CHF review Flashcards by Emily Hendrickson

Heart failure in women stats?

HF contributes to 35% of total female CVD deaths
women have more comordities - more HTN, valvular disease and thyroid dysfxn, less obstructive CAD, DM strong risk for CAD and HF in women, LVH increase RF for death in women
BNP over 500 more predictive of death in women
women w/ acute HF have more preserved EF (2x men), clinical course more benign
benefit more from CRT, donate 46% of tx heart and receive 36%, more complications w/ VAD implantation

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Definition of HF?

complex, heterogenous, and progressive syndrome characterized by structural and/or fxnl abnormalities in cardiac contraction, consequent adverse neuro-hormonal adaptations and remodeling and co-morbidities that collectively alter myocardial fxn, fluid regulation, respiration, and perfusion and overall hemodynamic stability

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Etiologies of HF w/ reduced EF?

non-myocardial: Valvular disease - AS, AR, MR, MS
high output: anemia, AV fistula
myocardial: HTN, CAD, DM, dilated cardiomyopathy, infiltrative myopathy

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Etiologies of of HF w/ preserved EF?

non-myocardial: valvular disease, postcardial constraint - constriction, tamponade
high output: anemia, AV fistula
myocardial:
HTN, CAD, diabetes, cardiomyopathy, ionfiltrative myopathy

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What are unusual causes of cardiomyopathy?

hypertrophic obstructive cardiomyopathy (HCM) - LV myocyte hypertrophy - genetic
AL amyloid cardiomyopathy - LVH w/o other causes - very poor prognosis
myocarditis - inflammatory disease from infectious or noninfectious process
Tachycardia induced cardiomyopathy - systolic or diastolic dysfxn due to rapid and/or irregular arrhythmia
Takotsubo cardiomyopathy: broken heart syndrome - transient apical ballooning syndrome post severe stress
peripartum cardiomyopathy - low EF heart failure in last month of preg to 5 months post delivery

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Co-morbid conditions assoc w/ HF?

up to 40% of HF pts have 5 or more chronic conditions -

anemia
gout
HTN
renal dysfxn
lung disease - sleep -disordered breathing
rapid or irregular dysrhythmias
diabetes
thyroid disorders

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Neuro-hormonal mechanisms and compensatory mechanisms in HF?

poor ventricular fxn/myocardial damage (post MI, dilated cardiomyopathy) -
leads to HF - this leads to decreased stroke volume and CO - this leads to neurohormonal response - this leads to activation of sympathetic sytem and RAAS - vasoconstriction, and sodium and fluid retention - increased vasopressin and aldosterone - this leads to further stress on ventricular wall and dilation (remodeling) - leads to worsening of ventricular fn - further HF

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2 diff types of remodeling inf HF?

hypertrophy (preserved EF heart failure) - LVEF over 50%

- dilation (reduced EF HF) - - LVEF less than 40%

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What is HFpEF?

increasing prevalence
HF sxs in those w/ LVEF over 50% or near normal LVEF (41-49%) - incidence about 50% of HF pt pop
clinical features of volume overload - decreased activity tolerance
morbidity/mortality nearly same as those w/ low EF heart failure
HFpEF almost always assoc w/ diastolic dysfxn -
diastolic dysfxn: increased LV wall stiffness and decreased compliance/impaired relaxation, decreased CO
pulmonary HTN almost always present, RV dysfxn equal to or greater than 25%

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3 stages of diastole?

isovolemic (active) relaxation and rapid early filling (reqr ATP)
diastasis (passive) filling: - dictated by how compliant the ventricle is, there is slowed LV relaxation and rise in LV diastolic pressure, stage worsens w/ age
active filling during atrial contraction, dependent on LV diastolic pressure
all phases affected by preload, afterload, HR and contractility: systolic flow greater than diastolic flow until diastolic dysfxn due to stiff ventricle and decreased atrial emptying

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Grading of diastolic dysfxn?

grade 1: impaired relaxation (suckers - normal DF and mild DD)
grade 2: pseudomonal, usually concomitant LAE, LVH, and/or decreased LVEF
grade III/IV: restrictive/constrictive - diff b/t III and IV is reversibility w/ medical therapy
(grade II, III/IV: pushers - impaired LV relaxation, increased LV stiffness, increased LA pressures

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What is cardiac remodeling - (HFrEF)?

dilation- compensate for poor cardiac output, ventricle dilates, becomes thinned and weakened
LVSD: impairment of LV myocardial contraction
EF less than 40%
decreased stroke volume
decreased cardiac output
backward failure due to decreased contractility, fluid buildup, engorgement of systemic veins
forward failure: secondary to inadequate cardiac output resulting in decreased perfusion to vital organs

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Definition of HFrEF?

EF: less than or equal to 40%

- also called systolic HF

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Definition of of HFpEF?

EF: 50% or greater, diastolic HF

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Definition of HFpEF, borderline?

41-49%

- outcomes similar to those of pts w/ HFpEF

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Definition of HFpEF, improved?

over 40%

- subset of pts w/ HFpEF previously had HFrEF.

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PP of arrhythmias?

weakened heart susceptible to arrhythmias
contribute to sxs and increased risk of sudden risk
AF: can lead to acute decompensated state, common cause of sxs - fatigue, dyspnea, especially in preserved EF pts
ventricular arrhythmias and bradycardia primary causes of syncope and sudden death
factors that contribute to arrhythmias: cardiac chamber enlargement, conduction system and anatomical heart abnormalities, adaptations of SNS, adverse responses to meds, electrolyte abnormalities

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HF disease progresion: ACC/AHA stages? Tx?

A: high risk - HTN, CAD, diabetes, family hx of cardiomyopathy - tx: HTN and lipids, smoking cessation, exercise, limit ETOH, ACEI
B: asx LVD: previous MI, LV systolic dysfxn, asx valvular diseaes - tx: plus ACEI, BB
C: sx HF: known structural heart disease, SOB and fatigue, reduced exercise tolerance - tx: plus ACEI, BB, diuretics, digoxin, aldosterone receptor antagonists, dietary salt restriction
D: refractory end stage: marked sxs at rest despite max medical therapy - tx: plus inotropes, transplant, VAD

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New York heart assoc fxnl classification?

class I: minimal (ordinary physical activity doesn’t cause undue sxs, no limitations)
class II: mild (ordinary activity causes sxs, no strenous exercise)
class III: moderate (less than ordinary activity causes sxs, activity limited to ADLs)
class IV: severe (sxs w/ any physical activity)

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CV status assessment involves what?

Broken down into 2 parts:

determination whether pt is wet or dry by assessing fluid status and congestion (indicates elevated filling pressure)
determination of whether pt is warm or cold by assessing indicators of perfusion
combo of these parameters equal 4 possible hemodynamic profiles

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Signs/sxs of congestion (wet) Heart failure:

orthopnea/PND
JVD
ascites
edema
rales (rare in HF)
S3
hepato-jugular reflex

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Possible evidence of low perfusion (cold)?

narrow pulse pressure
sleepy/obtunded
low serum sodium
cool extremities
hypotension w/ ACEI
renal dysfxn

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What questions should you ask in H and P?

SOB: at rest or exertion, waken you from sleep, increasing w/ daily activities now as opposed to 1 month ago, 6 months ago
cough:
is it productive, non productive, worse w/ exertion or when lying down, taking ACEI
CP: sharp, dull, stabbing, localized, radiating to jaw, teeth, arms, accomp by diaphoresis, SOB, N/V, w/ or w/o exertion
-palpitations: duration and description, accomp by dizziness, LOC, shock from ICD
dizziness, lightheadedness, syncope: does it occur w/ position changes, while bending over, accomp by palpitations, LOC
abdominal fullness: wt change, experiencing RUQ tenderness, feeling of pressure
dietary habits: is salt added to meals, processed meals, canned foods, restaurants
edema: resolve at noc, skin painful or seeping
sleep: able to lay flat, frequency of urination
mentation: diff thinking, concentration
substance abuse: smoking, ilicit drugs, ETOH
past disease/tx: recent infections, sxs, tx, rheumatic fever, chemo

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Dx testing for HF?

CXR
Lab (include BNP)
ECG
echo, MUGA, MRI (infiltrative)
risk stratification for CAD:
noninvasive imaging: nuclear stress test, stress echo
invasive imaging: cardiac cath
risk stratification for HF

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Lab testing done initially and as indicated?

renal fxn and electrolytes; magnesium
BNP (ni clinical uncertainty, to est prognosis/disease severity)
blood glucose: A1C
CBC w/o diff
TSH
serum albumin
LFTs
lipid panel
proteinuria, RBCs)
uric acid
CXR in suspected or new onset HF

Assoc BNP with probable HF?

pt presents w/ dyspnea - PE, CXR, ECG, BNP level

BNP: less than 100 - HF very improbable
100-500: clinical suspicion of HF or past hx of HF - 90%
BNP: over 500 - HF very probable (95%)

General management of HF?

stabilize pt w/ diuretic
stabilize disease: ACEI + BB
can also use digoxin to tx residual sxs if needed

Guidelines for diuretics use?

diuretics: used in sx pts to reduce fluid, no survival benefit
increase initial dose as necessary to relieve congestion. After effective diuretic is achieved w/ short acting loop diuretics, increasing admin to 2-3x a day may provide more diuresis w/ less physiologic upset than a larger single dose
torsemide and bumetanide which have higher bioavailability can be effective in pts w/ por absorption of oral meds or erratic diuretic effect, esp in right sided HF and refractory retention despite high doses of other loop diuretics
IV diuretics may be necessray to relieve congestion
add chlorthiadone or metolazone when high dose loop diuretic not effective - avoid chronic use
selected pts may be educated to adjust daily dose of diuretic in response to wt gain from fluid overload
diuretic refractoriness may represent pt non-adherence, a direct effect of diuretic use on kidney or profession of underlying cardiac dysfxn
observe for SEs including electrolyte abnormalities, sx hypotension, renal dysfxn, or worsening renal fxn

Use of ACEIs? Examples?

captopril, enalapril, lisinopril, ramipril
inhibits conversion of angiotensin I-II (dilates blood vessels and decrease SVR and BP)
reduces morbidity and mortality
improves cardiac fxn, sxs, and clinical status
all pts w/ LVEF less than 40% should receive an ACEI, ARBs used when intolerant of ACEI (Diovan, Atacand, losartan) for reasons other than hyperkalemia, renal insufficiency

CIs of ACEI/ARBs?

hx of intolerance, CI in pregnancy
serum K+ greater than 5 mEq/L
sx hypotension: asx SBP less than 80 or sx orthostatic BP when pt is euvolemic
caution in pts w/ Cr over 3.0 mg/dL

Surveillance for pts on ACEI/ARBs?

monitor BP, renal fxn and K+ w/in 1 wk of initiation of therapy and w/ med titration
modify Rx if increase in Cr of 0.5 mg/dL, if BUN/Cr increase less than 50%, maintain dose, if increases by 100% switch HYDZ/ISOS
assess vol status if pt develops renal insufficiency or hypotension
physicians/pt may need to toelrate mild to moderate renal insufficiency to maintain ACEI/ARB therapy

Use of BB in HF tx?

metoprolol XL, carvedilol, bisoprolol. toprol and zebeta may be better tolerated in pts w/ SBP
start when pt isn’t significantly congested - titrate q 2 wks, slower titration may be required
1st line therapy:
increase LVEF
global sx improvement
decrease hosp and mortality
decrease sympathetic tim: antiarrhythmic activity benefit
all pts w/ stable HF w/ LVEF less than 40% should receive a BB, beneficial in those w/ or w/o DM2 or CAD, ok use in COPD, PAD

SEs w/ BB up-titration?

coreg: vasodilator SEs:
usually temporary, sep dosing of BB and ACEI, if persistent, reduce vasodilators
fluid retention:
increase diuretic to restore baseline wt, delay up titration until wt is at baseline
bradycardia/AV block:
check dig level, if persistent, consider cardiac pacing

When is digoxin useful?

beneficial in pts w/ HFrEF, to decrease hospitalization for HF, no survival benefit
HF pts w/ AF, BB therapy usually more effective than digoxin in controlling ventricular rate, especially during exercise
don’t give in sig sinus or AV block unless pt has permanent pacemaker
reduce digoxin dose by 1/2 when used w/ amiodorone or BB therapy
lean body mass and impaired renal fxn can increase dig levels, toxcity may occur w/ lower dig levels w/ hypokalemia, hypomagnesmia, or hypothyroidism
## most often dose should be 0.125 mg qd

Use of Hydralazine/Nitrates?

Isosorbide dinitrate: NO donor, large and small artery dilator, venous dilator
Hydralazine: antioxidant (inhibits destruction of NO), arteriolar dilator, NO enhancer
combo of HYDZ/ISOS recommended to improve outcomes:
african-americans w/ HFrEF NYFC III-IV HF on optimal therapy w/ ACEI/ARB, BB
non-african american pts w/ HFrEF who remains sx despite optimized therapy
non african-americans, HYDZ/ISOS can be useful to decrease morbidity or mortality in pts w/ current or prior sx HFrEF who cannot be given ACEI/ARB b/c hypotension, renal insufficiency, unless CI

Use of aldosterone antagonists?

aldosterone has adverse effects on cardiac structure and fxn
low dose spironolactone/eplerenone (aldosterone antagonist) reduces mortality in moderate to severe heart failure pts
addition of aldosterone antagonist recommended in NYHA-FC II-IV and EF less than 35% who can be carefully monitored for renal fxn and normal K+ level

PT selection for aldosterone antagonists?

pt already on ACEI/ARB and BB therapy
K+ less than 5, Cr less than 2.5 in men and 2.0 in women
aldosterone antagonist in absence or concomitant loop diuretic not recommended
monitor renal fxn and K+
diarrhea or other cause of dehydration should be addressed urgently, stop aldosterone antagonists during dehydration or while loop diuretics is interrupted

WHat is Entresto? Indications, MOA?

new CHF drug
decreases CV deaths and morbidity from HF
indication: chronic HFrEF, HYHA-FC II-IV, used w/ other HF meds in place of ACEI or ARB
MOA: sacubitril - inhibits breakdown of vasoactive peptides including BNP, bradykinin - results in natriuresis, diuresis
valsartan: ARB, antagonizes angiotensin II at ATI recepotr, decrease in ATII dependent aldosterone release, increase vasodilation
monitor: BP, vol status, BUN/SCr
adverse effects: decrease in BP, hyperkalemia, cough, dizziness, ARF, angioedema

What is Corlanor? Indications? CI, SE?

just approved in 04/15
reduces slow diastolic depolarization phase
indications:
reduce risk of hospitalization for worsening HFrEF
SR w/ HR resting of over 70 bpm on max BB or CI for BB use
CI: ADHF, BP: less than 90/50, SSS, SA block, CHB, HR resting of less than 60, severe hepatic impairment
relative CI: negative chronotropes - amiodarone, digoxin, increased bradycardia
SE: AF, bradycardia, HTN, dizziness, fatigue, CHB

Other meds used for CHF?

vasodilators (nitro)
inotrope infusion:
dobutamine: stim B-adrenergic receptors, can’t be used w/ B blcokers, dopamine: NE release, promotes diuresis on receptors in renal vasculature
anticoag
dysrhythmics
lipid management, omega 3
screen for sleep disordered breathing

Managing co-morbidities of HFpEF dysfxn?

control BP (less than 130/80)
rate control in AF
alleviation of MI
managemnt of DM2
screen for sleep disordered breathing
Na+ restriction

Tx for R sided heart failure?

O2 therapy: increase RV fxn (SV), decrease RV after load, increase survival
inhalers: CPAP if indicated
digoxin: tx for rhythm problems that occur in R atria
diuretics
R sided HF often accompanied w/ preserved LV heart failure, occasionally low LVEF heart failure
tx sfor pulmonary HTN

Drugs that may hurt HF?

antiarrhymic drugs increase arrhythmias and negative inotropic affects (amiodorone doesn’t have these effects)
megestrol acetate - may exacerbate HF
NSAIDs, including COX2 inhibitors, ibuprofen, indocin
corticosteroids - cause Na and fluid retention, Dexamethasone causes min Na retention and may be safer alt

Early intervention: surgeries and medical devices for HF?

CABG, TAVR
cardiac transplantation
CRT (bi ventricular pacing)
ICD
LVAD - destination or bridge

VADs characteristics?

device sufficient to replace/assist pumping fxn of LV, rx for end stage HF
heartmate, Jarvik, heartware
MRI CI
continuous flow like water out of hose
narrowed or no pulse pressure
in case of emergency - get LVAD running if not, CPR can only be done if LVAD not running and cant be started
defibrillation can be done
complications: arrhythmias, RHF, hypovolemia, bleeding, infection, thrombus/stroke

Recommended Na restriction?

Na homeostasis alt in HF pts
HFrEF: study showeed lower Na intake assoc w/ worse outcomes in pts w/ HFrEF
HTN, LVH and CVD: 1500mg/day for most pts, stage A and B HF
stage C and D: less than 3 gm/day for sx improvement
food processing contains majority of the source of salt

Fluid restrictions for HF pts?

limit fluids in hyponatremic pts (gen 130 mg/dL or less)
common recommendation - 6-8 cups/day
any food that melts at room temp is considered a fluid
gelatin desserts, and frozen deserts (melted less vol than frozen)

Sleep disordered breathing assoc w/ HF?

75% of HF pts have poor sleep pattern
SDB: cheyne stokes - Central sleep apnea - CSB-CSA:
consequence of HF, more common in decompensated HF, more common in men, AF, HFrEF, white, ischemic
OSA:
possible cause of HF, more common in HFpEF (50%)
linked to increased CV morbidity and mortality
RFs: obesity, male gender, post menopausal women, neck larger than 16 inches, in men and 15 in women
CSB-CSA and OSA often co-exist - exacerbate MI, increase risk for arrhythmias (AF, ventricular arrhythmias, and SCD), fatigue, excessive daytime sleepiness, mood disturbance, decrease daytime FC, may decrease QOL, may worsen cog fxn, CSB-CSA not assoc w/ cognitive decline

Use of CPAP - in tx of SDB?

can be beneficial to improve heart fxn and fxnl status in HF pts w/ sleep apena
decrease apnea-hypopnea index, increase nocturnal O2, increase LVEF, decrease NE levels, increase 6 min walk test distance
berlin questionnaire: screen for SDB

Wt correlation w/ HF?

HF pts w/ BMI 30-35 kg/m2 -lower mortality, morbidity than normal range
wt loss:
cachexia - predicts worse prognosis, wt loss of more than 5% in 12 months or BMI of less than 20 w/ muscle wasting, fatigue, anorexia, anemia, low albumin, increased inflammation markers
morbidly obese pts may have worse outcomes
U shaped distribution curve suggested - mortality greates in cachectic pts, lower in normal, overt, and mildly obese pts and higher in severely obese pts

Exercise for HF pts?

exercise training (or regular physical activity) is recommended as safe/effective for pts w/ HF who are able to participate to improve fxnl status
cardiac rehab can be useful in clinically stable HFrEF (less than 35%) pts to improve fxn; capacity, exercise duration, QOL, mortality
stop exercise: rapid pulse, CP/pressure, unusual SOB, irregular or slow HR, weakness, faintness or dizziness, extreme fatigue

Possible mechanisms through which HF self care influences health outcomes?

neuro-hormonal deactivation: maintenacne of optimal vol, effectiveness of meds: NE, RAAS
limited inflammation: decrease in shear mechanical stress, decrease in tissue ischemia, decrease in TNF, CRP
avoidance of pharm: decrease likelihood of high dose diuretics, BB reduction
limited myocardial hibernation - decreased wall tension, decreased ischemic events, increased sub endocardial perfusion, increased myocardial viability

Self care for HF?

meds: take, don’t stop
follow lower Na diet: ADA. low fat diet, know how to shop, cook, eat out, adapt family customs
monitoring sxs of worsening HF: sx recognition and what to do/whom to call, which sxs are impt, when to act w/ sxs escalation
daily weighing
phsyical activity
alcohol, smoking, fluid intake

When should hosp be considered w/ CHF?

worsened congestion even w/o dyspnea
signs and sxs of pulmonary or systemic congestion even in absence of wt gain
major electrolyte disturbance
assoc comorbid conditions (pneumonia, PE, diabetic ketoacidosis)
sxs suggestive of TIA or stroke
Repeated ICD firings
previously undx HF w/ signs/sxs of systemic or pulmonary congestion

Emergency department care for CHF?

challenges: many co-morbidities
SOB pie: pneumonia, influenza, COPD, HF
tx: O2, lasix, nitrates, inotropes, admission

MOA of basic HF drugs?

diuretics: reduce fluid vol
vasodilators: decrease preload and or afterload
inotropes: augment contractility

Top 3 predictors of mortality for pts admitted w/ acute CHF?

BUN, SBP, SCr

When can HF pt leave hosp?

near optimal volume: stable wt, VS, adequate urine output, absence of crackles, S3, edema, HR under 100
stable after transition from IV to oral diuretics for at least 24 hrs
exacerbating factors addressed (non-adherence w/ diet, meds)
LVEF documented
near optimal med therapy - ACEI, BB, diuretic
pt and family ed initiated
FU clinic visit scheduled ideally w/in 7 days after d/c
additional criteria for advanced HF: no IV vasodilator or inotropic agents in 24 hrs, stable on oral meds for 24 hrs, ambulation b/f discharge, plan for post-d/c management at home

What are the factors that put HF pts at highest risk for readmission?

advanced age
comorbidities: renal disease, DM2, COPD, HF severity, psych dx (esp depression), frailty
low education/literacy level
prior admissions for HF
pt behaviors: lacking self care skills, adherence issues, substance abuse
not ready for D/C
absence of friends, family, religious, social, and financial support, access to transportation

What are the 3 phases of progressive HF?

chronic disease management: dx, focus on extended survival, concurrent palliation of sxs, promoting self care (NYFC I-III)
supportive and palliative care phase: approp when pts reqr recurrent hospitalizations, focus on promoting comfort and QOL, palliation of sxs and advanced care planning (NYFC III-IV)
terminal care phase: pt has poor response despite max appropriate intervention (renal insufficiency, hypotension, fatigue, cachexia, diuretic resistance), focus on clarificaiton of tx decisions, advanced directives, comfort, QOL, support pt, family, prep for EOL and bereavement

What are barriers to use of palliative care? Proposed Model of palliative care?

traditional model of medicine: cure and comfort are mutually exclusive, EOL discussions uncommon until days b/f death, half of DNR orders were written w/in 24 hrs of death
proposed integrated model of palliative care:
focus on sxs dosen’t preclude cont aggressive tx of disease
illness progresses, palliative care assumes larger role, is replaced w/ hospice at EOL
continues w/ bereavement care for survivors

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CHF review Flashcards

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