Heart failure treatment Flashcards
when does R heart failure only commonly occur?
in severe lung disease
not likely to be asked about in cardiovascular system question
heart failure tends to refer to LV heart disease
two types of heart failure?
systolic and diastolic
systolic heart failure (HFrEF - heart failure reduced ejection fraction)
heart has turned into a skinny bag that cannot function properly
Decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure
LVSD
usually occurs following myocardial damage ie post MI
diastolic heart failure (HFpEF - Heart Failure with a Preserved Ejection Fraction ie it is normal)
Involves a thickened and stiff heart muscle due to high BP
As a result, the heart releases all the blood but it does not fill with blood properly as it can’t relax properly
This results in fluid backup in the lungs and heart failure
heart failure usually occurs following sustained hypertension
Chronic heart failure
2-10% of population affected
People with severe heart failure are very symptomatic – QOL affected greatly.
Peripheral oedema, if severe, can reduce mobility
risk factors for heart failure
Coronary artery disease previous MI Hypertension (LVH) Valvular heart disease Alcoholism – v common cause Infection (viral) diabetes congenital heart defects
then general:- age, obesity, smoking, obstructive sleep apnoea
what is the most severe risk factor of heart failure
hypertension
LV diastolic dysfunction can be prevented if hypertension is tackled aggressively
frank starling law and systolic dysfunction?
if the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood.
Failing or damaged heart - lose this relationship
Healthy heart – contraction force is in proportion with the amount it is stretched
Damaged heart - More you stretch the heart due to increased circulatory volume (H20 and salt retention) the weaker the force of contraction and CO drops further
drop in CO activates vasoconstrictor system (sympathetic) and RAAS
how does a drop in CO due to HF cause further problems?
drop in CO activates RAAS system which then increases plasma vol and therefore increases venous return so cardiac performance deteriorates further
how does the heart weaken
As the heart starts to dilate the cardiac myocytes undergo hypertrophy and then fibrosis and thus the heart is further weakened
myocytes that become hypertrophic become ischaemic and die
The RAAS system causes the release of what?
angiotensin II – causes vasoconstriction
aldosterone
what does the Natriuretic peptide system ANP/BNP
cause salt watter loss
what does EDRF do?
muscle relaxation
vasodilation
treatment options to improve SYMPTOMS of heart failure? (2)
diuretics - no other drug that alters physical state of patient like them - gets rid of excess fluid so they don’t have peripheral oedema - also improves exercise capacity
digoxin - slows and controls heart rate
treatment options to improve SYMPTOMS AND SURVIVAL of heart failure? (3)
ACE inhibitors/ARBs
Spironolactone – mineralocorticoid - steroid hormone
Valsartan-sacubitril – expensive, inhibits the breakdown of natriuretic peptides resulting in varied effects including increased diuresis, natriuresis, and vasodilation.
treatment to improve HF survival
beta blockers
ivabradine
symptomatic treatment?
Loop Diuretics
FUROSEMIDE or BUMETANIDE
Furosemide- start on IV then move onto oral con is that they can;t leave house due to a lot of diuresis (urine output increases)
Bumetanide - takes 10 hours to reduce diuresis - Have to use these in the morning and early afternoon – so they don’t have to get up during the night to urinate – high fall risk at night etc for elderly
treatment options for blocking detrimental hormonal changes?
sympathetic activation by cavedilol, bisoprolol, metoprolol beta blockers - proven benefit in treatment of chronic HF
which two drugs can block the affects of angiotensin II
ACE Inhibitors (Ramipril )
Angiotensin antagonists (Valsartan, Losartan) but these are not as effective (ELITE II)
which drug can block the affect of aldosterone?
SPIRONOLACTONE
what is the treatment option if a patient is resistant to diuretics
use a diuretic in combination with thiazide diuretics - powerful combo - 5/10 litres a day - diuresis induced
how can a patient become resistant to diuretics?
Patients become resistant to furosemide because the body is trying to maintain balance by retaining more salt water
ADRs related to diuretic use (6)
Dehydration Hypotension Hypokalaemia Hyponatraemia Gout - formation of crystals in the joints Impaired glucose tolerance, diabetes
drug-drug interactions
furosemide and…
- aminoglycosides
- lithium
- NSAIDs
- antihypertensives
- vancomycin
- aural (ear) and renal toxicity
- renal toxicity
- renal toxicity
- profound hypotension
- renal toxicity
4 ways to reduce mortality?
angiotensin blockade - induces vasodilation - lowers BP
beta receptor blockade - lowers heart rate
ANP/BNP enhancement - vasodilation, natriuresis, and inhibition of RAA and sympathetic systems.
define natriuresis
process of sodium excretion in the urine through the action of the kidneys
it lowers the conc of Na+ in the blood and also tends to lower blood vol because osmotic forces drag H20 out of the body’s blood circulation and into the urine along with the Na+
which drugs prevent the conversion of angiotensin I to II by blocking the angiotensin converting enzyme?
Ramipril
Enalapril
Lisinopril
by doing this they reduce the preload and after load on the heart
what does using ACE inhibitors do for:-
patients with chronic HF
post MI patients
which studies looked into this?
CHF - reduces morbidity, mortality
Post MI - reduces morbidity, mortality, onset of heart failure
studies:- CONCENSUS, SOLVD,
ADRs with ace inhibitors
First dose hypotension Cough Angioedema Renal impairment Renal failure Hyperkalaemia
NSAIDs and ACEI
could be life threatening - acute renal failure
NSAIDs - aches and pains - elderly
role of angiotensin I
Vasoconstriction Vascular proliferation Aldosterone secretion Cardiac myocyte proliferation Increased sympathetic tone
role of angiotensin II
Vasodilation
Anti-proliferation
Apoptosis
how can beta blockers kill patients with severe HF
patients with severe HF rely on adrenergic system to survive. A beta blocker flattens them quickly and they die
what do you need to do before putting a patient on a beta blocker
stabilise them - should not be used during an acute presentation
need to get rid of peripheral oedema etc first
ivabradine
specific inhibitor of the pacemaker current in the SA node (binds to If receptors in pacemaker) - slows heart rate
reduces mortality and hospitalisations in people that cannot tolerate beta blockers (ie get too tired/lethargic) – it isn’t as effective though
warfarin
Anticoagulant - used if there is high risk of thromboembolic disease - prevents stroke
Dilated ventricle gives rise to thrombus formation and thrombo-embolic events
how do you monitor someone with HF
HF is evident due to fluid retention
monitor by measuring weight on daily basis - see how many kilos of weight they’re losing each day through urine/bowel movements etc
benefits of monitoring patient
Symptomatic relief
SOB, tiredness, lethargy
Clinical relief
Peripheral oedema, ascites, weight
Monitor weight regularly
Patient performs daily weight assessment
Increase medication according to symptoms or weight
Patient education
