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1
Q
  1. Why is BNP more focused on than ANP?
A
  •  Because it has a greater half-life than ANP

*  So, it is a much more stable monitor in chronic conditions like heart failure

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2
Q

What effects do these peptides have on renin secretion?

A
  •  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
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3
Q
  1. When are BNP/NT pro-BNP and ANP released?
A

•  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

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4
Q

How does pulmonary hypertension and subsequently RHS heart failure occur?

A

•  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

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5
Q

How does valve disease cause heart failure?

A

•  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

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6
Q

What are the two highest contributory factors to heart failure in the UK?

A
  •  Heart attacks

*  Uncontrolled hypertension

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7
Q
  1. What occurs in someone with uncontrolled hypertension?
A

•  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
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8
Q
  1. Why does an acute MI cause heart failure?
A
  •  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
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9
Q
  1. What causes the pit-like formation in pitting oedema?
A

•  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

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10
Q
  1. How does ascites and pitting oedema occur in RHS heart failure?
A

•  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

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11
Q
  1. How does a raised JVP occur in RHS heart failure?
A
  •  Due to elevated pressures in the right atrium

*  Causing the pulse in the jugular vein to appear higher up the jugular vein

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12
Q
  1. What is a cardiomegaly?
A
  •  An enlarged heart
  •  Because the end diastolic volume is increased so the ventricles swell and stretch
  •  Making the heart appear much larger
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13
Q
  1. What can be done to prevent breathlessness at night?
A

•  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

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14
Q
  1. What is the basis of the renin-angiotensin system in increase of blood volume?
A

 Causes salt and water retention which in turn increases blood volume

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15
Q
  1. Why would a patient with HF experience orthopnoea and paroxysmal nocturnal? How does this occur?
A

•  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

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16
Q
  1. 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?
A

•  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

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17
Q
  1. What is the consequence of a reduced EF in a failing heart?
A

•  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

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18
Q
  1. When in LHS heart failure does pulmonary congestion occur?
A

 It tends to occur when end diastolic volume increases towards the upper limits of what’s
possible

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19
Q
  1. What are the signs and symptoms of right sided heart failure (Cor Pulmonale)? 
A 
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
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20
Q
  1. What are signs and symptoms of left sided heart failure?
A 
•	  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
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21
Q

meant by “creps” in lungs?

A

 Crackles, bubbling sounds

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22
Q
  1. Why would a patient with heart failure become increasingly tired?
A

 SOB and decreased CO

 SOB presumably due to CO not being sufficient to meet demands of body

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23
Q
  1. What happens in moderate/severe heart failure as the afterload increases?
A

•  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.

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24
Q
  1. What happens in hypertension as the afterload increases?
A

•  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

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25
14. 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
26
13. 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
27
12. 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
28
11. 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
29
9. 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
30
61. What needs to be monitored during MRA therapy?
*  Renal function *  K+ *  Na+ *  Weight *  Fluid balance *  With spironolactone in particular, the presence of gynaecomastia in the male population
31
60. What are the NICE guidelines for using MRA’s
*  Add to ACEI + BB in HFrEF if still symptomatic *  If post ACS with EF <40% and symptoms of diabetes: add eplerenone *  If already being treated with MRA, can continue that drug
32
59. What was shown in the Emphasis-HF trial?
•  First hospitalisation for HF occurring less frequently, significantly less frequently in the trial group compared to the placebo
33
57. Why was the RALES trial stopped early?
 Stopped early due to reduction in mortality and reduction in sudden cardiac death 58. What was shown in the EPHESUS STUDY trial? •  Mortality benefit •  Reduction in hospitalisations
34
56. What are the 3 trials that support the use of MRA’s in the management of HFrEF?
*  RALES (1999) *  Emphasis-HF (2011) *  EPHESUS STUDY (2003)
35
55. What is the role of aldosterone in heart failure?
*  Increased levels of aldosterone are seen in patients with HFrEF *  This can lead to effects that worsen HF such as: * Oestrogen * Pathologic LV hypertrophy • Arrhythmia * Ischaemia
36
54. What needs to be monitored during BB therapy?
*  Heart rate *  BP *  Wheeze/bronchospasm *  Fatigue/cold extremities *  Impotence *  Diabetes – reduced response to hypoglycaemia
37
53. What is a caution of using beta-blockers?
•  Need to be careful in unstable heart failure •  Consideration into selecting the timing in those who are particularly unwell •  Only beta-blockers that are licensed for HFrEF in the UK should be used – carvedilol, bisoprolol and nebivolol
38
52. Between Beta-blockers and ACE inhibitors, which drug class shows a stronger mortality benefit?
 Beta-blockers
39
What do the beta-blocker trials show?
•  Shows clear evidence of benefit of adding BB to ACE inhibitor •  Regardless of which study is looked at, those patients that received a BB had a better outcome than those who received the placebo •  Magnitude of the benefit will be due to the different patients within the groups
40
50. Which beta-blockers should be used?
•  Should be looking to use beta-blockers that have been used in the clinical trials and have been subsequently licensed for the management of HFrEF •  Bisoprolol •  Carvedilol •  Nebivolol •  Metoprolol – has strong trial data, although it isn’t licensed in the UK for this indication
41
49. Who should start on BB therapy?
 All patients |  HFrEF (<40%) regardless of symptoms (unless contra-indications)
42
48. Where are B1 and B2 receptors located?
 B1 – heart |  B2 – lungs/vascular smooth muscle
43
47. What does beta therapy do?
•  Reduces the high levels of circulating adrenaline and noradrenaline •  Cause bradycardia which will improve the filling of ventricle, (increased coronary blood flow) cardiac output is maintained and the force of contraction is reduced •  Block the RAS system and aldosterone effects •  Reduce arrhythmias/SCD •  Reduce mortality
44
46. When should BB therapy be started? And what does this do?
 At the same time as ACE inhibitor
45
45. Why is it not advised to use an ACE inhibitor, MRA and ARB?
 Because using all three drugs in combination would cause much higher levels of renal
46
44. Why would the addition of an MRA be more beneficial?
 Because the addition of an MRA has a mortality benefit as well as a symptomatic benefit
47
43. What should be done if a patient remains symptomatic after ARB therapy?
 Add in MRA (rather than adding ACE and BB) |  Alternative therapy would be to switch patient to sacubitril-valsartan (+BB + MRA)
48
42. When should angiotensin II antagonists (aka ARBs) be used?
•  ACE inhibitors are the gold standard/first line and ARBs alone are not superior to them •  Therefore, ARBs should only be used if there is an intolerance of ACE inhibitors (e.g in afro- Caribbean patients)
49
41. What did the CHARM ADDED TRIAL (2003) look at and what did the findings show?
•  Looked at adding an ARBS to patients that were already on an ACE inhibitor and a beta- blocker •  Findings showed that: o • Using an ARB in addition to an ACE inhibitor reduces CV events in heart failure with reduced LVEF o • Drug combination reduced the total number of hospital admissions
50
40. What are two things to note in terms of ACE inhibitors?
*  To start at a low dose and titrate up | *  Monitor
51
39. When is ACE inhibitor contraindicated and why?
•  In bilateral renal artery stenosis (RAS) •  Because as the narrowing of the arteries that are supplying the kidneys occurs •  If you give an ACE inhibitor, it will cause a drop in the pressure gradient across the kidneys and push the patient into acute renal failure •  However, this is the case only in a small number of patients.
52
38. In which circumstances is specialist initiation/caution required?
*  Diuretic therapy *  Serum creatinine > 150 micromol/L (underlying renal impairment) *  Hyponatremia *  Hypotension
53
36. How long after every dose increase should the renal function and K+ level be measured?
 1-2 weeks after every dose increase
54
34. When can a patient get angioedema during ACE inhibitor therapy?  Patient can get angioedema at any point during ACE inhibitor therapy 35. What needs to be monitoring during ACE inhibitor therapy?
•  Renal function (baseline and on dose increase) •  K+ •  Cough •  BP (sitting and standing BP, specifically monitoring BP in those complaining of dizziness or those with hypotension)
55
33. What are the potential side effects of ACE inhibitors?
•  Hyperkalaemia •  Hypotension (particular first dose) •  Renal impairment •  Acute angioedema which can cause swelling of lips, tongues and the airway (being possibly potentially fatal) •  Chronic dry cough
56
32. What did the HOPE TRIAL (2000) show?
 It showed that even in patients who have not yet had a coronary event but are at high risk for CV events and no heart failure, ramipril showed a benefit compared to the placebo in terms of prevention of heart failure.
57
30. Which trial showed that there is more benefit with higher doses (dose importance)?  ATLAS TRIAL (1999) 31. Which groups were shown by the trials to have smaller benefit? What did this therefore indicate?
•  Post MI with no LVSD were shown to have smaller benefits •  This suggests that the ACE inhibitors are the gold standard treatment for patients with acute coronary syndrome
58
29. What are the trials that were shown to prove the benefit of ACE inhibitors in patients with
*  CONSENSUS TRIAL (1987) *  SOVLD TRIAL (1991) *  SAVE TRIAL (first trial ACEI post MI study) (1992)
59
28. Who should use ACE inhibitors?
*  All patients | *  HFrEF (EF<40%) regardless of symptoms (if no contra-indications)
60
27. What are the benefits of using ACE inhibitors?
*  Prevent myocardial hypertrophy/”remodelling” *  Relieve symptoms and hospitalisations *  Improve exercise tolerance *  Reduce acute exacerbations *  Reduce mortality *  Improve survival and prevent progression of symptoms
61
26. Why are the treatment options for HFpEF quite limited?
 Because all of the clinical trials that have been undertaken to date have not been able to offer us a treatment that confers a prognostic benefit in patients with HFpEF
62
25. In which instance is blocking aldosterone seen to be beneficial?
 In HFrEF
63
24. Why are MRA’s useful in patients on loop or thiazide diuretic’s?
•  Because MRA’s cause potassium retention •  So, they are useful in these patients on loop or thiazide diuretics to help retain potassium in their systems
64
23. Give a situation in which an MRA may be particularly helpful?
*  When a patient has abdominal oedema | *  Useful to reduce fluid retention
65
22. What are some consequences of raised aldosterone?
•  Sodium and water retention, which can lead to oedema/congestion •  Vasoconstriction which may lead to hypertension •  Hypokalaemia and hypomagnesaemia, which may induce electrical instability and death of cardiac myocytes •  Myocardial hypertrophy and fibrosis
66
20. What is the goal when choosing a diuretic?
 Looking at the minimum dose needed to manage congestive symptoms 21. Is metolazone still readily available? •  No, it is discontinued •  NP only
67
What is metolazone?
*  Thiazide diuretic *  When used alone it is a weak diuretic *  VERY potent when combined with a loop diuretic
68
17. What is a risk of using thiazides?
 Thiazides may exacerbate diabetes and gout (due to uric acid retention) 18. What needs to be monitored when using thiazides? •  Potassium, sodium, magnesium, calcium •  Renal function
69
When are Thiazides ineffective?
HFrEF?  Because they act on the distal tubule, they tend to be ineffective in patients with poor renal function (eGFR <30mls/min) mainly because there is limited sodium exchange left available to patient.
70
. When is bumetanide better absorbed?
. When is bumetanide better absorbed?
71
11. When is IV diuretic stepped down to oral?
•  Once the patient has received adequate diuresis •  “48-hour rule”: o • Looking to get some clinical stability prior to discharge for 48 hours o • Ensuring that fluid retention is not recurring
72
9. Which diuretic causes inter and intra patient variability of absorption?  Furosemide 10. How are diuretics given in a hospital setting?
*  Given I/V | *  Bolus or continuous infusion
73
8. Give examples of loop, thiazide and mineralocorticoid receptor antagonists (MRA)
*  Loop diuretics: furosemide, bumetanide *  Thiazide diuretics: Bendroflumethiazide, metolazone *  MRA: spironolactone, eplerenone
74
19. What is NT pro-BNP? |  N-terminal pro-B-type natriuretic peptide 20. What does NT pro-BNP do?
*  It is a natriuretic peptide so it promotes natriuresis *  Inhibits ADH and aldosterone release *  Synthesised in myocardial cells in response to raised ventricular filling pressure: * Levels can be raised in heart failure

Heart Failure (7 decks)

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