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treatment of cardiac failure Flashcards

1
Q

aims of treatment for HF?

A
  • relieve symptoms
  • improve exercise tolerance
  • reduce incidence of acute exacerbations
  • reduce mortality
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2
Q

strategies for treatment?

A
  • 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
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3
Q

what are lifestyle modifications that an be made for treatment of HF?

A
  • 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
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4
Q

what are “devise therapy for treatment of hypertension?

A
  • pacing
  • cardiac resynchronisation therapy
  • implantable cardiac defibrillators
  • coronary revascularisation
  • heart transplant
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5
Q

what are the 5 main drugs used in treatment of HF and Hf with receded ejection fraction (HFrEF)

A

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)

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6
Q

step 1 treatment of chronic HF?

A

DAB
D= diuretic if fluid retention
A= ace inhibitor or ARB
B = beta blocker

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7
Q

what is A and B alone in step one shown to do?

A

reduce mortality and improve the quality of life

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8
Q

what do kidney function modifiers do in HF?

A

they increase excretion of sodium and water

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9
Q

step 1 for modifying kidney function in HF?

A

loop dietetics - this will effect the thick ascending loop of henle

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10
Q

step 2 for modifying kidney function in HF?

A

spironolactone - this will effect the collecting tubule

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11
Q

what is the use and aim for flexible loop dietetic regimes?

A

use = if l=clinical signs/ symptoms of fluid overload/congestion
aim= achieve a ‘dry’ weight using the lowest diuretic dose possible

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12
Q

describe patient self management with edu?

A
  • daily weight = if it varies in either direction then alter the dose
  • symptom review = breathlessness, peripheral oedema
  • thirst level
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13
Q

what are loop diuretic common side effects?

A
  • electrolyte disturbances
  • hypotension
  • renal impairment
  • hypovolaemia
  • nocturia is taken too late in day
  • acute gout common with high dose
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14
Q

acute hypertension treatment?

A
  • Lasix (furosemide) IV
  • Morphine IV
  • Nitrates - sublingual or oral
  • Oxygen
  • Position - sit patient up
  • Treat cause of decompensation (MI, arrythmia, myocarditis)
  • β-blockers contraindicated
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15
Q

what is the nmominic to remember the main drugs used in HF?

A

ABBA
A= ACEI (angiotensin converting enzyme inhibitor)
B= Beta Blocker
A = Aldosterone antagonist

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16
Q

at what part of the kidney will loop diuretics have an effect?

A

thick ascending loop of henele

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17
Q

at what part of the kidney will thiazides have an effect?

A

distal tubule

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18
Q

at what part of the kidney will spironolactone have an aeffcect?

A

collecting tube

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19
Q

when would you use Renin Angiotensin System inhibitors?
what will it do?

A
  • use in heart failure with a reduced ejection fraction of all the NYHA classes
  • it will reduce morbidity/ mortality
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20
Q

what are the Angiotensin Converting enzyme inhibitors?

A

ramipril
lisinopril

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21
Q

what are the effects of using ACEI and ARB’s in HF?

A
  • reduce salt and water retention
  • reduce vasoconstriction
  • reduce vascular resistance
  • reduce after load
  • improve tissue perfusion
    -reduce ventricular remodelling and hypertrophy
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22
Q

in what group of patients is ACEI and ARB’s less effective?
what drugs should you use instead?

A

African or Caribbean ethnicity
- try hydralazine + nitrate

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23
Q

how would you administer ACEI and ARB’s?

A

start on a low dose, monitor the BP and blood chemistry and symptoms and uptitrating to maximum tolerated or target dose.

24
Q

common side effects of RAAS inhibitors?

A
  • dizziness
  • headache
  • hyperkalaemia
  • renal impairment
    avoid in bilateral renal artery stenosis
25
Q

side effects to ACE inhibitors?

A

persistent dry cough
tiredness
rare but serious = angioedema

26
Q

side effects of ARB’s (angiotensin AT1 receptor antagonists)?

A
  • back/leg pain
27
Q

what are the bad and good effects of using beta blockers in HF?

A

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.

28
Q

how d you start the administration of B-blockers in HF?

A

start if there is a reduced ejection fraction but stable NYHA class 2-4
- start low, go slow

29
Q

side effects of B-blockers?

A
  • bradycardia/heart block
  • fatigue
  • shortness of breathe
  • dizziness
  • cold peripheries
  • impotence/reduced libido
  • insomnia
30
Q

when are beta blockers contra indicated?

A

in asthmatics and people with a heart block

31
Q

describe step 2 for treating HF?

A
  • 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
32
Q

what drugs are used in step 2?

A

spironolactone, eplerenone

33
Q

what are common side effects of Aldosterone Receptor Antagonist?

A
  • hyperkalaemia
  • hyponatraemia
  • nausea
  • hypotension
  • gynaecomastia with spironolactone
  • renal impairment
    Use in class 2-5
34
Q

how do you manage HF drug adverse effects?

A
  • 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
35
Q

what is step 3 or 4 in treatment of HF?

A

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

36
Q

what are other drug options you can consider if concurrent sodium and water retention?

A

additional diuretics (thiazides like metolazone)

37
Q

what are other drug options you can consider if there is co-existing angina?

A
  • oral nitrates
  • amlodipine
38
Q

what type of drug is digoxin?

A

cardiac glycoside

39
Q

what is the mechanism of action of digoxin in Atrial fibirilation?

A
  • increased vagal effort activity to the heart
  • decreased SAN firing rate
  • decreased HR
  • decreased conduction velocity in the AV node
40
Q

what is the mechanism of action of digoxin in Heart failure?

A

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)

41
Q

what will digoxin inhibit?

A

it inhibits Na/K ATPase pump, affecting the Na/Ca exchanger
= increased force of myocardial contraction

42
Q

what are the side effects of digoxin?

A
  • GI upset
  • dizziness
  • conduction abnormalities
  • blurred or yellow vision
43
Q

what is a sodium glucose transport protein 2 inhibitor (SGLT2)

A

dapagliflozin
- normally used in the treatment of diabetes
- but decrease the risk of further CVS mortality or the likelihood of hispotilisation

44
Q

acute heart failure?

A

sudden worsening of signs and symptoms of heart failure as a result of severe congestion of multiple organs
= increased dyspnoea, oedema

45
Q

cause of acute heart failure?

A

MI
infection
anaemia
thyroid dysfunction
arrhythmia
uncontrolled hypertension
poor concordance

46
Q

aims of treatment of acute heart failure?

A
  • normalise ventricular filling pressures
  • restore adequate tissue perfusion
47
Q

overview of treatment of acute HF?

A

LMNOP
L= loop
M= morphine
N= nitrates
O= oxygen
P= positioning

48
Q

IV lOOP DIURETICS FOR ACUTE HF?

A

cause dilation and diuresis
reduces preload

49
Q

Iv opiates for treatment of acute HF?

A
  • reduce anxiety
  • vasodilator, reducing preload
  • reduces sympathetic drive
  • not routinely offered
50
Q

IV nitrates (Glyceryl trinatrate) in treatment of acute HF?

A
  • reduces the preload and after load
  • vasodilator
51
Q

oxygen and position for treatment of acute HF?

A
  • oxygen maintains O2 stats
  • positioning = keep patient upright.
52
Q

describe the second line of treatment for acute HF?

A

you want to increase contractility
- using inotropic agents
- increase contractility will …
- increase SV
- increase CO
- increase the clearance of pooled blood in the ventricles

53
Q

what happens as CO increases?

A

baroreceptors will sense a change in MABP and decrease sympathetic drive so there is a decrease in HR and TPR

54
Q

where are the main points in the pharmacological intervention for HF?

A
55
Q

ionotropes?

A

= 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)

56
Q

vasopressors?

A

noradrenaline (alpha>beta) = cause vasoconstriction, raises the BP, used in severe septic shock

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