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CDM > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is heart failure?

A

Inability of heart to sufficiently pump blood around the body. The heart compensates by beating harder, increasing stroke volume and beats faster. Over time, muscles become overworked leading to death of cardiomyocytes.

HF is a clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral oedema) caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress.

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2
Q

What is the ejection fraction?

A

% blood pumped out from the ventricles (usually left as it is oxygenated)

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3
Q

What is the EF for a normal heart?

A

60%

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4
Q

What is the EF for systolic dysfunction?

A

<40- 50%

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5
Q

What is systolic dysfunction?

What is it also known as?

A

Reduced ejection fraction

The ventricles can be filled with more blood, however the walls are thinner and weaker so less can be pumped out - impaired contractility of the ventricles

Left sided heart failure/ HF with reduced ejection fraction

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6
Q

Which type of heart failure is there evidence based medicine for?

A

Systolic dysfunction

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7
Q

What are the two different types of Heart failure?

A

Diastolic and systolic dysfunction

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8
Q

What is diastolic dysfunction?

What is it also known as?

A

Preserved ejection fraction

Stiff, thicker ventricles so volume is lower in ventricles but still pumping out at least 60% volume

Right sided heart failure/ HF with preserved ejection fraction

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9
Q

How do you treat diastolic dysfunction?

A

Can only be treated via symptoms eg) Hypertension, comorbidities

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10
Q

What is Frank Starling Law?

A

Cardiac output= HR x Stroke volume

The ability of the heart to chance its force of contraction (and therefore stroke volume) in response to changes in venous return

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11
Q

What is cardiac output?

A

Volume of blood leaving the heart per minute

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12
Q

What is stroke volume?

A

Volume of blood pumped out of the ventricle per beat

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13
Q

What is preload?

A

The pressure within the ventricles end of diastole (where the blood is being filled into the ventricles and the pressure gets so great that the aortic/pulmonary valve opens to push blood out of the heart)

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14
Q

Is stroke volume proportional to cardiac output?

How does this relate to venous return?

A

Yes

A greater end diastolic volume increases contractile strength of the ventricles and increase cardiac output

The higher the venous return, the more filling in the right atrium and ventricle increases pressure

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15
Q

What is Laplace’s law?

A

Larger heart - insufficient

Hypertrophy - increase muscle mass leads to increased workload and oxygen consumption of the heart (as there is more muscle)

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16
Q

What is the renin angiotensin aldosterone system?

A
  1. Liver produces angiotensinogen
  2. Renin (produced by kidneys in response to low BP) converts angiotensinogen to angiotensin 1
  3. ACE (from lungs) converts angiotensin 1 to angiotensin 2
  4. Angiotensin 2 causes release of aldosterone from adrenal glands
  5. Aldosterone acts on nephron to cause water and sodium retention. Blood volume and BP increases

Aldosterone also causes adrenaline to be released causing sympathetic NS activation, so HR and contractility increases.

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17
Q

What is the consequence of the heart working harder?

A

Cardiac remodelling takes place

Walls become thicker

Hypertrophy

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18
Q

What is bradypnoea? Is it a symptom of heart failure?

A

Low breathing rate

No- HF patients breathe faster

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19
Q

What are the symptoms of heart failure?

A 
Fatigue 
Dyspnoea (SOB)
Peripheral Oedema 
Orthopnoea (SOB when lying down) 
Faster breathing rate
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20
Q

Describe the New York Association classification of Heart failure

A

Class 1- No limitations with ordinary physical activity

Class 2- Slight limitation and SOB with moderate to severe exertion

Class 3 - Marked limitation less than ordinary activity causes dyspnoea

Class 4- Severe disability dyspnoea at rest

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21
Q

What does elevated jugular venous pressure?

A

It highlights increased pressure in the venous system

Right sided HF (diastolic dysfunction)

Jugular veins drain blood from the head and when pressure in right atrium is too high, blood glows back into this vein

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22
Q

What are the 7 causes of heart failure?

A
  1. Vascular disease
  2. Coronary artery disease (2/3 of cases)
  3. Hypertension
  4. Arrythmia
  5. Non-cardiac causes e.g. anaemia and pregnancy
  6. Cardiomyopathy
  7. Congenital heart disease
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23
Q

How can heart failure be diagnosed?

A

Serum BNP (brain naturetic peptide) -hormone by heart muscle when it is damaged. Not a definite diagnosis
> 400 - HF possible
> 2000 - Severe HF

Echocardiogram (ultrasound) - shows heart physiology including muscles, valves, EF, and pressures within the heart. The only diagnostic tool for HF.

Electrocardiogram (ECG)

Chest X-Ray to see if heart is enlarged

Biochemical results are monitoring rather than diagnosis

24
Q

What machine measures EF?

What would be the EFs that would lead to diagnosis of the two types of HF?

A

Echocardiogram

<40% - left systolic dysfunction with reduced EF

> 40% + symptoms - right diastolic dysfunction with preserved EF

25
Q

What 10 pieces of advice would you give to a HF patient?

A
  1. Smoking cessation
  2. Avoid alcohol
  3. Healthy diet- Mediterranean
  4. Lose weight, exercise
  5. Reduce saturated fats
  6. Low salt diet
  7. Daily weights to check oedema - 2kg weight gain is likely water retention
  8. Limit fluid intake
  9. Annual flu vaccine
  10. Cardiac rehab
26
Q

What are the 5 goals of HF treatment?

A
  1. Relieve/reduce symptoms
  2. Prevent hospital admission
  3. Improve QOL
  4. Improve survival
  5. Slow disease progression
27
Q

What is the treatment algorithm for HF?

A
  1. ACEi and titrate up
  2. Beta blocker and titrate up
  3. Aldosterone antagonist if poor symptom control (spironolactone/epeloronone)

Can add diuretic e.g. loop (bumetanide, furosemide)

Can add digoxin if AF and symptomatic with 1st and 2nd line medication (ACEi and BB)

Can add ivabradine in sinus rhythm, HR > 75 bpm and symptomatic with 1st and 2nd line

28
Q

What is the role of loop diuretic in HF and why are they used?

What is the MOA?

What is the side effect and why you wouldn’t you treat it with NSAIDs?

What are the side effects?

A
  • More intense and shorter diuresis than thiazides?
  • Works on the ascending limb of Loope of Henle, inhibits sodium/potassium/chloride co-transporter so increases water and sodium excretion
  • Also dilates capacitance veins - reduces preload and improves contractile function of the overstretched heart muscle
  • Due to the lowered excretion, uric acid concentration causing gout
  • Cannot treat gout with NSAIDs as they affect renal function and promotes water retention. You would use allopurinol for long term prevention if needed
  • Dehydration, hypovolemia, hyperkalemia
29
Q

ACEi, aldosterone antagonists and beta blockers reduce mortality and hospitalisation. True or false?

A

True

30
Q

The following are contraindicated in ACEi. True are false?

  1. Angiodema
  2. Bilateral renal artery stenosis
  3. Persistent cough
  4. Critical aortic stenosis
  5. Creatinine increase up to 50% above baseline
A
  1. True
  2. True
  3. False
  4. True
  5. False
31
Q

What are side effects of ACEi?

A
  • Hypotension
  • Dry cough
  • Hyperkalaemia
  • Angiodema
32
Q

What is angiodema?

A

Swelling under the skin

33
Q

When is the best time to take the first dose of ACEi and why?

A

At bedtime to reduce symptomatic hypotension

34
Q

Why does ACEi cause a cough?

A

Inhibits bradykinin breakdown

35
Q

What do you monitor with ACEi?

A
  • Creatinine (renal function)
  • Sodium
  • Potassium
  • BP
36
Q

What is the MOA of ACEi?

A

Inhibits conversion of angiotensin 1 to angiotensin 2

Angiotensin 2 is a vasoconstrictor increasing sodium and water retention via aldosterone (which causes adrenaline release)

Promotes vasodilation and reduces afterload (peripheral vascular resistance)

37
Q

Your patient has a dry cough on ramipril - what do you recommend they switch to and why?

A

ARB

Angiotensin 2 receptor blockers do not inhibit the bradykinin breakdown

Candesartan
Losartan
Valsartan

38
Q

Which 3 beta blockers are licensed in heart failure?

A

Bisoprolol and nebivolol (Cardioselective)

, carvedilol (non-selective)

39
Q

How do beta blockers work?

A

Reduces force of contraction and speed of conduction in the heart so reduces cardiac work and demand

40
Q

What additional effect does carvedilol have?

A

Vasodilatory effect due to alpha receptors

Preferable in vasoconstriction patients

41
Q

What additional effect does nebivolol have?

A

Vasodilatory effect due to nitric oxide release

Preferable in vasoconstriction patients

42
Q

What patient group are non cardioselective beta blockers contraindicated in?

A

Asthma as they can cause bronchospasm via beta 2 antagonism

43
Q

What class of CCB do beta blockers interact with?

A

Non-dihydropyridine CCBs

Verapamil and diltiazem

44
Q

What are side effects of beta blockers?

A
  • Bradycardia
  • Fatigue
  • Peripheral vasoconstriction
  • Erectile dysfunction
45
Q

What severity are aldosterone antagonists used in?

A

Moderate to severe

46
Q

Name examples of aldosterone antagonists

A

Spironolactone

Eplerenone

47
Q

How do aldosterone antagonists work?

A

Antimineralocorticoid

Increases water and sodium excretion

Also acts as a potassium sparing diuretic

48
Q

Using aldosterone antagonists and NSAIDs together increases renal failure risk. True or false?

A

True

49
Q

What are the side effects of aldosterone antagonists?

A

Hypotension and hyperkalaemia

50
Q

At what potassium would you hold and stop aldosterone antagonists?

A

Hold and review at 5

Stop at 6

51
Q

What do you need to monitor with aldosterone antagonists?

A

Renal function

BP

Potassium levels

Urine output vs fluid input balance

52
Q

When would you consider eplerenone over spironolactone?

A

MI patient with a low EF%

Or if patient is experiencing hormonal side effects e.g. erectile dysfunction, gycnecomastia (as spironolactone has a similar structure to oestrogen)

53
Q

How does digoxin work?

A

Used in AF patients

Negatively chronotropic (decreases heart rate) and positively ionotropic (increases force of contraction)

Inhibits sodium potassium ATPase pumps so sodium accumulates in the cell. Calcium then accumulates in the cell increasing contraction force

54
Q

What are the side effects of digoxin?

A
  • Bradycardia

- Arrythmias associated with digoxin toxicity- loop and thiazide diuretics increase the risk of this

55
Q

How does ivabradine work?

A

Decreases HR by inhibition of If (funny channels) in SA node

56
Q

How does Enteresto (Sacubitril / valsartan) work?

A

Sacubitril is produced by pregnant women and is a neprilysin inhibitor (vasodilatory effect)

Valsartan is an ARB

57
Q

When would you initiate Enteresto (sacubitril/valsartan)?

A
  • Used if optimal ACEi and beta blocker but still symptomatic
  • ACEi has to be stopped 2 days earlier as new drug contains ARB
  • Continue with beta blocker
  • Hospital only initiated, and after 3 months can refer to GP care

CDM (17 decks)

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