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FA CARDIO 3 > HFrEF > Flashcards

HFrEF Flashcards

1
Q

Etiologies of HFrEF

A

Loss of myocardium (MI, CAD)

Pressure overload (Chronic HTN, valvular dz)

Dilated cardiomyopathy (hyper metabolic, toxin exposure)

Myocarditis

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2
Q

HFrEF Epidemiology

A

HTN (women) and CAD (men)

45% of heart failure, not as many hospitalizations but worse prognosis

60% 5 year mortality rate

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3
Q

alterations in ventricular size and geometry causes secondary to:

A

valvular insufficiency (papillary muscle rearrangement)

subendocardial ischemia (decreased diastole = decreased coronary perfusion)

myocardial fibrosis (easier to develop arrhythmias)

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4
Q

cardiac renal anemia syndrome

A

decreased CO causes renal hypoperfusion

elevation in cytokine levels and bone marrow resistance to erythropoietin = anemia

increased plasma volume = worsening LV hypertrophy = cardiac dysfunction

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5
Q

myocardial stunning

A

ischemic events caused by prolonged systolic dysfunction

hours or days after event stops

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6
Q

myocardial hibernation

A

sustained reduction in blood flow = only enough to maintain viability but not enough to maintain normal contractility

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7
Q

myocyte apoptosis

A

combo of hibernation and stunning

progression of LV systolic dysfunction and reduced EF/CO

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8
Q

compensatory mechanisms heart uses (5)

A
  1. Frank Starling Law
  2. RAAS
  3. Norepinephrine
  4. ADH
  5. Vasodilator peptides/BNP
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9
Q

Frank Starling Law compensation in HF

A

excessive workload on heart causes normal cells to hypertrophy to increase contractile force

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10
Q

RAAS compensation in HF

A

afferent arterioles in kidneys respond to changes in arterial pressure via sympathetic release of renin to increase pressure

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11
Q

angiotensin II compensation in HF

A

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

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12
Q

norepinephrine compensation in HF

A

increases HR and contractility

eventually B-receptor density decreases so this compensation fails

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13
Q

ADH compensation in HF

A

simulated by norepinephrine and angiotensin II accumulation

increased water retention in kidney

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14
Q

BNP compensation in HF

A

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

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15
Q

s/s of congestion

A 
Pulmonary edema 
orthopnea 
PND
hepatojugular reflex 
pulmonary rales and wheezing
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16
Q

s/s of impaired perfusion

A 
fatigue/sleepiness
cool extremities 
narrow pulse pressure
low sodium 
increased CR
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17
Q

Left Sided HF symptoms

A 
Fatigue
mental status change
narrow pulse pressure
worsening renal function
dyspnea
pulmonary edema
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18
Q

R sided HF

A 
JVD
hepatomegaly
anorexia
weight gain
ascites/anasarca/peripheral edema
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19
Q

cardinal symptoms

A

dyspnea and fatigue that occur with exertion and/or at rest

may see acute pulmonary edema

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20
Q

PND

A

supine position, causes choking and air hunger

must sit upright to regain control

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21
Q

orthopnea

A

dyspnea within minutes after assuming supine position

affected patients sleep upright

22
Q

fatigue

A

due to low CO and muscle atrophy

increased numbers of easily fatigued fast twitch fibers

23
Q

Cardiac Cachexia

A

abdominal fullness decreases food intake

elevated norepinephrine causes increased metabolism and skeletal muscle atrophy

24
Q

physical exam findings (9)

A

cardiac cachexia

increased sympathetic activity

pulmonary rales

pleural effusions

pitting edema

stasis dermatitis

anasarca

JVD

S3

25
Q

Lab work up

A 
CBC
BMP
LFTs 
TSH/T3/T4
BNP/Troponin
26
Q

Diagnostic studies (7)

A

CXR

Echo

CPET

Cardiac Cath

Cardiac MRI

Endomyocardial Bx

genetic testing

27
Q

CXR

A

cardiac silhouette
pulmonary vasculature

cardiomegaly, interstitial and perivascular edema
kerley lines
pleural effusion

28
Q

echocardiogram

A

cardiac structure and function

cardiac component of HF symptoms

29
Q

CPET

A

measures pea kO2 consumption and slope of ratio of ventilation

peak VO2 <50% = LVAD

30
Q

major criteria of Framingham (9)

Wipes Poop

A

(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

31
Q

minor criteria of framingham (7)

cheap tp

A

(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

32
Q

NYHA

type I

A

no symptoms and no limitations with ordinary physical activity

SOB with exertion (i.e. climbing stairs)

33
Q

NYHA

type II

A

mild symptoms (mild SOB and/or angina) and slight limitations during ordinary activity

34
Q

NYHA

type III

A

moderate limitations in activity due to symptoms

even during less than ordinary activity (walking short distances, comfortable at rest)

35
Q

NYHA

type IV

A

severe limitations

experiences symptoms even while at rest

36
Q

AHA/ACC

stage A

A

@ risk of developing HF by no symptoms of structural dz

tx: weight reduction, smoking cessation, avoid cardiotoxins, control DM, lipid, HTN, AFib

37
Q

AHA/ACC

stage B

A

structural disease w/o overt symptoms

tx: addition of anti-HTN agents

38
Q

AHA/ACC

stage C

A

structural heart disease WITH overt symptoms

tx: non pharm interventions (lifestyle) + diuretics

39
Q

AHA/ACC

stage D

A

HF that req special interventions

tx: A + B + C + inotropes (digoxin), devices (ICD, CRT)m mechanical support, transplant

40
Q

pharm tx

A
  1. ACE
  2. ARB
  3. Beta Blocker
  4. Diuretics
  5. Aldosterone Agents
  6. Inotropes
  7. Angiotensin receptor-neprilysin
41
Q

ACEs used (3)

A

Enalapril (Vasotec)

Lisinopril (Zestril)

Ramipril (Altace)

42
Q

ACE HF tx

A

first line

se: cough, angioedema, hyperkalemia, hypotension

43
Q

ARBs used (3)

A

Iosartan (Cozaar)

Valsartan (Diovan)

Candesartan (Cilexetil)

44
Q

Beta blockers used (4)

A

Carvedilol (Coreg)

Metoprolol (Lopressor)

Bispropanolol (Zebeta)

Propranolol (Inderal)

45
Q

BB use in therapy

A

ONLY in HFrEF I, II, III

ci: severe HF, acute decompensated HF, cardiogenic shock, COPD

46
Q

Diuretics

A

Spironolactone (Aldactone)

Eplerenone (inspra)

Triamterene (Dyrenium)

47
Q

Inotropes drug name

A

Digoxin (lanoxin)

48
Q

Digoxin use

A

rate control in HF + AF, late stage (C, D) tx

improves contractility and systolic fxn

49
Q

digoxin CI/special considerations

A

CI: prior Tach or VFib

caution in pEF bc promote calcium influx= worsening of diastolic

50
Q

adjunct therapies (5)

A
  1. CABG/PCI
  2. CardioMEMs
  3. Ultrafiltration
  4. Heart Transplant
  5. LVAD

FA CARDIO 3 (5 decks)

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