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heart failure Flashcards

1
Q

what is stroke volume?

A

how many ml of blood is pumped per contraction

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2
Q

what initial blood tests would you do in someone presenting with oedema and why?

A

U+E: renal disease could lead to increased excretion of proteins
LFT and GGT -liver disease could lead to decreased synthesis of proteins
FBC
TFTs -hypothyroidism can cause oedema and fatigue
pro-BNP

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3
Q

what affects stroke volume?

A

preload
contractility
afterload

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4
Q

what is preload and what affects it?

A

end diastolic volume -amount of blood filling up ventricle before contracting-affected by venous return, fluid volume, ability of atria to contract and pass blood to ventricles

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5
Q

what affects contractility of heart muscle?

A

increase -positive inotropes eg noradrenaline
decrease -negative inotropes, beta blockers, CCBs

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6
Q

what is afterload and what affects it?

A

pressure required to pump blood from heart into arterial system -affected by BP, atherosclerosis, aortic valve stiffness

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7
Q

what is cardiac output and the equation for it?

A

amount of blood heart pumps out per minute
stroke volume x heart rate

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8
Q

what is ejection fraction and equation for it?

A

% of total blood in ventricle that gets pumped out by each systolic contraction
stroke volume/total ventricular volume

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9
Q

what is normal ejection fraction (EF)?

A

50-70%

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10
Q

what are the 3 types of heart failure (classified by ejection fraction) and their EFs?

A

1) systolic HF -HF with reduced ejection fraction -EF <40%
2) heart failure with mildly reduced ejection fraction -41-49%
3) diastolic HF -HF with preserved ejection fraction (hefpef) -EF>50%

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11
Q

what happens in HF with impaired ejection fraction and an example of a cause?

A

inability of ventricles to properly contract resulting in decreased cardiac output, eg IHD

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12
Q

what happens hefpef and examples of causes?

A

inability of ventricles to contract therefore fill properly
cardiac tamponade, restrictive cardiomyopathy, constrictive pericarditis

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13
Q

what happens in cor pulmonale/pulmonary heart disease?

A

enlargement and failure of right ventricle of heart as response to increased vascular resistance/ high BP in lungs. can happen due to respiratory disorder or buildup from left heart failure.

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14
Q

what are the 2 situations from which acute heart failure can arise?

A

1) previously healthy heart where something has caused in to fail
2) acute decompensation of already known heart failure

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15
Q

what are some triggers of acute heart failure?

A

ACS
tachys
PE
severe HTN
infection
drugs eg NSAIDs, steroids
not taking usual meds /dietary restrictions
renal insufficiency

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16
Q

how can acute heart failure be classified?

A

warm/cold -how peripherally perfused patient is
wet/dry -how fluid overloaded they are

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17
Q

what are some signs of poor peripheral perfusion?

A

low BP
cool peripheries
prolonged CRT
reduced UO

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18
Q

what are some signs of fluid overload?

A

pulmonary oedema -bibasal coarse crackles
raised JVP
peripheral oedema

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19
Q

what is he prognosis and management principle of warm and dry acute HF?

A

best prognosis
optimise meds and treat triggers

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20
Q

what is the management strategy of warm and wet acute HF?

A

give diuretics +/- vasodilators

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21
Q

what is the management strategy of cold and dry acute HF?

A

consider fluid bolus, may need inotropes

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22
Q

what is the prognosis and management strategy for cold and wet acute HF?

A

worst prognosis
consider diuretics if BP>90
may need vasopressors/inotropes

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23
Q

what are the symptoms of left heart failure?

A

congestion in lungs causing pulmonary oedema:
dyspnoea
orthopnoea
PND
cough
cardiac wheeze (wheeze caused by heart issues)

24
Q

what are some signs of right HF?

A

ankle oedema
raised JVP
ascites

25
Q

what are some non specific symptoms of HF?

A

fatigue
chest pain

26
Q

what do you hear on auscultation of pulmonary oedema?

A

bibasal course crackles

27
Q

what are some signs of acute HF?

A

pulmonary oedema
raised JVP
peripheral oedema
wheeze
S3 heart sound
ascites
signs of poor perfusion

28
Q

what is the classic disease course of heart failure?

A

period of relative stability followed by progressive decline. the decline is often punctuated by attacks of decompensated heart failure, from which the patient often recovers with medical support, but may not reach their previous level of independence and functioning.

29
Q

what bloods would you do for ?HF and why?

A

baso guided on symptoms +use common sense but:
- FBC -anaemia, infection
- U+E -renal function to check trigger in acute and affect drug choices
- LFTs -HF can cause raised LFTs but not specific, raised LFTs mean poorer prognosis
- TFTs -rule out differentials eg palpitations
- pro-BNP
- troponin -rule out ?MI in acute
- d-dimer -rule out ?PE in acute

30
Q

what are the NICE guidelines for different levels of NT pro-BNP?

A

NT-pro-BNP >400 should be referred for echo and specialist assessment within 6 weeks
>2000 -urgent review within 2 weeks

31
Q

what level of NT pro BNP is suggestive of heart failure?

A

> 400
not diagnostic tho

32
Q

what is the investigation of choice for diagnosis of HF?

A

echo

33
Q

what do you see on CXR of HF?

A

ABCDE:
alveolar oedema
kerley B lines
cardiomegaly
dilated upper lobe vessels
pleural effusion

34
Q

what system stages severity of heart failure?

A

NYHA

35
Q

what are the NYHA classifications of heart failure?

A

class I-no limitations, ordinary physical activity doesn’t cause symptoms
- class II-symptomatically mild, slight limitation of physical activity but comfortable at rest
- class III -symptomatically moderate, marked limitation of physical activity
- class IV -symptomatically severe, symptoms even present at rest.

36
Q

what is the management for acute heart failure?

A
  • sit patient up if they have pulmonary oedema -increases ventilation area
  • high flow 02 in patients who are hypoxic -don’t give if they have normal sats.
  • IV furosemide -for patients with signs of fluid overload -aim to give dose at least equal to/higher than the patient’s usual dose and monitor renal function closely.
  • diamorphine +antiemetic -if patient has chest pain/distress and not confused or drowsy
  • catheterisation and monitor UO
  • if BP low, consider ITU admission and inotropes, eg dobutamine. can also consider vasopressors under specialist guidance.
37
Q

what are the lifestyle interventions for chronic heart failure?

A

stop offending drugs
stop smoking and drinking
monitor fluid intake
diet -salt reduction
exercise -patients should be referred to cardiac rehab programme
imms -annual flu, single pneumococcal
weight tracking to look for unexpected weight gain

38
Q

what is the pharmacological treatment for chronic heart failure with preserved ejection fraction once diagnosed by a specialist?

A

diuretics for congestive symptoms and fluid retention-furosemide 1stline
manage all comorbidities in line with NICE guidance
personalised exercise based cardiac rehab programme (unless condition is unstable)

39
Q

what is the pharmacological treatment for chronic heart failure with reduced ejection fraction once diagnosed by a specialist?

A

1) diuretics for congestive sx and fluid retention
1) ACEi and BB
consider ARB if intolerant of ACEi, consider hydralazine and nitrate if intolerant of ACEi and ARB
2) MRA if symptoms continue
3) specialist advice

40
Q

what might a specialist consider for HF with reduced EF post firstline treatments?

A

-replace ACEi/ARB with sacubitril valsartan if EF <35%
-add ivabradine if HR >75 and EF <35%
-add hydralazine and nitrate-more highly considered if afro-carribean descent
-digoxin for HF with sinus rhythm to improve sx
-SGLT2s-if added to either triple therapy (ACE/ARB/sacubitril+BB+MRA)
-CRT
-ICD

41
Q

what are 2 examples of ACEis?

A

lisinopril
ramipril

42
Q

what are the 2 ARBs licensed for HF treatment?

A

candesartan
valsartan

43
Q

which beta blockers are licensed for HF ?

A

bisoprolol, carvedilol (old people), nebivolol

44
Q

what are MRAs and examples?

A

antimineralocorticoids -spironolactone, eplerenone

45
Q

what is hydralazine?

A

direct acting vasodilator

46
Q

what does digoxin actually do?

A

cardiac glycoside that increases force of myocardial contraction and reduces conductivity within the AVN, slowing heart rate.

47
Q

which SGLT2s are licensed for heart failure and in what situations?

A

empagliflozin and dapagloflozin
if added to triple therapy: ACE/ARB?sacubitril valsartan +BB+MRA

48
Q

what does sacubitril do?

A

inhibits breakdown of natriuretic peptides resulting in increased diuresis, natriuresis, and vasodilation.

49
Q

what is natriuresis?

A

process of sodium excretion in the urine through the action of the kidneys.

50
Q

what does ivabradine do?

A

pacemaker current inhibitor -slows HR via specific inhibition of the pacemaker current

51
Q

what are ICDs?

A

implantable cardiac defibrillators

52
Q

what do ICDs do?

A

device under the skin with leads going to heart
detect potentially fatal rhythms and give shocks -eg VT, VF, brady

53
Q

when are ICDs recommended?

A

people with LVSD (left ventricular systolic dysfunction) with EF <35% who are not likely to die in the next year

54
Q

what happens in CRT (cardiac resynchronisation therapy)?

A

device under skin with leads to heart
device registers atrial rate and stimulates ventricles to coordinatedly contract, bypassing the bundle branches.
some of them can also have a defibrillator (CRT-D) (CRT-P=pacing only)

55
Q

who is CRT appropriate for?

A

patients with poor ventricle coordination. most common cause =prolonged QRS with LBBB. generally QRS>150ms and LBBB are the patients who get it

56
Q

what is an LVAD?

A

left ventricle assist device -device which physically pumps blood from heart rather than delivering impulse, used to keep patient alive/optimise health pre heart transplant

cardiovascular (9 decks)

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