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Cardiology > Heart failure > Flashcards

Heart failure Flashcards

1
Q

Briefly describe the definition of HF

A

Of note - after a confirmed diagnosis, HF is categorised into HFreF vs. HFpeF (based on 2018 guidelines)

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2
Q

In addition to symptoms + signs of HF and an EF>50%, HFpEF requires additional objective parametres to favour in the diagnosis. What are the two categories of this?

A

Objective evidence of
1. Relevant structural heart disease
2. Evidence of diastolic dysfunction

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3
Q

Describe one finding that would be suggestive of stuctural heart disease

A
  • LV hypertrophy
  • left atrial enlargement
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4
Q

What are 2 features that may suggest diastolic dysfunction?

A

Some sort of raised filling pressure
- elevated BNP or NT proBNP
- evidence on exercise (invasive or stress TTE)
- evidence on TTE*
- findings on a cardiac cath

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5
Q

What is HF with improved EF?

A
  • note these patients have a better prognosis
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6
Q

The diagnosis of HF (as per strong recommendation) includes an ECG (looking for LVH/ischaemia), CXR, BNP and TTE. Which of these shows high quality of evidence?

A

BNP

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7
Q

What value of BNP rules out a likely HF diagnosis?

A

<100

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8
Q

What value of NT proBNP rules out a HF diagnosis?

A

<300

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9
Q

What value of BNP rules in a Dx of HF?

A

BNP>400

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10
Q

What value of NT pro-BNP rules in a Dx of HF?

A

note this is age dependent

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11
Q

Once HF appears to be a likely diagnosis, there is often Ix into the cause. One possible cause is CAD. Outline how you would approach this

A
  • consider angiogram for patients that are high risk (e.g. refractory angina, ventricular arrhythmiyas, intermediate - high probability of CAD)
  • for low-moderate risk can consider non-invasive Ix such as CTCA or cardiac MRI
  • if patients have ESTABLISHED CAD + HF, can consider SPECT, stress TTE, PET and CMR to assess the need for coronary vascularisation
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12
Q

A patient has a diagnosis of HF. What would be the next most useful Ix if it was found the patient has increased LV wall thickness on their TTE?

A
  • Cardiac MRI - would assist to identify inflammatory and infiltrative cardiomyopathies
  • PET + bone scintigraphy > the latter especially useful in amyloidosis
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13
Q

What is the mainstay treatment in decompensated CCF

A
  • loop diuretics
  • IV vasodilators if SBP>90
  • IV ionotropes if peripheral hypopersfusion and SBP<90, and treatment towards easing congestion has failed (contraindicated if no evidence of peripheral hypoperfusion)
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14
Q

Where do loop diuretics work (e.g. furoseimide)?

A

thick ascending limb of the loop of Henle

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15
Q

Briefly outline the channel that enables Na reabsorption

A
  • via transporting cells containing Na-K-ATPase pumps
    > allows Na to return to the systemic circulation
    > allows maintainence of Na concentration at low levels
    > raise K above its electrochemical equilibrium, thus enabling polarisation of the inside of the cell
    *Note sodium cannot move freely across a channel, it requires a tranposrter or channel
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16
Q

Which part of the nephron reabsorbs most of the sodium?

A

proximal tubule (approx 60-65%)

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17
Q

Outside of the proximal tubule, where else is Na reabsorbed?

A

loop of Henle (approx 20%)

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18
Q

Acetazolamide (a carbonic anhydrase inhibitor) acts at the proximal tubule. Why isn’t this an effective diuretic?

A
  • Most of the filtered sodium is reabsorbed in the proximal tubule (approximately 60 to 65 percent) and the loop of Henle (20 percent).
  • As a result, it might be expected that a proximally acting diuretic, such as the carbonic anhydrase inhibitor acetazolamide, could induce relatively large losses of sodium and water.
  • However, this does not occur, since almost all of the excess fluid delivered out of the proximal tubule can be reabsorbed more distally, particularly in the loop of Henle and to a lesser degree the distal tubule
    *sometimes distal reabsorption could also occur with a loop diuretic
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19
Q

List one other medication other than frusemide that is a loop diureitc

A
  • bumetanide
  • torsemide*
  • ethacrynic acid*
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20
Q

Outline the common side effect of furosemide

A
  • hypokalemia
    > this is because the Na-K-2Cl channel is blocked (preventing influx of 2K via transport). Additionally, as this cant come in, it cant also exit using a K channel to drive influx of sodium
  • hypocalcaemia
21
Q

How do loop diuretics affect calcium?

A
  • reabsorption of calcium is primarily passive, driven by the electrochemical gradient driven by NaCl transport
  • loop diuretics can therefore reduce calcium, thereby increasing calcium excretion (in the past furosemide + N.saline was thought to treat hypercalcemia!!!, but now anti-resoprtiove therapies are the mainstay of treatment
22
Q

What dose of frusemide is 1mg bumetanide equivalent to?

A

40mg

23
Q

What EF should triple/quadriple therapy be started for patients with reduced EF?

A

EF<40%

24
Q

Explain why the ARB/ARNI combination is currently used instead of an ACE/ARNI combination

A

The reason the neprilysin inhibitor was combined with ARB instead of ACE was due to higher rates of angioedema in the ACE/neprilysin inhibitor group

25
Q

When should you be cautions about starting an ARNI/ARB

A

If the patient has low blood pressure - If SBP<90, to consider starting at a low dose and ensuring close monitoring

26
Q

in 2018, the ARNI/ARB medication was introduced into the HF guidelines. What is this replacing?

A

ACE or ARB monotherapy

27
Q

in 2018, the ARNI/ARB medication was introduced into the guidelines. What is the washout period for an individual on ARB or ACE monotherapy and why?

A
  • to prevent angiooedema
  • 36 hour washout period recommended
28
Q

In what time frame would you expect to see benefit with treatment for HFreF?

A

within 30 days!

29
Q

List the 2 most common causes of left ventricular hypertrophy

A
  • aortic stenosis
  • systemic hypertension
30
Q

List 3 causes of LVH

A
  • Systemic hypertension
  • Aortic stenosis (valvular, supravalvular, or subvalvular)
  • Aortic regurgitation
  • Mitral regurgitation
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Ventricular septal defect
  • Some infiltrative cardiac processes (eg, Fabry disease, Danon disease)
31
Q

List one condition that demonstrates LVH without concurrent ECG changes

A
  • Amyloidosis
  • Sarcoidosis
  • Hemochromatosis
32
Q

Describe this ECG

A

suggestive of LVH
- increase LV voltages
- R wave peak is >50
- LV strain with STD and twi in 1, avL, v5 v6
- L) axis deviation
*consider how the ST elevation may be proportional to the deep S waves in LVH

33
Q

Describe the mechansim of sacubritil

A
  • neprilysin inhibitor > greater amounts of natureitic peptide
  • usual function of neprylysin is to break down breaks down naturetic peptides, angiotension II, bradykinin
34
Q

What do natureitc peptides do?

A

respond to ventricular stretch - cause vasodilation, naturesis (kidney excretion) and diuresis

35
Q

Why can’t sacubitril be paired with ACE inhibitor

A

leads to angioedema - both ACE and sacubitril lead to a build up of bradykinin

36
Q

Describe the mechanism of valsartan

A
  • Angiotensin I receptor blocker, therefore prevents angiotension II formation (Angiotensin I > angiotension II > acts on adrenal gland)
  • Neprilysin breaks down angiotensin II
  • This means a neprylisin inhibitor, causes excess angiotension II to build up – this is why the combination blocks the effect of angiotension II
37
Q

Explain how a side effect of an ARB can be hyperkalemia

A

ARBs inhibit angiotension II from binding to the adrenal receptor > inhibits production of angiotensin II within the adrenal cortex > decreases aldosterone and impairs potassium excretion
*note normal role of aldosterone is Na reabsorption and K excretion

38
Q

There are several drugs involved with RAAS blockage. How do ACE inhibitors work?

A

ACE inhibitors - block conversion of Ang1 to Ang 2 by blocking ACE enzyme

39
Q

How does an ARB work?

A

ARB antagonise effect of AngII on AT1 (angiotension I) receptor

40
Q

The four well known used ARBs are candesartan, irbesartan, telmesartan and valsartan. List one condition they are more commonly used for

A
  • Candesartan – HTN, heart failure
  • Irbesartan – HTN, diabetic nephropathy
  • Telmesartan – HTN, CVD patients who cant tolerate ace, stroke prophylaxis, MI prophylaxis
  • Valsartan – HF, Left ventricular dysfunction post MI
41
Q

what is the general role of beta receptors?

A

Inhibition of beta receptors reduced chronotropy (HR) and ionotropy (contractility) + reduces blood pressure. Decreased oxygen demand also helps with angina Sx

42
Q

Explain the difference between b1 and b2 receptors
a) what are the binding agents
b) what is the impact of b1?
c) what is the impact of b2?

A

B1 – cardio selective
- Binding agents are adrenaline, noradrenaline, catecolamines
- This induces cardiac automaticity + increased conduction velocity + renin release
- Prolonged atrial refractory periods can cause arrithmiyas

B2 – diverse location
- Bindings agents are adrenaline, noradrenaline, catecolamines
- This induces smooth muscle relaxation

43
Q

List two beta blockers that are non-selective

A

Propranolol, carvedilol, sotalol, labetalol

44
Q

List two beta blockers that have cardio-selective activity

A

Atenolol, bisoprolol, metoprolol, esmolol

45
Q

Alpha 1 receptors induce vasoconstriction and this leads to increase chronotropy. What 2 beta blockers have additional a1 activity

A
  • Carvidelol
  • labetolol

More pronounced effect in treating hypertension

46
Q

List one important contraindication of a beta blocker

A
  • beta-blockers are contraindicated specifically in systolic heart failure when pulmonary edema is present, when there are signs of cardiogenic shock, severe bradycardia, hypotension or wheezing related to asthma.
  • Beta-blockers are contraindicated during an acute myocardial infarction when there are signs of pending cardiogenic shock. These include systolic blood pressure < 110 mmHg and pulmonary edema.
  • other typical contraindications include severe bradycardia, heart block more advanced than first degree (unless a pacemaker is in place) and for use during a MI from cocaine use.
47
Q

Outline the mechanism of an SGLT2 inhibitor. What does your eGFR need to be to use it?

A
  • Act on SGLT inhibitors found in the proximal convultued tubule
  • Act by preventing reabsorption of glucose from the PCT
  • Can be used if eGFR>20
  • An important adverse effect is UTIs and therefore hygiene is important > often get build up of glycosuria
  • Associated with Euglycaemia DKA
48
Q

What part of the heart are naturetic peptides found

A
  • ventricular cells (site of primary release)

Cardiology (7 decks)

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