Critical Care Flashcards

1
Q

This syndrome is defined by end-organ hypoperfusion as a result of circulatory failure

A

Shock

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2
Q

This type of shock can be due to sepsis, anaphylaxis, spinal cord injury

A

Distributive

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3
Q

This type of shock can be due to acute MI, end-stage cardiomyopathy, severe valvular disease, myocarditis, or arrythmias

A

Cardiogenic

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4
Q

This type of shock can be due to PE, tamponade, tension pneumothorax, abdominal compartment syndrome

A

Obstructive

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5
Q

This type of shock can be due to hemorrhage or severe dehydration

A

Hypovolemic

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6
Q

What is a first-like agent for vasoactive drugs due to their rapid onset, high potency, and short half life?

A

Adrenergic agonists (NE)

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7
Q

Good and bad of use of NE for shock?

A

Stimulating B-adrenergic increases CO but also increases risk of MI

Stimulating a-adrenergic R increases vascular tone and MP but also impairs CO and flow to hepatosplanchnic region

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8
Q

What will happen if you give dobutamine when patients are not well volume resuscitated?

A

Blood pressure can decrease

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9
Q

These agents are PDE-III inhibitors, which decrease metabolism of cAMP and comines inotropic and vasodilating properties

A

Milrinone and enoximone

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10
Q

This study compared NE with NE + Vasopressin, showing no overall difference in survival between the treatment groups

A

VAAST study

 The
norepinephrine +
vasopressin group had
decreased norepinephrine
requirement. Mortality
benefit was seen in the
subgroup of patients with
less severe septic shock
receiving both
norepinephrine+
vasopressin when the
norepinephrine dose was <
15 μg/min
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11
Q

Side effects of NE?

A

Arrhythmias, bradycardia, peripheral ischemia

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12
Q

Side effects of Epi?

A

Arrythmias
Reduction in gut blood flow
Increases lactate

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13
Q

Side effects of dopamine?

A

More arrythmogenic than NE

↑ 28 day mortality with cardiogenic shock

Possible ↑ mortality in those with septic shock

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14
Q

Side effects of phenylephrine?

A

Reflex bradycardia

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15
Q

What happens if you titrate above the fixed dose of vasopressin?

A

Increased cardiac and peripheral ischemia

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16
Q

True/False: Intra-aortic balloon pump has shown a mortality benefit in cardiogenic shock

A

FALSE

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17
Q

Target Hgb for transfusion in most shock?

A

7 g/dL

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18
Q

Normal mixed venous O2 sat (Svo2)?

A

60-80%

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19
Q

Say you don’t happen to have a PA catheter to check a pure/majestic/unadulterated Svo2 and decide to check it off the central line in the right IJ instead (Scvo2). What is the normal Scvo2 compared to Svo2?

A

Scvo2 is slightly < Svo2

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20
Q

In the critically ill, what happens to Scvo2 compared to Svo2?

A

Scvo2 is often > Svo2

Giving you false hope that it isnt cardiogenic shock?

Also, there may be a benefit in targeting Scvo2 > 70% in the first 6 hours of shock.

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21
Q

Patient clinically improving overall from shock but lactates still elevated. What organ might have dysfunction?

A

Liver

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22
Q

Goal SBP in acute aortic dissection?

A

<120

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23
Q

Goal SBP in hemorrhagic CVA?

A

<140

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24
Q

Goal SBP in ischemic CVA?

A

<220

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25
Q

Goal MAP in hypertensive encephalopathy?

A

Decrease MAP by 20-25%

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26
Q

Goal DBP in pre-eclampsia?

A

<110

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27
Q

What % of upper GI bleed are caused by PUD?

A

50%

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28
Q

Urea:Cr in upper GI bleed?

A

> 100

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29
Q

How do vasoactive medications decrease bleeding in variceal hemorrhage?

A

They decrease portal blood flow

vasopressin, somatostatin and analogues like octreotide

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30
Q

What is the AIMS65 mnemonic for severity of upper GI bleed?

A
Albumin < 3.0
INR > 1.5
altered Mental status
SBP > 90
Age > 65
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31
Q

This intervention is reserved for unsuccessful endoscopic therapy for variceal bleeding

A

TIPS

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32
Q

True/False: prophylactic intubation before endoscopy has not shown to reduce the risk of aspiration

A

TRUE

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33
Q

What is the most common cause of lower GI bleed?

A

Diverticulosis

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34
Q

Drugs/toxins that can cause acute liver failure?

A
Acetaminophen
Alcohol
Amanita phalloides (mushroom)
Idiosyncratic drug reactions
Toxin exposure
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35
Q

Infections that can cause acute liver failure?

A

Hepatitis viruses (BCDE)
CMV
EBV

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36
Q

Perfusion problems that can cause acute liver failure?

A
Ischemic hepatitis
Shock liver
Veno-occlusive disease
HELLP
HLH
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37
Q

Genetic diseases that can cause acute liver failure?

A

Wilsons

AIH

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38
Q

Kings college criteria for liver transplant?

A

Arterial pH <7.3

Grade III/IV encephalopathy with PT >100sec and Cr >3.4

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39
Q

Most common cause of death in acute liver failure?

A

Cerebral edema

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40
Q

Treatment of cerebral edema in liver failure?

A

Hyperosmotic agents (mannitol)
Hyperventilation (PaCO2 targets 25-30)
Barbiturates

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41
Q

When to use antibiotics in pancreatitis?

A

If there is necrotizing pancreatitis.

Consider IR/surgical drainage

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42
Q

In most ICU patients, when should enteral nutrition be initiated?

A

Within 48hours of admission

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43
Q

When should TPN be considered?

A

1 week

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44
Q

Contraindications to enteral nutrition?

A

Hemodynamic instability in those predisposed to bowel ischemia, bowel obstruction, upper GI bleed, intractable vomiting, diarrhea

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45
Q

Contraindications to parenteral nutrition?

A

hyperosmolality, hypervolemia, severe hyperglycemia or electrolyte abnormalities

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46
Q

Indications for FFP administration?

A

Factor deficiency
Reverse warfarin
TTP (contains ADAMSTS13)
Coagulopathy in acute bleed

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47
Q

What are the components inside cryoprecipitate?

A

Fibrinogen, fibronectin, vWF, factor XIII, and factor VIII

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48
Q

What can be infused for patients with hemophilia A or B with life-threatening bleeds?

A

Factor VII

THATS 7

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49
Q

TRALI or TACO:

Fever, hypotension, pulmonary infiltrates, not likely to respond to diuretics

A

TRALI

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50
Q

Which type of HIT is immune mediated and takes longer to see?

A

Type II

Type I is more mild, a direct result of heparin on platelets, and occurs within the first 2 days of heparin exposure.

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51
Q

How long is anticoagulation indicated for patient swith HIT without thrombosis?

A

4-6 weeks

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52
Q

How long is anticoagulation indicated for patients with HIT with thrombosis?

A

3 months

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53
Q

Should you use warfarin for HIT?

A

NO

They exacerbate the prothrombotic state

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54
Q

3 different treatment options for TTP?

A

PLEX!!!!
Steroids if no evidence for drug-induced etiology or AKI despite PLEX
Rituximab with or without cyclophosphamide in refractory TTP-HUS

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55
Q

How long should PLEX be administered in TTP/HUS?

A

Until resolution of thrombocytopenia and hemolysis (LDH)

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56
Q

Which one of these has ↑PT/PTT, ↓platelets, ↓fibrinogen, ↑D-dimer:

TTP, HUS, DIC

A

DIC

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57
Q

According to the Cairo-Bishop definition, how many lab abnormalities do you need to be diagnosed with TLS?

A

2 or more

↑BUN, ↑K, ↑PO4, ↓Ca

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58
Q

Indications for emergent dialysis in TLS?

A

Severe oliguria/anuria, persistent hyperkalemia, or hyperphosphatemia-induced symptomatic hypocalcemia

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59
Q

How many blasts do you need on peripheral blood smear to be deemed to be in a blast crisis?

A

≥20%

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60
Q
47-year-old woman who
worked in a textile mill with
wool had malaise, fever,
and myalgia 5 days ago is
now presenting with severe
hypoxia and delirium.
Chest radiography shows
widened mediastinum.
What type of exposure is
suggested?
A

Bacillus anthracis

inhalation

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61
Q

Initial antibiotics for suspected bacterial meningitis in those >50, immunosupressed, alcoholics, or debilitated?

A

Ceftriaxone + vancomycin + ampicillin

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62
Q

Initial antibiotics for suspected bacterial meningitis in those after neurosuregery or have penetrating cranial trauma?

A

Ceftazidime + vancomycin

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63
Q

Dexamethasone dose and timing for meningitis?

A

0.15mg/kg Q6 for 4 days given before or with first antibiotic dose

64
Q

Treatment for RMSF encephalitis?

A

Doxycycline

65
Q

Treatment for neurosyphilis encephalitis?

A

PCN G

66
Q

Treatment for lyme encephalitis?

A

PCN or 3rd gen cephalosporin

67
Q

Treatment for herpes encephalitis?

A

ACV

68
Q

Treatment for VZV encephalitis?

A

ACV

69
Q

Treatment for brain abscess?

A

Ceftriaxone + metronidazole + surgery

70
Q

Needed Duke criteria for diagnosis of endocarditis?

A

2 major, or

1 major and 3 minor, or

5 minor

71
Q

Major Duke criteria for endocarditis?

A

Positive blood cultures:

  • Typical microorganism from 2 separate blood cultures
  • Persistently positive blood culture
  • Single blood culture for Coxiella burnetii or aniphase I immunoglobulin G antibody titer > 1:800

Evidence of endocardial involvement:

  • Positive echo findings
  • New valvular regurgitation
72
Q

Minor Duke criteria for endocarditis?

A

Predisposition (heart condition, IVDU)
Fever
Vascular phenomena (arterial emboli, septic pulmonary infarct, mycotic aneurysm, incracranial hemorrhage, conjunctival hemorrhage, Janeway lesions)
Immunologic phenomena (glomerulonephritis, Osler nodes, Roth spots, RF)
Positive blood cultures that do not meet major criteria

73
Q

Duration of antibiotics for native valve endocarditis?

Prosthetic valves?

A

Native - 4 weeks

Prosthetic - 6 weeks

74
Q

EKG abnormality that shows worsening endocarditis?

A

PR prolongation

75
Q

3 major indications for surgery for endocarditis?

A
  1. Heart failure (cardiogenic shock).
  2. Uncontrolled infection (abscess, enlarging vegetation, dehisence of prosthetic valve, persistent fever/blood cultures >7 days)
  3. Prevention of embolic event based on size (>15mm or > 10mm with complication).
76
Q

Duration of antibiotics for line infection after line removal for organisms that isnt S. aureus?

A

5-10 days

77
Q

Duration of antibiotics for line infection after line removal for organisms that is uncomplicated S. aureus?

A

14 days

78
Q

Duration of antibiotics for line infection after line removal for candidemia?

A

14 days

Make sure to check them eyes!

79
Q

Indications for surgery for C. diff infections?

A

Toxic megacolon
Perforation
Necrotizing colitis
Rapidly progressive or refractory disease with SIRS and multiple organ failure

80
Q

What type of soft tissue infection is likely given the following data:

Thin, dark, foul-smelling wound drainage with gas, pain, crepitus. Caused by clostridium species

A

Necrotizing cellulitis

81
Q

What type of soft tissue infection is likely given the following data:

Deep infection that spreads quickly, elevated CPK, crepitus, caused by mixed bacteria (type I) or group A strep (type II)

A

Nectrotizing fasciitis

82
Q

What type of soft tissue infection is likely given the following data:

Severe pain and induration of a muscle after skin abrasions, blunt trauma, or heavy exercise. Caused by group A strep.

A

Necrotizing myositis

83
Q

What type of soft tissue infection is likely given the following data:

Progression to red/yellow/green/black discoloration and bullae with crepitus. Causes acute sudden pain and swelling, sepsis, and serosanguineous drainage with sweet odor

A

Clostridial myonecrosis

84
Q
What antibiotic is included in the empiric antibiotic
treatment of severe soft
tissue infection because of
its antitoxin effects against
streptococci and
staphylococci species?
A

Clindamycin

85
Q

Protein and BP levels for the diagnosis of preeclampsia?

A

Proteinuria >300 mg/d

BP >140/90mmHg

86
Q

Single most important
predictor of hemorrhagic
stroke in patients with
preeclampsia?

A

SBP >160

87
Q

Antihypertensive treatment options in those with preeclampsia?

A

Labetalol
Nicardipine
Hydralazine

88
Q

Indications for delivery in HELLP?

A
DIC
Pulmonary edema
Liver hemorrhage/infarction
Renal failure
Placental abruption
Nonreassuring fetal status
89
Q

Most common cause of post-partum hemorrhage?

A

Uterine atony

God this is like doing medical school all over again. The worst.

90
Q

Young female patients present 3 months after delivering baby with fatigue, lethargy, secondary amenorrhea, and hyponatremia. What do you suspect?

A

Sheehan syndrome

91
Q

Treatment of Sheehan syndrome?

A

Make em hormonal again

92
Q

Which peripartum medications are associated with noncardiogenic pulmonary edema?

A

The tocolytics:

Terbutaline (ß2 agonist)
Ritodrine (ß2 agonist)

93
Q

This is the development of new-onset cardiomyopathy (LVEF <45%) that develops during the last month of pregnancy or up to 5 months postpartum

A

Peripartum cardiomyopathy

94
Q

Treatment for Peripartum cardiomyopathy?

A

Heart failure treatment guidelined except dont sue ACEi in pregnancy

95
Q

Outcomes for Peripartum cardiomyopathy?

A

1/3 recover

1/3 have residual cardiac failure

1/3 need transplant

96
Q

Preferred imaging modality for suspected PE in pregnancy?

A

VQ scan

97
Q

Preferred anticoagulation in PE with pregnancy?

A

LMWH

98
Q

How long to continue anticoagulation postpartum for a PE during pregnancy?

A

≥6 weeks (minimum 3-6 months)

99
Q

Young woman delivers and develops abrupt shock, profound hypoxemia, DIC, pulmonary edema, and coma. Suspected Dx?

A

Amniotic fluid embolism

100
Q

Treatment for Amniotic fluid embolism?

A

Supportive care for BP and hypoxemia, consider inhaled NO, control hemorrhage with blood products and factor VIIa

101
Q

Treatment for air embolism in pregnancy?

A

Place in left lateral decubitus position (prevents air from lodging in lungs) and trendelenburg (prevents going to brain)

102
Q

What is this clinical triad?

Bradycardia
Respiratory depression
Hypertension

A

Cushings triad

103
Q

Treatment for elevated ICP?

A
Treat cause (duh)
Elevated HOB
Hyperventilate (PaCO2 goal 25-30)
IV mannitol or hypertonic saline
Intubate using lidocaine
104
Q

After all other criteria for brain death are met and pt does not have hypothermia, hypercapnia, hypotension, or hypoxemia, what is the PaCO2 rise threshold for apnea test?

A

> 60mm Hg or 20 mmHg greater than baseline

105
Q

Which ancillary testing is indicated for brain death when clinical criteria cannot be done?

A
Cerebral angiography
Transcranial doppler
Magnetic MRA
CT angiography
EEG
106
Q

Suspected substance of overdose given the following clinical criteria?

Pupils ↑
Temp ↑
BP↑ 
HR↑
RR↑
Other: agitation, hallucinations, paranoia
A
Cocaine
Amphetamines
Pseudoephedrine
Caffeine
Theophylline
107
Q

Suspected substance of overdose given the following clinical criteria?

Pupils ↑ 
Temp↑
BP↑
HR↑
RR↑
Other: Myoclonus, hyperreflexia, diaphoresis, flushing, tremors, trismus, rigidity, confusion, agiation
A

MAOI, SSRI, TCA, dextromethophran

108
Q

Suspected substance of overdose given the following clinical criteria?

Pupils ↑
Temp↑
BP↑
HR↑
RR↑
Other: Nystagmus, perceptual distortions, hallucinations, agitation
A

Hallucinogens (LSD, ecstasy, PCP)

109
Q

Suspected substance of overdose given the following clinical criteria?

Pupils ↓
Temp↓
BP↓
HR↓
RR↓
Other: CNS depression, confusion, stupor, coma, hyporeflexia
A

Sedatives (benzos, alcohol, barbituates)

110
Q

Suspected substance of overdose given the following clinical criteria?

Pupils ↓
Temp↓
BP↓
HR↓
RR↓
Other: CNS depression, coma, hyporeflexia, pulmonary edema
A

Opioids

111
Q

Suspected substance of overdose given the following clinical criteria?

Pupils ↓
Temp ↔
BP↑
HR↓
RR ↨ 
Other: Salivation, incontinence, diarrhea, emesis, diaphoresis, lacrimation
A

Cholinergic agents (organophosphate, nicotine, verve agents, physostigmine, edrophonium)

112
Q

Suspected substance of overdose given the following clinical criteria?

Pupils↑
Temp↑
BP↑
HR↑
RR↑
Other: Dry/flushed skin and mucus membranes, urinary retention, myoclonus, hypervigilance, agiation, delirium
A

Anticholinergics (antihistamines, atrtopine, scopolamine, Jimson weed, TCA)

113
Q

NMS or serotonin syndrome:

Fevers, altered mental status, rigidity, hyperreflexia, myoclonus

A

Serotonin syndrome

NMS has hyporeflexia

114
Q

Treatment for NMS?

A

Dantrolene

Stop the drug

115
Q

Epinephrine dose for anaphylaxis?

A

0.3-0.5mg IM

Can repeat every 5-15 mins

116
Q

What are the pulmonary, neurologic, cardiovascular, and hematologic manifestations of near drowning?

A

Pulm- noncardiogenic pulmonary edema

Neurologic - cerebral edema and ↑ ICP

Cardiovascular - arrhythmias 2/2 hypothermia and hypoxemia

Heme- hemolysis and coagulopathy (rare)

117
Q

True/False: Heat stroke can be managed by cooling methods in addition to dantrolene, tylenol, and aspirin

A

FALSE

Meds dont work

118
Q

Drugs of choice for anthrax exposire?

A

Cipro or doxy

119
Q

Berlin definition of ARDS?

Onset
Imaging
Etiology
P:F

A

Onset - within 1 week of clinical insult
CXR- bilateral opacities
Etiology- non-cardiogenic
P:F - determines severity. Mild (200-300), Mod (100-200), Severe (<100).

120
Q
What condition is
associated with the
pathologic finding of diffuse
alveolar damage with no
known cause?
A

Acute interstitial
pneumonia (Hamman-Rich
syndrome)

121
Q

Direct lung injury causes of ARDS?

A
Pneyumonia
Aspiration
Neara drowning
Inhalation (smoke/toxin)
Pulmonary contusion
Embolism
Re-expansion injury
Reperfusion injury (after transplant)
122
Q

Indirect lung injury causes of ARDS?

A
Sepsis
Shock
Trauma
Blood transfusions
Cardiopulmonary bypass
Anaphylaxis
Medications (opioids, salicylates, amiodarone, tocolytics, chemotherapy)
Pancreatitis
123
Q

This phase of ARDS is characterized by release of inflammatory markers, leading to fluid leakage into the alveoli. Bx shows diffuse alveolar dmg.

A

Exudative phase

124
Q

Timeframe for exudative phase of ARDS?

A

<7-10d

125
Q

This stage of ARDS is characterized by resolution of pulmnary edema, proliferation of type II alveolar cells, squamous metaplasia, interstitial infiltration by myofibroblasts, early collagen deposition, and oblitration of pulmonary capillaries.

A

Proliferative stage

126
Q

Timeframe for proliferative stage of ARDS?

A

7d-2wk

127
Q

This stage of ARDS is characterized by obliteration of normal lung architecture, diffuse fibrosis, and cyst formation.

A

Fibrotic stage

128
Q

Timeline of fibrotic stage of ARDS?

A

> 2 weeks

129
Q

ARDSnet guidelines for TV, plateau pressure, PaO2 goal, pH goals?

A

TV 4-6mg/kg IBW
Plateau pressure < 30
PaO2 55-80
pH 7.3-7.45

130
Q

Risks of prostacyclin or NO in ARDS?

A

Can worsen shunt and oxygenation

131
Q

Patients that you want to avoid APRV due to short exhalation time?

A

Bronchospasm, obstructing secretions

132
Q

Initial inspiratory flow rates on volume control ventilation?

A

30-80 L/min

High flow rates has lower Ti but higher peak pressures

133
Q

Calculate resistance using peak and plateau pressures

A

R = peak - plateau

134
Q

Causes of large resistances on the vents (>5cmH2O)?

A

Increased airway resistance from bronchospasm, ET occlusion, patient biting tube

135
Q

Causes of elevated peak pressures but small difference between peak and plateau?

A

Decreased compliance:

pulmonary edema
pneumonia
PTX
Auto-PEEP
chest wall abnormality
increased abdominal pressure
136
Q

Calculate static compliance on the vent

A

TV/(plateau-PEEP)

137
Q

Calculate dynamic compliance on the vent

A

TV/(peak pressure - PEEP)

138
Q

Normal dynamic compliance on the vent?

A

50-100cm/H2O

139
Q

When paralyzed and mechanically ventilated peak airway pressure shows what?

A

the force required to overcome resistive and elastic recoil of the lung and chest wall

140
Q

Things you can do to adjust for double triggering on the vent?

A

Usually the Ti is shorter than the actual patients inspiratory time, so you can

increase TV, inspiratory time, or sedation and switching to a variable flow setting

141
Q

Most common cause of asynchrony where inspiratory effort that doesnt trigger a breath?

A

Auto-PEEP

Tx = increase PEEP. This reduces the amount of pressure drop needed for the patient to trigger a breath.

142
Q

Cause of autotriggering on the vent?

A

Vent is reading inspiratory effort but due to circuit leak, tube condensation, or vibration of ventilation

143
Q

Type of asynchrony where there is concave deflection on the pressure-time graphic

A

Inadequate flow rate

Tx = increase flow rate

144
Q

In cycling asynchrony, the duration of the breath is too short or long. What is the treatment?

A

Decrease Ti

Increase flow

145
Q

Cuff pressure goals to reduce the risk of tracheal stenosis or TE fistula?

A

18-25 mmHg

146
Q

2 methods to reduce risk of VAP?

A

CHG mouth scrubs

HOB elevation to >30 degrees

147
Q

True or False: an indication for NIPPV is fever and pulmonary infiltrates in immunocompromised host.

A

TRUE

This population is at an increased risk for VAP and alveolar hemorrhage if intubated, so OK to use NIPPV.

148
Q

Formula that relates CO2 production to alveolar ventilation?

A

PaCO2 = K (VCO2/VA)

K=0.863
VCO2 = CO2 ventilation
VA = alveolar ventilation

149
Q

THis is the concentration of CO2 at the end of each breath.

A

ETCO2

150
Q

Normal ETCO2?

A

35-45mmHg

151
Q

ETCO2 less than what # means poor quality CPR?

A

<10

152
Q

Why does ETCO2 rise when spontaneous circulation occurs during resuscitation?

A

Increased cardiac output

153
Q

What is the “20-30-40 rule” when you need ventilatory support with respiratory muscle weakness?

A

VC < 20 ml/Kg

NIF/MIP < -30 cm H2O

MEP < 40

154
Q

If a patient has unilateral diaphragmatic paralysis secondary to phrenic nerve injury, what happens to FVC and MIP on PFTs?

A

They decrease

155
Q

Patient post-CABG presents with fever, leukocytosis, elevated ESR, and pleural effusion. Thora reveals exudate with high neutrophil and eosinophil count. Diagnosis?

A

Post-pericardiotomy syndrome

This is thought to be due to an immunologic response to damaged cardiac tissue. Happens >1 wk post surgery.

156
Q

Bronchoscopic managment of bronchopleural fistula?

A

Gel foam, blood patch, fibrin glue

Valves

Ethanol injection

“laser”

157
Q

Hct threshold on pleural fluid to be deemed hemothorax?

A

> 50% of total body hct