Kuhl's: Evidence Based Infections in Ventilated Patients Flashcards

(50 cards)

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?

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?

24
Q

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

25
What are the 2 types of ARDS?
1. due to a primary lung injury or pneumonia | 2. associated with a systemic condition
26
Regardless of the etiology, ARDS represents a generalized (blank) of the inflammatory system
systemic activation
27
List some (8) conditions associated with ARDS
``` Shock of any type Trauma Infection/sepsis Transfusion Inhalation of toxic gases Aspiring gastric contents Intra-abdominal catastrophe Multi-organ failure ```
28
5 stages of ARDS
1. prodome 2. acute or exudative phase 3. proliferating phase 4. fibrosing alveolitis 5. recovery
29
Describe the prodrome phase of ARDS (12-36hrs). What drives the physiologic process that is occurring during this phase?
dyspnea, tachypnea, respiratory alkalosis with NORMAL pO2 often presents as agitation CXR shows mild increase in pulmonary vasculature **driven by inflammatory mediators
30
What is the hallmark of the acute or exudative phase of ARDS (up to 7 days)? What are the physiologic/histologic changes?
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
What happens to type 1 and type 2 pneumocytes in the acute phase of ARDS?
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
The acute or exudative phase basically activates the (blank) system
inflammatory
33
What will you see on CXR with ARDS?
bilateral white out
34
What stage is this? Increased alveolar thickness, increased shunt. Collagen replaces exudate-->beginning of alveolar fibrosis Hypercarbia is the hallmark
stage 3: proliferative phase **hypercarbia is the hallmark
35
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
stage 4: fibrosing alveolitis
36
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
Stage 5 - recovery
37
What do you use to treat sepsis in ARDS?
fluids | vasopressors
38
What are the two types of fluids?
crystalloid | colloids (containing blood products)
39
Does it matter if you give fluids conservatively or liberally?
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
How to treat sepsis?
send cultures start broad spectrum antibiotics immediately then narrow them down when you get specific testing results back
41
What antibiotics to use for resistant gram positives?
vancomycin | linezolid
42
T/F: Sepsis increases mortality to 50-80%
True
43
What is PEEP used for?
you increase PEEP to decrease Fi02 | PEEP keeps alveoli open
44
What level should p02 be at?
60's or 70's 60 = 90% O2
45
Goal is to decrease FiO2 to less than (blank)% to reduce O2 toxicity.
60%
46
What is the inverse ratio ventilation?
normal 1:2 (inspiration vs expiration)
47
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.
True
48
What tidal volume should be used in lung protective ventilation?
low tidal volume **associated with decreased mortality
49
What happens to patients who are constantly lying supine in beds? What can be done for these patients?
they get collapse of their posterior alveoli; prone these patients
50
Alternative that rotates patients nearly 270 degreess | Can improve oxygenation
rotational therapy