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Phase II - Pharmacology > 19. Cardiology - Heart Failure > Flashcards

19. Cardiology - Heart Failure Flashcards

1
Q

What is heart failure?

A

Where the heart fails to pump adequate blood to meet the needs of the body despite adequate filling pressure.

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2
Q

What are the cardinal symptoms of heart failure?

A

Dyspnoea, fatigue, fluid retention.

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3
Q

What are the causes of heart failure?

A

Arteriosclerotic heart disease, myocardial infarction, hypertension, valvular heart disease, dilated cardiomyopathy, congenital heart disease.

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4
Q

What are the physiologic compensatory mechanisms in the progression of HF?

A

SANS and RAAS activated chronically so remodelling of cardiac tissue, loss of myocytes, hypertrophy, and fibrosis. Leads to additional neurohormonal activation in a vicious cycle.

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5
Q

What are the goals of pharmacological intervention in HF?

A

Alleviate symptoms, slow disease progression, improve survival.

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6
Q

What are the seven classes of drugs effective in HF management?

A

ACE-i, ARB, aldosterone antagonists, B blockers, diuretics, direct vaso and venodilators, inotropic agents.

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7
Q

What are the benefits of pharmacological intervention in HF?

A

Reduced myocardial workload, decreased ECF volume, improved cardiac contractility, reduced rate of cardiac remodelling.

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8
Q

What is the naming rule of ACE-inhibitors? Give an example.

A

-pril, e.g. ramipril, lisinopril.

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9
Q

What is the naming rule of ARBs? Give an example.

A

-sartan, e.g. losartan, valsartan.

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10
Q

What is the naming rule of aldosterone antagonists? Give an example.

A

-one, e.g. spironolactone, eplerenone.

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11
Q

What is the naming rule of B-blockers? Give an example.

A

-lol, e.g. bisoprolol, carvedilol, metoprolol.

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12
Q

Which diuretics can be used in HF?

A

Bumetanide, furosemide, metolazone, torsemide.

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13
Q

Which vaso/venodilators can be used in HF?

A

Hydralzine, isosorbide dinitrate.

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14
Q

Which inotropic agents can be used in HF?

A

Digoxin, dobutamine, milrinone.

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15
Q

Where are pacemaker cells located?

A

In the sinoatrial and atrioventricular nodes.

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16
Q

What are the five phases of cardiac action potentials?

A

Phase 0 ‘fast upstroke’ - Na+ channels open and influx, Na+ channel are inactivated and upstroke ends.
Phase 1 ‘partial repolarisation’ - K+ channels open and close so transient efflux.
Phase 2 ‘plateau’ - Ca2+ open and slow influx balances slow efflux of K+.
Phase 3 ‘repolarisation’ - Ca2+ channels close and K+ channels open so efflux.
Phase 4 ‘forward current’ - back to threshold.

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17
Q

What is an inotropic effect?

A

Things that increase force of contraction by increasing free cytosolic calcium available.

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18
Q

What are the movements of Ca2+ during cardiac muscle contraction?

A
  1. Ca2+ entry from outside of cell triggers release of lots of Ca2+ from sarcoplasmic reticulum.
  2. Ca2+ removed by reuptake into sarcoplasmic reticulum and extrusion from cell by Ca2+/Na+ exchange.
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19
Q

What are the three compensatory physiological responses in HF?

A

Increased SANS, activation of RAAS, cardiac hypertrophy.

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20
Q

How is sympathetic activity increased in HF?

A

Baroreceptors sense a decrease in BP and activate SANS. Increased HR and force of contraction in heart muscle. Vasoconstriction to enhance venous return and therefore increase preload –> increased stroke volume.

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21
Q

How is the RAAS activated in HF?

A

Fall in CO means less blood to kidneys so renin is released. Angiotensin II is made and aldosterone is released. There is increased peripheral resistance (afterload) and retention of sodium and water so blood volume increases.

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22
Q

How does peripheral oedema occur in HF?

A

The RAAS increases the blood volume for the heart to pump by increasing sodium and water retention. The heart can’t pump the full volume so venous pressure increases and peripheral and pulmonary oedema occurs.

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23
Q

How does myocardial hypertrophy occur in HF?

A

Stretching the heart muscle more initially leads to stronger contraction. So the chambers dilate and the heart increases in size but eventually stretch too much and become weaker.

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24
Q

What is HF with reduced ejection fraction?

A

When the heart hypertrophies and the fibres are elongated excessively so have weaker contractions and reduced ejection. The ventricles are unable to pump effectively.

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25
Q

What is HF with preserved ejection fraction?

A

Ability of ventricles to relax and accept blood is impaired by structural changes. So thickening of the ventricular wall reduces volume and the heart muscle can’t relax. This means the ventricle doesn’t fill adequately.

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26
Q

What is acute/decompensated HF?

A

The compensatory adaptive mechanisms fail to maintain cardiac output so HF is decompensated and the patient develops worsening HF signs and symptoms.

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27
Q

What are the typical HF symptoms?

A

Dyspnoea on exertion, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, peripheral oedema.

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28
Q

What are the non-pharmacological strategies for HF management?

A

Fluid intake restriction, salt intake restriction, treat comorbid conditions.

29
Q

What are the actions of ACE-i on the heart in HF?

A

Decrease vascular resistance (afterload) and venous tone (preload), resulting in increased CO. Reduce AT-II mediated effects.

30
Q

What are the indications for ACE-i in HF?

A

HFrEH, all stages of LV failure. Use in combination with diuretics, B-blockers, digoxin etc if severe. Recent MI or high risk of cardiovascular event may benefit.

31
Q

What are the ADRs of ACE-i?

A

Postural hypotension, renal insufficiency, hyperkalaemia, persistent dry cough, angioedema (rare).

32
Q

What are the actions of ARB on the cardiovascular system?

A

Block ATII action without affecting bradykinin breakdown.

33
Q

What is the indication of use of ARBs?

A

In place of ACE-i in patients who don’t tolerate them in HF or hypertension.

34
Q

What are the ADRs of ARBs?

A

Postural hypotension, renal insufficiency, hyperkalaemia.

35
Q

Why do patients with HF have increased aldosterone?

A

RAAS system produces more and hepatic clearance is decreased.

36
Q

What are the actions of aldosterone antagonists in HF?

A

Prevent salt retention, myocardial hypertrophy, and hypokalaemia.

37
Q

When are aldosterone antagonists indicated in HF?

A

More severe stages of HFrEF or HFpEF and recent MI.

38
Q

What does evidence show about use of B blockers in HF?

A

Improved systolic function and reversed cardiac remodelling.

39
Q

Which three B-blockers are beneficial in HF?

A

Bisoprolol, metoprolol, carvedilol.

40
Q

Which patients with HF are B-blockers recommended for?

A

Chronic, stable HF. Particularly HFrEF.

41
Q

What drugs should make B-blockers in HF be used with caution?

A

Ones that slow AV conduction like amiodarone, verapamil, diltiazem.

42
Q

What is the purpose of diuretic use in HF?

A

Symptom management - reduce pulmonary congestion and peripheral oedema by decreasing plasma volume nad venous return to heart.

43
Q

Which type of diuretic is mostly used in HF?

A

Loop diuretics.

44
Q

Why are vaso- and venodilators useful in HF?

A

Dilation of blood vessels decreases cardiac preload by increasing venous capacitance.

45
Q

Which patients have indications for vaso/venodilator use in HF?

A

Black patients with HFrEF.

46
Q

What is the action of inotropic drugs in HF?

A

Increase cardiac contractility and therefore CO.

47
Q

What is the mechanism of action of calcium glycosides considering cytosolic calcium concentration?

A

Inhibits Na+-K+-ATPase so myocyte can’t pump Na+ from the cell so the Na+ concentration gradient is decreased. This reduces action of Na+/Ca2+ exchanger to move Ca2+ out of the cell. Intracellular Ca2+ increases as Na+ is exchanged for extracellular Ca2+ by the Na+/Ca2+ exchanger. The membrane is depolarised so more excitable.

48
Q

What is the mechanism of action of digoxin considering contractility of cardiac muscle?

A

Increased FOC causing CO to be higher. Vagal tone is increased so HR and myocardial O2 demand is decreased. Digoxin slows conduction velocity through AV node so useful in AF as well as HF.

49
Q

What is the mechanism of action of digoxin considering neurohormonal function?

A

Low-dose digoxin inhibits SANS activation.

50
Q

What is the indication of use of digoxin in HF?

A

HFrEF after ACE-i, B-blockers, diuretics. Or HFpEF only if with AF or flutter too.

51
Q

What are the ADRs of digoxin?

A

Main issue is it has a small therapeutic ratio so risk of digoxin toxicity. Anorexia, nausea, and vomiting are signs of toxicity. Blurred vision, yellowish vision (xanthopsia), arrhythmias.

52
Q

How can digoxin toxicity be reversed?

A

Stop digoxin and replenish potassium.

53
Q

Give an example of a B-agonist used in HF.

A

Dobutamine, dopamine.

54
Q

What is the mechanism of action of B-agonists in HF?

A

Increase cAMP –> activation of protein kinase which phosphorylates slow calcium channels and increases Ca2+ entry into cell therefore enhancing contraction.

55
Q

When are B-agonists used in HF?

A

Short-term treatment of acute HF in hospital.

56
Q

What is the action of Milrinone?

A

Phosphodiesterase inhibitor.

57
Q

What is the mechanism of action of phosphodiesterase inhibitors in HF?

A

Increases intracellular concentration of cAMP therefore increasing intracellular Ca2+ and cardiac contractility.

58
Q

What are the stages of managing HF?

A
  1. Risk factor reduction, patient education
  2. Treat hypertension, diabetes, dyslipidaemia - ACE-i or ARBs
  3. ACE-i or ARBs in all patients, B-blockers in some
  4. ACE-i and B-blockers in all patients, aldosterone antagonists and HYD/ISDN in some
  5. Dietary Na+ restriction, diuretics, digoxin
59
Q

Which drug mat exacerbate HF? Acetaminophen, cetirizine, chlorothalidone, ibuprofen.

A

Ibuprofen - NSAIDs –> increased fluid retention and increased BP.

60
Q 
Which best describes the action of ACE-i in HF?
A. increase vascular resistance
B. decrease CO
C. reduce preload
D. increase aldosterone
A

C. reduce preload - decrease vascular resistance, decrease preload, decrease afterload, increase CO, blunt aldosterone release.

61
Q 
What makes losartan different from other ARBs?
A. renally eliminated
B. active metabolite
C. short half-life
D. small volume of distribution
A

B. active metabolite - undergoes first-pass metabolism to convert to active metabolite.

62
Q 
How do B-blockers improve cardiac function in HF?
A. decrease cardiac remodelling
B. increase heart rate
C. increase renin release
D. activate adrenaline
A

A. decrease cardiac remodelling - improve cardiac function by reducing heart rate, decreasing renin, and preventing adrenaline effects on heart all to decrease remodelling.

63
Q

A 70yo female has HFrEF and has a PMHx of AF and HTN. Drug Hx: hydrochlorothiazide, lisinopril, metoprolol tartrate, warfarin. She has no symptoms, which medication should she change?
A. stop hydrochlorothiazide
B. lisinopril –> losartan
C. decrease warfarin dose
D. metoprolol tartate –> metoprolol succinate

A

D. metoprolol tartate –> metoprolol succinate as succinate is used in HF for mortality benefit.

64
Q 
75yo white male has HF. He presents with SOB, increased pitting oedema, 5-pound weight gain over 2 days. Drug Hx: losartan and metoprolol succinate. He has no chest pain and is stable for outpatient treatment. What's the best recommendation?
A. increase metoprolol succinate dose
B. start hydrohlorothiazide
C. start furosemide
D. stop losartan
A

C. start furosemide - HF exacerbation is a possibility so loop diuretics can be used for immediate diuresis.

65
Q 
How is spironolactone beneficial in HF?
A. promotes K+ secretion
B. agonises aldosterone
C. prevents cardiac hypertrophy
D. decreases blood glucose
A

C. prevents cardiac hypertrophy - antagonises aldosterone so prevents Na+/water retention, cardiac hypertrophy, and hypokalaemia.

66
Q 
Which is important to monitor in patients taking digoxin?
A. Cl-
B. K+
C. Na+
D. zinc
A

B. K+ - hypokalaemia can lead to life-threatening arrhythmias and precipitate digoxin toxicity.

67
Q 
Which describes the mechanism of action of milrinone in HF?
A. decreases intracellular Ca2+
B. increases cardiac contractility
C. decreases cAMP
D. activates phosphodiesterase
A

B. increases cardiac contractility - increases cAMP so increases intracellular Ca2+ and increases contractility.

68
Q 
What is the most common ADR of fixed-dose hydralazine/isosorbide dinitrate?
A. diarrhoea
B. drug-induced lupus
C. headache
D. heartburn
A

C. headache - lupus is also a possibility but far less common.

Phase II - Pharmacology (7 decks)

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