Lecture 26 Flashcards

1
Q
  1. failure of heart to pump adequate blood to satisfy body’s needs
  2. certain conditions or diseases lead to a decrease in CO
  3. can involve the right ventricle, left ventricle, or both (with time, failure of one ventricle leads to failure of the other)
A

heart failure

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2
Q

dysfunctional mechanical pumping (decreased contractility)

A

systolic heart failure

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3
Q

most often caused from coronary artery disease which reduces coronary blood flow to heart leading to hypoxia and impaired contractility → ↓SV → ↑ESV → ↑EDV/preload → with a chronic increase in EDV, the ventricle remodels by dilating → ↓force development→ ↓SV → ↓CO

A

systolic heart failure

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4
Q

reduced cardiac output and ejection fraction

A

systolic heart failure

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5
Q

inadequate relaxation and reduced filling

A

diastolic heart failure

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6
Q

Most often caused from hypertension → ↑ afterload → stimulation of ventricular hypertrophy → ↑ stiffness (↓ compliance) → ↓filling → ↓EDV → ↓SV → ↓CO

A

diastolic heart failure

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7
Q

reduced cardiac output, but ejection fraction may be near normal; this reduced EF is useful only as an indicator of systolic failure

A

diastolic heart failure

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8
Q

compensation of HF due to activation of SNS and RAAS causes ____________

A

progressive weakening of the heart

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9
Q

how does long term activation of the SNS and RAAS contribute to weakening of the heart?

A

SNS and RAAS ultimately increase the work of the heart which puts a strain on the heart muscle. if the SNS and RAAS increase the oxygen demand of the heart muscle, it has to work harder to deliver that oxygen or the muscle will become hypoxic and hypoxia will cause weakening

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10
Q
  1. tachycardia (increases O2 consumption
  2. increases contractility (increases O2 consumption)
  3. vasconstriction (increases afterload, which increases O2 consumption)
  4. chronic norepinephrine exposure is toxic to myocardial cells (causes apoptosis)
  5. increases risk of arrhythmias which can decrease CO
A

effects of SNS

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11
Q
  1. vasoconstriction (increases afterload)
  2. stimulates renal sodium and water reabsorption (increases blood volume and preload)
  3. stimulates SNS
  4. stimulates ventricular remodeling (which causes dysfunction)
A

effects of RAAS: Ang II

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12
Q
  1. stimulates renal sodium and water reabsorption (increases blood volume and preload)
  2. stimulates interstitial cardiac fibrosis (causing stiffness and dysfunction)
  3. increases risk for arrhythmias
A

effects of RAAS: aldosterone

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13
Q

other hormones also contribute to HF, such as ____

A

ADH

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14
Q

loss of cardiac reserve

A

decompensation

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15
Q

compensation can occur for several years in attempt to main an adequate CO the best it can. but as the heart progressively weakens over time, the CO eventually decreases to an inadequate level; the SNS and RAAS can no longer compensate. this is called the ____________ stage

A

decompensation

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16
Q
  1. tachycardia
  2. decreased cardiac reserve and decreased exercise tolerance
  3. shortness of breath
  4. peripheral and/or pulmonary edema
  5. cardiomegaly (dilation of heart)
A

signs and symptoms of HF

17
Q

treatment strategies-depends on the stage of dieease

A
  1. Beta blockers
  2. ACE inhibitors
  3. ARBs
  4. Aldosterone antagonists
  5. Diuretics
  6. decrease salt and water intake
18
Q

inhibit actions of SNS

A

Beta blockers

19
Q

Inhibit actions of RAAS

A
  1. ACE inhibitors
  2. ARBs
  3. Aldosterone antagonists
20
Q

increased afterload causes:

A

hypertrophy

21
Q

why does pathological hypertrophy cause HF?

A

decreases filling

22
Q

during what phase of the cardiac cycle is the fourth heart sound heard?

A

atrial contraction

23
Q

what effect to vasodilator drugs tend to have to have on afterload?

A

decrease it