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BLOCK 9; Week 4-M > Evidence Based Infections in Ventilated Patients > Flashcards

Evidence Based Infections in Ventilated Patients Flashcards

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1
Q

Do patients often aspirate when they are ventilated? What are some factors to decrease aspiration?

A

yes. esp if they have eaten within the last 6 hours.
factors to decrease aspiration:
rapid sequence intubation
holding cricoid pressure

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2
Q

What is so bad about stomach contents getting into the lungs?

A

There is…
ACID–>can cause chemical pneumonitis
BACTERIA-gram neg., can get infection
both damage respiratory endothelial cells

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3
Q

How do the oral secretions of hospitalized patients change?

A

they become more negative.

the receptors on epithelial cells of mouth bind pathogenic organisms…

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4
Q

Where is the pool of death located? What does that mean?

A

located behind the balloon of the endotracheal tube

this is filled with oral secretions that can get in to the lung & wreck havoc

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5
Q

What can you do to help this aspiration problem?

A
  1. decontaminate the oral cavity

2. subglottic suctioning-decreases puddle of death

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6
Q

What is involved in decontaminating the oral cavity?

A

chlorhexidine antiseptic for mouth–decreases gram + organisms
H2 blockers to decrease acid secretions.
**decreases pneumonia 31-10% & bacteremia decreased by 1.9%

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7
Q

What is the most common nosocomial infection?

A

ventilator associated pneumonia, 65%

>90% occur with mechanical ventilation

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8
Q

What is the usual microbiology of hospital acquired pneumonia?

A

mostly gram neg naerobic bacilli (75%)-ex: pseudomonas

some gram +

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9
Q

What is the usual microbiology of community acquired pneumonia?

A

Pneumococci
Atypical organisms
Viruses

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10
Q

T/F Many of the gram neg. bacteria in VAP are multi drug resistant.

A

True.

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11
Q

What are 2 things that antibiotics must cover for hospital acquired pneumonia, specifically VAP?

A

gram neg. bacilli & MRSA/Staph Aureus

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12
Q

What is involved in the diagnosis of pneumonia?

A

Fever or hypothermia
Leukocytoses or leukopenia
Increased respiratory secretions
New or worsened infiltrate on chest x-ray

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13
Q

In patients on ventilators there a bunch of causes of pulmonary infiltrates. What are some of them? What % of them are included under the category of pneumonia?

A

1/3 pneumonia

Atelectesis-someone not breathing deeply enough, alveoli don’t open up=opacity
Effusions
Pulmonary edema looks similar to pneumonia
Pulmonary contusion (trauma). Bruises on lungs can look like pneumonia.
ARDS

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14
Q

What are you looking for when you test tracheal aspirate?

A

WBCs-infection
macrophages-infection
more than 10 squamous cells–>indicates more oral than tracheal aspirate

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15
Q

What is the accuracy of tracheal aspirate in diagnosing VAP?

A

sensitive but not specific
sens: if neg. no VAP
not specific–>if pos. could just be normal colonization of sputum in intubated patients

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16
Q

What is involved in bronchoalveolar lavage?

A

can test for pathogen & is therapeutic

Bronchoscopy and occlude the distal airway that appears to have pneumonia
Instill sterile saline
Suction fluid and send for quantitative culture (104)

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17
Q

How is acute respiratory distress syndrome diagnosed?

A
  1. bilateral infiltrates on CXR
  2. wedge<18; no clinical signs of LA HTN
  3. hypoxemia even with high PEEP
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18
Q

WHat is the PO2/FIO2 ratio of normal people? For a definition of ARDS, what must your PO2/FIO2 be? How about for ARDS diagnosis after acute lung injury?

A

Normal; PO2/FiO2=500

ARDS diagnosis: <300

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19
Q

What are the 2 types of ARDS?

A
  1. primary–injury of lung thru trauma or pneumonia etc.
  2. systemic-associated with a system wide deal
    * *systemic activation of inflammation–CRP would be present
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20
Q

What are some systemic conditions associated with ARDS?

A
  1. Shock
  2. Trauma
  3. Sepsis/Infection (even nonpulmonary)
  4. Transfusion
  5. Inhalation of Toxic Gases: smoke, meth
  6. Aspiration of Gastric Contents (esp if there are drugs there or it is super acidic)
  7. Intra-abdominal catastrophe-infarcted bowel or pancreatitis)
  8. multiorgan failure
21
Q

What are the stages of ARDS?

A
  1. Prodrome-feel sick
  2. Acute or Exudative Phase
  3. Proliferative Phase
  4. Fibrosing Alveolitis (10+ days)
  5. Recovery
22
Q

What period of time makes up the prodrome? What are the symptoms at this time?

A

12-36 hrs
dyspnea, tachypnea, resp alkalosis (low pCO2 w/ normal pO2)
agitation

23
Q

What does the CXR show in the prodrome phase of ARDS? What is happening physiologically at this time?

A

CXR: mild increase in pulmonary vasculature
Physiologic: inflammatory mediators present, platelet aggregates, fibrin plugs

24
Q

What period of time makes up the acute or exudative phase? What is the main symptom in this phase?

A

up to 7 days

Hallmark: HYPOXEMIA

25
Q

What is shown on CXR & what is happening physiologically @ acute/exudative phase of ARDS?

A

CXR: bilateral infiltrates-can look like cardiac edema
Physio: capillary endothelial damage–>alveolar edema
neutrophil activation
alveolar epithelial disruption: lots of protein, blood, hyaline, water w/ exudates

26
Q

What’s going on @ the histo level during the acute/exudative phase of ARDS?

A

Type 1 Alveolar Cells–>denuded & contributing to pulmonary edema, allows bacteria into bloodstream
Type 2 Alveolar Cells–>surfactant loss–>atelectesis

27
Q

What is an important thing to give to babies who are born prematurely?

A

artificial surfactant

28
Q

What happens to the inflammatory system during the acute/exudative phase of ARDS?

A

Activation of Inflammatory System:
Macrophage Inhibitory Factor (Anterior Pituitary)
Pro-inflammatory: Increases IL-8 and a-TNF.

29
Q

What is the timeframe for the proliferative phase of ARDS? What’s the hallmark of this period? What else is going on?

A 
7-10+ times
Hallmark: hypercarbia
increased alveolar thickness, increased shunt
collagen is laid down, less exudate
alveolar fibrosis begins
30
Q

What’s the deal with the hypercarbia in the proliferative phase of ARDS?

A

CO2 always exchanges better than O2. At this stage of collagen proliferation etc. even CO2 can’t be exchanged.

31
Q

WHat is the timeframe for the fibrosing alveolitis stage of ARDS?

A

10+ days
increased alveolar thickness
once again, hypercarbia
**thickening & narrowing of vessels

32
Q

What are some possible complications of the fibrosing alevolitis stage of ARDS?

A

some develop a pneumothorax
pulmonary HTN
right heart failure
increased mortality

33
Q

What happens during the recovery phase of ARDS?

A

macrophages go to work in protein removal
neutrophil apoptosis
type II cells can differentiate into type 1
**Gradual improvement in hypercarbia & hypoxemia

34
Q

How long does it take for patients to return to normal after ARDS?

A

6-12 months

35
Q

What is a treatment during sepsis in patients with ARDS?

A

vasopressors-increase CO

fluid resuscitation–sometimes blood products w/ increased Hb for oxygen carry capacity

36
Q

T/F It is best to use osmotic fluids, such as dextrose or albumin, in patients with lung damage, compared to regular IV fluids.

A

False. Sometimes it can do damage. So use regular IV fluids.
Conservative fluid groups in research have fewer ICU days.

37
Q

After you send cultures for a patient with sepsis, what do you do next?

A

STart them on super broad spectrum antibiotics. Then after you get the culture results you can narrow it down.

38
Q

Which antibiotics can address resistant gram +?

A

vancomycin

linezolid

39
Q

Which antibiotics address gram - & anaerobes?

A

cefipime (a 4th gen cephalosporin)

merepenem

40
Q

Which drugs can address fungal infections?

A

fluconazole, caspofungin

41
Q

T/F Early enteral feeding may reduce sepsis in critically ill patients. ALso, arginine may help.

A

True.

42
Q

What is PEEP? What is this value in a healthy person?

A

positive end expiratory pressure
glottis closes–>PEEP
Healthy person: 5 PEEP, low value
higher PEEP, allows us to keep alveoli open all the time b/c if it is opening & closing can cause shearing in an unhealthy person

43
Q

What does an increased PEEP do to FiO2? What is a goal FiO2 for a sick person?

A

increased PEEP=decreased FiO2

you want FiO2<60% to reduce O2 toxicity

44
Q

What type of tidal volume do you want to use for lung protective ventilatoin?

A

low tidal volumes (6cc/kg)
decreases the inflammatory response
protect the fragile lungs b/c our alveoli are open the whole time

45
Q

T/F Permissive hypercapnia is harmful.

A

False. low pH can be controlled by dialysis.

46
Q

What are other forms of ventilator support?

A

high frequency jet ventilation
high frequency oscillator ventilation
airway pressure release ventilation (pretty effective)

47
Q

Which position is most therapeutic for ill patients w/ lung issues? WHy?

A

prone position-on stomach is best

when supine: posterior alveoli collapse & get V/Q mismatch w/ too much perfusion to these posterior alveoli

48
Q

What is an alternative to prone positioning?

A

rotational therapy–rotate patient 270 degrees to improve oxygenation
**Can do with 4 people or super fancy machine

BLOCK 9; Week 4-M (8 decks)

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