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Cardiovascular System > Heart Failure - Therapy > Flashcards

Heart Failure - Therapy Flashcards

1
Q

Chronic heart failure is a syndrome. What is it characterised by?

(4)

A
  • progressive cardiac dysfunction
  • breathlessness (congestion)
  • fatigue
  • neurohormonal disturbances
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2
Q

Heart failure results in a reduction of ________ ________. This is also know as the _________ fraction.

A

cardiac output

ejection

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3
Q

There are two types of heart failure. Name them both.

A

Systolic heart failure

Diastolic heart failure

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4
Q

What are the characteristics of systolic heart failure?

A
  • HF with reserved ejection fraction
  • decreased pumping action of the heart
  • ejection fraction of less than 40%
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5
Q

What are the characteristics of diastolic heart failure?

A
  • HF with preserved ejection fraction
  • the left ventricle loses its ability to relax normally therefore the ejection fraction is normal or only mildly reduced.
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6
Q

What is common with both types of heart failure?

A
  • they present with the same symptoms

- that is, they both involve fluid back up into the lungs.

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7
Q

What are the main risk factors for heart failure?

5

A 
Hypertension (main one!!)
CAD/previous MI
valvular heart disease
alcoholism
congenital heart defects
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8
Q

Outline the pathological progression of CVD.

[hint: think about risk factors, neurohormones and types of heart failure]

A
  • increase in some risk factor(s) e.g. hypertension, diabetes
  • increased myocardial injury
  • neurohormonal stimulaiton
  • physiological response is pathological remodelling
  • leads to lower ejection fraction (systolic HF)
  • symptomatic (dyspnoea, fatigue, oedema)
  • pump failure = chronic heart failure
  • could lead to SCD/death
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9
Q

If the muscle of a healthy heart is stretched it will contract with _______ ________ and pump out ______ blood.

A reduction in cardiac output activates ___________________ and therefore the circulatory __________ ___________.

A

greater force
more

the RAAS further
volume increases

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10
Q

Why does activation of the RAAS lead to further heart deterioration.

A

It is a cycle.

  • HF = reduced CO
  • RAAS activation = increased blood volume
  • cardiac dilation = deterioration of myocardium (hypertrophy)
  • ejection fraction is reduced
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11
Q

Which type of heart failure is most likely to occur from sustained hypertension?

A

diastolic heart failure/preserved EF i.e. issue with relaxation

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12
Q

Which type of heart failure is most likely to occur following myocardial damage e.g. MI?

A

Systolic dysfunction/reduced EF

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13
Q

How does the body physiologically respond to HF i.e. reduced CO/circulatory volume?

A
  • SNS activation (vasoconstriction/increased HR)

- RAAS activation (Na+ and water retention)

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14
Q

What path does renin take?

A

renin - AT I - AT II

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15
Q

Outline how AT II affects the preload?

A
  • increased Na+ and water retention
  • increased PV
  • increased preload
  • increased work load
    = HF
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16
Q

Outline how AT II affects the afterload i.e. what is causing the change in afterload?

A
  • peripheral vasoconstriction
  • increased afterload
  • reduced CO (as pressure gradient between LV and aorta is reduced)
    = HF
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17
Q

What happens to the myocardium when the afterload is increased?

A

LV hypertrophy/fibrosis

- diastolic dysfunction

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18
Q

Activation of the SNS causes the release of which neurohormones?

What are the effects and results of the release of these hormones? (3)

A

adrenaline
noradrenaline

  • vasoconstriction
  • stimulates renin release
  • myocyte hypertrophy (due to increased afterload)
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19
Q

What is the function of the natriuretic peptide system?

A

A natriuretic peptide is a peptide which induces natriuresis - the excretion of sodium by the kidneys.

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20
Q

Give examples of natriuretic peptides.

A

ANP (atrial NP)

BNP (brain NP)

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21
Q

Give examples of hormones which act as physiological responses to HF? (3)

[hint: they act to make things better, not worse]

What are the effects of these hormones being released?

A
  • EDRF (endothelium-derived relaxing factor)
  • ANP
  • BNP
  • Na+ and water excretion (from natriuretic peptides)
  • potent vasodilation (reduce afterload)
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22
Q

Usual treatment for heart failure today has two main aims. What are they?

A
  • improve symptoms

- inhibit effect of detrimental physiological responses (improve survival)

23
Q

Give examples of drugs used to improve symptoms e.g. oedema?

A

diuretics (e.g. furosemide)

digoxin (cardiac glycoside)

24
Q

Which drugs are used to prevent detrimental hormonal changes from SNS activation?

A

beta blockers (e.g. bisoprolol)

25
Q

Which drugs are used to block the effects of angiotensin II?

A

ACE inhibitors

ARBs (angiotensin II receptor blockers) - nat as effective as ACEi

26
Q

Which drug is used to block the effects of aldosterone?

A

spironolactone

27
Q

Which drug increases the amount of bradykinin by preventing its degradation?

What is the effects of bradykinin?

A

ACE inhibitors

vasodilation, NO release

28
Q

Which drug is used to enhance the effect of benificial hormonal changes?

[hint: vasodilation and Na+/water excretion]

A

neprilysin - prevents metabolism of ANP/BNP

29
Q

Which drug is used to improve the ability of the heart to pump and so improve cardiac status?

[hint: there is only one of this drug type in current use]

What type of drug is this?

A

digoxin - cardiac glycoside (positive inotrope)

30
Q

What do nitrovasodilators do that improve cardiac function?

Give an example.

Which drug is often considered alongside a nitrate?

A
  • vasodialtion
  • reduced preload/afterload

isosorbide mononitrate (long acting nitrate)

hydralazine

31
Q

What is the most common loop diuretic used?

What is its effect?

A

furosemide

  • inhibits Na-K-Cl transporter in the loop of Henle
  • increased urine output
  • works at low GFR
32
Q

If a diuretic resistant patient, which drug might be used in combination to a loop diuretic?

What is the combined effect?

What are the adverse drug reactions?

A

thiazide-type diuretic

powerful/synergistic

ADRs:

  • dehydration
  • hypotension
  • hypokalaemia
  • hyponatraemia
33
Q

What are some drug-drug interactions involving frusemide?

A 
frusemide
\+ aminoglycosides
\+ lithium
\+ NSAIDs
\+ vancomycin

= renal toxicity

34
Q

What are some drug-drug interactions involving frusemide which result in profound hypotension?

A

Frusemide + antihypertensives

35
Q

AT I conversion to AT II can be blocked by ACE inhibitors. What other route can AT I take to become AT II?

[hint: enzyme]

A

chymase

36
Q

What end organ damage can AT II cause in the brain?

2

A

atherosclerosis (carotids)

stroke

37
Q

What end organ damage can AT II cause in the heart?

3

A

LV hypertrophy
fibrosis
remodelling

38
Q

What end organ damage can AT II cause in the kidneys?

5

A
  • CO decreases
  • renal blood flow decreases
  • GFR decreases
  • increase proteinuria
  • increased aldosterone release
39
Q

Give examples of the most commonly used ACE inhibitors. (3)

What are the effects of them?

A

Ramipril (main one)
Enalapril
Lisinopril

  • prevent conversion of AT I to AT II (vasoconstriction, PV increase)
  • reduce preload/afterload
40
Q

What are the adverse drug reactions of ACE inhibitors? (4)

A
  • cough
  • hyperkalaemia
  • first dose hypotension
  • renal failure
41
Q

What are possible drug-drug interactions with ACE inhibitors? (3)

A

+ NSAIDs = renal failure
+ K supplements = hyperkalaemia
+ K-sparing diuretics (e.g. spironolactone) = hyperkalaemia

42
Q

Which receptor is blocked on AT II by ARBs?

A

AT1

43
Q

When are ARBs administered?

A

When patient is intolerant to ACE inhibitors.

44
Q

What are the roles of the AT1 receptor on AT II?

A

vasoconstriction
aldosterone secretion
increased sympathetic tone

(basically all the things you don’e want in HF)

45
Q

What are the roles of the AT2 receptor on AT II?

A

vasodilation

ahh the good stuff

46
Q

There is a new class of drugs with combined effects for treating HF. What is the new class called?

What are the therapeutic effects of this drug?

A

ARNI (angiotensin receptor-neprilysin inhibitor)

VALSARTAN (ARB) - blocks AT1 receptor

NEPRILYSIN - blocks the breakdown of ANP and BNP (vasodilators/Na+ excreters)

47
Q

Name the common aldosterone antagonist used in treating HF?

What type of diuretic is this?

What is it used in combination with?

A

spironolactone

K sparing diuretic

loop diuretics

48
Q

What beta blockers are used in the treatment of chronic HF?

What are the contraindications to beta blocker use?

A

bisoprolol
atenolol
carvedilol
metoprolol

sudden cessation can lead to MI, bradycardia, should not be used with acute presentation of HF, should only be used once a patient has been stabilised

49
Q

What are the effects of ivabradine?

What are the contraindications to its use?

A
  • Ivabradine works by affecting your heart’s electrical activity in order to slow the heart rate.
  • reduced HF hospital admissions in patients with stable chronic systolic HF.

contrindications: slow resting HR <70bpm, hypotension

50
Q

What drug class is digoxin?

What are the effects of this drug?

What are the adverse drug reactions/side effects (3)

A

cardiac glycoside/positive inotrope

  • increases availability of Ca2+ in the myocyte
  • reduces hospitalisation

ADRs:

  • nausea
  • arrhythmias
  • delirium
51
Q

Why is it necessary sometimes to include an anticoagulant into the drug therapy regime of HF treatment?

A
  • dilated ventricle gives rise to thrombosis (more areas for blood stasis)
  • anticoagulant decreases this risk
52
Q

Which anticoagulant is likely to be included in the drug therapy regime for HF?

A

warfarin

53
Q

What is the treatment regime for chronic heart failure?

class and example drug

A

ABCD SWAD

  • ACE inhibitor (e.g. ramipril) or (C)
  • Beta-blocker (e.g. bisoprolol)
  • Candesartan (ARB)
  • Digoxin (positive inotrope)
  • Spironolactone (Aldosterone antagonist) - (HFrEF)
  • Warfarin (anticoagulant)
  • ARNI (e.g. valsartan & neprilysin)
  • Diuretic (e.g. furosemide) +/- thiazide-type diuretic

Cardiovascular System (37 decks)

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