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Drafts of absite from online deck > Chapter 16: Critical Care COPY > Flashcards

Chapter 16: Critical Care COPY Flashcards

1
Q

Normal value: cardiac output (CO) (L/min)

A

4-8

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2
Q

Normal value: cardiac index (CI) (L/min)

A

2.5 - 4

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3
Q

Normal value: systemic vascular resistance (SVR)

A

800 - 1,400

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4
Q

Normal value: pulmonary capillary wedge pressure (PCWP)

A

11 +/- 4

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5
Q

Normal value: central venous pressure

A

7 +/- 2

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6
Q

Normal value: pulmonary artery pressure (PAP)

A

25/10 +/- 5

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7
Q

Normal value: mixed venous oxygen saturation (SvO2)

A

75 +/- 5

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8
Q

MAP?

A

MAP = CO x SVR

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9
Q

CI?

A

CI = CO/BSA

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10
Q

% Cardiac output:

  • Kidney
  • Brain
  • Heart
A
  • Kidney: 25%
  • Brain: 15%
  • Heart: 5%
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11
Q

Left ventricular end-diastolic length, linearly related to left ventricular end-diastolic volume (LVEDV) and filling pressure

A

Preload

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12
Q

Resistance against the ventricle contracting (SVR)

A

Afterload

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13
Q

What determines stroke volume?

A

LVEDV, contractility and afterload

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14
Q

Stroke volume?

A

Stroke volume = LVEDV - LVESV

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15
Q

Ejection fracture?

A

EF = SV / LVEDV

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16
Q

What determines EDV (end-diastolic volume)?

A

Preload and distensibility of the ventricle

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17
Q

What determines ESV (end-systolic volume)?

A

Determined by contractility and after load

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18
Q

Why does cardiac output start to decreased with HR 120-150?

A

Decreased diastolic filled time

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19
Q

Accounts for 20% of LVEDV

A

Atrial kick

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20
Q

Automatic increase in contractility secondary to increased afterload

A

Anrep effect

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21
Q

Automatic increase in contractility secondary to increased afterload

A

Anrep effect

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22
Q

Automatic increased in contractility secondary to increased heart rate

A

Bowditch effect

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23
Q

Equation: arterial oxygen content

A

CaO2 = HgB x 1.34 x O2 saturation + (Po2 x 0.003)

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24
Q

Equation: oxygen delivery

A

oxygen delivery = CO x arterial oxygen content (caO2) x 10

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25
Q

Equation: oxygen consumption

A

(VO2) = CO x (CaO2 - CvO2); CvO2 = venous O2 content

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26
Q

Normal oxygen delivery-to-consumption ratio

A

5: 1. CO increases to keep this ratio constant.

- Oxygen consumption is usually supply dependent (consumption does not change until low levels of delivery are reached)

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27
Q

Causes of right shift on oxygen-hemoglobin dissociation curve (oxygen unloading)

A

Increased CO2, increased temperature, increased ATP production, increased 2,3-DPG, decreased pH

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28
Q

Normal p50 (O2 at which 50% of oxygen receptors are saturated)

A

27 mmHg

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29
Q

What causes increased SvO2?

A

Increased shunting of blood or decreased oxygen extraction (e.g., sepsis, cirrhosis, cyanide toxicity, hyperbaric oxygen, hypothermia, paralysis, coma, sedation)

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30
Q

What causes decreased SvO2?

A

Increased oxygen extraction or decreased oxygen delivery (e.g., decreased O2 saturation, decreased CO, malignant hyperthermia)

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31
Q

What can throw off the PCWP?

A

May be thrown off by pulmonary hypertension, aortic regurgitation, mitral stenosis, mitral regurgitation, high PEEP, poor LV compliance

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32
Q

Where should Swan-Ganz catheter be placed?

A

Zone III (lower lung)

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33
Q

Treatment: hemoptysis after flushing Swan-Ganz catheter

A

Increase PEEP, which will tamponade the pulmonary artery bleed, mainstem intubate non-affected side; can try to place Fogarty balloon down mainstem on affected side; may need thoracotomy and lobectomy

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34
Q

Relative contraindications to Swan-Ganz catheter placement

A

Previous pneumonectomy, left bundle branch block

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35
Q

Approximate Swan-Ganz catheter distance to wedge

  • R SCV
  • R IJ
  • L SCV
  • L IJ
A
  • R SCV: 45 cm
  • R IJ: 50 cm
  • L SCV: 55 cm
  • L IJ : 60 cm
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36
Q

How can you measure the pulmonary vascular resistance (PVR)?

A

PVR can be measured only by using a Swan-Ganz catheter (ECHO does not measure PVR)

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37
Q

When should wedge pressure be taken?

A

At end-expiration (for both ventilated and non ventilated patients)

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38
Q

Primary determinants of myocardial oxygen consumption (can lead to myocardial ischemia)

A

Increased ventricular wall tension (#1) and HR

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39
Q

Why is LV blood 5mmHg (PO2) lower than pulmonary capillaries?

A

Unsaturated bronchial blood empties into pulmonary veins

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40
Q

Normal alveolar-arterial gradient

A

10 - 15 mmHg in a normal nonventilated patient

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41
Q

Blood with the lowest venous oxygen saturation

A

Coronary sinus blood (30%)

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42
Q

Most basic definition of shock

A

Inadequate tissue oxygenation

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43
Q

When do you see tachypnea and mental status changes in shock?

A

Tachypnea and mental status changes occur with progressive shock

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44
Q

MCC adrenal insufficiency

A

Withdrawal of exogenous steroids

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45
Q

Cardiovascular collapse; characteristically unresponsive to fluids and pressers; nausea and vomiting, abdominal pain, fever, lethargy, decreased glucose, increased potassium

A

Adrenal insufficiency

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46
Q

Tx: adrenal insufficiency

A

Dexamethasone

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47
Q

Steroid potency:
1x?
5x?
30x?

A
  • 1x: cortisone, hydrocortisone
  • 5x: prednisone, prednisolone, methylprenisolone
  • 30x: dexamethasone
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48
Q
  • Loss of sympathetic tone; usually associated with spine or head injury
  • Usually have decreased heart rate, decreased blood pressure, warm skin
A

Neurogenic shock

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49
Q

Tx: neurogenic shock

A

Give volume first, then phenylephrine after resuscitation

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50
Q

Initial alteration in hemorrhagic shock

A

Increased diastolic pressure

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51
Q

Beck’s triad

A

Cardiac tamponade

  • Hypotension
  • JVD
  • Muffled heart sounds
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52
Q

Mechanism of hypotension in cardiac tamponade

A

Decreased ventricular filling due to fluid in the pericardial sac around the heart

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53
Q

Echo: cardiac tamponade

A

Impaired diastolic filling of right atrium initially (first sign)

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54
Q

Does pericardiocentesis blood in cardiac tamponade form a clot?

A

No. Pericardiocentesis blood does not form clot.

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55
Q

Tx: cardiac tamponade

A

Fluid resuscitation to temporize situation; need pericardial window or pericardiocentesis

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56
Q

Hemorrhagic shock:

  • CVP and PCWP
  • CO
  • SVR
A

Hemorrhagic shock:

  • CVP and PCWP: decreased
  • CO: decreased
  • SVR: increased
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57
Q

Septic shock (hyperdynamic):

  • CVP and PCWP
  • CO
  • SVR
A

Septic shock (hyperdynamic):

  • CVP and PCWP: decreased (usually)
  • CO: increased
  • SVR : decreased
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58
Q

Cardiogenic shock:

  • CVP and PCWP
  • CO
  • SVR
A

Cardiogenic shock:

  • CVP and PCWP: increased
  • CO: decreased
  • SVR: increased
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59
Q

Neurogenic shock:

  • CVP and PCWP
  • CO
  • SVR
A

Neurogenic shock:

  • CVP and PCWP: decreased
  • CO: decreased
  • SVR: decreased
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60
Q

Adrenal insufficiency:

  • CVP and PCWP
  • CO
  • SVR
A

Adrenal insufficiency:

  • CVP and PCWP: decreased (usually)
  • CO: decreased
  • SVR: decreased
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61
Q

Early sepsis triad

A

Hyperventilation
Confusion
Hypotension

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62
Q

Early gram-negative sepsis

A

Decreased insulin, increased glucose (impaired utilization)

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63
Q

Late gram-negative sepsis

A

Increased insulin, increased glucose (secondary to insulin resistance)

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64
Q

When does hyperglycemia occur in sepsis?

A

Hyperglycemia often occurs just before the patient becomes clinically septic

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65
Q

Neurohormonal response to hypovolemia

A
  • Rapid: epi and norepi release (adrenergic release; results in vasoconstriction and increased cardiac activity)
  • Sustained: renin (from kidney; renin-angiotensin pathway activated resulting in vasoconstriction and water resorption); ADH (from pituitary; reabsorption of water) and ACTH release (from pituitary; increases cortisol)
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66
Q

Hormones involved in rapid neurohormonal response to hypovolemia

A

Epinephrine and norepinephrine

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67
Q

Hormones involved in sustained neurohormonal response to hypovolemia

A

Renin, ADH, ACTH

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68
Q

Petechiae, hypoxia and confusion

- MC with lower extremity (hip, femur) fractures / orthopedic procedures

A

Fat emboli

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69
Q

Stain: may show fat in sputum and urine

A

Sudan red stain

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70
Q

Chest pain and dyspnea; decreased PO2 and PCO2; respiratory alkalosis; increased heart rate and increased respiratory rate; hypotension and shock if massive

A

Pulmonary emboli

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71
Q

Where do most PE’s arise from?

A

Iliofemoral region

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72
Q

Tx: Pulmonary embolism

A

Heparin, coumadin; consider open or percutaneous (suction catheter) embolectomy if patient is in shock despite massive pressers and inotropes

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73
Q

Treatment: air emboli

A

Place patient head down and roll to the left (keeps air in RV and RA) then aspirate air out with central line or PA catheter to RA/RV

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74
Q

When does intra-aoritc balloon pump inflate and deflate?

A

Inflates on T wave (diastole) and deflates on P wave (systole)

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75
Q

Contraindication to IABP

A

Aortic regurgitation

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76
Q

Where does tip of IABP sit?

A

Place tip of catheter just distal to left subclavian (1-2 cm below the top of the arch)

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77
Q

What is IABP used for?

A

Used for cardiogenic shock (after CABG or MI) or in patients with refractory angina awaiting revascularization

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78
Q

Advantages of intra-aortic balloon pump (IABP)

A
  • Decreased after load (deflation during ventricular systole)
  • Improves diastolic BP (inflation during ventricular diastole), which improves diastolic coronary perfusion
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79
Q

Receptor: vascular smooth muscle constriction, gluconeogenesis, and glycogenolysis

A

Alpha-1

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80
Q

Receptor: venous smooth muscle constriction

A

Alpha-2

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81
Q

Receptor: myocardial contraction and rate

A

Beta-1

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82
Q

Receptor: relaxes bronchial smooth muscle, relaxes vascular smooth muscle; increases insulin, glucagon, and renin

A

Beta-2

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83
Q

Receptor: Relax renal and splanchnic smooth muscle

A

Dopamine receptors

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84
Q

Dopamine

  • 2-5 ug/kg/min
  • 6-10 ug/kg/min
  • > 10 ug/kg/min
A

Dopamine

  • 2-5 ug/kg/min: dopamine receptors (renal)
  • 6-10 ug/kg/min: beta-adrenergic (heart contractility)
  • > 10 ug/kg/min: alpha-adrenergic (vasoconstriction and increased BP)
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85
Q

Beta-1

- Increases contractility mostly, tachycardia with higher doses

A

Dobutamine

Initial dose: 3 ug/kg/min

86
Q
  • Phosphodiesterase inhibitor (increased cAMP)
  • Results in increased Ca flux and increased myocardial contractility
  • Also causes vascular smooth muscle relaxation and pulmonary vasodilation
A

Milrinone

87
Q
  • 10 ug/kg/min

- Alpha-1, vasoconstriction

A

Phenylephrine

88
Q
  • Initial dose: 5 ug/min
  • Low dose: beta-1 (increased contractility)
  • High dose: alpha-1 and alpha -2
  • Potent splanchnic vasoconstrictor
A

Norepinephrine

89
Q
  • 1-2 ug/min initially
  • Low dose: beta1 and beta2 (increase contractility and vasodilation) - Can decrease BP at low doses
  • High dose: alpha 1 and alpha 2 (vasoconstriction). Increases cardiac ectopic pacer activity and myocardial oxygen demand
A

Epinephrine

90
Q
  • Beta 1 and beta2, increases HR and contractility, vasodilates
  • Side effects: extremely arrhythmogenic; increases heart metabolic demand (rarely used); may actually decrease BP
A

Isoproterenol (1-2 ug/min initially)

91
Q

Vasopression receptor: vasoconstriction of vascular smooth muscle

A

V-1 receptor

92
Q

Vasopressin receptor: water reabsorption at collecting ducts

A

V-2 receptors (intrarenal)

93
Q

Vasopressin receptor: mediate release of factor 8 and von Willebrand factor (vWF)

A

V-2 receptors (extrarenal)

94
Q

MOA: nipride

A

Arterial vasodilator

95
Q

When do you have to be concerned about Nipride?

A

Cyanide toxicity at doses > 3 ug/kg/min for 72 hours, can check thiocyanate levels and signs of metabolic acidosis

96
Q

Tx for cyanide toxicity

A

Amyl nitrite, then sodium nitrite

97
Q

Predominantly venodilation with decreased myocardial wall tension from decreased preload; moderate coronary vasodilator

A

Nitroglycerin

98
Q

Alpha-blocker; lowers BP

A

Hydralazine

99
Q

Initial dose phenylephrine

A

10 ug/min

- alpha-1 vasoconstriction

100
Q

Initial dose norepinephrine

  • Low dose?
  • High dose?
A

Initial: 5 ug/min

  • Low dose: beta 1 (increased contractility)
  • High dose: alpha-1 and alpha -2
101
Q

Initial dose epinephrine

  • Low dose?
  • High dose?
A

Initial dose: 1-2 ug/min

  • Low dose: beta-1 and beta-2 (increase contractility and vasodilation)
  • High dose: alpha 1 and alpha 2 (vasoconstriction)
102
Q

Effects of low dose epinephrine

A

Can decrease BP at lower doses

103
Q

Effects of high dose epinephrine

A

Increases cardiac ectopic pacer activity and myocardial oxygen demand

104
Q

Initial dose isoproterenol

A

1-2 ug / min

105
Q

Initial dose dobutamine

A

3 ug/kg/min

106
Q

Definition compliance

A

Compliance = change in volume / change in pressure

107
Q

What does high pulmonary compliance mean?

A

Lungs are easy to ventilate (change in volume / change in pressure)

108
Q

What decreases pulmonary compliance?

A

ARDS, fibrotic lung diseases, reperfusion injury, pulmonary edema, atelectasis

109
Q

How does aging affect pulmonary physiology?

A

Decreased FEV1 and vital capacity, increased functional residual capacity (FRC)

110
Q

How do the upper lung lobes differ from lower lung lobes in regards to V/Q ratio (ventilation/perfusion ratio)?

A

V/Q ratio is highest in upper lobes, lowest in lower lobes

111
Q

Ventilator: improves oxygenation (alveoli recruitment) -> improves FRC

A

Increased PEEP

112
Q

Ventilator: actions to decrease CO2

A

Increased rate or volume

113
Q

Normal weaning parameters

A
  • Negative inspiratory force > 20
  • FiO2 60 mmHg, PCO2 93%
  • Off pressors, follows commands, can protect airway
114
Q

Decreases work of breathing (inspiratory pressure is held constant until minimum volume is achieved)

A

Pressure support

115
Q

FiO2: prevents O2 radical toxicity

A

FiO2

116
Q

High risk of barotruama

A

Plateaus > 30 and peaks > 50 -> need to decrease TV: consider pressure control ventilation

117
Q

Improves FRC and compliance by keeping alveoli open -> best way to improve oxygenation

A

PEEP

118
Q

Excessive PEEP complications

A

Decreased RA filling, decreased CO, decreased renal blood flow, decreased urine output, and increased PVR

119
Q

When is high-frequency ventilation used?

A

Used a lot in kids; tracheoesophageal fistula, bronchopleural fistula

120
Q

Lung volume after maximal inspiration

A

Total lung capacity (TLC)

121
Q

Equation total lung capacity

A

TLC = FVC + RV

122
Q

Maximal exhalation after maximal inhalation

A

Forced vital capacity (FVC)

123
Q

Lung volume after maximal expiration (20% TLC)

A

Residual volume (RV)

124
Q

Volume of air with normal inspiration and expiration

A

Tidal volume (TV)

125
Q

Lung volume after normal exhalation

A

Functional residual capacity (FRC)

126
Q

Equation FRC

A

FRC = ERV + RV

127
Q

What decreases FRC?

A

Surgery (atelectasis), sepsis (ARDS), and trauma (contusion, atelectasis, ARDS)

128
Q

Volume of air that can be forcefully expired after normal expiration

A

Expiratory reserve volume (ERV)

129
Q

Maximum air breathed in from FRV

A

Inspiratory capacity

130
Q

Forced expiratory volume in 1 second (after maximal inhalation)

A

FEV1

131
Q

Minute ventilation

A

MV = TV x RR

132
Q

Decreased TLC
Decreased RV
Decreased FVC
- FEV1?

A

Restrictive lung disease

- FEV1 can be normal or increased

133
Q

Increased TLC
Increased RV
Decreased FEV1
- FVC?

A

Obstructive lung disease

- FVC can be normal or decreased

134
Q

Normally to the level of the bronchiole (150mL)

A

Dead space

135
Q

Area of lung that is ventilated but not perfused

A

Dead space

136
Q

What can increase dead space?

A

Drop in cardiac output, PE, pulmonary HTN, ARDS, and excessive PEEP.
- Can lead to high CO2 buildup (hypercapnia)

137
Q

Increases work of breathing due to prolonged expiratory phase

A

COPD

138
Q

Mediated primarily by PMNs, get increased proteinaceous material, increased A-a gradient, increased pulmonary shunt

A

ARDS

139
Q

What cell primarily mediates ARD?

A

PMNs

140
Q

MCC ARDS

A

Pneumonia - other causes: sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC

141
Q

ARDS Criteria

A

Acute onset
BL pulmonary infiltrates
PaO2 / FiO2

142
Q

What pH and volume is associated with increased degree of damage in aspiration?

A

pH 0.4 cc/kg is associated with increased degree of damage

143
Q

Chemical pneumonitis from aspiration of gastric secretions

A

Mendelson’s syndrome

144
Q

Most frequent site of aspiration

A

Superior segment of the right lower lobe (RLL)

145
Q

Collapse of alveoli resulting in reduced oxygenation; usually caused by poor inspiration postop

A

Atelectasis

146
Q

MCC fever in first 48 hours after operation

A

Atelectasis

147
Q

s/s Atelectasis

- Tx?

A

S/S: fever, tachycardia, hypoxia

- Tx: incentive spirometry, pain control, ambulation

148
Q

What increases incidence of atelectasis?

A

Increased in patients with COPD, upper abdominal surgery, obesity

149
Q

What can throw off a pulse oximeter?

A

Nail polish, dark skin, low-flow states, ambient light, anemia, vital dyes

150
Q

Cause pulmonary vasodilation (drugs x 4)

A

PGE1
Prostacyclin (PGI2)
Nitric oxide
Bradykinin

151
Q

Cause pulmonary vasoconstriction

A 
Hypoxia (#1)
Acidosis
Histamine
Serotonin
TXA2
152
Q

Alkalosis: affect on pulmonary vasculature

A

Pulmonary vasodilator

153
Q

Acidosis: affect on pulmonary vasculature

A

Pulmonary vasoconstrictor

154
Q

What causes pulmonary shunting?

A

Occurs with nitroprusside (Nipride), nitroglycerin, and nifedipine

155
Q

MCC postoperative renal failure

A

Hypotension intra-op

156
Q

% nephrons damaged before renal dysfunction occurs

A

70% of nephrons need to be damaged before renal dysfunction occurs

157
Q

Best test for azotemia

A

FeNa (fractional excretion of sodium) = (urine Na/Cr)/(plasma Na/Cr)

158
Q

Prerenal renal failure

  • Urine osmolarity
  • U/P osmolality
  • U/P creatinine
  • Urine Sodium
  • FeNa
A

Prerenal renal failure

  • Urine osmolarity: > 500
  • U/P osmolality: > 1.5
  • U/P creatinine: > 20
  • Urine Sodium:
159
Q

Parenchymal renal failure

  • Urine osmolarity
  • U/P osmolality
  • U/P creatinine
  • Urine Sodium
  • FeNa
A

Parenchymal renal failure

  • Urine osmolarity: 250-350
  • U/P osmolality: 40
  • FeNa: > 3%
160
Q

Treatment: oliguria

A
  • 1st: make sure patient is volume loaded (CVP 11 - 15 mmHg)
  • 2nd: try diuretic trial -> furosemide (Lasix)
  • 3rd: Dialysis if needed
161
Q

Indications for dialysis

A

Fluid overload, increased K, metabolic acidosis, uremic encephalopathy, uremic coagulopathy, poisoning

162
Q

Rapid, can cause large volume shifts

A

Hemodialysis

163
Q

Slower, good for ill patients who cannot tolerate the volume shifts (septic shock, etc); Hct increases by 5-8 for each liter taken off with dialysis

A

CVVH

164
Q

What causes release of renin?

A
  • Decreased pressure sensed by juxtaglomerular apparatus in kidney
  • Increased sodium concentrations sensed by the macula dense
  • Beta-adrenergic stimulation and hyperkalemia
165
Q

Converts angiotensinogen (synthesized in liver) to angiotensin I

A

Renin

166
Q

Converts angiotensin I to angiotensin II

A

Angiotensin-converting enzyme (lung)

167
Q

Relaxes aldosterone in response to angiotensin II

A

Adrenal cortex

168
Q

Acts at the distal convoluted tubule to reabsorb water by up-regulating the Na/K ATPase on the membrane (Na re-absorbed, K secreted)

A

Aldosterone

169
Q

Vasoconstricts as well as increases HR, contractility, glycogenolysis and gluconeogenesis; inhibits renin release

A

Angiotensin II

170
Q
  • Released from atrial wall with atrial distention
  • Inhibits Na and water resorption in the collecting ducts
  • Also a vasodilator
A

Atrial natriuretic pepetide

171
Q
  • Released by posterior pituitary gland when osmolality is high
  • Acts on collecting ducts for water resorption
  • Also a vasoconstrictor
A

Antidiuretic hormone (ADH; vasopressin)

172
Q

What limb of the kidney controls GFR

A

Efferent limb of the kidney controls GFR

173
Q

Cause renal damage by inhibiting prostaglandin synthesis, resulting in renal arteriole vasoconstriction

A

NSAIDs

174
Q

Antibiotic: direct tubular injury

A

Aminoglycoside

175
Q

Direct tubular injury

- Tx: alkalinize urine

A

Myoglobin

176
Q

Direct tubular injury

- Tx: pre-hydration before contrast exposure best; HCO3-, N-acetylcysteine

A

Contrast dyes

177
Q

Four examples of renal toxic drugs

A

NSAIDs, aminoglycosides, myoglobin, contrast dyes

178
Q

Causes of SIRS

A

Shock, infection, burns, multi-trauma, pancreatitis, severe inflammatory responses

179
Q

Most potent stimulus for SIRS

A

Endotoxin (lipopolysaccharide - lipid A)

180
Q

Very potent stimulator of TNF release

A

Lipid A

181
Q

Mechanism of SIRS

A

Inflammatory response is activated systemically (TNF-alpha and IL-1 major components) and can lead to shock and eventually multi-organ dysfunction

182
Q

Results in capillary leakage, microvascular thrombi, hypotension and eventually end-organ dysfunction

A

SIRS

183
Q

SIRS + Infection

A

Sepsis

184
Q

SIRS criteria

A
  • Temp > 38C or 90 bpm

- RR > 20/min or PaCO2 12k or

185
Q

Arterial hypotension despite adequate volume resuscitation (inadequate tissue oxygenation)

A

Shock

186
Q

Progressive but reversible dysfunction of 2 or more organs arising from an acute disruption of normal homeostasis

A

MOD (multisystem organ dysfunction)

187
Q

Diagnostic criteria for significant organ dysfunction: Pulmonary

A

Need for mechanical ventilation, PaO2:FiO2 ratio

188
Q

Diagnostic criteria for significant organ dysfunction: Cardiovascular

A

Need for inotropic drugs or CI

189
Q

Diagnostic criteria for significant organ dysfunction: Kidney

A

Creatinine > 2 times baseline or 2 consecutive days or need for dialysis

190
Q

Diagnostic criteria for significant organ dysfunction: Liver

A

Bilirubin > 3 mg/dL on 2 consecutive days or PT > 1.5 control

191
Q

Diagnostic criteria for significant organ dysfunction: Nutrition

A

10% reduction in lean body mass; albumin

192
Q

Diagnostic criteria for significant organ dysfunction: CNS

A

Glasgow Coma Scale score

193
Q

Diagnostic criteria for significant organ dysfunction: Coagulation

A

Platelet count

194
Q

Diagnostic criteria for significant organ dysfunction: Host defenses

A

WBC

195
Q

Precludes diagnosis: brain death

A

Temperature

196
Q

Brain death: following must exist for 6-12 hours

A

Unresponsive to pain, absent cold caloric oculovestibular reflexes, absent oculocephalic reflex (patient doesn’t track), no spontaneous respirations, no corneal reflex, no gag reflex, fixed and dilated pupils, positive apnea test

197
Q

Brain death: EEG / MRA

A
  • EEG: shows electrical silence.

- MRA: will show no blood flow to brain

198
Q

What is the apnea test?

A

The patient is pre-oxygenated, a catheter delivering O2 at 8L/min is placed at the carina thru the ETT and CO2 should be normal before the start of the test. Disconnect the patient from the ventilator for 10 minutes.

199
Q

Brain death: What is a positive apnea test?

A

A CO2 > 60mmHg or increase in CO2 by 20 mmHg at the end of the test is positive test for apnea (meets brain death criteria)

200
Q

Brain death: What is a negative apnea test?

A

If BP drops ( place back on the ventilator (cannot declare brain death).

201
Q

Can you still have deep tendon reflexes with brain death?

A

Yes, you can still have deep tendon reflexes with brain death (PS: I love Alireza.)

202
Q
  • Can falsely increase oxygen saturation reading on pulse oximeter
  • Binds hemoglobin directly (creates carboxyhemoglobin - HA, nausea, confusion, coma, death)
A

Carbon monoxide

203
Q

Treatment: carbon monoxide

A

Can usually correct with 100% oxygen on ventilator (displaces carbon monoxide); rarely need hyperbaric oxygen

204
Q

Abnormal carboxyhemoglobin levels

A

> 10% in normal.

> 20% in smokers

205
Q

O2 saturation reads 85%

- Tx: methylene blune

A

Methemoglobinemia (from nitrites such as Hurricaine spray, nitrites bind Hgb)

206
Q
  • Motor > sensory neuropathy
  • Occurs with sepsis
  • Can lead to failure to wean from ventilation
A

Critical illness polyneuropathy

207
Q
  • In endothelial cells, forms toxic oxygen radicals with reperfusion, involved in reperfusion injury
  • Also involved in the metabolism of purines and breakdown to uric acid
A

Xanthine oxidase

208
Q

Most important mediator of reperfusion injury

A

PMNs

209
Q

Nausea and vomiting, thirst, polyuria, increased glucose / ketones, decreased sodium, increased potassium
- Tx: normal saline and insulin initially

A

DKA

210
Q

HTN, tachycardia, delirium, seizures after 48 hours

- Tx: thiamine, folate, B12, Mg, K, PRN lorazepam (Ativan)

A

ETOH withdrawal

211
Q

Generally occurs after third postoperative day and is frequently preceded by lucid interval.

A

ICU (or hospital) psychosis

212
Q

What do you need to rule out in ICU (or hospital psychosis)?

A

Metabolic (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes

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