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KLowe Pharm 2 > Lecture 3-Positive Inotropes > Flashcards

Lecture 3-Positive Inotropes Flashcards

1
Q

Positive inotropes improve ___

A

The strength of contraction—they improve the squeeze out of the LV to get blood out into the body

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2
Q

___ is peripheral circulatory failure that results in underperfusion of tissues

A

Shock

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3
Q

Shock results in ___ (increased/decreased) oxygen delivery to tissues; ___ (increase/decrease) in anaerobic metabolism; more ___ (acidic/alkalotic) pH; ___ (increased/decreased) lactate

A

Shock results in decreased O2 delivery to tissues; increase in anaerobic metabolism; more acidic pH; increased lactate

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4
Q

Shock is a low cardiac output state—T/F?

A

True

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5
Q

3 types of shock =

A
  • Septic
  • Hypovolemic
  • Cardiogenic
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6
Q

Septic shock = ___ (increased/decreased) CI; ___ (increased/decreased) PCWP; ___ (increased/decreased) SVR

A

Increased CI; decreased PCWP; decreased SVR

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7
Q

Hypovolemic shock = ___ (increased/decreased) CI; ___ (increased/decreased) PCWP; ___ (increased/decreased) SVR

A

Decreased CI; decreased PCWP; increased SVR

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8
Q

Cardiogenic shock = ___ (increased/decreased) CI; ___ (increased/decreased) PCWP; ___ (increased/decreased) SVR

A

Decreased CI; increased PCWP; increased SVR

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9
Q

In CHF, there is ___ (increased/decreased) intracellular cAMP

A

Decreased intracellular cAMP

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10
Q

CHF responds to ___ reduction, ___ reduction, and improved ___

A

Preload reduction, afterload reduction, and improved contraction

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11
Q

Low cardiac output syndrome (LCOS) can occur in patients coming off of CPB—T/F?

A

True

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12
Q

LCOS results in inadequate ___ delivery to tissues; hemo___; mild ___calcemia; ___magnesemia; ___uresis; tissue ___ gradients; variable levels of ___

A

Inadequate oxygen delivery to tissues; hemodilution; mild hypocalcemia; hypomagnesemia; kaliuresis (elimination of potassium through the kidneys); tissue thermal gradients; variable levels of systemic vascular resistance

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13
Q

Risk factors for LCOS—___; increasing age above ___; ___ (male or female?); pre-op decreased ___; increased duration of CPB (> ___ hours quickly increases the risk)

A

Diabetes; increasing age above 65; female; pre-op decreased LVEF; increased duration of CPB (> 6 hours quickly increases the risk)

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14
Q

LCOS is caused by a stunned myocardium—___contractile myocardium in response to ___ and ___

A

hypocontractile myocardium in response to ischemia and reperfusion

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15
Q

Beta receptor down regulation has been reported with LCOS—T/F?

A

True, but this takes weeks to occur

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16
Q

Treatment of LCOS = ___ (what drug class?)

A

Positive inotropes to increase the contractility of normal and stunned myocardium

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17
Q

Hypotension in LCOS responds well to vasodilators alone—T/F?

A

False—hypotension in LCOS (UNLIKE CHF) responds POORLY to vasodilators alone

In CHF, you can use vasodilators to reduce preload/afterload and reduce the workload on the heart—this helps to improve the strength of contraction/helps with hypotension

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18
Q

Goal of LCOS treatment in critically ill patients is to increase levels of O2 ___ (keep SvO2 > ___%) and increase O2 ___ (arterial blood lactate level < or equal to ___ mmol/L)

A

Increase levels of O2 delivery (keep SvO2 > 70%) and increase O2 consumption (arterial blood lactate level < or equal to 2 mmol/L)

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19
Q

(2) classes of positive inotropes:

A
  • cAMP dependent

- cAMP independent

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20
Q

(3) cAMP dependent positive inotropes:

A
  • Beta agonists
  • Dopaminergic agonists
  • Phosphodiesterase inhibitors
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21
Q

(2) cAMP independent inotropes:

A
  • Cardiac glycosides

- Calcium

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22
Q

Hemodynamic effects of positive inotropes—___ (increased/decreased) contractility with ___ (increased/decreased) SV and often ___ (increased/decreased) LVEDP and volume

A

Increased contractility with increased SV and often decreased LVEDP and volume

Have reduced LV pressure/volume because you are pumping more blood out

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23
Q

“Pure” beta-1 agonists AKA inodilators = ___ and ___

A

Dobutamine and isoproterenol

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24
Q

Hemodynamic effects of “pure” beta-1 agonists/inodilators—___ (increased/decreased) HR; ___ (increased/decreased) AV conduction; ___ (increased/decreased) SVR and PVR; variable effect on myocardial ___

A

Increased HR; increased AV conduction; decreased SVR and PVR (beta 2 effect causing peripheral vasodilation in skeletal muscle/periphery); variable effect on myocardial O2 consumption

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25
Q

Mixed alpha/beta agonists AKA inoconstrictors = ___, ___, and ___

A

Norepi, epi, and dopamine

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26
Q

Hemodynamic effects of mixed alpha/beta agonists AKA inoconstrictors—___ (increased/decreased) vascular resistance; ___ (increased/decreased) myocardial O2 consumption; ___ (increased/decreased) HR

A

Increased vascular resistance; increased myocardial O2 consumption; increased HR

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27
Q

If you have both a reduction in cardiac output and SVR, it would be best to use an inodilator like dobutamine or isoproterenol—T/F?

A

False—it would be best to use an inoconstrictor like norepi, epi, or dopamine

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28
Q

Contraindications/complications of positive inotropes—isoproterenol, dobutamine, and dopamine may worsen ___

A

Tachyarrhythmias

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29
Q

Contraindications/complications of positive inotropes—high doses of NE and epi for prolonged periods with persistent low CO will ___ (increase/decrease) perfusion to many tissue beds and contribute to ___ failure

A

Decrease perfusion to many tissue beds and contribute to renal failure

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30
Q

Contraindications/complications of positive inotropes—digoxin should be used cautiously in patients with ___kalemia, ___ failure, ___cardia, and drug ___

A

Hypokalemia, renal failure, bradycardia, and drug interactions

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31
Q

Goal with positive inotropes is to use the lowest dose possible for the shortest period of time possible—T/F?

A

True

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32
Q

Arrhythmogenic potential of positive inotropes (in order of least to greatest risk):

A

Dobutamine < dopamine < epi < isoproterenol

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33
Q

Which positive inotrope has the greatest arrhythmogenic potential?

A

Isoproterenol

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34
Q

Norepi has high risk of arrhythmias—T/F?

A

False—norepi improves CO/SV but does not come with significant increases in HR, so it has less arrhythmogenic potential

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35
Q

CAMP dependent positive inotropes MOA—catecholamines bind to beta receptors and activate a membrane-bound guanine nucleotide binding protein; this activates ___ and generates ___; ___ increases ___ influx via slow channels and increases sensitivity of regulatory proteins; result is ___ (increased/decreased) force of contraction and velocity of relaxation through the movement of ___ (what electrolyte?)

A

This activates adenylyl cyclase and generates cAMP; cAMP increases Ca influx via slow channels and increases sensitivity of regulatory proteins; result is increased force of contraction and velocity of relaxation through the movement of Ca

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36
Q

Review—epi stimulates ___, ___, and ___ receptors

A

Alpha 1, beta 1, and beta 2 receptors

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37
Q

Low dose epi = primarily ___ effects in the ___

A

Primarily beta 2 effects in the peripheral vasculature

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38
Q

Low dose epi—the net effect is ___ (increased/decreased) SVR and distribution of blood to ___; MAP essentially remains ___

A

The net effect is decreased SVR and distribution of blood to skeletal muscle; MAP essentially remains the same

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39
Q

Low dose epi is essentially a vaso___

A

Vasodilator

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40
Q

Intermediate dose epi = ___ effects; increased ___, ___, and ___

A

Inotropic/beta 1 effects; increased HR, contractility, and CO

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41
Q

High dose epi > 10 mcg/min = ___ effects; potent vaso___; used to maintain ___ and ___ perfusion; reflex ___cardia can occur

A

Alpha 1 effects; potent vasoconstrictor; used to maintain myocardial and cerebral perfusion; reflex bradycardia can occur

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42
Q

Norepi is primarily an ___ agonist

A

Alpha 1 agonist

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43
Q

Norepi—cardiac output may ___ (increase/decrease) at low doses, but at higher doses may ___ (increase/decrease) because of ___ and ___

A

Cardiac output may increase at low doses, but at higher doses may decrease because of increased afterload and baroreceptor-mediated reflex bradycardia

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44
Q

What is the vasoconstrictor of choice for septic shock?

A

Norepi—maintains peripheral vasculature/improves cardiac output

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45
Q

Isoproterenol has ___ and ___ receptor effects

A

Beta 1 and beta 2 receptor effects…beta all day

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46
Q

Isoproterenol increases ___, ___, and ___

A

Heart rate, contractility, and cardiac automaticity

Positive chronotrope, inotrope, and dromotrope

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47
Q

Isoproterenol ___ (increases/decreases) SVR and diastolic BP because of negative feedback

A

Decreases SVR and diastolic BP because of negative feedback

When you increase the workload on the heart like isoproterenol does, then the vasculature will relax in response to that

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48
Q

Isoproterenol is an ino___

A

Dilator

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49
Q

Net effect of isoproterenol is ___ (increased/decreased) cardiac output and ___ (increased/decreased) MAP

A

Increased cardiac output and decreased MAP

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50
Q

Side effects of isoproterenol—___cardia; diastolic ___tension; ___ (increased/decreased) myocardial oxygen consumption; ___ (increased/decreased) incidence of cardiac dysrhythmias

A

Tachycardia; diastolic hypotension; increased myocardial oxygen consumption; increased incidence of cardiac dysrhythmias

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51
Q

Isoproterenol should be avoided in patients in ___ or in patients with ___

A

Avoided in patients in cardiogenic shock or in patients with ischemic heart disease

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52
Q

Uses of isoproterenol—chemical pacemaker after ___ or in ___; broncho___ management during anesthesia; decrease ___ in patients with pulmonary HTN/RV failure

A

Chemical pacemaker after heart transplant or in complete heart block; bronchospasm management during anesthesia; decrease PVR in patients with pulmonary HTN/RV failure

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53
Q

Dobutamine is a synthetic catecholamine with structural characteristics of ___ and ___

A

Dopamine and isoproterenol

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54
Q

Dobutamine acts primarily on ___ receptors

A

Beta 1 receptors (with small effects on beta 2 and alpha 1 receptors)

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55
Q

Dobutamine has no clinically significant vaso___ activity; ___ (more/less) increase in conduction compared to isoproterenol; less likelihood of adverse increase in myocardial ___ requirements; dilates ___ vasculature; no ___ receptor activation

A

No clinically significant vasoconstrictor activity; less increase in conduction compared to isoproterenol; less likelihood of adverse increase in myocardial O2 requirements; dilates coronary vasculature; no dopaminergic receptor activation

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56
Q

Dobutamine may NOT be effective in patients who need increased ___ to increase ___

A

Increased SVR to increase BP (because it is an inodilator and only improves cardiac output)

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57
Q

What should you use for a patient who needs increased SVR/BP?

A

Inoconstrictor (norepi, epi, dopamine)

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58
Q

Dobutamine must be prepared in ___ solution

A

D5W

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59
Q

Dobutamine can be inactivated if prepared in ___ IV solutions

A

Alkaline IV solutions (i.e.: NS)

60
Q

Two types of dopaminergic agonists:

A
  • D1 like

- D2 like

61
Q

D1 like dopaminergic agonists ___ (stimulate/inhibit) adenylate cyclase and ___ (activate/inhibit) cAMP; results in smooth muscle vaso___

A

Stimulate adenylate cyclase and activate cAMP; results in smooth muscle vasodilation

62
Q

D2 like dopaminergic agonists ___ (stimulate/inhibit) adenylate cyclase and ___ (activate/inhibit) cAMP; promotes vaso___

A

Inhibit adenylate cyclase and inhibit cAMP; promotes vasodilation

63
Q

D1 like dopaminergic agonists ___ (increase/decrease) gastric secretion/acidity; D2 like dopaminergic agonists ___ (increase/decrease) gastric secretion/acidity

A

D1 decreases, D2 increases gastric secretion/acidity

64
Q

Both D1 and D2 dopaminergic agonists ___ (stimulate/inhibit) aldosterone secretion from the adrenal glands

A

Inhibit

65
Q

Low dose (renal dose) dopamine may increase RBF, GFR, Na+ excretion and urine output but is NOT renal protective—T/F?

A

True

66
Q

Low dose (renal dose) dopamine is not predictable; tolerance to renal effects develops after 2-48 hours; and there has been no benefit of renal dose dopamine for the prevention/treatment of renal failure—T/F?

A

True

67
Q

Intermediate dose dopamine has ___ receptor effects—results in ___ (increased/decreased) myocardial contractility/CO without marked changes in ___ or ___

A

Beta receptor effects—results in increased myocardial contractility/CO without marked changes in HR or BP

68
Q

Part of the beta effects of intermediate dose dopamine is due to the release of endogenous stores of ___, which predisposes patients to cardiac ___

A

Release of endogenous stores of NE, which predisposes patients to cardiac dysrhythmias

69
Q

Dopamine may be used in clinical situations where the patient presents with decreased ___, decreased systemic ___, or increased ___

A

Decreased CO, decreased systemic BP, or increased LVEDP

70
Q

Dopamine interferes with the ventilatory response to ___ through its inhibitory role at the ___

A

Interferes with the ventilatory response to hypoxemia through its inhibitory role at the carotid bodies

71
Q

High doses of dopamine inhibit the release of ___, causing ___

A

Inhibit the release of insulin, causing hyperglycemia

72
Q

Dopamine must be prepared in ___

A

D5W (just like dobutamine)

73
Q

Side effects of dopamine—___/___; ___cardia; ___ pain d/t increased myocardial oxygen consumption; ___ (less than isoproterenol, higher risk than dobutamine); ___ache; ___tension; peripheral vaso___

A

Nausea/vomiting; tachycardia; angina pain d/t increased myocardial oxygen consumption; arrhythmias (less than isoproterenol, higher risk than dobutamine); headache; hypertension; peripheral vasoconstriction

74
Q

Dopamine can cause nausea/vomiting through its ___ receptor activation

A

D2 receptor activation

75
Q

Fenoldopam (corlopam) is a selective ___ agonist with moderate affinity for presynaptic ___ receptors

A

Selective D1 agonist with moderate affinity for presynpatic alpha 2 receptors

76
Q

Fenoldopam (corlopam) ___ (increases/decreases) SVR and renal vasculature resistance, resulting in ___ (increased/decreased) BP and ___ (increased/decreased) LVEF and RBF

A

Decreases SVR and renal vasculature resistance, resulting in decreased BP and increased LVEF and RBF

77
Q

What can occur if fenoldopam (corlopam) is titrated up too quickly?

A

Reflex tachycardia

78
Q

Fenoldopam (corlopam) is a last resort medication to treat severe ___

A

Hypertension

79
Q

Fenoldopam (corlopam) can be titrated quickly—T/F?

A

False—needs to be titrated very slowly otherwise you may have a lot of complications with BP/HR

80
Q

Fenoldopam (corlopam) can be given as a bolus—T/F?

A

False—do NOT bolus

81
Q

Fenoldopam (corlopam) preserves RBF, UO, and is renal protective—T/F?

A

False-ish—it does preserve RBF and UO, but it is NOT renal protective

82
Q

With slow titration of fenoldopam (corlopam), there is no increase in HR or arrhythmias—T/F?

A

True

83
Q

Side effects of fenoldopam (corlopam) include ___ache, ___ syndrome, sweating/flushing, nausea, ___ wave inversion, dizziness, and slight increase in ___

A

Headache, restless leg syndrome, sweating/flushing, nausea, T wave inversion, dizziness, and slight increase in IOP

84
Q

Hemodynamics summary—phenylephrine ___ (increases/decreases) PWP; ___ (increases/decreases/has no effect) on CO; ___ (increases/decreases) SVR; ___ (increases/decreases) MAP

A

Increases PWP; has no effect on CO; increases SVR; increases MAP

85
Q

Hemodynamics summary—norepinephrine ___ (increases/decreases) PWP; ___ (increases/decreases/has no effect) on CO; ___ (increases/decreases) SVR; ___ (increases/decreases) MAP

A

Increases PWP; has no effect on CO; increases SVR; increases MAP

86
Q

Hemodynamics summary—epinephrine ___ (increases/decreases) PWP; ___ (increases/decreases) CO; ___ (increases/decreases) SVR; ___ (increases/decreases) MAP

A

Decreases or increases PWP; increases CO; decreases or increases SVR; increases MAP

87
Q

Hemodynamics summary—dopamine ___ (increases/decreases) PWP; ___ (increases/decreases) CO; ___ (increases/decreases) SVR; ___ (increases/decreases) MAP

A

Increases PWP; increases CO; increases SVR; increases MAP

88
Q

Hemodynamics summary—dobutamine ___ (increases/decreases) PWP; ___ (increases/decreases) CO; ___ (increases/decreases) SVR; ___ (increases/decreases/has no effect) MAP

A

Decreases PWP; increases CO; decreases SVR; has no effect on MAP

89
Q

Hemodynamics summary—isoproterenol ___ (increases/decreases) PWP; ___ (increases/decreases) CO; ___ (increases/decreases) SVR; ___ (increases/decreases/has no effect) MAP

A

Decreases PWP; increases CO; decreases SVR; has no effect on MAP

90
Q

Phosphodiesterase breaks down ___, which stops the action of bringing ___ into the cell

A

Cyclic AMP, which stops the action of bringing calcium into the cell

91
Q

Phosphodiesterase inhibitors increase ___, resulting in continued ___ effects

A

Increase cAMP, resulting in continued calcium effects

92
Q

CAMP dependent positive inotropes are AKA phosphodiesterase ___ inhibitors

A

Phosphodiesterase 3 inhibitors

93
Q

Phosphodiesterase 3 inhibitors increase intracellular ___ concentrations; increase the ___ sensitivity of contractile proteins; increase ___ influx; peripherally, cause arterial and venous vaso___; results in increased ___

A

Increase intracellular cAMP concentrations; increase the Ca sensitivity of contractile proteins; increase Ca influx; peripherally, cause arterial and venous vasodilation; results in increased CO

94
Q

Inamrinone causes dose-dependent increases in ___ and ___ and decreases in ___ and ___ after CABG

A

Increases in SV and CI and decreases in SVR and PVR after CABG

95
Q

Inamrinone has proven to be more effective with fewer complications than dobutamine during separation from CPB—T/F?

A

True

96
Q

In patients with poor LV function, inamrinone is as effective as epi, but inamrinone and epi are superior to either drug alone—T/F?

A

True

97
Q

Adverse reactions/cautions with inamrinone—can cause ___ in 10% of patients; elevated ___; ___; do NOT administer to patients with ___; may aggravate outlet obstruction in patients with ___

A

Can cause thrombocytopenia in 10% of patients; elevated LFTs; arrhythmias; do NOT administer to patients with aortic stenosis (results in bad outcomes); may aggravate outlet obstruction in patients with idiopathic hypertrophic subaortic stenosis (IHSS)

98
Q

If patient has platelet count < 150K and is on inamrinone, how should you adjust the inamrinone dose?

A

Reduce inamrinone dose

99
Q

Milrinone (primacor) has inotropic and vasodilator properties similar to inamrinone, but it is ___-___ times more potent with a shorter half-life (___ hours) and without the risk of ___

A

15-20 times more potent with a shorter half-life (2.5 hours, so it would be completely out of someone’s system in ~12 hours) and without the risk of thrombocytopenia

100
Q

Loading dose of milrinone (primacor) is not really recommended if you are using it for a longer duration/going to be putting the patient on a milrinone infusion—T/F?

A

True

Can use loading dose of milrinone when separating the patient from CPB

101
Q

Milrinone side effects—___ache, ___tension, ___ope; ventricular ___ (~___%); increased ventricular response rate in ___ and ___

A

Headache, hypotension, syncope; ventricular arrhythmias (~10%); increased ventricular response rate in A-fib and A-flutter

102
Q

Glucagon acts at ___ receptor on the myocardium to increase ___

A

Glucagon receptor on the myocardium to increase cAMP

103
Q

Glucagon ___ (increases/decreases) CI, HR, BP and ___ (increases/decreases) SVR and LVEDP

A

Increases CI, HR, BP and decreases SVR and LVEDP

104
Q

Glucagon is useful in cardiac failure precipitated by ___

A

Beta blockade

105
Q

Glucagon use is limited due to side effects—___/___; increased ___; increased ___ and ___ vascular resistance

A

Nausea/vomiting; increase blood sugar; increase coronary and pulmonary vascular resistance

106
Q

Glucagon can be used to treat ___ and ___ toxicity

A

Beta blocker and CCB toxicity

107
Q

Glucagon drug interactions—___ medications enhance glucagon GI side effects (nausea/vomiting); ___ increase INR

A

Anticholinergic medications enhance glucagon GI side effects (nausea/vomiting); vitamin K antagonists (i.e.: warfarin) increase INR

108
Q

Digoxin is a ___

A

Cardiac glycoside

109
Q

Digoxin is a positive ___, negative ___, and negative ___

A

Positive inotrope (increases strength of contraction), negative dromotrope (decreases speed of conduction through AV node), and negative chronotrope (decreases HR)

110
Q

How does digoxin work? It inhibits ___; the reduced ___ gradient slows ___ removal

A

It inhibits Na+/K+ ATPase (3 Na+ out for 2 K+ in); the reduced Na gradient slows Ca removal (so more Ca stays inside the cardiac myocyte to improve contractility)

111
Q

Use of digoxin—positive inotrope for treatment of mild to moderate ___ (often used in combo with a ___ and ___); control of ventricular response rate in patients with chronic ___

A

Positive inotrope for treatment of mild to moderate heart failure (often used in combo with a diuretic and ACE inhibitor); control of ventricular response rate in patients with chronic AFib

112
Q

No clinical trials have demonstrated that digoxin improves mortality for patients with CHF—T/F?

A

True

113
Q

Patients with CHF on digoxin may experience less hospitalizations—T/F?

A

True

114
Q

Beta blockers/CCBs are much more effective at reducing heart rate than digoxin—T/F?

A

True

115
Q

Digoxin has a very narrow therapeutic range—___-___ ng/mL

A

0.8-2 ng/mL

116
Q

Digoxin toxicity can occur at plasma levels > ___ ng/mL

A

> 3 ng/mL

117
Q

Digoxin toxicity is associated with a decrease in intracellular ___

A

Potassium (because it is blocking the Na+/K+ ATPase pump)

118
Q

Predisposing causes of digoxin toxicity—___kalemia; ___magnesemia; ___emia; ___calcemia; ___thyroid

A

Hypokalemia; hypomagnesemia; hypoxemia; hypercalcemia; hypothyroid

119
Q

Digoxin toxicity presentation—early signs = ___, ___/___

A

Anorexia, nausea/vomiting

120
Q

What is the most common dysrhythmia associated with digoxin toxicity?

A

Paroxysmal atrial tachycardia with block

121
Q

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

A

VFib

122
Q

Treatment of dig toxicity—correct ___ causes; administer drugs—___ or ___ to suppress ventricular dysrhythmias; ___ to increase HR; ___ to suppress increased automaticity; temporary ___ if complete heart block is present

A

Correct predisposing causes (i.e.: electrolyte imbalances, hypoxemia); administer drugs—phenytoin or lidocaine to suppress ventricular dysrhythmias; atropine to increase HR; beta blocker to suppress increased automaticity; temporary pacing if complete heart block is present

123
Q

What is the antidote for digoxin?

A

Digibind

124
Q

How does digibind work?—___ bind to the drug and decrease plasma concentrations of cardiac glycosides

A

Fab (antibody fragments) bind to the drug

125
Q

Fab-digitalis complex is eliminated by the ___

A

Kidneys

126
Q

You should check digoxin levels shortly after administering digibind?—T/F?

A

False—do not check levels for several days

Patients with kidney failure will take several days to remove the digoxin/digibind complex from the body; if you check levels too early, you will still see high levels of digoxin because it hasn’t been removed from the body yet.

127
Q

When bound to digibind, digoxin is still active until the whole complex is removed by the kidneys—T/F?

A

False—digoxin becomes inactive when bound up by digibind

128
Q

Digoxin drug interactions—quinidine, amiodarone, verapamil, propafenone, coreg, cyclosporine, and conivaptan ___ (increase/decrease) clearance of digoxin

A

DECREASE clearance of digoxin (so would increase your risk of digoxin toxicity)

129
Q

Digoxin drug interactions—macrolides, PPIs, conazoles, ranolazine ___ (enhance/decrease) digoxin absorption

A

Enhance

130
Q

Digoxin drug interactions—resin binders, acarbose/miglitol, kaolin-pectins, reglan, sulfasalazine, and sucralfate ___ (enhance/decrease) digoxin absorption

A

Decrease

131
Q

Therapeutic plan for low cardiac output—goal is to optimize heart ___ and ___

A

Optimize heart rate and rhythm

132
Q

Therapeutic plan for low CO—first thing you want to do is optimize ___

A

Preload

Increase intravascular volume as long as these additions increase SV and don’t produce excessive increases in ventricular filling pressures that lead to pulmonary edema or myocardial ischemia

133
Q

Therapeutic plan for low CO—what medication class should you use to optimize preload?

A

Venous vasodilators (i.e.: nitroglycerine)

134
Q

Therapeutic plan for low CO—if BP is acceptable after increasing preload, administer an ___ dilator to increase SV (optimize ___); if further support is needed, add an ___; alternatively, can add an ino___

A

Administer an arteriolar dilator to increase SV (optimize afterload); if further support is needed, add an inotrope; alternatively, can add an inodilator (i.e.: inamrinone, milrinone, dobutamine)

135
Q

Therapeutic plan for low CO—for low BP, add an ___; once BP is acceptable, if SV is still depressed, add an ___ vasodilator; if SVR is low, add an ___

A

Inotrope; once BP is acceptable, if SV is still depressed, add an arteriolar vasodilator; if SVR is low, add an inoconstrictor (i.e.: norepi, epi, dopamine)

136
Q

Positive inotropes—initial drug selection—if patient has pulmonary and/or systemic HTN, use ___, ___ or ___, ___

A

Dobutamine, inamrinone or milrinone, or isoproterenol

137
Q

Positive inotropes—initial drug selection—if low SVR, use ___

A

Inoconstrictor—norepi, epi, dopamine

138
Q

Positive inotropes—initial drug selection—if normal PVR and SVR, can use ___ or ___

A

Dopamine or epi

139
Q

Positive inotropes—initial drug selection—if tachycardic, can use ___ or ___, ___, ___, ___

A

Can use inamrinone or milrinone, calcium, norepi, epi (epi is not really best choice for patient who is already tachycardic)

140
Q

Persistent low CO or myocardial ischemia with maximal medical therapy indicates the need for ___ or ___

A

IABP or LVAD

141
Q

ALARM-HF Trial—found there was ___ (lower/higher) mortality for patients receiving vasodilator + diuretic vs. diuretic alone

A

Lower mortality

7.6% mortality for vasodilator+diuretic vs. 14.2% mortality for diuretic alone

142
Q

ALARM-HF Trial—found there was ___ (lower/higher) mortality for IV inotropes vs. no inotropes

A

Higher mortality for IV inotropes vs. no inotropes

25.9% mortality for IV inotropes vs. 5.2% mortality for no inotropes

143
Q

ALARM-HF Trial—found there was a ___ fold increase in mortality for patients receiving dopamine or dobutamine; ___ fold increase in mortality for patients receiving NE or epi

A

1.5 fold increase in mortality for patients receiving dopamine or dobutamine; 2.5 fold increase in mortality for patients receiving NE or epi

144
Q

___ are great for HF patients

A

Vasodilators

145
Q

Inotropes increase mortality for HF patients—T/F?

A

True

146
Q

If patient has high pressures (PAOP/MAP), use a ___ to improve ___; can also remove fluid with a ___ to decrease high pressures

A

Use a venous vasodilator (i.e.: NTG) to improve preload; can also remove fluid with a diuretic to decrease high pressures

147
Q

If patient has low pressures (PAOP/MAP), use ___ if HR is normal; if HR is low, use ___ or ___

A

Use norepi if HR is normal; if HR is low, use dopamine or epi

KLowe Pharm 2 (10 decks)

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