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Block 9 Week 4 > Kuhl's: Evidence Based Infections in Ventilated Patients > Flashcards

Kuhl's: Evidence Based Infections in Ventilated Patients Flashcards

1
Q

When patients are intubated, they commonly aspirate stomach contents. What can be done to decrease the incidence and amount of aspiration?

A

rapid sequence intubation & holding cricoid pressure

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2
Q

How can stomach contents get into the respiratory tract and cause pathology?

A

stomach contents are acidic, and the acid can damage and denude respiratory endothelial cells –> denuded endothelial cells create an opportunity for bacteria to invade

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3
Q

What can happen to patients with endotracheal tubes?

A

puddle of death - oral flora pool in secretions above the balloon of the endotracheal tube

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4
Q

Hospitalized patients change their oral flora to this…

A

gram negative flora, like pseudomonas

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5
Q

This can be used to decontaminate the oral cavity

A

chlorhexidine antiseptic agent

**only effective against gram positive organisms

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6
Q

Oral decontamination decreases pneumonia occurance from 31% to (blank)%

A

10%

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7
Q

This is another form of decontamination which can decrease bacteremia to 1.9%

A

gut decontamination

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8
Q

Why is decontamination used more often in Europe that in the US?

A

In the US, there is a concern about bacterial resistance

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9
Q

This is another intervention that can be used to decrease the rate of pneumonia in patients who are intubated

A

subglottic suctioning - suctions the oral secretions that pool above the cuff of the endotracheal tube

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10
Q

the most common nosocomial infection in the ICU – 65% of all nosocomial infections

A

ventilator associated pneumonia

**over 90% occur during mechanical ventilation, 50% begin w/i the first four days of intubation

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11
Q

Lengthens hospital and ICU stay

A

ventilator-associated pneumonia

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12
Q

Which bacteria are most often associated with ventilator-associated pneumonia?

A

gram negative bacilli: pseudomonas aeruginosa and E. Coli

gram positive cocci: Staph aureus

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13
Q

T/F: Many gram negative bacteria are multi-drug resistant

A

True

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14
Q

Antibiotic therapy should cover this type of bacteria

A

aerobic gram negative bacilli

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15
Q

How to traditionally diagnose pneumonia?

A

fever or hypothermia
leukocytoses or leukopenia
increased respiratory secretions
new or worsened infiltrate on CXR

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16
Q

In patients who are on ventilators, there are many causes of pulmonary infiltrates. Name a few.

A 
Atelectesis: alveoli collapse
Effusions
Pulmonary edema
Pulmonary contusion
ARDS
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17
Q

(blank) represents 1/3 of all pulmonary infiltrates in ICU patients

A

pneumonia

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18
Q

When you do a tracheal aspirate, what number of WBCs indicates infection? What other cells indicate infection if present in the aspirate?

A

> 25 neutrophils per HPF
lung macrophages are an indication of infection
10 squamous epithelial cells per LPF is suggestive of oral contamination (saliva mixes with coughed up sputum)

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19
Q

If you have a negative culture from a tracheal aspirate, does this rule out pneumonia? Is a positive culture diagnostic for ventilation-associated pneumonia?

A

yes, a negative culture excludes pneumonia; a positive culture is not diagnostic for VAP bc all intubated pts have some colonies growing in their sputum

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20
Q

What is bronchoalveolar lavage?

A

do a bronchoscopy, instill sterile saline, suction the fluid and send for a culture (look for 10^4 CFU/mL)

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21
Q

What is the diagnostic threshold for bronchoalveolar lavage culture?

A

10^4

22
Q

What are the diagnostic criteria for ARDS?

A
  1. bilateral infiltrates of CXR
  2. wedge pressure less than 18 or no clinical signs of left atrial hypertension
  3. hypoxemia regardless of amount of PEEP being used
23
Q

In ARDS, what is the PO2/iO2F ratio?

A

200 or less

24
Q

For acute lung injury, what is the PO2/iO2F ratio?

A

300 or less

25
Q

What are the 2 types of ARDS?

A
  1. due to a primary lung injury or pneumonia

2. associated with a systemic condition

26
Q

Regardless of the etiology, ARDS represents a generalized (blank) of the inflammatory system

A

systemic activation

27
Q

List some (8) conditions associated with ARDS

A 
Shock of any type
Trauma
Infection/sepsis
Transfusion
Inhalation of toxic gases
Aspiring gastric contents
Intra-abdominal catastrophe
Multi-organ failure
28
Q

5 stages of ARDS

A
  1. prodome
  2. acute or exudative phase
  3. proliferating phase
  4. fibrosing alveolitis
  5. recovery
29
Q

Describe the prodrome phase of ARDS (12-36hrs). What drives the physiologic process that is occurring during this phase?

A

dyspnea, tachypnea, respiratory alkalosis with NORMAL pO2
often presents as agitation
CXR shows mild increase in pulmonary vasculature

**driven by inflammatory mediators

30
Q

What is the hallmark of the acute or exudative phase of ARDS (up to 7 days)?

What are the physiologic/histologic changes?

A

HYPOXEMIA
CXR shows bilateral infiltrates that are indistinguishable from cardiac edema;

increased capillary endothelial damage –> alveolar epithelial disruption –> alveoli flooded with protein, blood, hyaline membranes, etc

31
Q

What happens to type 1 and type 2 pneumocytes in the acute phase of ARDS?

A

Type 1 alveolar cells are denuded –> loss of protective barrier allows the bacteria to cross into the bloodstream, causing bactermia and septic shock

type 2 alveolar cells are damaged –> decreased surfactant –> atelectesis

32
Q

The acute or exudative phase basically activates the (blank) system

A

inflammatory

33
Q

What will you see on CXR with ARDS?

A

bilateral white out

34
Q

What stage is this?

Increased alveolar thickness, increased shunt.
Collagen replaces exudate–>beginning of alveolar fibrosis
Hypercarbia is the hallmark

A

stage 3: proliferative phase

**hypercarbia is the hallmark

35
Q

What stage is this?

Increased alveolar thickness, increased shunt
Difficulty with CO2 exchange–>hypercarbia
Thickening and narrowing of vessels
10-13% develop pneumothoraces
Pulmonary Hypertension
Right Heart Failure
Increased mortality, especially if superimposed pneumonia

A

stage 4: fibrosing alveolitis

36
Q

What stage is this?

Gradual improvement in hypercarbia and hypoxemia.
Interestingly many patients return to normal pulmonary function in 6-12 months.
Macrophages play key role in protein removal.
Type II epithelial cells proliferate and differentiate into Type I cells.
Neutrophil apoptosis (death) key to recovery

A

Stage 5 - recovery

37
Q

What do you use to treat sepsis in ARDS?

A

fluids

vasopressors

38
Q

What are the two types of fluids?

A

crystalloid

colloids (containing blood products)

39
Q

Does it matter if you give fluids conservatively or liberally?

A

nahhh, no need to crush em! Besides, you can save on hospital bill

**ventilator free days and ICU free days are higher in conservative group

40
Q

How to treat sepsis?

A

send cultures
start broad spectrum antibiotics immediately
then narrow them down when you get specific testing results back

41
Q

What antibiotics to use for resistant gram positives?

A

vancomycin

linezolid

42
Q

T/F: Sepsis increases mortality to 50-80%

A

True

43
Q

What is PEEP used for?

A

you increase PEEP to decrease Fi02

PEEP keeps alveoli open

44
Q

What level should p02 be at?

A

60’s or 70’s

60 = 90% O2

45
Q

Goal is to decrease FiO2 to less than (blank)% to reduce O2 toxicity.

A

60%

46
Q

What is the inverse ratio ventilation?

A

normal 1:2 (inspiration vs expiration)

47
Q

T/F: High versus low peep as long as oxygenation is maintained does not make a difference in mortality, vent free and ICU free days.

A

True

48
Q

What tidal volume should be used in lung protective ventilation?

A

low tidal volume

**associated with decreased mortality

49
Q

What happens to patients who are constantly lying supine in beds? What can be done for these patients?

A

they get collapse of their posterior alveoli; prone these patients

50
Q

Alternative that rotates patients nearly 270 degreess

Can improve oxygenation

A

rotational therapy

Block 9 Week 4 (8 decks)

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