Chapter 16: Critical Care Flashcards
1
Q
Normal value: cardiac output (CO) (L/min)
A
4-8
2
Q
Normal value: cardiac index (CI) (L/min)
A
2.5 - 4
3
Q
Normal value: systemic vascular resistance (SVR)
A
800 - 1,400
4
Q
Normal value: pulmonary capillary wedge pressure (PCWP)
A
11 +/- 4
5
Q
Normal value: central venous pressure
A
7 +/- 2
6
Q
Normal value: pulmonary artery pressure (PAP)
A
25/10 +/- 5
7
Q
Normal value: mixed venous oxygen saturation (SvO2)
A
75 +/- 5
8
Q
MAP?
A
MAP = CO x SVR
9
Q
CI?
A
CI = CO/BSA
10
Q
% Cardiac output:
- Kidney
- Brain
- Heart
A
- Kidney: 25%
- Brain: 15%
- Heart: 5%
11
Q
Left ventricular end-diastolic length, linearly related to left ventricular end-diastolic volume (LVEDV) and filling pressure
A
Preload
12
Q
Resistance against the ventricle contracting (SVR)
A
Afterload
13
Q
What determines stroke volume?
A
LVEDV, contractility and afterload
14
Q
Stroke volume?
A
Stroke volume = LVEDV - LVESV
15
Q
Ejection fracture?
A
EF = SV / LVEDV
16
Q
What determines EDV (end-diastolic volume)?
A
Preload and distensibility of the ventricle
17
Q
What determines ESV (end-systolic volume)?
A
Determined by contractility and after load
18
Q
Why does cardiac output start to decreased with HR 120-150?
A
Decreased diastolic filled time
19
Q
Accounts for 20% of LVEDV
A
Atrial kick
20
Q
Automatic increase in contractility secondary to increased afterload
A
Anrep effect
21
Q
Automatic increase in contractility secondary to increased afterload
A
Anrep effect
22
Q
Automatic increased in contractility secondary to increased heart rate
A
Bowditch effect
23
Q
Equation: arterial oxygen content
A
CaO2 = HgB x 1.34 x O2 saturation + (Po2 x 0.003)
24
Q
Equation: oxygen delivery
A
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
