heart failure therapeutics Flashcards
chronic HF diagnosed by specialist what do you give
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
what is heart failure
where the heart cannot pump enough to meet the bodies needs
reduced systolic contractions and decreased diastolic compliance
end diastolic volume
heart at fullest
preload
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
after load
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
if system overstretched and ventricle filled to brim shown by cardiomegaly what can you do
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
what drugs reduce volume
diuretics
how do you reduce afterlaod - to make the pipes bigger to pump same volume
what can do this
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.
how else can you increase SV
increase contractility of the heart - positive inotrophe
crhontorphe is HR
ACEi - vasodilator - afterload
diuretics - preload
beta blocker - after load
digoxin - cardiac muscle contractility
drugs used in HR vasodilators ACEi , ARB , PDEIs diuretics Lopp, thiazides and MRAs postive inotropes beta agonists, PDEI, cardiac glycosides cardioinhibors beta blockers
vasodilators
relax smooth. muscle in BV causing dilation and reducing systemic vascular resistance
ACEi SE - after load
dry cough
hypotension
angioedema - due to kinin build up
hyperkalamia and impaired auto regulation
ARB avoid this kinin side effects
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
hypokalaemia
deafness
renal toxicity with dehydration
limited effectiveness on own
mineralocorticoid receptor antagonists
aldosterone mechanism s
block itnracellaurl aldosterone receptors causing sodium excretion and ECF volume reduced
such as spironolactone SE
hyperkalamia
used with furseomide
gynaecomastia
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
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
phosphodiesterase einhribors
PDEIs beta 1 afrenoreceptros
icnrease intraceulalr 2nd messengers by preventing their breakdown
e.g. milrinone
also vasoidaltion via Beta 2
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
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
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)
don’t give beta blocker in chronic HF
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
beta blockers - bisoprolol, carvedilol
reduces cardiac wok, improve LV filling, improves O2 supply, inhbits rennin , lowers mortality
SE worsens contractility acutely bronchospasm in asthmatics cold hands and feet fatigue
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
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
treatment of acute heart failure
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
treatment of chronic HF
ACEi
beta blocker is stable add slow
MRA
loop diuretic if fluid overloaded
goal of treatment of HF
goal is to improve cardiac output while reducing associated symptoms like oedema
pre renal cause of AKI
Pre-renal- SEPSIS, hypovolaemia, renal artery stenosis
