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MO1 > Heart failure > Flashcards

Heart failure Flashcards

1
Q

define heart failure

A

Heart failure is not a single pathological diagnosis, but a clinical syndrome consisting of
* cardinal symptoms
* Dyspnoea, ankle oedema and fatigue
* and signs
* Elevated JVP, pulmonary crackles and peripheral oedema

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2
Q

what causes heart failure?

A

Due to structural +/- functional abnormality of the heart

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3
Q

what does heart failure result in?

A

Elevated intracardiac pressure
* And/or inadequate cardiac output
* At rest and/or during exercise

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4
Q

what conditions damage the heart muscle/ limit its ability to function normally?

A

CHD, HTN, Cardiomyopathies
* Drugs, Toxins
* Endocrine conditions & infiltrative conditions

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5
Q

what conditions reduce cardiac output?

A
  • Increased vascular resistance with hypertension
  • Abnormal heart rhythm
  • Aortic stenosis (severe)
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6
Q

what conditions result in a high cardiac output?

A
  • Anaemia
  • Thyrotoxicosis
  • Septicaemia
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7
Q

what happens in left Heart failure?

A

there is an increase in CO and pulmonary congestion
this results in pulmonary oedema, breathlessness and exercise intolerance

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8
Q

what happens in right sided HF?

A

congestion of peripheral
tissues)
* Distended JVP
* Hepatomegaly,
* Ascites
* Dependent ankle oedema

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9
Q

how is left ventricular ejection fraction classified?

A

– Heart failure with reduced ejection fraction (HFrEF)
* LVEF ≤40%
– Heart failure with mildly reduced ejection fraction (HFmrEF)
* LVEF 41 – 49%
– Heart failure with preserved ejection fraction (HFpEF)
* LVEF ≥50% (associated with HF symptoms/structural or functional
abnormalities or raised natriuretic peptides

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10
Q

what is acute/decompensated heart failure?

A

New or deterioration in patient with chronic HF

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11
Q

what are the different classes of the new york heart classification?

A

1- no limitation of physical act. ordinary physical activity does not cause fatigue, palpitation or dyspnoea.
2- slight limitation of physical activity. Comfortable at rest but ordinary physical activity results in fatigue, palpitations or dyspnoea
3- marked limitation of physical activity. comfortable at rest but less than ordinary activity results in fatigue, palpitation or dyspnoea
4- unable to carry out physical activity without discomfort. symptoms at rest. if any physical activity is undertaken, discomfrot is increased

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12
Q

what are the levels of aldosterone like in HF?

A

aldosterone levels 20x normal in HF

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13
Q

what is kidney hypoperfusion result from?

A

reduced cardiac output- ie HF
thus leads to the activation of the RAAS

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14
Q

what does a decrease in CO result in ?

A

activation of the SNS and release of catecholamines

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15
Q

what is the initial benefit of a activation of the SNS?

A

Activation of B1 receptors will increase HR and
contractility
– Activation of alpha1 receptors causes
vasoconstriction
– » Redistributes blood flow to essential organs
(heart, brain, lungs)
– » Maintains BP in the face of decreased CO

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16
Q

what is the eventual harm that occurs when the SNS is activated?

A

Prolonged catecholamine stimulation results in:
* » Increased myocardial O2 demands
* » Down-regulation of B1 recs/decreased contractile function
* » Cardiac ischemia/arrhythmias (b/c heart working harder)

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17
Q

how would a HF patient presentation differ in a hospital than community?

A

Hospital
* Typically SOB, exercise intolerance, swollen
legs +/- other clinical features, dyspnoea,
fatigue, fluid retention
Community
* Usually less acute
* More challenging diagnosis
* Differential?

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18
Q

what are the complications in HF?

A
  • Arrhythmias – common at any stage.
  • Atrial fibrillation — prevalence increases with severity of HF
  • Ventricular arrhythmias — common with dilated left ventricle and reduced LVEF
  • Depression-
  • Sexual dysfunction
  • Common – may be caused by HF or drugs (e.g. beta-blockers).
  • Cachexia (wasting) – serious complication
  • Usually occurs together with severe dyspnoea and weakness.
  • Life expectancy is worse for people with cachexia and HF than that for
    most cancers.
  • Sudden death – about half of HF deaths
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19
Q

what is the stay and management for decompensated HF?

A

around 10 days
* Inpatient management:
– Bed rest – facilitates diuresis
– LMWH
– Strict fluid balance – input and output
– Daily weights
– Fluid restriction – 1.5L/day
– Daily U&E’s during IV therapy
– IV diuretics
– Catheter

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20
Q

when should diuretics be given in HF?

A

dyspnoea, ankle or pulmonary oedema
before or with an ACEI
before a BB
adjust dose according to response

21
Q

what should you monitor with diuretics?

A
  • Monitor electrolytes and renal function
22
Q

what are the common diuretics used in HF?

A
  • Loop
  • Furosemide, Bumetanide, Torasemide
  • Oral preferred route or IV if severely congested (congestion affects absorption)
  • Thiazides
  • Bendroflumethiazide
  • Metolazone (short-term or low dose for resistant pts)
23
Q

what is the pharmacological therapy for HF?

A

NICE recommended ACEI or beta-blocker should be
initiated first and up-titrated to target dose or maximum
tolerated dose, although ESC propose a new
sequencing, starting with beta-blocker and SGLT2i.

24
Q

is the sequence initiation of therapy important?

A

The exact order of initiation is likely to be unimportant,
as long as quadruple therapy is achieved.

25
Q

when should you do baseline U/Es?

A

1/2 weeks > 3 monthly

26
Q

how is the max dose of ACEi reached? what do you do after that?

A

he dose of ACE inhibitor can be increased every two weeks until the maximum dose is achieved
* Once the maximum dose is achieved add one of the recommended β
blockers

27
Q

what is sacubitril/valsartan?

A

First-in-class angiotensin receptor neprilysin inhibitor

28
Q

how does sacubitril/valsartan work?

A
  • Neprilysin degrades vasoactive peptides
  • Inhibition causes vasodilation, diuresis, reduces remodelling
29
Q

when would sacubitril/ valsartan be used?

A

Recommended as an option for treating symptomatic chronic heart failure in patients with reduced ejection fraction who meet criteria as specified by NICE TA388.
May also be considered in patients with HFrEF in those who are ACE inhibitor/ARB naïve with a LVEF of ≤35%. Treatment must be initiated
by heart failure specialist.

30
Q

how should you initiate sacubitril/valsartan if patient is already on an ACEi?

A

Do not start treatment until 48 hours after discontinuing ACE inhibitor therapy to minimise the risk of angioedema.

31
Q

what do mineralocorticoid receptor antagonists prevent?

A

Prevent remodeling and fibrosis, sudden cardiac death (VTs), & improve
hemodynamics (used alone or with ACEis or ARBs)

32
Q

what are the two examples of mineralocirticoid receptor antagonists for HF?

A

Currently spironolactone & eplerenone

33
Q

when would MRAs be given?

A

In addition to ACE and Beta Blocker as first line therapy if reduced ejection fraction and symptoms continue

34
Q

what is the danger associated with MRAS?

A

Danger of hyperkalaemia and worsening renal function
* Extra caution with diarrhoea, vomiting etc.

35
Q

what is spironolactone? when would you use it?

A
  • Spironolactone is a non-selective inhibitor of aldosterone
  • Consider after initial HF treatment steps
36
Q

what is the dose of spironolactone?

A
  • Initial dose 25mg daily
  • Baseline U&Es, recheck ~1wk
  • Can ↑to 50mg or ↓12.5mg daily
  • Symptomatic improvement may not be for some weeks
37
Q

what is eplerenone?

A

Selective aldosterone antagonist
* Prevents binding of aldosterone to mineralocorticoid cell receptors

38
Q

when would eplernone be given?

A

Adjunct in stable patients with left ventricular ejection fraction ≤40% with evidence of
heart failure, following myocardial infarction

39
Q

what side effects does eplernone have?

A

– Hyperkalaemia, dizziness, diarrhoea, nausea
– Drug interactions (Cytochrome P450 3A4 interactions)

40
Q

what monitoring is required for ACEi, BB, MRA?

A
  • Start therapy at a low dose and titrate until target dose
    (or max tolerated) is achieved. e.g. every 2 weeks
  • Monitor sodium, potassium and renal function at
    baseline and 7-14 days after dose increments
  • Measure BP before and after dose increments
41
Q

when are SGLT2 inhibitors C/I?

A

type 1 diabetes mellitus: do not use

42
Q

what do you have to remember to council on with SGLT2 inhibitors?

A

– Genito-urinary infections
– DKA
– Sick day rules

43
Q

what dose of SGLT2 inhibitors should a patient be initiated on by a SPECALIST?

A

10mg od

44
Q

when is digoxin used?

A

use for all patients with atrial fibrillation and any degree of
heart failure
* Consider for patients on maximal therapy and worsening HF
due to LVSD

45
Q

when is ivabradine used?

A

chronic HF

46
Q

how does ivabradine work?

A

Selective and specific inhibition of the cardiac pacemaker If
current
* – NYHA stage II to IV, with systolic dysfunction, SR with 75
bpm or greater, with LVEF of 35% or less

47
Q

what other management of HF should be taken into account?

A
  • Assess and manage cardiovascular risk
  • Review current medicines that may affect heart
    failure:
    manage co-morbidities
48
Q

what meds may affect hF?

A

o NSAIDs (associated with fluid retention and renal toxicity).
o Calcium-channel blockers (may cause fluid retention
and have no mortality benefit).
o Pioglitazone
o Antiarrhythmics.

49
Q

what co-morbidities should be managed in HF?

A
  • Angina
  • Asthma or COPD
  • Atrial Fibrillation
  • Diabetes mellitus
  • Gout
  • Renal impairment

MO1 (50 decks)

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