HF & Pulmonary Edema Flashcards
HF
-impaired ability of ventricle to fill or eject blood
HF Sx
dyspnea
fatigue
fluid retention (d/t lack of BF to kidneys –> RAAS goes into overdrive, Na is retained, thus water is retained)
One cause of HF
MI causes myocardial death –> nonfunctional tissue
Explain how pulmonary edema develops w/ L. HF
Blood pools in LV bc LV fails to eject blood through AV valve –> Blood gets backed up into LA and into pulmonary veins –> pulm edema
Predominant sx of L. HF
-sx of low CO and elevated pulmonary venous pressure
-dyspnea is predominant sx
Predominant sx of R. HF
fluid retention (specifically peripheral edema/positional edema of extremities)
HF classification
SYSTOLIC dysfunction (HFrEF): low EF (<40%), dilated LV (pumping problem)
DIASTOLIC dysfunction (HFpEF): preserved EF (>50%) and contractility, impaired filling of ventricles (filling problem)
*both lead to pulm congestion
HF Stages
Stage A: high risk but no structural abnormality
Stage B: structural abnormality but no sx
Stage C: structural abnormality w/ sx
Stage D: end-stage HF that is refractory to tx
Epidemiology of HF
-very common
-more common in men 60+, esp 80+ (women too at 80+)
Etiology (cause) of HF
-CAD causes 2/3 of cases (systolic HF)
-Non-ischemic causes: HTN, DM, valvular dz, arrhythmias, myocardial toxins (metals, chemo), myocarditis (commonly d/t virus), CT d/o, thyroid d/o
-Infiltrative causes: restrictive cardiomyopathy (diastolic HF) (amyloidosis-pr builds up in heart, hemochromatosis-iron builds up in organs, and sarcoidosis-inflamm & scarring of heart)
Acute decompensated HF (may be new or may be an exacerbation of chronic HF): Sx
DYSPNEA
orthopnea
paroxysmal nocturnal dyspnea d/t high LA pressure
Acute decompensated HF: Px findings
-displaced apical impulse (if HFrEF bc likely to have LVH)
-many signs have okay specificity but low sensitivity (if they have the finding, then they’re likely to have acute decomp HF, but if they don’t have the finding then it’s unknown): extra heart sounds (S3 w/ systolic or S4 w/ diastolic), hepatomegaly, rales, edema, high JVP
*worse prognosis if cool extremities, AMS, a low urine output, and a narrow pulse pressure
Acute Decompensated HF: Dx tests
-EKG
-Labs: CBC (anemia), BMP (kidney fxn, electrolytes), thyroid panel, iron (r/o hemochromatosis)
-CXR: pulm edema, enlarged heart
-ECHO: assess cause A (measures EF) - LVH, wall motion abnormalities, valvular abnormalities
-Cardiac catheterization if CAD is a possibility
cephalization of vessels
may see on CXR in pt w/ HF
-caused by pulmonary congestion causing blood to leak out of pulmonary veins
-looks like branching (“stag sign”)
Kerley B lines on CXR
-appear as horizontal lines (laterally)
-fluid accumulation around the septa (which is on top of pleura)
what can make BNP low
obesity
Acute decompensated HF: Natriuretic peptides
BNP and NT-proBNP are GOLD standard biomarkers for evaluation and management of HF
-should NOT be used in isolation to dx or exclude CHF
-more valuable than EKG, CXR, and other blood tests
*when there’s pressure/volume overload in the ventricles they will release BNP
*BNP causes vasodilation, natriuresis, diuresis, and decreases BP and the RAAS
HF drugs
ACE-I: decrease Na by blocking aldosterone, decrease myocyte hypertrophy, increase vasodilation by blocking angiotensin
Angiotensin receptor neprilysin inhibitors (ARNIs): Sacubitril/Valsartan (Entresto)
B-blockers: decrease NE (decrease symNS)
Aldosterone antagonists: decrease Na, NE uptake, and myocyte fibrosis
SGLT2 inhibitors: decrease Na, improve cardiac metabolism, prevent inflammation
Loop diuretics: freq used to quickly offload fluid
MOA of Sacubitril/Valsartan (Entresto)
Sacubitril (Neprilysin inhibitor) blocks ANP (decreased BP & cardiac hypertrophy) and BNP (decreases cardiac fibrosis) and BRADYKININ (increases vasodilation & vascular permeability)
Valsartan blocks angiotensin II
-decreases excess bradykinin (if bradykinin builds up it can lead to angioedema)
*if pt is on ACE-I you need to d/c and wash out before starting Entresto to avoid build up of bradykinin
Acute decompensated HF: Management/Tx
-try to give IV loop diuretics w/in the first hour (furosemide, bumetanide, torsemide
*monitor K & Mg (worry about arrhythmias), and BP
-ACE-I or Entresto (ideally)
-B-blockers
-Spironolactone
-SGLT2 inhibitors
*goal is to (eventually) get pt on all of these
-Inotropic agents (Dobutamine and milrinone) in those who have signs of hypoperfusion, such as neurologic or severe renal dysfunction, lactic acidosis, cool extremities, a narrow pulse pressure, or in those who fail diuresis
*wait to start certain meds in certain cases (ex. if pt is hypotension hold off on B-blockers or Entresto; ex. if hyperkalemic hold off on spironolactone)
Management of CHF w/ reduced EF
Similar to acute decompensation:
-ACE-I or Entresto (ideally)
-B-blockers
-Spironolactone
-SGLT2 inhibitors
(may be on a diuretic at home as well)
Other tx options, besides meds, for pt with CHF w/ reduced EF
-ICDs if NYHA II-III (class B or C) sx of HF + EF 30% or less
-Cardiac resynchronization therapy (w/ biventricular pacing) if QRS is 120msec+ (wide) (pts often receive combo of resynchronization device + ICD)
-Heart transplants
-LV assist devices (LVAD)
Management of HF w/ preserved EF (diastolic)
-control RFs: HTN, CAD, DM, HLD, smoking, alcohol ingestion, & use of cardiotoxic drugs
-Diuretics (loop, but if volume overload is mild then an SGLT2 inhibitor may work)
-SGLT2 inhibitor is often administered first
-spironolactone
-if pt has stable Cr and K levels on spironolactone, then start Entresto
pulmonary edema causes (2)
- increased capillary pressure (hydrostatic) - MI, severe HTN, AKI, volume overload, mitral stenosis
- increased capillary permeability
cardiogenic pulmonary edema
fluid accumulation in interstitial and alveolar spaces d/t increased LA/pulmonary vein pressure
RF for cardiogenic pulmonary edema
any condition that predisposes to acute decompensated HF is a RF: mitral regurgitation, aortic stenosis, arrhythmias, myocarditis, cardiomyopathy
diagnosis cardiogenic pulmonary edema (clinical features, dx tests)
Clinical features: breathlessness, tachypnea, signs of increased symNS activity (tachycardia, HTN, diaphoresis)
Dx tests:
-CXR (butterfly pattern of alveolar edema)
-ECHO
-BNP and NT-proBNP
what is the most practical and useful means of assessing and quantifying pulmonary edema
CXR:
1. upper lobe diversion (“cephalization” - can see branching of pulmonary veins d/t excess fluid, “stag sign”)
2. interstitial edema (“Kerley B lines”)
3. alveolar edema (“butterfly pattern”)
