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CVS drugs > Heart Failure drugs > Flashcards

Heart Failure drugs Flashcards

1
Q

How to choose between drugs that reduce workload of heart vs drugs that increase workload?

A
  • Drugs that reduced workload = compensatory stage of HF
  • Drugs that increase workload = chronic HF

As the pump becomes less effective, more blood remains in the ventricles at the end of each cycle. Gradually, end-diastolic volume (preload) increases. Initially, increase in preload may promote increased force of contraction (Frank-Starling Curve)
But as preload increases, further, the heart is overstretched and contracts less forcefully (chronic HF)

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2
Q

Drugs used in HF

A
  1. Beta blockers
  2. Sacubitril-Valsartan
  3. Diuretics (Loop, K+ sparing)
  4. Hydralazine
  5. Isosorbide mononitrate/dinitrate
  6. Ivabradine
  7. Cardiac Glycosides
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3
Q

Examples of beta blockers

A

Non-selective: carvedilol
(Cardvedilol also blocks a1 receptors → reducing peripheral vascular resistance)

Beta-1 selective: bisoprolol, metoprolol XL

Dose-dependent: Nebivolol (b1 selective in low doses, non selective in high doses)

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4
Q

MOA of beta blockers

A

Beta-adrenoreceptor antagonists decreases the HR → more time for ventricular filling during diastole → increase CO

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5
Q

What classes of drugs ends with -lol?

A

beta blockers

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6
Q

Beta blockers contraindicated in?

A
  1. Contraindicated in asthmatic patients as they can cause bronchoconstriction (b1 selective only)
  2. Contraindicated in diabetics as they can mask the effects of hypoglycaemia (palpitations, tremors etc.) preventing them from getting appropriate intervention
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7
Q

Clinical uses of beta blockers

A

1.Hypertension
2.HF (slower HR → increase time for ventricular filling → increase CO)
3.Abnormal heart rhythms
4.Following myocardial infarction
5.Anxiety disorders

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8
Q

MOA of Sacubitril

A

BNP antagonise the RAAS and has favourable effects on HF

BNP are broken down by neprilysin

Sacubitril inhibits neprilysin → prolongs BNP effects (antagonise RAAS which is activated under HF)

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9
Q

Why is Valsartan added

A

Neprilysin also breaks down angiotensin II (Sacubitril inhibiting neprilysin prevents the breakdown of angiotensinII)

Therefore add Valsartan (a AT1 receptor blocker)

Valsartan avoids the negative effects of angiotensin II that is prolonged by Sacubitril

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10
Q

Clinical uses of Sacubitril- Valsartan

A

HFrEF (decreases workload of the heart → preserves the heart’s function and prevent further damage)

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11
Q

Adverse effects of Sacubitril- Valsartan

A
  1. dry cough and angioedema (Neprilysin is also involved in the breakdown of Bradykinin, which is inhibited by Sacubitril)
  2. Hypotension
  3. Hyperkalaemia
  4. Renal failure
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12
Q

Examples of Loop diuretics

A

Furosemide, Bumetanide, Ethacrynic acid, Sulfonamide derivatives

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13
Q

Which channels of the nephron do loop diuretics act on

A

Na/K/2Cl cotransporter at the thick ascending limb

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14
Q

Which ions are affected by loop diuretics

A

Reduce absorption of Na+, K+, Cl-, Mg2+ and Ca2+

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15
Q

Adverse effects of Loop diuretics

A
  1. Hypokalemic metabolic alkalosis
  2. Ototoxicity (avoid use with aminoglycosides)
  3. Hyperuricemia
  4. Hypomagnesemia
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16
Q

Clinical uses of Furosemide

A
  1. Acute pulmonary oedema
  2. Acute hyperkalaemia (reduces K+ absorption from lumen)
  3. Anion overdose
  4. Acute renal failure
17
Q

Do the Nitrates reduce the workload of the heart directly or indirectly

A

Indirectly.
Donates NO which activates guanylyl cyclase, increasing cGMP and causing inactivation of myosin-LC

a. Vasodilation → venodilation (decrease preload)
b. Vasodilation → arteriolar dilation (decrease afterload)
Overall decreases workload of the heart

18
Q

Potassium sparing diuretics and which part of the nephron they work on

A

Spironolactone, Epierenone: blocks aldosterone receptor –> no activation of Na+ channel –> no reabsorption of Na+ at the collecting duct –> no water retention

Triamterene, Amiloride: blocks Na+ channels at the collecting duct directly

19
Q

Do they K+ sparing diuretics have a slower onset of action than loop diuretics?

A

YES

20
Q

Clinical uses of K+ sparing diuretics

A
  1. diuretics
  2. hyperaldosteronism
21
Q

Side effects of Spironolactone and Triamterene

A
  1. Hyperkalaemia (decreasing Na+ reabsorption decreases K+ secretion by the Na+/K+/Atpase pump)
  2. Gynecomastia (only spironolactone which may block the testosterone receptor)
  3. Acute renal failure (triamterene + indomethacin)
  4. Kidney stones (triamterene)
22
Q

Clinical use of Hydralazine

A

Second line hypertensive, first line for HF

  1. Essential hypertension (2nd line)
  2. HFrEF (in combination with isosorbide dinitrate, orally)
  3. Acute-onset, severe peripartum or postpartum hypertension (IV)
23
Q

Adverse effects of Hydralazine

A
  1. Baroreflex associated sympathetic activation: flushing, tachycardia
  2. Hypotension
  3. HILS – arthralgia, myalgia, serositis, fever
  4. Contraindicated in coronary disease due to stimulation of SNS → increase CO output → increase myocardial oxygen demand
24
Q

MOA of hydralazine

A

Direct vasodilator → decreasing total peripheral resistance → decrease afterload

  1. Vasodilator by inhibiting IP3-induced Ca2+ release from the smooth muscle cell sarcoplasmic reticulum
  2. Can trigger compensatory release of NE/adrenaline → increase CO
25
Q

MOA of Isosorbide dinitrate/ Mononitrate

A

Donates NO which activates guanylyl cyclase, increasing cGMP and causing inactivation of myosin-LC

a. Vasodilation → venodilation (decrease preload)
b. Vasodilation → arteriolar dilation (decrease afterload)
Overall decreases workload of the heart

26
Q

Comment on the duration of action and onsent of action of ISDN and ISMN

A
  • long duration of action and long onset of action
  • ISMN has a faster onset of action (30-45 min) compared to ISDN (60 min)
27
Q

Clinical uses of ISMN/ISDN

A
  1. Angina pectoris prophylaxis (decreasing workload of heart reduce oxygen consumption + decrease end diastolic pressure for better blood flow to coronary arteries)
  2. HF
28
Q

Side effects of ISMN/ISDN

A
  1. Reflex tachycardia (due to baroreceptors picking up lower BP)
  2. Hypotension
  3. Headache (meningeal artery vasodiation)
29
Q

MOA of Ivabradine

A

A heart rate lowering agent
Does not reduce preload, afterload or contractility, just reduces heart rate

Inhibits cardiac pacemaker I(f) current that controls the spontaneous diastolic depolarisation in the SA node → slows down/regulates heart rate

30
Q

Clinical uses of Ivabradine

A

Useful in HFrEF, in patients in sinus rhythm whose heart rate > 75 bpm (increase time for ventricular filling, improving overall cardiac function )

31
Q

Does Ivabradine reduce preload, afterload or contractility?

A

No. just reduces heart rate

32
Q

Adverse effects of ivabradine

A
  1. Visual problems: Luminous phenomena, transient enhanced brightness in a limited area of the visual field
  2. Dizziness (bradycardia)
  3. Hypotension, fatigue, malaise (all related to bradycardia)
33
Q

Examples of Cardiac glycosides

A

Faster onset, shorter half life: Digoxin
Slower onset, longer half life: Digitoxin

34
Q

MOA of Digoxin

A

Inhibits the Na+/K+/Atpase pump in cardiac muscle cells

Prevents efflux of Na+ → increase Na+ intracellularly → decrease efflux of Ca2+ (through the Ca2+ Na+ channel) → increased CICR from sarcoplasmic reticulum → increased myocyte contraction → increase CO

35
Q

Clinical uses of DIGOXIN

A
  1. Late stage HF
  2. Systolic dysfunction
  3. Atrial fibrillation
36
Q

Adverse effect of cardiac glycosides

A

1.Progressive, more severe dysrhythmia (AV block, AF, VF)
2.GI effects: anorexia, nausea, vomiting
3.CNS: headache, fatigue, confusion, blurred vision

37
Q

How to treat Digitalis toxicity

A
  • Discontinue cardiac glycoside therapy
  • Correction of K+ or Mg+ deficiency
  • Antiarrhythmic drugs (as it can increase automaticity leading to AF or VF)
  • if automaticity is predominant: lidocaine, propranolol
    Digoxin antibody (FAB fragments, digibind)
38
Q

Do ACE inhibitors, sacubitril and valsartan cause dry cough?

A

Only ACE inhibitors (e.g. Lisinopril) and Sacubitril

CVS drugs (6 decks)

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