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Board Review > IVDrugsFluidsAntidotesFC > Flashcards

IVDrugsFluidsAntidotesFC Flashcards

1
Q

What are the two main types of catheters?

A

Peripheral and central

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2
Q

How long is the peripheral catheter?

A

A few centimeters

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3
Q

Where is the peripheral catheter inserted?

A

through the skin into the peripheral vein, usually in the hand or arm.

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4
Q

Where is the central catheter inserted?

A

It is placed in a large vein (eg. subclavian, internal jugular, inferior vena cava) located in the chest, neck, or groin. The tip of the catheter sits in the vena cava.

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5
Q

What are the advantages of using a central IV line over a peripheral line?

A
  1. It can deliver fluids/medications that are overly irritating to peripheral veins
  2. Multiple parallel compartments (or lumens) within the catheter so multiple medications can be given at once. Larger volumes and rates of drugs
  3. Some central lines can measure central venous pressure and other hemodynamics (cardiac output, etc)
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6
Q

What are disadvantages to central lines?

A
  1. higher risks of bleeding
  2. infection
  3. thromboembolism
  4. more difficult to insert correctly
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7
Q

What is a commonly used central line?

A

Peripherally inserted central catheter (PICC line)

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8
Q

When are PICC lines best used?

A

They are used when access to the vein is required for a prolonged period of time or when the infused substance would damage a peripheral vein (eg patients that require long-term TPN or long courses of IV antibiotics)

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9
Q

What does PVC stand for?

A

Polyvinyl chloride

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10
Q

What are the two concerns with the use of PVC infusion bags?

A

Leaching and sorption

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11
Q

What does leaching mean?

A

Leaching means one substance is pulled from another, in this case, the primary concern is the leaching of diethylhexyl phthalate (DEHP) from PVC bags.

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12
Q

What does DEHP stand for?

A

diethylhexyl phthalate.

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13
Q

What is DEHP?

A

DEHP is a plasticizer used to make PVC bags softer and more flexible.

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14
Q

What effect does DEHP have shown in animal studies?

A

In animal studies, DEHP has been shown to adversely affect the male reproductive system. There is very little known data on humans.

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15
Q

What should be done with drugs known to cause leaching?

A

Put in non-PVC bags and use polyethylene-lined, non-DEHP administration tubing.

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16
Q

Drugs known to have leaching issues: (6)

A
  1. tacrolimus
  2. temsirolimus
  3. teniposide
  4. cabazitaxel
  5. docetaxel
  6. paclitaxel
    tic tac toe, craving delicious pho
  7. amiodarone
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17
Q

What does sorption mean?

A

Sorption means one substance pulls in another, in this case, the PVC bag pulls in some of the drug, which reduces the concentration of the drug in solution.

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18
Q

What should be done with drugs known to cause sorption?

A

pharmacists should use the newer polyolefine containers, which have reduced sorption and leaching potential. Occasionally, with some of these drugs, glass containers are used.

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19
Q

Drugs that cause sorption: (7)

A
  1. amiodarone (infusion >2 hours)
  2. carmustine
  3. lorazepam
  4. sufentanil
  5. thiopental
  6. regular human insulin
  7. nitroglycerin

ACLS TIN

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20
Q

What are intravenous fluids used to treat?

A
  1. hypoperfusion
  2. shock
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21
Q

What are 2 types of fluids?

A
  1. Crystalloids
  2. Colloids
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22
Q

What does crystalloids consist of?

A
  1. Salt solution (NS, 1/2 or 1/4 NS with or without KCl, and hypertonic saline solutions (3%, 7.5%, 23.4%))
  2. Lactate Ringer’s
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23
Q

True or False: After crystalloids administration, only about 25% of the volume in the solution will remain intravascular 30 minutes after administration.

A

true

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24
Q

True or false Crystalloids can be isotonic (0.9% NaCl), hypertonic (3% NaCl), or hypotonic (0.45% NaCl)

A

TRUE

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25
Q

What can a hypertonic solution be used to treat?

A

Hyponatremia or intracranial hypertension (elevated intracerebral pressures from trauma or non-traumatic causes).

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26
Q

How should hypertonic solution be administered? (peripheral or central)

A

Central

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27
Q

Do colloids freely diffuse across a semi-permeable membrane?

A

No, in doing so it keeps the fluid within the intravascular space.

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28
Q

(Colloids or crystalloids) are used to increase the osmotic pressure in patients and are substantially more expensive than (colloids or crystalloids).

A

Colloids are used to increase the osmotic pressure in patients and are substantially more expensive than crystalloids.

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29
Q

What are in colloids?

A

Colloids includes albumin 5% and 25%, hetastarch 6%, pentastarch 10%, dextran and others.

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30
Q

True or false: Crystalloids and colloids cannot be used for fluid resuscitation.

A

False. Crystalloids and colloids can be used for fluid resuscitation.

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31
Q

(Smaller or larger) volume of crystalloids are needed to adequately resuscitate patients with shock as compared to colloids.

A

Larger volume.

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32
Q

What risk factors are associated with the use of colloids?

A

Hypersensitivity reactions and bleedings disorders.

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33
Q

What are crystalloids used for?

A

Crystalloids are used for maintaining fluid status and keeping the IV lines open.

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34
Q

What causes shock syndrome?

A

Shock results from a lack of oxygen due to hypoperfusion.

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35
Q

What are signs of shock?

A

hypotension, or low blood pressure (SBP <90 mmHg)

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36
Q

What are the 4 main types of shock?

A
  1. Hypovolemic (hemorrhagic)
  2. Cardiogenic
  3. Distributive (septic)
  4. Obstructive (massive pulmonary embolism)
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37
Q

How are pts with hypovolemic shock treated?

A
  1. First line is colloids or crystalloids (fluid resuscitation)
  2. Vasopressors may be used if the pt does not respond to fluid challenge. (Vasopressors will not be effective without adequate fluid administration - at least 30 mL/kg)
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38
Q

How are pts with cardiogenic shock treated?

A

Vasopressors or ionotropes

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39
Q

How are pts with sepsis shock treated?

A
  1. Colloids or crystalloids
  2. Vasopressors
    and/or
  3. Inotropes
  4. Antibiotics
  5. Corticosteroids
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40
Q

How do inotropes work?

A

By increasing contractility either through beta-adrenergic stimulation or through inhibition of phosphodiesterase. These mechanisms lead to an increase in cardiac output (CO).

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41
Q

How do vasopressors work?

A

Vasoconstriction and thereby increasing systemic vascular resistance (SVR)

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42
Q

List inotropes used in shock syndromes.

A
  1. Dobutamine
  2. Milrinone
  3. Dopamine
  4. Epinephrine (Adrenalin)
  5. Norepinephrine (Levophed)
  6. Phenylephrine (Neo-synephrine)
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43
Q

List vasopressors used in shock syndrome.

A

Vasopressin (Pitressin)

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44
Q

What medical emergency may occur with the use of vasopressors/inotropes?

A

Extravasation (leakage of IV into surrounding tissue) may lead to tissue damage or necrosis.

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45
Q

What drug has antagonist effects on norepinephrine?

A

phentolamine (Regitine) for Extravasation

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46
Q

How is phentolamine taken?

A

Dilute 5-10 mg of phentolamine in 10 mL in NS and give SC to infiltrated area.
Blanching should reverse immediately.

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47
Q

Sedation/analgesia is commonly used for patients in the ICU, particularly if the patient is receiving _________ __________.

A

Mechanical ventilation

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48
Q

Why is sedation/analgesia used in mechanically ventilated pts?

A
  1. Limit anxiety and agitation.
  2. Maintain synchronized breathing (prevent “bucking” the ventilator).
  3. Keep pt free of pain and suffering.
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49
Q

What agents are used for ICU sedation and analgesia?

A

Combination of:
1. Opioids (morphine, hydromorephone, and fentanyl)
2. Benzodiazepines (midazolam, lorazepam)
3. Antipsychotics (haloperidol, quetiapine, risperidone)
4. Hypnotics (propofol, dexmedetomidine)

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50
Q

True or False: It’s generally NOT recommended to administer and optimize analgesia first.

A

False.

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51
Q

What opioid is preferred drug for achieving rapid analgesia?

A

Fentanyl

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52
Q

Which drugs are recommended for sedation?

A

Benzodiazepines and propofol

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53
Q

Which drug is preferred for rapid achievement of sedation?

A

Midazolam

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54
Q

Which drug is preferred for procedural sedation and rapid awakening?

A

Propofol

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55
Q

How is benzodiazepine administered?

A

intermittent bolus doses or by continuous infusion.

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56
Q

How is propofol administered?

A

Continuous infusion

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57
Q

Care should be taken to limit the dose and duration of propofol due to the risk of propofol-related infusion syndrome, which can result in________ ____________ and _________.

A

cardiac arrhythmias and death.

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58
Q

Dexmedetomidine has been studied as an alternative to the traditional sedative agent. It shown to produce (more/less) sedation, and (more/less) sleep-like state.

A

Dexmedetomidine shown to produce less sedation, and more sleep-like state.

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59
Q

What are the advantage and disadvantage of Dexmedetomidine to benzodiazepines and propofol.

A

Advantages of dexmedetomidine:
- fewer days of mechanical ventilation
- less incidence of delirium

Disadvantages of dexmedetomidine:
- more expensive than benzodiazepines and propofol.

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60
Q

How frequent are pts monitored?

A

generally every 2-3 hours

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61
Q

Why are daily interruptions of continuous infusions of sedative drugs recommended?

A

to limit the duration of mechanical ventilation, doses of drugs administered, and length of ICU stay

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62
Q

How is delirium assessed?

A

Using the Confusion Assessment Method (or CAM-ICU)

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63
Q

How is delirium treated in the ICU?

A

antipsychotics (haloperidol)

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64
Q

Lorazepam brand name drugs used in ICU

A

Ativan, Lorazepam Intensol

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65
Q

Lorazepam side effects

A

Respiratory depression, oversedation, hypotension

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66
Q

Lorazepam monitoring

A

BP, HR, sedation scale

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67
Q

Lorazepam price

A

Inexpensive

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68
Q

when to use lorazepam over midazolam

A

Used for long-term sedation (>48 hours)
No active metabolite
Longer t1/2 than midazolam

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69
Q

midazolam side effects

A

Respiratory depression, oversedation, hypotesion

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70
Q

midazolam contraindications

A

Use small, initial doses in elderly (e.g. 1 mg, not to exceed 2.5 mg).

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71
Q

why avoid rapid administration with midazolam

A

Contains benzyl alcohol, avoid rapid injection or prolonged infusion

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72
Q

midazolam monitoring

A

BP, HR, sedation scale

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73
Q

midazolam DDI / renal interaction

A

many drug interaction (major 3A4 substrate)
increase levels with 3A4 inhibitors
active metabolite accumulates in renal failure

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74
Q

when to use midazolam over lorazepam

A

use for short-term sedation (<48 hours), shorter acting than lorazepam if pt has preserved organ function (no hepatic or renal impairment or CHF)
drug is highly lipophilic and may accumulate in obese pts
active metabolite accumulates in renal dysfunction

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75
Q

Propofol brand name drug

A

Diprivan

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76
Q

Propofol dosing ICU

A

MD: 5-80 mcg/kg/min

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77
Q

Propofol side effects

A

hypotension, apnea
hypertriglyceridemia
green urine
-propofol-related infusion syndrome (PRIS-rare but can be fatal)

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78
Q

Propofol monitoring

A

BP
respiration
-triglycerides (if on longer than 2 days)
signs and symptoms of pancreatitis
sedation scale

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79
Q

Propofol how to handle? When to throw out vial? What type of filter to use? What if the emulsion separates, what do you do?

A

Shake well before use
use strict aseptic technique due to potential for bacterial growth
-Discard vial and tubing within 12 hours of use.
Do not use if there is separation of phases in the emulsion.
-Do not use filter of <5 micron for administration

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80
Q

propofol formulation consistency

A

Formulated in 10% lipid emulsion (provides 1.1 kcal/mL)

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81
Q

Fospropofol brand name drug

A

Lusedra

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82
Q

Fospropfol controlled substance class

A

C IV

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83
Q

Fospropofol side effects

A

Paresthesias, pruritus, hypotension

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84
Q

Fospropofol monitoring

A

BP, respiration, patient responsiveness

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85
Q

Fospropofol MOA

A

Prodrug of propofol; delayed onset due to need for conversion to active metabolite.

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86
Q

dexmedetomidine brand name drug

A

Precedex

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87
Q

dexmedetomidine drug class MOA

A

alpha2-adrenergic agonist

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88
Q

dexmedetomidine Fluid compatibility

A

Mix with NS only

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89
Q

dexmedetomidine side effects

A

transient hypertension during loading dose (may need to decrease infusion rate)
hypotension
bradycardia
dry mouth

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90
Q

dexmedetomidine monitoring

A

BP, HR, sedation scale

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91
Q

dexmedetomidine, what is the sedation like and for which patients it used for?

A

Used for sedation in intubated and non-intubated patients
Pts are arousable and alert when simulated

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92
Q

max infusion time for precedex

A

-*Duration of infusion should not exceed 24 hours

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93
Q

advantage of precedex

A

Does not cause respiratory depression

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94
Q

Morphine dosing

A

LD: 2-4 mg IV push
MD: 2-30 mg/hr

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95
Q

Morphine side effects

A

respiratory depression
hypotension
oversedation
bradycardia
pruritus
xerostomia
constipation
others

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96
Q

Morphine monitoring

A

BP, HR, respiratory status, sedation/pain scale

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97
Q

Why is renal funciton to mx with morhpine?

A

-*Has an active metabolite (morphine-6-glucuronide) which can accumulate in renal impairment
causes a histamine release (hypotension)
preferred agent in Pts who are hemodynamically stable

98
Q

Fentanyl dosing

A

LD: 25-50 mcg IV push
MD: 0.7-10 mcg/kg/hr

99
Q

Fentanyl side effects

A

respiratory depression
bradycardia
oversedation
constipation
rigidity with high doses

100
Q

Fentanyl monitoring

A

BP, HR, respiratory status, sedation/pain scale

101
Q

Fentanyl advantages

A

-*Less hypotension than morphine due to no histamine release
Fast onset of action and short duration of action
-100x more potent than morphine
preferred agent in Pts with unstable hemodynamics

102
Q

Hydromorphone brand name drug

A

Dilaudid

103
Q

Hydromorphone dosing

A

LD: 0.2-0.6 mg IV push
MD: 0.5-3 mg/hr

104
Q

Hydromorphone side effects

A

respiratory depression, oversedation, high potential for abuse

105
Q

Hydromorphone monitoring

A

Breathing rate, HR, respiratory status, sedation/pain scale

106
Q

Hydromorphone notes

A

No active metabolites; not commonly used for ICU sedation

107
Q

Remifentanil brand name drug

A

Ultiva

108
Q

Remifentanil monitoring

A

Breathing rate, HR, respiratory status, sedation/pain scale

109
Q

Remifentanil advantage

A

Metabolized by tissue esterases, no accumulation

110
Q

Haloperidol brand name drug

A

Haldol

111
Q

Haloperidol dosing

A

2-10 mg IV push
may repeat Q15-30 minutes until calm,

then administer 25% of last dose Q6h

112
Q

Haloperidol side effects

A

hypotension
QT prolongation
Tachycardia
Extrapyramidal symptoms (EPS)
Anticholinergic effects
Neuroleptic malignant syndrome
others

113
Q

Haloperidol monitoring

A

QT interval and ECG
EPS
Abnormal involuntary movement
Vital signs

114
Q

Haloperidol hw not to administer

A

Not to be given via continuous infusion

115
Q

Normal pH of blood is:

A

7.4 (range 7.35-7.45)

116
Q

What is the primary buffering system of the body?

A

Bicarbonate/carbonic acid system

117
Q

What organ help maintain a neutral pH by controlling bicarbonate (HCO3-) resorption and elimination?

A

kidney

118
Q

What is normal bicarbonate level?

A

24 mEq/L (range 22-26)

119
Q

Which organ help maintain a neutral pH by controlling carbonic acid?

A

Lung

120
Q

What is the normal partial pressure of carbon dioxide?

A

40 mmHg (range 35-45 mmHg)

121
Q

Bicarbonate acts as a buffer and as (a base/an acid), whereas carbon dioxide acts as a buffer and (a base/an acid).

A

Bicarbonate acts as a buffer and as a base, whereas carbon dioxide acts as a buffer and an acid.

122
Q

True or False: Alterations from the normal values lead to acid-base disorders.

A

TRUE

123
Q

What lead to a large production of H ion that needs to be excreted to maintain acid-base balance?

A

Diet and cellular meteabolism

124
Q

What can determine acid-base status of a pt?

A

arterial blood gas (ABG)

125
Q

pH < 7.35 is called:

A

acidosis

126
Q

pH >7.45 is called:

A

alkalosis

127
Q

Acidosis and alkalosis can be classified as:

A

metabolic or respiratory in origin

128
Q

How does metabolic acidosis present?

A

low plasma bicarbonate (HCO3-) and may have increased anion gap (>12)

129
Q

How is anion gap calculated?

A

AG = Na - (Cl- + HCO3-)

130
Q

How does metabolic alkalosis present?

A

high plasma bicarbonate (HCO3-)

131
Q

How does respiratory acidosis present?

A

high PaCO2

132
Q

How does respiratory alkalosis present?

A

low PaCO2

133
Q

What are the etiologies of metabolic acidosis non-elevated anion gap?

A

renal tubular acidosis, diarrhea
administration of acidic substance

134
Q

What are the etiologies of metabolic acidosis elevated anion gap?

A

cyanide
uremia
toluene
ethanol (alcholic ketoacidosis)
diabetic ketoacidosis
isoniazid
methanol
propylene glycol
lactic acidosis
ethylene
salicylates

CUTE DIMPLES

135
Q

What are the etiologies of metabolic alkalosis?

A

loop and thiazide diuretics
high doses of penicillins
vomiting
cystic fibrosis

136
Q

What are the etiologies for respiratory acidosis?

A

opioids
sedatives
anesthetics
stroke
asthma/COPD

137
Q

What are the etiologies for respiratory alkalosis

A

pain
fever
brain tumors
salicylates
catecholamines
theophylline

138
Q

What is used to treat metabolic acidosis to raise pH to >/= 7.2

A

sodium bicarbonate

139
Q

True or False: Treating pts with metabolic acidosis with sodium bicarb has no benefit in morbidity and mortality compared to general supportive care.

A

TRUE

140
Q

What is used in severe metabolic alkalosis?

A

hydrochloric acid, however it’s very rare.

141
Q

What is normal sodium concentration in blood?

A

135-145 mEq/L

142
Q

What serum osmolality is sodium maintained?

A

275-290 mOsm/kg H20. Changes in serum sodium are usually from changes in water concentration.

143
Q

How is hyponatremia defined?

A

Na <135 mEq/L

144
Q

What etiologies causes hypertonic hyponatremia?

A

hyperglycemia
or
use of hypertonic solutions that Do not contain sodium.

145
Q

What etiologies causes hypotonic hyponatremia?

A

hyperlipidemia

146
Q

What are the etiologies for hypovolemia hypotonic hyponatremia?

A

diuretic usesalt-wasting syndromes
adrenal insufficiency
blood loss
vomiting/diarrhea

147
Q

How is hypovolemia hypotonic hyponatremia treated?

A

Correct the underlying cause and to administer saline solutions.
3% NaCl is preferred if Na <120 mEq/L or if severe symptoms are present.

148
Q

What are the etiologies for hypervolemic hypotonic hyponatremia?

A

fluid overload (usually with cirrhosis, heart failure, or renal failure)

149
Q

How is hypervolemic hypotonic hyponatremia treated?

A

diuresis with fluid restriction is usually preferred to treat this type of hyponatremia

150
Q

What are the etiologies for isovolemic (euvolemic) hypotonic hyponatremia?

A

Syndrome of inappropriate antidiuretic hormone (SIADH)
THis results in the normal excretion of sodium with impaired free-water excretion by the kidney.

151
Q

What does SIADH stand for?

A

Syndrome of inappropriate antidiuretic hormone

152
Q

How is SIADH treated?

A

directed to water restriction, and in some cases diuresis.
Conivaptan (Vaprisol) and tolvaptan (Samsca) may be used.

153
Q

What is the mechanism of action of conivaptan and tolvaptan?

A

They antagonize arginine vasopressin receptors (vasopressin V2=receptor antagonists), resulting in excretion of free water and maitenance of sodium.

154
Q

What group of people should conivaptan and tolvaptan be used in caution and avoided?

A

pts with heart failure and should be avoided in pts with hypotension or hypovolemia.

155
Q

Conivaptan brand name drug

A

Vaprisol

156
Q

Conivaptan dose

A

LD: 20 mg IV over 30 minutes; followed by 20 mg IV continuous infusion over 24 hours (0.83 mg/hr).
Do not exceed 4 days

157
Q

Conivaptan contraindications?

A

allergy to corn/corn products
use in hypovolemic hyponatremia
-concurrent use with strong 3A4 inhibitors
anuria

158
Q

Conivaptan side effects

A

orthostatic hypotension
fever
hypokalemia
hyponatremia

159
Q

Conivaptan monitoring

A

rate of serum Na increase
BP
volume status
urine output

160
Q

Tolvaptan brand name

A

Samsca

161
Q

Tolvaptan dosing

A

15 mg PO daily
Max 60 mg PO daily

162
Q

Tolvaptan Black Box Warning

A

Should be initiated and re-initated in a hospital under close monitoring of serum Na+

163
Q

what is the limit of sodium correction for hyponatremia and what could happen?

A

Too rapid correction of hyponatremia (>12 mEq/L/24 hours) can be life-threatening

164
Q

Tolvaptan contraindications

A

Do not use in pts who are
unable to sense or respond appropriatedly to thirst
hypovolemic hyponatremia
-concurrent use with strong 3A4 inhibitors
anuria

165
Q

Tolvaptan side effects

A

thirst
dry mouth
asthenia
constipation
pollakiuria
poyluria
hyperglycemia

166
Q

Tolvaptan monitoring

A

rate of serum Na increase
BP
volume status
urine output

167
Q

Define hypernatremia.

A

Na>145 mEq/L associated with a water deficity and hypertonicity.

168
Q

What cause hypovolemic hypernatremia?

A

Dehydration
vomiting
diarrhea

169
Q

How is hypovolemic hypernatremia usually treated?

A

-Hypotonic solution (0.45% NaCl)
Dextrose (to replace free water deficit)

170
Q

What cause hypervolemic hypernatremia?

A

administration of hypertonic solution

171
Q

How is hypervolemic hypernatremia treated?

A

Diuresis
-5% dextrose

172
Q

What cause isovolemic (euvolemic) hypernatremia?

A

Diabetes insipidus (DI)

173
Q

What are the two types of diabetes insipidus?

A

Central (impaired release of antidiuretic hormone)
Nephrogenic (impaired response to antidiuretic hormone)

174
Q

How is central diabetes insipidus treated?

A

Desmopressin (IV or SC)

175
Q

How is nephrogenic diabetes insipidus treated?

A

Remove any causative medications
HTCZ or indomethacin

176
Q

True or False: Caution should be taken in treating patients with sodium disorders to prevent correcting too slowly.

A

False.

177
Q

what happens if your correct the sodium too quickly ?

A

Caution should be taken in treating patients with sodium disorders to prevent correcting too QUICKLY.
Corrections of sodium >12 mEq/L over 24 have been associated with central pontine myelinosis, which may lead to quadriparesis, seizures, and death.

178
Q

What is normal potassium level?

A

K = 3.5 - 5 mEq/L

179
Q

Define hyperkalemia.

A

Depending on the source it may be defined as a K level above 5.3 or above 5.5 mEq/L, although most clinicians are concerned with any level above 5 mEq/L

180
Q

Where is most potassium found? Intracellular or extracellular?

A

Intracellular.

181
Q

What drugs causes potassium excretion to increase?

A

Aldosterone
diuretics (strongly by loops, weakly by thiazides)

182
Q

What does insult do to potassium?

A

Shift potassium into cells.

183
Q

What is the most common cause of hyperkalemia?

A

Decreased renal excretion due to renal failure.

184
Q

What drugs cause potassium to increase in serum?

A

Potassium-sparing diuretics
ACEis
ARBs
NSAIDS
Oral Contraceptives containing drospirenones (Yaz)
Cyclosporine
Tacrolimus
Heparin
Pentamidine
Trimethoprim/sulfamethoxazole
Potassium supplements

185
Q

Symptoms of hyperkalemia

A

Elevated potassium may be asymptomatic or symptomatic depending on the level.
Muscle weakness
bradycardia
fatal arrhythmia

186
Q

True or False: ECG may be needed to check for cardiotoxicity (monitor heart rhythm).

A

TRUE

187
Q

_______ _______ is administered to stablize the cardiac tissue if there is ECG abnormalities.

A

IV Calcium

188
Q

How is potassium lowered?

A
  1. Glucose and/or insulin
  2. Beta-agonists (such as nebulized albuterol)
  3. Loop diuretic, such as furosemide
  4. fluidrocortisone (Florinef)
  5. Cation exchange resin, sodium polystyrene sulfonate (SPS) (Kayexelate)
  6. Emergency dialysis
  7. Sodium bicarbonate, if metabolic acidosis is present.
189
Q

How does does glucose decrease potassium?

A

Increase insulin. Insulin pushes potassium into cells.

190
Q

What is beta-agonists monitor parameters?

A

Tachycardia
Chest pain

191
Q

What is loop diuretic monitor parameter?

A

Volume status

192
Q

What kind of pts fludrocortison (Florinef) is best used for to decrease potassium?

A

pts with hypoaldosteronism

193
Q

How long does it take for Kayexelate take to work?

A

within 2 hours

194
Q

How much can a single enema of Kayexelate decrease potassium?

A

by 2 mEq/L

195
Q

SPS (Kayexelate) route of administration.

A

Rectal or oral

196
Q

What route of administration is preferred for high treatment (emergency)?

A

rectal

197
Q

What should SPS (Kayexelate) not be mixed with?

A

Sorbitol due to risk of GI necrosis

198
Q

SPS (Kayexelate) side effects

A

decrease appetite
Nausea
vomiting
or
constipation (less commonly diarrhea)

199
Q

What does SPS stand for?

A

Sodium PolystyreneSulfonate

200
Q

Define hypokalemia

A

K < 3.5 mEq/L

201
Q

Hypokalemia management

A

Treat underlying cause (e.g. metabolic alkalosis, overdiuresis)
Administer oral or IV potassium

202
Q

When administering potassium for hypokalemia, which route (oral, IV) is preferred?

A

Oral

203
Q

IV potassium should be administered no more than ___ - ___ mEq/hr with intermittent doses.

A

10-20 mEq/hr

204
Q

Concentrations > ____ mEq/L should be administered through a central line.

A

80 mEq/L

205
Q

Pts with critical illness have reduced blood flow to the gut as blood flow is diverted to the major organs of the body. This results in: (3)

A

breakdown of gastric mucosal defense mechanisms including:
1. Prostaglandin synthesis
2. bicarbonate production
3. cell turnover

206
Q

Which drugs are recommended for stress ulcer prophylaxis?

A

-Histamine 2-receptor antagonist (H2RAs)
Proton pump inhibitors (PPIs)

207
Q

What are the risk factors for H2RAs

A

Thrombocytopenia
-Mental status change (esp in pts >65 yrs c liver and kidney impairment)
Tachyphylaxis

208
Q

What are the risk factors for PPIs

A

Nosocomial pneumonia
GI infections (c. dif)

209
Q

non-pharmacologic therapy for VTE prophylaxis

A

Intermittent pneumatic compression (IPC)
Graduated compression stockings (GCS)
Venous foot pump (VFP)

210
Q

Low dose unfractionated heparin dose

A

5,000 units SC BID or TID

211
Q

LMWH dose

A

-30 mg SC BID
-40 mg SC daily

Crcl < 30 mL/min
-30 mg SC daily

212
Q

(LMWH) Dalteparin dose

A

2,500 - 5,000 units SC daily

213
Q

Factor Xa inhitors

A

Fondaparinux
Rivaroxaban

214
Q

Fondaparinux dose

A

2.5 mg SC daily

Avoid in pts CrCl < 30 or pts weights < 50 kg

215
Q

Rivaroxaban dose

A

10 mg PO daily
Avoid in pts with CrCl < 30 mL/min

216
Q

Route of administration for anesthetics

A

Topical
Inhaled
IV
Epidural
Spinal

217
Q

Main side effects of anesthetics

A

hypotension
bradycardia
Nausea
vomiting
Mild drop in body temperature that cause shivering

218
Q

Inhaled anesthetics can cause __________ __________ (rare)

A

Malignant hyperthermia

219
Q

How is malignant hyperthermia treated

A

Dantrolene

220
Q

If anesthetics are given too much or too high of a dose, it may cause _________ _________ and ________ _________.

A

respiratory depression and cardiac arrest

221
Q

Commonly used anesthetics: (Topical: 2; Inhaled: 4; Injectable: 3)

A

Topical: Lidocaine, Benzacaine
Inhaled: Isofurane, sevofurane, desofurane, nitrous oxide, others

Injectable: bupivacine, lidocaine, ropivacaine, others

222
Q

Bupivacine brand name drug

A

Marcaine
Sensorcaine

223
Q

Lidocaine brand name drug

A

Xylocaine

224
Q

Ropivacine brand name drug

A

Naropin

225
Q

True or false: Epidurals containing bupivacaine can quickly be fatal if given via IV route.

A

TRUE

226
Q

When is neuromuscular blocking agents used?

A
  1. Facilitate mechanical intubation
  2. Manage increased intracranial pressure
  3. Treat muscle spasm (tetany)
  4. Prevent shivering in pts undergoing therapeutic hypothermia after cardiac arrest
227
Q

True or false: NMBAs are first line in critically ill pts

A

False.
NMBAs is typically recommended when other methods have been proven ineffective and are not to be routinely used in critically ill pts.

228
Q

True or false: NMBAs provide sedation or analgesia.

A

FALSE

229
Q

True or false: Pts should receive NMBAs prior to additional sedation and analgesia.

A

False. Pts should receive adequate sedation and analgesia PRIOR to starting a NMBA.

230
Q

Pts must be _________ _________ as these agents ________ the _________.

A

Pts must be mechanically ventilated as these agents paralyze the diaphragm.

231
Q

True or False: NMBAs are considered high risk medications by ISMP.

A

TRUE

232
Q

NMBAs should be labeled with bright red auxiliary labels stating: WARNING, _____________ _________.

A

Paralyzing agent

233
Q

What are the two types of NMBAs

A

depolarizing and non-depolarizing

234
Q

The only depolarizing agent is:

A

Succinylcholine, which is typically reserved for intubation and not used for continuous neuromuscular blockade.

235
Q

Succinylcholine has been rarely associated with causing __________ ___________.

A

Malignant hyperthermia (particularly with inhaled anesthetics

236
Q

Depolarizing NMBA mechanism of action

A

Succinylcholine resembles acetylcholine. It binds to and activates the acetylcholine receptors and desensitizes them.

237
Q

Non-depolarizing NMBAs mechanism of action

A

Bind to acetylcholine receptor and block the action of endogenous acetylcholine

238
Q

Non-depolarizing NMBA side effects

A

Flushing
bradycardia
hypotension
Tachyphylaxis

Long term use
Acute quadriplegic myopathy syndrome (ACMS)

239
Q

Examples of nondepolarizing NMBAs

A

Atracurium
Cisatracurium
Pancuronium
Rocuronium
Vecuronium

240
Q

Cisatracurium brand name

A

Nimbrex

241
Q

Rocuronium brand name

A

Zemuron

Board Review (65 decks)

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