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Cardiovascular System > Heart Failure - Therapy > Flashcards

Heart Failure - Therapy Flashcards

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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?

Study These Flashcards
A
  • improve symptoms

- inhibit effect of detrimental physiological responses (improve survival)

23
Q

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

Study These Flashcards
A

diuretics (e.g. furosemide)

digoxin (cardiac glycoside)

24
Q

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

Study These Flashcards
A

beta blockers (e.g. bisoprolol)

25
Which drugs are used to block the effects of angiotensin II?
ACE inhibitors | ARBs (angiotensin II receptor blockers) - nat as effective as ACEi
26
Which drug is used to block the effects of aldosterone?
spironolactone
27
Which drug increases the amount of bradykinin by preventing its degradation? What is the effects of bradykinin?
ACE inhibitors vasodilation, NO release
28
Which drug is used to enhance the effect of benificial hormonal changes? [hint: vasodilation and Na+/water excretion]
neprilysin - prevents metabolism of ANP/BNP
29
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?
digoxin - cardiac glycoside (positive inotrope)
30
What do nitrovasodilators do that improve cardiac function? Give an example. Which drug is often considered alongside a nitrate?
- vasodialtion - reduced preload/afterload isosorbide mononitrate (long acting nitrate) hydralazine
31
What is the most common loop diuretic used? What is its effect?
furosemide - inhibits Na-K-Cl transporter in the loop of Henle - increased urine output - works at low GFR
32
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?
thiazide-type diuretic powerful/synergistic ADRs: - dehydration - hypotension - hypokalaemia - hyponatraemia
33
What are some drug-drug interactions involving frusemide?
``` frusemide + aminoglycosides + lithium + NSAIDs + vancomycin ``` = renal toxicity
34
What are some drug-drug interactions involving frusemide which result in profound hypotension?
Frusemide + antihypertensives
35
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]
chymase
36
What end organ damage can AT II cause in the brain? | 2
atherosclerosis (carotids) | stroke
37
What end organ damage can AT II cause in the heart? | 3
LV hypertrophy fibrosis remodelling
38
What end organ damage can AT II cause in the kidneys? | 5
- CO decreases - renal blood flow decreases - GFR decreases - increase proteinuria - increased aldosterone release
39
Give examples of the most commonly used ACE inhibitors. (3) What are the effects of them?
Ramipril (main one) Enalapril Lisinopril - prevent conversion of AT I to AT II (vasoconstriction, PV increase) - reduce preload/afterload
40
What are the adverse drug reactions of ACE inhibitors? (4)
- cough - hyperkalaemia - first dose hypotension - renal failure
41
What are possible drug-drug interactions with ACE inhibitors? (3)
+ NSAIDs = renal failure + K supplements = hyperkalaemia + K-sparing diuretics (e.g. spironolactone) = hyperkalaemia
42
Which receptor is blocked on AT II by ARBs?
AT1
43
When are ARBs administered?
When patient is intolerant to ACE inhibitors.
44
What are the roles of the AT1 receptor on AT II?
vasoconstriction aldosterone secretion increased sympathetic tone (basically all the things you don'e want in HF)
45
What are the roles of the AT2 receptor on AT II?
vasodilation | ahh the good stuff
46
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?
ARNI (angiotensin receptor-neprilysin inhibitor) VALSARTAN (ARB) - blocks AT1 receptor NEPRILYSIN - blocks the breakdown of ANP and BNP (vasodilators/Na+ excreters)
47
Name the common aldosterone antagonist used in treating HF? What type of diuretic is this? What is it used in combination with?
spironolactone K sparing diuretic loop diuretics
48
What beta blockers are used in the treatment of chronic HF? What are the contraindications to beta blocker use?
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
What are the effects of ivabradine? What are the contraindications to its use?
- 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
What drug class is digoxin? What are the effects of this drug? What are the adverse drug reactions/side effects (3)
cardiac glycoside/positive inotrope - increases availability of Ca2+ in the myocyte - reduces hospitalisation ADRs: - nausea - arrhythmias - delirium
51
Why is it necessary sometimes to include an anticoagulant into the drug therapy regime of HF treatment?
- dilated ventricle gives rise to thrombosis (more areas for blood stasis) - anticoagulant decreases this risk
52
Which anticoagulant is likely to be included in the drug therapy regime for HF?
warfarin
53
What is the treatment regime for chronic heart failure? | class and example drug
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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