SAQ QS Flashcards
- Why is BNP more focused on than ANP?
- Because it has a greater half-life than ANP
* So, it is a much more stable monitor in chronic conditions like heart failure
What effects do these peptides have on renin secretion?
- These peptides reduce renin secretion, which reduces the production of angiotensin and aldosterone
- By reducing the production of these substances, there is a loss of salt and water
- Loss of salt and water causes blood volume to decrease
- If blood volume decreases, then venous return, EDV and BP will decrease
- These peptides also have vasodilatory actions which will also decrease blood pressure
- When are BNP/NT pro-BNP and ANP released?
• When the heart muscle cells become abnormally stretched
• When someone has HF, they can compensate the reduced CO by increasing venous return,
end diastolic volume and therefore increasing stroke volume
• Increase in end diastolic volume is going to stretch the ventricles and as it stretches the
ventricles, BNP and ANP are released
How does pulmonary hypertension and subsequently RHS heart failure occur?
• Due to chronic pulmonary problems
• COPD
• Lung cancer
• Part of the lung might have trouble with gaseous exchange
• In COPD, gaseous exchange may be impaired because of mucus build up in the airways
• In lung cancer, the tumour becomes disrupted
• In the pulmonary circulation, if a piece of tissue is not receiving a high level of oxygen
• Either because mucus in airways or because the tumour is disrupting gaseous exchange
• The blood vessels in the airways, clamp off
• They constrict, so the blood supply to that damaged area is reduced and the blood going to
the lungs is redistributed to parts of the lungs that are healthy and where gaseous exchange
is occurring more naturally
• Because part of the vascular bed has been constricted off, there is increase in the blood
pressure in the lungs
• This increase in blood pressure is what can lead to damage in the RHS of the heart
How does valve disease cause heart failure?
• As valves get older, they can become stenotic – so requires much more pressure in the atria to open the valve to allow the blood to flow into the ventricles
• When the ventricles contract, they require much more work to be done to open the valve and to allow blood to flow to the aorta
• Stenotic valves make the heart work much harder than its healthy counterparts
• This work is going to increase muscle size, leading to reduction in chamber volume and an
inefficient heart
• Valves become difficult to open and may not close properly
What are the two highest contributory factors to heart failure in the UK?
- Heart attacks
* Uncontrolled hypertension
- What occurs in someone with uncontrolled hypertension?
• The heart is having to work much harder to pump the blood out of the systemic circulation
• Overtime, the increase in work is going to increase the size of muscle fibres in the heart
• When the muscle cells become larger, they tend to reduce volume of the ventricular
chamber and so grow inwards
• So, chamber volume becomes less and therefore CO becomes less
- Increase in the size of the heart muscle cells is not matched by an increase in blood supply to those muscle cells.
- So, although they are bigger, they are not as efficient as their smaller counterparts
- Why does an acute MI cause heart failure?
- Damage to heart muscle fibres, typically in the LHS of the heart in the left ventricle
- Therefore, the left ventricle is unlikely to work as efficiently as it has done prior to the MI
- What causes the pit-like formation in pitting oedema?
• Stick a thumb into somebody’s leg
• Rather than the skin springing back when you release your thumb
• It leaves a pit
• This is because it takes a while for the fluid to redistribute itself and for the indentation to
disappear
- How does ascites and pitting oedema occur in RHS heart failure?
• If the RHS of the heart has failed, then blood returning to the RHS will pool in the right
ventricle and not much of it will be removed
• More blood returns
• The pressure increases in the right ventricle, this increases pressure in the right atrium
• And then that increases the pressure in the venae cavae, that bring blood from..
• Areas above the heart such as the superior vena cava and areas below the heart such as the
superior vena cava
• So, because of the build up in pressure
• That causes a build up in the pressure of the capillaries in the abdomen causes ascites
• Can cause build up in the capillaries in the peripathy causes pitting oedema
- How does a raised JVP occur in RHS heart failure?
- Due to elevated pressures in the right atrium
* Causing the pulse in the jugular vein to appear higher up the jugular vein
- What is a cardiomegaly?
- An enlarged heart
- Because the end diastolic volume is increased so the ventricles swell and stretch
- Making the heart appear much larger
- What can be done to prevent breathlessness at night?
• Propping the patient up with pillows
• Severity of heart failure can be determined by how many pillows, the patient requires to get
a comfortable night’s sleep
• The more pillows, the more the patient will be propped up
• So, the more their blood pressure is going to increase
• Venous pressure is going to decrease and therefore movement of fluid in lungs is going to be
inhibited
- What is the basis of the renin-angiotensin system in increase of blood volume?
Causes salt and water retention which in turn increases blood volume
- Why would a patient with HF experience orthopnoea and paroxysmal nocturnal? How does this occur?
• When lying down, some of the fluid, if not all of it
• Due to the pressure changes that occur when lying down
• Will allow the fluid to move back into the CVS
• This will increase blood volume and therefore increase venous return
• If venous return is increased to the RHS of the heart, it will then get pumped to the LHS
• In the case of LHS heart failure, the additional blood that is returning to the heart is going to
cause an increase in pressure to the left ventricle, the left atrium, the pulmonary veins, the
capillaries of the lungs
• And is going to drive fluid out into the lungs
• Coupled with this
• When lying down, the CV system, in order to return blood to the heart isn’t having to work against gravity
• This increases venous return, which is going to increase the pressure in LHS of the heart
• Which will eventually cause more fluid to move out into the lungs
- Why is an increased hydrostatic/blood pressure at the venous end of the capillaries a bad thing in the case of heart failure? How does this result in fluid appearing in the lungs?
• In the case of heart failure, there is an increase of blood/hydrostatic pressure at the venous
end
• This is due to the backlog of blood that was increasing the pressure in the pulmonary vein,
and therefore the capillaries in the lungs
• If the hydrostatic pressure is increased at the venous end, then less fluid is going to be
reabsorbed
• The same amount of fluid will still be filtered out, but less is going to be taken back into
capillary
• Fluid that remains in the intracellular space eventually gets into the alveoli and causes
pulmonary congestion, impaired gaseous exchange and difficulty breathing – SOB
- What is the consequence of a reduced EF in a failing heart?
• In a patient with HF, the amount of blood returning to the heart is typically increased over
what is normally seen
• This is because the heart isn’t functioning as well as it should be
• A lot of blood returning to the heart, makes its way into the left ventricle
• Then the heart contracts to try and pump that blood out
• Because of systolic dysfunction, the contraction is relatively weak and it only removes 35% of
blood that has appeared in the left ventricles
• And therefore, more blood returns and the left ventricle fill up even more and starts to
stretch
• Pressure builds up and that pressure forces blood back into the left atrium
• The increase of pressure in the left atrium then feeds back up the pulmonary vein to the
venous end of the capillaries in the lungs
• So, the venous end of the capillaries are seeing a much higher hydrostatic pressure than they
normally would – a much higher blood pressure
- When in LHS heart failure does pulmonary congestion occur?
It tends to occur when end diastolic volume increases towards the upper limits of what’s
possible
- What are the signs and symptoms of right sided heart failure (Cor Pulmonale)?
Fatigue Increase in peripheral venous pressure Ascites Enlarged liver and spleen May be secondary to chronic pulmonary problems Distended jugular veins Anorexia and complaints of GI distress Weight gain Dependent oedema NOTE: In some patients, failure in LHS can lead to failure in RHS sometime later
- What are signs and symptoms of left sided heart failure?
• Paroxysmal nocturnal dyspnoea • Elevated pulmonary capillary wedge pressure • Pulmonary congestive: o • Cough o • Crackles o • Wheeze o • Blood-tinged sputum o • Tachypnoea • Restlessness • Confusion • Orthopnoea • Tachycardia • Exertional dyspnoea • Fatigue • Cyanosis
meant by “creps” in lungs?
Crackles, bubbling sounds
- Why would a patient with heart failure become increasingly tired?
SOB and decreased CO
SOB presumably due to CO not being sufficient to meet demands of body
- What happens in moderate/severe heart failure as the afterload increases?
• The drop off in stroke volume is far more rapid when the heart is challenged with an increasing afterload
• There’s not much reserve in the hearts, in these conditions
• If the heart challenged to work harder, it struggles to do that
• Therefore, uncontrolled hypertension in a patient with heart failure is a real problem
• Whereas, acutely uncontrolled hypertension in a patient with a healthy heart isn’t going to
have much of an impact on stroke volume.
- What happens in hypertension as the afterload increases?
• There are still relatively little changes in stroke volume
• This is because the heart muscle is healthy and can generate quite a high degree of force
over and above what it would usually achieve
• And it can therefore compensate for this increase in outflow resistance
• However, if blood pressure becomes very high and the vasculature becomes very constricted
• Then, the heart will struggle to maintain the same level of stroke volume
• There is seen to be about a 25-30% decrease in stroke volume up at the very high levels of
flow resistance
- What happens if outflow resistance/afterload is increased?
o Afterload – is the force that the heart has to generate in order to pump blood into the
systemic circulation
o If the blood vessels are constricted, then the amount of force that the heart has to generate
in order to pump out blood is increased
o Because it is pumping it out into a much higher resistance
- What the two extrinsic mechanisms underlying how an increase in ventricular end- diastolic volume can increase stroke volume?
o Sympathetic nervous system
o Renin-angiotensin system
- What are two mechanisms underlying how an increase in ventricular end-diastolic volume can increase stroke volume?
• These are the two intrinsic mechanisms that the heart uses to match venous return to stroke volume
• First mechanism:
o • At rest and when the diastolic volume is relatively low, there is very little stretch of the
muscle fibres in the ventricle
o • Therefore, sarcomere length is relatively short and there is a high degree of overlap of
the actin and myosin filaments
o • Therefore, if the heart muscle cell wanted to contract, it can only move a relatively small
distance
o • The more blood that returns to the heart, the more it stretches the sarcomere
o • And therefore, the more contraction is possible, allowing the heart to pump out the
same amount of blood as enters the heart
• Second mechanism:
o • Based around the sensitivity of troponin C to calcium
o • When troponin C binds to calcium, it pulls tropomyosin out of the way because there is a
conformational change in troponin C
o • It pulls it out of the way of myosin binding sites
o • Therefore, the actin and the myosin can interact and the muscle can contract
o • Calcium binding causes a conformational change which pulls tropomyosin away from the
myosin binding sites
o • As end diastolic volume is increased, troponin C is able to move the tropomyosin at
increasingly lower concentrations of calcium
o • So, stretching the muscle fibres, sensitizes troponin C to calcium
o • So, at far lower levels of intracellular calcium, tropomyosin will be removed allowing
contraction to occur
- Describe the typically seen on a frank-starling curve
• As the end diastolic volume increases, the stroke volume increases
• With exercise, the curve is shifted up and to the left:
o • Predominantly due to the activity of the sympathetic nervous system
o • Because the sympathetic nervous system increases the force of contraction of the
ventricles
• Typical curve for a HF patient:
• Shifted to the right
• • Maximum stroke volume that can be achieved is very much less than seen in a normal patient at exercise or rest
• • If end diastolic volume is increased too much, then stroke volume starts to go down
Compensated heart failure:
• • Shift of frank-starling curve downwards and to the right in a failing heart
• • Maximum is decreased
• • If end diastolic volume is increased, same stroke volume as a normal heart can be
acheived
- In people with HFPEF, what % of blood volume is pumped out into systemic circulation? Does it meet circulatory demands?
• Only 60-70% of a much smaller than normal volume of blood is pumped out into the systemic circulation
• So therefore, circulatory demands of the body are not being met 10. What occurs in people with HFREF?
• Ventricles are very much enlarged, typically because lots of blood is returning to the
ventricles
• There is a dysfunction in the ability of the heart to contract – systolic dysfunction
• Therefore, in someone with HF, they are typically only ejecting less than 35% of blood that is
present in their ventricles
