10: Pathophysiology of Heart Failure Flashcards

1
Q

What is the effect of the valsalva maneuver?

A
  • ↑intrathoracic pressure –> ↓venous return –> ↓preload
  • ↓intensity of most heart murmurs
  • ↑intensity of MVP, HTCM murmurs
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2
Q

What is capacitance?

A

Volume at a specified pressure; the slope at that point is stiffness = 1/compliance

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3
Q

What is arterial elastance?

A
  • Ea = ESP/SV
  • Ea = HR*TPR
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4
Q

What is the basic pathophysiology of heart failure?

A
  • Myocardial insult/stimuli/damage causes pump dysfunction.
  • Pump dysfunction activates neurohormones:
    • Catecholamines
    • Angiotensin II
    • Cytokines
  • Heart remodels by hypertrophy, fibrosis and apoptosis
  • Process cycles
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5
Q

Describe the neurohormonal activation in heart failure.

A
  • Initial fall in LV performance –> ↑wall stress
  • Activates RAS and SNS
  • Remodeling and progressive worsening of LV function leads to arrhythmias, pump failure, death
  • Fibrosis, apoptosis, hypertrophy, cellular/molecular alterations, myotoxicity
  • Peripheral vasoconstriction, sodium retention and hemodynamic alterations lead to heart failure Sx:
    • Fatigue
    • Activity altered
    • Chest congestion
    • Edema
    • SOB
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6
Q

Describe the adrenergic pathway in heart failure progression.

A
  • ↑CNS sympathetic outflow
    • ↑Cardiac sympathetic activity
      • Beta-1
      • Beta-2
      • Alpha-1
        • Myocyte hypertrophy
        • Myocyte injury
        • ↑arrhythmias
    • ↑vascular sympathetic activity
      • Alpha-1
        • Vasoconstriction
    • ↑renal sympathetic activity
      • Beta-1
        • Activation of RAS
          • Vasoconstriction
      • Alpha-1
        • Sodium retention
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7
Q

Describe the neurohormonal balance in heart failure.

A

Vasoconstrictive hormones (endothelin, aldosterone, angiotensin II, epinephrine) outweigh naturitic peptides (ANP, BNP).

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8
Q

Describe the pathophysiology of myocardial remodeling.

A
  • Insult/remodeling stimuli
  • ↑wall stress, cytokines, neurohormones, oxidative stress
    • Myocyte hypertrophy
    • Altered interstitial matrix
      • Ventricular enlargement
    • Fetal gene expression
      • Diastolic dysfunction
    • Altered calcium handling proteins
    • Myocyte death
      • Systolic dysfunction
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9
Q

What are the four basic mechanisms of heart failure?

A
  1. ↑blood volume (XS preload)
  2. ↑resistance to flow (XS afterload)
  3. ↓contractility
  4. ↓filling
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10
Q

What are the etiologies of increased blood volume? What do they result in?

A

Mitral or aortic regurgitation, volume overload (IV fluid), L to R shunts, chronic kidney disease

Reduced CO to peripheries results in sodium retention, vasoconstriction –> increased preload –> ventricular remodeling (eccentric).

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11
Q

What are the etiologies of increased afterload? What do they result in?

A

Caused by aortic stenosis, aortic coarctation, HTN.

Reduced CO from diastolic dysfunction results in sodium retention, vascoconstriction and concentric remodeling.

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12
Q

What are the etiologies of decreased contractility? What do they result in?

A

Caused by ischemic cardiomyopathy (infarcion or ischemia), myocarditis, or toxins (anthracycline, alcohol, cocaine).

Reduced CO results in sodium retention and vasoconstriction, resulting in eccentric ventricular remodeling.

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13
Q

What are the etiologies of decreased filling? What do they result in?

A

Caused by mitral stenosis, constriction, restrictive cardiomyopathy, cardiac tamponade, HTCM, ICM

Concentric ventricular remodeling causes a decrease in filling pressure, reduced capacitance.

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14
Q

Systolic vs. diastolic heart failure

A
  • Systolic
    • Impaired contraction
    • Eccentric remodeling
    • All ages
    • 2/2 CAD, MI
    • Decreased EF
    • Third heart sound
  • Diastolic
    • Impaired filling
    • Concentric remodeling
    • >60y/o, women
    • 2/2 HTN
    • Unchanged EF
    • Fourth heart sound
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15
Q

What is evidence for low perfusion?

A
  • Narrow PP
  • Pulsus alterations
  • Cool forearms/legs
  • Sleepy/obtunded
  • ACEI-related
    • Symptomatic HoTN
  • Declining serium sodium level
  • Worsening renal function
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16
Q

What is evidence for congestion (elevated filling pressure)?

A
  • Orthopnea
  • High JVP
  • Increasing S3
  • Loud P2
  • Edema
  • Ascites
  • Abdominojugular reflux
  • Valsalva square wave
17
Q

Distinguish between dilated, **hypertrophic **and restrictive heart failure.

A
  • Dilated
    • Dilated left/both ventricles w/ impaired contraction (ischemic, idiopathic, familial, viral, alcoholic, toxic, valvular)
  • Hypertrophic
    • L/R ventricular hypertrophy (familial w/ AD inheritance)
  • Restrictive
    • Restricted filling, reduced diastolic filling of one/both ventricles, normal/near-normal systolic function (idiopathic, amyloidosis, endomyocardial fibrosis)
18
Q

Describe the NYHA Classification of heart failure.

A
  • Class I: asymptomatic
  • Class II: Sx w/ moderate activity
  • Class III: Sx w/ minimal activity
  • Class IV: Sx at rest
19
Q

Describe the **ACC/AHA Staging System **of heart failure.

A
  • Stage A: High risk for developing HF (HTN, CAD, DM, FHx, obesity)
  • Stage B: Asymptomatic LV dysfunction
  • Stage C: Past/current Sx of HF
    • Once at C, cannot go back to B/A
  • Stage D: End-stage HF
20
Q

What are the ACA treatment guidelines for Stage A HF?

A
  • OPT
    • Aspirin
    • ACEI
    • Statins
    • B-Blockers
21
Q

What are the ACA guidelines for **Stage B **HF?

A
  • OPT
  • ICD if LV dysfunction present
22
Q

What are the AHA guidelines for Stage C HF?

A
  • OPT
  • ICD if LV dysfunction present
  • Cardiac resynchronization therapy (CRT) if QRS wide, LVEF=35%
23
Q

What are the AHA guidelines for **Stage D **HF?

A