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

Heart failure (see DM) Flashcards

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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)

Study These Flashcards
A

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

25
what is left ventricular assist device (LVAD) and when is it indicated
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
how does acute HF present and how should it be managed
presents in decompensation stage (low output and congestion); IV treatment is needed (depends on other comorbidities)
27
how does chronic HF present (frank-starling)
low output but not congested
28
what are the 4 main indications for ACEi use
HTN; chronic HF; ischaemic heart disease/CAD; diabetic nephropathy adn CKD with proteinuria (reduced proteinuria and progression)
29
what is the MOA of ACEi and what does it result in
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
common side effects of ACEi (4)
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
who should avoid ACEi (4)
pts w renal artery stenosis (rely of contraction of elomerular arterioles); AKI; pregnant; breastfeeding
32
4 indications of ARBs
HTN; chronic HF; ischaemic heart disease; diabetic neuropathy and CKD
33
why would ARBs be used over ACEis
if ACEi is not tolerated e.g. due to dry cough
34
what do ARBs act on
block the action of angiotensin II on angiotensin type 1 (AT1) receptors
35
common side effects of ARBs (3)
hypotension; hyperkalemia; renal failure
36
indications for aldosterone antagonists (3)
1. ascites & oedema due to liver cirrhosis 2. chronic HF 3/ primary hyperaldosteronism
37
MOA of aldosterone
acts on mineralcorticoid receptors in the DCL of kidneys to increase ENaC activity --> ↑ Na+ and water reabsorption --> ↑BP
38
MOA of aldosterone antagonists
competitively inhibits alosterone receptro binding --> ↑ Na+ and water excretion, ↑K+ retension --> reduced BP --> fluid around heart
39
side effects of aldosterone antagonists
hyperkalemia (leads to muscle weakness, arrythmias and cardiac arrest); gynaecomastia (impotence in men); liver impairment and jaundice leading to steven johnson sydnrome
40
what is steven-johnson syndrome
T cell mediated hypersensitivity reaction; skin errupts w rash/blisters
41
who should avid aldosterone antagonists
pts w severe renal impairment; hyperkalaemia; addison's disease
42
side effects of BBs (6)
fatigue; cold extremities; GI disturbances; sleep disturbances; impotence
43
who should avoid BBs
pts w asthma; haemodynamic instability; significant hepatic failure; heart block
44
when is digoxin indicated (2)
1. AF/ A flutter; 2. severe HF - if other drugs are failing or if pt has AF and HF
45
digoxin MOA
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
side effects of digoxin (5)
bradycardia; GI disturbance; rash; dizziness; visual disturbances (blurred yellow vision); digoxin toxicity with associated arrythmias
47
who should not take digoxin (3)
pts w 2nd degree/complete heart block; risk of ventricular arrythmias; electrolyte abnormalities (esp. hypokalaemia, hypomagnesaemia and hypercalcaemia)
48
what drugs increase the risk of digoxin toxicity
hypokalaemia causing - loop/thiazide diuretics; incr digoxin plasma conc - amioderone; CCBs; spironolactone; quinine
49
when are loop diuretics indicated (3)
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
loop diuretics MOA
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
side effects of loop diuretics
dehydration and hypotension; low electrolyte state (e.g. hyponatraemia, hypokalemia etc.); tinnitus + hearing loss (same transporter regulates endolymph)
52
who are loop diuretics contraindicated in
pts w severe hypovolaemia/dehydration; risk of hepatic encephalopathy; severe hypokalaemia/hyponaturaemia; pts w gout
53
what is Systolic (HFrEF)
Reduce proportion of blood that fills ventricles in diastole; Incr in blood at end of systole → ventricular stretch, dilatation, eccenetric remodelling
54
what is Diastolic (HFpEF)
Impaired ventricular relaxation or filling; Ventricular hypetrophy tends to develop
55
what is cardiac remodeling
changes in cardiac size, shape & function in response to cardiac injury or increased load
56
compensatory mechs for decreased CO (5)
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
how does peripheral oedema occur in HF
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
cons of using BNP as a marker (2)
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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