Evidence Based Infections in Ventilated Patients

Question 1

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

Answer 1

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

Question 2

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

Answer 2

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

Question 3

How do the oral secretions of hospitalized patients change?

Answer 3

they become more negative.

the receptors on epithelial cells of mouth bind pathogenic organisms…

Question 4

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

Answer 4

located behind the balloon of the endotracheal tube

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

Question 5

What can you do to help this aspiration problem?

Answer 5

1. decontaminate the oral cavity

2. subglottic suctioning-decreases puddle of death

Question 6

What is involved in decontaminating the oral cavity?

Answer 6

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

Question 7

What is the most common nosocomial infection?

Answer 7

ventilator associated pneumonia, 65%

>90% occur with mechanical ventilation

Question 8

What is the usual microbiology of hospital acquired pneumonia?

Answer 8

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

some gram +

Question 9

What is the usual microbiology of community acquired pneumonia?

Answer 9

Pneumococci
Atypical organisms
Viruses

Question 10

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

Answer 10

True.

Question 11

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

Answer 11

gram neg. bacilli & MRSA/Staph Aureus

Question 12

What is involved in the diagnosis of pneumonia?

Answer 12

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

Question 13

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?

Answer 13

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

Question 14

What are you looking for when you test tracheal aspirate?

Answer 14

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

Question 15

What is the accuracy of tracheal aspirate in diagnosing VAP?

Answer 15

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

Question 16

What is involved in bronchoalveolar lavage?

Answer 16

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)

Question 17

How is acute respiratory distress syndrome diagnosed?

Answer 17

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

Question 18

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?

Answer 18

Normal; PO2/FiO2=500

ARDS diagnosis: <300

Question 19

What are the 2 types of ARDS?

Answer 19

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

Question 20

What are some systemic conditions associated with ARDS?

Answer 20

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

Question 21

What are the stages of ARDS?

Answer 21

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

Question 22

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

Answer 22

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

Question 23

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

Answer 23

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

Question 24

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

Answer 24

up to 7 days

Hallmark: HYPOXEMIA

Question 25

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

Answer 25

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

Question 26

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

Answer 26

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

Question 27

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

Answer 27

artificial surfactant

Question 28

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

Answer 28

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

Question 29

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

Answer 29

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

Question 30

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

Answer 30

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

Question 31

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

Answer 31

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

Question 32

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

Answer 32

some develop a pneumothorax pulmonary HTN right heart failure increased mortality

Question 33

What happens during the recovery phase of ARDS?

Answer 33

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

Question 34

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

Answer 34

6-12 months

Question 35

What is a treatment during sepsis in patients with ARDS?

Answer 35

vasopressors-increase CO | fluid resuscitation--sometimes blood products w/ increased Hb for oxygen carry capacity

Question 36

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

Answer 36

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

Question 37

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

Answer 37

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

Question 38

Which antibiotics can address resistant gram +?

Answer 38

vancomycin | linezolid

Question 39

Which antibiotics address gram - & anaerobes?

Answer 39

cefipime (a 4th gen cephalosporin) | merepenem

Question 40

Which drugs can address fungal infections?

Answer 40

fluconazole, caspofungin

Question 41

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

Answer 41

True.

Question 42

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

Answer 42

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

Question 43

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

Answer 43

increased PEEP=decreased FiO2 | you want FiO2<60% to reduce O2 toxicity

Question 44

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

Answer 44

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

Question 45

T/F Permissive hypercapnia is harmful.

Answer 45

False. low pH can be controlled by dialysis.

Question 46

What are other forms of ventilator support?

Answer 46

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

Question 47

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

Answer 47

prone position-on stomach is best | when supine: posterior alveoli collapse & get V/Q mismatch w/ too much perfusion to these posterior alveoli

Question 48

What is an alternative to prone positioning?

Answer 48

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