Heart Failure - Therapy Flashcards
Chronic heart failure is a syndrome. What is it characterised by?
(4)
- progressive cardiac dysfunction
- breathlessness (congestion)
- fatigue
- neurohormonal disturbances
Heart failure results in a reduction of ________ ________. This is also know as the _________ fraction.
cardiac output
ejection
There are two types of heart failure. Name them both.
Systolic heart failure
Diastolic heart failure
What are the characteristics of systolic heart failure?
- HF with reserved ejection fraction
- decreased pumping action of the heart
- ejection fraction of less than 40%
What are the characteristics of diastolic heart failure?
- HF with preserved ejection fraction
- the left ventricle loses its ability to relax normally therefore the ejection fraction is normal or only mildly reduced.
What is common with both types of heart failure?
- they present with the same symptoms
- that is, they both involve fluid back up into the lungs.
What are the main risk factors for heart failure?
5
Hypertension (main one!!) CAD/previous MI valvular heart disease alcoholism congenital heart defects
Outline the pathological progression of CVD.
[hint: think about risk factors, neurohormones and types of heart failure]
- 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
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 __________ ___________.
greater force
more
the RAAS further
volume increases
Why does activation of the RAAS lead to further heart deterioration.
It is a cycle.
- HF = reduced CO
- RAAS activation = increased blood volume
- cardiac dilation = deterioration of myocardium (hypertrophy)
- ejection fraction is reduced
Which type of heart failure is most likely to occur from sustained hypertension?
diastolic heart failure/preserved EF i.e. issue with relaxation
Which type of heart failure is most likely to occur following myocardial damage e.g. MI?
Systolic dysfunction/reduced EF
How does the body physiologically respond to HF i.e. reduced CO/circulatory volume?
- SNS activation (vasoconstriction/increased HR)
- RAAS activation (Na+ and water retention)
What path does renin take?
renin - AT I - AT II
Outline how AT II affects the preload?
- increased Na+ and water retention
- increased PV
- increased preload
- increased work load
= HF
Outline how AT II affects the afterload i.e. what is causing the change in afterload?
- peripheral vasoconstriction
- increased afterload
- reduced CO (as pressure gradient between LV and aorta is reduced)
= HF
What happens to the myocardium when the afterload is increased?
LV hypertrophy/fibrosis
- diastolic dysfunction
Activation of the SNS causes the release of which neurohormones?
What are the effects and results of the release of these hormones? (3)
adrenaline
noradrenaline
- vasoconstriction
- stimulates renin release
- myocyte hypertrophy (due to increased afterload)
What is the function of the natriuretic peptide system?
A natriuretic peptide is a peptide which induces natriuresis - the excretion of sodium by the kidneys.
Give examples of natriuretic peptides.
ANP (atrial NP)
BNP (brain NP)
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?
- EDRF (endothelium-derived relaxing factor)
- ANP
- BNP
- Na+ and water excretion (from natriuretic peptides)
- potent vasodilation (reduce afterload)
Usual treatment for heart failure today has two main aims. What are they?
- improve symptoms
- inhibit effect of detrimental physiological responses (improve survival)
Give examples of drugs used to improve symptoms e.g. oedema?
diuretics (e.g. furosemide)
digoxin (cardiac glycoside)
Which drugs are used to prevent detrimental hormonal changes from SNS activation?
beta blockers (e.g. bisoprolol)
Which drugs are used to block the effects of angiotensin II?
ACE inhibitors
ARBs (angiotensin II receptor blockers) - nat as effective as ACEi
Which drug is used to block the effects of aldosterone?
spironolactone
Which drug increases the amount of bradykinin by preventing its degradation?
What is the effects of bradykinin?
ACE inhibitors
vasodilation, NO release
Which drug is used to enhance the effect of benificial hormonal changes?
[hint: vasodilation and Na+/water excretion]
neprilysin - prevents metabolism of ANP/BNP
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)
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
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
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
What are some drug-drug interactions involving frusemide?
frusemide \+ aminoglycosides \+ lithium \+ NSAIDs \+ vancomycin
= renal toxicity
What are some drug-drug interactions involving frusemide which result in profound hypotension?
Frusemide + antihypertensives
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
What end organ damage can AT II cause in the brain?
2
atherosclerosis (carotids)
stroke
What end organ damage can AT II cause in the heart?
3
LV hypertrophy
fibrosis
remodelling
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
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
What are the adverse drug reactions of ACE inhibitors? (4)
- cough
- hyperkalaemia
- first dose hypotension
- renal failure
What are possible drug-drug interactions with ACE inhibitors? (3)
+ NSAIDs = renal failure
+ K supplements = hyperkalaemia
+ K-sparing diuretics (e.g. spironolactone) = hyperkalaemia
Which receptor is blocked on AT II by ARBs?
AT1
When are ARBs administered?
When patient is intolerant to ACE inhibitors.
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)
What are the roles of the AT2 receptor on AT II?
vasodilation
ahh the good stuff
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)
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
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
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
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
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
Which anticoagulant is likely to be included in the drug therapy regime for HF?
warfarin
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
