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Pham II > Postive Inotropes > Flashcards

Postive Inotropes Flashcards

1
Q

What are the functions of Phosphodiesterase III Inhibitors?

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
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2
Q

What positive inotropes will worsen tachyarrythmias?

A

Isoproterenol

DA and Dobutamine

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3
Q

High doses of NE and Epi for long periods with low CO will __________ perfusion to many tissue beds and contribute to _______ __________.

A

decrease; renal failure

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4
Q

What population requires caution with the use of Digoxin?

A

Patients with hypokalemia, renal failure or a history of pre-op dig (because of the potential for toxicity)

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5
Q

When using Sympathomimetic drugs in combination with inhalation agents there is an increased potential for what complication? List meds lowest to highest

A

Arrhythmogenics

- Dobutamine<isoproterenol

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6
Q

What is the most potent activator of Alpha-1 receptors?

A

Epinephrine

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7
Q

What does Epi (Inoconstrictor) do?

A

It is a prototypical catecholamine, which stimulates Alpha-1, Beta-1 and Beta-2 receptors

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8
Q

Describe the pathway of cAMP Dependent Postive Inotropes

A
  • Catecholamines bind to beta receptors and activate a membrane-bound guanine nucleotide binding protein
  • this activates adenyl cyclase and generates cAMP
  • cAMP increases Ca influx via slow channels and increases Ca sensitivity of Ca regulatory proteins
  • Increase the force of contraction and velocity of relaxation
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9
Q

What effects occur with low doses (1-2mcg/min) of Epinephrine?

A

Beta-2 effects

  • essentially vasodillatory
  • stimulate Alpha-1 receptors in the skin, mucosa and hepatorenal system while Beta-2 receptors are stimulated in skeletal muscle
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10
Q

What are the Beta-2 effects of low dose Epi?

A
  • Beta-2 effects in peripheral vasculature predominate
    - the net effect is decreased SVR and distribution of blood to skeletal muscle
    - MAP remains essentially the same
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11
Q

What effects will you see with intermediate doses of Epi (2-10mcg/min)?

A

Beta-1

  • Inotrope
  • Increased HR, CO and contractility
  • increased automaticity, which may lead to PVCs in sensitized myocardium
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12
Q

What effects will you see with high dose Epi (>10mcg/min)?

A

Alpha-1

  • Potent vasoconstrictor including cutaneous, splachnic and renal vascular beds
  • used to maintain myocardial and cerebral perfusion (increases aortic dBP)
  • Reflex bradycardia can occur
  • Vasoconstriction
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13
Q

Epinephrine is used for. . .

A
  • continuous IV infusion to treat decreased myocardial contractility
  • SQ vasoconstriction with local anesthetics
  • Anaphylaxis treatment
  • refractory bradycardia (high spinal)
  • Cardiac arrest
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14
Q

What are the effects of Levophed (NE)?

A
  • Primarily an Alpha-1 agonist
  • Beta-1 effects are overshadowed by Alpha-1
  • Beta-2 effects are minimal
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15
Q

Low doses of Levophed do what to CO?

A

increase

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16
Q

Higher doses of Levophed do what to CO?

A

decrease CO, because of increased afterload and baroreceptor-mediated reflex bradycardia

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17
Q

How should Levophed be used for BP control?

A

Titrate dose to flow!!! Rather than a specific BP

-it is used IV to treat refractory hypotension

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18
Q

Levophed at 2mcg/min has what effects?

A

increases CO, may uncover Beta stimulation

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19
Q

Levophed at >3mcg/min has what effects?

A

Alpha-1 peripheral vasoconstriction, decrease CO

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20
Q

T/F Levophed binds more readily to Alphas and Beta-1 receptors than Beta-2

A

True

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21
Q

Which inotrope is better at increasing CO, epi or NE?

A

Epi

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22
Q

NE is used as a relative Beta-1 agonist when combined with what med, in order to counteract its potent Alpha-1 and 2 agonist activities?

A

Phentolamine

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23
Q

This is a synthetic catecholamine with structural characteristics of Dopamine and Isoproterenol?

A

Dobutamine (Dobutex)- inodilator

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24
Q

Dobutamine acts primarily on what receptors?

A

Beta-1 with small effects on Beta-2 and Alpha-1

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25
Q

What are the general effects of Dobutamine?

A

no significant vasoconstrictor activity
small increase in HR compared to isoproterenol
less likelihood of adverse increase in Mvo2
dilates coronary vasculature
No dopaminergic receptor activation (increases RBF by increasing CO)

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26
Q

At what doses of Dobutamine are patients predisposed to tachycardia and cardiac dysrhythmias?

A

> 10mcg/kg/min

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27
Q

Does Dobutamine have indirect effects?

A

No, Inotropic properties with less cardiac dysrhythmogenic activity
- have a dose dependent increase in CO and HR and decrease in filling pressure

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28
Q

Does Dobutamine alone increase BP in patients with decreased SVR?

A

maybe not, it is used with DA to increase SVR and UO

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29
Q

Dobutamine and Dopamine should be prepared in what way to prevent inactivation?

A

D5w

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30
Q

Isoproterenol works on what receptors?

A

Beta 1- Beta 2 (no Alphas)

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31
Q

What effects are seen with Isoproterenol?

A

increased HR, contractility, BP and cardiac automaticitiy
decreased SVR and dBP
net effect is increased CO and Decreased MAP
bronchodilator
tachycardia
increased Myocardial O2 consumption
increased incidence of cardiac dysrhythmias

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32
Q

T/F increase Isoproterenol’s use in patients with ischemic heart disease

A

False, decrease use

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33
Q

DOA of isoproterenol

A

onset <5 min
peak 15 min
duration 3 hours

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34
Q

What is Isoproterenol commonly used for?

A

Chemical pacemaker after heart transplant or in complete heart block
to attempt to decrease PVR in Pts with Pulmonary HTN and RV failure

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35
Q

Does D1:G coupled stimulate or inhibit adenylate cyclase alpha to activate cAMP?

A

stimulate- causing smooth muscle of blood vessels (vasodilation), naturesis, diuresis

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36
Q

Does D2:G coupled simulate or inhibit AC alpha to inhibit cAMP?

A

Inhibit- Presynaptic: inhibit NE release and promote vasodilation
-attenuate the beneficial effects o DA on renal blood flow

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37
Q

Dopamine has “dose dependent” effects: what are they?

A

0.5-3mcg/kg/min DA1 and DA2
3-10mcg/kg/min beta
10-20mcg/kg/min beta and alpha effects
>20mcg/kg/min alpha effects

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38
Q

T/F Dopamine increases RBF, GFR, Na+ excretion and UO, but is NOT renal protective (at 0.5-3mcg/kg/min)

A

True

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39
Q

Renal Dose Dopamine studies are based on pts. with sepsis or SIRS, what have these studies shown?

A

-renal dose is not predictable
tolerance seen after 2-48hours
no benefit for prevention of renal failure
DA blunts resp. drive
DA worsens splanchnic O2 and impairs GI function
necrosis with peripheral infiltrate

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40
Q

what are the hormonal effects of Renal dose DA?

A

increased renin counters the effects of DA
DA suppresses the endocrine system
DA may cause immunosuppression

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41
Q

Dopamine at 0.5-3mcg/kg/min effects. . .

A

DA1 stimulation producing vasodilation in the renal, mesentry, coronary, and cerebral arteries

  • inhibit secretion of aldosterone
  • has been used a lot during periods of renal stress
  • but is considered BAD MEDICINE
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42
Q

What are the effects of Dopamine at 2-20mcg/kg/min?

A

increased contractility and CO without changes in HR or BP

  • release of endogenous stores of NE which predisposes to dysrhythmias
  • Alpha receptor activation starting
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43
Q

At what doses do we start seeing an Indirect effect from DA?

A

> 5mcg/kg/min- which stimulates the release of NE

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44
Q

At 10-20mcg/kg/min of DA, what receptor effects are seen?

A

alpha and beta

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45
Q

At what doses of DA, do Alpha effects take over?

A

> 20mcg/kg/min

46
Q

When Dopamine is used, what is the patient presentation like?

A

Decreased CO and BP

Increased LVEDP

47
Q

T/F DA does not interfere with ventilator response of hypoxemia

A

False, it does interfere

48
Q

High doses of __________ inhibit the release of ________ causing hyperglycemia

A

Dopamine, insulin

49
Q

What are characteristics of Dopexamine (Dopacard)?

A

Inodilator
lacks direct alpha receptor agonist activity, but expressed Beta-2 and DA1 receptor activity
-inhibits presynaptic reuptake of NE (indirect inotropic activity)

50
Q

This med is as effective at increasing CI after CBP as Dopamine, but tachycardia is more common

A

Dopexamine

51
Q

What is Dopexamine used for?

A

Treating CHF when SVR is high

52
Q

How is Dopexamine dosed?

A

1-6mcg/kg/min

>4mcg/kg/min causes dose dependent tachycardia

53
Q

This selective D1 agonist is 10-100 times more potent than Dopamine, with moderate affinity for presynaptic Alpha-2 receptors

A

Fenoldopam (Corlopam)

54
Q

Characteristics of Fenoldopam. . .

A

It decreases SVR and renal vascular resistance resulting in decreased BP and increased LVEF and RBF

  • reflex tachycardia with rapid increases
  • dose related increase in RBF
55
Q

This med is as effective as SNP in controlling BP with the added benefit of increased RBF

A

Fenoldopam

56
Q

Fenoldopam should only be used for how long?

A

< 48 hours for severe HTN

57
Q

What are some benefits of Fenoldopam?

A 
rapid onset and offset (slower than SNP)
no Aline required
can use a peripheral IV
low doses (0.03-0.1mcg/kg/min) have less reflex tachycardia than initial higher doses
no coronary steal
58
Q

Adverse effects of Fenoldopam

A 
Does not prevent renal failure after contrast administration
hypokalemia can occur
high cost
dose related tachycardia
HA, RLS, sweating, nausea, Twave inversion, flushing, dizziness
Slight increase in ICP
ECG changes
mild tolerance after long infusion
59
Q

T/F Fenoldopam has negative inotropic/chronotropic effects

A

false- no negative

60
Q

This cAMP Dependent Positive Inoptrope slows the metabolism of cAMP to 5’-AMP increasing intracellular cAMP concentration

A

Phosphodiesterase III inhibitors

  • They also increase the Ca++ sensitivity of contractile proteins
  • increase Ca++ influx
  • Antagonize adenosine
61
Q

What are the different PDE inhibitors?

A

Inamrinone (Inocor)

Milrinone (Primacor)

62
Q

Characteristics of Inamrinone. . .

A

dose dependent increases in SV and CI- decreases in SVR and PVR after CABG

  • more effective with fewer complications than dobutamine during separation ffrom CPB
  • increases intrapulmonary shunting and decreases paO2
63
Q

In pts with poor LV function, _________ is as effective as Epi

A

Inamrinone

64
Q

What is the dosing of Inamrinone?

A

Loading dose- 0.75mg/kg IV over 2-3min
Infusion: 5-10mcg/kg/min
-may give an additional bolus 30min after starting therapy
max dose 10mg/kg

65
Q

What are the adverse reactions to Inamrinone?

A 
Thrombocytopenia (10%)
elevated LFTs
arrhythmias
CAN NOT use with pts with AS/PS
may aggrevate outlet obstruction in pts with IHSS
66
Q

What are the characteristics of Milrinone?

A

Inotropic and vasodilator properties similar to inamrinone
-shorter 1/2 life without risk of thrombocytopenia
loading dose: 50mcg/kg
-infusion 0.375-0.75mcg/kg/min
decreased dose in renal failure

67
Q

T/F Inamrinone is 15-20times more potent than Milrinone.

A

False, Milrinone is more potent

68
Q

What are the side effects of Milrinone?

A

HA, hypotension, syncope, ventricular arrhythmias, increased ventricular response to afib/flutter

69
Q

What class of drug is Glucagon?

A

cAMP Dependent Inotrope

70
Q

What receptor does Glucagon work on?

A

At a receptor other than Beta to increase cAMP

???? glucagon Receptor

71
Q

What are glucagon effects?

A

Increases CI, HR, BP while decreasing SVR and LVEDP

-good for use in Heart failure precipitated by beta blockade

72
Q

Side effects of Glucagon include. . .

A

N/V, increased BG, coronary and pulm. Vascular resistance

$$$costly

73
Q

what are the Natriuretic Peptides?

A

Brain Natriuretic Peptide (BNP)

Neseritide (Natrecor)

74
Q

Where is BNP synthesized?

A

in the atrium and released when overdistended

75
Q

Where is BNP Stored?

A

in the brain and excreted in response to venous congestion

76
Q

What are the effects of BNP?

A

promotes:

  • potent sodium excretion
  • diuresis
  • vasodilation
  • suppression of the R-A-A axis
  • lowers sympathetic tone
  • lowers the activation threshold of vagal afferents
  • inhibits secretion of vasopressin
77
Q

Neseritide stimulates _______ production resulting in vascular smooth muscle ____________.

A

cGMP; relaxation

78
Q

What is Neseritide used for and its dosing?

A

Acute decompensated CHF

  • 2mcg IV
  • 0.01-0.03mcg/kg/min IV
79
Q

This is a positive Inotrope for the treatment of mild to moderate heart failure

A

Digoxin

80
Q

Digoxin is often combined with ____ _________ and a ___________

A

ace inhibitor; diuretic

81
Q

Besides heart failure treatment what else is Digoxin used to treat?

A

control of ventricular rate with chronic a fib

82
Q

Digoxin has a cardiac glycoside profile which includes. . .

A

Positive inotrope
negative dromotrope
negative chronotrope

83
Q

Digoxin’s direct myocardial action inhibits _________ increasing intracellular _______ and indirectly intracellular _________.

A

Na-K ATPASE; Na; Ca

84
Q

In CHF what dose digoxin do to LV function and EF

A

Increases LV shortening and increases EF

85
Q

What is the Vagomimetic effect of Digoxin?

A

Indirect

-Slowing of the HR and decreased conduction velocity thru the AV node

86
Q

What is the Baroreceptor sensitization of Digoxin?

A

Neurohormonal deactivation

increased afferent inhibitory activity and decreased activity of the SNS and RAS for any given increment of MAP

87
Q

Digoxin toxicity is plasma levels. . .

A

> 3ng/ml

-associated with a decrease in intracellular K

88
Q

What are the predisposing causes for Digoxin toxicity?

A

hypokalemia
hypomagnesemia
hypoxemia

89
Q

what are causes of hypokalemia?

A

K+ wasting diuretics
diuresis after CPB
Alkalosis secondary to Mechanical ventilation

90
Q

What is the presentation of Digoxin toxicity?

A 
anorexia, N/V
PVCs
Paroxysmal atrial tachycardia with block (most common dysrhythmia)
mobitz type 2 av-block
v-fib
91
Q

How do you treat digoxin toxicity?

A

correct causes: K, Mag, hypoxemia
admin. of drugs: Phenytoin or lidocaine to suppress ventricular dysrhythmias
atropine to increase HR
BB to suppress increased automaticity
temporary pacing for complete heart block

92
Q

How is fab-digitalis complex eliminated?

A

kidneys- levels are useless to check for several days

93
Q

What drugs decrease clearance of digoxin?

A 
Quinidine
amiodarone
verapamil
propafenone
coreg
cyclosporine
conivaptan
94
Q

What drugs enhance digoxin absorption?

A

macrolides
PPIs
conazoles
ranolazine

95
Q

What drugs decrease digoxin absorption?

A 
resin binders
acarboes/miglitol
Kaolin-pectins
reglan
sulfasalazine
sucralate
96
Q

What are the benefits of calcium salts?

A

above the normal Ca level improves contractility of isolated cardiac muscle

  • ca increases SVR
  • INteracts with vasoactive drugs
  • Ca can inhibit Beta agonists by direct inhibition of AC
97
Q

Does Ca+ blousing have any consistent effect on CO coming off CPB?

A

NO-

98
Q

What are complications for Catecholamines?

A 
ischemia from SQ infiltration of inoconstrictors
increased MV02
enhance lipolysis and gluconeogenesis
alter electrolyte concentrations
override microvascular control mechanisms
alter distribution of CO
increase myocardial work
increase the risk of cardiac arrhythmias
99
Q

What is the therapeutic plan for low CO?

A

optimize HR and rhythm
optimize preload
increase SV (optimize afterload)

100
Q

If Bp is not optimal after increasing preload what can be done?

A

administer an arteriolar dilator to increase SV (optimize afterload)

  • may add an Inotrope
  • or add an inodilator
101
Q

If once BP is acceptable, but SV still depressed what can be added?

A

an Arteriolar vasodilator

102
Q

What drugs should be added for pts with Pulmonary &/or systemic HTN?

A

Dobutamine, inamrinone or milrinone, isoproternol

103
Q

What drugs should be added for pts with low SVR?

A

NE, DA, EPI

104
Q

What drugs should be added for pts with Normal PVR and SVR?

A

DA, Epi

105
Q

What drugs should be added for pts with tachycardia?

A

inamrinone or milrinone, calcium, NE, Epi

106
Q

Persistant low CO or MI with maximal medical therapy indicates the need for. . .

A

IABP or LVAD

107
Q

If your pt has MI, decreased BP and SVR, Normal CO without heart failure what should you use to treat them?

A

They are afterload INSENSITIVE

  • start vasoconstrictor (phenylephrine)
  • NTG
108
Q

If your pt has MI, decreased BP and SVR, Normal CO WITH heart failure what should you use to treat them?

A

They are afterload SENSITIVE

-Phenylephrine reverses the benefit of NTG to relieve ischemia

109
Q

Vasoconstrictors should be used with small hearts. . .

A

preload sensitive/afterload insensitive

110
Q

How do you treat a pt with low BP, MI and Low CO?

A

If not in SR convert, speed up bradycardia

111
Q

How should you treat a PCWP <18?

A

fluid challenge to volume expand

-increase SV, CO, and dBP (but increase LVEDP too)

112
Q

How should low SV and PCWP >18, in a pt with low CO and MI be treated?

A

Add vasodilator to improve SV and BP

  • Add inotrope to increase SV and CPP
  • if increased HR with inotropes or vasodilators add BBs

Pham II (1 decks)

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