LV dysfunction and heart failure 2 Flashcards
When is RAAS and the SNS stimulated?
When cardiac output drops, either due to:
blood loss
heart failure
Whats the renin-angiotensin-aldosterone system?
Angiotensinogen->RENIN-> Angiotensin 1-> ACE-> Angiotensin 2-> salt retention thru aldosterone release & vasoconstriction
angiotensin 2 is synergistic with the SNS- promotes the release of noradrenaline from nerve endings
What does the sympathetic nervous system do?
Releases noradrenaline-> vasoconstriction (leading to peripheral resistance) and increased cardiac output
also synergistic with RAAS- promotes the release of renin
How do changes in RAAS and the SNS benefit us when we lose blood?
tachycardia- increased CO
positive inotropic effect- increased CO
vasoconstriction- increased blood pressure- maintain flow
sodium and water retention- increased circulatory volume
How do changes in RAAS and the SNS make it worse when we have heart failure?
Tachycardia- increased workload and oxygen demand
positive inotropic effect- “ “
vasoconstriction- increase afterload
sodium and water retention- increased preload and oedema
chronic adrenergic stimulation- myocyte toxicity and arrhythmia
What are the main types of treatment for heart failure?
Diuretics vasodilators aldosterone antagonists ACE inhibitors ARB- angiotensin 2 receptor blocker beta blocker- interferes with SNS and thus noradrenaline production
What effects do ACE inhibitors have and when are they used? Examples of ACE inhibitors
Reduce mortality significantly -hypertension -heart failure -diabetic nephropathy ramipril, enalapril, perindopril, trandolapril
What are ACE inhibitors adverse effects?
Related to angiotensin 2- hypotension acute renal failure hyperkalemia teratogenic effects in pregnant women related to kinins- cough- dry and persistent rash anaphylactic reactions
Why do ACE inhibitors increase kinin levels?
ACE catalyzes the conversion of bradykinin to inactive peptides
inhibiting ACE means you potentiate the effects of bradykinin
What effects do beta blockers have and when are they used? Examples of beta blockers
reduce mortality (carvedilol, bisoprolol and metaprolol)
can also improve the chances of developing HF or having an event & being hospitalized
angina
heart failure
arrhythmias
hypertension
propanolol, atenolol, nadolol
How are beta blockers selective?
Either beta 1 selective or non selective (both beta 1 and 2)
increase the dose of the drug- becomes non selective
selectivity is relative rather than absolute
Why is the term cardioselective beta 1 incorrect?
up to 40% of the receptors in the heart are beta 2 receptors
thus cardioselective technically means beta 1 and 2
What are beta blockers main adverse effects?
central NS effects:
fatigue, headache, sleep disturbance, nightmares, depression
vascular effects:
bradycardia, hypotension, cold peripheries, erectile dysfunction, worsening of asthma or COPD, PVD-claudication or Raynauds
How can beta blockers cause heart failure?
When the heart is failing- SNS is doing its best to stimulate the heart and keep it going- if you use a standard dose of beta blocker (IN ACUTE HEART FAILURE)-> blocks these effects and causes a drop is pressure which is bad
can kill people with acute heart failure
thus it is only used in chronic heart failure and in very small doses
How does sacubitril and valsartan affect heart failure?
Combination therapy- known as entresto
sacubitril= neprilysin inhibitor- potentiate the effects of cardiac natriuretic peptides
valsartan= angiotensin 2 inhibitor- ARB
What effect does digoxin have on heart failure patients?
Doesnt effect mortality- wont make you live longer
less likely to be hospitalised
What is ivabradine? How does it effect heart failure?
Blocks the funny current (part of cardiac action potential) in the sinus node
thus it slows down heart rate by decreasing sinus node firing
used in angina and HF
has no benefit in terms of CVD
significant benefit in terms of death from heart failure
significant benefit in terms of hospitalization due to HF
What is acute heart failure?
heart failure that occurs suddenly and often without warning, unlike chronic heart failure
could be due to a heart attack, or a ruptured valve etc
What drugs need to be given to a person with serious pulmonary oedema?
oxygen
diamorphine- relaxing cerebral effects and is a vasodilator
nitrates- vasodilation
loop diuretics- work quickly, acute effect= vasodilation, followed by diuresis
When and why would we give someone an inotrope?
When a person has acute heart failure due to a known cause- ruptured valve etc
tide the person over if they were going to die imminently (wouldn’t last for surgery)
2 types:
-adrenergic agonists- catecholamine type drugs
-PDE 3 inhibitors- PDE causes the breakdown of cAMP- block the breakdown- potentiate the effect of cAMP- stimulates the CNS
Examples of adrenergic agonists
Inoconstrictors- noradrenaline, adrenaline and dopamine (ino- work on beta 1 receptors) (constrictors- work on beta alpha 1 receptors) Inodilators- dobutamine, dopexamine, isoproterenol (dilators- work on beta 2 receptors)
Why are PDE3 inhibitors only administered for a couple of days?
Long term use- associated with increased mortality
die more frequently on this drug if used long term
What are the typical drugs a heart failure patient would be on
Beta-blocker- low dose gradually building uo
ACE inhibitors- low dose gradually building up
spironolactone- aldosterone antagonist
diuretic- furosemide etc
if patient still has symptoms- fast heart rate etc- administer ivabradine and digoxin
