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Flashcards in Chapter 16: Critical Care Deck (212):
1

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

4-8

2

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

2.5 - 4

3

Normal value: systemic vascular resistance (SVR)

800 - 1,400

4

Normal value: pulmonary capillary wedge pressure (PCWP)

11 +/- 4

5

Normal value: central venous pressure

7 +/- 2

6

Normal value: pulmonary artery pressure (PAP)

25/10 +/- 5

7

Normal value: mixed venous oxygen saturation (SvO2)

75 +/- 5

8

MAP?

MAP = CO x SVR

9

CI?

CI = CO/BSA

10

% Cardiac output:
- Kidney
- Brain
- Heart

- Kidney: 25%
- Brain: 15%
- Heart: 5%

11

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

Preload

12

Resistance against the ventricle contracting (SVR)

Afterload

13

What determines stroke volume?

LVEDV, contractility and afterload

14

Stroke volume?

Stroke volume = LVEDV - LVESV

15

Ejection fracture?

EF = SV / LVEDV

16

What determines EDV (end-diastolic volume)?

Preload and distensibility of the ventricle

17

What determines ESV (end-systolic volume)?

Determined by contractility and after load

18

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

Decreased diastolic filled time

19

Accounts for 20% of LVEDV

Atrial kick

20

Automatic increase in contractility secondary to increased afterload

Anrep effect

21

Automatic increase in contractility secondary to increased afterload

Anrep effect

22

Automatic increased in contractility secondary to increased heart rate

Bowditch effect

23

Equation: arterial oxygen content

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

24

Equation: oxygen delivery

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

25

Equation: oxygen consumption

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

26

Normal oxygen delivery-to-consumption ratio

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)

27

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

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

28

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

27 mmHg

29

What causes increased SvO2?

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

30

What causes decreased SvO2?

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

31

What can throw off the PCWP?

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

32

Where should Swan-Ganz catheter be placed?

Zone III (lower lung)

33

Treatment: hemoptysis after flushing Swan-Ganz catheter

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

34

Relative contraindications to Swan-Ganz catheter placement

Previous pneumonectomy, left bundle branch block

35

Approximate Swan-Ganz catheter distance to wedge
- R SCV
- R IJ
- L SCV
- L IJ

- R SCV: 45 cm
- R IJ: 50 cm
- L SCV: 55 cm
- L IJ : 60 cm

36

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

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

37

When should wedge pressure be taken?

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

38

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

Increased ventricular wall tension (#1) and HR

39

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

Unsaturated bronchial blood empties into pulmonary veins

40

Normal alveolar-arterial gradient

10 - 15 mmHg in a normal nonventilated patient

41

Blood with the lowest venous oxygen saturation

Coronary sinus blood (30%)

42

Most basic definition of shock

Inadequate tissue oxygenation

43

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

Tachypnea and mental status changes occur with progressive shock

44

MCC adrenal insufficiency

Withdrawal of exogenous steroids

45

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

Adrenal insufficiency

46

Tx: adrenal insufficiency

Dexamethasone

47

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

- 1x: cortisone, hydrocortisone
- 5x: prednisone, prednisolone, methylprenisolone
- 30x: dexamethasone

48

- Loss of sympathetic tone; usually associated with spine or head injury
- Usually have decreased heart rate, decreased blood pressure, warm skin

Neurogenic shock

49

Tx: neurogenic shock

Give volume first, then phenylephrine after resuscitation

50

Initial alteration in hemorrhagic shock

Increased diastolic pressure

51

Beck's triad

Cardiac tamponade
- Hypotension
- JVD
- Muffled heart sounds

52

Mechanism of hypotension in cardiac tamponade

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

53

Echo: cardiac tamponade

Impaired diastolic filling of right atrium initially (first sign)

54

Does pericardiocentesis blood in cardiac tamponade form a clot?

No. Pericardiocentesis blood does not form clot.

55

Tx: cardiac tamponade

Fluid resuscitation to temporize situation; need pericardial window or pericardiocentesis

56

Hemorrhagic shock:
- CVP and PCWP
- CO
- SVR

Hemorrhagic shock:
- CVP and PCWP: decreased
- CO: decreased
- SVR: increased

57

Septic shock (hyperdynamic):
- CVP and PCWP
- CO
- SVR

Septic shock (hyperdynamic):
- CVP and PCWP: decreased (usually)
- CO: increased
- SVR : decreased

58

Cardiogenic shock:
- CVP and PCWP
- CO
- SVR

Cardiogenic shock:
- CVP and PCWP: increased
- CO: decreased
- SVR: increased

59

Neurogenic shock:
- CVP and PCWP
- CO
- SVR

Neurogenic shock:
- CVP and PCWP: decreased
- CO: decreased
- SVR: decreased

60

Adrenal insufficiency:
- CVP and PCWP
- CO
- SVR

Adrenal insufficiency:
- CVP and PCWP: decreased (usually)
- CO: decreased
- SVR: decreased

61

Early sepsis triad

Hyperventilation
Confusion
Hypotension

62

Early gram-negative sepsis

Decreased insulin, increased glucose (impaired utilization)

63

Late gram-negative sepsis

Increased insulin, increased glucose (secondary to insulin resistance)

64

When does hyperglycemia occur in sepsis?

Hyperglycemia often occurs just before the patient becomes clinically septic

65

Neurohormonal response to hypovolemia

- 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)

66

Hormones involved in rapid neurohormonal response to hypovolemia

Epinephrine and norepinephrine

67

Hormones involved in sustained neurohormonal response to hypovolemia

Renin, ADH, ACTH

68

Petechiae, hypoxia and confusion
- MC with lower extremity (hip, femur) fractures / orthopedic procedures

Fat emboli

69

Stain: may show fat in sputum and urine

Sudan red stain

70

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

Pulmonary emboli

71

Where do most PE's arise from?

Iliofemoral region

72

Tx: Pulmonary embolism

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

73

Treatment: air emboli

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

74

When does intra-aoritc balloon pump inflate and deflate?

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

75

Contraindication to IABP

Aortic regurgitation

76

Where does tip of IABP sit?

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

77

What is IABP used for?

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

78

Advantages of intra-aortic balloon pump (IABP)

- Decreased after load (deflation during ventricular systole)
- Improves diastolic BP (inflation during ventricular diastole), which improves diastolic coronary perfusion

79

Receptor: vascular smooth muscle constriction, gluconeogenesis, and glycogenolysis

Alpha-1

80

Receptor: venous smooth muscle constriction

Alpha-2

81

Receptor: myocardial contraction and rate

Beta-1

82

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

Beta-2

83

Receptor: Relax renal and splanchnic smooth muscle

Dopamine receptors

84

Dopamine
- 2-5 ug/kg/min
- 6-10 ug/kg/min
- > 10 ug/kg/min

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)

85

Beta-1
- Increases contractility mostly, tachycardia with higher doses

Dobutamine
(Initial dose: 3 ug/kg/min)

86

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

Milrinone

87

- 10 ug/kg/min
- Alpha-1, vasoconstriction

Phenylephrine

88

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

Norepinephrine

89

- 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

Epinephrine

90

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

Isoproterenol (1-2 ug/min initially)

91

Vasopression receptor: vasoconstriction of vascular smooth muscle

V-1 receptor

92

Vasopressin receptor: water reabsorption at collecting ducts

V-2 receptors (intrarenal)

93

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

V-2 receptors (extrarenal)

94

MOA: nipride

Arterial vasodilator

95

When do you have to be concerned about Nipride?

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

96

Tx for cyanide toxicity

Amyl nitrite, then sodium nitrite

97

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

Nitroglycerin

98

Alpha-blocker; lowers BP

Hydralazine

99

Initial dose phenylephrine

10 ug/min
- alpha-1 vasoconstriction

100

Initial dose norepinephrine
- Low dose?
- High dose?

Initial: 5 ug/min
- Low dose: beta 1 (increased contractility)
- High dose: alpha-1 and alpha -2

101

Initial dose epinephrine
- Low dose?
- High dose?

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

Effects of low dose epinephrine

Can decrease BP at lower doses

103

Effects of high dose epinephrine

Increases cardiac ectopic pacer activity and myocardial oxygen demand

104

Initial dose isoproterenol

1-2 ug / min

105

Initial dose dobutamine

3 ug/kg/min

106

Definition compliance

Compliance = change in volume / change in pressure

107

What does high pulmonary compliance mean?

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

108

What decreases pulmonary compliance?

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

109

How does aging affect pulmonary physiology?

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

110

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

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

111

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

Increased PEEP

112

Ventilator: actions to decrease CO2

Increased rate or volume

113

Normal weaning parameters

- Negative inspiratory force > 20
- FiO2 60 mmHg, PCO2 93%
- Off pressors, follows commands, can protect airway

114

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

Pressure support

115

FiO2: prevents O2 radical toxicity

FiO2

116

High risk of barotruama

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

117

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

PEEP

118

Excessive PEEP complications

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

119

When is high-frequency ventilation used?

Used a lot in kids; tracheoesophageal fistula, bronchopleural fistula

120

Lung volume after maximal inspiration

Total lung capacity (TLC)

121

Equation total lung capacity

TLC = FVC + RV

122

Maximal exhalation after maximal inhalation

Forced vital capacity (FVC)

123

Lung volume after maximal expiration (20% TLC)

Residual volume (RV)

124

Volume of air with normal inspiration and expiration

Tidal volume (TV)

125

Lung volume after normal exhalation

Functional residual capacity (FRC)

126

Equation FRC

FRC = ERV + RV

127

What decreases FRC?

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

128

Volume of air that can be forcefully expired after normal expiration

Expiratory reserve volume (ERV)

129

Maximum air breathed in from FRV

Inspiratory capacity

130

Forced expiratory volume in 1 second (after maximal inhalation)

FEV1

131

Minute ventilation

MV = TV x RR

132

Decreased TLC
Decreased RV
Decreased FVC
- FEV1?

Restrictive lung disease
- FEV1 can be normal or increased

133

Increased TLC
Increased RV
Decreased FEV1
- FVC?

Obstructive lung disease
- FVC can be normal or decreased

134

Normally to the level of the bronchiole (150mL)

Dead space

135

Area of lung that is ventilated but not perfused

Dead space

136

What can increase dead space?

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

137

Increases work of breathing due to prolonged expiratory phase

COPD

138

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

ARDS

139

What cell primarily mediates ARD?

PMNs

140

MCC ARDS

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

141

ARDS Criteria

Acute onset
BL pulmonary infiltrates
PaO2 / FiO2

142

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

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

143

Chemical pneumonitis from aspiration of gastric secretions

Mendelson's syndrome

144

Most frequent site of aspiration

Superior segment of the right lower lobe (RLL)

145

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

Atelectasis

146

MCC fever in first 48 hours after operation

Atelectasis

147

s/s Atelectasis
- Tx?

S/S: fever, tachycardia, hypoxia
- Tx: incentive spirometry, pain control, ambulation

148

What increases incidence of atelectasis?

Increased in patients with COPD, upper abdominal surgery, obesity

149

What can throw off a pulse oximeter?

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

150

Cause pulmonary vasodilation (drugs x 4)

PGE1
Prostacyclin (PGI2)
Nitric oxide
Bradykinin

151

Cause pulmonary vasoconstriction

Hypoxia (#1)
Acidosis
Histamine
Serotonin
TXA2

152

Alkalosis: affect on pulmonary vasculature

Pulmonary vasodilator

153

Acidosis: affect on pulmonary vasculature

Pulmonary vasoconstrictor

154

What causes pulmonary shunting?

Occurs with nitroprusside (Nipride), nitroglycerin, and nifedipine

155

MCC postoperative renal failure

Hypotension intra-op

156

% nephrons damaged before renal dysfunction occurs

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

157

Best test for azotemia

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

158

Prerenal renal failure
- Urine osmolarity
- U/P osmolality
- U/P creatinine
- Urine Sodium
- FeNa

Prerenal renal failure
- Urine osmolarity: > 500
- U/P osmolality: > 1.5
- U/P creatinine: > 20
- Urine Sodium:

159

Parenchymal renal failure
- Urine osmolarity
- U/P osmolality
- U/P creatinine
- Urine Sodium
- FeNa

Parenchymal renal failure
- Urine osmolarity: 250-350
- U/P osmolality: 40
- FeNa: > 3%

160

Treatment: oliguria

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

161

Indications for dialysis

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

162

Rapid, can cause large volume shifts

Hemodialysis

163

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

CVVH

164

What causes release of renin?

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

165

Converts angiotensinogen (synthesized in liver) to angiotensin I

Renin

166

Converts angiotensin I to angiotensin II

Angiotensin-converting enzyme (lung)

167

Relaxes aldosterone in response to angiotensin II

Adrenal cortex

168

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

Aldosterone

169

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

Angiotensin II

170

- Released from atrial wall with atrial distention
- Inhibits Na and water resorption in the collecting ducts
- Also a vasodilator

Atrial natriuretic pepetide

171

- Released by posterior pituitary gland when osmolality is high
- Acts on collecting ducts for water resorption
- Also a vasoconstrictor

Antidiuretic hormone (ADH; vasopressin)

172

What limb of the kidney controls GFR

Efferent limb of the kidney controls GFR

173

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

NSAIDs

174

Antibiotic: direct tubular injury

Aminoglycoside

175

Direct tubular injury
- Tx: alkalinize urine

Myoglobin

176

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

Contrast dyes

177

Four examples of renal toxic drugs

NSAIDs, aminoglycosides, myoglobin, contrast dyes

178

Causes of SIRS

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

179

Most potent stimulus for SIRS

Endotoxin (lipopolysaccharide - lipid A)

180

Very potent stimulator of TNF release

Lipid A

181

Mechanism of SIRS

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

182

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

SIRS

183

SIRS + Infection

Sepsis

184

SIRS criteria

- Temp > 38C or 90 bpm
- RR > 20/min or PaCO2 12k or

185

Arterial hypotension despite adequate volume resuscitation (inadequate tissue oxygenation)

Shock

186

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

MOD (multisystem organ dysfunction)

187

Diagnostic criteria for significant organ dysfunction: Pulmonary

Need for mechanical ventilation, PaO2:FiO2 ratio

188

Diagnostic criteria for significant organ dysfunction: Cardiovascular

Need for inotropic drugs or CI

189

Diagnostic criteria for significant organ dysfunction: Kidney

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

190

Diagnostic criteria for significant organ dysfunction: Liver

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

191

Diagnostic criteria for significant organ dysfunction: Nutrition

10% reduction in lean body mass; albumin

192

Diagnostic criteria for significant organ dysfunction: CNS

Glasgow Coma Scale score

193

Diagnostic criteria for significant organ dysfunction: Coagulation

Platelet count

194

Diagnostic criteria for significant organ dysfunction: Host defenses

WBC

195

Precludes diagnosis: brain death

Temperature

196

Brain death: following must exist for 6-12 hours

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

Brain death: EEG / MRA

- EEG: shows electrical silence.
- MRA: will show no blood flow to brain

198

What is the apnea test?

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

Brain death: What is a positive apnea test?

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

Brain death: What is a negative apnea test?

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

201

Can you still have deep tendon reflexes with brain death?

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

202

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

Carbon monoxide

203

Treatment: carbon monoxide

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

204

Abnormal carboxyhemoglobin levels

> 10% in normal.
> 20% in smokers

205

O2 saturation reads 85%
- Tx: methylene blune

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

206

- Motor > sensory neuropathy
- Occurs with sepsis
- Can lead to failure to wean from ventilation

Critical illness polyneuropathy

207

- 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

Xanthine oxidase

208

Most important mediator of reperfusion injury

PMNs

209

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

DKA

210

HTN, tachycardia, delirium, seizures after 48 hours
- Tx: thiamine, folate, B12, Mg, K, PRN lorazepam (Ativan)

ETOH withdrawal

211

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

ICU (or hospital) psychosis

212

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

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