HFrEF Flashcards
Etiologies of HFrEF
Loss of myocardium (MI, CAD)
Pressure overload (Chronic HTN, valvular dz)
Dilated cardiomyopathy (hyper metabolic, toxin exposure)
Myocarditis
HFrEF Epidemiology
HTN (women) and CAD (men)
45% of heart failure, not as many hospitalizations but worse prognosis
60% 5 year mortality rate
alterations in ventricular size and geometry causes secondary to:
valvular insufficiency (papillary muscle rearrangement)
subendocardial ischemia (decreased diastole = decreased coronary perfusion)
myocardial fibrosis (easier to develop arrhythmias)
cardiac renal anemia syndrome
decreased CO causes renal hypoperfusion
elevation in cytokine levels and bone marrow resistance to erythropoietin = anemia
increased plasma volume = worsening LV hypertrophy = cardiac dysfunction
myocardial stunning
ischemic events caused by prolonged systolic dysfunction
hours or days after event stops
myocardial hibernation
sustained reduction in blood flow = only enough to maintain viability but not enough to maintain normal contractility
myocyte apoptosis
combo of hibernation and stunning
progression of LV systolic dysfunction and reduced EF/CO
compensatory mechanisms heart uses (5)
- Frank Starling Law
- RAAS
- Norepinephrine
- ADH
- Vasodilator peptides/BNP
Frank Starling Law compensation in HF
excessive workload on heart causes normal cells to hypertrophy to increase contractile force
RAAS compensation in HF
afferent arterioles in kidneys respond to changes in arterial pressure via sympathetic release of renin to increase pressure
angiotensin II compensation in HF
myocyte hypertrophy, apoptosis, intercostal fibrosis, promotion of fibroblasts proliferation and collagen deposits
this is when RAAS compensation goes bad, results in stiffening of ventricles and arteries
norepinephrine compensation in HF
increases HR and contractility
eventually B-receptor density decreases so this compensation fails
ADH compensation in HF
simulated by norepinephrine and angiotensin II accumulation
increased water retention in kidney
BNP compensation in HF
vasodilator peptide
released by heart during HF to stimulate vasodilation and reduce pressures (RA, pulmonary a., pulmonary v.)
more common in rEF
release stimulates vascular resistance and CO, eventually overwhelmed by RAAS and norepinephrine
s/s of congestion
Pulmonary edema orthopnea PND hepatojugular reflex pulmonary rales and wheezing
s/s of impaired perfusion
fatigue/sleepiness cool extremities narrow pulse pressure low sodium increased CR
Left Sided HF symptoms
Fatigue mental status change narrow pulse pressure worsening renal function dyspnea pulmonary edema
R sided HF
JVD hepatomegaly anorexia weight gain ascites/anasarca/peripheral edema
cardinal symptoms
dyspnea and fatigue that occur with exertion and/or at rest
may see acute pulmonary edema
PND
supine position, causes choking and air hunger
must sit upright to regain control
orthopnea
dyspnea within minutes after assuming supine position
affected patients sleep upright
fatigue
due to low CO and muscle atrophy
increased numbers of easily fatigued fast twitch fibers
Cardiac Cachexia
abdominal fullness decreases food intake
elevated norepinephrine causes increased metabolism and skeletal muscle atrophy
physical exam findings (9)
cardiac cachexia
increased sympathetic activity
pulmonary rales
pleural effusions
pitting edema
stasis dermatitis
anasarca
JVD
S3
Lab work up
CBC BMP LFTs TSH/T3/T4 BNP/Troponin
Diagnostic studies (7)
CXR
Echo
CPET
Cardiac Cath
Cardiac MRI
Endomyocardial Bx
genetic testing
CXR
cardiac silhouette
pulmonary vasculature
cardiomegaly, interstitial and perivascular edema
kerley lines
pleural effusion
echocardiogram
cardiac structure and function
cardiac component of HF symptoms
CPET
measures pea kO2 consumption and slope of ratio of ventilation
peak VO2 <50% = LVAD
major criteria of Framingham (9)
Wipes Poop
(1) Weight loss on diuretics (> 10 lb in 5 days)
(2) Increased venous pressure > 16 cm H2O (assessed via a central line)
(3) Pulmonary rales
(4) Elevated jugular venous pressure
(5) S3 gallop
(6) Pulmonary edema on CXR
(7) Observe Hepatojugular reflux w/ JVD
(8) Overlapping & enlarged heart silhouette on consecutive CXR
(9) Paroxysmal nocturnal dyspnea or orthopnea
minor criteria of framingham (7)
cheap tp
(1) Cough at night
(2) Hepatomegaly
(3) Exertional dyspnea
(4) Apparent B/L extremity edema
(5) Pulmonary vascular engorgement on CXR
(6) Tachycardia > 120 bpm
(7) Pleural effusion on CXR
NYHA
type I
no symptoms and no limitations with ordinary physical activity
SOB with exertion (i.e. climbing stairs)
NYHA
type II
mild symptoms (mild SOB and/or angina) and slight limitations during ordinary activity
NYHA
type III
moderate limitations in activity due to symptoms
even during less than ordinary activity (walking short distances, comfortable at rest)
NYHA
type IV
severe limitations
experiences symptoms even while at rest
AHA/ACC
stage A
@ risk of developing HF by no symptoms of structural dz
tx: weight reduction, smoking cessation, avoid cardiotoxins, control DM, lipid, HTN, AFib
AHA/ACC
stage B
structural disease w/o overt symptoms
tx: addition of anti-HTN agents
AHA/ACC
stage C
structural heart disease WITH overt symptoms
tx: non pharm interventions (lifestyle) + diuretics
AHA/ACC
stage D
HF that req special interventions
tx: A + B + C + inotropes (digoxin), devices (ICD, CRT)m mechanical support, transplant
pharm tx
- ACE
- ARB
- Beta Blocker
- Diuretics
- Aldosterone Agents
- Inotropes
- Angiotensin receptor-neprilysin
ACEs used (3)
Enalapril (Vasotec)
Lisinopril (Zestril)
Ramipril (Altace)
ACE HF tx
first line
se: cough, angioedema, hyperkalemia, hypotension
ARBs used (3)
Iosartan (Cozaar)
Valsartan (Diovan)
Candesartan (Cilexetil)
Beta blockers used (4)
Carvedilol (Coreg)
Metoprolol (Lopressor)
Bispropanolol (Zebeta)
Propranolol (Inderal)
BB use in therapy
ONLY in HFrEF I, II, III
ci: severe HF, acute decompensated HF, cardiogenic shock, COPD
Diuretics
Spironolactone (Aldactone)
Eplerenone (inspra)
Triamterene (Dyrenium)
Inotropes drug name
Digoxin (lanoxin)
Digoxin use
rate control in HF + AF, late stage (C, D) tx
improves contractility and systolic fxn
digoxin CI/special considerations
CI: prior Tach or VFib
caution in pEF bc promote calcium influx= worsening of diastolic
adjunct therapies (5)
- CABG/PCI
- CardioMEMs
- Ultrafiltration
- Heart Transplant
- LVAD
