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Y2S1-Pharmacology > Drugs used for the management of heart failure > Flashcards

Drugs used for the management of heart failure Flashcards

1
Q

Clinical trials proved which medication is best for improving the CO?

A

Vasodilators, and not positive inotropes

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2
Q

What is the clinical importance of digoxin?

A

Digoxin/cardiac glycoside will reduce the times the patient is hospitalized but it will not prolong the life expectancy when compared to vasodilators or (ACEi, ARB, and BB to a lesser extent)

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3
Q

What are the indications of positive ionotropic drugs?

A
  • They increase the workload on the heart, used in:

1) Heart Failure

2) In refractory when other drugs are not working

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4
Q

What are the non-pharmacological therapy of HF?

A

1) Sodium restriction

2) Aerobic exercise (mild, and under supervision)

3) Weight loss

4) Treat the hypertension and the comorbidities

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5
Q

What are the pharmacological treatments of HF?

A

1) ACEIs

2) ARBs

3) Aldosterone antagonists

4) B-blockers

5) Vasodilators (like hydralazine)

6) Diuretics (very imp in acute pulmonary edema and we give it in huge doses of furosemide (most potent) to decongest the lung that is of course if the BP can handle it)

7) Digoxin

8) Device therapy

9) Cardiac resynchronization therapy

10) Implantable defibrilators

11) Left ventricular assist devices

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6
Q

What is the body’s compensatory mechanism for HF?

A
  • In case of decreased CO

1) Increase in the sympathetic outflow due to decreased carotid sinus firing rate, which will ultimately increase the rate, force, preload and afterload of the heart, increasing the CO

2) Activation of the RAAS, increasing the secretion of renin and thus angiotensin-2, which will ultimately increase the afterload and preload increasing the CO

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7
Q

What is meant by the vicious circle?

A
  • When the CO DECREASES THIS WILL INDUCE VASOCONSTRICTION WHICH WILL INCREASE THE AFTERLOAD, however, the heart cannot pump against that increased afterload decreasing the CO further
  • To break this cycle vasodilators are used
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8
Q

What is the effect of beta-adrenergic blockers in HF?

A

At specific dosages, BB improves HF by blocking the increased outflow of the sympathetic system, but only specific BB

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9
Q

Which BB is used in HF?

A
  • MBC3

1) B1 selective blocker

  • Bisoprolol
  • Metoprolol

2) Non-selective third generation BB

  • Carvedilol
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10
Q

Why is it important to use vasodilators in HF?

A
  • They decrease both the preload and afterload
  • Oral vasodilators usually are used in patients with chronic HF and parenteral agents are reserved for those who have severe HF or are unable to take oral medications
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11
Q

What are the positive ionotropic agents used in HF?

A

1) Digitalis glycoside

  • Mainly digoxin (Oral or intravenous)

2) Phosphodiesterase inhibitors

  • Inamrinone
  • Milrinone IV

3) Dobutamine and Dopamine

4) Human natriuretic peptide

  • Nesiritide

5) Endothelin receptor antagonists

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12
Q

What is the pharmacology of digoxin on the CVS?

A

1) Positive ionotropic action (as it inhibits the Na+/K+ ATPase pump)

2) Increases the parasympathetic activity

3) It has a negative chronotropic effect

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13
Q

What is the mechanism of action of digoxin?

A

1) It blocks the sodium-potassium pump (which pumps 3 Na+ out and two K+ in)

2) Intracellular Na+ would be high, inhibiting the Na+/Ca2+ pump and increasing the intracellular levels of calcium

  • Which will all lead to more contractility due to the binding and blocking of digoxin to the Na+-K-ATPase pump
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14
Q

What are the effects of digoxin on the heart?

A

1) Improves the pumping ability of the heart in HF

2) Increases the myocardial contractility allowing the ventricles to empty more completely with each beat

3) Improves the CO by decreasing the (Heart size, rate, end-systolic/diastolic pressure, etc)

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15
Q

What is the pharmacokinetic of digoxin?

A

60% of it is excreted renaly, and largely unchanged

  • Give loading dose as its half-life is 36-40 hours with normal renal function
  • It also crosses the placenta, and serum levels in neonates are similar to those in the mother
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16
Q

What are the therapeutic uses of digoxin?

A

1) Management of HF

2) Atrial fibrillation and atrial flutter

17
Q

When is digoxin contraindicated?

A

1) Severe myocarditis

2) Ventricular tachycardia

3) Heart block

4) Wolff-Parkinson-white syndrome

5) In hypokalemia

6) Renal impairment

18
Q

What are the adverse effects of digoxin toxicity?

A
  • Since it has a narrow therapeutic index (0.8-2.0 ng/ml)
  • GIT and CNS adverse effects are the most common
  • In regards to the CNS they will see the world as yellow
  • It can also cause gynecomastia and allergic skin reactions
19
Q

What is the management of digoxin toxicity?

A

1) Without serious arrhythmia

  • Withdrawl from digoxin
  • Correction of the electrolyte disturbace

2) Moderate to severe toxicity with arrhythmia

  • Withdraw digoxin
  • Correct the electrolyte imbalance
  • Cardia pacing for bradycardia
  • Antiarrhythmic drugs, lidocaine, phenytoin, propranolol
  • Digoxin antibodies
20
Q

What are the phosphodiesterase inhibitors?

A

Inamrinone, and milrinone IV, are cardiotonic-ionotropic agents that are used in the short-term management of acute, severe HF and it is not controlled by digoxin, diuretics, and vasodilators

  • Both drugs are given IV by bolus injection followed by continuous infusion
21
Q

What is the mechanism of action of the phosphodiesterase inhibitors?

A

1) They increase the levels of cyclic adenosine monophosphate (cAMP) in the myocardial cells by inhibiting the phosphodiesterase (which normally metabolizes cAMP)

2) They relax the smooth muscle of the BV, producing vasodilation, decreasing the preload and afterload

22
Q

What are the side effects of phosphodiesterase inhibitors?

A

1) Tachycardia

2) Atrial/ventricular dysrhythmias

3) Hypotension

4) Hepatotoxicity with inamrinone

23
Q

What is an example of an aldosterone antagonist drug?

A

1) Spironolactone, it reduces the aldosterone-induced retention of sodium and water

2) Eplerenone, is a better choice as it causes less hypokalemia

24
Q

Which drug is given in acute severe heart failure?

A

Adrenergic/sympathomimetics, given when circulatory support is required, like dopamine or dobutamine

25
Q

What is dopamine?

A

It is a natural sympathomimetic catecholamine, that is administered IV, as it is not absorbed orally and it does not cross the BBB

26
Q

What is the mechanism of action of dopamine?

A

1) Small dose

  • Induces vasodilation via the D1-receptors

2) Moderate dosage

  • Induces vasodilation via D1-receptors
  • Acts on B1-receptors with a positive ionotropic effect, increasing the CO

3) Large dosage

  • Induces vasodilation via D1-receptors
  • Acts on B1-receptors with a positive ionotropic effect, increasing the CO
  • Activates the a1-receptors inducing vasoconstriction (not wanted)
27
Q

What are the therapeutic uses of dopamine?

A

1) Cardiogenic shock

2) Septic shock

3) Refractory heart failure

28
Q

What is dobutamine?

A
  • Synthetic sympathomimetic
  • a Selective B1-agonist
  • It has a +ve ionotropic, chronotropic & dromotropic effects
  • It increases the force of contraction rather than the HR
29
Q

When is dobutamine used?

A
  • IV infusion

1) cardiogenic shock

2)Resistant heart failure

  • It improves the contractility with minimal tachycardia
30
Q

What is the human natriuretic peptide B-type?

A

Nasiritide is the first class of drug used in the management of acute HF, it is identical to endogenous human B-type natriuretic peptide

31
Q

What is the mechanism of action of Nasiritide?

A
  • It compensates for deteriorating cardiac function by:

1) Reduces the preload and afterload

2) Increases the diuresis and secretion of sodium

3) It suppresses the renin-angiotensin-aldosterone system

4) Suppresses the secretion of neurohormones like endothelin and norepinephrine

  • The onset of action is immediate, followed by a bolus dose and continuous IV infusion.
32
Q

What are the endothelin receptor antagonists?

A
  • Endothelin-1 causes vasoconstriction, forcing the heart to work harder during HF
  • They are drugs that relax the blood vessels and improve blood flow by targeting endothelin-1, which is produced in excess in HF
  • Bosentan a endothelin receptor antagonist is approved for the use in pulmonary hypertension only
33
Q

What are the steps for managing acute heart failure?

A

1) Sit the patient upright

2) Oxygen

3) Monitor ECG and treat arrhythmias

4) Diamorphine slowly via IV

5) Furosemide slowly IV

6) GTN spray if systolic is below 90mmHg

7) is systolic >100mmHg start nitrate infusion

  • If the patient is worsening

8) Further furosemide

9) CPAP

10) Increase nitrate infusion

  • If systolic BP <100 mmHg

11) Cardiogenic shock refer to ICU

34
Q

How to manage a cardiogenic shock?

A

1) Oxygen

2) Diamorphine

3) Correct arrhythmia

  • Assess the filling pressure with clinical assessment

4a) Underfillled = give plasma expander

4b) well/overfilled = give ionotropic support

Y2S1-Pharmacology (14 decks)

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