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Pharmacology > EXAM #2: CONGESTIVE HEART FAILURE > Flashcards

EXAM #2: CONGESTIVE HEART FAILURE Flashcards

1
Q

What is preload?

A

Tension developed on the wall of the ventricles before the start of contraction

This is equal to the end diastolic volume, and EDV is equal to the atrial pressure

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2
Q

What is the Frank Starling Principle?

A

More preload = more contractility TO A POINT

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3
Q

What is afterload?

A

The pressure the ventricle has to push against i.e. arterial pressure/ peripheral vascular resistance

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4
Q

What is the relationship between afterload and contractility?

A

Increasing afterload increases contractility to a point

This is called the anrep phenomenon

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5
Q

What is the relationship between the contractility and heart rate?

A

Faster heart rate will be associated with increased contraction

This is called the Bowditch phenomenon*

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6
Q

Draw the relationship between ventricular EDV and stroke volume. How is this changed in HF?

A

N/A

Generally, in HF you need MORE preload to produce the same amount of WORK.

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7
Q

Draw the pathophysiology of Heart Failure and the major drug action sites.

A

N/A

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8
Q

What is the main cause of HF?

A

Cardiac remodeling

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9
Q

What is stage A Heart Failure?

A

High risk for developing HF

  • HTN
  • CAD
  • DM
  • FHX of Cardiomyopathy
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10
Q

What is stage B Heart Failure?

A

Asymptomatic HF

  • S/p MI
  • LV systolic dysfunction
  • Asymptomatic valvular disease
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11
Q

What is stage C Heart Failure?

A

Symptomatic HF

  • Known structural heart disease
  • Dyspnea/ Fatigue
  • Reduced exercise tolerance
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12
Q

What is stage D Heart Failure?

A

Refractory End-Stage HF

- Symptoms at rest despite max. medical therapy

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13
Q

What drugs classes are used to treat Stage A HF?

A

1) ACEI or ARB

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14
Q

What drugs classes are used to treat Stage B HF?

A

1) ACEI or ARB

2) Beta-blocker

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15
Q

What drugs classes are used to treat Stage C HF?

A

1) ACEI or ARB
2) Beta-blocker
3) Diuretics

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16
Q

What drugs classes are used to treat Stage D HF?

A

1) ACEI or ARB
2) Beta-blocker
3) Diuretics
4) Digoxin
5) Positive ionotrope

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17
Q

What is the effect of diuretics alone on the pathophysiology of HF?

A

Shift to lower cardiac filling pressure on the same ventricular function curve

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18
Q

What is the effect of ionotropes alone on the pathophysiology of HF?

A

Shift to higher ventricular function curve BUT increased workload

19
Q

What is the effect of vasodilators alone on the pathophysiology of HF?

A

Shift to improved ventricular function curve AND reduce cardiac filling pressure

20
Q

What is the effect of vasodilators and ionotropes on the pathophysiology of HF?

A

Shift to improved ventricular function curve AND sight reduction in cardiac filling pressure

21
Q

What is the effect of vasodilators, diuretics, and ionotropes on the pathophysiology of HF?

A

Shift to improved ventricular function curve AND significant reduction in cardiac filling pressure

22
Q

What are the effects of beta agonists on myocardial contractility?

A
  • Gs stimulation
  • Increased cAMP
  • Phosphorylation of the Ca++ channel in the sarcolemma
  • Increased Ca++ induced Ca++ release

Positive ionotropy

23
Q

How can intrinsic myocardial activity be increased?

A

1) Increase cytosolic Ca++
2) Increased myocardial cAMP
3) Agonism of B1 receptors
4) Increase B1 density

24
Q

What drugs increase cytosolic Ca++?

A

Cardiac Glycosides i.e. Digoxin

25
Q

What drugs increase myocardial cAMP?

A

Phosphodiesterase inhibitors

26
Q

What drugs agonise B1 receptors?

A 
Isupreal 
Dobutamine
DA 
Epi 
NE
27
Q

What drugs increase B1 receptor denisty?

A

Beta-1 ANTAGONISTS

28
Q

What is the mechanism of action of digoxin?

A

1) Block Na+/K+ ATPase
2) Accumulation of intracellular Na+
3) Reduction in Na+/Ca++ exchange
4) INFLUX of Ca++ from extracellular space

Net ionotropic effect

29
Q

What are the cardiac effects of Digoxin?

A

1) Positive ionotropy
2) Direct vagal effect
3) Increased coronary blood flow
4) Proarrhythmic

30
Q

Why is digoxin used in patients with A-fib w/ RVR?

A

Direct vagal effect decreases AV conduction

31
Q

What EKG change is characteristic of Digoxin?

A

Hockey stick ST depression

32
Q

What is the proarrhythmic effect of digoxin related to?

A

K+

33
Q

What is the half-life of digoxin?

A

36-48 hours

34
Q

How long does it take to achieve steady-state blood levels of digoxin?

A

7 days

35
Q

How is digoxin excreted?

A

Kidney

36
Q

What are the adverse effects of Digoxin?

A

1) Hypokalemia
2) Acid-base disbalance
3) Arrhythmia (AV block)

37
Q

What are the first symptoms that patients complain of with digoxin that should be concerning to you?

A

Anorexia
Nausea
Vomiting
Visual distrubance

38
Q

What is the role of Digoxin in the treatment of HF?

A

Used frequently in HF, especially in CHF and a-fib w/ RVR; however
- Improves quality of life but NOT all-cause mortality

39
Q

How is Digoxin overdose reversed?

A

Cholestyramine

40
Q

List the phosphodiesterase 3 inhibitors.

A

Inamrione

Milrinone

41
Q

What is the mechanism of action of the phosphodiesterase 3 inhibitors?

A
  • Type III Phosphodiesterase degrades cAMP

- inhibition INCREASES cAMP

42
Q

What is the effect of cAMP in the heart?

A

Increased intracellular Ca++ leading to enhanced contractility

43
Q

What are the cardiovascular effects of the phosphodiesterase 3 inhibitors?

A
  • Positive ionotrope
  • Positive lusotropy
  • Balanced venous and arterial dilation

All increase CO

44
Q

What setting are Inamrinone and Milrinone used in?

A

ICU i.e. only for short-term support of advanced CHF

Pharmacology (64 decks)

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