Heart Failure - treatment Flashcards

1
Q

when does R heart failure only commonly occur?

A

in severe lung diseasenot likely to be asked about in cardiovascular system questionheart 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 properlyDecreased pumping function of the heart, which results in fluid back up in the lungs and heart failureLVSD 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 BPAs a result, the heart releases all the blood but it does not fill with blood properly as it can’t relax properlyThis results in fluid backup in the lungs and heart failureheart failure usually occurs following sustained hypertension

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5
Q

Chronic heart failure

A

2-10% of population affectedPeople 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 diseaseprevious MIHypertension (LVH)Valvular heart diseaseAlcoholism – v common causeInfection (viral)diabetescongenital heart defectsthen general:- age, obesity, smoking, obstructive sleep apnoea

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7
Q

what is the most severe risk factor of heart failure

A

hypertensionLV 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 relationshipHealthy heart – contraction force is in proportion with the amount it is stretchedDamaged heart - More you stretch the heart due to increased circulatory volume (H20 and salt retention) the weaker the force of contraction and CO drops furtherdrop 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 weakenedmyocytes 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 vasoconstrictionaldosterone

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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 relaxationvasodilation

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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 capacitydigoxin - 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/ARBsSpironolactone – mineralocorticoid - steroid hormoneValsartan-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 blockersivabradine

17
Q

symptomatic treatment?

A

Loop Diuretics FUROSEMIDE or BUMETANIDEFurosemide- 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

DehydrationHypotensionHypokalaemiaHyponatraemiaGout - formation of crystals in the joints Impaired glucose tolerance, diabetes

24
Q

drug-drug interactions furosemide and…1. aminoglycosides2. lithium3. NSAIDs4. antihypertensives5. vancomycin

A
  1. aural (ear) and renal toxicity2. renal toxicity3. renal toxicity4. profound hypotension5. renal toxicity
25
Q

4 ways to reduce mortality?

A

angiotensin blockade - induces vasodilation - lowers BPbeta receptor blockade - lowers heart rateANP/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 kidneysit 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

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

28
Q

what does using ACE inhibitors do for:-patients with chronic HFpost MI patients which studies looked into this?

A

CHF - reduces morbidity, mortalityPost MI - reduces morbidity, mortality, onset of heart failurestudies:- CONCENSUS, SOLVD,

29
Q

ADRs with ace inhibitors

A

First dose hypotensionCoughAngioedemaRenal impairmentRenal failureHyperkalaemia

30
Q

NSAIDs and ACEI

A

could be life threatening - acute renal failureNSAIDs - aches and pains - elderly

31
Q

role of angiotensin I

A

VasoconstrictionVascular proliferation Aldosterone secretionCardiac myocyte proliferationIncreased sympathetic tone

32
Q

role of angiotensin II

A

VasodilationAnti-proliferationApoptosis

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 presentationneed 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 ratereduces 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 reliefSOB, tiredness, lethargyClinical reliefPeripheral oedema, ascites, weightMonitor weight regularlyPatient performs daily weight assessmentIncrease medication according to symptoms or weightPatient education