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Pharmacology > Drugs for Heart Failure 2 > Flashcards

Drugs for Heart Failure 2 Flashcards

1
Q

What is the effect of beta blockers?

A
  • reduces heart rate and oxygen consumption
  • cardiac output is increased after several months
  • chance of irregular heart beat reduced
  • mortality reduced post MI-> treatment of choice post-infarct
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2
Q

What are the benefits of beta-adrenergic receptor blockade?

A
  • decrease adverse effects of high catecholamine levels on the heart
  • decreased cardiomyocyte apoptosis (cell death)
  • decreased cardiac remodelling (decreased mitogenic activity)
  • — mechanism is not completely understood
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3
Q

Describe the action of carvedilol?

A
  • blocks beta and alpha adrenergic receptors
  • alpha adrenergic receptor blockade helps to relax (dilate) arteries
  • the heart does not have to work as hard to eject blood (decreased after load)
  • beta adrenergic receptor blockade slows the heart and decreases force of contraction
  • first line treatment in heart failure
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4
Q

What is the main difference between metoprolol and carvedilol?

A

– metoprolol selectively blocks beta 1 adrenergic receptors

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5
Q

Beta blockers should be avoided in what conditions?

A
  • avoid in asthma, COPD, peripheral vascular disease, insulin dependent diabetes, physically active
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6
Q

What diseases are beta blockers mostly used in?

A
  • hypertension
  • glaucoma
  • certain arrhythmia
  • MI
  • angina
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7
Q

What is the drug interaction between carvedilol and ventolin?

A
  • interaction with ventolin worsens breathing problems due to a narrowing of the airways
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8
Q

What is the interaction between carvedilol/metoprolol and verapamil?

A

interaction can cause an irregular heart beat

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9
Q

Antiretroviral medications can cause an _____

A

arrhythmia

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10
Q

Why is alcohol dangerous to take with blood pressure lowering agents?

A
  • has an additive effect on lowering blood pressure
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11
Q

What is the action of ionotropes?

A
  • alter the force of contraction of the heart (increase contraction)
  • positive ionotropes are of interest here
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12
Q

What is the effect of long term use of ionotropes?

A
  • increased mortality
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13
Q

What are the 2 examples of ionotropes?

A

-digoxin and dobutamine

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14
Q

Explain the mechanism of action of dobutamine?

A
  • must be given via IV
  • stimulates beta adrenergic receptors in the heart to increase heart rate and more importantly contractility
  • must carefully monitor- may increase heart rate, myocardial oxygen consumption and blood pressure
  • may aggravate ischemia and promote arrhythmias
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15
Q

Explain the mechanism of digoxin?

A
  • increases heart contractility (increases calcium release in myocardial cells)
  • blocks Na/K ATPase
  • must closely monitor (can increase heart rate, myocardial O2 consumption, BP. Can also aggravate schema and provoke arrhythmias)
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16
Q

What is the symptomatic improvement that digoxin provides?

A
  • improved exercise capacity and decreased hospitalization for heart failure
17
Q

When taking digoxin, it is important to monitor ____ levels

A

potassium

(hypokalemia increases digoxin toxicity, as both inhibit the Na/K ATPase

18
Q

What drugs must you be careful with when giving digoxin?

A
  • diuretics: may produce hypokalemia (increases digoxin toxicity)
  • ACEIs/ARBs or B-adrenegric receptor antagonists: may increase potassium levels
  • Potassium sparing diuretics: do not cause hypokalemia, not as good at increasing sodium excretion
  • interactions with some medications can dangerously increase blood levels of digoxin resulting in cardiac arrhythmias (antibiotics such as amoxicillin and erythromycin, amiodarone)
19
Q

What is the action of the proximal tubule of the kidney?

A
  • reabsorbs almost all glucose and amino acids and about 60% of sodium
  • Na is reabsorbed through a Na/K ATPase
  • CL exchanged for formate or oxalate anions
  • water follows passively to maintain osmolarity
20
Q

What ist he action of the ascending loop of henle?

A
  • impermeable to water

- Na/K/2Cl co-transporter reabsorbs 30% of these ions

21
Q

What is the action of the collecting tubule and duct?

A
  • reabsorbs Na and water from the urine and secretes K

- Na/K ATPast is performing this function

22
Q

What is the primary site of action of thiazide diuretics?

A

distal tubule

23
Q

What happens in the distal tubule when a thiazide diuretic is added as a treatment option?

A
  • inhibition of the Na/Cl transporter
  • decreasing Na/Cl reabsorption (increase in Na excretion)
  • increase in Ca reabsorption (decrease in Ca excretion)
24
Q

What are the main problems associated with thiazide diuretics?

A
  • hypokalemia- increased Na in urine at distal tubule causes more K to be exchanged for Na causing loss of K from the body
  • hyperglycemia - problem for type 2 diabetes (decreases insulin release, decreases tissue utilization)
  • increase in LDL levels
  • increased incidence of erectile dysfunction
  • volume contraction
  • interaction with the anti-arrhythmic agent amiodarone can lead to a more irregular heartbeat
25
Q

What are the advantages of using a thiazide diuretic over other medications to treat blood pressure?

A
  • orally active
  • no postural hypertension
  • potentiate other anti-hypertensives
26
Q

What do thiazide diuretics do to K? Uric acid? BP? Na? Ca?

A

K: due to increased aldosterone - sodium reabsorption at expense of potassium loss
Uric acid: increases
BP: decreses
Na: lowers due to the direct effect to increase sodium excretion
Ca: due to direct effect to decrease calcium excretion

27
Q

What is the mechanism of action of loop diuretics?

A
  • inhibit the Na/K/2Cl co-transporter in the ascending loop of henle
  • very potent and efficacious- high ceiling diuretics. Up to 20% of the filtered load if excreted
  • prostaglandins are very important - useful in acute pulmonary edema
  • increases Na, Cl, K, Mg and Ca excretion (note Ca effect)
28
Q

The effect on ___ is opposite in loop diuretics and thiazide diuretics?

A

calcium

29
Q

What are the main side effects of loop diuretics?

A
  • deafness and kidney damage - never combine loop diuretics with amino glycoside antibiotics
  • interaction with the antiarrhythmatic agent amiodarone can lead to a more irregular heartbeat
30
Q

When are loop diuretics typically used?

A
  • preferred in renal insufficiency
  • glomerular filtration rate of under 50 ml/min
  • edema, hypertension, hypercalcemia, heart failure
31
Q

Describe potassium sparing diuretics?

A
  • weak diuretics
  • give with other diuretics to decrease potassium loss
  • may cause hyperkalemia
  • never combine with K supplements
32
Q

Describe the action of spironolactone

A
  • aldosterone receptor antagonists
  • prevents aldosterone from binding to the receptor
    (decreases sodium reabsorption, decreases potassium excretion)
  • may cause hyperkalemia
  • prevents cardiac remodeling associated with high levels of aldosterone in heart failure
33
Q

How potassium sparing diuretics manage ___ is opposite of loop and thiazide diuretics

A

K

34
Q

What are the steps of managing a patient with heart failure?

A
  • managing conditions that contribute to heart failure (hypertension, diabetes, lipids)
  • diet physical activity and lifestyle changes
    1. start with ACEI or Beta-adrenegeric receptor blockade (lowers bp and reduces stress on the heart)
    2. Diuretic- in patients with edema (remove excess fluids and sodium from the body)
    3. Extreme failure- add an ionotrope (increases contractility to alleviate heart failure symptoms)
35
Q

Beta blockers are only started once patients are _____ on ACEI- should start at a low dose

A

stable

36
Q

Describe the different stages of heart failure (A-D)

A

A: High risk heart failure with no symptoms
B: Structural heart disease, no symptoms
C: structural heart disease, previous or current symptoms
Stage D: end stage-just trying to improve quality of life

Pharmacology (23 decks)

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