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Drugs: from molecules to man > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is chronic heart failure?

A

ongoing condition, symptoms change fairly slowly over a long period of time

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2
Q

What is acute heart failure?

A

sudden onset of heart failure symptoms or more rapid worsening of chronic heart failure

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3
Q

What is heart failure?

A

the inability of the heart to pump enough blood to meet body’s O2 demands

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4
Q

Why is heart failure complex?

A

it is not a single condition – divided into two separate types with different treatment options

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5
Q

What happens with someone’s Frank-Starling relationship when they have heart failure?

A

When someone has heart failure their Frank-Starling relationship is shifted to the right and their maximum is depressed – they have a higher end diastolic pressure for a lower stroke volume. This makes it hard to exercise.

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6
Q

What are symptoms of heart failure?

A
  • Fatigue
  • Blood backing up from heart into lungs – pulmonary oedema which causes shortness of breath and coughing
  • Right side of blood receives blood from rest of the body but doesn’t eject enough blood
     Don’t get enough blood from right side to left side exacerbating tiredness
     Blood backs up into the rest of the body, leading to effusion of blood into the tissues – e.g. fluid accumulates in ankles and legs, swelling in abdomen
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7
Q

What is the epidemiology of heart failure?

A
  • Prevalence 1.3-4% (Europe, N. America)
  • Estimated that up to 900000 people in the UK have HF
  • Global costs estimated to be $108 billion (2012)
  • Five year survival rate is 50% (worse than many cancers)
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8
Q

What are the key problems in heart failure?

A
  • The heart doesn’t contract well: systolic failure
  • The heart doesn’t fill well: diastolic failure
  • Both result in reduced cardiac output
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9
Q

What is the ejection fraction and what is the normal ejection fraction?

A
  • 100(stroke volume)/ ventricle volume

- Normally ejection fraction of around 60%

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10
Q

What ejection fractions do you see in diastolic and systolic heart failure?

A
  • In systolic failure you see reduced ejection fraction less than 40%
  • In diastolic failure you see preserved ejection fraction.
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11
Q

What do we see with reduced ejection fraction heart failure?

A
  • With heart failure with reduced EF we see a larger left ventricle with thinner walls
  • When left ventricle contracts we get much less blood pumped out into the aorta
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12
Q

What are the risk factors for reduced ejection fraction heart failure?

A

previous MI, diabetes, valvular disease, hypertension, CAD, dilated cardiomyopathy (genetic), male, age smoking

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13
Q

What do we see with preserved ejection fraction heart failure?

A
  • See thickening or stiffening of wall of left ventricle
  • Stops ventricle from filling properly
  • EF around >50% but low stroke volume
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14
Q

What are the risk factors for preserved ejection fraction heart failure?

A

hypertension, age, atrial fibrillation, hypertrophic cardiomyopathy (genetic), female, diabetes

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15
Q

What are genetic forms of heart failure?

A
  • Dilated cardiomyopathy
     Enlarged and ‘baggy’ ventricle
     Gives HFrEF (heart failure with reduced ejection fraction): diagnosed when causes like hypertension excluded
     About 50% familial (frequency 1:250 people)
     Rest due to cardiac injury from other causes
  • Hypertrophic cardiomyopathy
     Ventricle has thick muscle walls -> filling problems
     Diagnosed when other causes of HFpEF (heart failure with preserved ejection fraction) rules out
     Mostly inherited: autosomal dominant (1:500)
  • Cardiomyopathy mutations known in most sarcomere proteins
     Actin, myosin, MLCK, titin
  • Same mutation can lead to DCM (dilated cardiac myopathy) or HCM (hypertrophic cardiac myopathy) even in the same family
     Genetic and environmental modifiers
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16
Q

What is another classification system (not about ejection fraction?

A
  • left side
  • right side
  • Forward: aren’t pushing enough blood out of that side of the heart
  • Backward: backing up of blood from that side of the heart
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17
Q

What are the symptoms of left forward heart failure?

A

Easily tired
Cyanosis
Under perfused kidney -> salt, water retention

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18
Q

What are the symptoms of left backwards heart failure?

A

pulmonary oedema

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19
Q

What are the symptoms of right forward heart failure?

A

easily tired

20
Q

What are the symptoms of right backward heart failure?

A

Engorged liver, spleen
Peripheral oedema
Pulmonary effusion

21
Q

What happens with the initial insult (e.g. ischaemia) that produces heart failure?

A
  • We have a decreased cardiac output
  • The sympathetic and angiotensin systems are activated
  • vasoconstriction, tachycardia and increased salt and water retention help with short term compensation
22
Q

What does short term compensation induce?

A

Further remodelling long term

23
Q

What is decompensation?

A

The adaptive processes are no longer able to compensate for the compromised heart function. Patient enters state where they don’t have enough blood reaching their tissues.

24
Q

What are risk factors for arrhythmias?

A

Cardiac ischaemia, increased sympathetic activation and muscle remodelling

25
Q

What is the CONSENSUS; SOLVD trial?

A

 Cooperative north Scandinavian Enalapril Survival study
 Studies of Left ventricular dysfunction
 ACE inhibitors improve survival, slow progression

26
Q

What is the COMET; CIBIS II trial?

A

 Cardiac insufficiency Bisoprolol Trial II
 Carvedilol or Metoprolol European Trial
 Bisoprolol improves survival; carvedilol better than metoprolol

27
Q

What is the RALES trial?

A

 Randomised Aldactone Evaluation Study

 Spironolactone improves survival, slows progression vs placebo

28
Q

What is the CHARM trial?

A

 Candesartan in Heart Failure Assessment of Reduction in Mortality and morbidity
 ARBs share benefits of ACE I; ARB + ACE I no additional benefit

29
Q

What is the PARADIGM-HF trial?

A

 Prospective comparison of ARNI with ACEI (enalapril) to determine impact on global mortality and morbidity in heart failure
 Angiotensin Receptor/ Neprilysin inhibitor (ANRI – alsartan/sacubitril) vs ACEI (enalapril)
 ANRI superior to ACEI (trial terminated early)

30
Q

What was the SHIFT trial?

A

 Systolic heart failure treatment with the IF inhibitor Ivabradine Trial
 Ivabradine sometimes used to treat angina
 Ivabradine gave a reduction in deaths and hospitalization vs placebo (being given a standard treatment)

31
Q

What was the A-HEFT trial?

A

 African-American heart failure trial
 Isosorbide dinitrate + hydralazine vs placebo
 Trial terminated early as isosorbide dinitrate + hydralazine superior

32
Q

What does Sacubitril do?

A 
- Cardiac natriuretic peptides 
 Opposes effects of RAAS 
 Increase salt and water excretion 
 Broken down by neprilysin 
- Sacubitril inhibits neprilysin 
- Increases salt and water excretion
33
Q

What do Ivabradine and hydralazine do?

A
  • Ivabradine inhibits SA node pacemaker current (If – funny current), slows heart, allows for better filling
  • Hydralazine interferes with IP2-stimulated Ca2+ release from vascular smooth muscle SR (vasodilator)
34
Q

What are the NICE guidelines for heart failure?

A
  • Diuretics used to control congestive symptoms for all HF patients
  • First line treatment for HFrEF: ACEI and beta blocker
     Beta blocker licenced for HF. Start with a low dose and increase it very slowly (otherwise you may kill patient)
     Bisoprolol, carvedilol, nebivolol
     Use ARB if ACEI not tolerated
  • If symptoms not controlled add spironolactone
  • More serious cases
     Ivabradine
     Sacubitril/valsartan
     Hydralazine + nitrate (especially if Afro Caribbean ancestry)
     Digoxin
35
Q

What are the NICE recommendations for HFpEF treatments?

A
  • NICE: diuretics…then refer to specialist

- Don’t yet have a drug to treat HFpEF

36
Q

What are some examples of loop diuretics and what is their mechanism?

A
  • Examples: furosemide (aka frusemide), bumetanide

* Mechanism: inhibit Na+, K+, Cl- transport in ascending limb of the Loop of Henle

37
Q

What are the main uses of loop diuretics?

A

heart failure, oedema. Also licenced for hypertension that does not respond to other drugs (resistant hypertension). Can be used in hypertension when patient also has kidney problems or heart failure

38
Q

what are the side effects of loop diuretics?

A

hypokalaemia, high volume of urine production (most powerful class of diuretics), fatigue, headache, muscle spasms

39
Q

What are some main examples of Thiazide and thiazide related diuretics and what is their mechanism?

A
  • Examples: Bendroflumethiazide, Chlortalidone, indapamide (for information only)
  • Mechanism: inhibit Na+, Cl- transport in the distal convoluted tubule
40
Q

What are some pain uses of thiazide and thiazide related diuretics?

A
  • Low doses: used in hypertension (main chlortalidone, indapamide)
  • Higher doses: used in oedema and sometimes in heart failure
41
Q

What are some side effects of thiazide and thiazide related diuretics?

A

hypokalaemia, hypochloraemia (at higher doses), moderately high volume of urine production (not as powerful as the loop diuretics), fatigue, headache, GI tract disturbance, postural hypotension

42
Q

What are some examples of potassium sparing diuretics?

A
  • Spironolactone (also known as Aldactone), eplerenone (a similar drug: for information only)
  • Amiloride, triamterene (a similar drug: for information only)
43
Q

What are the mechanisms of spironolactone and amiloride?

A
  • Spironolactone is an aldosterone antagonist

- Amiloride blocks the epithelial sodium channel (ENaC)

44
Q

What are the main uses of amiloride and spironolactone?

A
  • Amiloride: added to loop and thiazide diuretics to prevent potassium loss
  • Spironolactone: to treat oedema in heart failure: used as an adjunct treatment in moderate to severe heart failure; adjunct in resistant hypertension; oedema due to liver dysfunction. Also used in aldosteronism
45
Q

What are the side effects of potassium sparing diuretics?

A
  • Hyperkalaemia, GI tract disturbance, more frequent urination (milder diuretics than thiazide or loop drugs)
  • Spironolactone can also act as an antiandrogen at high doses which can cause feminization in men. It can disrupt the menstrual cycle in woman.
46
Q

What is regenerative medicine?

A
  • replacing missing limbs or organs

- primarily centres around the use of stem cells

47
Q

What has been used extensively in regenerative medicine research and why?

A
  • the zebrafish
    • Zebrafish grow rapidly, have relatively simple hearts (two chambers) and the zebrafish genome has been sequenced
    • Zebrafish embryos are virtually transparent allowing the development of the CVS system to be followed very easily
    • The main reason why zebrafish have become popular for regenerative medicine research is that they are capable of great feats of organ repair and replacement

Drugs: from molecules to man (22 decks)

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