Heart failure Flashcards
Briefly describe the definition of HF
Of note - after a confirmed diagnosis, HF is categorised into HFreF vs. HFpeF (based on 2018 guidelines)
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?
Objective evidence of
1. Relevant structural heart disease
2. Evidence of diastolic dysfunction
Describe one finding that would be suggestive of stuctural heart disease
- LV hypertrophy
- left atrial enlargement
What are 2 features that may suggest diastolic dysfunction?
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
What is HF with improved EF?
- note these patients have a better prognosis
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?
BNP
What value of BNP rules out a likely HF diagnosis?
<100
What value of NT proBNP rules out a HF diagnosis?
<300
What value of BNP rules in a Dx of HF?
BNP>400
What value of NT pro-BNP rules in a Dx of HF?
note this is age dependent
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
- 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
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?
- Cardiac MRI - would assist to identify inflammatory and infiltrative cardiomyopathies
- PET + bone scintigraphy > the latter especially useful in amyloidosis
What is the mainstay treatment in decompensated CCF
- 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)
Where do loop diuretics work (e.g. furoseimide)?
thick ascending limb of the loop of Henle
Briefly outline the channel that enables Na reabsorption
- 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
Which part of the nephron reabsorbs most of the sodium?
proximal tubule (approx 60-65%)
Outside of the proximal tubule, where else is Na reabsorbed?
loop of Henle (approx 20%)
Acetazolamide (a carbonic anhydrase inhibitor) acts at the proximal tubule. Why isn’t this an effective diuretic?
- 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
List one other medication other than frusemide that is a loop diureitc
- bumetanide
- torsemide*
- ethacrynic acid*
Outline the common side effect of furosemide
- 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
How do loop diuretics affect calcium?
- 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
What dose of frusemide is 1mg bumetanide equivalent to?
40mg
What EF should triple/quadriple therapy be started for patients with reduced EF?
EF<40%
Explain why the ARB/ARNI combination is currently used instead of an ACE/ARNI combination
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
When should you be cautions about starting an ARNI/ARB
If the patient has low blood pressure - If SBP<90, to consider starting at a low dose and ensuring close monitoring
in 2018, the ARNI/ARB medication was introduced into the HF guidelines. What is this replacing?
ACE or ARB monotherapy
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?
- to prevent angiooedema
- 36 hour washout period recommended
In what time frame would you expect to see benefit with treatment for HFreF?
within 30 days!
List the 2 most common causes of left ventricular hypertrophy
- aortic stenosis
- systemic hypertension
List 3 causes of LVH
- 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)
List one condition that demonstrates LVH without concurrent ECG changes
- Amyloidosis
- Sarcoidosis
- Hemochromatosis
Describe this ECG
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
Describe the mechansim of sacubritil
- neprilysin inhibitor > greater amounts of natureitic peptide
- usual function of neprylysin is to break down breaks down naturetic peptides, angiotension II, bradykinin
What do natureitc peptides do?
respond to ventricular stretch - cause vasodilation, naturesis (kidney excretion) and diuresis
Why can’t sacubitril be paired with ACE inhibitor
leads to angioedema - both ACE and sacubitril lead to a build up of bradykinin
Describe the mechanism of valsartan
- 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
Explain how a side effect of an ARB can be hyperkalemia
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
There are several drugs involved with RAAS blockage. How do ACE inhibitors work?
ACE inhibitors - block conversion of Ang1 to Ang 2 by blocking ACE enzyme
How does an ARB work?
ARB antagonise effect of AngII on AT1 (angiotension I) receptor
The four well known used ARBs are candesartan, irbesartan, telmesartan and valsartan. List one condition they are more commonly used for
- 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
what is the general role of beta receptors?
Inhibition of beta receptors reduced chronotropy (HR) and ionotropy (contractility) + reduces blood pressure. Decreased oxygen demand also helps with angina Sx
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?
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
List two beta blockers that are non-selective
Propranolol, carvedilol, sotalol, labetalol
List two beta blockers that have cardio-selective activity
Atenolol, bisoprolol, metoprolol, esmolol
Alpha 1 receptors induce vasoconstriction and this leads to increase chronotropy. What 2 beta blockers have additional a1 activity
- Carvidelol
- labetolol
More pronounced effect in treating hypertension
List one important contraindication of a beta blocker
- 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.
Outline the mechanism of an SGLT2 inhibitor. What does your eGFR need to be to use it?
- 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
What part of the heart are naturetic peptides found
- ventricular cells (site of primary release)
