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Cardiovascular > Heart Failure - Pathophysiology and Treatment > Flashcards

Heart Failure - Pathophysiology and Treatment Flashcards

1
Q

What is chronic heart failure characterised by?

A

Progressive cardiac dysfunction, breathlessness, tiredness, neurohormonal disturbances and sudden death

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2
Q

What are types of heart failure?

A

Left ventricular systolic dysfunction (HFrEF)
Left ventricular diastolic heart failure (HFpEF)

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3
Q

What is left ventricular systolic dysfunction (HFrEF)?

A

Decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure

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4
Q

What is left ventricular diastolic (relaxation) heart failure (HFpEF)?

A

Involves a thickened and stiff heart muscle
As a result, the heart does not fill with blood properly and fluid build up in the lungs and heart failure

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5
Q

What are 2 major risk factors for HF?

A

Hypertension - leads to diastolic dysfunction then progresses to reduced ejection failure systolic dysfunction
MI - damage to LV so systolic dysfunction

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6
Q

What does Heart failure usually occur as a result of?

A

Sustained hypertension
MI
Or both - CO falls and body registers as loss in circulatory volume so vasoconstriction and RAAS activation

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7
Q

What does the Frank-Starling Law state?

A

If the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood

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8
Q

Describe the loss of relationship (Frank-starling Law) in the failing or damaged heart?

A

Heart dilates as circulatory volume increases, force of contraction weakens and CO drops further
CO then activates the sympathetic and RAAS so further vasoconstriction and salt and water retention

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9
Q

What is the result of the vicious cycle where there is sympathetic system and RAAS activation?

A

Circulatory volume increases and cardiac performance deteriorates further

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10
Q

What does peripheral vasoconstriction lead to?

A

Increased afterload so decreased CO leading to heart failure
Progressive vasoconstriction leads to myocyte death and fibrosis

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11
Q

What does increased salt and water retention lead to?

A

Increased plasma volume and increases preload
So increased cardiac workload leading to HF and oedema

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12
Q

What are the aim for the treatment?

A

Improve clinical status, functional capacity and QoL, prevent hospital admission and reduce mortality

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13
Q

What is the mechanism for loop diuretics?

A

Induce profound diuresis by inhibiting the Na-K-Cl transporter in the Loop of Henle
Work at very low glomerular filtration rates
They prevent reabsorption of 20% of filtered sodium and water

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14
Q

What is loop diuretics used for?

A

Main stay of treatment for patients with salt and water retention to reduce symptoms of tiredness, fatigue and improve exercise capacity

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15
Q

What is the name of loop diuretic mainly used?

A

Furosemide

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16
Q

What do you use in patients who are diuretic resistant?

A

Can use loop in combo. with thiazide diuretics
May induce a diuresis of 5-10l a day

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17
Q

What are some adverse drug reactions with diuretics?

A

Dehydration, hypotension, hypokalaemia, hyponatraemia, gout and impaired glucose tolerance - diabetes

18
Q

What are some drug drug interactions of frusemide?

A

Aminoglycosides - aural and renal toxicity
Lithium - renal toxicity
NSAIDs - renal toxicity
Antihypertensive - profound hypotension
Vancomycin - renal toxicity

19
Q

What are some neuro-hormonal antagonists?

A

ACE inhibitors/ Angiotensin Receptor Blockers
Beta blockers
Mineralocorticoid receptor blockers
Combined angiotensin blockage plus ANP/BNP enhancement

20
Q

What are some angiotensin converting enzyme inhibitors?

A

Ramipril is most common
Enalapril and Lisinopril

21
Q

What is the mechanism of action of angiotensin converting enzyme (ACE) inhibitors?

A

Competitively block angiotensin converting enzyme which prevents conversion of angiotensin I to II
Reduces preload and afterload on heart

22
Q

What is reduced in patients given ACE inhibitors?

A

Significant reduction in morbidity and mortality

23
Q

What are some adverse drug reaction of ACE inhibitors?

A

Cough, angioedema, renal impairment, renal failure and hyperkalaemia

24
Q

What are some drug-drug interactions of ACE inhibitors?

A

NSAIDs - acute renal failure
Potassium supplements - hyperkalaemia
Potassium sparing diuretics -hyperkalaemia

25
Q

Describe Angiotensin Receptor Blockers

A

ARBs selectively block the angiotensin II at AT1 receptor
Are effective but not proven to reduce mortality in patients with HFrEF
Not as effective as ACEi

26
Q

When is angiotensin receptor blockers given?

A

Restricted to patients who are intolerant of an ACEi

27
Q

What is Valsartan-Sacubitril (ARNI)?

A

Combined valsartan and ARB and Neprilysin inhibitor
ARB blocks At1 receptor
Neprilysin inhibitor stops breakdown of ANP and BNO by neutral endopeptidases

28
Q

Is Valsartan-Sacubitril (ARNI) effective?

A

Reduces mortality and hospital admissions
Doubles benefits of current inhibitors of RAAS

29
Q

When is Valsartan-Sacubitril (ARNI) recommended as an option for treatment?

A

Treating symptomatic chronic HF with recued ejection fraction in people with - NYHA class II to IV symptoms, LVEF of 35% or less, and who are already on stable does of ACEi or angiotensin II receptor blockers and remaining symptoms

30
Q

What is the mechanism of action for mineralocorticoid receptor antagonists (MRAs)?

A

Block receptors that bind aldosterone and other steroid hormone receptors
Spironolactone and eplerenone mainly used

31
Q

When is MRAs recommended?

A

All symptomatic patients with HFrEF (despite treatment with an ACEi and a BB) and LVEF <35% to reduce mortality and HF hospitalisation

32
Q

What does spironolactone and eplerenone cause?

A

Are potassium sparing diuretics and inhibit action of aldosterone
Acts on distal tubule

33
Q

What are common beta blockers used?

A

Carvedilol and Bisoprolol

34
Q

Describe beta blockers

A

Block actions of sympathetic system
Have demonstrated to reduce morbidity and mortality in HF by 30%

35
Q

When should a Beta blocker be used in treatment?

A

Patient is stabilised and not during an acute presentation as precipitate severe deterioration in CHF if the patient is in fluid overloaded

36
Q

Describe Ivabradine

A

Slows down HR through inhibition of the If channels in the sinus node and therefore should only be used in patients with sinus rhythm

37
Q

Is Ivabradine beneficial in patients with HFrEF?

A

Can be beneficial in reducing HF hospitalisations for patients who are symptomatic stable chronic HFrEF who are receiving standard therapy - incl. bb at max. dose and who are in sinus rhythm which HR at 70 bpm

38
Q

What is a positive inotrope used in treatment?

A

Digoxin

39
Q

Describe Digoxin

A

Increases availability of Ca in the myocyte and reduce hospitalisations
No effect on mortality
Narrow therapeutic index - toxicity can happen

40
Q

What can Digoxin cause?

A

Arrhythmias, nausea and confusion

41
Q

What is a standard therapeutic regime in treatment of HFrEF?

A

Furosemide and possible thiazide
ACE inhibitor
ARB if allergic to ACEi
ARNI if still symptomatic
BB and maybe ivabradine
MRA - spironolactone

42
Q

Describe monitoring benefit?

A

Symptomatic relief - SOB, tiredness and lethargy
Clinical relief - oedema, ascites and weight
Monitor weight regularly
Patient education also important

Cardiovascular (33 decks)

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