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Pharmacology- Test 3 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is the equation of C.O.?

A

CO= HR x SV

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2
Q

What is HR regulated by?

A

ANS

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3
Q

What is preload (filling pressure)?

A

The volume of blood flowing back to the heart; i.e. venous return going back to the heart

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4
Q

What is the relationship between the preload and the SV?

A

There is a direct relationship; if you increase the preload, you increase the SV (and opposite)

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5
Q

What is afterload (PR)?

A

The resistance against which the heart has to pump against (the ventricle has to pump the blood into the systemic circulation); the peripheral vascular resistance (i.e. how constricted the arterioles are);

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6
Q

What is the relationship between afterload and SV?

A

Inverse relationship; if you increase the resistance of the flow, the lower the SV will be and vice versa

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7
Q

What is contractility?

A

The amount of force that the ventricle can produce per fixed volume of blood in the ventricle

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8
Q

Contractility is regulated by what? When would you get more contractility?

A

ANS (the ventricles are innervated by sympathetic nerves); when you activate B-1 receptors increases contractility (i.e. if you increase SNS, the pump is going to generate more force into the systemic circulation)

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9
Q

What are the 3 things that can alter SV?

A

(1) Preload
(2) Afterload
(3) Contractility

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10
Q

What is the qualitative definition of heart failure?

A

Inability of heart to pump sufficient blood to meet the metabolic demands of the body

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11
Q

What is the quantitative definition of heart failure?

A

Decreased mechanical efficiency (decrease in contractility); reduced ability to generate force into the systemic circulation

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12
Q

Starling’s Law

A

(1) Increase the preload –>
(2) heart is going to dilate to accomodate, and as you do that you increase the volume of blood and the
(3) pump has to generate more force to pump it out (increase pump contractility)

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13
Q

What are the two ways the body tries to compensate for heart failure?

A

(1) Intrinsic- what happens within the heart muscle itself

(2) Extrinsic- the neural-chemical activation

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14
Q

What are the two ways that Intrinsic factors try and compensate?

A

(1) Ventricular dilation

(2) Ventricular hypertrophy

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15
Q

Ventricular dilation- why does this happen?

A

To increase the ventricular volume which increases S.V. (You get venoconstriction (increase contractility) which means that more blood goes back to the heart, which means the preload is increased, which means the heart dilates, and force you have to use to pump out will increase)

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16
Q

Ventricular hypertrophy- why does this happen?

A

Each myocyte grows in size (they don’t divide) which increases the number of contractile elements within each cell in the heart’s attempt to increase the force of contraction
- net result is cells get bigger= ventricular wall gets bigger

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17
Q

Are the intrinsic compensation factors better short term or long term?

A

short term (acutely)

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18
Q

What are the extrinsic compensations of heart failure?

A

Decrase BP is sensed by the baroreceptors to increase sympathetic nervous system

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19
Q

What, in turn from the baroreceptor extrinsic compensation, will happen when you stimulate the sympathetic nervous system?

A

(1) Increase heart rate- B-1 receptors which increases CO
(2) Increase Preload (A-1 constriction from veins)
(3) Increase Afterload (A-1 constriction of arteries- increase BP)
(4) Increase in Ang-II (B-1 renin release in kidney; stimulates release of aldosterone causing salt and water retention)
(2-3-4) Increases blood volume

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20
Q

What will happen if the extrinsic compensation happens chronically?

A

It will accelerate the progression of heart failure

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21
Q

What happens when the sympathetic nerves stimulate the B-1 receptors in the ventricle?

A

Increases contractility and stimulates growth of the myocytes (hypertrophy and remodeling)

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22
Q

What 2 things stimulate myocyte growth in extrinsic compensation pathway which stimulate hypertrophy and remodeling?

A

(1) B-1 receptor activation in the ventricle

(2) Ang-II receptor bind to myocytes and stimulate growth

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23
Q

What is maladaptive/ventricular remodeling?

A

Alteration in dimension, shape or mass in response to hemodynamic stress/injury in association with neurohormonal activation

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24
Q

What happens during maladaptive remodeling? Why is this bad?

A

The shape of the ventricle changes (goes from elliptical to a circular shape and the wall gets thicker); due to pure physics it doesn’t pump as well

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25
Q

What are the 4 things that happen during ventricular remodeling?

A

(1) Myocyte hypertrophy
(2) Myocyte apoptosis- cells die faster
(3) Fibroblast proliferation (collagen)- take over for the myocytes (inactive); reduces ability to pump
(4) Oxidative stress- instead of producing ATP, produces species that will increase cell death

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26
Q

What are the mediators involved in ventricular remodeling?

A

(1) Ang-II
(2) Catecholamines (NE)
(3) Aldosterone (mineralocorticoid receptors in myocytes)
(4) Cytokines

27
Q

How do Inotropic agents work?

A

Directly act with the heart to increase contractility; useful acutely (once case chronically) but they are going to increase workload on heart

28
Q

How do Beta-blockers work?

A

Can over time decrease S.V.

29
Q

How do the ACE inhibitors and AII receptor blockers work?

A

Interferes with the R-A system to block it’s effects

30
Q

How do Diuretics work?

A

lowers blood volume back towards normal

31
Q

How do Vasodilators work?

A
  • Reduces afterload (vasodilates the arterioles)

- Selectively decrease preload (venodilators- relieves pulmonary congestion)

32
Q

What are the inotropic agents?

A

(1) Cardiac Glycosides (Digoxin)
(2) Epinephrine, Isoproterenol
(3) Dobutamine
(4) Phosphodiesterase inhibitor (Milrinone)

33
Q

What goes Digoxin do to the heart?

A

(1) Increases contractility which increases SV

(2) Decreases HR by increasing vagal tone, slows A-V conduction

34
Q

Digoxin- Mechanism

A

inhibits Na-K-ATPase (a small amount) which increases intracellular calcium

35
Q

What is the problem of Digoxin?

A

T 1/2 is 36 hours with a low therapeutic index (give by doing loading dose and then maintenance doses)

36
Q

Dogoxin- Toxicities; How do you combat these toxicities (parentheses)?

A

(1) Nausea, vomiting, diarrhea, visual changes
(2) Arrhythmias
- Bradycardia, (Atropine)
- A-V block (Atropine)
- Ventricular premature beats/Tachycardia (Digibind- antibody to digoxin)

37
Q

Why don’t you use Epinephrine or Isoproterenol in the treatment of heart failure?

A

Because it overworks the heart, increases the contractility by causes severe tachycardia

38
Q

What type of drug is Dobutamine?

A

dopamine derivative

39
Q

What dosage do you use for Dobutamine? Why?

A

Low to moderate dose; because the Beta receptors are utilized at a low dose and alpha are utilized at a high dose (agonists)

40
Q

What does Dobutamine do to the heart?

A

Increases contractility which increases C.O.

41
Q

T/F Isoproterenol causes more severe tachycardia than Dobutamine.

A

TRUE

42
Q

How is Dobutamine given? How long should it be used for/Why?

A

IV only (has big first pass metabolism); has a short-term cardiac support because chronic use desensitizes the B- receptors

43
Q

T/F Only Digoxin is the only inotropic agent that is pro-arrhythmic.

A

FALSE; Digoxin, Dobutamine, and Milrinone

44
Q

Phosphodiesterase inhibitor (Milrinone)- Mechanism; why is this important?

A

Prevents the breakdown from cAMP from AMP which produces a cellular effect that you’ve activated the receptor even though you haven’t actually activated it; it doesn’t develop tolerance like Dobutamine

45
Q

What does Milrinone do? Why do you get opposite reactions from cardiac muscle to vascular smooth muscle?

A

(1) Inhibits PDE which increase cAMP
(2) Increases cAMP (in cardiac muscle) which increases contractility and SV
(3) Increases cAMP (in vascular smooth muscle) which decreases afterload (vasodilation)
- you get an increase in intracellular calcium in the cardiac muscle, while you get a decrease in intracellular calcium in the venous system-

46
Q

What is the limitations of Milrinone?

A

Hypotension

47
Q

What are the Neurohormonal Modulators?

A

Angiotensin II Modifiers-

1) ACE inhibitors (Captopril, Enalapril);
(3) Ang-II receptor blockers (Losartan

48
Q

What do the Angiotensin-II modifiers do to the heart?

A

(1) Decrease afterload (vasodilation)= increase SV
(2) Venodilation= decrease preload= decrease congestion
(3) Decrease aldosterone= decrease blood volume
(4) Slows progression of hypertrophy/remodeling (which decreases mortality)

49
Q

What are the differences in mechanisms between ACE inhibitors and Ang-II blockers?

A

ACE inhibitors block the receptor from receiving the signal while ACE inhibitors block the conversion of Ang-I to Ang-II

50
Q

What are the adverse effects of Angiotensin-II modifiers?

A

(1) Hypotension (1st dose, salt depleted- low salt diet for HTN or diuretic for heart failure)- reduce dose and increase slowly over time
(2) Fetopathic potential (renal roxicity)- contraindicated for pregnant women
(3) Cough with *ACE inhibitors (bradykinin goes up)
(4) Angioedema with *ACE inhibitors

51
Q

What are the beta-blockers?

A

(1) Metoprolol (B-1 selective)

2) Carvedilol (Beta-nonselective, alpha-1 antagonist

52
Q

What do Beta blockers do to the heart?

A

(1) Acute effect: low dose initiation decreases the ejection fraction (decrease SV)
(2) Chronic effect: gradual dose escalation which increases the ejection fraction (increase SV)
~blockade of toxic catecholamine effects (antiarrhythmic)
~ slows progression of ventricular hypertrophy (decreases mortality)

53
Q

T/F the beta blockers are given in varying doses.

A

TRUE; given at a low dose for acute effect and with a gradual dose elevation afterwards.

54
Q

What are the limitations and adverse effects of beta blockers?

A

(1) Limitations- asthma (nonselective blockers; bronchospasm), diabetes (prolongation of hypoglycemia)
(2) Adverse effects- bradycardia (S-A and A-V nodal), insomnia, nightmares

55
Q

What are the Aldosterone Antagonists?

A

Spironolactone (K sparing diuretic)

56
Q

What does Spironolactone do to the heart?

A

(1) Blocks mineralocorticoid receptor that aldosterone stimulates to cause salt and water retention
(2) Decreases sodium and water reabsorption in the kidney
(3) Decreases potassium excretion
(4) Reduces sympathetic tone (mineralocorticoid receptors in the sympathetic nerve terminals- less NE being released in heart)
(5) Decrease L remodeling which increases EF and decreases apoptosis and fibrosis

57
Q

What are the limitations of Spironolactone?

A

(1) Hyperkalemia (imporant for people who have pre-existing renal problems)
(2) Male impotence

58
Q

What is the standard therapy for heart failure?

A

ACE inhibitor or Ang-II receptor blocker WITH Beta-blocker

59
Q

What are the Vasodilators?

A

(1) Nitroglycerin

(2) Hydralazine

60
Q

T/F Nitroglycerin and Hydralazine cannot be used in combination.

A

FALSE

61
Q

What does Niroglycerin do to the heart?

A

Dilator: veins> arterioles (NO)

- decreases preload which decreases filling pressure, decreases congestion

62
Q

What is the limitation of the vasodilators?

A

Hypotension

63
Q

What does Hydralazine do in the heart?

A

Dilator: arterioles> veins (NO)

- decreases TPR which decreases afterload which increases SV

Pharmacology- Test 3 (7 decks)

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