Lecture 13 - Heart failure Flashcards
What is chronic heart failure defined as?
A chronic inability of the heart to maintain adequate perfusion of the tissues at a normal filling pressure.
What is the main pathophysiological cause of chronic cardiac failure?
Reduced myocardial contractility (a less efficient pump)
What does reduced myocardial contractility result in? (Relate to the starling curve)
Starling curve shifts down the page.
This means that for a given end diastolic pressure, there is a lower stroke volume compared to if the heart wasn’t failing .
However the change may or may not reduce resting stroke volume depending on compensatory responses.
In heart failure, why may SV be maintained by compensatory responses?
In mild heart failure there will be an increased in ED pressure due to increased filling - this means we can maintain the same SV despite having a reduced contractility.
However this compensation can’t last forever.
Therefore at rest, cardiac output in cardiac failure can be:
- Almost normal (compensated failure)
- Subnormal (decompensated failure)
Why might SV not be a good indication of cardiac function cardiac failure?
What measurement should be done instead?
Since it’s maintained to normal levels due to compensatory responses.
We use the ejection fraction (EF) (%)
EF = SV/EDV
This puts the SV in contect of the EDV
At rest the normal ejection fraction is ~50-70%
Why does EF increase in exercise?
- Increased EDV - cause increase in SV by frank-starling mechanism
- SNS activity - increases contractility, making it rise higher on the starling curve
What happens to the EF during exercise of someone with a failing heart?
And why doesn’t increased venous return have much of an affect?
EF decreases with exercise.
A large change in EDP gives a relatively small change in SV, this is why SV virutally doesn’t increase with exercise in failing hearts.
In a person with cardiac failure cardiac output fails to increase on exercise - causing exercise intolerance
Why doesn’t increased SNS activity have much of an affect on the failing heart?
Because B1-adrenoreceptors in myocardial cells are downregulated.
Describe how heart vairables change during exercise, and compare this to what would happen with a failing heart
Describe how cardiac variables change during exercise in a person with heart failure?
What 2 compensation mechanisms occur in cardiac failure
- Increased adrenergic activity
- Renal retention of sodium/water
What does the compensatory mechanism of increased adrenergic activity compensate for? and how it work
It causes vasoconstriction leading to an increase in TPR, which helps maintain BP (MABP = COxTPR).
How does the compensation mechanism of renal retention of sodium/water work?
It increases extracellular fluid volume which will increase mean criculatory filling pressure to the heart (by starlings law) will help maintain CO (increased EDV, increased SV)
Since in cardiac failure CO is reduced, what happens to blood distribution?
CO is preferentially distrubuted to
- Heart (coronary blood flow)
- Brain (cerebral blood flow)
- skeletal muscle
Where is blood flow reduced to in Cardiac failure?
Blood flow is reduced to
- The kidney (renal blood flow)
- Skin (cutaneous blood flow
- Gut (splanchnic blood flow)
How do the kidneys respond to the reduced perfusion in cardiac failure?
They reatin salt and water. This will expand ECF volume by up to 30%.
This salt and water retention is due to activation of the RAAS
What are the concequences of fluid rentetion in chronic cardiac failure?
- Fluid retention supports cardiac function to some extent (starlings law)
- But reduced cardiac function and increased plasma volume elevates venous pressure
- elevation in venous pressure leads to a rise in capillary pressure
- Disturbs starlings equilibrium
- Increases interstitial fluid volume
- Oedema formation - need 4-5 litres of excess fluid for oedema to be detectable.
- Oedema of the lungs and/or the periphery is a prominent feature in chronic cardiac failure
How does increasing venous pressure affect the capillary hydrostatic pressure?
Filtration will be favoured over reabsorption
- If the net rate of filtatration exceeds lymph fow, fluid will accumulate in the interstitial space causing oedema.
- We need 4-5 extra litres of ECF
How does pulmonary oedema occur (Sequence of steps)
Pulmonary oedema
Left heart failure
- Increased EDV
- Increased EDP
- Decreased LAP-LVP pressure gradient
- Increased LA volume/LAP
- Increased pulmonary venous pressure
- Increased pulmonary capillary pressure -> shift of fluid out pulmonary capillaries to lung interstitium -> Pulmonary oedema
How is pulmonary oedema caused? (in LVF)
There is increased pulmonary capillary pressure. This shifts fluid out from pulmonary capillaries into lung intersitium, and oedema develops in the lungs.
This pulmonary interstitial congestion reduces lung compliance and makes them stiffer, and this affects ventilaition. - causing dyspnoea and SOB
Can eventually get fluid leaking into alveolar spaces
Why does the dyspnoea get worse at night? (Paroxysmal nocturnal dyspnoea)
- Supine position makes the blood distributed more centrally
- This exacerbates failure
- This increases pulmoanry congestion
- Which increases filtration
- Which increases oedema, causing an increased SOB
In severe pulmonary oedema fluid floods into the alveolar spaces, impairing O2 transport.
What sequence of events leads to peripheral oedema in RVF
Peripheral oedema
Right heart failure
- Increased EDV
- Increased EDP
- Decreased RAP-RVP pressure gradient
- Increased RA volume/RAP
- Increased systemic venous pressure
- Increased systemic capillary pressure
What problems does dilatation of the heart cause?
The muscle tension that must be generated to develop a given ventricular pressure (P) depends upon the radius of the ventricle (r) and the thickness of the ventricle wall (w) (Law of Laplace).
When the L ventricle fails during heart failure what variables change in laplaces law
