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PHA 222 > heart failure3/4/5 > Flashcards

heart failure3/4/5 Flashcards

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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
what is the MOA of ACEIs?
inhibition of ACE by: decreasing ang 2 production INCREASING bradykinin activity
26
how does ACEIs increase bradykinin activity?
by inhibiting Kinase 2- to prevent the inactive form being formed
27
what happens when you suppress ANG 2 formation?
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
28
what happens when you promote bradykinin activity?
1 increase peripheral vasodilatation increase SVR 2increase prostaglandin release- increase vasodilatation- increase SVR
29
what happens when aldosterone is released?
decrease in PV - decrease congestive symptoms
30
when do you give ACE inhibitors?
all patients with LV systolic dysfunction (LVEF less than 40%) Asymptomatic patients with LV dysfunction All NYHA II-IV patients (unless contraindicated)
31
how do you dose ACE inhibitors?
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
32
should dose of ACE inhibitors be determined by symptoms?
no
33
adverse effects of ang 2 formation
Hypotension (1st dose effect) Worsening renal function Hyperkalaemia
34
adverse effects of inhibition of breakdown of bradykinin
Cough | Angioedema
35
what do b-adrenoceptor antagonists do?
chronic SNS activation in HF | potential benefits of inhibition of chronic SNS activation
36
what is the MOA of b-adrenoceptor antagonists?
blockade of b-adrenoreceptors
37
what are the possible mechanisms of B-adrenoceptor antagonist therapy?
increase Density of ß1 receptors Inhibit cardiotoxic effects of catecholamines decrease Neurohormonal activation decrease HR Anti-ischaemic & antiarrhythmic effects Antioxidant & antiproliferative effects
38
what are the indications to give b-adrenoceptor antagonists?
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
how do you dose B-adrenoceptor antagonists?
start at low doses up-titrate slowly to clinically proven effective doses assess HR, BP & clinical status aftereach dose titration
40
what are the 3 UK licensed b-adrenoceptor
bisoprolol, carvedilol, nebivolol
41
what are extra precautions of B-adrenoceptor antagonists?
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
what are the adverse effects of B-adrenoceptor antagonists?
Hypotension Fluid retention -worsening heart failure Bradycardia / heart block Fatigue
43
what are ARB's?
angiotensin 2 receptor blockers
44
what are ARB's MOA?
angiotensin II ‘escape’ during ACE inhibition ACEIs as ‘blunt instruments’ selective blockade of AT1 receptors improves adverse s/e
45
what do AT1 receptors block?
aldosterone release vasoconstriction proliferative actions
46
what effects do AT2 receptors mediate in this chain?
vasodilation and antiproliferative actions
47
what happens when you decrease vasoconstrictions with ARBs?
increases peripheral volume | decreases SVR
48
what happens when you decrease aldosterone release?
decrease plasma volume
49
what happens when you decrease proliferative events?
you decrease cardiac remodelling
50
what are the 4 ways ARBs produce their clinical effects?
arteriolar vasodilation= decrease in afterload venodilation =decrease in preload decrease in aldosterone release prevention of cardiac remodelling
51
what are the 3 licensed agents of ARBs?
Candesartan Losartan Valsartan
52
what are the 3 adverse effects of ARBs?
Hypotension (1st dose effect) Worsening renal function Hyperkalaemia (same as ACE effects)
53
what is the MOA of aldosterone receptor agonists?
blockade of aldosterone receptors
54
why is decreasing aldosterone clinically effective?
decrease PV- decrease in congestive symptoms= dec in cardiac remodelling and increase in survival
55
what do you use ARAs in conjunction with?
ACEIs, B-blockers, diuretics
56
What are the 2 licensed ARAs?
spironolactone, eplerenone
57
what are the adverse effects of ARAs?
impotence & gynaecomastia menstrual disorders & hirsutism hyperkalaemia
58
what is ANRIs?
Angiotensin Receptor-Neprilysin Inhibitors (ARNIs)
59
what 2 drugs is ANRIs a combination of?
Sacubitril/Valsartan
60
What is the MOA of ANRIs?
Combined selective inhibition of neprilysin and AT1angiotensin II receptors
61
why is ANRIs beneficial in heart failure?
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
what are the clinical effects of ANRIs?
Improved symptoms Reduced HF hospitalization Reduced CV mortality & prolonged survival
63
when would we use ANRIs?
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
what are the side effects of ANRIs?
Hypotension Hyperkalemia Renal impairment Angioedema
65
should ANRIs be given with ACE /ARBS?
NOO. must take off ACE/ARB at least 36 hours before administration
66
what is the MOA of Ivabradine?
selectively inhibits Ifchannel in SA node -reduced heart rate in patients in sinus rhythm
67
when would you give ivabradine?
``` NYHA class II–IV HF-REF patients (LVEF ≤35%) in sinus rhythm & with resting heart rate ≥75 beats/min - optimised with ACE/ ARB ```
68
what are the adverse effects of ivabradine?
bradycardia AV block, headache, dizziness visual disturbances –phosphenes, blurred vision
69
what are Hydralazine-Nitrate Combination?(Hydralazine-ISDN Combination)
they are vasodilators
70
what are hydralazine- ASDN MOA?
Hydralazine -arterial vasodilatation | Isosorbide dinitrate -venous vasodilatation
71
What is Hydralazine-ISDN's clinical use?
adjunctive therapy for symptom control | alternative first-line in patients intolerant of ACEIs & ARBs
72
what are the adverse effects of H-ISDN?
development of tolerance reflex neurohormonal activation vasoconstriction myocardial stimulation hypotension, headache, dizziness & GIT disturbances
73
What are the two types of ionotropic agents?
Cardiac Glycosides= Digitalis –digoxin | Phosphodiesterase inhibitors =Milrinone&Enoximone
74
what are the only licensed ionotropic agents?
digitalis
75
what are the two type of effects digitalis have?
cardiac mechanical and cardiac digital effects
76
what effect to cardiac mechanical digitals have?
increase myocardial contractility | Results from inhibition of Na+/K+pump increase [Ca++]i
77
what effect does cardiac digital effects have?
low doses: inc PN activity high doses: inc SN activity direct increase in automaticity
78
how do digitals produce their clinical effect?
Contractility inc CO dec hypoperfusion symptoms Natriuresis dec PV dec congestive symptoms Neurohormonal control
79
what are the adverse effects of digitals?
Cardiac arrhythmias Neurological disturbances GIT disturbances
80
what are the 2 licensed PDEI's?
Milrinone & Enoximone
81
what is the MOA of PDEI's?
Inhibition of PDE III and increase in intracellular cAMP inc myocardial contractility inc peripheral vasodilatation

PHA 222 (40 decks)

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