11/14 Heart Failure - Almendral Flashcards

1
Q

heart failiure

A

result of myocardial muscle dysfx or loss

  • can be systolic, diastolic, or mixed → leads to neurohormonal and circulatory abnormalities
  • progressive, often fatal
  • stabilization → myocardial dysvx and remodeling may improve (spontaneous or as consequence of tx

symptoms:

  • fluid retention
  • shortness of breath
  • fatigue, esp on exertion’

severity of sx can vary substantially during course of disease

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2
Q

course of HF

A
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3
Q

NYHA functional classes

vs

stages of heart failure

A

functional classes can move up and down

stages only move in one direction

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4
Q

Stage A-D

A

A: high risk for HF without structural heart disease or sx

  • HTN
  • atherosclerotic HD
  • diabetes
  • obesity
  • metabolic syndrome
  • family hx of cardiomyopathy

B: structural heart disease without devpt of HF

  • prior MI
  • depressed LV ejection fraction
  • LVH
  • asymptomatic valvular HD

C: structural heart disease with CURRENT OR PRIOR symptoms

D: end-stage HF

refractory sx requiring special intervention like:

  • inotropes
  • LVAD
  • transplant
  • hospice
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5
Q

normal EF

A

EF = ejection fraction = fraction of blood ejected by ventricle relative to its end diastolic volume

normal EF > 50-60%

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6
Q

cardiac output

A

CO = SV * HR

heart rate

  • influenced by SNS and PSNS

stroke volume

  • influenced by preload, contractility, afterload
    • incr preload → incr stretch → incr SV
    • incr afterload → more impedance to flow → decr SV
    • contractility: indep of preload/afterload, influenced by chem/neurohormonal factors
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7
Q

heart failure

distinguish between factors that cause preserved IF and reduced EF

A

preserved EF

  • impaired diastolic filling
    • LVH
    • restrictive CM
    • myocardial fibrosis
    • transient ischemia
    • pericardial constriction
    • tamponade

reduced EF

  • incrased afterload
    • aortic stenosis
    • severe HTN
  • impaired contractility
    • CAD
    • chronic volume overload
    • dilated CM
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8
Q

HF with reduced EF

A

(HFrEF)

LVEF < 40-50%

  • dereased capacity to eject blood
  • due to decr contractility
    • myocyte loss
    • incr fibrosis
    • abnormal systolic fx
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9
Q

HF with preserved EF

A

(HFpEF)

LVEF > 5%

abnormal diastolic fx due to :

  • incr stiffness (passive)
  • impaired relaxation (active)

incr diastolic pressures are transmitted retrograde to pulmonary and systemic veins → HF sx

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10
Q

RV failure

A

RV is thin-walled and more compliant

  • accepts wide rane of volumes without significant change in filling pressures
  • ejects to low resistance system (pulmo circuit) → not used to high afterload!
    • most common cause of RV failure = LV failure
    • other causes: lung processes (COPD, PE, etc)

symptoms of right sided failure:

  • leg edema
  • abdominal bloating
  • ascites
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11
Q

compensatory mechanisms in heart failure

A
  1. Frank-Starling mechanism
    • decr contractility → decr SF → incr LV end diastolic volume → incr stretch → incr contractility!
  2. Neuro-hormonal activation
    • components:
      • sympathetic nervous system (SNS)
      • renin-angiotensin-aldosterone system (RAAS)
      • anti-diuretic hormone (ADH)
    • serves to maintain perfusion to vital organs by effecting:
      • incr SVR
      • incr intravastular volume
    • acute effects = good, chronic effects = deleterious
      • incr volume → congestion
      • incr vasoconstriction → incr afterload → decr CO
      • incr Ang II and incr aldosterone → incr cytokines, fibroblasts → cardiac fibrosis
  3. Natriuretic peptides (ANP, BNP)
    • respond to stretch →
      • incr Na and water excretion!
      • promotes vasodil
      • inhibits renin secretion
    • good mech but usually not sufficient :(
  4. Ventricular hypertrophy and remodeling
    • reduces wall stress and maintains contractlity
    • myocardial hypertrophy + ECM deposition → incr wall thickness (reduction in wall stress)
    • incr thickness → incr stiffness → incr diastolic pressure
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12
Q

neurohormonal activation:

SNS activity

A

role of SNS in HF is to increase activity

incr SNS, decr PSNS output to heart and periphery

  • incr HR, incr contractility, incr vasoconstriction
  • alpha receptor distribution in periphery aids with peripheral vasoconstriction → maintenance of central perfusion!
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13
Q

neurohormonal activation:

RAAS activity

A
  • decrease in CO → decr renal perfusion → incr reninrenin cleave antiogensinogen to Ang I, which can then be converted into Ang II [ACE[
  • Angiotensin II
    • potent vasoconstrictor (incr SVR)
    • thirst stimulator
    • incr aldosterone →incr Na retention → incr volume
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14
Q

neurohormonal activation:

ADH activity

A
  • ADH is secreted by posterior pituitary
    • mediated by arterial baroreceptor and AngII
  • fx: incr water retention in distal nephron
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15
Q

sx of left sided HF

A
  1. congestion
  2. low output
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16
Q

sx of right sided HF

A
17
Q

physical findings in…

L sided HF

R sided HF

A

left sided HF

  • cardiac cachexia, tachypnea, tachycardia
  • rales, decreased breath sounds
  • diffuse apical impulse
  • S3/S4, mitral regurg murmur
  • weak pulse

right sided HF

  • RV heave
  • right sided S3/S4
  • incr JVD, hepatic enlargement
  • ascites, leg edema
18
Q

diagnostic studies in HF

chest film

A

CXR

  • upper zone vascular redistribution
  • pleural effusions
  • cardiomegaly

see others in slide

19
Q

management of HFrEF

tx (medication) for HFrEF

A
  1. sx relief
  2. ID of underlying cause
  3. recog of precipitant for HF decompensation
  4. long-term modulation of neuro-hormonal response
  5. prolong survival
  • diuretics
  • vasodilators
  • inotropes
  • beta-blockers
  • aldosterone antagonists
20
Q

HFrEF tx:

diuretics

A

mechanism: water and Na elimination

  • decr intravascular volume
  • decr diastolic volume → decr congestion

*use judiciously! overdiuresis can lower CO even more

most potent = loop diuretics

less potent, additive = thiazides

21
Q

HFrEF tx:

vasodilators

A

venous vasodilators (ex. nitrates)

  • incr venous capacitance
  • decr LV preload

arteriolar vasodilators (ex. hydralazine, prazosin)

  • decr SVR/afterload
    • incr CO, incr BP!
22
Q

HFrEF tx:

ACEI and ARBs

A

ACEI (ACE inhibitors)

  • decr: Ang II, aldosterone
  • incr: bradykinins
  • limit maladaptive remodeling
  • improve survival

ARBs (Ang II receptor blocker)

  • total inhibition of Ang II, no effect on bradykinins
  • similar efficacy and survival benefit as ACEI

hydralazine/nitrates

  • alternative if intolerant to ACEI, ARB
23
Q

HFrEF tx:

inotropes

A

inotropes

beta-agonists: dobutamine, dopamine

PDE inhibitor: milrinone

  • no oral form!
  • long term use is ltd by tolerance

digoxin

  • IV or oral
  • blunts SNS drive, slows AVN conduction
  • inhibits Na/K ATPase → incr intracellular Ca
  • improves sx, reduces hospitalizations
  • no effect on survival
24
Q

HFrEF tx:

aldosterone antagonists

A

spironolactone and eplerenone

  • blunt cardiac fibrosis and remodeling
  • incremental survival venefit as add-on treatment

need to moitor K level, side effects

25
Q

HFpEF

A

no real treatment options

general recs:

  • volume control
  • bp control
  • rate/rhythm control
  • revascularization if needed
  • address comorbidities
26
Q

R sided HF keys

A

usually due to LV failure → use HF tx

if due to cor pulmonale → address pulmonary issues

avoid overdiuresis, might drop preload

last resort: inotropes

27
Q

acute decompensated HF

A

look at:

  • congestion at rest
  • low perfusion at rest
28
Q

acute decompensated HF

wet and warm

A
  • makes up majority of patients
  • DIURESE THEM
    • if they fail to response do diuretics: increase dose, Na and fluid restriction, add another diuretic
    • if no hypotension, can use IV vasodilators!
  • keep on beta blockers and other home meds
29
Q

acute decompensated HF

wet and cold

A
  • IV inotropes if..
    • low EF and low CO syndrome with
      • marginal bp less than 90mm Hg
      • unresponsive to vasodil
      • poor response to diuretics
      • worsening renal fx
30
Q

acute decompensated HF

dry and cold

A
  • usually don’t get admitted unless they’re at end-stage
  • make sure they’re not too dry
  • vasodilators if BP is ok
  • inotropes if BP is low
31
Q

acute decompensated HF

dry and warm

A
  • stable chronic HF
  • want to double check to make sure they are not wet
    • if theyre actually dry, then their sx are from something else
32
Q

acute decomp heart failure keys

A

treatmend depends on hemodynamic status

  • mainstay: IV diuretics
  • if low output: vasodilators and inotropes
  • address precipitating factors, optimize meds once stable