Lecture - CVS (Bevin Physiology 12 Heart Failure)

Question 1

Chronic Cardiac Failure

1. Chronic heart failure (or congestive heart failure) may be defined as what?
2. Is there is only one cause?
   - what’s the main pathophysiological feature of it?
3. What does the Starling curve look like in cardiac failure?
   - what goes on the x and y axis on the starling curve graph?
4. Okay so the curve shifts down becuase reduced contractility so you expect a decrease a SV (CO) but initally, things arent as bad as they seem depending on c____ responses
   - so if failure is only mild, how is the SV maintained?
5. What’s the failure called when the CO in cardiac failure is (a) almost normal and (b) subnormal
6. So SV/CO may or may not be reduced at rest……So will SV be a good indication of cardiac function in cardiac failure?
   - What’s a more useful measure of cardiac performance?
   - What’s the valvue of this in a normal resting heart?
7. What two things lead to increased EF in exercise?
   - what mechaism for the first reason? Where do you move the starling curve?
   - what about the mechanism of the second reason? Where do you move the starling curve?
8. What does the EF look like of the ventricle of a pateint with cardiac failure at rest and during exercise?
   - explain this using the starling curve (with the venous return)
   - what happens with the SNS mediated increase in contractility?
9. How do you measure EF?
   - so just rememeber that for someone with cardaic failure the CO fails to increase on exercise
10. Okay on the slide 24, there are a number of cardiovascular variables. For each other them (that I will list), tell me how the normal person responds vs how a person with ischaemic cardiac failure will respond:
    - CO
    - HR
    - SV
    - Volume left in heart after end-diastole
    - Volume left in heart after end-systolic
    - EF
11. After what HR does it become counter productive aka not enough time to fill up enough?
12. What will dilate the ventricle in a pateint with cardiac failure?
13. What leads to the limited increase in HR during exercise?

Answer 1

8. Increase EDV but SV same so decrease EF in exercise with pateint who has heart failure

Question 2

Compensation in cardiac failure

1. Increased adrenergic activity - I know that the myocardial cells have a downregulation of the B1 adrenoreceptors buuut the vessels still respond to the SNS so what will increasing the adrenergic activity do?
   - two effects here
   - what are these effects achieved by?
2. What does the kidney do?
   - why does the kidney respond? LIke, isn’t it getting enough blood? (Slide 31)
   - which other organs is the blood flow reduced to since CO down (the body will preference certain organs)
   - what system activated by the kidneys leads to the retention of the salt and water?

Answer 2

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Question 3

Consequences of fluid retention in chronic cardiac failure

1. Okay, so we know that fluid retention supports the cardiac function to some extent (Starling’s Law - increase EDV to keep SV maintained)
2. Buuuuut you have reduced CO and increased plasma volume so what do you elevate?
   - what pressure from that pressure inceases?
   - what equillibrim is disturbed?
   - How much does the volume of the interstitial fluid need to increase to see clinically detectable oedema?
   - where do you usually see the oedema and what is that odeme assocaited with (like which side of the heart)?
3. Starling’s equilibrium
   - what is fluid driven out of the caps and into the interstitial space by?
   - what is fluid drawn back into the caps by?
   - so there is a b____ between filtration and reabs
   - how does this change when you increase venous pressure (by not pumping blood out and having more volume, I think)

Pulmonary oedema

1. Which side of the heart’s failure is this related to?
2. What happens to:
   - EDV
   - EDP
   - LAP-LVP pressure gradient?
   - LA volume, LAP
   - Pul venous pressure
   - Pul cap pressure
   - how does that lead to oedema?
3. So where is the congestion?
4. What happens to lung compliance? Why?
5. What happens to ventilation?
6. Will the fluid get to the alveolar spaces?
7. What does it look like on chest x-ray?
8. What does the supine position exacerbate the failure?
   - so what happens with shortness of breath?
   - so when is the dyspnoea more marked? What’s the clinical term for this?

Peripheral oedema

1. Which side of the heart is this related to?
2. What happens to these values:
   - EDV
   - EDP
   - RAP-RVP pressure gradient
   - RA volume/RAP
   - systemic venous pressure
   - systemic cap pressure
3. So pateints with RHF or b_____ failure develop this oedema
   - where do you see the oedema?
   - what happens to JVP?
   - Why does the liver become enlarged?

Answer 3

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Question 4

Increase EDV is of some use via Starling’s Lae buuuuut resusltation dilatation causes other problems

1. So you will dilate the ventricle bc you keep having increased EDV. According to the Law of Laplace - what happens to the tension and therefore myocardial O2 demand?
2. How does this relate to the lenght-tension curve?
3. What about the valves?

So principle of treatment of cardiac failure

1. What’re the main aims of treatment from a phyiological POV?
2. But you need to make sure the treatment doesnt undermind what?

Answer 4

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