treatment of cardiac failure Flashcards
aims of treatment for HF?
- relieve symptoms
- improve exercise tolerance
- reduce incidence of acute exacerbations
- reduce mortality
strategies for treatment?
- increase contractility
- decrease preload and/or after load in order to decrease cardiac work demand:
by relaxing vascular smooth muscle and by reducing blood volume. - inhibit the RAAS
- prevent inappropriate increase HR
- mobilise the oedematous fluids
what are lifestyle modifications that an be made for treatment of HF?
- Smoking cessation
- Salt and fluid restriction (improves mortality)
- Supervised cardiac rehabilitation
- Keep vaccines up to date
- Lorry/bus drivers need to notify the DVLA if they are symptomatic
what are “devise therapy for treatment of hypertension?
- pacing
- cardiac resynchronisation therapy
- implantable cardiac defibrillators
- coronary revascularisation
- heart transplant
what are the 5 main drugs used in treatment of HF and Hf with receded ejection fraction (HFrEF)
1- loop diuretics (furosemide, bumetanide)
2- ACE inhibitors (ramipril, lisinopril)
3- angiotensin 2 receptor blockers (candesartan, losartan)
4- beta blockers (bisprolol)
4- aldosterone receptor antagonists (spironolactone)
step 1 treatment of chronic HF?
DAB
D= diuretic if fluid retention
A= ace inhibitor or ARB
B = beta blocker
what is A and B alone in step one shown to do?
reduce mortality and improve the quality of life
what do kidney function modifiers do in HF?
they increase excretion of sodium and water
step 1 for modifying kidney function in HF?
loop dietetics - this will effect the thick ascending loop of henle
step 2 for modifying kidney function in HF?
spironolactone - this will effect the collecting tubule
what is the use and aim for flexible loop dietetic regimes?
use = if l=clinical signs/ symptoms of fluid overload/congestion
aim= achieve a ‘dry’ weight using the lowest diuretic dose possible
describe patient self management with edu?
- daily weight = if it varies in either direction then alter the dose
- symptom review = breathlessness, peripheral oedema
- thirst level
what are loop diuretic common side effects?
- electrolyte disturbances
- hypotension
- renal impairment
- hypovolaemia
- nocturia is taken too late in day
- acute gout common with high dose
acute hypertension treatment?
- Lasix (furosemide) IV
- Morphine IV
- Nitrates - sublingual or oral
- Oxygen
- Position - sit patient up
- Treat cause of decompensation (MI, arrythmia, myocarditis)
- β-blockers contraindicated
what is the nmominic to remember the main drugs used in HF?
ABBA
A= ACEI (angiotensin converting enzyme inhibitor)
B= Beta Blocker
A = Aldosterone antagonist
at what part of the kidney will loop diuretics have an effect?
thick ascending loop of henele
at what part of the kidney will thiazides have an effect?
distal tubule
at what part of the kidney will spironolactone have an aeffcect?
collecting tube
when would you use Renin Angiotensin System inhibitors?
what will it do?
- use in heart failure with a reduced ejection fraction of all the NYHA classes
- it will reduce morbidity/ mortality
what are the Angiotensin Converting enzyme inhibitors?
ramipril
lisinopril
what are the effects of using ACEI and ARB’s in HF?
- reduce salt and water retention
- reduce vasoconstriction
- reduce vascular resistance
- reduce after load
- improve tissue perfusion
-reduce ventricular remodelling and hypertrophy
in what group of patients is ACEI and ARB’s less effective?
what drugs should you use instead?
African or Caribbean ethnicity
- try hydralazine + nitrate
how would you administer ACEI and ARB’s?
start on a low dose, monitor the BP and blood chemistry and symptoms and uptitrating to maximum tolerated or target dose.
common side effects of RAAS inhibitors?
- dizziness
- headache
- hyperkalaemia
- renal impairment
avoid in bilateral renal artery stenosis
side effects to ACE inhibitors?
persistent dry cough
tiredness
rare but serious = angioedema
side effects of ARB’s (angiotensin AT1 receptor antagonists)?
- back/leg pain
what are the bad and good effects of using beta blockers in HF?
bad = may slow HR, this would decrease CO
good = allows ventricles to fill more completely during diastole
- some beta blockers will cause vasodilation through blockage of alpha receptors, therefore decreased after load.
- reduce renin release by kidney.
how d you start the administration of B-blockers in HF?
start if there is a reduced ejection fraction but stable NYHA class 2-4
- start low, go slow
side effects of B-blockers?
- bradycardia/heart block
- fatigue
- shortness of breathe
- dizziness
- cold peripheries
- impotence/reduced libido
- insomnia
when are beta blockers contra indicated?
in asthmatics and people with a heart block
describe step 2 for treating HF?
- add aldosterone antagonist (mineralocritcoid receptor antagonist)
- add if they are still symptomatic after step 1
- in NYHA class 2-4 (effective win severe HF)
- use a low dose
- it will reduce symptoms and mortality
what drugs are used in step 2?
spironolactone, eplerenone
what are common side effects of Aldosterone Receptor Antagonist?
- hyperkalaemia
- hyponatraemia
- nausea
- hypotension
- gynaecomastia with spironolactone
- renal impairment
Use in class 2-5
how do you manage HF drug adverse effects?
- there is a flexible dose for DAB’s, can put it up or down titrate
- review the BP = this may be low
- bradycardia = if symptomatic may need to stop B-blockers or review any other rate controlling drugs the patient is on.
If HR <45 bpm, stop B- blocker and call specialist
what is step 3 or 4 in treatment of HF?
sacubitril-valsartan (combination)
= neprilysin inhibitor & ARB (entresto)
Ivabridine = specialist use only
- reduces the HR but not contractility
- acts on sinus nodes
- only use if HR is <75
what are other drug options you can consider if concurrent sodium and water retention?
additional diuretics (thiazides like metolazone)
what are other drug options you can consider if there is co-existing angina?
- oral nitrates
- amlodipine
what type of drug is digoxin?
cardiac glycoside
what is the mechanism of action of digoxin in Atrial fibirilation?
- increased vagal effort activity to the heart
- decreased SAN firing rate
- decreased HR
- decreased conduction velocity in the AV node
what is the mechanism of action of digoxin in Heart failure?
it will increase the force of myocardial contraction
- inhibits Na/K ATPase pump, this will effect the Na/Ca exchanger.
- elevating the intracellular calcium levels in the SR then when calcium is released it results in strengthened contractility.
(it indirectly increases calcium levels and subsequent storage in the SR)
what will digoxin inhibit?
it inhibits Na/K ATPase pump, affecting the Na/Ca exchanger
= increased force of myocardial contraction
what are the side effects of digoxin?
- GI upset
- dizziness
- conduction abnormalities
- blurred or yellow vision
what is a sodium glucose transport protein 2 inhibitor (SGLT2)
dapagliflozin
- normally used in the treatment of diabetes
- but decrease the risk of further CVS mortality or the likelihood of hispotilisation
acute heart failure?
sudden worsening of signs and symptoms of heart failure as a result of severe congestion of multiple organs
= increased dyspnoea, oedema
cause of acute heart failure?
MI
infection
anaemia
thyroid dysfunction
arrhythmia
uncontrolled hypertension
poor concordance
aims of treatment of acute heart failure?
- normalise ventricular filling pressures
- restore adequate tissue perfusion
overview of treatment of acute HF?
LMNOP
L= loop
M= morphine
N= nitrates
O= oxygen
P= positioning
IV lOOP DIURETICS FOR ACUTE HF?
cause dilation and diuresis
reduces preload
Iv opiates for treatment of acute HF?
- reduce anxiety
- vasodilator, reducing preload
- reduces sympathetic drive
- not routinely offered
IV nitrates (Glyceryl trinatrate) in treatment of acute HF?
- reduces the preload and after load
- vasodilator
oxygen and position for treatment of acute HF?
- oxygen maintains O2 stats
- positioning = keep patient upright.
describe the second line of treatment for acute HF?
you want to increase contractility
- using inotropic agents
- increase contractility will …
- increase SV
- increase CO
- increase the clearance of pooled blood in the ventricles
what happens as CO increases?
baroreceptors will sense a change in MABP and decrease sympathetic drive so there is a decrease in HR and TPR
where are the main points in the pharmacological intervention for HF?
ionotropes?
= beta agonists which will increase myocardial contractility
- dobutamine (beta 1&2) = in patients with cariogenic shock to maintain blood pressure
- dopamine (DA>beta>alpha) = increases renal perfusion at low doses, can increase BP at high doses
- isoprenaline = in bradycardia =/heart block emergencies
- adrenaline (beta>alpha)
vasopressors?
noradrenaline (alpha>beta) = cause vasoconstriction, raises the BP, used in severe septic shock
