Pathophysiology of CHF Flashcards

1
Q

What is forward failure?

A

The inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body

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2
Q

What is backward failure?

A

The ability to pump blood forward at a sufficient rate only if the cardiac filling pressures are abnormally high

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3
Q

What is the single most important determinant of cardiac output?

A

Heart Rate

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4
Q

What are the determinants of cardiac output?

A

Preload
Afterload
Contractility
Heart Rate

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5
Q

Preload

A

The ventricular wall tension at the end of diastole. In mechanical terms, the stretch on the muscle fibers prior to contraction.

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6
Q

Afterload

A

Aortic impedance

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7
Q

Contractility

A

A measure of the magnitude of contractile force at any given resting fiber length

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8
Q

How is cardiac output calculated?

A

Heart Rate x Stroke Volume = CO

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9
Q

What is Stroke Volume comprised of?

A

Preload
Afterload
Contractility

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10
Q

What is Ca2+ trigger?

A

Calcium entry triggers Ca release from intracellular storage pool within the Sarcoplasmic Reticulum (SR)

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11
Q

What are the 3 categories of CHF?

A
  1. Disorders of impaired contractility
  2. Disorders with markedly increased afterload
  3. Disorders with impaired ventricular relaxation and/or reduced filling
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12
Q

How does systolic HF manifest?

A

Manifested as a HF with Decreased Ejection Fraction

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13
Q

How does diastolic HF manifest?

A

Manifested as HF with normal EF

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14
Q

What are the causes of systolic HF?

A
  • impaired contractility

- pressure overload

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15
Q

What can cause impaired contractility in systolic HF?

A

Loss of contractility can result from destruction of cardiomyocytes (ex. acute MI) or abnormal myocyte function (ex. alcohol-induced cardiomyopathy)

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16
Q

What are the causes of diastolic HF?

A
  • impaired relaxation

- reduced filling

17
Q

What can cause the reduced compliance of the heart?

A

LV hypertrophy, ischemia, fibrosis, or restrictive

cardiomyopathy

18
Q

What is the difference in compliance and pressure in the RV?

A

Right Ventricle (RV) is much more compliant than the LV, but generates much less pressure

19
Q

What can the RV tolerate better than the LV? What can the LV tolerate better than the RV?

A

RV can tolerate much larger changes in filling without changes in pressure, but does not tolerate changes in afterload nearly as well as the LV. This makes the RV is very susceptible to acute changes in pulmonary vascular resistance.

20
Q

What is the most common cause of RV failure?

A

LV Failure

21
Q

What are some other causes of RV failure?

A
Pulmonic Stenosis
Acute MI with RV Infarction
COPD
Interstitial lung diseases 
Pulmonary embolism
Primary pulmonary hypertension
22
Q

What are the main compensatory mechanisms in CHF?

A

Frank-Starling Mechanism
Autonomic Nervous System Effects
Renin-Angiotensin-Aldosterone System

23
Q

How does the Frank-Starling Mechanism work?

A

LV dysfunction ⇒ Decreased stroke volume (SV) ⇒ Increased LVEDV ⇒ Increased fiber stretch ⇒ tends to restore SV

24
Q

How do Autonomic Nervous System Effects work?

A

Baroreceptor Reflex ⇒ Sympathetic stimulation and withdrawal of parasympathetic tone ⇒ Increased heart rate and contractility tends to restore SV and increase C.O.

25
Q

How does the Renin-Angiotensin-Aldosterone System work?

A

Decreased C.O. ⇒ Decreased Renal Perfusion ⇒ Increased Renin release ⇒ Increased Angiotensin II-Aldosterone Production ⇒ Increased Na and Water Retention ⇒ Increased preload tends to restore increase SV and C.O.

26
Q

What is post-MI ventricular remodeling?

A

Hypertrophy and dilatation of noninfarcted segments

occurring weeks to years after acute MI.

27
Q

How does an increase in ventricular afterload reduce cardiac output?

A

It will decrease the SV

28
Q

How does an increase in ventricular preload increase cardiac output?

A

It will increase the SV

29
Q

What happens to the heart with chronic sympathetic stimulation?

A
  • Increased afterload (Norepinephrine-induced vasoconstriction)
  • Beta-1 receptor down-regulation (decreased response to ß1-stimulation)
30
Q

What are symptoms of L-sided CHF?

A
  1. Dyspnea on Exertion (DOE)
  2. Orthopnea (Inability to lie flat in bed)
  3. Paroxysmal Nocturnal Dyspnea (awaken SOB due to mobilization of fluid)
  4. Fatigue
31
Q

What are symptoms of R-sided CHF?

A
  1. Peripheral edema

2. RUQ Abdominal Discomfort (hepatic congestion)

32
Q

What is the effect of remodeling on CHF?

A

Remodeling often PRECEDES the development of symptoms of CHF. Efforts directed at preventing or slowing the progression of ventricular remodeling will prevent or delay the development of CHF.