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Pharm 2 > Postive Inotropes > Flashcards

Postive Inotropes Flashcards

1
Q

What is the defintion of shock?

A

Peripheral circulatory failure resulting in underperfusion of tissues

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2
Q

Shock results from decreased ____ delivery to tissues and an increase in ____ metabolism

A
  • O2

- Anaerobic

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3
Q

3 types of shock

A
  1. Septic
  2. Cardiogenic
  3. Hypovolemic
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4
Q

Septic shock is the the result of ____ CI, ____ PCWP, and _____ SVR

A
  • Increased
  • Decreased
  • Decreased
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5
Q

Hypovolemic shock is the the result of ____ CI, ____ PCWP, and _____ SVR

A
  • decreased
  • decreased
  • increased
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6
Q

Cardiogenic shock is the the result of ____ CI, ____ PCWP, and _____ SVR

A
  • decreaed
  • increased
  • increased
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7
Q

CHF is the result of decreased _____

A

intracellural cAMP

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8
Q

What two processes are responsible for the the decreased intracellular cAMP in CHF?

A
  1. Downregulation of Beta receptors

2. Impaired coupling between beta receptors and adenyl cyclase

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9
Q

CHF responds to what 3 treatments?

A

preload reduction, afterload reduction, and improved contraction

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10
Q

The risk Low Cardiac Output Syndrome (LCOS) increases if a patient is on CPB longer than ___-

A

6 hours

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11
Q

Risk factors for developing LCOS

A
  • DM
  • Increased age
  • Female
  • Pre-op decreased LVEF
  • Increased duration of CPB
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12
Q

LCOS is a combination of what 7 factors?

A
  1. Inadequate oxygen delivery to tissues
  2. Hemodilution
  3. Mild hypocalcemia
  4. Hypomagnesemia
  5. Kaliuresis
  6. Tissue thermal gradients
  7. Variable levels of systemic vascular resistance
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13
Q

What is the pathophysiogy of LCOS?

A

Stunned myocardium (hypocontractile myocardium in response to ischemia and reperfusion)

Beta receptor down-regulation has been reported

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14
Q

What is the treatment of LCOS?

A

Positive inotropes to increase the contractility of normal and stunned myocardium

Hypotension, unlike CHF, responds poorly to vasodilators alone.

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15
Q

What are the 2 goals of LCOS?

A

Increase levels of O2 delivery (keep SvO2 >70%)

Increase O2 consumption (arterial blood lactate level < 2 mmol/L).

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16
Q

T/F

LCOS is similar to cardiogenic shock

A

True

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17
Q

What are the two major classes of positive inotropes?

A

cAMP Dependent and cAMP independent

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18
Q

What drug classes are contained in cAMP dependent positive inotropes?

A
  1. Beta Agonists
  2. Dopaminergic Agonists
  3. Phosphodiesterase Inhibitors
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19
Q

What drug classes are contained in cAMP independent positive inotropes?

A
  1. Cardiac Glycosides

2. Calcium

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20
Q

What are the hemodynamic effects of positive inotropes that are “pure” beta 1 agonists?

A
  1. Increased HR
  2. Increased A-V conduction
  3. Decreased SVR and PVR (Beta 2 effects)
  4. Variable effect on MRO2 (dependent on HR effect)
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21
Q

Which drug has the most arrhythmogenic potential?

A

Isoproterenol>Epinephrine>Dopamine>Dobutamine

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22
Q

What enzyme stops contraction and breaks down cAMP into AMP?

A

Phosphodiesterase

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23
Q

MOA of cAMP dependent Positive inotropes?

A

Catecholamine binds to beta receptor and activates membrane bound guanine nucleotide. This activates AC which generates cAMP. cAMP increases CA++ and therefore increases the force of contraction and velocity of relaxation

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24
Q

Which receptors are stimulated at low-dose epi?
Intermediate-dose epi?
High-dose epi?

A

Low dose= Beta 2
Intermediate dose=Beta 1
High dose= Alpha 1

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25
Q

What epi dose would ideally be used to a patient with low cardiac output?

A

Intermediate dose epinephrine.

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26
Q

What receptors are activated by norepinephrine?

A

Alpha-1>Beta 1>Beta 2

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27
Q

T/F: Cardiac output may decrease at low doses, but at high doses may increased because of increased afterload and baroreceptor mediated reflex bradycardia with norepinphrine infusion?

A

False; CO increases with low dose, and can decrease with high dose

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28
Q

Which medication can be given along with norepinephrine to produce predominantly Beta 1 agonism from the NE only?

A

Phentolamine

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29
Q

Why might NE be used following cardio-pulmonary bypass?

A

to be used as a vasoconstrictor to counter the vasoplegic syndrome that can follow CPB

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30
Q

What are complications of catecholamine administration

A
  1. Local tissue ischemia from SQ infiltration
  2. Increased MRO2
  3. Enhanced lipolysis and gluconeogenesis
  4. Alter electrolytes
  5. Activate coagulation
  6. Override microvascular control mechanisms
  7. Alter distribution of CO
  8. Increase myocardial work
  9. Increase the risk of cardiac arrythmias
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31
Q

Which receptors does isoproterenol stimulate?

A

Beta-1 and Beta-2

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32
Q

What is the net effect of isoproterenol on CO and MAP?

A 
CO Increases
MAP Decreases (d/t drop in SVR)
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33
Q

Does the diastolic or systolic BP change with isoproterenol infusions?

A

Systolics may stay the same (or mildly elevate), but diastolics will decrease

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34
Q

What is the reason for diastolic/MAP decrease with isoproterenol infusions?

A

It is due to Beta-2 agonism

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35
Q

What are the 3 main uses of isoproterenol?

A
  1. Chemical pacemaker after heart transplant or in complete heart block
  2. Bronchospasm management during anesthesia
  3. Decrease PVR in patients with pulmonary hypertension and RV failure
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36
Q

Name a synthetic catecholamine with structural characteristics of dopamine and isoproterenol?

A

Dobutamine

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37
Q

Dobutamine works on which receptors?

A

Beta 1»>beta 2=alpha 1

Almost primarily Beta 1

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38
Q

What is dobutamine’s effect on coronary vasculature?

A

Dilates coronaries

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39
Q

Is dobutamine effective in patients with septic shock?

A

No; not effective d/t the need for increased SVR to increase BP

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40
Q

Dobutamine should only be mixed in what IV solution?

A

D5W

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41
Q

D1-like or D2-like:

Stimulates adenylate cyclase?

A

D1-like

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42
Q

D1-like or D2-like:

Causes naturesis and diuresis?

43
Q

D1-like or D2-like:

vasodilation?

44
Q

D1-like or D2-like: Inhibits cAMP?

45
Q

What other dopamine receptors are “like” D1?

46
Q

What other dopamine receptors are “like” D2?

47
Q

What other positive inotrope does dopamine mimic in it’s incremental receptor effects?

A

Epinephrine

48
Q

What is the infusion rate for “renal dose” dopamine?

A

0.5 to 3mcg/kg/min

49
Q

What is “renal dose” dopamine’s effect on the kidneys?

A

Increase RBF, GFR, Na+ excretion, and UO, but is not renal protective

50
Q

What are the effects typically seen from dopamine infusion at 2-10mcg/kg/min?

A

Beta receptor effects

51
Q

Are there indirect or direct effects from beta receptor agonism with dopamine?

A

Both. Indirect effects increase release of NE stores

52
Q

At doses greater than 20mcg/kg/min, dopamine has primarily what effect?

A

Alpha receptor effects

53
Q

In what three clinical situations is dopamine typically used?

A
  1. Decreased CO
  2. Decreased systemic BP
  3. Increased LVEDP
54
Q

What is dopamine’s effect on breathing?

A

Dopamine inferferes with the ventilatory response to hypoxemia

55
Q

What is dopexamine’s use?

A

Treat CHF when SVR is high

56
Q

What are the effects seen with dopexamine infusions?

A
  1. Beta 2 activity
  2. D1 activity
  3. Inhibits presynaptic reuptake of NE
57
Q

What are fenoldopam’s effects?

A
  1. Selective D1 agonist
  2. Alpha 2 agonism
  3. Decrease SVR
  4. Dose related increase in RBF
58
Q

T/F: Fenoldopam is 10-100 times more potent than Dopamine?

59
Q

Is fenoldopam a renal protective?

A

No, preserves RBF and UO

60
Q

What is unique about the administration of IV fenolodopam compared to other positive inotropes?

A
  1. A-line not required

2. Can use peripheral IV

61
Q

What are 4 cautions with fenoldopam infusions?

A
  1. Dose related tachy with infusions >0.1mcg/kg/min
  2. Hypokalemia
  3. Costly
  4. Slight increase IOP
62
Q

Are phosphodiesterase inhibitors cAMP dependent or independent?

63
Q

What are the cellular effects of PDE3 inhibitors?

A
  1. Slow the metabolism of cAMP to 5-AMP with increases intracellaulr cAMP
  2. Increase Ca++ sensitivity of contractile proteins
  3. Increase Ca++ influx
64
Q

What are the overall hemodynamic affects of PDE3 Inhibitors?

A
  1. Peripheral, arterial, venous vasodilation

2. Increased CO

65
Q

Inamrinone is effective at treating poor LV function; however, what other drug can be administered at the same time to improve outcome?

A

Epinephrine

66
Q

What are adverse side effects with Inamrinone?

A
  1. Thrombocytopenia
  2. Elevated LFTs
  3. Arrythmias
67
Q

Inamrinone is absolutely contraindicated with which diagnosis?

A

Aortic stenosis

68
Q

Which drug has inotropic and vasodilator properties and is similar to inamrinone?

69
Q

Which side effect is NOT related to Milrinone, but is a side effect of inamrinone?

A

No risk of thrombocytopenia with Milrinone

70
Q

What are the SEs of milrinone?

A
  1. H/A, HoTN, syncope
  2. Ventricular arrhythmias
  3. Increased ventricular response rate in Afib/flutter
71
Q

Which drug act at a receptor other than the beta to increase cAMP?

72
Q

MOA of Glucagon?

A

Activates Glucagon receptor and through G-protein 2nd messengers, it accelrates AC and increase cAMP.

73
Q

Where is Glucagon secreted from in the body?

A

Alpha Pancreatic cells

74
Q

What arrhythmia is glucagon specifically helpful in treating?

A

Brady-arrhythmias and beta-blocker induced heart failure

75
Q

What are the hemodynamic effects of glucagon?

A

Increase CI, HR, BP

Decreases SVR and LVEDP

76
Q

Why is glucagon’s use limited?

A

Side effects: N/V, increased blood sugar, increased coronary and pulmonary vascular resistance

77
Q

What medication class does digoxin belong to?

A

Cardiac Glycoside?

78
Q

What are Digoxin’s three major effects on CV system

A
  1. Positive inotrope
  2. Negative dromotrope
  3. Negative chronotrope
79
Q

What are the only two approved uses for digoxin?

A
  1. Heart failure

2. Atrial fibrillation

80
Q

Does digoxin primarily work on the SA or AV node?

81
Q

MOA of Digoxin?

A

Digoxin stops the Na+ from leaving the cardiac cell so that less Na+ needs to come back in. Less Na+ movement means less Ca++ will leave the cell over all.

In a sentence, digoxin blocks the sodium which stops the calcium from leaving the cell

82
Q

What is the therapeutic range for Digoxin?

A

0.8-2ng/ml

83
Q

What EKG change can be seen with digoxin?

A

Swooping ST segment (expected and non-pathological)

84
Q

At what level is digoxin considered toxic?

A

Plasma levels >3ng/ml

85
Q

For what treatment is digoxin plasma level often above toxic levels?

A

When treating A fib. Treat to results (desired ventricular rate)

86
Q

What are 5 predisposing factors for digoxin toxicity?

A
  1. Hypokalemia
  2. Hypomagnesemia
  3. Hypoxemia
  4. Hypercalcemia
  5. Hypothyroid
87
Q

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

88
Q

What is the most common dysrrythmia with digoxin toxicity?

A

Paroxysmal atrial tachycardia with Mobitz Type II block

89
Q

Treatment for CV issues causes from digoxin toxicity?

A
  1. Phenytoin/lidocaine to suppress ventricular dysrrythmias
  2. Atropine to increase HR
  3. Beta blocker
  4. Temporary pacing for complete heart block
  5. Digibind
90
Q

How does digibind work?

A

Fragmented antibodies (FAB) bind to the drug and decrease the plasma concentrations of cardiac glycosides

91
Q

How is FAB=digitalis complex eliminated from the body?

92
Q

What drugs enhance digoxin absorption?

A
  1. Macrolides
  2. PPIs
  3. Conazoles
  4. Ranolazine
93
Q

What drugs decrease digoxin absorption?

A
  1. Resin binders
  2. Acorboes/miglitol
  3. Kaolin-pectins
  4. Reglan
  5. Sulfasalazine
  6. Sucralfate
94
Q

3 conclusions from ALARM-HF trial?

A
  1. Lower in house mortality fro patients receiving vasodilator+diuretic vs diuretic alone
  2. Great in house mortality for IV inotropes vs no inotropes
  3. 1.5 fold increase for patients receiving dopamine or dobutamine, 2.5 fold increase for patients receiving NE or EPI
95
Q

What are the step to treating low CO?

A
  1. Appropraite heart rate (pacing)
  2. Optimize ventricular filling (preload)
  3. Reduce afterload if BP is appropriate
  4. Improve contractility (inotrope)
  5. Recheck adequacy of ventricular filling
  6. Combination therapy (inotropes and vasodilators)
  7. IABP
  8. LVAD
96
Q

What is the MOA of Levosimendan?

A

Increases the sensitivity of the myocardium to Ca+

Not approved in USA, but used to treat hypotension and arrhythmias from LCOS

97
Q

Are pure beta-1 agonists (Isoproterenol, dobutamine) inodilators or inoconstrictors?

A

Inodilators

98
Q

Are mixed alpha and beta agonists (NE, Epi, Dopamine) inodilators or inoconstrictors?

A

Inoconstrictors

99
Q

What substance breaks down cAMP into AMP?

100
Q

What is the prototypical catecholamine?

A

Epinephrine

101
Q

According to the Frank Starling curve, stroke volume improves with ______

A

Blood volume

102
Q

T/F

Dopexamine is a inoconstrictor

A

False

It is a inodilator

103
Q

T/F

When starting Fenoldopam, you need to start with a bolus dose

A

False

DO NOT BOLUS

104
Q

T/F

MAP will stay the same with low dose epinephrine

Pharm 2 (19 decks)

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