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Exam 2: Critical Care Flashcards

1
Q

What defines hemodynamic instability in shock?

A

SBP< 90mmHg

MAP< 65 mmHg

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2
Q

What are signs of poor tissue perfusion/anaerobic metabolism?

A

Lactate > 4mmol/L

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3
Q

What characterizes shock?

A

Hypo-perfusion of tissues leading to anaerobic metabolism (impaired cellular metabolism). This will lead to inadequate tissue perfusion, cellular injury and dysfunction and ultimately multiple organ failure.

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4
Q

What happens with impaired oxygen utilization?

A

Anaerobic metabolism kicks in leading to

  1. ATP stores reduced and decreased Na/K ATPase Pump usage and decreased amplitude of action potential.
  2. Increased Na leading to hypovolemia (fluid entering cells due to higher Na levels), cellular edema and leaking lysosomal enzymes (damages the cells more)
  3. Decreased fluid in vascular system (hypovolemia) which will lead to decreased O2 delivery causing the activation of clotting cascade, ATN, ARDS, DIC.
  4. Anaerobic metabolism leads to metabolic acidosis/acidemia causing membrane disruption, enzyme disassociation and decreased O2 carrying capacity
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5
Q

Impaired Glucose Utilization

A
  1. Decreased delivery of glucose will increase cortisol, growth hormone and catecholamine release.
  2. Leads to hyperglycemia and insulin resistance.
  3. Glycogenolysis, gluconeogenesis and lipolysis cause high energy costs that contribute to cell failure.
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6
Q

What are the issues with gluconeogenesis in shock?

A

Protein is not longer available to maintain cell structure, function, repair, replication.

  1. Decreased albumin leads to reduced osmotic pressure
  2. decreased immunoglobulins = immunosuppression
  3. alanine release produces lactate
  4. byproducts of ammonia and urea
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7
Q

What happens to muscle tissue as a result of gluconeogenesis in shock?

A

Muscle wasting (diaphragm and cardiac muscle)

  1. respiratory dysfunction (decreased O2/CO2 exchange)
  2. Myocardial dysfunction (decreased glucose delivery)
  3. Decreased removal of waste products
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8
Q

What is shock driven by?

A

Reduced cardiac output, reduced systemic vascular resistance, or both

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9
Q

How do you determine blood pressure?

A

CO x SVR

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10
Q

How do you determine cardiac output?

A

SV x HR

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11
Q

What determines central venous pressure (Preload)?

A

Pressure of blood returning to the heart through the venous system

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12
Q

How do you determine mean arterial pressure (MAP)?

A

MAP = (1/3)SBP + (2/3)DBP

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13
Q

What does MAP represent?

A

Average of systolic and diastolic pressure in the arterial system, it is a surrogate marker of issue perfusion.

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14
Q

How do you calculate SVR?

A

80* (MAP-CVP)/CO

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15
Q

What does SVR represent?

A

the total resistance of the circulatory system (the amount or resistance the heart must overcome to create forward flow)

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16
Q

What are the types of shock?

A

Cardiogenic, Hypovolemic, Neurogenic, Anaphylactic (distributive), Septic (distributive), Sustained shock

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17
Q

What is the etiology of cardiogenic shock?

A

(Problem with the pump) Decompensated HF, MI, PAH, PE, valvular dysfunction, dysrhythmias, myocarditis

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18
Q

How do we treat cardiogenic shock?

A

Inotrope, vasopressor, cautious diuresis, correct underlying cause.

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19
Q

What compensatory mechanisms occur in cardiogenic shock?

A

Increases to SVR (e.g. vasoconstriction) resulting in further cardiac output.

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20
Q

How do you treat hypovolemic shock?

A
  1. Stop bleeding/fluid loss,
  2. give fluids (crystalloid or colloid
  3. Blood Products: whole blood, or packed red blood cells+ platelets + fresh frozen plasma) (if needed)
  4. Vasopressors (temporize)
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21
Q

Etiology: Neurogenic shock

A

Profound vasodilation and lack of compensatory tachycardia.

  1. too much parasympathetic activity leading to bradycardia.
  2. too little sympathetic stimulation of vascular smooth muscle leading to decreased SVR.
    3: mostly caused by SCI: C-spine, high T-spine (T1-T6)
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22
Q

How do you treat neurogenic shock?

A
  1. Fluids
  2. Vasopressors (increase vascular tone)
  3. Inotropes (treat bradycardia)
  4. Stabilize spine if SCI
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23
Q

What is the etiology of anaphylactic shock?

A

Allergy leads to an immune/inflammatory response (IgE mediated), leads to vasodilation (decreased SVR) and vascular permeability (tissue edema/hypovolemia), extra-vascular smooth muscle constriction leading to bronchoconstriction/laryngospasm

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24
Q

How do you treat anaphylactic shock?

A
  1. Remove the antigen or anti-venom (if available)
  2. Glucocorticoids, antihistamines (blunt inflammatory response)
  3. Fluid resuscitation (correct hypovolemia)
  4. Epinephrine (vasoconstriction (alpha 1 agonist), bronchodilation (Beta 2 agonist))
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25
Q

What is the etiology of septic shock?

A

Bacteremia leading to endo/exo-toxins, lipopolysaccharide (LPS) gram negative, peptidoglycan and lipoteichoic acid gram positive.

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26
Q

How do you treat septic shock?

A
  1. Remove/suppress infection (ABX)
  2. Fluids
  3. Vasopressors
  4. Source control (I&D, remove infected heart valve, debridement/amputation)
  5. Renal replacement therapy, mechanical ventilation
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27
Q

What happens if a patient sustains shock for a long period of time?

A

Multi-organ dysfunction syndrome (MODS): progressive dysfunction of two or more organ systems resulting from uncontrolled inflammatory response to severe illness or injury

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28
Q

What are some common triggers that can lead to MODS?

A
  • Severe trauma
  • Major surgery
  • Burns
  • Shock
  • Pancreatitis
  • AKI
  • ARDS
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29
Q

What are the three main types of shock?

A

Hypovolemic, cardiogenic, distributive

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30
Q

What is hypovolemic shock?

A

Decreased CO due to inadequate blood or plasma volume.

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31
Q

How is hypovolemic shock presented as?

A

Thirst, nausea, anxiousness, weakness, light headedness, dizziness, decrease UOP.

Severe: tachycardia, elevated RR, hypotension, altered mental status

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32
Q

What types of fluids are given in hypovolemic shock?

A

Crystalloids (NS, LR, D5W, and 3% NaCl), Colloids (Albumin), blood products

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33
Q

How is NS and LR distributed into the body?

A

100% ECF,

75% into the interstitial and 25% into the intravascular space.

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34
Q

How is D5W distributed into the body?

A

40% ECF and 60% ICF

75% into the interstitial and 25% into the intravascular space (break down of the ECF)

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35
Q

How is Albumin 5% distributed in the body?

A

100% ECF

100% interstitial

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36
Q

How is Albumin 25% distributed in the body?

A

100% ECF

500% intravascular (concentrated albumin will pull fluid into the intravascular space)

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37
Q

When would we use D5W in hypovolemia?

A

Dehydration with minor s/s of volume deplesion

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38
Q

When would we use 3% NS in hypovolemia?

A

In addition to LR/NS, for head trauma. Caution due to osmolarity, risk of cellular crenation and damage

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39
Q

Why would we use packed red blood cells in shock?

A

To increase oxygen carrying capacity in blood.

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40
Q

Why would we use fresh frozen plasma in shock?

A

To replace the clotting factors

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41
Q

Why would we use platelets in shock?

A

To administer for thrombocytopenia

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42
Q

How does Cardiogenic shock present?

A

altered mental status, pulmonary edema, hypotension, weak pulses, cool extremities, decreased urine output

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43
Q

How do we diagnose cardiogenic shock?

A

Sustained hypotension (SBP <90), reduced Cl (<2.2 l/min/m2) with an elevated PCWP > 18 (pulmonary capillary wedge pressure)

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44
Q

How do we generally treat cardiogenic shock?

A

Fluid resuscitation (unless frank pulmonary edema is present), furosemide for pulmonary edema, correct rhythm abnormalities (Mg/K), consider vasopressor therapy.

Avoid BB and CCB

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45
Q

How do we treat cardiogenic shock with STEMI pts?

A

PCI or CABG, fibrinolytic therapies for unstable patients, intra aortic balloon pump, alternative LV assist devices for circulatory support.

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46
Q

How is distributive shock defined as?

A

Excessive vasodilation resulting in impaired distribution of blood flow.

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47
Q

What is SIRS? What are the criteria?

A

Systemic Inflammatory response syndrome (SIRS), criteria (2 or more):

  • Temperature of >38.3 or <36
  • HR >90 bpm
  • RR > 20 or mechanical vent
  • WBC >12,000 or <4,000 or >10% immature forms (bands)
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48
Q

How do you determine qSOFA?

A

2 or more:
- RR >/= 22
- altered mentation
SBP = 100 mmHg

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49
Q

How should you initially resuscitate a sepsis induced hypoperfusion?

A
  • Measure lactate (repeat if elevated (>2 mmol/L)
  • Blood cultures and broad spectrum abx
  • fluids for hypotension or lactate >4 mmol/L
  • Vasopressors for MAP >/= 65 mmHg (to maintain 65 mmHg or greater)
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50
Q

At what rate and what types of fluids should a septic patient receive?

A

Crystalloids are preferred, 30 mL/kg
Albumin may be used for pts with substantial requirements of crystalloids after initial resuscitation.
CVP is used for fluid status (goal 8-12 mmHg or 12-15 if mechanically ventilated)

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51
Q

What is the target goal for vasopressor therapy in shock?

A

MAP >/= 65

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52
Q

Norepinephrine:
Dose:
Rate:

A

Dose: 0.02-3 ug/kg/min
Rate: 4-30 ug/min

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53
Q

Why is norepinephrine considered first line therapy?

A

Increases MAP/SVR via vasoconstriction and causes little change in heart rate and stroke volume, may be a little more effective at reversing hypotension than dopamine

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54
Q

Vasopressin

Rate:

A

0.04 units/min, can do 0.03 units/min to NE to raise MAP or decrease NE
>0.03-0.04 units/min is considered salvage therapy.

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55
Q

What are some considerations to think about with vasopressin?

A

increases BP in pts refractory to other vasopressors, antidiuretic properties via V2 receptors, may increase serum cortisol via V3 receptors (proinflammatory and increases BP), higher doses associated with cardiac, digital and splanchnic ischemia

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56
Q

Epinephrine
Dose:
Rate:

A

Dose: 0.01-0.5 mcg/kg/min
Rate: 2-10 mcg/min

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57
Q

What’s epinephrine’s role in therapy?

A

Either added to possibly substituted for NE

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58
Q

What are some considerations to think about with epinephrine?

A

Decreases renal and splanchnic blood flow, increases lactate levels via stimulation of skeletal B2 receptors

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59
Q

Phenylephrine
Dose:
Rate:

A

Dose: 0.5-9 mcg/kg/min
Rate: 40-300 mcg/min

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60
Q

Why would you use phenylephrine?

A

Not normally recommended.
Only use if NE is associated with serious arrhythmias
High CO and persistently low BP
Salvage therapy

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61
Q

What are some considerations if thinking about using phenylephrine?

A

It’s purely an alpha activator and the least likely drug to cause tachycardia.
May decrease stroke volume (limited use)

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62
Q

Dopamine

Rate:

A
  • 1-3 mcg/kg/min
  • 3-10 mcg/kg/min
  • 10-20 mcg/kg/min
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63
Q

What’s dopamine’s role in shock?

A

It is an alternate to NE when there is a low risk of tachyarrhythmias and absolute or relative bradycardia.
- Do not use low doses for renal perfusion

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64
Q

What are some considerations when thinking of using dopamine?

A
  • increases MAP and CO due to increase in stroke volume and HR.
  • may be useful with compromised systolic function, but causes more tachycardia and may be more arrhythmogenic than NE
  • Influences endocrine response via hypothalamic pituitary axis and has immunosuppressive effects
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65
Q

When can you use dobutamine?

A

myocardial dysfunction as suggested by elevated cardiac filling pressures and low CO. Ongoing signs of hypoperfusion despite adequate intravascular volume and adequate MAP

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66
Q

When should you use hydrocortisone therapy?

A

Hemodynamic instability despite fluid resuscitation and vasopressor therapy.

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67
Q

When should you initiate glucose control? What is the goal?

A

When two blood glucose measures are >180 mg/dL, target for = 180 mg/dl. Monitor q1-2 hours until glucose and insulin infusion is stable then every 4 hours thereafter.

68
Q

When should you use stress ulcer prophylaxis?

A

W/ bleeding risk factors:

- coagulopathy (INR >1.5, platelets <50,000), mechanical ventilation >48 hours, and possibly hypotension.

69
Q

What is an indication for rapid sequence intubation?

A

Aspiration, or loss of airway (protect the airway!)

70
Q

What steps should you take for rapid sequence intubation?

A

Induction then paralyze

71
Q

What are the types of induction meds?

A

Etomidate, Ketamine, midazolam, propofol

72
Q

What is the onset and duration of etomidate?

A

Onset: 10-30 sec
Duration: 4-10 min

73
Q

What are some adverse effects of etomidate?

A

Adrenal insufficiency (controversial), myoclonic activity (brief, minimal)

74
Q

What is the dosing for etomidate?

75
Q

What is the dosing for Ketamine?

A

1.5 mg/kg (1-2 mg/kg)

76
Q

What is the onset and duration for ketamine?

A

Onset: 45-60 seconds
Duration: 10-20 minutes

77
Q

What are some adverse effects of ketamine?

A

Increased HR, BP, caution with CV disease and hypertensive patients.
increased intraocular pressure
Increased ICP
Bronchodilator (theoretical)

78
Q

What is the dosing for midazolam?

A

0.3 mg/kg (0.1-0.3 mg/kg)

79
Q

What is the onset and duration of midazolam?

A

Onset: 60-90 sec
Duration: 30-80 minutes (up to several hours)

80
Q

What are some adverse effects of midazolam?

A

Hypotension, respiratory depression, paradoxical agitation. Dose and patient response can vary.

81
Q

What is the dosing for propofol?

A

1.5 mg/kg (1-2 mg/kg)

82
Q

What is the onset and duration of propofol?

A

Onset: 15-45 sec
Duration: 5-10 minutes

83
Q

What are some adverse effects of propofol?

A

Hypotension, myocardial depressant and decreases in SVR, caution with egg allergy, reduces ICP

84
Q

What are the types of paralytic medications?

A

Succinylcholine, rocuronium, vecuronium

85
Q

What is the dosing for succinylcholine?

86
Q

What is the onset and duration for succinylcholine?

A

Onset: 30-60 sec
Duration: 6-10 min

87
Q

What is the onset and duration for rocuronium?

A

Onset: 45-60 sec
Duration: 45-70 minutes

88
Q

What is the dosing for rocuronium?

A

0.6-1.2 mg/kg (usually around 1)

89
Q

What are the adverse effects of succinylcholine?

A

Rhabdomyolysis, hyperkalemia, fasciculations, elevated intraocular pressure, malignant hyperthermia (rare), caution in pts with neuromuscular disease

90
Q

What is the dosing for vecuronium?

91
Q

What is the onset and duration for vecuronium?

A

onset: 120-180 s
Duration: 40-60 min

92
Q

What are some adverse effects of rocuronium?

A

longer onset compared to succinylcholine, few adverse effects.

93
Q

What are some adverse effects of vecuronium?

A

longer onset compared to succinylcholine, few adverse effects.

94
Q

How should you monitor pain in communicating patients?

A

Numeric rating scale

95
Q

How can you monitor for pain in non communicative patients/

A

Behavioral pain scale, critical care pain observation tool

96
Q

What is the gold standard for pain assessment?

A

Pt self assessment, also use vital signs to cure further assessments of pain

97
Q

What is the first line treatment for non-neuropathic pain in acute settings?

A

Fentanyl, morphine, hydromorphone

98
Q

How is fentanyl metabolized?

A

Hepatically, N-dealkylation, CYP3A4/5 substrate

99
Q

How is morphine metabolized?

A

Hepatically, glucuronidation

100
Q

How is hydromorphone metabolized?

A

hepatically, glucuronidation

101
Q

What is the onset and duration of fentanyl?

A

onset: 1-2 minutes
Duration: 30 min-1 hour

102
Q

What is the onset and duration of morphine?

A

Onset: 5-10 min
Duration: 4 hours

103
Q

What is the onset and duration of hydromorphone?

A

Onset: 5-15 min
Duration: 3-4 hours

104
Q

What are the active metabolites for morphine?

A

6- and 3-glucuronide (respiratory depression)

105
Q

How is fentanyl, morphine and hydromorphone excreted?

106
Q

When can fentanyl accumulate in the body?

A

with hepatic impairment

107
Q

When can morphine accumulate in the body?

A

with renal/hepatic impairment

108
Q

When can hydromorphone accumulate in the body?

A

in hepatic impairment

109
Q

Which opioids can cause histamine release?

A

morphine, hydromorphone (minimally)

110
Q

When should you avoid morphine?

A

Hemodynamic instability d/t histamine release

111
Q

What are the major side effects of fentanyl?

A

resp depression, tachyphylaxis, constipation, chest wall rigidity and largygospasm.

112
Q

What are the major side effects of morphine and hydromorphone?

A

respiratory depression and constipation.

113
Q

What are some underlying causes of agitation?

A

Pain, delirium, hypoxemia, hypoglycemia, hypotension, withdrawal

114
Q

What are some ways to nonpharmacologically treat patients with agiation/confusion?

A

minimize light and noise, cluster patient care activities, decrease stimuli at night

115
Q

What is considered light sedation?

A

arousable, able to follow commands

116
Q

What is considered deep sedation?

A

unresponsive to painful stimuli

117
Q

How can you measure patient responsiveness/awareness during a daily sedation interruption?

A

Open eyes
Maintain eye contact
Squeeze hand/ stick tongue out
wiggle toes (meet 3/4 of the requests). Restart meds at half dose

118
Q

How can we reduce mechanical ventialation time?

A
  • daily sedation interruption

- light sedation over deep sedation

119
Q

What types of sedatives are preferred? why?

A

Non-benzodiazepines in mechanically ventilated patients. Reduces risk of delirium

120
Q

When might you consider benzos in sedation therapy?

A

seizures, alcohol or benzo withdrawal

121
Q

What is a contraindication against midazolam use?

A

Severe hepatic impairment.

122
Q

How is midazolam metabolized?

A

Hepatic phase I

123
Q

how is lorazepam metabolized?

A

Hepatic phase II, less affected by liver impairment

124
Q

How is midazolam and lorazepam excreted?

125
Q

What is some considerations for lorazepam?

A

risk of propylene glycol toxicity

126
Q

What are the side effects for midazolam and lorazepam?

A

resp depression, paradoxical psychosis, hypotension

127
Q

how is propofol metabolized?

A

hepatically

128
Q

how is propofol excreted?

129
Q

what are the side effects of propofol?

A

resp depression, brady cardia, hypertriglyceridemia, hypotension, overfeeding, discolored urine, PRIS

130
Q

what are the side effects of dexmedetomidine?

A

bradycardia, hypotension, loss of airway reflexes

131
Q

how is dexmedetomidine metabolized and excreted?

A

hepatically metabolized and renally excreted

132
Q

Does midazolam have active metabolites?

A

Yes, may accumulate in renal impairment

133
Q

what considerations do you have to think about with dexmedetomidine?

A

minimal respiratory depression, cannot achieve deep sedation

134
Q

what is the onset and half life of midazolam?

A

onset: 2-5 min

half life: 3-11 hr

135
Q

what is the onset and half life of lorazepam

A

onset:15-20 min

half life: 8-15 hr

136
Q

what is the onset and half life of propofol

A

onset: 1-2 min

half life: 3-10 min

137
Q

what is the onset and half life of dexmedetomidine?

A

onset: 5-10 minutes
duration: 1.8-3.1 hr

138
Q

what is the mechanism of propofol infusion syndrome (PRIS)?

A

prolonged (>48 hours) of high dose administration (>70 mcg/kg/min) leading to dysfunction of mitochondria, fatty acid oxidation impairment, diversion of carb metabolism to fat substrate and propofol metabolite accumulation

139
Q

what is the presentation of PRIS?

A

metabolic acidosis, hypertriglyceridemia, hypotension, arrhythmia, rhabdomyolysis, acute renal injury, hyperkalemia

140
Q

what causes propylene glycol toxicity

A

accumulation of higher dosed lorazepam infusions (15-25 mg/hr), lower doses can also cause toxicity

141
Q

how is propylene glycol toxicity presented as?

A

Metabolic acidosis, acute kidney injury, seizures

142
Q

how can you monitor for glycol toxicity?

A

osmol gap >10-12 mOsm/L can help identify the accumulation

143
Q

What causes DKA?

A

Absolute insulin deficiency leading to utilization of ketones for energy and causing ketoacidosis. Patient is also hyperglycemic.

144
Q

What causes hyperosmolar hyperglycemic state (HHS)?

A

Relative insulin deficiency leading to minimal (or absent) ketogenesis. Hyperglycemia leads to loss of water and electrolytes (glycosuria) causing hyperosmolarity from dehydration and decreased fluid intake.

145
Q

How do you diagnose for DKA?

A 
Blood glucose >250
Arterial pH <7.3
Bicarb <18
Anion gap >10
Positive Ketones
146
Q

How do you diagnose for HHS?

A

Blood glucose >600

Serum osmolarity >320

147
Q

What can cause euglycemic DKA?

A

SGLT-2 inhibitors, ketosis, acidosis

148
Q

How do you calculate anion gap?

A

Na-Cl- HCO3 = anion gap

149
Q

What is a normal anion gap? and defines metabolic acidosis?

A

Normal: 7-9

Metabolic acidosis: >10-12

150
Q

What is a normal serum osmolarity? What defines hyperosmolar?

A

Normal: 285-295
Hyperosmolar: >/= 320

151
Q

how do you calculate serum osmolarity?

A

2(Na) + glu/18 + BUN/2.8 = serum osmolality

152
Q

What are the treatment goals for DKA and HHS?

A

Rehydration, insulin, manage electrolyte and acid/base imbalances (consider bicarb in severe acidosis and prevent hypokalemia), Identify precipitating events (underlying infection, non-adherence, heavy drug/alcohol use)

153
Q

How should you fluid resuscitate a patient for DKA or HHS?

A
  • NS IV 15-20 ml/kg over the first hour
  • NS or 1/2 NS 250-500 ml/hr until blood glucose is normalized (NS if Na is low, 1/2 NS if Na is normal)
  • D5 in 1/2 NS at 125-250 ml/hr until DKA is resolved.
154
Q

How do you calculate for corrected Na?

A

Measured Na + [(serum glucose- 100)/100] x1.6

155
Q

What is the goal for potassium replacement in DKA and HHS?

156
Q

When should you begin to replace potassium in DKA and HHS? How much should you administer?

A

when K< 5.2, 20-30 mEq K per L of fluid, (10 mEq is ~0.1 mEq/L), withhold insulin treatment if K <3.3 mEq/L

157
Q

What should you do for an acid/base imbalance?

A

Acidosis usually will resolve with fluids and insulin.
pH >/= 6.9 does not need any sodium bicarbonate.
pH <6.9: 100 mEq of sodium bicarb in 400 ml sterile water with 20 mEq KCl administered at a rate of 200 ml/h for 2 h until the venous pH is >7.0

158
Q

What is the initial insulin treatment for DKA and HHS?

A

0.1 units/kg IV bolus + 0.1 units/kg/hr continuous IV infusion

or

0.14 units/kg/hr of continuous IV infusion

(Goal is to decrease glucose by 50-75 mg/dl/hr)

159
Q

When do you transition to the second step of insulin treatment for DKA and HHS?

A

DKA: glucose <200 mg/dL

HHS: glucose <300 mg/dL

160
Q

What is the second step of insulin in treating DKA and HHS?

A

Decrease to 0.02-0.05 units/kg/hr continuous IV infusion (also switch to D5 and 1/2 NS).

161
Q

Where should you maintain blood glucose for DKA and HHS until resolution?

A

DKA: 150-200
HHS: 200-300

162
Q

What determines resolution of DKA?

A

Serum glucose <200
pH >7.3
Anion gap closure <12
Serum bicarb >18

163
Q

What determines resolution of HHS?

A

Normal osmolality, return to normal mental status

164
Q

How should you transition to SQ insulin from IV after hyperglycemic crisis is resolved?

A

Dose:

  • insulin naiive: 0.5-0.8 units/kg/day
  • previous use: may use previous dose if adequate.

Overlap IV and SQ insulin by 1-2 h to prevent the return to DKA/HHS

Make sure patient can tolerate oral food

165
Q

What are some adverse drug effects that can cause ADHF?

A

NSAIDs (AKI?), decongestants (hypertension, increased afterload), Alka-seltzer (high sodium), beta agonists (risk of exacerbation)

166
Q

How do you calculate cardiac index? What is considered normal?

A

CI =CO/BSA

Normal CI = 2.8 - 4.2 L/min/m2

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