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PHA 222 > heart failure3/4/5 > Flashcards

heart failure3/4/5 Flashcards

1
Q

what are the 5 treatments of heart failure?

A 
Diuretics
Neurohormonal blocking agents
If channel inhibitors –ivabradine
Vasodilators –hydralazine-ISDN combination
Inotropic agents –digoxin
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2
Q

what are the aims of HF-REF treatment?

A

discover cause/ precipitating factors
relieve/ control signs and symptoms
prevent and reduce risk of hospitalisation
arrest or slow the risk of progressive HF
prolong survival/ reduce mortality

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3
Q

what is the integrated approach to treating HF-REF ?

A

general: reduce cardiac workload/ decrease salt intake/ smoking and alcohol moderation
drug treatment
other: heart transplant

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4
Q

what are the hallmarks( indications) of CHF?

A

reduced cardiac output
raised atrial / ventricular filling pressures
progressive deterioration in cardiac function

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5
Q

what are the 3 treatment goals of HF-CHF?

A

improve cardiac output (i.e. decrease forward failure)
reduce atrial / ventricular filling pressures (i.e. decrease venous return/preload decrease backward failure)
arrest or reverse myocardial remodelling

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6
Q

what are the 3 treatment strategies for CHF?

A
  • myocardial stimulation
  • reduce cardiac workload
  • arrest or reverse of cardiac remodelling
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7
Q

how do you myocardial stimulate?

A

increase myocardial contractility- with inotropic agents(digoxin, -adrenoceptor agonists, etc)

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8
Q

how do you reduce cardiac workload?

A

reduce afterload / preload-with diuretics, vasodilators, etc

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9
Q

how do you arrest or reverse cardiac remodelling?

A

inhibit chronic neurohormonal activation –with ACEIs, -blockers, ARBs, ARNIs, & aldosterone antagonists

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10
Q

which models are symptom relief?

A

cardiorenal model (Diuretics•Inotropes) and cardiocirculatory model(Inotropes•Vasodilators)

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11
Q

which model aims to prevent disease?

A

neurohormonal model (ACEIs•bblockers•ARBs•Aldosterone antagonists•ARNIs)

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12
Q

what are diuretics?

A

anionic, cationic or uncharged molecules at physiological pH
enter renal tubules via glomerular filtration or active secretion
interfere with tubular solute and/or water reabsorption

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13
Q

what are the 5 main subtypes of diuretics and what are they classified according to?

A

classified according to chemistry, site of action and MOA

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14
Q

what are the 5 subtypes of diuretics?

A

1-Osmotic diuretics –mannitol
2-Carbonic anhydrase inhibitors –acetazolamide
3-Thiazides & thiazide-related agents -Bendroflumethiazide*
4-Loop diuretics, types I & II –ethacrynic acid, furosemide*
5-Potassium sparing agents

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15
Q

what is the site and MOA of thiazide diuretics?

A

inhibit active exchange of Na+, Cl-in the distal convoluted tubule

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16
Q

what is the site and MOA of potassium sparing diuretics?

A

Inhibit reabsorption of Na+in the distal convoluted and collecting tubule

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17
Q

what is the site and MOA of loop diuretics?

A

Inhibit exchange of Na+, K+, 2Cl-in the thick segment of the ascending loop of Henle

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18
Q

what is the mechanism of diuretics?

A

1- increase salt and water excretion (diuresis)
- decrease effective plasma vol/ dec venous return and preload
2-arterial/ venodilation

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19
Q

what are the clinical uses of diuretics in CHF?

A

to prevent fluid retention and the elimination of congestive symptoms
indicate CHF patients with predisposition to fluid retention

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20
Q

what should be avoided with diuretics?

A

avoid COX 2 inhibitors and NCAIDS

avoid monotherapy-combine with ACEIs, -blockers, ARBs, ARNIs, etc

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21
Q

what are the adverse effects of thiazide and loop diuretics?

A

depletion phenomenon –hypokalaemia, hyponatremia hypomagnesaemia, hypovolaemia (L)
retention phenomenon –hyperuricemia, hypercalcemia (T)
metabolic changes –hyperglycaemia & hyperlipidaemia (T)hypersecretion of renin & aldosterone

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22
Q

what are the adverse effects of potassium-sparing diuretics?

A

retention phenomenon –hyperkalaemia

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23
Q

what 3 neurotransmitters contribute to neurohormonal activation HF

A

ANG 2, aldosterone and norephrine

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24
Q

what are the 5 available drugs for the neurohormonal blockade?

A

1-Angiotensin converting enzyme inhibitors (ACEIs)-
2-b-adrenoceptor antagonists (b-blockers)
3-Angiotensin II receptor antagonists (ARBs)
4-Aldosterone receptor antagonists
5-Angiotensin II receptor-neprilysin inhibitors (ARNIs)

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25
Q

what is the MOA of ACEIs?

A

inhibition of ACE by:
decreasing ang 2 production
INCREASING bradykinin activity

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26
Q

how does ACEIs increase bradykinin activity?

A

by inhibiting Kinase 2- to prevent the inactive form being formed

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27
Q

what happens when you suppress ANG 2 formation?

A

decrease in peripheral vasoconstriction- decrease SVR
decreased aldosterone release
decrease plasma volume - decrease cardiac stimulation decrease cardiac remodelling decrease SNS activation -decrease SVR & cardiac remodelling

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28
Q

what happens when you promote bradykinin activity?

A

1 increase peripheral vasodilatation increase SVR 2increase prostaglandin release- increase vasodilatation- increase SVR

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29
Q

what happens when aldosterone is released?

A

decrease in PV - decrease congestive symptoms

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30
Q

when do you give ACE inhibitors?

A

all patients with LV systolic dysfunction (LVEF
less than 40%)
Asymptomatic patients with LV dysfunction
All NYHA II-IV patients (unless contraindicated)

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31
Q

how do you dose ACE inhibitors?

A

start at low doses
up-titrate to clinically proven effective doses (every 2 weeks)
heck BP, renal function and serum K+& Na+–at initiation, 1-2 weeks after initiation, and after each dose increment
avoid fluid retention

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32
Q

should dose of ACE inhibitors be determined by symptoms?

A

no

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33
Q

adverse effects of ang 2 formation

A

Hypotension (1st dose effect)
Worsening renal function
Hyperkalaemia

34
Q

adverse effects of inhibition of breakdown of bradykinin

A

Cough

Angioedema

35
Q

what do b-adrenoceptor antagonists do?

A

chronic SNS activation in HF

potential benefits of inhibition of chronic SNS activation

36
Q

what is the MOA of b-adrenoceptor antagonists?

A

blockade of b-adrenoreceptors

37
Q

what are the possible mechanisms of B-adrenoceptor antagonist therapy?

A

increase Density of ß1 receptors
Inhibit cardiotoxic effects of catecholamines
decrease Neurohormonal activation
decrease HR
Anti-ischaemic & antiarrhythmic effects
Antioxidant & antiproliferative effects

38
Q

what are the indications to give b-adrenoceptor antagonists?

A

Patients with LV systolic dysfunction (EF less than 40%)
Asymptomatic patients with LV systolic dysfunction after AMI
All stable NYHA II-IV patients (unless contraindicated)

39
Q

how do you dose B-adrenoceptor antagonists?

A

start at low doses
up-titrate slowly to clinically proven effective doses
assess HR, BP & clinical status aftereach dose titration

40
Q

what are the 3 UK licensed b-adrenoceptor

A

bisoprolol, carvedilol, nebivolol

41
Q

what are extra precautions of B-adrenoceptor antagonists?

A

Patient should be stable
has no physical evidence of fluid retention
has no need for i.v.inotropic drug treatment use
clinical judgement in deciding whether or not to start ACEi first
ensure there are no contraindications
initiate in hospital

42
Q

what are the adverse effects of B-adrenoceptor antagonists?

A

Hypotension
Fluid retention -worsening heart failure
Bradycardia / heart block
Fatigue

43
Q

what are ARB’s?

A

angiotensin 2 receptor blockers

44
Q

what are ARB’s MOA?

A

angiotensin II ‘escape’ during ACE inhibition
ACEIs as ‘blunt instruments’
selective blockade of AT1 receptors
improves adverse s/e

45
Q

what do AT1 receptors block?

A

aldosterone release
vasoconstriction
proliferative actions

46
Q

what effects do AT2 receptors mediate in this chain?

A

vasodilation and antiproliferative actions

47
Q

what happens when you decrease vasoconstrictions with ARBs?

A

increases peripheral volume

decreases SVR

48
Q

what happens when you decrease aldosterone release?

A

decrease plasma volume

49
Q

what happens when you decrease proliferative events?

A

you decrease cardiac remodelling

50
Q

what are the 4 ways ARBs produce their clinical effects?

A

arteriolar vasodilation= decrease in afterload
venodilation =decrease in preload
decrease in aldosterone release
prevention of cardiac remodelling

51
Q

what are the 3 licensed agents of ARBs?

A

Candesartan
Losartan
Valsartan

52
Q

what are the 3 adverse effects of ARBs?

A

Hypotension (1st dose effect)
Worsening renal function
Hyperkalaemia
(same as ACE effects)

53
Q

what is the MOA of aldosterone receptor agonists?

A

blockade of aldosterone receptors

54
Q

why is decreasing aldosterone clinically effective?

A

decrease PV- decrease in congestive symptoms= dec in cardiac remodelling and increase in survival

55
Q

what do you use ARAs in conjunction with?

A

ACEIs, B-blockers, diuretics

56
Q

What are the 2 licensed ARAs?

A

spironolactone, eplerenone

57
Q

what are the adverse effects of ARAs?

A

impotence & gynaecomastia
menstrual disorders & hirsutism
hyperkalaemia

58
Q

what is ANRIs?

A

Angiotensin Receptor-Neprilysin Inhibitors (ARNIs)

59
Q

what 2 drugs is ANRIs a combination of?

A

Sacubitril/Valsartan

60
Q

What is the MOA of ANRIs?

A

Combined selective inhibition of neprilysin and AT1angiotensin II receptors

61
Q

why is ANRIs beneficial in heart failure?

A

Reflex activation of the natriuretic peptide system
Boosting the NP system via inhibition of the enzymatic breakdown of natriuretic peptide should be beneficial
Neprilysin inhibition also increases angiotensin II, which is undesirable

62
Q

what are the clinical effects of ANRIs?

A

Improved symptoms
Reduced HF hospitalization
Reduced CV mortality & prolonged survival

63
Q

when would we use ANRIs?

A

Only recommended as an option for NYHA class II–IV patients with LVEF ≤35%Who are symptomatic despite already taking a stable dose of an ACE inhibitor or ARB

64
Q

what are the side effects of ANRIs?

A

Hypotension
Hyperkalemia
Renal impairment
Angioedema

65
Q

should ANRIs be given with ACE /ARBS?

A

NOO. must take off ACE/ARB at least 36 hours before administration

66
Q

what is the MOA of Ivabradine?

A

selectively inhibits Ifchannel in SA node -reduced heart rate in patients in sinus rhythm

67
Q

when would you give ivabradine?

A 
NYHA class II–IV HF-REF patients (LVEF ≤35%) in sinus rhythm & with resting heart rate ≥75 beats/min
- optimised with ACE/ ARB
68
Q

what are the adverse effects of ivabradine?

A

bradycardia
AV block, headache, dizziness
visual disturbances –phosphenes, blurred vision

69
Q

what are Hydralazine-Nitrate Combination?(Hydralazine-ISDN Combination)

A

they are vasodilators

70
Q

what are hydralazine- ASDN MOA?

A

Hydralazine -arterial vasodilatation

Isosorbide dinitrate -venous vasodilatation

71
Q

What is Hydralazine-ISDN’s clinical use?

A

adjunctive therapy for symptom control

alternative first-line in patients intolerant of ACEIs & ARBs

72
Q

what are the adverse effects of H-ISDN?

A

development of tolerance
reflex neurohormonal activation vasoconstriction
myocardial stimulation
hypotension, headache, dizziness & GIT disturbances

73
Q

What are the two types of ionotropic agents?

A

Cardiac Glycosides= Digitalis –digoxin

Phosphodiesterase inhibitors =Milrinone&Enoximone

74
Q

what are the only licensed ionotropic agents?

A

digitalis

75
Q

what are the two type of effects digitalis have?

A

cardiac mechanical and cardiac digital effects

76
Q

what effect to cardiac mechanical digitals have?

A

increase myocardial contractility

Results from inhibition of Na+/K+pump increase [Ca++]i

77
Q

what effect does cardiac digital effects have?

A

low doses: inc PN activity
high doses: inc SN activity

direct increase in automaticity

78
Q

how do digitals produce their clinical effect?

A

Contractility inc CO dec hypoperfusion symptoms
Natriuresis dec PV dec congestive symptoms
Neurohormonal control

79
Q

what are the adverse effects of digitals?

A

Cardiac arrhythmias
Neurological disturbances
GIT disturbances

80
Q

what are the 2 licensed PDEI’s?

A

Milrinone & Enoximone

81
Q

what is the MOA of PDEI’s?

A

Inhibition of PDE III and increase in intracellular cAMP
inc myocardial contractility
inc peripheral vasodilatation

PHA 222 (40 decks)

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