Heart Failure Flashcards

1
Q

Heart Failure (HF)

A

Decreased pumping or filling ability of the heart

Results in:

  1. Decreased CO
  2. Fluid build-up in the lungs (LHF) and/or peripheries (RHF)
  3. Hypoperfusion
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2
Q

Pathophysiology of HF

A

RAAS over-activity:

  1. HF
  2. Decreased CO (decreased effective circulating volume)
  3. Excess secretion of renin, angiotensin II, and aldosterone
  4. Increased sodium and water reabsorption
  5. Increased plasma volume
  6. Increased preload and afterload
  7. Increased pulmonary (LHF) and peripheral edema (RHF)

SNS over-activity:

  1. HF
  2. Decreased CO (decreased effective circulating volume)
  3. Excess secretion of (1) catecholamines and (2) insulin
  4. Increased (1) HR, BP, muscle tone etc., and (2) sodium and water reabsorption
  5. Vasoconstriction
  6. Increased preload and afterload
  7. Further decreases CO
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3
Q

Causes of HF

A

CAD (most common cause), MI, HTN, smoking, obesity, DM, cardiomyopathy, heart valvular disease

Other causes: Congenital heart disease, dysrhythmias, endocarditis, anemia, lung disease, drugs/medications

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4
Q

Cardiac Output (CO)

A

The amount of blood the heart pumps through the circulatory system in a minute (SV x HR)

Factors:

  1. Preload: ventricular stretch prior to contraction
  2. Afterload: resistance to ejection of blood from the heart
  3. Cardiac contractility
  4. HR
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5
Q

Stroke Volume (SV)

A

Volume of blood ejected during systole

Factors:

  1. Preload
  2. Afterload
  3. Nervous system alterations
  4. Myocardial oxygen supply
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6
Q

Frank-Starling Law

A

Increased preload results in INCREASED (1) contractility, (2) force of contraction, and (3) SV (to a limit)

However, if preload continues to rise, muscle fibers become over-stretched and ultimately DECREASE contractility, force of contraction, and SV (and CO)

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7
Q

Laplace’s Law

A

Contractile force within a chamber is directly proportional to (1) the RADIUS of the chamber and (2) the THICKNESS of its wall

Ex.: Small, thick-wall chamber = Increased contraction force; compared to a thin-wall chamber

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8
Q

Neurohumoral mechanisms in response to HF

A
  1. Catecholamines: SNS attempts to compensate for decreased CO by increasing HR, BP, and PVR (blood flow from pulmonary artery to LA)
  2. Vasopressin (ADH): causes water reabsorption in renal tubules (increases plasma blood volume), which results in vasoconstriction; increases preload and afterload
  3. RAAS: decreased renal blood flow and BP promotes sodium and water reabsorption; increases preload and afterload
  4. Brain natriuretic peptides: increase to attempt to decrease preload (by promoting sodium and water EXCRETION); compensation is generally inadequate
  5. Cytokines: inflammatory; cause vasoconstriction
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9
Q

Right-sided HF (RHF)

A

Reduced output from the RV; inability of the heart to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure

Common cause: LHF

Right = Rest-of-body (back flow)

S/S: JVD, peripheral edema, hepatosplenomegaly, ascites, GI venous congestion (anorexia, bloating, N/, constipation), continued fatigue and weakness

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10
Q

Left-sided HF (LHF)

A

Reduced output from the LV; inability of the heart to generate adequate CO to perfuse vital tissues

More common; LHF typically ends up involving both ventricles

Left = Lungs (back flow)

S/S: DOE and PND (paroxysmal nocturnal dyspnea), blood-tinged sputum, orthopnea, cough, cyanosis, rales/crackles, fatigue, S3 gallop, oliguria

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11
Q

Systolic LHF

A

Pathway:

  1. LV pumping is impaired
  2. Blood is backed up into the LA
  3. LA has reduced filling capacity to accept blood from pulmonary veins
  4. Back flow of blood into the pulmonary vascular bed
  5. Increased hydrostatic pressure in the pulmonary vascular bed
  6. Accumulation of fluid in interstitial and alveolar spaces (pulmonary congestion)
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12
Q

Diastolic LHF

A

HF characterized by:

  1. Impaired LV diastolic filling
  2. PRESERVED ejection fraction

Clinical manifestation: DOE, fatigue

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13
Q

Pulmonary edema

A

Capillary fluid moves into alveoli; decreased gas exchange

S/S: Lungs become stiffer, harder to inhale, crackles, frothy pink sputum, “wet cough”, hypoxemia

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14
Q

Diagnosing HF

A

H&P

Lab (CMP)

EKG (Visualized electrical activity)

CXR

Echocardiography

BNP

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15
Q

FACES

A

Fatigue

Activities impaired

Chest congestion

Edema or ankle swelling

SOB

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