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2C Week 4,7 - heart failure and cardiomyopathy > Heart failure (see DM) > Flashcards

Heart failure (see DM) Flashcards

1
Q

what is heart failure

A

a clinical syndrome caused by a structural/functional abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures (inherent leaks increases intracardiac pressure)

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2
Q

new york heart association classification for HF (4)

A

I - no limitations in activity;
II - comfortable at rest, ordinary physical activity results in symptoms (mild);
III - comfortable at rest, pts have a marked limitation of physical activity (moderate);
IV - pts have symptoms even at rest, mortality of 15-20% which is worse than most cancers (severe)

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3
Q

3 most common causes of HF

A
  1. CAD
  2. hypertension (+diabetes + whole syndrome X)
  3. valve disease (AS/MR usually)
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4
Q

what is whole syndrome X?

A

a type of ischemic heart condition which results in the LV and myocardium not contracting properly

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5
Q

other causes of HF (10)

A

arrhythmias; cardiomyopathies; congenital heart defects; infective; drug induced; infiltrative; storage disorders; endomyocardial disease; pericardial disease; metabolic; neuromuscular disease

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6
Q

HF pathophysiology pathway

A

MI/aging/HTN etc. –> muscle injury –> ↓CO –> ↓ renal perfusion, ↓carotid baroreceptor –> ↑ sympathetic ↑ RAAS –> ↑ HR, ↑myocardial O2 consumption, ↑vasoconstriction –> ↑ preload, ↑ afterload –> ↑adverse remodelling –> muscle injury

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7
Q

how does loss of elasticity in LV muscle result in ↓ CO

A

impaired relaxation of LV –> ↓ change in pressure –> blood not pulled into the LV as fast –> decreased volume in LV –> decreased CO

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8
Q

types of HF (by EF) and their distinguishing factors (3)

A

HFpEF - LVEF >50% + ↑NTproBNP +LVH/↑LA or LV diastolic dysfunction + symptoms;
HFmEF - LVEF 40-49% + ↑NTproBNP + LVH/↑LA or LV diastolic dysfunction + symptoms;
HFrEF - LVEF <40%

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9
Q

treatment for HFpEF

A

dont yet have a good treatment - nonspecific treatment; treat primary cause (HTN, diabetes, obesity, cardiomyopathy etc.); diuretics

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10
Q

what 4 drugs (classes) are always given in treatment of HFmEF/HFrEF +examples

A

ACEi - ramapril; B blocker - bisoprolol; MRA (aldosterone antagonist) - spiranolactone; SGLT2 inhibitor - dapagliflozin (take care w renal impairment)

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11
Q

what is the main cause of HFmEF and HFrEF

A

ishaemic heart disease

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12
Q

why is the incidence of HFmEF and HFrEF decreasing

A

better treatment of heart attacks

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13
Q

what are the common causes of HFmEF and HFrEF (not ischaemia - 5)

A

dilated cardiomyopathy; alcohol induced cardiomyopathy; nutritional; auto-immune; arrhythmia induced

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14
Q

what are the primary care investigations for HF (4)

A

ECG; NTproBNP; bloods - FBC, U&Es, LFTs, thiamine, B12/folate, vit D, Ca2+, mg2+, HBA1c); CXR

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15
Q

what are the secondary care investigations for HF (5)

A

echo; cardiac MRI; invasive angiogram; cardiac CT coronary angiogram; nuclear imagine

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16
Q

what effect does a vasodilator have on the frank-starling mech

A

moves heart function from low output + high preload to lower preload and higher CO

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17
Q

what effect does a ionotrope have on the frank-starling mech

A

raises CO (increased LVED) without changing preload

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18
Q

what effect does a diuretic have on the frank-starling mech

A

increases preload but not enough to reduce HF as there is no effect on the contractility

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19
Q

what should be taken with caution alongside ACEi/ARBs and why

A

K+ sparing diuretics due to risk of hyperkalemia

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20
Q

what is the main aim of drug treatment in HF

A

decrease afterload and preload

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21
Q

what 7 drug classes are commonly given in HFrEF

A

ACEi; ARB; angiotensin-neprilysin inhibitors; BBs; loop diuretics/thiazides; MRA; ivabradine; nitrates

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22
Q

what drugs should not be given in HF and why, and what other type of drug should it not be combined with

A

CCBs (e.g. verapamil) - can result in abrupt decompensation and development of overt pulmonary edema and hypotension; should not be given with BBs

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23
Q

why are ACEi bad for pts w kidney impairment

A

dialte both the venous and arterial systems which can cause renal impairment

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24
Q

what non drug treatments are available for HF (6)

A

valve surgery; PCI/CABG; CRT; ICD; nodal ablation (if causing arrythmias); cardiac transplant

25
Q

what is left ventricular assist device (LVAD) and when is it indicated

A

a device that pumps the blood outside the LV - only used in extreme cases (e.g. dilated cardiomyopathy, MI in <40yro) and usually as a bridge for a heart transplant

26
Q

how does acute HF present and how should it be managed

A

presents in decompensation stage (low output and congestion); IV treatment is needed (depends on other comorbidities)

27
Q

how does chronic HF present (frank-starling)

A

low output but not congested

28
Q

what are the 4 main indications for ACEi use

A

HTN; chronic HF; ischaemic heart disease/CAD; diabetic nephropathy adn CKD with proteinuria (reduced proteinuria and progression)

29
Q

what is the MOA of ACEi and what does it result in

A

inhibits angiotensin I –> angiotensin II (and therefore aldosterone release); results in reduced peripheral vascular resistance, lowers BP, dilates efferent glomerular aterioles in particular and works to slow the effects of CKD; aldosterone reductions results in increased water and sodium excretion –> reduced venous return (preload) which is beneficial to HF

30
Q

common side effects of ACEi (4)

A

hyotension (esp after first dose); peristent dry cough (due to incr bradykinin which is usually inactivated by ACE); hyperkalemia (decr aldosterone promotes K+ retention); cause/worsen renal failure

31
Q

who should avoid ACEi (4)

A

pts w renal artery stenosis (rely of contraction of elomerular arterioles); AKI; pregnant; breastfeeding

32
Q

4 indications of ARBs

A

HTN; chronic HF; ischaemic heart disease; diabetic neuropathy and CKD

33
Q

why would ARBs be used over ACEis

A

if ACEi is not tolerated e.g. due to dry cough

34
Q

what do ARBs act on

A

block the action of angiotensin II on angiotensin type 1 (AT1) receptors

35
Q

common side effects of ARBs (3)

A

hypotension; hyperkalemia; renal failure

36
Q

indications for aldosterone antagonists (3)

A
  1. ascites & oedema due to liver cirrhosis
  2. chronic HF
    3/ primary hyperaldosteronism
37
Q

MOA of aldosterone

A

acts on mineralcorticoid receptors in the DCL of kidneys to increase ENaC activity –> ↑ Na+ and water reabsorption –> ↑BP

38
Q

MOA of aldosterone antagonists

A

competitively inhibits alosterone receptro binding –> ↑ Na+ and water excretion, ↑K+ retension –> reduced BP –> fluid around heart

39
Q

side effects of aldosterone antagonists

A

hyperkalemia (leads to muscle weakness, arrythmias and cardiac arrest); gynaecomastia (impotence in men); liver impairment and jaundice leading to steven johnson sydnrome

40
Q

what is steven-johnson syndrome

A

T cell mediated hypersensitivity reaction; skin errupts w rash/blisters

41
Q

who should avid aldosterone antagonists

A

pts w severe renal impairment; hyperkalaemia; addison’s disease

42
Q

side effects of BBs (6)

A

fatigue; cold extremities; GI disturbances; sleep disturbances; impotence

43
Q

who should avoid BBs

A

pts w asthma; haemodynamic instability; significant hepatic failure; heart block

44
Q

when is digoxin indicated (2)

A
  1. AF/ A flutter;
  2. severe HF - if other drugs are failing or if pt has AF and HF
45
Q

digoxin MOA

A

it is a negatively chronotropic (decr HR) and positively ionotropic (incr contratility) drug;
AF - increases vagal tone and blocks AVN conduction;
HF - has a direct effect on myocytes through inhibiton of Na+/K+ ATPase pumps causing Na+ to accumulate in the cell, low Na+ conc is required for Ca2+ extrusion -> Ca2+ accumulates within the cell and increases the force of contraction

46
Q

side effects of digoxin (5)

A

bradycardia; GI disturbance; rash; dizziness; visual disturbances (blurred yellow vision); digoxin toxicity with associated arrythmias

47
Q

who should not take digoxin (3)

A

pts w 2nd degree/complete heart block; risk of ventricular arrythmias; electrolyte abnormalities (esp. hypokalaemia, hypomagnesaemia and hypercalcaemia)

48
Q

what drugs increase the risk of digoxin toxicity

A

hypokalaemia causing - loop/thiazide diuretics;
incr digoxin plasma conc - amioderone; CCBs; spironolactone; quinine

49
Q

when are loop diuretics indicated (3)

A
  1. relief of SOB in acute pulmonary oedema (alongside O2 and nitrates)
  2. symptomatic fluid overload in chronic HF
  3. symptomatic fluid overload in other oedematous states e.g. liver failure
50
Q

loop diuretics MOA

A

act on ascending loop of Henle, inhibit Na+/K+/2Cl- co-transporter - responsible for transporting sodium, potassium & chloride ions from tubular lumen into epithelial cell, Water then follows by osmosis → Inhibiting this process has a potent diuretic effect;
effect bvs - dilatation of capacitance veins;
acute HF - reduces preload & improves contractile function of ‘overstretched’ heart muscle

51
Q

side effects of loop diuretics

A

dehydration and hypotension; low electrolyte state (e.g. hyponatraemia, hypokalemia etc.); tinnitus + hearing loss (same transporter regulates endolymph)

52
Q

who are loop diuretics contraindicated in

A

pts w severe hypovolaemia/dehydration; risk of hepatic encephalopathy; severe hypokalaemia/hyponaturaemia; pts w gout

53
Q

what is Systolic (HFrEF)

A

Reduce proportion of blood that fills ventricles in diastole; Incr in blood at end of systole → ventricular stretch, dilatation, eccenetric
remodelling

54
Q

what is Diastolic (HFpEF)

A

Impaired ventricular relaxation or filling; Ventricular hypetrophy tends to develop

55
Q

what is cardiac remodeling

A

changes in cardiac size, shape & function in response to cardiac injury or increased load

56
Q

compensatory mechs for decreased CO (5)

A
  1. increasing preload - increased contraction to compensate for decreased EF, Severe disease results in large increases → pulmonary oedema, ascites &
    peripheral oedema;
  2. increase HR (CO = SV x HR)
  3. RAAS activation - renal hypoperfusion from decr CO. Contributes to increased
    venous pressures through vasoconstruction & retention of water & Na+
    contributing to oedema;
  4. sympathetic activation - Increases myocardial contractility & HR, Chronic activation is detrimental triggering myocyte death & further activation of RAAS
  5. hypertrophy of stressed myocardium
57
Q

how does peripheral oedema occur in HF

A

fall of circulatory volume and arterial filling -> activation of RAAS (regulates blood pressure, activation of this system causes ADH release and salt + water retention); Renal sympathetic nerves are also activated due to baroreceptors which also increases RAAS activation -> This together leads to increased peripheral and renal arteriolar resistance alongside water and Na+ retention -> This leads to increased venous volume and therefore expansion resulting in oedema

58
Q

cons of using BNP as a marker (2)

A

obesity may mask it; elevation may be caused by other things e.g. MI - it is non specific to HF

2C Week 4,7 - heart failure and cardiomyopathy (6 decks)

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