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Pharmacology fall 2024 > Congestive Heart Failure (Exam III) > Flashcards

Congestive Heart Failure (Exam III) Flashcards

1
Q

What’s the 5 year mortality rate for heart failure?

A

50%

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2
Q

What is the most common cause of heart failure?
What is the progression of this disease process?

A

Coronary Artery Disease

CAD → Angina → MI → Scarring/Remodeling → HF

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3
Q

Differentiate systolic HF vs diastolic HF.

A

Systolic HF = reduced cardiac function (i.e. pumping)
Diastolic HF = reduced diastolic filling (usually hypertrophy)

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4
Q

What happens to Ejection Fraction (EF) in systolic vs diastolic failure?

A

Systolic HF: ↓ EF ↓ CO
Diastolic HF: ↓ CO, normal EF.

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5
Q

What is the rarest form of heart failure?

What 4 examples were given that can cause this heart failure?

A

“High-Output” Failure = normal CO, insufficient for bodily demands.

  1. Hyperthyroidism
  2. Beriberi disease
  3. Anemia
  4. Arteriovenous shunts.
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6
Q

How is End-Diastolic Volume (EDV) calculated?

A

Passive Filling + Atrial Contraction + End-Systolic Volume (ESV) = EDV

Ex. 65ml + 25ml + 50ml = 140ml EDV

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7
Q

How is stroke volume calculated?

A

EDV - ESV = SV

140ml - 60ml = 80ml

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8
Q

What 3 examples were given in lecture for decreasing preload?

A
  1. Na⁺ restriction
  2. Diuretics
  3. Venodilation (nitroglycerin, etc.)
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9
Q

Describe the pathologic positive feedback mechanism of heart failure associated with excessive afterload.

A

↓ CO = ↑ NE/Epi → ↑ afterload = ↓ CO

rinse and repeat

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10
Q

Which compensatory mechanism is the first to respond in a situation of decreased cardiac output (CO) ?

A

↑ Heart Rate

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11
Q

Which 3 mechanisms influence stroke volume?

Which of these 3 negatively affects CO?

A

Preload, contractility, and afterload.

↑ afterload = ↓ CO

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12
Q

Which pump is going to influx Ca⁺⁺ into the sarcoplasmic reticulum for storage?

A

SERCA (Sarcoplasmic Reticulum Ca⁺⁺ ATPase Pump)

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13
Q

What molecule binds to and holds Ca⁺⁺ in the sarcoplasmic reticulum?

A

CalS (Ca⁺⁺ Sequestrin)

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14
Q

In broad strokes, what is the process for Ca⁺⁺ to affect myocardial contractility?

A
  1. “Trigger” Ca⁺⁺ enters cell via action potential.
  2. Ca⁺⁺ binds to SR, releasing Ca⁺⁺ stores.
  3. Ca⁺⁺ binds w/ myosin = contraction
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15
Q

What 3 factors effect the amount of “trigger” Ca⁺⁺ that enters a sarcomere/myocardial cell?

A
  1. Amount of L-Type Ca⁺⁺ channels
  2. Duration of channel opening
  3. SNS stimulation.
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16
Q

How do β1 agonists affect trigger Ca⁺⁺ levels?

A

β-1 agonists ↑ time that Ca⁺⁺ L-channels are open = ↑ trigger Ca⁺ to enter the cell.

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17
Q

What drug has been stipulated as being both pro-arrythmic and anti-arrythmic?

A

Digoxin

18
Q

What is the mechanism of action of digoxin?

A
  1. Digoxin binds to and inhibits Na⁺K⁺ATPase Pump.
  2. ↓ intracellular K⁺ = ↑ intracellular Na⁺
  3. Na⁺/Ca⁺⁺ antiporter is reversed.
  4. ↑ intracellular Ca⁺⁺
19
Q

Which drug is a cardiac glycoside?
What is this drug used for?
What is it derived from?
What is its therapeutic index

A
  • Digoxin
  • Only + oral inotrope
  • Foxglove plant
  • Narrow TI = 2
20
Q

What is the bioavailability of digoxin?
What is the T½ of digoxin?
What is the excretion of digoxin?

A
  • 65-80%
  • T1/2= 36-40 hours
  • 2/3 excreted unchanged by kidneys
21
Q

What are the electrical effects of digoxin?
What does toxic dosing of digoxin cause?
What is the “digitalis effect” on an EKG?

A
  • ↑ PR interval, ↓ QT interval
  • Tachycardia, fibrillation, cardiac arrest
  • Downward “swoop” on ST segment
22
Q

How does hyperkalemia affect digoxin?

How does this compare with hypercalcemia and hypomagnesemia?

A

↑ K⁺ competes with digoxin and decreases effect.

↑ Ca⁺⁺ and ↓ Mg⁺⁺ = arrhythmias

23
Q

What does phosphodiesterase-3 inactivate?

Knowing this, what would a PDE-3 inhibitor do to these?

A

cAMP and cGMP

PDE-3 Inhibition = ↑ cAMP & ↑ cGMP

24
Q

Which PDE-3 Inhibitor is a bipyridine?

How does this drug produce myocardial contraction and smooth muscle relaxation?

A

Milrinone

PDE-3 Inhibition:
1. ↑ cAMP = myocyte contraction
2. ↑ cGMP = smooth muscle relaxation

25
Q

What should be known about the pharmacokinetics of milrinone (i.e. route of administration, T½, and site of excretion) ?

A
  • Parenteral (IV) only
  • T½ = 2-3 hours
  • Urinary excretion
26
Q

Why might a phosphodiesterase inhibitor be preferred over digoxin?

A

No inhibition of the Na⁺ K⁺ ATPase pump.

27
Q

Which β agent is the most utilized drug for acute HF?

A

Dobutamine

28
Q

Which drug class reduces preload, edema, and cardiac size?
How does this class accomplish this?
Is the process of reduction of cardiac size a rapid one?

A
  • Diuretics
  • Reduction of salt and H₂O retention
  • Cardiac remodeling is a very gradual process.
29
Q

Which two drugs might be good choices to reduce compensatory responses to decreased cardiac output (i.e. HF)?

A

ACE Inhibitors (Captopril) & ARBs (Losartan)

30
Q

How do all vasodilators, to one degree or another, treat heart failure?

A

Reduction of preload & afterload

31
Q

How do nitroprusside, hydralazine, and nitrates produce vasodilation?

A

Release of NO from drug or endothelium

32
Q

How do verapamil, diltiazem, and nicardipine produce vasodilation?

A

Ca⁺⁺ influx reduction

33
Q

How do minoxidil and diazoxide produce vasodilation?

A

↑ pK⁺ to hyperpolarize smooth muscle membrane.

34
Q

How does Fenoldepam produce vasodilation?

A

Activation of dopamine receptors

35
Q

How do β-blockers treat HF?
Which β-blockers are preferred for HF?
Should β-blockers be used in severe HF?

A
  • Reduction of CO = less O₂ demand
  • β-1 selective and/or vasodilatory (nebivolol)
  • No
36
Q

How do Ca⁺⁺ Sensitizers work?

A

↑ inotropy + vasodilate
* Stabilize Ca⁺⁺ bound conformation
* Open K⁺ channels (hyperpolarize cell)

37
Q

Which drugs should be avoided in HF?

What is the exception?

A
  • NSAIDs (except aspirin)
  • Thiazolidinediones (Rosiglitazone & Pioglitazone)
  • Metformin (causes lactic acidosis)
  • Non-selective β-blockers for severe HF
38
Q

What are the stages of heart failure?

A
  • Stage A - High risk, no symptoms
  • Stage B - Structural disease, no symptoms
  • Stage C - Structural disease, symptoms
  • Stage D - Refractory symptoms
39
Q

What is the best treatment for Stage A heart failure?

A

Risk-factor reduction and education

40
Q

If someone were to be treated for acute heart failure and be hyponatremic, would you use diuretics?

A
  • No, could lower Na⁺ too much.
  • Conivaptan (ADH inhibitor) instead.

Pharmacology fall 2024 (23 decks)

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