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Emily: Pharm 2 > Quiz 3: Positive Inotropes and Myocardial Oxygen Balance > Flashcards

Quiz 3: Positive Inotropes and Myocardial Oxygen Balance Flashcards

1
Q

During shock there is an increase in _______ metabolism which creates a more acidic pH and increases _____.

A
  • anaerobic

- Lactate

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2
Q

What are the three types of shock?

A
  • Septic
  • Hypovolemic
  • Cardiogenic
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3
Q

What type of hemodynamic would you see with septic shock?

A

INCREASE
-Cardiac Index

DECREASE

  • PCWP
  • SVR
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4
Q

What type of hemodynamic changes would you see with hypovolemic shock?

A

INCREASE
-SVR

DECREASE

  • CI
  • PCWP
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5
Q

What type of hemodynamic changes would you see with cardiogenic shock?

A

INCREASE

  • PCWP
  • SVR

DECREASE
-CI

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6
Q

T/F: The end result of CHF could be ischemic heart disease and hypertension.

A

TRUE

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7
Q

With congestive heart failure at the inter cellular level there would be __________ intracellular cAMP, ______ of beta receptors and _____ ______ between beta receptors and adenyl cyclase.

A
  • Decreased
  • downregulation
  • impaired coupling
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8
Q

Hemodynamically what does congestive heart failure respond to:

A
  • decrease preload
  • decrease afterload
  • improved contraction
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9
Q

Risk factors for low cardiac output syndrome would be:

A
  • DM
  • increased age
  • female
  • preop decreased LVEF
  • Increased duration of CPB
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10
Q

What is the pathophysiology of Low cardiac output syndrome (LCOS):

A

-stunned heart causing hypocontractility due to ischemia and reperfusion

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11
Q

T/F: With low cardiac output syndrome there is up regulation of beta receptors.

A

FALSE (…..there is down regulation of ….)

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12
Q

What is the line of treatment for low cardiac syndrome:

A

-positive inotropes

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13
Q

What is the goal in low cardiac output syndrome:

A

INCREASE

  • O2 delivery (SvO2 >70%)
  • O2 consumption (arterial blood lactate level =< 2mmoL)
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14
Q

Positive inotropes that are cAMP dependent are:

A
  • beta agonist
  • Dopaminergic agonists
  • Phosphodiesterase inhibitors
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15
Q

Positive inotrope that are cAMP indepent are:

A
  • cardiac glycosides

- calcium

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16
Q

What are the hemodynamic effects of positive inotropes:

A
  • increased SV

- decrease in LVEDP

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17
Q

Positive inotropes that are considered “PURE” beta 1 agonist are:

A
  • doBUTAMINE

- isoproterenol

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18
Q

Positive inotropes that are considered mixed alpha and beta agonists are:

A
  • Noriepinepherine
  • Epinepherine
  • doPAMINE
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19
Q

Positive inotropes that are “PURE” beta 1 agonists would be a inodilator or inoconstrictor:

A

Inodilator

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20
Q

Positive intropes that are mixed alpha and beta agonist would be a inodilator or inoconstrictor:

A

Inoconstrictor

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21
Q

Positive inotropes ion a failing circulation, effects of inotropes are likely to be more _________.

A

-pronounced

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22
Q

T/F: Isoproterenol (DA and dobutamine) will worsen tachyarrhythmias.

A

TRUE

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23
Q

T/F: High doese of noriepinephine and epinephrine for prolonged periods with persistent low cardiac output will increase perfusion to many tissue beds and contribute to renal failure

A

FALSE (…output will decrease perfusion…)

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24
Q

T/F: Digoxin should be used cautiously in patient with hypokalemia, reanl failure, and bradycardia.

A

TRUE

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25
Q

What are the arrhythmogenic postential for postive inotropes for medication such as dobutamine, epinephrine, isoproterenol, and DA.

A

Dobutamine< DA<isoproterenol

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26
Q

What are the steps at the cellular level to make beta agonist work on the cAMP edpendent positive inotrope?

A
  1. Catecholamine bind to beta receptors and activate a membrane-bound guanine nucleotide binding protein
  2. This activate adenyl cyclase and generates cAMP
  3. cAMP increases Ca influx via slow channels and increases Ca sensitivity of Ca-regulatory proteins.
  4. Increase the force of contraction and velocity of contraction and velocity of relaxation
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27
Q

Epinephrine works on what receptors and is an agonist or antagonist:

A
  • Alpha 1
  • Alpha 2
  • Beta 1
  • Beta 2
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28
Q

Low doses of epinephrine (1-2 mcg/min) will do what with receptors and body:

A
  • Stimulate (less) Alpha 1 receptors in skin,mucosa,hepatorenal sytem
  • Stimulate (MORE) BETA 2 receptor in skeletal system which will decrease SVR and distribute blood to skeletal system
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29
Q

Will MAP stay the same at low does epinephrine:

A

YES

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30
Q

Intermediate does of epinephrine (4 mcg/min) will do what:

A
  • WORKS MORE ON BETA 1 RECEPTORS
  • inotropes
  • Increase HR
  • Increase contractility
  • Increase C.O.
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31
Q

At low dose epinephrine will work as a vasodilator.

A

TRUE

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32
Q

At high dose epinephrine will work as a vasoconstrictor.

A

TRUE

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33
Q

T/F: Epinephrine is the least potent activator of the Alpha 1 receptors.

A

FALSE (..the most potent…)

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34
Q

High dose of epinephrine w(> 10 mcg/min) will do what:

A

-Works most on the ALPHA 1 RECEPTOR
-constict at the cutaneous, splanchnic, and renal vascular beds
-maintain myocardial and cerebral perfusion
-Increase aortic DBP
-

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35
Q

What type of reflex can epinephrine cause:

A

BRADYCARDIA

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36
Q

Norepinephrine primary job works on what receptors. What receptors are most effected?

A
  • Alpha 1 agonist (MOST)
  • Beta 1 agonist (overshadowed by alpha 1)
  • Beta 2 least effected
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37
Q

At low doses norepinephrine will cause and ____ with cardiac output, but at high doses norepinephrine will cause _____ with cardiac output.

A
  • increase

- decrease

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38
Q

Why does norepinephrine cause a decrease with CO at high doses.

A
  • increased afterload

- baroreceptor mediated reflex bradycardia

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39
Q

Which causes a greater cardiac output effect epinephrine or noriepinephrine.

A

Epinephrine

40
Q

What receptor would noriepinephrine work on primarily when phentolamine is used in conjunction:

A

-Beta 1 agonist

41
Q

Isoproterenol works on what receptors:

A
  • Beta 1

- Beta 2

42
Q

T/F: Isoproterenol can work as a bronchodilator.

A

TRUE

43
Q

The net effect hemodynamically of isoproterenol causes:

A
  • increase in C.O.

- Decrease M.A.P.

44
Q

What are the uses of isoproterenal:

A
  • chemical pacemaker after a heart transplant or complete heart block
  • bronchospasm management during anesthesia
  • Used to attempt to decrease PVR in patient with pumonary hypertension and RV failure
45
Q

DoBUTAMINE works on what receptor:

A
  • Beta 1 (MORE)
  • Beta 2 (less)
  • Alpha 1 (less)
46
Q

T/F: Dobutamine has a small percent of dopaminergic receptor activation.

A

FALSE (Dobutamine has no dopaminergic…)

47
Q

How does dobutamine increase renal blood flow:

A

-increase C.O.

48
Q

Is dobutamine effective in patient who need increased SVR to increase BP.

A

NO

49
Q

What would happen to dobutamine if prepared in an alkaline IV solution.

A

Dobutamine would be inactivated.

50
Q

Dopaminergic agonist D1 process is:

A
  1. G coupled
  2. stimulate adenylate cyclase
  3. activate cAMP
51
Q

Dopaminergic agonist D1 works on:

A
  • Smooth muscle of blood vessles: vasodilation
  • Naturesis
  • Diuresis
52
Q

Dopaminergic agonist D2 process is:

A
  1. G coupled
  2. inhibits adenylate cyclase
  3. inhibits cAMP
53
Q

Dopaminergic agonist D2 works on:

A
  • Presynaptic: inhibits NE release and promote vasodilation

- Attenuate the beneficial effects of DA on renal blood flow

54
Q

Dopamine dose at 0.5-3 mcg/kg/min effects:

A
  • DA1

- DA2

55
Q

Dopamine dose at 3-10mcg/kg/min effects:

A

-beta effect

56
Q

Dompamine dose at 10-20mcg/kg/min effects:

A

-beta and alpha effect

57
Q

Dopamine dose over 20 mcg/kg/min effects:

A

-Alpha effects

58
Q

T/F: Dopamine in low doses is renal protective.

A

FALSE

59
Q

T/F: Dopamine in low dose inhibits aldosterone secretion.

A

TRUE

60
Q

Dopamine ___ the respitory drive.

A

blunts

61
Q

Dopamine _____ splanchnic oxygenation and impairs GI function.

A

-worsens

62
Q

How long until tolerance of dopamine on renal effects develope.

A

-2-48 hours

63
Q

What neurohormonal effects does dopamine have that are detrimental:

A
  • suppresses endocrine system

- immunosupression

64
Q

How much dopamine is needed to cause a noriepinephrine release:

A

over 5 mch/kg/min

65
Q

A dose of Dopamine (2-10 mcg/kg/min) causes what:

A
  • increase contractility
  • increase C.O.
  • no change in HR or BP
  • ALPHA activation starting
66
Q

High doses of dopamine ______ release of insulin causing ______.

A
  • inhibit

- Hyperglycemia

67
Q

Clinical situation dopamine is used in is:

A
  • decreased CO
  • Decreased systemic B.P.
  • Increased L.V. end diastolic pressure
68
Q

Dopexamine is a inodilator or inoconstrictor.

A

Inodilator

69
Q

What receptor does dopexamine work on:

A
  • Beta 2

- DA 1 receptor

70
Q

Dopexamine _____ presynaptic reuptake of noriepinephrine.

A

inhibits

71
Q

Dopexamine is a (indirect/direct) inotropic activity.

A

-indirect

72
Q

Tachycardia is more prevalent in dopamine or dopexamine.

A

-Dopexamine

73
Q

What is the use of Dopexamine?

A

-treat CHF when SVR is high

74
Q

What are some phosphodiesterase III inhibitors.

A
  • Inamrinone

- milrinone

75
Q

How does phosphodiesterase III inhibitors work:

A
  • Slow the metabolism of cAMP to 5’-AMP increasing intracellular cAMP concentrations
  • increase the Ca sensitivity of contractile proteins
  • Increase Ca influx
  • Antagonize adenosine
76
Q

Inamrinone _____ intrapulmonary shunting and ____ PaO2.

A
  • increases

- decreases

77
Q

T/F: Inamine is more effective with fewer complications than dobutamine during separation from CABG.

A

TRUE

78
Q

Inamrines is dose dependent _____ in SV and CI and _____ in SVR and PVR after CABG.

A
  • increases

- Decreases

79
Q

What are adverse reaction of inamines?

A
  • thrombocytopenia (10%)
  • elevated LFT
  • Arrhythmias
  • Do NOT administer to patient with AORTIC STENOSIS
  • May aggravate outlet obstruction in patient with IHSS
80
Q

Milrinone has _____ inotropic and vasodilator properties to inamrines but ______ times more potent, with a shorter t1/2 and without the risk of __________

A
  • similar
  • 15 to 20
  • thrombocytopenia
81
Q

What are the side effect of milrinone?

A
  • HA
  • Hypotension
  • syncope
  • ventricular arrhythmias
  • increased ventricular response rate in A. FIB/FLUTTER
82
Q

What receptor does glucagon work at?

A

-Glucagon receptor

83
Q

What hemodynamic effects does glucagon have?

A
  • INCREASE
  • CI
  • HR
  • BP

DECREASE

  • SVR
  • LVEDP
84
Q

What are the side effects of glucagon:

A
  • EXPENSE
  • N/V

INCREASE

  • blood sugar
  • coronary resistance
  • pulmonary resistance
  • vascular resistance
85
Q

Digoxin is a cardiac _____.

A

-glycoside

86
Q

Digoxin has what effect on inotrope, dromotrope, chronotrope.

A
  • positive (Inotrope)
  • negative (Negative)
  • negative (Negative)
87
Q

How does digoxin work:

A

-inhibits Na K-ATPase pump increasing intracellular Na and indirectly intracellular CA

88
Q

What kind of level would you see in K if Digoxin level were high?

A

-low K

89
Q

What are the presentation of digoxin toxicity:

A
  • Anorexia, N/V
  • PVC
  • Paroxysmal atrial tachycardia with block
  • mobitz type 2 AV block
  • V. Fib
90
Q

What is the early presentation of digoxin toxicity?

A
  • anorexia

- N/V

91
Q

What is the most common dysrrhythmia for digoxin toxicity?

A

-Paroxysmal atrial tachycardia with block

92
Q

What is the most frequent cause of death for digoxin toxicity?

A

-V. FIB

93
Q

How do you correct digoxin toxicity?

A
  • correct electrolyte balance
  • administer phenytoin
  • administer lidocaine
  • atropine
  • beta blocker may be used to suppress increased automaticity
  • temporary pacing if complete heart block is present
94
Q

What does digiband do:

A

-fab antibody fragment bind to the drug and dcrease plasma consentration of cardiac glycosides

95
Q

What eliminate the fab antibody:

A

kidneys

96
Q

T/F: Ca can inhibit beta agonists by direct inhibition of adenyl cyclase.

A

TRUE

97
Q

What do inotropes often cause for low C.O.?

A

-tachycardia

Emily: Pharm 2 (11 decks)

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