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Neonatal Pharmacology > Cardiac > Flashcards

Cardiac Flashcards

1
Q

What is Preload?

A

Amount of pressure in heart at the end of diastole

or amount of blood distending the ventricles prior to the next contraction

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2
Q

What is Afterload?

A

Amount of pressure produced by the heart after contraction

or resistance to the outflow of blood-what the heart has to pump against

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3
Q

What does Inotropic affect?

A

Myocardial contractility

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4
Q

What does Chronotropic affect?

A 
Heart rate
(chrono=time)
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5
Q

What does Lusitropic affect?

A

Relaxation

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6
Q

What does a vasopressor affect?

A

Causes vasoconstriction–>Increase b/p

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7
Q

What does a vasodilator affect?

A

Causes vessels to dilate–>decreases SVR & lowers B/P

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8
Q

The autonomic nervous system has 2 parts, name them.

A

SNS-sympathetic

PNS-parasympathetic

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9
Q

Name the neurotransmitters in the SNS

A

Norepinephrine
Epinephrine
Dopamine

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10
Q

The sympathetic NS stimulates different ________ receptors depending on sructure

A

Adrenergic

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11
Q

Activation of the SNS produces _____ or _____ response

A

Fight or Flight

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12
Q

Alpha 1 receptors are present in?

A

Vascular beds

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13
Q

When activated, Alpha 1 receptors cause?

A

Vasoconstriction of arteries and veins (increased b/p)

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14
Q

Alpha 2 receptors are present on?

A

presynaptic nerve endings

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15
Q

What do Alpha 2 receptors do? (2 things)

A
  1. Inhibit presynaptic release of norepinephrine through feedback mechanism
  2. Decreases sympathetic outflow
    - –it regulates fight/flight response
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16
Q

Name the 7 types of Adrenergic receptors

A
  1. Alpha 1
  2. Alpha 2
  3. Beta 1
  4. Beta 2
  5. Dopaminergic
  6. Vasopressin 1
  7. Vasopressin 2
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17
Q

Where are Beta 1 receptors located?

A

Cardiac muscle

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18
Q

What do Beta 1 receptors do?

A 
Increase Heart Rate
Increase Contractility (inotropic effect)
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19
Q

Where are Beta 2 receptors located?

A

Bronchial muscle
Peripheral vasculature
Liver

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20
Q

What do Beta 2 receptors do?

A

Bronchodilate lungs
Vasodilate peripheral vasculature-(sometimes see this as s/e)
Increase glucose release from Liver

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21
Q

Where are Dopaminergic receptors located?

A

Kidneys & viscera

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22
Q

What do Dopaminergic receptors do?

A

Dilate arterioles in Renal and Splanchnic (mesenteric/splenic/hepatic beds) circulation.

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23
Q

Where are Vasopressin 1 receptors located?

A

Smooth muscle
Liver
Tissues

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24
Q

What do Vasopressin 1 recpetors do?

A

Cause vasoconstriction–> Increase b/p

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25
Q

Where are Vasopressin 2 receptors located?

A

Kidneys

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26
Q

What do Vasopressin 2 receptors do?

A

Increase water permeability and reabosption in the collecting tubules–> Increase b/p

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27
Q

True/False: Some medications actually have to touch the receptor to work (actual physical contact).

A

True

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28
Q

Name 2 Inotropes

A
  1. Dobutamine (Beta 1 activity)

2. Isoproterenol

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29
Q

Name 2 types of vasopressors/inotropes with mixed effects that act directly on the receptor.

A
  1. Dopamine

2. Epinephrine

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30
Q

True/False: the infant heart differs in how it responds to meds to tx CHF vs older child/adult

A

True

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31
Q

Why is an infant’s response to CHF meds different than child/adult? (2 things)

A

Limited response to Inotropes &

Electrolyte and metabolic reaction differences in their heart.

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32
Q

Why do infants have limited response to inotropes? (6 things)

A
  1. Immature heart
  2. Restricted functional reserve
  3. Lower ratio of active myofilaments to noncontractile elements
  4. Greater stiffness of ventricle
  5. Underdeveloped sympathetic nerves
  6. Higher CO per unit Surface Area
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33
Q

Name the Pure Inotropes used in NICU

A

Digoxin
Dobutamine
Milrinone
Isoproterenol

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34
Q

True/False: Digoxin has a very narrow therapeutic range

A

True

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35
Q

What are the MOA’s of Digoxin? (5 things)

A
  1. By inhibiting Na+/K+ ATPase pump
  2. Slows conduction through SA & AV nodes
  3. Decreases HR by increasing Vagal activity
  4. Decreases Cardiac filling pressures and capillary pressures
  5. Has anti-arrhythmic properties
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36
Q

When the Na+/K ATPase pump is inhibited, what does this cause?

A

Increased intracellular Na+ & Ca++

Increased Contractility

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37
Q

Why is there increased contractility with Digoxin?

A

The heart likes Ca++ to pump and there is increased intracellular Ca++

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38
Q

Digoxin is used to tx?

A

L-sided heart failure

Atrial fibrillation/flutter

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39
Q

Is Digoxin used to tx R-sided heart failure?

A

No

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40
Q

Are loading doses of Digoxin typically used?

A

No-d/t risk of toxicity

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41
Q

When might a loading dose of Digoxin be used?

What must be done with a Dig load?

A

Arrhythmias
Acute heart failure

Dose must be split

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42
Q

Are IV and PO Digoxin doses equivalent?

A

NO

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43
Q

With IV Digoxin, it’s given slowly over 5-10 min. What should the order include? Why?

A

HR cut off for holding dose.

Can be a tip off for toxicity.

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44
Q

Where is Digoxin absorbed?

A

GI

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45
Q

GI absorption of Digoxin is affected by?

A

Immature gut flora affected by:

  • Age
  • Feeding type
  • Drug therapy (i.e. acid suppression)
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46
Q

True/False: Because of immature gut flora in infants, there can be a reduction in the metabolism of Digoxin

A

True

Only 10% of Dig is metabolized by gut flora in adults

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47
Q

The distribution of Digoxin is Larger/Smaller in infants vs. adults?

A

Larger

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48
Q

Digoxin is Eliminated how?

A

Urine (active tubular secretion) via Renal P-glycoprotein

-monitor closely w/renal dysfunction

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49
Q

What does Renal P-glycoprotein do?

A

It’s a transporter involved in tubular secretion of drugs

***Drug-drug interactions possible: inhibitors & inducers—i.e. Dig (substrate) + Erythromycin (inhibitor)=increased Dig levels

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50
Q

When should Dig levels be checked? (5 things)

A
  1. Toxicity
  2. Accidental ingestions
  3. Renal Failure
  4. Compliance
  5. Absoprtion issues
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51
Q

What is the best time for Dig level?

A

Trough-right before next due dose.

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52
Q

What are EDLS?

A

Endogenous Digoxin-like substances. Sometimes found in infants.

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53
Q

What do EDLS do?

A

Interfere w/interpretation of serum concentrations

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54
Q

True/False: EDLS decrease with increasing GA?

A

True

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55
Q

What consideration to EDLS might you want to take?

A

Draw blood level before starting Dig therapy. Will tell you if EDLS present. If not, serum testing may be a useful guide.

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56
Q

What are the adverse effects of Dig?

A

Bradycardia, Ventricular arrhythmias, SA/AV block
Feeding intolerance
Hypokalemia potentiates Dig toxicity
Hyperkalemia w/Acute Dig toxicity

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57
Q

Besides K+, what other electrolytes can predispose infant to Dig toxcity?

A

Hypomagnesemia

Hypercalcemia

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58
Q

What drugs decrease the absorption of Dig?

A

Antiacids, Metoclopramide, Sucralfate

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59
Q

What drugs increase concentration of Dig?

A

Erythromycin, azithromycin, Amiodarone, Verapamil, Nifedepine, Spironolactone, Carvedilol

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60
Q

What drug causes decreased clearance of Dig?

A

Indomethacin (decreased GFR)

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61
Q

Dobutamine is a synthetic __________

So it does not what?

A

Catecholamine

Depend on release of endogenous catecholamines for it’s activity

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62
Q

Dobutamine primarily stimulates what receptors?

A

Beta 1

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63
Q

The Beta 1 action of Dobutamine causes what effects?

A

-Increases contractility and therefore CO
(positive inotrope)
-Little effect on HR (mild chronotropic effect)
-Increased Stroke Vol.
-Mild increase in myocardial O2 consumption

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64
Q

With Dobutamine, besides Beta 1 receptor action, what other receptors may have mild activity?

So what might you see?

A 
Beta 2 (vasodilation of periphery)
Alpha 1

Could see a little: hypertension, Increased SVR, b/c can have an opposite effect from Beta 1 with Alpha 1

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65
Q

Does Dobutamine cause increased U.O.? Why

A

Yes

Increased CO

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66
Q

Does Dobutamine increase SVR?

A

No, mild at high doses.

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67
Q

What situations is Dobutamine used for?

A

Shock, hypotension, congestive heart failure

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68
Q

What are the adverse effects of Dobutamine?

A
  • Tachycardia (monitor HR, B/P, C.O.)–use caution in pts w/A fib. (can see increased conduction)–
  • IV extravasation (not as severe since no Alpha effects)
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69
Q

Milrinone is a _________ inhibitor.

A

Phosphodiesterase (Ino-dilator)

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70
Q

Milrinone causes increased Ca++ entry into myocardial cells which causes increased ____________.

A

Contractility

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71
Q

Milrinone causes relaxation of ________ _____ & ___________ which reduces both preload and afterload (lusitropic effect)

A

Vascular muscle & Vasodilation

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72
Q

In what situations is Milrinone used?

A
  • Septic shock
  • Short-term for acute decompensated heart-failure
  • Low CO after surgery
  • Pulmonary Hypertension
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73
Q

Is a loading dose of Milrinone used?

A

No, d/t resulting increased b/p

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74
Q

Milrinone is ___________ eliminated.

A

Renally, so need to adjust the dose with dysfunction

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75
Q

What are the side effects of Milrinone?

A

Hypotension & Arrhythmias
Thrombocytopenia & Hepatotoxicity
Hypokalemia

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76
Q

What is an advantage of Milrinone?

A
  • Longer half-life than Dopa, Dobuta, etc

- Can just stop the drip (no wean usually needed)

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77
Q

Isoproterenol like Dobutamine is…?

A

Synthetic

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78
Q

Isoproterenol stimulates what receptors?

A

Beta 1 & Beta 2

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79
Q

Does Isoproterenol stimulate Alpha receptors?

A

No

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80
Q

The Beta 1 action of Isoproterenol causes an increase in? (3 things)

A

Rate of contraction (HR)
Force of contraction (Contractility)
Cardiac output

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81
Q

The stimulation of Beta 1 by Isoproterenol results in ____________ by Beta 2, causing what effects?

A 
Bronchodilation
Increased SBP
Increased CO
Decreaesed MAP
Decreased DBP
Increased myocardial consumption (increased HR)
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82
Q

In what situations might Isoproterenol be used?

A

Cardiac Shock
Post-heart transplant to increase CO
Emergency situations to stimulate heart

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83
Q

What are the adverse effects of Isoproterenol?

A
  • Tachycardia
  • Ventricular Arrhythmias
  • Systemic vasodilation–>decreased afterload & b/p, flushing
  • Hypoglycemia d/t blunting the B2 receptor
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84
Q

Name the 2 drugs that are both vasopressors and inotropes.

A

Dopamine

Epinephrine

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85
Q

Dopamine directly stimulates what receptors?

A

Dopaminergic
Beta
Alpha 1

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86
Q

Dopamine is a metabolic precursor which indirectly causes the release of ________ _________

A

Endogenous Norepinephrine

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87
Q

True/False: Dopamine has dose-dependent effects

A

True

88
Q

Low dose Dopamine 2-5 mcg has what effect?

So what might you see?

A

Dopaminergic (D1 & D2 receptors)

see increased renal perfusion; vasodilation of vascular beds: renal, mesenteric, coronary

89
Q

The Beta 1 effects of Dopamine do what at what dosing?

A

Increase contractility & HR

At moderate dosing 5-10 mcg/kg/min

90
Q

The Alpha 1 effects of Dopamine do what at what dosing?

A

Vasoconstriction–>increased SVR & b/p

>10mcg/kg/min

91
Q

Clearance of Dopamine is prolonged in what 2 situations?

A

Renal and Hepatic dysfunction

92
Q

What is the first-line agent for shock, hypoperfusion & hypotension?

Why?

A

Dopamine

Increases CO, B/P, peripheral perfusion, possibly U.O.

93
Q

What are some infant-specific issues r/t Dopamine?

A
  • May be less effective as Inotorope <6 mos
  • Vasoconstriction may occur at lower doses
  • Primary vasoconstriction vs effect on contractility (may have decreased perfusion to some organs)
94
Q

True/false: with Dopamine use it’s possible to get more Alpha effect when you thought you were getting more Beta effect.

A

True:

May see better b/p’s at a cost to other organs

95
Q

What are the adverse effects of Dopamine?

A

Tachycardia, hypertension, arrhythmias
Decreased peripheral perfusion w/high doses
IV infiltration: vasoconstriction, ischemia, necrosis, tissue shoughing

96
Q

With Dopamine infiltration what med is used to prevent further damage and block further Alpha effects?

How must it be given?

A

Phentolamine

Central line (no UAC)

97
Q

Epinephrine stimulates what receptors?

A

Alpha 1, Beta 1, Beta 2

receptor-mediated

98
Q

At low doses of Epinephrine, what receptors are effected?

So what is seen?

A

Beta 1 & 2
Increased HR & Contractility;
Decreased SVR, Bronchodilation

99
Q

At high doses of Epinephrine, what receptors are affected?

So what is seen?

A

Alpha 1

Increased SVR, MAP & myocardial oxygen demand

100
Q

Epinephrine is used for what 3 things?

A

Cardiac arrest
Bradycardia
Hypotension

101
Q

What are the adverse effects of Epinephrine?

A

Arrhythmias & Hypertension
Decreased peripheral, renal and gut perfusion
Hyperglycemia
IV infiltration: vasoconstriction, ischemia, necrosis, tissue sloughing

102
Q

If you have an IV infiltrate of Epinephrine, what medication is used?
How must it be given?

A

Phentolamine

Given via central line (not UAC)

103
Q

What is important to know about Epinephrine’s sensitivity and it’s expiration?

A

It is photosensitive (light sensitive)

Cover & expires in 3 days

104
Q

What is the T2 of Epinephrine?

A

Just a few minutes

105
Q

Epinehprine for cardiac resuscitation can be given in what 3 ways?

A

IV, IO, ETT

106
Q

Milrinone is an inotrope and also a __________. It can be used in 2 different ways “ino-dilator”

A

Vasodilator

So- if using for inotropic effects, don’t forget at high doses–>see decreased b/p in periphery

107
Q

How does Milrinone cause vasodilation?

A

Causes Ca++influx into the cells–> Vasodilation in the lungs (helps w/PPHN)

108
Q

What is the mechanism of action of Nitroprusside?

A

It is converted to Nitric Oxide

109
Q

Name the Vasodilator meds. (7 of them)

A 
Milrinone
Nitroprusside
Nitroglycerine
iNO
ACE Inhibitors
Angiotensin II blockers (ARB's)
Hydralazine
110
Q

Nitroprusside is a mixed ______-_______ vasodilator.

It has the following functions (4).

A

Mixed aterial-venous

  1. Decreased vascular resistance
  2. Increases CO
  3. Decreases preload and afterload
  4. Dilates coronary vasculature
111
Q

When is Nitroprusside used?

A

Hypertensive crisis
Afterload reduction in refractory CHF
ECMO

112
Q

What kind of toxicity can you have with Nitroprusside?

When might you suspect this?

A

Cyanide toxicity

Sudden tachyphylaxis and the drug is NOT working (increased SVO2 sats, metabolic acidosis–cyanide increases Lactate production)

113
Q

What are the adverse effects of Nitroprusside?

A

Profound hypotension

Thyroid suppression

114
Q

Does Nitroprusside work fast?

A

Yes, very fast & short duration of action

115
Q

When might you have increased risk of cyanide toxicity?

A

Renal or Hepatic dysfunction of if the infusion is used a long time (should only be temporarily used)

116
Q

What is the antedote for Cyanide posioning?

A

Sodium Thio-Sulfate–produces the metabolite cyanite (less toxic and able to be eliminated by the kidneys)

117
Q

How does Nitroglycerin work

A

Nitrate–>NO–>vascular smooth muschle relaxation

118
Q

What is the hemodynamic effect of Nitroglycerin?

A
  1. Dilate large veins–>pooling of blood/decreased preload
  2. Dilate coronary vasculature
  3. Decreased myocardial O2 consumption
119
Q

True/False: Nitroglycerin can be used topically to increase perfusion to ischemic tissue

A

True

120
Q

When is Nitroglycerin infusion used?

A

Low CO syndrome after cardiac surgery

121
Q

Does Nitroglycerin have more effect on veins or arteries?

A

VEINS

122
Q

What are the adverse reactions/side effects of Nitroglycerin?

A

Hypotension and reflux Tachycardia
Headache/flushing
Unwanted hypotension when used topically

123
Q

What should the RN/NNP do if applying topical Nitroglycerine to a pt?

A

Wear gloves! It can affect the person applying it too.

124
Q

iNO is a ________ ____________ drug used in what condition?

A

Pulmonary vasodilator

PPHN

125
Q

What is the MOA of ACE inhibitors?

A

Blocks the conversion of Angiotensin I to Angiogensin II (blocks systemic vasoconstriction)

126
Q

What are the hemodynamic effects of ACE inhibitors?

A

Decreases preload and afterload

Increases CO

127
Q

In what situations might an ACE inhibitor be used?

A

Hypertension
Afterload reduction in CHF
Neonatal renovascular HTN
Valvular Regurgitation

128
Q

If Angiotension II is produced, what is the result?

A

Increased Afterload and Aldosterone Secretion–>Increased Na+ & H2O retention–>Increased preload

129
Q

Name the ACE inhibitors mentioned in lecture (1 is PO, 1 IV)

A

Enalapril (PO)–prodrug hydrolyzes to active
enalaprilat
Enalaprilat (IV)

130
Q

With Enalapril and Enalaprilat is the dosing equivalent when switching modes?

A

NO
Watch mcg/mg!!!
It is a compound suspension

131
Q

Is captopril used frequently in NICU?
Does it have a shorter or longer T2 than enalapril? So,what might be seen?
Is it compounded?

A

NO
Shorter
Might see more b/p swings
Yes

132
Q

What are the adverse effects of ACE inhibitors? (6)

A
  1. Dry cough
  2. Maculopapular rash
  3. Hypotension
  4. Hyperkalemia
  5. Renal complications in pts w/renal aftery stenosis
  6. Teratogenic
133
Q

How so Angio II receptor blockers (ARB’s) work?

Are they used frequently in NICU?

A

Blockade of Angiotension I receptors

No

134
Q

Hydralazine is a direct ___________

It primarily affects ________

A

Vasodilator

Arteries

135
Q

When is Hydralazine used in NICU?
Can it be used PRN?
Is it available IV & PO?

A

Initially for HTN control
Yes–not long-term, will change to another drug
Yes

136
Q

Name the Anti-Arrhythmics. (3)

A

Beta-Blockers
Na+ Blockers
Other (Adenosine)

137
Q

What is the MOA of beta-blockers?

A

Blocks Epinephrine and Norepinephrine at Beta receptors–>Decreased: HR, CO, Contractility

138
Q

What are the adverse effects of Beta-blockers?

A

Bronchospasm (Beta 2 blockade)
Bradycardia (Beta 1 blockade)
Hypoglycemia (Beta 2 blockade)

139
Q

True/False: there are Selective Beta blockers and non-selective Beta blockers?

A

True
Beta 1 selective (cardio-selective)** with max doses can see B2 effects**
Non-selective (broad spectrum B1 & B2)

140
Q

Beta blockers have Intrinsic ____________ activity

A

sympathomimetic (ISA for short)

141
Q

What is ISA activity?

A
  • Small but significant Beta agonist effect (so get B blocker but also a little B agonist effect).
  • Good Antihypertension effects
  • Reduced side-effects (bradycardia)
142
Q

True/False: Some Beta-blockers have Alpha adrenergic blocking activity

A

True

143
Q

Name the Beta-blockers used in NICU

A

Propranalol

Esmolol

144
Q

Propranalol is a selective/non-selective beta blocker?

A

Non-selective (B1 & B2)

145
Q

What effects does Propranalol cause?

A
  • Decreased HR, myocardial contractility, B/P, & myocardial O2 demand
  • Negative Inotrope and Chronotrope
146
Q

What is Propranalol used for? (7 things)

A
  1. Hypertension
  2. A fib
  3. SVT
  4. V tachycardia
  5. TOF cyanotic spells
  6. Neonatal thryotoxicosis
  7. Hemangiomas
147
Q

What are the adverse effects of propranalol? (3)

A
  1. Hypoglycemia (usually seen 1st dose)
  2. Hypotension and Bradycardia
  3. Bronchospasm (non-specific B activity)
148
Q

Can you suddenly stop Propranalol?

A

No, gradual taper needed

149
Q

Esmolol is given via ___________ _____.

A

Continuous Drip

150
Q

Esmolol is used in what pts (though infrequently in NICU)

A

Post-op Cardiac Pts

151
Q

Name the 3 Na+ channel blockers in NICU

A

Procainamide
Propafenone
Flecainide

152
Q

Procainamide works by?

A

Depressing myocardial contractility by increasing electrical stimulation threashold of the ventricle (making the heart less excitable).

153
Q

Procainamide what type of drug?

A

Class 1A Antiarrhythmic w/Anticholinergic and local anesthetic effects

154
Q

When would you use reduced dosing?

A

Renal & Hepatic impairment

155
Q

When is Procainamide used?

A

Ventricular arrhythmias
A Fib
SVT

156
Q

What are s/e’s of Procainamide?

A
  • Prolonged Q-T, A-V block, hypotension

- Agranulocytosis, hemolytic anemia, neutropenia, thrombocytompenia

157
Q

What is important to monitor for when giving Procainamide?

A

Drug interactions (additive Q-T prolongation)

158
Q

How is Procainamide metabolized?

A

By acetylation in the liver–>N-acetyl procainamide (NAPA, an active metabolite)

159
Q

The half-life of Procainamide is dependent on?

A

Liver acetylator hpenotype, cardiac fxn, renal fxn (NAPA)

160
Q

How is Procainamide excreted?

A

Urine

161
Q

How is Procainamide monitored?

A

Procainamide levels in the blood

N-Acetyl procainamide (NAPA) levels

162
Q

Propafernone is a class _____ antiarrhythmic agent

A

1C

163
Q

How does Propafenone work?

A
  1. Blocks the fast inward Na+ current
  2. Slows the rate of increase of action potential
  3. Prolongs conduction and refractoriness
164
Q

When might Propafenone be used?

A

PO option for paroxysmal SVT

165
Q

How is the dosing of Propafeneone different from typical meds?

A

Dosed in meters squared, so must calculate it.

166
Q

Is propafenone compounded?

A

yes

167
Q

What are the s/e’s of Propafenone?

A

Prolonged QT interval (proarrhythmic)

Bradycardia, Hypotension

168
Q

What is important to monitor when giving Propafenone?

A

Drug interactions (cummulative QT prolongation)

169
Q

What type of pharmacokinetics is a/w Propafenone?

A

Nonlinear (d/t saturable kinetics profile)

-so might bump up dose a little and get 10-fold effect

170
Q

Is Flecainide the 1st line drug for SVT’s?

A

No, but has been used when other meds failed

171
Q

Flecainide is metabolized by?
Excreted unchanged in?
Can you measure serum levels?

A

Liver
Urine
Yes

172
Q

True/False: there are reports of decreased absorption of Flecainide w/dairy milk/infant formula feeds.

A

True

173
Q

Must Flecainide be compounded?

Is there an IV form?

A

yes

Not availble in U.S.

174
Q

What is the s/e of Flecainide?

A

proarrhythmic

175
Q

Adenosine works on what receptor?

Which is linked to what channels via the G-protein system?

A

A1 (Adenosine receptor)

linked to K+ channels

176
Q

What does Adenosine do?

A
  • Slows conduction time/re-entry pathwyas through A-V node

- Restores normal rhythm

177
Q

In what situations is Adenosine used?

A

Sustained paroxysmal SVT after no self-resolution & vagal maneuvers have been tried

178
Q

What is the T2 of Adenosine?

So give slow/fast?

A

1-5 seconds (<10 for sure)

Fast 1-2 seconds in line closest to heart, immediately flush with NS

179
Q

When monitoring baby getting Adenosine, what might bee seen briefly?

A

“flat line” when heart re-sets

180
Q

Name the Ca+ channel blocker meds used or hypertension. (2)

A
  1. Amlodipine

2. Nicardipine

181
Q

True/False: Amlodipine is compounded?

A

True

182
Q

Amlodipine is dosed either _____ or ___ x’s / day

A

1 or 2

183
Q

Is Amlodipine used often?

A

No, mainly in Renal pts.

184
Q

Nicardipine inhibits entry of Ca++ into the cardiac and smooth muscle causing:

A

Relaxation of coronary and vascular smooth muscle

Vasodilitation of coronary arteries (increases myocardial O2 delivery)

185
Q

When is Nicardipine used?

A

Hypertension

Arrhythmias

186
Q

What are the s/e’s of Nicardipine?

A

Flushing, Vasodilation, Palpitations, Hypotension, Headache

187
Q

Nicardipine is incompatibile w/what typical NICU meds?

A

Ampicillin
Cefepime
Furosemide

188
Q

Are drug interactions typical w/Nicardipine?

A

Yes, so check

189
Q

Like Propafenone, Nicardipine has what type of pharmacokinetics?

A

Saturable, (non-linear metabolism) so the longer the pt is on it, the longer the effect

190
Q

Name the Alpha 2 receptor Agonist

A

Clonidine

191
Q

Clonidine stimulates what receptors?

A

Central Alpha 2 receptors (feedback mechanism receptor)

192
Q

Clonidine is used for?

A

Centrally mediated HTN

Adjunct in NAS (can also help w/increased b/p in these pts)

193
Q

Can you abruptly stop Clonidine?

A

No, taper slowly to avoid rebound HTN

194
Q

Diuretics are used frequently in post-op period in what pts?

Why?

A

CHF

Decrease pulmonary edema
Maintain euvolemic state
Anti-hypertensive

195
Q

What are the 4 main classes of diuretics?

A

Loop (most common)
Thiazide
K+ sparing
Carbonic anhydrase inhibitors

196
Q

Thiazides and K+ -sparing diuretics act mainly where in the kidney?

A

Cortex of the kidney

197
Q

Loop diuretics act mainly where in the kidney?

A

Medulla

198
Q

Thiazides work by?

A

Inhibiting active exchange of Cl- & Na+ in cortical dilating segment of the ascending loop of Henle

199
Q

K+ sparing work by?

A

Inhibiting reabsorption of Na in the distal convoluted tubule and collecting duct

200
Q

Loop diuretics work by?

A

Inhibiting exchange of Cl-/Na+/K+ in the thick segment of the ascending loop of Henle

201
Q

Name the 2 most common Loop diuretics

A

Furosemide (lasix)

Bumetanide (Bumex)

202
Q

How much Na is reabsorbed int he ascending limb of the loop of henle w/Loop diuretics?

A

25-35%

203
Q

IV furosemide is ___ x’s as potent as IV dose

A

2 x’s

204
Q

Adverse effects of Loop diuretics?

A

1: Hypokalemia

  • Hypomagnesemia
  • Hypocalcemia (bad for bones)
  • Hyperuricemia
  • Nephrocalcinosis
  • Ototoxicity
  • Long-term: Osteopenia
205
Q

Name 2 Thiazide diuretics

A
  1. Hydrochlorothiazide

2. Chlorothiazide

206
Q

Thiazides act in the distal tubule to decrease reabsorption of?

A

Na+

207
Q

Thiazides have loose efficacy in what pts?

A

Renal dysfunction

208
Q

Thiazides might be used with what other type to obtain synergisitc diuretic effect?

A

Loop Diuretics

209
Q

Thiazides are typically used in neonates to decrease the risk of?

A

Nephrocalcinosis and Osteopenia seen w/Loop Diuretics

210
Q

What are the adverse effects of Thiazides?

A 
Hypokalemia
Hypomagnesemia
Hypercalcemia
Hyperglycemia
-Reduced vascular resistance due to both blood volume reduction &amp; relaxation of smooth muscle arterioles
211
Q

Which Thiazide is expensive?

A

Chlorothiazide

212
Q

Name a K+ sparing Diuretic

A

Spironolactone

213
Q

How does Spironolactone work?

A
  • Aldosterone antagonist
  • Competes w/receptor sites in distal renal tubules
  • Increasing Na+ & H2O excretion while preserving K+
214
Q

Are K+ sparing diuretics potent?

What might they be used with?

A

No

Might be used w/other diuretics to prevent excretion of K+

215
Q

What are the adverse effects of K+ sparing diuretics?

A

GI upset/nausea
Hyperkalemia
Lethargy

216
Q

Are K+ sparing diuretics compounded? Name?

A

Yes, Aldactazide

is Aldactone & Hydrochlorothiazide in equal amounts

Neonatal Pharmacology (17 decks)

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