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Cardiovascular system > Heart Failure Treatment > Flashcards

Heart Failure Treatment Flashcards

1
Q

define congestive heart failure

A

a state in which the heart is unable to pump blood at a rate commensurate with requirements of the tissue or can do so only from high pressures

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2
Q

define systolic heart failure

A

decreased pumping function of the heart which results in fluid back up in the lungs and heart failure

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3
Q

define diastolic heart failure

A

thickened/stiff heart muscles resulting in the heart being unable to fill with blood properly. this results in fluid backup in the lungs and heart failure

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4
Q

what are the risk factors for heart failure?

A 
> coronary heart disease
> hypertension
> valvular heart disease
> alcoholism
> infection
> diabetes
> congenital heart defects
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5
Q

what is the frank-starling law that is lost on heart failure?

A

if the muscle of a healthy heart is stretched it will contact with greater force and pump out more blood

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6
Q

describe what changes occur to lead to systolic dysfunction heart failure

A

the circulatory volume increases dilating the heart and weakening the force of contraction dropping the cardiac output. as a result the RAAS is activating increasing the circulatory volume even more and further deteriorating cardiac performance. cardiac myocytes also then undergo hypertrophy and fibrosis further weakening the heart.

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7
Q

what is the final result of the RAAS cycle in heart failure?

A

there is progressive retention of salt and water creating peripheral and pulmonary oedema. this leads to progressive myocyte death and fibrosis.

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8
Q

what drugs improve symptoms of heart failure?

A

> diuretics

> digoxin

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9
Q

what drugs improve survival of heart failure?

A

> beta blockers

> ivabradine

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10
Q

what drugs improve symptoms and survival?

A

> ACE inhibitors
spironolactone
valsartan-sacubitril

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11
Q

what do symptomatic treatment regimes target?

A

> inhibition of detrimental neuro-hormonal adaptions
enhancement of beneficial neuro-hormonal adaption
enhancement of cardiac function

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12
Q

what drugs block sympathetic activation?

A

beta-blockers
> carvedilol
> bisoprolol
> metoprolol

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13
Q

what two drugs groups block the effects of angiotensin 2?

A

> ACE inhibitors (Ramipril)

> angiotensin antagonists (valsartan, losartan)

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14
Q

what blocks the effects of aldosterone?

A

spironolactone

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15
Q

what metabolises ANPs and BNPs?

A

neutral endopeptidase

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16
Q

what does the drug neprolysin do?

A

it enhances beneficial hormonal changes by preventing metabolism and enhancing the actions of ANP/BNP.

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17
Q

what are the effects of positive inotropes?

A

they improve the ability of the heart to pump and so improve cardiac status (digoxin)

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18
Q

what are the effects of vasodilators on cardiac function?

A

they improve cardiac function by reducing preload and after load

19
Q

give some examples of vasodilators used to treat heart failure

A

> nirtovasodilators: isosorbide mono, dinitrate

> hydralazine (arterial dilator)

20
Q

describe the actions of loop diuretic drugs

A

they removes excess slat and water by inducing profound diuresis. they inhibit the Na-K-CL transport in the loop of Henle and work at low glomerular filtration rates. they prevent reabsorption of 20% of filtered sodium and water.

21
Q

name a loop diuretic

A

furosemide

22
Q

what drugs can you use in diuretic resistant patients?

A

in combination with thiazide diuretics

23
Q

what are the adverse drug reactions associated with thiazide diuretics?

A 
> dehydration
> hypotension
> hypokalaemia
> hyponatraemia
> gout
> impaired glucose tolerance
24
Q

what drugs does frusemide interact with to create renal toxicity?

A

> aminoglycosides
lithium
NSAIDs
vancomycin

25
Q

what does frusemide interact with to create hypotension?

A

anti-hypertensives

26
Q

what actions reduce mortality?

A

> angiotensin blockade
beta receptor blockade
aldosterone blockade
ANP/BNP enhancement

27
Q

name the pathways that generate angiotensin 2

A

> angiotensinogen converted by renin in the liver

> chymase pathway

28
Q

what effects does angiotensin 2 have on the heart?

A

> left ventricle hypertrophy
fibrosis
remodelling
apoptosis

29
Q

name three angiotensin converting enzyme inhibitors

A

> Ramipril
enalapril
lisinopril

30
Q

what do angiotensin converting enzyme inhibitors reduce?

A

the preload and afterload on the heart. morbidity and mortality of patients with CHF.

31
Q

what are the adverse drug reactions of ACE inhibitors?

A 
> first dose hypotension
> cough
> angioedema
> renal impairment
> renal failure
> hyperkalaemia
32
Q

what drug-drug interactions are there with ACE inhibitors?

A

> NSAIDs, acute renal failure
potassium supplements, hyperkalaemia
potassium sparing diuretics, hyperkalaemia

33
Q

what is the actions of angiotensin receptor blockers?

A

they selectively block the angiotensin 2, AT1 receptor.

34
Q

what are the roles of AT1 receptor?

A 
> vasoconstriction
> vascular proliferation
> aldosterone secretion
> cardiac myocyte proliferation
> increased sympathetic tone
35
Q

what are the roles of AT2 receptors?

A

> vasodilation
anti-proliferation
apoptosis

36
Q

what is valsartan-sacubitril?

A

it is combined valsartan and ARB and neprilysin

37
Q

what is the action of spironolactone?

A

this is a potassium sparing diuretic which acts in the distal tube, inhibiting the actions of aldosterone.

38
Q

name three beta-blockers

A

> carvedilol
bisoprolol
metoprolol

39
Q

when should beta blocker be used?

A

when the patient has been stabilised as they block the actions of the sympathetic system not to be used in acute presentation.

40
Q

what does ivabradine inhibit?

A

If current in the sinoatrial node

41
Q

to which patients is ivabradine given?

A

symptomatic stable chronic HFrEF who are receiving standard therapy including beta blocker at maximum tolerated dose and who are sinus rhythm with a heart rate of 70bpm or greater

42
Q

what is the action of digoxin?

A

it increases the availability of calcium in the myocyte

43
Q

what events does warfarin help prevent?

A

thrombus formation and thrombo-embolic events caused by dilated ventricles.

44
Q

what is monitored to monitor benefit of treatment?

A

> symptomatic relief
clinical relief
weight
patient education

Cardiovascular system (34 decks)

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