HF & Pulmonary Edema

Question 1

HF

Answer 1

-impaired ability of ventricle to fill or eject blood

Question 2

HF Sx

Answer 2

dyspnea
fatigue
fluid retention (d/t lack of BF to kidneys –> RAAS goes into overdrive, Na is retained, thus water is retained)

Question 3

One cause of HF

Answer 3

MI causes myocardial death –> nonfunctional tissue

Question 4

Explain how pulmonary edema develops w/ L. HF

Answer 4

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

Question 5

Predominant sx of L. HF

Answer 5

-sx of low CO and elevated pulmonary venous pressure
-dyspnea is predominant sx

Question 6

Predominant sx of R. HF

Answer 6

fluid retention (specifically peripheral edema/positional edema of extremities)

Question 7

HF classification

Answer 7

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

Question 8

HF Stages

Answer 8

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

Question 9

Epidemiology of HF

Answer 9

-very common
-more common in men 60+, esp 80+ (women too at 80+)

Question 10

Etiology (cause) of HF

Answer 10

-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)

Question 11

Acute decompensated HF (may be new or may be an exacerbation of chronic HF): Sx

Answer 11

DYSPNEA
orthopnea
paroxysmal nocturnal dyspnea d/t high LA pressure

Question 12

Acute decompensated HF: Px findings

Answer 12

-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

Question 13

Acute Decompensated HF: Dx tests

Answer 13

-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

Question 14

cephalization of vessels

Answer 14

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”)

Question 15

Kerley B lines on CXR

Answer 15

-appear as horizontal lines (laterally)
-fluid accumulation around the septa (which is on top of pleura)

Question 16

what can make BNP low

Answer 16

obesity

Question 17

Acute decompensated HF: Natriuretic peptides

Answer 17

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

Question 18

HF drugs

Answer 18

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

Question 19

MOA of Sacubitril/Valsartan (Entresto)

Answer 19

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

Question 20

Acute decompensated HF: Management/Tx

Answer 20

-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)

Question 21

Management of CHF w/ reduced EF

Answer 21

Similar to acute decompensation:
-ACE-I or Entresto (ideally)
-B-blockers
-Spironolactone
-SGLT2 inhibitors
(may be on a diuretic at home as well)

Question 22

Other tx options, besides meds, for pt with CHF w/ reduced EF

Answer 22

-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)

Question 23

Management of HF w/ preserved EF (diastolic)

Answer 23

-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

Question 24

pulmonary edema causes (2)

Answer 24

1. increased capillary pressure (hydrostatic) - MI, severe HTN, AKI, volume overload, mitral stenosis
2. increased capillary permeability

Question 25

cardiogenic pulmonary edema

Answer 25

fluid accumulation in interstitial and alveolar spaces d/t increased LA/pulmonary vein pressure

Question 26

RF for cardiogenic pulmonary edema

Answer 26

any condition that predisposes to acute decompensated HF is a RF: mitral regurgitation, aortic stenosis, arrhythmias, myocarditis, cardiomyopathy

Question 27

diagnosis cardiogenic pulmonary edema (clinical features, dx tests)

Answer 27

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

Question 28

what is the most practical and useful means of assessing and quantifying pulmonary edema

Answer 28

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”)