Heart Failure Flashcards
What is heart failure
CO insufficient, unsustainably with increased EDP
Describe RHF
- systemic veins
- pulmonary artery
- pulmonary vein
- aorta
Any edema and why
Systemic veins
-increase pressure, maintain CO, increased EDP
Pulmonary artery, vein, aorta
-maintained by reflexes
CVP increases as RVEDP increases => peripheral edema
Describe LHF
- systemic veins
- pulmonary artery
- pulmonary vein
- aorta
Any edema and why
Systemic veins
-may increase if severe
Pulmonary artery, vein
-pressure increases
Aorta
-maintained by reflexes
Pulmonary capillary filtration => net mv into interstitium =.> pulmonary effusion
Describe congestive HF
- stsemic veins
- pulmonary artery
- pulmonary vein
- aorta
Any edema and why
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
How does pressure overload lead to heart failure
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
How does volume overload lead to heart failure
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
Why do we have contractile issues in heart failure after major cardiac events
Describe the vicious cycle involved in HF
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
Describe the natural compensatory mechanisms that act on HF
Why is this good in acute settings and bad in chronic settings
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
How would you treat HF
B blocker
-decrease SNS input
ACEi
-decrease RAAS
Spirinolactone
-decrease aldosterone, counter NH mech