNS— epi and NE binds mainly to B1 receptors in heart causing positive inc in heart rate and enhancing contracilty

what does inc in heart rate called

positive chronotropy

what inc in contractility caleld

positive inotrope

what are the THREE BIGGEST THINGS effecting stroke volume

1. preload— degree of stretch of cardiac muscle fibers at end of diastole

2. conttactility — force with which teh heart muscle contracts

3. afterlaod— resistance heart must overcome to eject blood during systolic

waht does frank-starling law mean

more heart fills with blood, harder it has to squeeze (as EDV goes up, stroke volume goes up)

example of negative chronotrophy

non-dhps

when are natriuretic peptides released

when heart is toooo stretched, ie to counteract RAAS, to get off some fluid

when is ANP vs BNP released

• ANP— atrial nat pep— whne blood volume incrased, fluid overlaod

• BNP— rleased from ventricles when ventricle is stretched (heart failure, volume overload, ventricle filling pressures)

what effects do natriuretic peptides have on the body

• vasodilation

• blood pressure, SNS tone, aldosterone levels

what are the three steps or phases in journey to HFrEF

1. insult— left ventricle damaged (like MI damages heart, HTN causes overload, etc)

2. compensation— heart tries to maintain cardiac output

3. decompensation— the compensation no longer helping— SOB/fatigue manifests

what is a way we can decrease preload

diuerteitcs

• less end-diastolic volume so less you hvae to overcome

list four compensatory mechs in HFrEF

1. increase preload through RASAS

2. vasoconstriction

3. tachy and increased contract

4. ventricular hypertrophy and remodelling

cardiac output is dropping so the body is trying to fix it!

benefits of compensatory RAAS increase? bad effects

• increase SV bc frank-starling mechs

• preload stretches the ventricle so can’t pump effctively, leading to congestion/back up in lungs, edema

what stimualtes release of aldosteron

release of ang 2!

• more Na/h20 retention

ANG 2 is huge vasoconstrictor

what are some exmaples of vasodialtors that reduce afterload

hydralazine, nitrates, dhps

why would vasoconstriction be helpful compensate and what goes wrong

• maintain BP despite reduced CO, gets blood mostly to essential organs

  • increased heart oxygen demand, increased afterload making everything worse

why owuld tachy and more contract be helpful compens? why bad?

• maintains CO

• increases oxygen demand, shortens diastolic filling time, increaes risk of cardiac cell death

ventricular hypertrophy and remodelling why beneficial compen and why NOT

• maintain CO reduces myocardial wall stres

• diastolic dysfunction, systolic dysfunction, icnreased risl of ischemia, fibrosis

in heart failure do you want to inc/dec preload?

decreaseeee too much fluid

in heart failure do you want to inc/dec contractility?

increaseee the power the heart has

in heart failure do you want to inc/dec afterload?

decreaseee what you have to overcome

what meds affect preload

diueretics, RAAS meds, sglt2 inhibitors, nitrates bc they prevent stuff getting back to the heart

• goal is DEC

what meds affect contractility

IV inotropes, digoxin

• goal is INC

what meds affect afterload

raas, nitrates, ccbs, bbs (the non-selective ones that also dilate veins)

• goal is DEC

what is the neprilysin inhib

sacubitril

• increases half -life of nat peptides

why do we want to decrease NE? what drugs we use to decrease NE?

• decrease NE bc it increases intracellular Ca, which is cardiotox to myocytes

• drugs:beta blockers

what do we want to decrease ang 2? what drugs do that?

• vasoconstricts, keeps Na/h20

• drugs:aceis, arbs, can be arni

should we use alpha blockers for HTN and heart failure

NO increased mortality and increase in heart failure

why do we not want to have aldosterone

• cause Na/H20 retention

• drugs: minearlocorticoid receptor antagonists (spironolactone, eplerenone)

do we want to increase or decrease nat peps? what drugs do that

you want to increase be stops raas, promotes vasodilation

• drugs: sacubitril!

what is NT-proBNP

a precursor to BNP so they directly related

what one drug also has some alpha action and is ok in heart failure

carvedilol

what are meds we KNOW redcrease remodelling

beta blockers to decrease NE/epi

Aceis, arbs, aldosterone antaga: decrease ang 2/aldosterone

ARNI: INCREASE nat peps

what are arnis/example

sacubitil/neprilysin inhib/ its in entresto

what are the heart failure bbs— HFrEF ONLY

• carvediolol

• metoprolol succinate

• bisoprolol

what are the nonselective b-blockers

• NOT bammin

• prop, nad, tim, pin, sota

what classic clinical presentation of HFrEF

• SOB (esp with exertion, orthopnea or hard to breath when lie down)

  • orthopbea— how many pillow are you sleeping on

• fatigue

• fluid overload— crackles on lung baes

• intolerance of daily-life activities

do diuertics reduce HF mortality? do sglt-2 i’s reduce mortality?

diueretics— NO

sglt-2i’s— YES

what are some main drugs to remember are disease modifying (not just symptom control)

aceis, arbs, arnis, bbs, sglt-2is, aldosteorne antags

is dig. disease modifying

no

what does systemic congestion look like

peripeheral edema

wet gain

jugular venous distension

noctuira

ascites

hepatic congestion

constipation

how does pulmonary congestion present

dyspnea

orthopnea

nocturnal dyspnea (paraoxymyasl— off and on)

nagging cough

wt gain

pulmonary edema

cehyne-stokes repsiration

does nat pep diagnose? what are elevated values for nt vs BNP

NO

• NT BNP— 125

• BNP 35

what is valuea t least or under which is HFrEf value ejection fraction

under 40!

what does BNP stand for

brain-type natriuretic peptide

where is BNP released from

ventricular myocytes

• esp in response to stress related injury

• from volume overload

what is the recommendation releated to BNP lab

use to EXCLUDE a diagnosis or SUPPORT diag of HEART FAIL

• as side quest, can alos be used to establish prognosis

what would need to diag HF

echo

• then BNP

range for LVEF for HFmEF

41-49%

• recall this represents how much blood left in left ventricle

range for HFpEF

>50%

• recall this represents how much blood left in left ventricle

what can falsely elevted BNP

• BW— higher BW have LESS BNP

• RENAL dysfunction— it is renally elminated so could stick around

• AFib

cardiac MRI why would be used

clarify EF when echo unclear— shows were heart injury might be

MUGA scan why would be used

tracks EF over tme

what is nucelar stress test /why used

evaluate ischemia and calcuate EF, valuves can differ from ECHO

sacubitril how effects BNP

INCREASES— blcoks neprilysin that degrades BNP

what are two types of echo?

• transthoracic — NONinvasive on chest

• transesophagela — INVASIVE in throat

which type of echo is first line

transthoracic

• meavues LVEF

  • assess heart structure

why would we need to be invasive and use transesophageal

• valve abnormalities

• suspected endocarditis

  • intracardiac thrombus

what does HFimpEF mean

impvoed EF

• was <40% , now over 40%

DIFFERENT THAN HFpEF— need to know if this is a follow up or not

what is stage A for HF

AT RISK

• no current OR PAST s/s

  • HTN, DM, obesity, cardiotox, genetic variant

what would qualify you for stage A (at risk for HF?)

HTN, CVD, DM, obesity, cardiotoxic agents, genetic variant for cardiomyopathy

what is stage B HF?

without current or previous s/s but evidence of one of these three things!:

1. strucutral heart dsiease

2. evidence of increased filling pressures

3. risk factors— increased BP or elevated cardiac troponin

what is stage C

symptomatic heart failure

• pts with current OR PREVIOUS s/s

what is stage D HF

marked HF symptoms that prevent daily activites

what stages would HF (mr, r, or p) EF include? what about HFimpEF?

stages B-C

• stage C

what does NYHA stand for

new york heart assocation functional class

NYHA class 1

no limitation