26 Flashcards

1
Q

Define HF

A
  • Inadequate blood flow for metabolic needs
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2
Q

Primary HF

A
  • Cause: cardiac origin, peripherally affected
  • Can’t empty –> systolic

–> weakened contractility (low ejection fraction)

  • Can’t fill –> diastolic

–> muscular hypertrophy (low volume)

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3
Q

describe the pathophsiology of HF

A
  • Begins with decreased cardiac output
  • compensate by increased volume (retain Na+ and H20)
  • Heart response limited to:

–> increase volume (filling) - increase left ventricular end diastolic volume

–> increased fiber length (spilling) - increase force of contraction

–> starlings law (SV and LVEDV increase together)

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4
Q

describe the bodies response to tissue ischemia

A
  • increases contractility, rate, peripheral resistance (epinephrine, norepinephrine)
  • Increase ischemia (systolic) or hypertorphy (diastolic) (increased O2 demand, increased work load)
  • renen/angiotensin activated as if hypovolemic
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5
Q

describe symptoms of LV Failure

A
  • Dyspnea (exertion, recumbent, nocturnal, resting)
  • Diminished exercise capacity (output down)
  • nocturia (recombent diuresis)
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6
Q

describe sysmptoms of RV failrue

A
  • peripheral edema
  • Edema of bowel wall can impair med absorption
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7
Q

describe NYHA functional classification

A
  • Class 1 - no limitation
  • Class 2 - slight limitation of activity (ordinary activity precipitates dyspnea, fatigue, angina)
  • Class 3 = makred limitation (less than normal activity)
  • Class 4 - symptoms at rest
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8
Q

describeing physical exams of LEFT HF

A
  • Pallor, cool extremities
  • anxiety, dyspnea at rest
  • pulses normal to rapid, weak
  • blood pressure varies
  • Pulmonary rales, pleural effusion
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9
Q

physical exam of Right HF

A
  • Hepatojugular reflux
  • kassmauls sign

–> paradoxical JVD from increased R chest pressure (inhallation normally increases blood return (rise in JVD)

  • congestive hepatomegally (ascites)
  • Edema (symmetrical, pitting, dependent)
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10
Q

describe goals of therapy for HF

A
  • relieve symptoms
  • improve NYHA functional class
  • decrease frequency and intesnity of tx
  • delay progression of myocardial dysfunction
  • reduce premature HF mortality
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11
Q

therapy at Stage A

A
  • Stage A = pre-symptoms, at risk, heart ok

- ACE inhibitors

  • beta blockers may be benefit
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12
Q

therapy at stage B

A
  • Stage B = no symptoms, cardiac structure changes)
  • Goals

–> prevent worsening dysfunction

–> improve symptoms

–> reduce disability and hospitalizations

  • Drugs = ACEIs, beta blockers, diuretics, digoxin (?)
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13
Q

Therapy at stage C

A
  • Stage C = structural changes and symptoms present)
  • Goals:

–> reduce premature HF mortality

–> reduce diability and hospitalization

–> improve symptoms and functional capacity

  • Drugs = ACEI, spironolactone, diuretics, beta blockers
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14
Q

therapy at stage D

A
  • Stage D = advnaced disease, continued symptoms, require aggressive therapy)
  • goals:

–> palliation (feel better)

–> reduce hospitalizations

  • Drugs = improve symptoms (cannot salvage the patient)
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15
Q

Describe adverse effects of angiotensin II in HF

A
  • mediated by AT-1 receptors
  • Myocyte hypertrophy
  • myocyte apoptosis
  • proliferation of fibroblasts

**ACEI are now MANDATORY agents for tx of HF**

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