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NAPLEX Review > Acute & Critical Care Medicine > Flashcards

Acute & Critical Care Medicine Flashcards

1
Q

What are IV fluids used for?

A

IV fluids are used to replace fluid losses and treat various conditions

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2
Q

What are the two categories of IV fluids?

A

Crystalloids or colloids

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3
Q

What are crystalloids?

A

Crystalloids contain various concentrations of sodium and/or dextrose that pass freely between semipermeable membranes

*Most of the administered volume does not remain in the intravascular space (inside the blood vessels) but moves into the extravascular space or interstitial space

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4
Q

What are some benefits of using crystalloids?

A
  • Crystalloids are less costly and generally have fewer adverse reactions than colloids
  • Some data suggest that balanced solutions may be preferred in certain disease states like sepsis, as the chloride load from sodium chloride can be high enough to contribute to cell injury, including renal damage in ICU patients
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5
Q

What are colloids?

A

Colloids are large molecules (typically protein or starch) dispersed in solutions that primarily remain in the intravascular space and increase oncotic pressure

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6
Q

What is a benefit of colloids?

A

Colloids provide greater intravascular volume expansion than equal volumes of crystalloids

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7
Q

What is the downside of colloids?

A

Colloids are more expensive and have not shown clear clinical benefit over crystalloids

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8
Q

What are some examples of crystalloids?

A

5% dextrose (D5W), 0.9% NaCl (normal saline), Lactated Ringer’s (LR), Multiple electrolyte injection

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9
Q

What are some examples of colloids?

A

Albumin 5%, 25%, Dextran, Hydroxyethyl starch

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10
Q

When are dextrose-containing products used?

A

When water is needed intracellularly, as these products contain “free water”

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11
Q

What are Lactated Ringer’s and normal saline used for?

A

Lactated Ringer’s and normal saline are the most common fluids used for volume resuscitation in shock states

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12
Q

When is albumin most useful?

A

Albumin is the most commonly used colloid and is particularly useful when there is significant edema

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13
Q

When should albumin not be used?

A

Albumin should not be used for nutritional supplementation when serum albumin is low

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14
Q

What is the boxed warning with hydroxyethyl starch?

A

Hydroxyethyl starch use is limited secondary to its boxed warning to avoid use in critical illness (including sepsis) due to mortality and renal injury

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15
Q

What is the definition of hyponatremia?

A

Na < 135 mEq/L

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16
Q

When are patients typically symptomatic from hyponatremia?

A

It is usually not symptomatic until the sodium is < 120 mEq/L, unless the serum level falls rapidly

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17
Q

What are the causes of hypotonic hypovolemic hyponatremia?

A

Hypotonic hypovolemic hyponatremia can be caused by diuretics, salt-wasting syndromes, adrenal insufficiency, blood loss or vomiting/diarrhea

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18
Q

What is the treatment to correct hypotonic hypovolemic hyponatremia?

A

Administer sodium chloride IV solutions

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19
Q

What is the cause of hypotonic hypervolemic hyponatremia?

A

Fluid overload (e.g. cirrhosis, heart failure or renal failure)

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20
Q

What is the preferred treatment of hypotonic hypervolemic hyponatremia?

A

Diuresis with fluid restriction is the preferred treatment

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21
Q

What is the cause of hypotonic isovolemic (euvolemic) hyponatremia?

A

Hypotonic isovolemic hyponatremia can be caused by the syndrome of inappropriate antidiuretic hormone (SIADH)

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22
Q

What is the treatment of hypotonic isovolemic hyponatremia?

A

Treatment includes stopping drugs that can induce SIADH, diuresis or restricting fluids

*Demeclocycline can be used off-label for SIADH

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23
Q

What can happen if you rapidly correct sodium?

A

Correcting sodium more rapidly than 12 mEq/L over 24 hours can cause osmotic demyelination syndrome or central pontine myelinolysis, which can cause paralysis, seizures and death

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24
Q

What is the role of desmopressin in correcting sodium?

A

Administration of desmopressin reduces water diuresis and can help avoid overcorrection

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25
Q

What can be used to treat SIAH and hypervolemic hyponatremia?

A

The arginine vasopressin (AVP) receptor antagonists (conivaptan and tolvaptan) may be used to treat SIADH and hypervolemic hyponatremia

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26
Q

How does AVP receptor antagonists work?

A

They increase excretion of free water while maintaining sodium

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27
Q

What is the downside of AVP receptor antagonists?

A

The role of these drugs is still being determined, as they are more expensive than 3% saline and use beyond 30 days with the oral product, tolvaptan, is not recommended

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28
Q

What are examples of arginine vasopressin receptor antagonists?

A

Conivaptan, Tolvaptan

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29
Q

What is a contraindication of conivaptan?

A

Hypovolemic hyponatremia, concurrent use with strong CYP3A4 inhibitors, anuria

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30
Q

What is a warning with conivaptan?

A

Overly rapid correction of hyponatremia is associated with ODS

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31
Q

What are some side effects of conivaptan?

A

Orthostatic hypotension, fever, hypokalemia, infusion site reactions (>60%)

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32
Q

What do you need to monitor when using conivaptan?

A

Rate of Na increase, BP, volume status, urine output

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33
Q

What are the boxed warnings of Tolvaptan?

A
  • Should be initiated and re-initiated in a hospital under close monitoring of serum Na
  • Overly rapid correction of hyponatremia is associated with ODS (consider slower correction with severe malnutrition, alcoholism or advanced liver disease
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34
Q

What are some contraindications to tolvaptan?

A

Patients who are unable to sense or respond appropriately to thirst, urgent need to raise Na, hypovolemic hyponatremia, use with strong CYP3A4 inhibitors, anuria

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35
Q

What is a warning associated with Tolvaptan?

A

Hepatotoxicity (avoid use > 30 days and in liver disease/cirrhosis)

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36
Q

What are some side effects of Tolvaptan?

A

Thirst, nausea, dry mouth, polyuria, weakness, hyperglycemia, hypernatremia

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37
Q

What are some monitoring parameters of Tolvaptan?

A

Rate of Na increase, BP, volume status, urine output, signs of drug-induced hepatotoxicity

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38
Q

What is hypernatremia?

A

Hypernatremia (Na > 145 mEq/L) is associated with a water deficit and hypertonicity

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39
Q

What is hypovolemic hypernatremia caused by?

A

Dehydration, vomiting, or diarrhea

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40
Q

How do you treat hypovolemic hypernatremia?

A

Fluids

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41
Q

What are the causes of hypervolemic hypernatremia?

A

Intake of hypertonic fluids

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42
Q

How is hypervolemic hypernatremia treated?

A

Diuresis

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43
Q

What is the cause of isovolemic (euvolemic) hypernatremia?

A

Diabetes insipidus which can decrease antidiuretic hormone

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44
Q

How is isovolemic hypernatremia treated?

A

With desmopressin

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45
Q

What is a common cause of hyperkalemia?

A

Chronic kidney disease

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46
Q

What is hypokalemia?

A

Hypokalemia, or K < 3.5 mEq/L, is a common occurrence in hospitalized patients

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47
Q

What is the general management of hypokalemia?

A

Management includes treating the underlying causes (metabolic alkalosis, overdiuresis and some medications such as amphotericin and insulin) and administering oral or IV potassium

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48
Q

What is the general rule of thumb in potassium deficit?

A

A drop of 1 mEq/L in serum K below 3.5 mEq/L represents a total body deficit of 100-400 meQ

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49
Q

What is generally used for potassium replacement?

A

Potassium chloride premixed IVs are generally used for IV replacement

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50
Q

What are the safe recommendations for IV potassium replacement through a peripheral line?

A

Safe recommendations for IV potassium replacement through a peripheral line include a maximum infusion rate < 10 mEq/hr and a maximum concentration of 10 mEq/100 mL

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51
Q

When are rapid infusions and higher concentrations of potassium warranted?

A

In severe or symptomatic hypokalemia

*these require a central line and cardiac monitoring

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52
Q

When can IV potassium be fatal?

A

If administered undiluted or IV push

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53
Q

What should be checked if hypokalemia is resistant to treatment and why?

A

Serum Mg should be checked becuase magnesium is necessary for potassium uptake so hypomagnesemia can worsen or prevent correction of hypokalemia

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54
Q

What should be replaced first when hypokalemia and hypomagnesemia are present?

A

Magnesium

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55
Q

What is hypomagnesemia?

A

Mg < 1.3 mEq/L

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56
Q

What are common causes of hypomagnesemia?

A

Chronic alcohol use, diuretics, vomiting and diarrhea

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57
Q

What is the most common cause of hypermagnesemia?

A

Renal insufficiency

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58
Q

When is IV replacement of magnesium recommended?

A

When serum Mg is <1 mEq/L with life-threatening symptoms (e.g. seizure, arrhythmias), IV replacement is recommended

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59
Q

What is used for IV replacement of magnesium?

A

Magnesium sulfate

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60
Q

What is recommended when serum Mg < 1 mEq/L without life-threatening symtpoms?

A

Therapy can be administered IV or IM

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61
Q

What is recommended when serum Mg is > 1 mEq/L and <1.5 mEq/L?

A

Magnesium is replaced orally, most commonly with magnesium oxide

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62
Q

How long should magnesium replacement regimens be?

A

Magnesium replacement regimens should continue for 5 days to fully replace body stores

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63
Q

What is a common cause of hypophosphatemia?

A

Chronic kidney disease

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64
Q

What is hypophosphatemia?

A

Hypophosphatemia is considered severe and is usually symptomatic when serum phosphate (PO4) is usually < 1 mg/dL

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65
Q

What are some symptoms of hypophosphatemia?

A

Symptoms can include muscle weakness and respiratory failure

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66
Q

What are some causes of hypophosphatemia?

A

Hypophosphatemia can be caused by phosphate-binding drugs (calcium, sevelamer, antacids), chronic alcohol intake and hyperparathyroidism

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67
Q

What is recommended when serum PO4 is < 1 mg/dL?

A

When serum PO4 is < 1 mg/dL, IV phosphorus is used for replacement

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68
Q

What is a common regimen for phosphorus replacement?

A

0.08-0.16 mmol/kg in 500 mL of NS or D5W over 6 hours

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69
Q

How long does full replacement of severe hypophosphatemia take?

A

Full replacement often takes one week or longer

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70
Q

What is intravenous immune globulin?

A

Intravenous immune globulin (IVIG or IGIV) contains pooled immunoglobulin (IgG) that is administered intravenously

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71
Q

How is IgG extracted?

A

IgG is extracted from the plasma of a thousand or more blood donors

*typically the IVIG is derived from between 3000-10000 donors

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72
Q

What is IVIG used for?

A

IVIG is given as plasma protein replacement therapy for immune-deficient patients who have decreased or abolished antibody production capabilities

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73
Q

What are some indications of IVIG?

A
  • immunodeficiency conditions

- off label: multiple sclerosis, myasthenia gravis, Guillain-Barre syndrome

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74
Q

What can IVIG impair the response to?

A

Vaccines

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75
Q

What is the boxed warning of IVIG?

A
  • Acute renal dysfunction can occur (rare) and has been associated with fatalities; it usually occurs within 7 days (more likely with products stabilized with sucrose)
  • Use caution in the elderly, renal disease, diabetes, volume depletion, sepsis, paraproteinemia and those taking nephrotoxic medications
  • Thrombosis can occur even without risk factors (for patients at risk, administer the minimum dose)
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76
Q

What are contraindications of IVIG?

A

IgA deficiency (can use product with lowest amount of IgA)

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77
Q

What is a warning about use of IVIG?

A

Use with caution in CV disease (use isotonic products and low infusion rate)

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78
Q

What are some side effects associated with IVIG?

A

Headache, nausea, diarrhea, injection site reaction, infusion reaction (facial flushing, chest tightness, fever, chills, hypotension) - slow/stop infusion, renal failure or blood dycrasias (both rare)

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79
Q

What are some monitoring parameters of IVIG?

A

Renal function, urine output, volume status, Hgb

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80
Q

What are some counseling points of IVIG?

A
  • Patients that should be asked about past IVIG infusions, including product used and any reactions that occurred; slow titration and premedication may be used
  • Lot numbers of administered IVIG products must be tracked (it is a blood product)
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81
Q

What is APACHE II and what is it used for?

A

The Acute Physiologic Assessment and Chronic Health Evaluation II is a scoring tool used to determine prognosis and estimate ICU mortality risk

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82
Q

How do vasopressors work?

A

Most vasopressors work by stimulating alpha receptors, which causes vasoconstriction and increases systemic vascular resistance which increases BP

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83
Q

What are some examples of vasopressors?

A

Dopamine, Epinephrine, Norepinephrine, Phenylephrine, Vasopressin

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84
Q

How does phenylephrine work?

A

Phenylephrine is a pure alpha-agonist that increases SVR without increasing HR

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85
Q

How does epinephrine and norepinephrine work?

A

Epinephrine and norepinephrine are mixed alpha- and beta- agonists, causing both an increase in SVR as well as an increase in CO and HR

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86
Q

When would you use dopamine?

A

Dopamine is a natural precursor of norepinephrine and is recommended for use in symptomatic bradycardia

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87
Q

How does vasopressin work?

A

Vasopressin acts directly on vasopressin receptors

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88
Q

How does Angiotensin II work?

A

Angiotensin II, approved for septic and distributive shock, raises blood pressure by vasoconstriction and aldosterone release, which results in sodium and water retention

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89
Q

What is a boxed warning of dopamine and norepinephrine?

A

Dopamine and norepinephrine have a boxed warning regarding extravasation; all vesicants when administered IV; treat extravasation with phentolamine

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90
Q

What are some warnings associated with dopamine, epinephrine and norepinephrine?

A

Use extreme caution in patients taking an MAO inhibitor; prolonged hypertension may result

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91
Q

What are some side effects of vasopressors?

A

Arrhythmias, tachycardia (especially dopamine, epinephrine), necrosis (gangrene), bradycardia (phenylephrine), hyperglycemia (epinephrine), tachyphylaxis, peripheral and gut ischemia

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92
Q

What are monitoring parameters for vasopressors?

A

Continuous BP monitoring (with continuous infusions), HR, mean arterial pressure (MAP), ECG, urine output, infusion site for extravasation

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93
Q

What are some important counseling points about vasopressors?

A
  • Solutions should not be used if they are discolored or contain a precipitate
  • All vasopressors are Y-site compatible with each other except angiotensin II
  • Some institutions use non-weight based infusions (mcg/min) instead of weight-based infusions (mcg/kg/min)
  • All vasopressors should be administered via central IV line
  • No clear evidence that low dose dopamine (renal dosing) provides benefit
  • Epinephrine used for IV push is 0.1 mg/mL (1:10,000 ratio strength); epinephrine used for IM injection or compounding IV products is 1 mg/mL (1:1,000 ratio strength); ratio strength has been removed from labeling per the FDA
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94
Q

What can vesicants cause?

A

Vesicants can cause severe tissue damage/necrosis with extravasation

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95
Q

What is extravasation?

A

Leakage of drug from the blood vessel into the surrounding tissue (medical emergency)

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96
Q

How do you reduce the risk of extravasation?

A

To reduce the risk, every attempt should be made to infuse vasopressors through a central line

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97
Q

How do you treat vasopressor extravasation?

A

Treat extravasation with phentolamine, an alpha-1 blocker that antagonizes the effects of the vasopressor

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98
Q

What should you use if extravasation occurs with norepinephrine, epinephrine or phenylephrine?

A
  • Stop the infusion but do not disconnect the needle/cannula and do not flush the line
  • Gently aspirate (remove) the drug
99
Q

What is an alternative to phentolamine?

A

Nitroglycerin ointment is sometimes used topically (off-label) as an alternative if phentolamine is unavailable

100
Q

What are some examples of vasodilators?

A

Nitroglycerin and Nitroprusside

101
Q

What is something that needs to be monitored when using IV vasodilators?

A

Frequent or continuous BP monitoring is required when using IV vasodilators, and the dose must be decreased if there is hypotension or worsening renal function

102
Q

When is nitroglycerin typically used?

A

Nitroglycerin is often used when there is active myocardial ischemia or uncontrolled hypertension, but effectiveness may be limited to 24-48 hours due to tachyphylaxis (tolerance)

103
Q

What is Nitroprusside?

A

Nitroprusside is a mixed (equal) arterial and venous vasodilator at all doses and has greater effect on BP than nitroglycerin

104
Q

Why should nitroprusside not be used in active myocardial ischemia?

A

It should not be used in active myocardial ischemia because it can cause blood to be diverted away from the diseased coronary arteries (“coronary steal”)

105
Q

What does the metabolism of nitroprusside result in?

A

The metabolism of nitroprusside results in thiocyanate and cyanide formation, which can cause toxicity (especially in renal and hepatic insufficiency, respectively)

106
Q

What can Hydroxocobalamin be used for?

A

Hydroxocobalamin can be administered to reduce the risk of thiocyanate toxicity or to treat cyanide toxicity

107
Q

What is something that can be used for cyanide toxicity?

A

Sodium thiosulfate and sodium nitrite (Nithiodote)

108
Q

What is a contraindication of Nitroglycerin?

A

SBP < 90 mmHg, use with PDE-5 inhibitors or riociguat

109
Q

What are some warnings associated with Nitroglycerin?

A

Severe hypotension and increased intracranial pressure

110
Q

What are some monitoring parameters of Nitroglycerin?

A

BP, HR

111
Q

What is an important note about Nitroglycerin?

A

Requires non-PVC container; use administration sets (tubing) intended for NTG

112
Q

What is the boxed warning associated with Nitroprusside?

A

Metabolism produces cyanide (uses the lowest dose for the shortest duration necessary), excessive hypotension (continuous BP monitoring required), not for direct injection (must be further diluted; D5W preferred)

113
Q

What is a warning associated with Nitroprusside?

A

Increases ICP

114
Q

What are some side effects of Nitroprusside?

A

Headache, tachycardia, thiocyanate/cyanide toxicity (risk increase in renal and hepatic impairment)

115
Q

What are some monitoring parameters of Nitroprusside?

A

BP (continuous), HR, renal/hepatic function, urine output, thiocyanate/cyanide toxicity, acid-base status, venous oxygen concentration

116
Q

What are some notes associated with Nitroprusside?

A

Requires light protection during administration; use only clear solutions, a blue color indicates degradation to cyanide - do not use

117
Q

How do inotropes work?

A

Inotropes increase the contractility of the heart

118
Q

What is the MOA of Dobutamine?

A

Dobutamine is a beta-1 agonist that increases HR and force of contraction, which increases CO

*Has weak beta-2 (vasodilation) and alpha-1 agonist activity

119
Q

What is the MOA of Milrinone?

A

Milrinone is a selective phosphodiesterase-3 inhibitor in cardiac and vascular tissue and produces inotropic effects with significant vasodilation

120
Q

When should Dobutamine and Milrinone be used?

A

Dobutamine and Milrinone should only be sed when BP is adequate because they produce vasodilation

121
Q

What are some side effects of Dobutamine?

A

Hyper/hypotension, ventricular arrhythmias, tachycardia, angina

122
Q

What are some side effects of Milrinone?

A

ventricular arrhythmias, hypotension

123
Q

What are some monitoring parameters of inotropes?

A

Continuous BP and ECG monitoring, HR, central venous pressure (CVP), MAP, urine output, LFTs and renal function (with milrinone)

124
Q

What are some counseling points of Milrinone?

A
  • Dose must be reduced for renal impairment
  • Dobutamine and Milrinone often referred to as “inodilators”
  • Risk of hypotension; use for inotropic effect only after adequate perfusion is achieved
125
Q

What are some counseling points of Dobutamine?

A
  • Dobutamine may turn slightly pink due to oxidation, but potency is not lost
  • Dobutamine and Milrinone often referred to as “inodilators”
  • Risk of hypotension; use for inotropic effect only after adequate perfusion is achieved
126
Q

What is shock?

A

Shock is a medical emergency characterized by hypoperfusion, usually in the setting of hypotension, defined as SBP < 90 mmHg or MAP < 70 mmHg

127
Q

What are the four main types of shock?

A

Hypovolemic (hemorrhagic), distributive (septic, anaphylactic), cardiogenic (post-myocardial infarction), obstructive (massive pulmonary embolism)

128
Q

What is the general treatment for hypovolemic shock?

A

To treat hypovolemic shock, restore intravascular volume, and improve oxygen-carrying capacity

129
Q

What is the first-line therapy for hypovolemic shock?

A

Fluid resuscitation with crystalloids is generally recommended as first-line therapy for hypovolemic shock that is not caused by hemorrhage

130
Q

What is the target MAP and how do you calculate it?

A

MAP = [(2 x DBP) + SBP]/3

  • Goal is > 65 mmmHG
131
Q

What are some medications used for shock?

A
  • Alpha-1 agonist activity (peripheral vasoconstriction) to increase systemic vascular resistance (SVR)
  • Beta-1 agonist activity to increase myocardial contractility and cardiac output (CO)
132
Q

When should blood products be administered for hypovolemic shock?

A

Blood products (packed red blood cells and fresh frozen plasma) should be administered in hypovolemic shock with intravascular depletion due to bleeding

133
Q

What can be used if patient does not respond to the initial crystalloid or blood product therapy (“fluid challenge”)?

A

Vasopressors

*will not be effective unless intravascular volume is adequate

134
Q

What is distributive shock?

A

Distributive shock is characterized by low SVR, and initially high CO followed by low or normal CO

135
Q

What are some examples of distributive shock?

A

Septic, anaphylactic and neurogenic shock

136
Q

What is sepsis?

A

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection

137
Q

How can organ dysfunction be defined as?

A

Organ dysfunction can be identified by an acute change in the total Sequential Organ Failure Assessment (SOFA) score by > 2 points due to infection

138
Q

How can organ dysfunction be identified?

A

Organ dysfunction can be identified by an acute change in total Sequential Organ Failure Assessment (SOFA) score by > 2 points due to infection

139
Q

What is the qSOFA?

A

The quickSOFA is simplified version that uses only three criteria: altered mental status, systolic blood pressure < 100 mmHg and respiratory rate > 22 breaths per min

140
Q

What is septic shock?

A

Septic shock is sepsis in the presence of persistent hypotension requiring a vasopressor to maintain MAP > 65 mmHg and serum lactate level > 2 mEq/L despite adequate fluid resuscitation

141
Q

What is the Surviving Sepsis Campaign?

A

An initiative calling for early administration of broad-spectrum antibiotics and fluid resuscitation with IV crystalloids when combine with additional measures to lower overall mortality

142
Q

What is considered the vasopressor of choice in septic shock?

A

Norepinephrine

*Vasopressin is commonly used in addition to norepinephrine in the setting of septic shock

143
Q

What are two common causes of ICU infections?

A

Mechanical ventilation and foley catheters

144
Q

How do mechanical ventilators work?

A

Mechanical ventilators allow air flow into the trachea through an endotracheal tube placed though mouth or nose

145
Q

What is weaning?

A

Weaning refers to the process of getting the patient off the ventilator when they are ready to breathe on their own again

146
Q

How does time on mechanical ventilation increase risk of infection?

A

Pseudomonas (and a few other organisms) thrive in the moist air in the ventilator

147
Q

How do foley catheters increase risk of infection?

A

Increased time with foley catheter increases risk of bladder infection

148
Q

What happens when a patient experiences acute decompensated heart failure?

A

Patients with heart failure may experience episodes of worsening symptoms such as sudden weigh gain, inability to lie flat without becoming short of breath, decreasing functionality (unable to perform their daily routine)

149
Q

What is cardiogenic shock?

A

Acute decompensated heart failure with hypotension and hypoperfusion present

150
Q

What can cause ADHF?

A

ADHF is caused by worsening HF, a cardiac event (e.g. MI, arrhythmia, valvular disease, uncontrolled hypertension) or a non-cardiac cause (e.g. non-adherence with medications or dietary restrictions, worsening renal function, infection, illicit drug use)

151
Q

What can worsen cardiac function and cause/exacerbate HF?

A

Negative inotropes, drugs that cause fluid retention (e.g. NSAIDs, COX-2 inhibitors) and cardiotoxic drugs can worsen cardiac function and cause/exacerbate HF

152
Q

When should beta-blockers be stopped in an ADHF episode?

A

Beta-blockers should only be stopped in an ADHF episode if hypotension or hypoperfusion is present

153
Q

What is the presentation of ADHF?

A

ADHF presents with volume overload, hypoperfusion or both

154
Q

What is the use of a Swan-Ganz or pulmonary catheter?

A

It is guided though the right side of the heart into the pulmonary artery and provides hemodynamic measurements of congestion (pulmonary capillary wedge pressure or PCWP), hypoperfusion (cardiac output) and other measurements (SVR, CVP) useful for guiding treatment

155
Q

What is the general treatment of ADHF?

A

Diuretics, inotropes and vasodilators, used in various combinations depending on the patient’s sign/symptoms

156
Q

How is volume overload in an ADHF patient treated?

A

Volume overload is treated with diuretics and possibly vasodilators

157
Q

Why are loop diuretics given IV in volume overload?

A

Loop diuretics are initially given IV since volume overload also affects the vessels of the gut and can decrease their oral absorption

158
Q

What can be used if diuretic resistance develops for volume overload?

A

If diuretic resistance develops, the dose can be increased or thiazide-type diuretic (e.g. metolazone, chlorothiazide) can be added to the loop diuretic

159
Q

What is the most common cause of cardiogenic shock?

A

The most common cause of cardiogenic shock is an MI, with resulting failure of the left ventricle

160
Q

How is cardiogenic shock generally treated?

A

Cardiogenic shock requires treatment with vasopressors and/or inotropes

161
Q

How are Dobutamine and Milrinone useful in patients with ADHF?

A

The vasodilatory and inotropic properties of dobutamine and milrinone make them uniquely suited to treat ADHF in patients with both congestion and hypoperfusion when BP is adequate

162
Q

What can be used if BP is inadequate in a patient with ADHF?

A

If BP is inadequate, inotropes will often be used in combination with vasopressors

163
Q

What must be avoid in patients with hypoperfusion and why?

A

Avoid vasodilattors because these can decrease BP and worsen hypoperfusion

164
Q

What is an important note about inotropes?

A

Inotropes are associated with worse heart failure outcomes and should be stopped as soon as the patient is stabilized

165
Q

What is the first-line agent of the treatment of pain in the ICU?

A

Opioids given IV (such as morphine, hydromorphone and fentanyl) are first-line for analgesia in the ICU

166
Q

What dictates the choice of agent for treatment of analgesia in a patient in the ICU?

A

The pharmacokinetic properties of the drug and the renal/hepatic function of the patient will dictate the choice of agent because all IV opioids exhibit similar analgesic efficacy when dosed correctly

167
Q

How often should pain be assessed in the ICU?

A

Assessment of pain (with a validated pain scale) should be performed at least every 2-4 hours in the ICU and all ICU patients should be evaluated for pain at rest

168
Q

What is analgesia-based sedation?

A

Analgesia-based sedation or “analgosedation” is a sedation strategy that uses analgesia first to relieve pain and discomfort, which are primary causes of agitation

*Associated with less time on the ventilator and short ICU length of stay in comparison to benzos

169
Q

Why is sedation required for some ICU patients?

A

Sedation is necessary for some ICU patients to maintain synchronized breathing with the ventilator (prevent “bucking” the ventilator) and to limit suffering in the harsh ICU environment

170
Q

How can agitation be managed in the ICU?

A

Benzodiazepines (lorazepam, midazolam) and/or non-benzodiazepine hypnotics (propofol, dexmedetomidine)

171
Q

What is preferred in the treatment of agitation in the ICU?

A

Non-benzodiazepines are preferred for sedation and are associated with improved ICU outcomes, shorter mechanical ventilation duration and decreased LOS

172
Q

What is Dexmedetomidine (Precedex) approved for?

A

Dexmedetomidine (Precedex) is the only sedative approved for use in intubated and non-intubated patients

173
Q

When do benzodiazepines have an important role in ICU patients?

A

Benzodiazepines have an important role in sedation in the presence of seizures or alcohol/benzodiazepine withdrawal

174
Q

How are sedatives used in the ICU?

A

Sedatives are used with validated sedation scales that allow for titration to light or deep sedation

*Light sedation (unless contraindicated) is preferred

175
Q

What are some commonly used sedation scales?

A

Richmond Agitation Sedation Scale (RASS), the Ramsay Agitation Scale (RAS) and the Riker Sedation-Agitation Scale (SAS)

*Glasgow Coma Scale is used to determine the level of consciousness (often after traumatic brain injury)

176
Q

How often should patients be monitored while receiving sedation?

A

Patients should be monitored every 2-3 hours while receiving sedation to make sure they are receiving the least amount of drug to keep them calm and pain-free

177
Q

How is assessment done on an ICU patient using sedative drugs?

A

Daily interruptions of continuous infusions of sedative drugs (“sedation vacations”) are used to assess the readiness to wean off/stop the sedative as soon as possible

178
Q

What are some analgesics used in the ICU?

A

Fentanyl, Hydromorphone, Morphine, Remifentanil, Oliceridine

179
Q

What are some monitoring parameters of analgesics in the ICU?

A

BP, HR, respiration, pain and sedation

180
Q

What are some medications used for agitation/sedation in the ICU?

A

Dexmedetomidine (Precedex), Propofol (Diprivan), Lorazepam, Midazolam, Etomidate, Ketamine

181
Q

What are some warnings associated with Precedex?

A

Use with caution in patients with hepatic impairment, diabetes, heart block, bradycardia, severe ventricular dysfunction, hypovolemia or chronic hypertension

182
Q

What are some side effects of Precedex?

A

Hypo/hypertension, bradycardia, dry mouth, nausea, constipation

183
Q

What are some monitoring parameters of Precedex?

A

BP, HR, sedation scale

184
Q

What are some important notes about Precedex?

A
  • Does not require refrigeration
  • Duration of infusion should not exceed 24 hours per FDA labeling
  • Used for sedation in intubated and non-intubated patients (patients are arousable and alert when stimulated [less respiratory depression than other sedatives])
185
Q

What are some contraindications to Propofol?

A

Hypersensitivity to egg, egg product, soy or soy product

186
Q

What are some side effects of Propofol?

A

Hypotension, apnea, hypertriglyceridemia, green urine/hair/nail beds, propofol-related infusion syndrome, myoclonus, pancreatitis, pain on infection (particularly peripheral vein), QT prolongation

187
Q

What are some notes associated with Propofol?

A
  • Shake well before use; do not use if there is separation of phases in the emulsion
  • Use strict aseptic technique due to potential for bacterial growth; discard vial and tubing within 12 hours of use
  • If transferred to a syringe prior to administration, must discard syringe within 6 hours
  • Do not use a filter < 5 microns for administration
  • Does not required refrigeration
  • Oil in water emulsion (opaque, white solution); provides 1.1 kcal/mL
188
Q

What are some notes associated with Lorazepam?

A

Injection is formulated in propylene glycol; TDD as low as 1 mg/kg/day can cause propylene glycol toxicity (acute renal failure and metabolic acidosis)

189
Q

What are some monitoring parameters of Lorazepam?

A

In critical care patients, monitor BP, HR, RR, sedation scale, s/sx of propylene glycol toxicity (BUN, SCr, lactate, anion gap) if receiving continuous infusion; limit use for delirium

190
Q

What are some boxed warnings associated with Midazolam?

A

Respiratory depression, respiratory arrest, apnea

*Start at lower end of dosing range in debilitated patients and geriatric population and do not administer by rapid IV injection in neonates

191
Q

What are contraindications of Midazolam?

A

Intrathecal or epidural administration (benzyl alcohol in formulation), acute narrow-angle glaucoma, use with potent CYP3A4 inhibitors

192
Q

What is a side effect of Midazolam?

A

Hypotension

193
Q

What are some monitoring parameters of Midazolam?

A

BP, HR, RR, sedation scale

194
Q

What are some notes associated with Midazolam?

A
  • Shorter acting than lorazepam if patient has normal organ function (no hepatic or renal impairment or HF)
  • Can accumulate in obese patients (highly lipophilic) and renal impairment (active metabolite) - caution with continuous infusion
195
Q

What is a warning associated with Etomidate?

A

Inhibits 11-B-hydroxylase which can lead to decreased cortisol production for up to 24 hours

196
Q

What are some monitoring parameters of Etomidate?

A

S/sx of adrenal insufficiency (hypotension, hyperkalemia), respiratory status, BP, HR, infusion site, sedation scale

197
Q

What are some warnings associated with Ketamine?

A

Emergence reactions (vivid dreams, hallucinations, delirium), CSF pressure elevation, respiratory depression/apnea, dependence/tolerance

198
Q

What are some monitoring parameters of Ketamine?

A

BP, HR, respiratory status, emergence reactions, sedation scale

199
Q

What is a note associated with Ketamine?

A

Pretreatment with benzodiazepine can decrease incidence of emergence reactions by 50%

200
Q

What are some medications used for delirium in the ICU?

A

Haloperidol, Quetiapine

201
Q

Why do stress ulcers occurs in patients in the ICU?

A

Patients with critical illness have reduced blood flow to the gut, so blood flow is diverted to the body’s major organs, resulting in a breakdown of gastric mucosal defense mechanisms, including prostaglandin synthesis, bicarbonate production and cell turnover

202
Q

What are some risk factors for the development of stress ulcers?

A

Mechanical ventilation > 48 h, major burns, coagulopathy, acute renal failure, sepsis, high dose systemic steroids, traumatic brain injury

203
Q

What are the recommended agents for the prevention of stress-related mucosal damage?

A

Histamine-2 receptor antagonists and proton pump inhibitors are the recommended agents for the prevention of stress-related mucosal damage

204
Q

What are some possible adverse effects of H2RAs?

A

H2RAs can cause thrombocytopenia and mental status changes in the elderly or those with renal/hepatic impairment (tachyphylaxis has also been reported)

205
Q

What are some adverse effects associated with PPIs?

A

PPIs have been associated with an increased risk of GI infections, fractures and nosocomial pneumonia

206
Q

Why are anesthetics used in the ICU?

A

Anesthetics are used for a variety of effects including numbing or an area (local anesthesia), to block pain (regional anesthesia) or to cause a reversible loss of consciousness and sleepiness during surgery (general anesthesia)

207
Q

What are some commonly used local anesthetics?

A

Lidocaine, benzocaine, liposomal bupivacaine

208
Q

What are some inhaled anesthetics?

A

Desflurane, sevoflurane, isoflurane, nitrous oxide, others

209
Q

What are some injectable anesthetics?

A

Bupivacaine, lidocaine, ropivacaine

210
Q

How do anesthetics work?

A

They work by decreasing the neuronal permeability to sodium ions, which blocks the initiation and conduction of nerve impulses

211
Q

What are some monitoring parameters of anesthetics?

A

Vital signs and respiration

212
Q

What are the main side effects of anesthetics?

A

Hypotension, bradycardia, nausea and vomiting and a mild drop in body temperature that can cause shivering

*Overdose can cause respiratory depression

213
Q

What can anesthetics cause?

A

Allergic reactions are possible, and though rare, inhaled anesthetics can cause malignant hyperthermia

214
Q

What is an important note about Bupivacaine?

A

Bupivacaine, commonly used in epidurals, can be fatal if administered intravenously

215
Q

What is an important counseling point about lidocaine?

A

Lidocaine should not be given by dual routes of administration (IV and topical)

216
Q

What is the combination product of lidocaine/epinephrine used for?

A

Lidocaine/epinephrine combination products are used for some local procedures that require an anesthetic, such as inserting an IV line

217
Q

How does the lidocaine/epinephrine combination product work?

A

Epinephrine is added for vasoconstriction, which keeps lidocaine localized to the area where the numbing is needed

218
Q

What do neuromuscular blocking agents do?

A

These agents cause paralysis of the skeletal muscle, including those used for respiration

219
Q

When are neuromuscular blocking agents used?

A

Patients can require the use of a NMBA in surgery conducted under general anesthesia to facilitate mechanical ventilation, to treat muscle spasms (tetany) or to prevent shivering when other methods have proven ineffective

220
Q

What must patients receive before starting an NMBA?

A

Patients should receive adequate sedation and analgesia prior to starting an NMBA

*Patients must be mechanically ventilated as these agents paralyze the diaphragm

221
Q

What should all NMBAs be labeled with?

A

All NMBAs should be labeled with a colored auxiliary label stating “WARNING, PARALYZING AGENT”

222
Q

What are the two types of NMBAs?

A

Depolarizing and non-depolarizing

223
Q

What is the only available depolarizing agent?

A

Succinylcholine is the only available depolarizing agent and is typically reserved for intubation

224
Q

What are some important notes about Succinylcholine?

A
  • Short-acting, fast onset (30-60 seconds)

- Associated with causing MH particularly when used with inhaled anesthetics

225
Q

How does Succinylcholine work?

A

Resembling ACh, succinylcholine binds to and activates ACh receptors and desensitizes them

226
Q

What is the MOA of non-depolarizing NMBAs?

A

Non-depolarizing NMBAs work by binding to the ACh receptors and blocking the actions of endogenous ACh

227
Q

What are some important notes about NMBAs?

A
  • Patients receiving NMBAs are unable to breath, move, blink or cough
  • Special care must be taken to protect skin, lubricate the eyes and suction the airway frequently to clear secretions while NMBAs are being used
228
Q

What is an anticholinergic drug that can be used to reduce secretions?

A

Glycopyrrolate

229
Q

What are some examples of non-depolarizing NMBAs?

A

Atracurium, Cisatracurium, Pancuronium, Rocuronium, Vecuronium

230
Q

What are some side effects of non-depolarizing NMBAs?

A

Flushing, bradycardia, hypotension, tachyphylaxis, acute quadriplegic myopathy syndrome with long-term use

231
Q

What are some monitoring parameters of non-depolarizing NMBAs?

A

Peripheral nerve stimulator to assess depth of paralysis during continuous infusions (also called train-of-four), vital signs (BP, HR, RR)

232
Q

What is hemostasis?

A

The term hemostasis means causing bleeding to stop

233
Q

What are some hemostatic methods?

A

Simple manual pressure with one finger, electrical tissue cauterization or the systemic administration of blood products or hemostatic agents

234
Q

How do systemic hemostatic drugs work?

A

Systemic hemostatic drugs work by inhibiting fibrinolysis or enhancing coagulation

235
Q

What are. some topical hemostatic agents?

A

Thrombin in bandages, liquids and sprays, fibrin sealants, acrylates

236
Q

What are some examples of hemostatic agents?

A

Aminocaproic acid, Tranexamic acid, Recombinant Factor VIIa

237
Q

What are some contraindications of Aminocaproic acid?

A

Disseminated intravascular coagulation (without heparin); active intravascular clotting process

238
Q

What are some side effects of aminocaproic acid?

A

Injection-site reactions, thrombosis

239
Q

What is a note associated with Aminocaproic acid?

A

FDA-approved for excessive bleeding associated with cardiac surgery, liver cirrhosis and urinary fibrinolysis

*Do not use in patients with active clots and do not give with factor IX complex concentrates due to increased risk for thrombosis

240
Q

What are some contraindications of Tranexamic acid?

A

IV: acquired defective color vision, active intravascular clotting, subarachnoid hemorrhage

Oral: previous or current thromboembolic disease, current use of combination hormonal contraception

241
Q

What are some side effects of Tranexamic Acid?

A

Injection: vascular occlusion, thrombosis

Oral: retinal clotting

242
Q

What are some notes about Tranexamic acid?

A
  • Lysteda (oral) is approved for heavy menstrual bleeding
  • Injection is approved for bleeding with hemophilia and is often used off-label to control surgical bleeding and. trauma-associated hemorrhage
243
Q

What is the boxed warning of Recombinant Factor VIIa?

A

Risk of thrombotic events, particularly when used off-label

244
Q

What is a note associated with Recombinant Factor VIIa?

A

FDA-approved for hemophilia and factor VII deficiency; has been used successfully off-label for patients with hemorrhage from trauma and warfarin-related bleeding events

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