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Block 9 Week 4 > Evidence Based Infections in Ventilated Patients-Kuhls > Flashcards

Evidence Based Infections in Ventilated Patients-Kuhls Flashcards

1
Q

When patients are intubated, they commonly aspirate (blank), particularly if they have eaten within the last (blank).
How can you reduce the incidence?

A

stomach contents
6 hours
-rapid sequence intubation and holding cricoid pressure (use drugs with quick onset of action and paralyzes patient to reduce gagging and valsalva AND puts pressure on esophagus to present gastric contents for coming up)

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2
Q

When will you use a rapid sequence intubation?

A

when you need to immediately intubate

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3
Q

What does acid do to your lungs?

A

damages and denudes respiratory endothelial cells creating a chemical pneumonitis

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4
Q

When happens if you have denuded endothelial cells? What types of bacteria will typically do this?

A

creates an opportunity for bacteria to invade

-Gram negative (oral flora)

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5
Q

Where is the majority of your bacteria in your GI tract?

A

mouth

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6
Q

What is the puddle of death?

A

Puddle of death-> set up for pneumonia cuz oral secretions collect about the ET balloon.

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7
Q

How do intubated patients develop pneumonia?

A
  • hospitalized pnts change oral flora to gram negative flora like pseudomonas
  • receptors on epithelial cells in mouth change to bind pathogenic organisms
  • oral floor pools above ET tube
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8
Q

People on ventilators are at risk for (blank)

A

gastric ulcers (put them on proton pump inhibitor)

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9
Q

What should you do if you are worried about your patient aspirating? What is this effective against?

A

decontaminate oral cavity with chlorhexidine

ONLY GRAM POSITIVE

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10
Q

In europe, they use gentamicin, colistin, and vanco to prevent ventiator-associated pneumonia, why dont we?

A

we are afraid of creating antibiotic resistance.

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11
Q

What were the results of oral decontamination?

A

pneumonia decreased from 31% to 10%

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12
Q

People have also tried gut decontamination, does this help reduce ventilator associated pneumonia?

A

YES! decreases bacteremia to 1.9%

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13
Q

If you have a patient who is intubated what three things must you do for them to keep them from aspirating? WHy?

A

have the heads of their beds up 30 degrees
have oral care
and frequent suctioning

Because these patients who are ill or sedated have a suppressed cough reflex

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14
Q

(blank) suctioning decreases the rate of pneumonia. Suctions the oral secretions that pool above the cuff of the endotracheal tube.

A

Subglottic

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15
Q

What is the most common nosocomial infection in the ICU?

A

Ventilator-associated pneumonia (VAP)

-65% of all nosocomial infections

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16
Q

Over 90% of VAP infections occur during (blank) ventilation. 50% begin within the first (blank) days of being intubated

A

mechanical

4

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17
Q

What is the crude mortality of VAP?

Why does it suck besides that it may cause death?

A

5-65%

lengthens hospital and ICU stay

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18
Q

What are the microbes found in hospital acquired pneumonia?

A

75% are gram negative aerobic bacilli (like pseudomonas) and gram positive

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19
Q

What are microbes found in community acquired pneumonia?

A

pneumococci
atypical organisms
viruses

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20
Q

Are gram positive or gram negatives more common in VAP?
What is the most common gram negative?
What is the most commmon gram positive?

A

gram negatives

Pseudomonas aeruginosa
Staph aureus

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21
Q

How should you treat VAP?

A

should cover aerobic gram neg bacilli

and staph aureus

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22
Q

How do you diagnose pneumonia?

Is this accurate?

A

clinically:

  • fever or hyperthermia
  • leukocytoses or leukopenia
  • increased respiratory secretions
  • new or worsened infiltrate on chest x-ray

NO, post-mortem exam on pnts diagnosed with pneumonia using this criteria is only 30-40%

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23
Q

Patients on ventilators have many causes of pulmonary infiltrates. Pneumonia represents (blank) of all pulmonary infiltrates in ICU patients. WHat are the other causes of pulmonary infiltrates?

A 
1/3rd
Atelctasis
Effusions
Pulmonary Edema
Pulmonary contusion (trauma)
ARDS
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24
Q

When doing a tracheal aspirate, what findings will lead you to pneumonia?

A

-presence of WBCS
(more than 25 neutrophils per HPF (high power field)
-Lung macrophages
-More than 10 squamos epithelial cells per LPF (suggestive of oral contamination)

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25
What is the accuracy of tracheal aspirate? So what will a negative culture tell you? What will a positive culture tell you?
cultures have high sensitivity (90%) but low specificity (5-40%) - negative culture excludes pneumonia - positive culture does not diagnoses VAP . In fact all intubated patients have colonized sputum.
26
What is a good way to diagnose pneumonia and is therapeutic? How does it work?
bronchoalveolar lavage Bronchoscopy and occlude distal airways that appears to have pneumonia. Insert sterile saline and suction fluid and send for quantitative culture (10^4)
27
How do you do a bronchoalveolar lavage without bronchoscopy?
protected brush sample | suction fluid and send for quantitative culture (10^4)
28
What is the most accurate test for detecting VAP?
BAL 10^4 (73% sensitive and 82% specific)
29
What is this: after at least 3 days of mechanical ventilation and within 2 days of worsening oxygenation the patient has body temp of 38C or< 36 or WBC count 12,000/mm^3 or 4,000/mm^3
Infection-related ventilator associated complication (IVAC)
30
What is this: after 2 days of stability or improvement on the ventilator, the patient has at least one of the following indications of worsening oxygen: increase in daily minimm FiO2 20% for at least 2 days or increase in daily minimum PEEP 3 cm H20 for at least 2 days
Ventilator Associated Condition
31
After at least 3 days of mechanical ventilation, and within 2 days of worsening on oxygenation the patient has purulent secretions and positive cultures
Probably Ventilator-Associated Pneumonia
32
What is the definition of acute respiratory distress syndrome (ARDS)?
- bilateral infiltrates CXR - wedge less than 18 or no clinical signs of left atrial HTN - hypoxemia regardless of amount of PEEP being used
33
ARDS = PO2/iO2F ratio of (blank) or less
200
34
Acute lung injury= pO2/FiO2 ratio of (blank) or less
300
35
Normal humans on room air have a pO2/FiO2 of (blank) or less
500
36
What is the incidence of ARDS? | What are the 2 types of ARDS?
75 per 100,000 per year (not very common, only seen when people are very ill) - Primary lung etiology of injury or pneumonia - Associated with systemic disease (caused by systemic disease)
37
Which type of ARDS represents a generalized systemic activation of the inflammatory system?
BOTH DO!!!
38
What are the systemic conditions associated with (CAUSE) ARDS?
1) shock of any type 2) trauma 3) infection/sepsis 4) transfusion
39
What are some common types of shock that causes ARDS?
Abdominal compartment syndrome and post cardiopulmonary bypass
40
What are some commom types of trauma that cause ARDS?
thoracic, fat emboli, soft tissue injury
41
What are the 2 categories of infection/sepsis that cause ARDS?
non pulmonary vs pulmonary
42
How can transfusion cause ARDS?
reaction to granulocyte 5b antibody (1 in 5000 transfusions)
43
What toxic gases can you inhale and get ARDS?
methamphetamine, smoke
44
What can you aspirate and get ARDS?
gastric contents or drug ingestion
45
What drugs can you aspirate and cause ARDs?
cocaine, salicylates
46
What are some intra-abdominal catastrophes that can cause ARDS?
pancreatitis, acalculous cholecystitis (inflammation of gall bladder without stones), infarcted bowel, etc.
47
What are the 5 stages of ARDS
- prodrome - acute or exudative phase - proliferative phase - fibrosing aveolitis (10+ days) - recovery
48
How long does the prodome phase last?
12-36 hours
49
How does the prodrome phase present?
- dyspnea, tachypnea, respiratory alkalosis (low pCO2) with normal pO2 - often presents as agitation - CXR shows mild increase in pulmonary microvasculature - physiologic-driven by inflammatory mediators.
50
What does the prodrome phase of ARDs look like histologically?
-infiltration of neutrophils, platelet aggregates, fibrin plugs (plugs up capillaries in the lungs and the alveoli)
51
How long does the acute or exudative phase of ARDS last?
up to 7 days
52
What is the hallmark sign of the acute or exuative phase? | What will the CXR show?
hypoxemia | bilateral infiltrates indistinguishable from cardiac edema
53
What are the physiologic/histologic changes of the acute or exudative phase of ARDS?
- increased capillary endothelial damage and permeability--> alveolar edema - neutrophil activation - alveolar epithelial disruption
54
When you have alveolar epithelial disruption as seen with ARDS, what will your alveoli look like?
flood with protein, blood, hyaline membranes, water-containing exudates
55
Summarize what happens in the acute or exudative phase?
causes fluid to go into alveoli and activation of neutrophils
56
What are the histological changes seen in type I alveolar cells (90% of epithelium in alveoli)?
they become denuded and contribute to pulmonary edema
57
How come when type I alveoli become denuded you get bacteremia and septic shock?
because the los of these cells allows bacteria to cross into the bloodstream causing bacteremia and sepsis
58
What alveolar cells produce surfactant? and what does ARDS do to these cells? What happens because of it?
type II alveolar cells dereased surfactant production atelectesis
59
What does ARDS activate and how?
inflammatory system - macrophage inhibitor factor (anterior pituitary) - Pro-inflammatory: increases IL-8 and a-TNF
60
What do you have if you see bilateral white out?
ARDS
61
When does the proliferative phase begin? | What is the hallmark of this phase?
day 7-10+ -Hypercarbia (usually its easy to get rid of CO2 in your lungs but you arent able to which means your lungs are really really bad...poor lungs)
62
In the proliferative phase what happens to the exudate?
collagen replaces it and thus begins fibrosis of the alveoli
63
What are the new pathological changes associated with the proliferative phase?
Collagen replaces exudate-> alveolar fibrosis Hypercarbia Increased alveolar thickness Increased shunt
64
When does the fibrosing stage begin and how long does it last?
10 days +
65
What are the findings of fibrosing alveolitis?
- increased alveolar thickness - increased shunt - hypercarbia - thickening and narrowing of vessels - 10-13% develop pneumothoraces - pulmonary HTN - Right heart failure - Increased mortality (especially if superimposed pneumonia)
66
What is the recovery stage of ARDS like?
- gradual improvement in hypercarbia and hypoxemia - macrophages remove protein - neutrophil apoptosis (key to recovery) - type II epithelial cells proliferate and differentiate into type I cells (weee!!!! more surfactant)
67
What is the key to recovery of ARDS and how long does it take to recover?
Neutrophil apoptosis | -pnts return to normal pulmonary function in 6-12 months
68
How do you treat hypotension or shock associated with ARDS?
- vasopressors + fluids + levophed (norepinephrine) - invasive catheter (help w/ fluids) - increase Hb
69
When you are giving a septic ARDS patient fluids, what type of fluids should you give them?
intravascular ones such as blood products and albumin
70
What is the difference in giving liberal vs conservative fluid management in ARDS patients?
no change in mortality | Conservative= less days on ventilator and in ICU
71
How should treat the sepsis associated with ARDS?
- culture - BROAD spec empiric antibiotics (dont delay) - de-escalate antibiotics based upon culture results
72
What antibiotics do you give to treat sepsis associated with ARDS?
GIVE ALL OF THESE: - Vanco or linezolid (for gram pos resistant bacteria) - Cefipime (4th generation cephalosporin) and merepenem (for gram negative and anaerobes) - fluconazole and caspofungin (for fungus)
73
Sepsis in patient increases mortality to (blank). What may reduce sepsis in critically ill patients?
50-80% -early enteral feeding (arginine is controversial)
74
To improve oxygenation in ARDS what do you do?
- increase PEEP (keeps alveoli open between breaths) to decrease FiO2 - get pO2 to 60s or 70s (=90% O2 sat) - inverse ratio ventilation (normal is 1 inspire to 2 expire, reverse this for inverse)
75
Why do you want to decrease FiO2 and by how much do you want to decrease it?
reduce O2 toxicity | less than 60%
76
T or F High versus low peep as long as oxygenation is maintained does not make a difference in mortality, vent free and ICU free days.
T
77
Why kind of tidal volume do you want to use in ARDs patients and why? What are the results of this related to?
low tidal volume decreases mortality (6cc is better than 12cc) -inflammatory response (6cc gives you lower IL-6)
78
What should you give an ARDS patient when peak pressures are above 35?
pressure control ventilation
79
ARDS patients have hypercapnia which isnt generally harmful but Low pH can be controlled by (blanK)
dialysis
80
Tell which of these are beneficial: High frequency jet ventilation? High frequency oscillator ventilation? Airway pressure release ventilation (APRV)?
- No proven benefit - may benefit if used early - beneficial * decreased ventilator days by 6 * decreaed ICU days by 7 * less sedation, paralytics
81
When you are laying supine with ARDS what happens?
your posterior alveoli collapse due to gravity and you get greater posterior profusion (v/q mismatch)
82
What happens when you are laying prone in ARDS?
recruits posterior alveoli and improves profusion - improved oxygenation - P/F ratios were improved - Mortality was unchanged
83
What is rotational therapy?
rotates patients nearly 270 degrees | can improve oxygenation
84
How long should patients be prone? supine?
2/3rds of the time | 1/3 of the time

Block 9 Week 4 (9 decks)

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