heart failure therapeutics Flashcards

1
Q

chronic HF diagnosed by specialist what do you give

A

offer diuretics for congestive symptoms and fluid retention

if preserved ejection fraction - manage cormobidites e.g. hypertension and offer exercise

if reduced ejection fraction ofFer ACEi and BB

DIGOXIN FOR HEART FAILURE WITH SINUS RHYTHM TO IMRPOVE SYMTPOMS

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2
Q

what is heart failure

A

where the heart cannot pump enough to meet the bodies needs

reduced systolic contractions and decreased diastolic compliance

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3
Q

end diastolic volume

A

heart at fullest

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4
Q

preload

A

Preload is the force that stretches the cardiac muscle prior to contraction. This force is composed of the volume that fills the heart from venous return.

in heart failure if you have a an insufficient pump and still same force and pressure of blood coming in you need to reduce the preload and reduce hydrostatic pressure so you don’t get leaky capillaries

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5
Q

after load

A

The afterload is the amount of pressure that the heart needs to exert to eject the blood during ventricular contraction.

if you have tight pumps to move out you are going to need to work harder to move out

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6
Q

if system overstretched and ventricle filled to brim shown by cardiomegaly what can you do

A

reduce preload - bring them down starling curve therefor increasing the stroke volume

use diuretics to reduce volume

also reduces pulmonary capillary hydrostatic pressure - IV shot of frusemide

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7
Q

what drugs reduce volume

A

diuretics

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8
Q

how do you reduce afterlaod - to make the pipes bigger to pump same volume

what can do this

A

reduce resistance after pump to cause SV to rise

a vasodilator

Sodium nitroprusside is an intravenous vasodilator commonly used in the past in patients with refractory heart failure.

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9
Q

how else can you increase SV

A

increase contractility of the heart - positive inotrophe

crhontorphe is HR

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10
Q

ACEi - vasodilator - afterload
diuretics - preload
beta blocker - after load
digoxin - cardiac muscle contractility

A
drugs used in HR 
vasodilators 
ACEi , ARB , PDEIs
diuretics 
Lopp, thiazides and MRAs
postive inotropes 
beta agonists, PDEI, cardiac glycosides
cardioinhibors 
beta blockers
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11
Q

vasodilators

A

relax smooth. muscle in BV causing dilation and reducing systemic vascular resistance

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12
Q

ACEi SE - after load

A

dry cough
hypotension
angioedema - due to kinin build up
hyperkalamia and impaired auto regulation

ARB avoid this kinin side effects

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13
Q
diuretics - preload 
loop diuretics - stop reabsorbing of ions from tubule back into institium which drags water in to be excreted reduces extraceulalr volume reducing preload 
this results in 
sodium excretion, water excretion 
SE
A

hypokalaemia
deafness
renal toxicity with dehydration
limited effectiveness on own

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14
Q

mineralocorticoid receptor antagonists
aldosterone mechanism s
block itnracellaurl aldosterone receptors causing sodium excretion and ECF volume reduced
such as spironolactone SE

A

hyperkalamia
used with furseomide
gynaecomastia

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15
Q

positive ion tropes - increase force of contrition thereof increasing SV - only used in date HF as uses HUGE amount of oxygen - also a vasodilator so pumping harder on less resistance

sympathomimetics
increase afterload example is dobutamine ( used in acute HF with reduced EF ( cariogenic shock)
SE

A

mimic action of adrenaline and noradrenaline
B1 cardiac specific

which one is more effective adrenaline or noreadneliae

tachycardia - dose related
no benefit in chronic HF

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16
Q

phosphodiesterase einhribors
PDEIs beta 1 afrenoreceptros

icnrease intraceulalr 2nd messengers by preventing their breakdown
e.g. milrinone

also vasoidaltion via Beta 2

A

hardly used

SE 
hypotension 
reflex tachycardia 
arrhymias 
worsens survival in chronic HF 

this is PDE3 inhibition
PDE5 - smooth muscle in penis affected by sidenifil - pulmonary and penile - vasodilation in specific

17
Q

cardiac glycosides
digoxin

increases contraciltiy but slows rate especially in AF
mild dieresis , improves sx
does not improve survival

SE arrhythmias, contradicted in hypokalaemia, renal impairment of AV block

A

ion exchange in cardiac mycoses
sodium and potassium pump inhibited
secondary inhibition of calcium and sodium exchange from intracellular sodium increase
rise in intracellular calcium results in positive ion trophy

slows AV conduction pariualry useful in AF ( negative chronotropicity)

18
Q

don’t give beta blocker in chronic HF

A
Compensatory activation of sympathetic nerves during heart failure can cause:
Arterioconstriction
Venoconstriction
Tachycardia
Increased cardiac work
Renin release

Blocking excessive sympathetic activation (with beta blockers) has proven to be beneficial

19
Q

beta blockers - bisoprolol, carvedilol

reduces cardiac wok, improve LV filling, improves O2 supply, inhbits rennin , lowers mortality

A
SE 
worsens contractility acutely 
bronchospasm in asthmatics 
cold hands and feet 
fatigue
20
Q

bisporlol - highly selective beta1 receptors less SE

carvedilol - mild alpha 1 receptors blocking action reducing preload

nebivolol - highly selective fro beta1 but also enhances vasodilation mediated by NO

A

loop diuretics given first - clear up extra fluid

If patients blood pressure drops what type of drug would you give - positive ionotrope e.g. digoxin

long term to manage symptoms

21
Q

treatment of acute heart failure

A

oxygen
plus IV furosemide
IV vasodilator with GTN
positive iontorphes ( if BP has dropped)
postifi3 pressure ventilation in extremities
more severity add ACEi and beta blockers when stable

plus treat underlying cause

22
Q

treatment of chronic HF

A

ACEi
beta blocker is stable add slow
MRA
loop diuretic if fluid overloaded

23
Q

goal of treatment of HF

A

goal is to improve cardiac output while reducing associated symptoms like oedema

24
Q

pre renal cause of AKI

A

Pre-renal- SEPSIS, hypovolaemia, renal artery stenosis