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1ST YEAR SYSTEMS: Cardiovascular > Heart failure treatment > Flashcards

Heart failure treatment Flashcards

1
Q

when does R heart failure only commonly occur?

A

in severe lung disease
not likely to be asked about in cardiovascular system question

heart failure tends to refer to LV heart disease

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2
Q

two types of heart failure?

A

systolic and diastolic

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3
Q

systolic heart failure (HFrEF - heart failure reduced ejection fraction)

A

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

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4
Q

diastolic heart failure (HFpEF - Heart Failure with a Preserved Ejection Fraction ie it is normal)

A

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

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5
Q

Chronic heart failure

A

2-10% of population affected

People with severe heart failure are very symptomatic – QOL affected greatly.

Peripheral oedema, if severe, can reduce mobility

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6
Q

risk factors for heart failure

A 
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

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7
Q

what is the most severe risk factor of heart failure

A

hypertension

LV diastolic dysfunction can be prevented if hypertension is tackled aggressively

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8
Q

frank starling law and systolic dysfunction?

A

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

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9
Q

how does a drop in CO due to HF cause further problems?

A

drop in CO activates RAAS system which then increases plasma vol and therefore increases venous return so cardiac performance deteriorates further

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10
Q

how does the heart weaken

A

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

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11
Q

The RAAS system causes the release of what?

A

angiotensin II – causes vasoconstriction

aldosterone

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12
Q

what does the Natriuretic peptide system ANP/BNP

A

cause salt watter loss

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13
Q

what does EDRF do?

A

muscle relaxation

vasodilation

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14
Q

treatment options to improve SYMPTOMS of heart failure? (2)

A

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

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15
Q

treatment options to improve SYMPTOMS AND SURVIVAL of heart failure? (3)

A

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.

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16
Q

treatment to improve HF survival

A

beta blockers

ivabradine

17
Q

symptomatic treatment?

A

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

18
Q

treatment options for blocking detrimental hormonal changes?

A

sympathetic activation by cavedilol, bisoprolol, metoprolol beta blockers - proven benefit in treatment of chronic HF

19
Q

which two drugs can block the affects of angiotensin II

A

ACE Inhibitors (Ramipril )

Angiotensin antagonists (Valsartan, Losartan) but these are not as effective (ELITE II)

20
Q

which drug can block the affect of aldosterone?

A

SPIRONOLACTONE

21
Q

what is the treatment option if a patient is resistant to diuretics

A

use a diuretic in combination with thiazide diuretics - powerful combo - 5/10 litres a day - diuresis induced

22
Q

how can a patient become resistant to diuretics?

A

Patients become resistant to furosemide because the body is trying to maintain balance by retaining more salt water

23
Q

ADRs related to diuretic use (6)

A 
Dehydration
Hypotension
Hypokalaemia
Hyponatraemia
Gout - formation of crystals in the joints 
Impaired glucose tolerance, diabetes
24
Q

drug-drug interactions
furosemide and…

  1. aminoglycosides
  2. lithium
  3. NSAIDs
  4. antihypertensives
  5. vancomycin
A
  1. aural (ear) and renal toxicity
  2. renal toxicity
  3. renal toxicity
  4. profound hypotension
  5. renal toxicity
25
Q

4 ways to reduce mortality?

A

angiotensin blockade - induces vasodilation - lowers BP

beta receptor blockade - lowers heart rate

ANP/BNP enhancement - vasodilation, natriuresis, and inhibition of RAA and sympathetic systems.

26
Q

define natriuresis

A

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+

27
Q

which drugs prevent the conversion of angiotensin I to II by blocking the angiotensin converting enzyme?

A

Ramipril
Enalapril
Lisinopril

by doing this they reduce the preload and after load on the heart

28
Q

what does using ACE inhibitors do for:-

patients with chronic HF
post MI patients

which studies looked into this?

A

CHF - reduces morbidity, mortality

Post MI - reduces morbidity, mortality, onset of heart failure

studies:- CONCENSUS, SOLVD,

29
Q

ADRs with ace inhibitors

A 
First dose hypotension
Cough
Angioedema
Renal impairment
Renal failure
Hyperkalaemia
30
Q

NSAIDs and ACEI

A

could be life threatening - acute renal failure

NSAIDs - aches and pains - elderly

31
Q

role of angiotensin I

A 
Vasoconstriction
Vascular proliferation 
Aldosterone secretion
Cardiac myocyte proliferation
Increased sympathetic tone
32
Q

role of angiotensin II

A

Vasodilation
Anti-proliferation
Apoptosis

33
Q

how can beta blockers kill patients with severe HF

A

patients with severe HF rely on adrenergic system to survive. A beta blocker flattens them quickly and they die

34
Q

what do you need to do before putting a patient on a beta blocker

A

stabilise them - should not be used during an acute presentation

need to get rid of peripheral oedema etc first

35
Q

ivabradine

A

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

36
Q

warfarin

A

Anticoagulant - used if there is high risk of thromboembolic disease - prevents stroke

Dilated ventricle gives rise to thrombus formation and thrombo-embolic events

37
Q

how do you monitor someone with HF

A

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

38
Q

benefits of monitoring patient

A

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

1ST YEAR SYSTEMS: Cardiovascular (39 decks)

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