Heart Failure Flashcards

1
Q

What is heart failure

A

CO insufficient, unsustainably with increased EDP

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2
Q

Describe RHF

  • systemic veins
  • pulmonary artery
  • pulmonary vein
  • aorta

Any edema and why

A

Systemic veins
-increase pressure, maintain CO, increased EDP

Pulmonary artery, vein, aorta
-maintained by reflexes

CVP increases as RVEDP increases => peripheral edema

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3
Q

Describe LHF

  • systemic veins
  • pulmonary artery
  • pulmonary vein
  • aorta

Any edema and why

A

Systemic veins
-may increase if severe

Pulmonary artery, vein
-pressure increases

Aorta
-maintained by reflexes

Pulmonary capillary filtration => net mv into interstitium =.> pulmonary effusion

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4
Q

Describe congestive HF

  • stsemic veins
  • pulmonary artery
  • pulmonary vein
  • aorta

Any edema and why

A

Systemic veins
-increased pressure

Pulmonary artery, vein
-increased pressure

Aorta
-maintained by reflexes

Increased LVEDP => net mv of fluid into interstitium => pleural effusion and edema
-fluid in alveoli => decreased gas exchange

Peripheral edema due to increased RH pressure, RHF => SVP increase

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5
Q

How does pressure overload lead to heart failure

A

Increased LVP => increased wall stress
Increased concentric hypertrophy to reduce radius => decrease wall stress
But new muscle is not normal muscle, prone to stretch => increased wall stress

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6
Q

How does volume overload lead to heart failure

A

Increased radius => increased wall stress
Increased eccentric hypertrophy to increase width of muscle => decrease wall stress
But new muscle is not normal muscle, prone to stretch => increased wall stress

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7
Q

Why do we have contractile issues in heart failure after major cardiac events
Describe the vicious cycle involved in HF

A

CHD, MI, congenital issues => cardiac scars

Can lead to either hypertrophy/dilated cardiomyopathy

Increased hypertrophy 
Increased muscle capillary inadequacy 
Imbalance of supply and demand
Ischemia, collagenous scar formation
Decreased contractility, increased stiffness
Increased wall stress
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8
Q

Describe the natural compensatory mechanisms that act on HF

Why is this good in acute settings and bad in chronic settings

A

LVEDP increases but contractility is poor
CO decreases
BP decreases
Fall in BP detected by baroceptors

RAAS
VC, fluid Na retention to increase BP, CO

SNS
VC, HR, contractility increase

Acute, keep us alive
But compensated HF is unsustainable

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9
Q

How would you treat HF

A

B blocker
-decrease SNS input

ACEi
-decrease RAAS

Spirinolactone
-decrease aldosterone, counter NH mech

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