Heart Failure Flashcards

Help define definitions; complications; interventions and evidence for treatment

1
Q

Definition of heart failure

A

Clinical syndrome with current or prior a structural or functional impairment of the heart WITH either raised BNP and objective evidence of pulmonary/systemic congestion

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2
Q

Washout period when transitioning from ACEi to ARNI? and why?

A

36hrs washout period - studies showed an associated risk of development of angioedema

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3
Q

Indication for starting ivabradine in eCCF and the study showing it’s indication

A

SHIFT study-
Showed improvement when commenced in HFrEF <35% and HR up to 70bpm with SR after ACEi and B-blocker with/without MRA.
This showed reduced cardiac mortality and hospitalizations

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4
Q

When should you consider advanced heart failure therapies

A

1.NYHA 3-4 sx
2.Recurrent Hospital Admissions
3.Episodes of vascular congestion
4. These sx persist despite optimised therapy

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5
Q

What are the type of beta blockers in the market?

A

Beta-1 receptor-selective blockers like atenolol, bisoprolol, metoprolol, and esmolol only bind

Non-selective agents bind to both beta-1 and beta-2 receptors and induce antagonizing effects via both receptors. Examples include propranolol, carvedilol, sotalol, and labetalol.

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6
Q

What defect is associated with Hypertrophic Obstructive Cardiomyopahty?

A

the most common defects involve a mutation in the gene encoding
i.β-myosin heavy chain protein ii.myosin-binding protein C

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7
Q

What are the ECHO findings associated with HOCM

A

Echo findings - mnemonic - MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)

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8
Q

What is the mechanism of action of Nicorandil

A

The correct answer is Potassium-channel activator. Nicorandil is a vasodilatory drug that acts as both
i.a nitrate
ii.non-selective potassium channel activator. It opens up ATP-sensitive potassium channels in the smooth muscle of coronary and peripheral blood vessels, leading to hyperpolarisation and relaxation.

This results in an increase in blood flow to the myocardium (heart muscle) and a reduction of the heart’s workload, thus alleviating angina symptoms.

Side effects include:
dizziness, nausea, vomiting and headache. This ulceration may occur anywhere along the gastrointestinal tract

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9
Q

What are the pathological findings found in HOCM

A

Myofibrillar hypertrophy, myocyte disarray and interstitial fibrosis

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10
Q

mechanism of action of ACE-i

A

Mechanism of action:
inhibits the conversion angiotensin I to angiotensin II
→ decrease in angiotensin II levels → to vasodilation and reduced blood pressure
→ decrease in angiotensin II levels → reduced stimulation for aldosterone release → decrease in sodium and water retention by the kidneys
renoprotective mechanism
angiotensin II(which effects have been decreased) constricts the efferent glomerular arterioles
ACE inhibitors therefore lead to dilation of the efferent arterioles → reduced glomerular capillary pressure → decreased mechanical stress on the delicate filtration barriers of the glomeruli
this is particularly important in diabetic nephropathy
ACE inhibitors are activated by phase 1 metabolism in the liver

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11
Q

In the event of Native valve endocarditis what is the most likely infective organism, and best therapy

A

Most likely Staphy Aureus.
Ideal blind therapy would be
IV Amoxicillin and IV gentamycin

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12
Q

Mechanism of action of Vericiguat?

A

This is a novel sGC stimulator that enhances cyclic GMP and NO signaling by stimulating sGC and sensitizing sGC to enodgenous NO

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13
Q

What are the effects of BNP?

A

Effects of BNP
i.vasodilator
ii.diuretic and natriuretic
iii.suppresses both sympathetic tone and the renin-angiotensin-aldosterone system

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14
Q
A
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