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Acute Care II - Summer 2017 > Weeks 7 & 8: Acute Respiratory Failure > Flashcards

Weeks 7 & 8: Acute Respiratory Failure Flashcards

1
Q

definition of acute respiratory failure

A

inadequate oxygenation OR ventilation which threatens function of vital organs

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2
Q

diagnostic criteria for acute respiratory failure

A
  • hypoxemia: PaO2 < 60 mm Hg

and/or

  • hypercapnia: PaCO2 > 50 mm Hg
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3
Q

what are the two types of acute respiratory failure

A

Type I ARF (hypoxic)

Type II ARF (hypoxic hypercarbic)

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4
Q

Description of Type I ARF (hypoxic)

A
  • PaO2 < 60 mm Hg
  • PA-PaO2 (A/a gradient) > 25 mm Hg
  • increased shunt (PaO2/FiO2 ratio < 300)
  • PaCO2 normal or < 50 mm Hg
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5
Q

Causes of Type I ARF (hypoxic)?

A
  • V/Q mismatch
  • alveolar hypoventilation
  • diffusion defect
  • R to L shunt
  • low ambient oxygen
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6
Q

Description of Type II ARF (hypoxic hypercarbic).

A
  • PaO2 < 60 mm Hg
  • PaCO2 > 50 mm Hg
  • acidosis
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7
Q

Causes of Type II ARF (hypoxic hypercarbic)

A
  • alveolar hypoventilation
  • increased airway resistance
  • loss of lung surface area
  • chest deformity
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8
Q

what is an intrapulmonary shunt

A

Percent of total veous blood that BYPASSES gas exchange (alveoli) and returns unoxygenated to systemic arterial system

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9
Q

what is a normal value for intrapulmonary shunt?

A

Normal 3-5% up to max of 10%

increased with each decade of life

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10
Q

Visual of intrapulmonary shunt

A
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11
Q

what do you need for a true shunt calculation?

A

mixed venous blood (from a Swan)

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12
Q

how do you estimate intrapulmonary shunt?

A
  • A-a gradient: least accurate with increasing FiO2, but most common
  • a/A ratio (Arterial to alveolar ratio): most accurate, allows for changes in PaCO2
  • PaO2/FiO2 ratio: most accurate, can be easiest (if PaCO2 is stable)
  • Respiratory index: not common
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13
Q

what do you need to do in order to be able to estimate shunt using a/A ratio?

A

must calculate Alveolar gas using standard equation

PAO2=[FiO2(Patm - PH2O)-(PaCO2/RQ)]

then divided PaO2/PAO2

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14
Q

what can you use to look at the diffusion defect?

A

A-a gradient = PAO2 - PaO2

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15
Q

what is a normal arterial - alveolar ratio

A

Normal > 0.8-0.9

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16
Q

is higher or lower a/A ratio make the shunt worse?

A

the lower the a/A ratio the worse the shunt

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17
Q

where do you obtain the PaCO2 & PaO2 values needed to calculate the diffusion defect/estimate the shunt?

A

ABG

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18
Q

what is normal PaO2/FiO2 ratio

A

550

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19
Q

what is the assumption for estimating shunt using PaO2 / FiO2 ratio?

A

that the patient is on 100% oxygen

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20
Q

what is the PaO2/FiO2 value for acute lung injury

A

<300

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21
Q

what is the PaO2 / FiO2 ratio value for ARDS

A

< 200

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22
Q

does a lower ratio for PaO2 / FiO2 ratio mean a larger or smaller shunt?

A

the lower the PaO2 / FiO2 ratio the larger the shunt

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23
Q

what is approximate shunt for PaO2 / FiO2 ratio for: 500, 300, 200?

A

500 - 5% shunt

300 - 15% shunt

200 - 20% shunt

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24
Q

clinical symptoms of ARF

A

dyspnea

orthopnea

anxiety

chest pain/stiffness

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25
Q

clinical signsof ARF

A
  • pulse oximetry, capnography & ABG: hypoxemia, hypercapnia
  • Tachypnea, increased WOB, accessory muscle use, nasal flaring, suprasternal or supraclavicular retractions paradoxical ‘abdominal’ breathing
  • confusion, restlessness, somnolence or AMS
  • crackles, rhonchi, ‘silent chest’
  • JVD
  • stress response: tachycardia, HTN, diaphroesis
  • Late: peripheral or central cyanosis, cardiac arrhythmia and coma
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26
Q

what is the most common cause of hypoxemic ARF?

A

a V/Q mismatch

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27
Q

what is a V/Q mismatch?

A

alveolar ventilation & pulmonary perfusion mismatch

perfusion of an unventilated lung

there is blood flow to the lung but it doesn’t have O2 in it, you’re wasting the blood going to that lung

it’s a problem of OXYGENATION as opposed to elimination of CO2

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28
Q

what are the most common causes of V/Q mismatch

A

PNA, aspiration, acute pulmonary edema, airway obstruction & severe stelectasis

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29
Q

what are less common causes of hypoexmic ARF?

A
  1. diffusion defect
  2. alveolar hypoventilation/inadequate minute ventilation
  3. high altitude
  4. low mixed venous oxygenation
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30
Q

definition of diffusion defect?

A

prevents O2 diffusion into blood

*

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31
Q

example of diffusion defect?

A

interstitial edema

inflammation

fibrosis

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32
Q

what do you do to fix diffusion defect?

A

treat causes: diuretics for cardiogenic pulmonary edema, corticosteroids for inflammatory disorder

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33
Q

examples of alveolar hypoventilation/inadequate minute ventilation?

A

anesthetic agents

opioid overdose

neuromusclar block/defect (myasthenia gravis)

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34
Q

how to treat alveolar hypoventilation/inadequate minute ventilation?

A

treat respiratory depression: stimulation, reversal getns, etc.

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35
Q

definition of high altitude hypoxemic ARF?

A

low inspired partial pressure of O2

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36
Q

definition of low mixed venous oxygenation?

A

extremely desaturation blood returning to lungs –> not adequately re-oxygenated

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37
Q

what is a potential cause of low mixed venous oxygenation, a less common cause of hypoxemic ARF?

A

low flow state could be causing extremely desaturated blood returning to lungs

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38
Q

what is V in V/Q mismatch?

A

v - ventilation: the air that reaches the alveoli

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39
Q

what is Q in V/Q mismatch

A

Q - perfusion: the blood that reaches the alveoli

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40
Q

Low V/Q?

A

limited ventilation relative to perfusion

Low PaO2

normal or low PaCO2

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41
Q

reasons for Low V/Q?

A

impaired gas exchange

venous admixture

cause of low PaO2 - should be corrected with O2

intrapulmonary shunt

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42
Q

examples of Low V/Q?

A

airway obstruction

atelectasis

consolidation

pulmonary edema

ARDS

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43
Q

basic definition of high V/Q?

A

better ventilation than perfusion

low PaO2, with high PaCO2

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44
Q

causes of high V/Q

A

blood circulation is impaired

dead space ventilation

less of an effect on PaO2 levels than PaCO2 levels (initially)

(later) PaO2 will decrease due to lack of re-oxygenation

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45
Q

example of high V/Q

A

pulmonary embolism

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46
Q

other caues of hypoxemic ARF

A

airway obstruction: neoplams, bronchospams

infection: PNA (viral, bacteria, fungal, mycoplasma)
trauma: pulmonary contusion, pulmonary laceration, hemopneumothorax

heart failure

ALI/ARDS

pulmonary embolism

interstitial lung disease

cystic fibrosis

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47
Q

causes of hypercapnic ARF?

A
  • tissue enlargement (tonsil/adenoid, hyperplasia, malignant neoplasm, polyps, goiter)
  • infections
  • trauma: flail chest
  • b/l vocal cord paralysis, laryngeal edema, tracheomalacia, OSA, cricoarytenoid arthritis
  • increased ICP, seizures, rigors
  • kyphoscoliosis, scleroderma, spondylitis, PTX, pleural effusion, fibrothorax, supine position, obesity, pain, ascites
  • Drugs: opoids, benzos, propofol
  • metabolic: decreased Na+, decreased Ca++, alkalosis
  • fever, burns, overfeeding
  • central alveolar hypoventilation, central sleep apnea
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48
Q

what should the evaluation of hypercapnic look like?

A

assess minute ventilation, RR & tidal volume

work of breathing: accessory respiratory muscle use, in drawing, retractions, abdominal paradox

NIF (negative inspiratory force): measure of muscle strength.

metabolic cart

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49
Q

is a higher or lower NIF (negative inspiratory force) associated with a better prognosis?

A

the more negative the number the better they can take in a breath, the greater likelihood for successful extubation

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50
Q

what are these CXR findings assocaited with: clear with hypoxemia and normocapnia (initially)?

A

pulmonary embolus, R to L shunt, shock

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51
Q

what are these CXR findings assocaited with: clear with hypercapnia

A

COPD

asthma

overdose

neuromuscular weakness

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52
Q

what are these CXR findings assocaited with: diffusely white (opacified) with hypoxemia and normocapnia?

A

ARDS

NCPE (non-cardiogenic pulmonary edema)

CHF
pulmonary fibrosis

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53
Q

what are these CXR findings assocaited with: localized infiltrate

A

pneumonia

atelectasis

infarct

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54
Q

pros and cons to CXR?

A

you can rule out a lot of things, but there is a lot that you can’t see on CXR. it can lag behind 24-48 hours of pathologic issues.

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55
Q

COPD related DDxs for acute on chronic respiratory failure

A

acute exacerbation COPD

bronchitis

PNA

LV failure (pulmonary edema)

pneumothorax

pulmonary embolus

drugs (beta blockers)

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56
Q

first phase of treatment of ARF?

A
  • urgent resuscitation
  • supplemetal oxygen
  • supported repiration (Non-invasive vs invasive)
    • ventilator management
    • PEEP
  • stabilization of circulation
  • reverse sedatives
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57
Q

what are different things you can use to treat etiology that are tailored to the cause of ARF?

A

bronchodilators

steroids

antibiotics

diurese

inotropes

anticoagulation

treat metabolic / electrlyte

look for toxins

neuromusclar (CNS cause)

chest tube for PTX

drain effusion

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58
Q

ongoing care for treatment of ARF

A

differential diagnosis: idenitfy the cause - therapeutic plan tailored to diagnosis

supportive care

minimize atelectasis: IS, flutter valve, chest PT, IPPB (intermittent positive pressure breathing - giving help & opening their alveoli) treatments, HOB up, turn every 1-2 hours, OOB as much as possible, treat incisional pain

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59
Q

indications for non-invasive positive ventialation?

A

it should be used early!

  • COPD with hypercapneic acidosis PaCO2 > 45 or pH < 7.0
  • cardiogenic pulmonary edema
  • post estubation respiratory failure
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60
Q

what is good about Bi-level positive airway pressure (BPAP/BiPAP)

how are the settings written?

A

delivers inspiratory airway pressure and expiratory airway pressure

setting is written as I=15 E=10

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61
Q

what are contraindciations to non-invasive postive ventilation

A

need for emergent intubation

cardiac/respiratory arrest

inability to cooperate

inability to protect airway/manage secretions

severe decreased LOC

high aspiration risk

prolonged need for vent anticipated

recent esophogeal anastomosis

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62
Q

what are traditional modes for mechanical ventialation?

A

Assist control (AC)

IMV/SIMV

pressure control/pressure support (PC/PS)

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63
Q

what are newer modes for mechanical ventilation

A

high frequency oscillation - delivers small tidal volume (TV) at 60-120 bpm

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64
Q

what are alternate modes of mechanical ventilation

A

pressure controlled inverse ratio ventilation

airway pressure release ventilation (APRV) and BiPhasic Airway Pressure

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65
Q

what are the benefits of PEEP

A

increase transpulmonary distending pressure, alveolar recruitment

decrease atelectasis

displace edema fluid into interstitium

decrease shunt

improved compliance

improved oxygenation

66
Q

what are risks of PEEP

A

increased intrathoracic pressure

reduced systemic venous return & hypotension (concern for if they are in shock)

Alveolar overdistention

increase in dead space

pulmonary barotrauma (worse with high levels of PEEP)

increased cerebral venous pressre - this is questionable

67
Q

what is hospital acquired pneumonia (HAP)

A

episode of PNA not associated with mechanical ventialation acquired after 48 hours of admission to hospital

68
Q

what are the main causes of hospital acquired pneumonia

A

GN bacilli such as Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, Acinetobacter species

69
Q

symptoms/signs of HAP

A

fever (or hypothermia)

leukocytosis (or leukopenia)

increased tracheal secretions

poor oxygenation

70
Q

what type of imaging supports HAP

A

alveolar shadowing on CXR or CT scan supports diagnosis

71
Q

should you obtain a culture for HAP?

A

a lower respiratory culture should be obtained before initiating antibiotics

result of the culture should be used to de-escalate antibiotics and focus on the offending pathogen - there is still a lot of talk about how long to give IV antibiotics

72
Q

what kind of antibiotics should be used for patients with risk ractors for MDR pathogens?

A

broad specturm antimicrobials should be used initially for patients with risk factors for MDR pathogens

73
Q

what is initial empiric antibiotics for HAP for those not at high risk of mortality and no factors increasing likelihood of MRSA?

A

any single of the below medications

  • Piperacillin-tazbactram (Zosyn) 4.5 gm IV Q6hours
  • Cefepime 2 gm IV Q8 hours
  • Levofloxacin 750 mg IV daily
  • Imipenem 500 mg IV Q6 hours
  • Meropenem 1 gm IV Q8 hours
74
Q

what is initial empiric antibiotic therapy for individuals not at high risk of mortality but with factors increase the likelihood of MRSA?

A

one of the following

  • piperacillin-tazbactam (Zosyn) 4.5 gm IV Q 6 hours

OR

  • cefepemine OR ceftazidime 2 gm IV Q8 hours

OR

  • levofloxacin 750 mg IV dialy
  • ciprofloxacin 400 mg IV Q8hours

OR

  • Imipenem 500 mg IV q6 hours
  • Meropenem 1 gm IV Q8 hours

OR

  • Aztreonam 2 gm IV Q8hours

PLUS

  • vancomycin 15 mg/kg IV Q8 - 12 hours (consider loading dose of 25-30 mg/kg x 1 for severe illness)

OR

  • Linezolid 600 mg IV Q12 hours
75
Q

what is initial empiric antibiotics for HAP for high risk of mortality or receipt of IV antibiotics during prior 90 days?

A

Two of the following (but avoid 2 beta lactams - EX: PCN, cephalosporins, carbapenems, monobactam)

  • piperacillin-tazobactam (Zosyn) 4.5 grams IV Q6H

OR

  • Cefepime or Ceftazidime 2 gm IV Q8H

OR

  • Levofloxacin 750 mg IV daily
  • Ciprofloxacin 400 mg IV Q8H

OR

  • Imipenem 500 mg IV Q6H
  • Meropenem 1 gm IV Q8h

OR

  • Amikacin 15-20 mg/kg IV Qday
  • Gentamycin or Tobramycin 5-7 mg/kg IV Qday

OR

  • Aztreonam 2 gm IV Q8H

PLUS

  • vancomycin 15 mg/kg IV Q8-12H (consider loading dose of 25-30 mg/kg x 1 for severe illness)

OR

  • Linezolid 600 mg IV Q12H

*If MRSA coverage not used, include MSSA coverage

76
Q

how much is spent on hospital acquired infections

A

$9.8 billion / year spent on treating hospital acquired infections

77
Q

what is #2 HAI?

A

ventilator associated PNA (31.6%)

78
Q

how much does HAI increase cost per case?

A

averaged $40,144

79
Q

what are some general measures for infection control?

A

handwashing, alcohol based hand sanitizers

use of microbial surveillance

early removal of invasive devices (cental lines, foley catheters)

80
Q

what is mortality risk for VAP?

A

10% (6-27%) = 30,000 VAP attributable deaths/year

81
Q

what is #1 ICU infection?

A

VAP

25% of all ICU infections and 50% of ICU antibiotic use

82
Q

how many cases of VAP are there a year?

A

300,000

83
Q

in what percentage of ventilated patients does VAP produe complications?

A

8-28% of mechanically ventilated patients

84
Q

does VAP increase ICU LOS?

A

yes, by 4-13 days, avergae increase is 6 days

85
Q

what is the cost of VAP?

A

per case cost est. $40,000

= $112 billion in US/year

86
Q

why is there such a wide range of estimates in VAP?

A

lack of universally accepted, reliable definition & diagnotic criteria

87
Q

on what is the diagnosis of VAP based?

A

combination/variety of definitions

surveillance defition, clinical definition, microbiologically confirmed defintion

88
Q

what is the OLD VAP definition

A

> 48 hours after hospital admission

absence of signs/symptoms of PNA at admission after endotracheal intubation

hospital admission is day 1, not date of intubation

diagnosis is based on lack of evidence that infection developed before intubation

89
Q

what is NEW VAP definition

A

new, progressive & persistent CXR infiltrate plus 2 of the following

abnormal WBC (<4K or > 12K)

fever or hypothermia (>38 or < 36)

purulent sputum

deterioration in gas exchange

90
Q

are the current definitions of VAP adequate?

A

no, current standards of VAP definition are fraught with issues

91
Q

what is the most accurate radiographic sign for PNA?

A

air bronchogram is most accurate radiographic sign for PNA

92
Q

what is diagnostic accuracy for air bronchogram?

A

64%

93
Q

what is the adequacy clinical signs/symptoms of VAP for definition?

A

2 of 3 clnical features of infection (fever, leukocytosis, purulent sputum) sensitivity & specificty ranged beteen 69-75%

94
Q

is it difficult to distinguish between colonization & infection in VAP?

A

yes! difficult to distinguish between colonization & infection in VAP

95
Q

what is the CDC ventilator assocaited events (VAE)?

A

a CDC task force developed surveillance strategy

defined as:

  • all significant & sustaing deterioration in oxygenation
  • includes infectious and non-infectious (atelectasis ,PE, pulmonary edema, ventilator induced lung injury) conditions

public reporting and pay for performance calcuations

96
Q

what is Tier 1 of VAE?

A

>/= 2 days of stable or decreasing daily minimum PEEP or FiO2 followed by:

>20% increase in the daily minimum FiO2

OR

increase of >/= 3 cm H2O daily minimum PEEP to maintain oxygentation for >/= 2 days

97
Q

tier 2 IVAC

A

IVAC (infection-related ventilator assocaited condition)

  • previously diagnosed with VAE
  • temperature <36 or >38 OR leukocytosis = 4000 or >/= 12,000
  • one or more new antibiotics continued for at least 4 days within 2 calendar days before or after onset of VAE, excluding the frist 2 days of mechanical ventilation
98
Q

tier 3 possible/probably VAP

A

Possible VAP

  • patient with IVAC and purulence alone or pathogenic cultures alone

Probably VAP

  • patient with both purulence and positive quantitative or semi-quantitative cultures, or suggestive histopathological features, positive pleural-fluid cultures, or diagnostic tests for legionella
99
Q

benefits of CDC surveillance system

A
  • inclusive of all mechanical ventilator assocaited complications
  • automatable/easily computerized
  • chest radiograph not required
  • objective parameters defining diagnosis
  • minimal risk of gamesman ship
  • homogenous inter-facility VAE rates comparison
100
Q

who is at risk for VAE/VAP

A

those at high risk for developing infectious pulmonary disease

  • depressed LOC d/t head injry & sedation
  • need for emergent surgery and anesthesia
  • need for emergent intubation

**delay in treatment with antibiotcs assocaited w/ poorer outcomes

101
Q

basic guidelines for VAE/VAP

A

if at all possible send sputum culture (BAL preferred) before starting antibiotics

start with broad spectrum and narrow once organisms speciate

102
Q

what is the CPIS score?

A

clinical pulmonary infeciton score

  • assess the likelihood of VAP - based entirely on expert opinion
  • 50% specificity
  • can use this at JHH to start empiric antibiotics
103
Q

what are other differential diagnosis to think of when acute respiratory failure?

A

CHF

pulmonary embolus

drug fever

ARDS

inflammatory disease (SLE, BOOP)

malignacy

104
Q

Rx recommeatios for presumed VAP

A
  • simultaneous Dx work up with starting of treatment for presumed VAP
  • sputum culture (BAL preferred) if at all possible & before starting antibiotics
  • blood cultures since VAP with bacteremia is assocaited with increased mortality
  • start broad specturm antibiotics & narrow once organisms speciated
    • a delay in starting antibiotics is associated with poorer outcomes
  • clinical signs of infection in patients with negative lower respiratory tract cultures should prompt investigation for extra pulmonary sites of infection
105
Q

pathogens causing VAP

A
  1. pseudomonas (24.4%)
  2. S aureus (20.4%, > 50% MRSA)
  3. enterobactericeae (14.1% - includes Klebsiella, E coli, Proteus, Enterobacter, Serratia, Citrobacter)
  4. Streptococcus (12.1%)
  5. Hemophilus (9.8%)
  6. Acinetobacter (7.9%)
  7. Neisseria (2.6%)
  8. Stenotrophomonas (1.7%)
  9. coagulae negative staphylococcus (1.4%)
  10. others (4.7% -Corynebacterium, Moraxella, Enterococcus, fungi)
106
Q

what is the most common organism in healthy patients?

A

H. influenza & S. pneumo.

107
Q

what are other common organisms for VAP

A

Gram Negative bacilli:

  • P. aeruginosa
  • Escherichia coli
  • Klebsiella pneumoniae
  • Acinetobacter species

Gram positive cocci:

  • staphylococcus aureus
  • MRSA more common in DM, TBI & those hospitalizaed in ICUs
108
Q

what type of infection should you consider for VAP in immunocompromised patients

A

fungal infections

109
Q

facts about sensitivity of organinisms

A
  • determining whether patient has risk factors for multi-drug resistant (MDR) strains is KEY (distinction between early and late onset) as critical to initial drug therapy
  • Early onset (within 96 hours): organisms are more likley to be antibiotic sensitive
  • late onset (after 96 hours): organisms tend to be more antibiotic resistant –> higher mobidity & mortality
110
Q

what are risk factors for MDR VAP

A

prior IV antibiotics within 90 days

septic shock at time of VAP

ARDS preceding VAP

5 or more days of hospitalization prior to occurrence of VAP

acute RRT prior to VAP onset

111
Q

risk factors for MDR HAP

A

prior IV antibiotics within 90 days

112
Q

risk factors for MRSA/VAP/HAP

A

prior IV antibiotic use within 90 days

113
Q

risk factors for MDR pseudomonas vap/hap

A

prior IV antibiotic use within 90 days

114
Q

what are the 4 key managment strategies to prevent vap?

A
  1. subglottic suctioning endotracheal tubes
  2. oral care using chlorhexidine BID
  3. sedation vacation and spontaneous breathing trials
  4. HOB up at least 30 degrees (45 degrees better)
  • most effectively reduced by bundling recommendations for synergistic effect
  • consistent applicaiton of all bundle elements to all patients who qualify is essential to success (think checklists)
115
Q

what are some other treatment strategies for vented patients

A

closed in line endotracheal suctioning systems

humidification systems and ventilation circuit routine changes (every 5-7 days)

orotracheal route for intubation

116
Q

what are non-VAP specific interventions

A
  • DVT/PE prophylaxis due to increased risk
  • PUD prophylaxis - selective gastro-intestinal decontamination ->overall may affect antibiotic sensitivity, leading to more resistant organisms and increased risk of VAP
117
Q

is sucralfate for VAP a prevention strategy?

A

it’s inconclusive, but does not decrease risk of GIB

H2 blockers better for GIB risk, because of this risk sucralfate is no longer recommended.

118
Q

What do you use for VAP empiric therapy in ICU for MRSA and double anti-pseudomonal / Gram negative coverage

A

Use gram positive antibiotics with MRSA activity, which include

  • glycopeptides (choose one)
    • vancomycin 15 mg/kg IV Q8-12 hours (consider loading dose of 25-30 mg/kg x 1 for severe illness)
    • Linezolie 600 mg IV Q12 hours

Gram negative antibiotics with antipsuedomal activity (beta lactams) (CHOOSE ONE)

  • Piperacillin-tazobactam (Zosyn) 4.5 gm IV Q6H (Antipseudomonal PCN)
  • Cephalosporins
    • Cefepime 2 gm IV Q8H
    • Ceftazidime 2 gm IV Q8H
  • Carbapenems
    • Imipenem 500 mg IV Q6H
    • Meropenem 1 gm IV Q8H
  • Monobactam
    • Aztreonam 2 gm IV Q8H

Gram Negative antibiotics with antipseudomonal activity (non-beta lactams) (CHOOSE ONE)

  • Fluoroquinolones
    • Cirpofloxacin 400 mg IV Q8H
    • Levofloxacin 750 mg IV Q24H
  • Aminoglycosides
    • Amikacin 15-20 mg/kg IV Q24H
    • Gentamycin 5-7 mg/kg IV Q24H
    • Tobramycin 5-7 mg/kg IV Q24H
  • Polymixins
    • Colistin 5 mg/kg IV x 1 (Load) followed by 2.5 mg x (1.5 x CrCl + 30) IV Q12H
119
Q

gram negative antibiotics with antipseudomonal activity (beta lactam)

A

One of the following:

antipseudomonal PCN

  • Piperacillin taxobactam (zosyn) 4.5 gm IV Q 6 hours

cephalosporins

  • Cefepime 2 gm IV Q8 hours
  • Ceftazidime 2 gm IV Q8 Hours

carbapenems

  • Imipenem 500 mg IV Q6 hours
  • Meropenem 1 gm IV Q 8 hours

monbactams

  • aztreonam 2 grams IV Q8 hours
120
Q

gram negative antibiotics with antipseudomonal activity (non Beta lactam)

A

one of the following:

fluoroqinolones

  • ciprofloxacin 400 mg IV Q8 hours
  • levofloxacin 750 mg IV Q24 hours

aminoglycosides

  • amikacin 15-20 mg/kg IV Q24 hours
  • gentamycin 5-7 mg/kg IV Q24 hours
  • tobramycin 5-7 mg/kg IV Q24 hours

polymyxins

  • Colistin 5 mg/kg IV x 1 (load) followed by 2.5 mg x 1 IV Q12 hours
121
Q

what is ARDS

A

a life threatening respiratory condition characterized by hypoxemia, and stiff lungs, without mechanical ventilation most patients would die

122
Q

epidemilogy of ARL/ARDS

A

mortality down to 35%-45% from high of 60-70% in past

lower with quicker and better treatment

African Americans & Latinos have increased mortality (genetic factors vs increased severity of illness?)

123
Q

long term outcomes of ALI/ARDS

A

PFTs return to normal by 5 yearspersisten physical and cognitive deficiets

  • fitness measured by 6 minute walk tests - frequently reduced
  • up to 1/3 show signs of clinically relevant depression
  • impact on fmaily - depression & decreased productivity
124
Q

OLD criteria of ALI

A

severe hypoxemia

PaO2/FiO2 < 300 mm Hg

125
Q

Old criteria of ARDS

A

acute severe hypoxemia

PaO2/FiO2 < 200 mmHg

126
Q

ARDS/ALI old criteria

A

bilateral pulmonary infiltrates on CXR (radiographic interpretation lacks sensitivity & specificity)

decreased pulmonary compliance

AND

no cardiac cause

-pulmonary artery wedge pressure <18 mmHg or no evidece of left atrial hypertension

exclusion of cardiogenic pulmonary edema can be difficuly –>both conditions may co-exist

127
Q

other questions regarding validity - reliability of old criteria

A
  • no definition of ‘acute’
  • no standardized level of PEEP for P/F ratio
    • level of PEEP could re-classify from one category to another
  • does the distinction of ALI from ARDS provide prognostic value?
  • does not distinguish group with severe ARDS –>have higher mortiality
    • may benefit from advanced therapies
128
Q

Berlin definition of ARDS?

A

within 1 week of known insult or onset of new respiratory symptoms

bilateral opacities: not solely due to effusions, lung collapse, or nodules

degree of respiratory failure not explained by cardiac failure or pulmonary edema (may coexist)

129
Q

definition of mild ARDS?

A

PaO2/FiO2 between 200 - 300 mm Hg with PEEP/CPAP >/= 5 cm H2o

130
Q

definition of moderate ARDS

A

PaO2/FiO2 between 100 - 200 mm Hg with PEEP/CPAP >/= 5 cm H2o

131
Q

definition of severe ARDS

A

PaO2/FiO2 < 100 mmHg w/ PEEP >/= 5 cm H2O

132
Q

How is Berlin definition different

A
  • classifies as mild, moderate, severe based on P/F ratio
  • specifies onset: within 1 week of known clinical insult or worsening respiratory symptoms
  • sets minimal PEEP levels during P/F ratio evaluation
  • chest imaging must include bilateral opacities not fully explained by effusions, lobar collapse or nodules, and origin of edema which cannot be fully explained by cardiac failure or fluid overload
133
Q

ARDS direct injury triggers

A

PNA

aspiration of gastric contents

trauma with pulmonary contusion

drowning

reperfusion injury (transplant)

toxic inhalation (smoke, gas)

Sepsis & PNA account for 60% of cases

134
Q

indirect injury triggers for ARDS

A

shock

sepsis

transufions

pancreatitis

Sepsis & PNA account for 60% of cases

135
Q

what are ARDS predisposing conditions

A

intracranial HTN

blood products

catheter sepsis

drugs

PNA

pulmonary contusion

cardiopulmonary bypass

pancreatitis

translocation endotoxemia

urosepsis

amniotic fluid embolism

long bone fracture

136
Q

pathophysiology of ARDS

A

damage to alveolar capillary membrane

increased capillary permeability

interstititial and alveolar exudate - surfactant damage, decreased FRC & diffusion defect & shunting)

137
Q

what is the first stage of ARDS

A

exudative stage

acute

hallmark is leakage of protein rich inflammatory edema fluid into the interstitial and alveolar space

unfolds over the first 2-4 days after onset of lung injury

decrease in compliance

138
Q

2nd stage of ARDS?

A

proliferative

sub acute

connective tissue proliferates in response to the initial injury

danger of PNA sepsis and rupture of the lungs causing leakage of air into surrounding areas

decrease in compliance and an increase in interstitial fibrolysis

139
Q

3rd stage of ARDS?

A

resolution & recovery

chronic

lung reorganizes and recovers –> dependent on severity

function may contnue to improve 6-12 months or longer (overal outcome is very individualized)

long term problems: cough, limited exervise tolerance, depression & fatigue

140
Q

clinical features of ARDS

A
  • early condition: reflects cause (fever, hypotension, acute abdominal pain)
  • pulmonary dysfunction 24-48 hours after insult
    • tachypnea, dyspnea, hypoexemia, tachyacardia, diffuse rales
    • severe hypoxemic ARF non-repsonsive to high FiO2
  • impaired gas exchange
    • V/Q mismatch and pulmonary shunting
  • decreased lung compliance
  • pulmonary hypertension
141
Q

radiologic features of ARDS

A

CXR presense of:

  • diffuse, fluffy alveolar infiltrates
  • prominent air broncograms
  • bilateral infiltrates of ANY severity –> not just complete white out

CXR absence of

  • Kerly B lines
  • cardiomegaly
  • pulmonary venous congestion
  • pleural effusion
142
Q

ARDS diagnostic differentials

A
  • r/o severe hemodynamic pulmonary edema
    • clinical distinction, not radiographic: pro-BNP, Echo, PCWP (cardiac is going to be most likely culprit)
  • other DDx
    • pulmonary vasculitis
    • diffuse alveolar hemorrhage (acute drop in Hgb)
    • acute interstitial PNAs
    • acute eosinophilic PNA
    • cancers (acute leukemia, lymphoma, some solid)
143
Q

management of ARDS

A
  • multidisciplinary approach
  • treat the underlying predisposing medical illness
  • appropriate ventilator strategy (low tidal volume, PEEP, tolerate a fair amount of hypoxemia with these patients, high levels of O2 has hurt patients over longer periods of time)
  • fluid management
  • sedation
  • supportive care
  • severe refractory hypoxemia–>requires indivdiualized approach –> resuce therapies
144
Q

what is the cornerstone of ARDS therapy?

A

lung protection

ARDSnet group: 15 years of clinical trials; lung protective strategy & supportive measures

2000 ARDSnet: 6 mL/kg vs 12 mL/kg tidal volume

plateau pressures <30 cm H2O

permissive hypercapnia

some tidal volumes as low as 4 mL/kg; use predicted rather than actual body weight (which is based on patient’s height)

<2/3 received tidal volume 8mL/kg or less

145
Q

ARDSnet protocol

A

matches escalation of PEEP and FiO2 based on measure of oxygenation & utilized higher PEEP levels

Low tidal volume produced:

  • decreased mortality (from 40-31%)
  • shorter duration of ventilation
  • fewer ICU days
  • fewer non-pulmonary system organ failure

​still under utilized (>50% in select patients). subsequent trials compared high vs low PEEP levels and showed no difference

146
Q

when might a higher PEEP be beneficial?

A

ARDS with atelectasis, higher PEEP might be beneficial

147
Q

NIH ARDS network low tidal volume protocol

A

vent mode: volulme assist control

tidal volume: < 6 mL/kg ideal body weight

plateau pressure: <30 cm H2O

vent rate: 6-35 bpm, adjusted for atrial pH >/= 7.30 if possible

inspiratory flow, I:E: adjust flow to achieve time of 1:1 or 1:3

oxygenation goal: PaO2 >55 mmHg or SpO2: 88% - 95%

weaning: attempts to wean by pressure support when FiO2/PEEP <0.4/8

148
Q

ARDS ventilation management

A
  • use assist control
  • contraindications: increased ICP, sickle cell disease
  • calculate predicted/ideal body weight
  • FiO2, PEEP & PaO2: maintain PaO2 55-80 or SpO2 88-95%
    • use only approved PEEP/FiO2 combinations
  • tidal volume
    • adjust to 6 mL/kg predicted/ideal body weight, if above this decrease by 1mL/kg Q1-2 hours until 6mL/kg
  • Respiratory rate
    • make with initial tidal volume to meet minute ventilation (5-8 L/min)
    • do not exceed RR > 35 and do not increase RR if PaCO2 < 25 w pH 7.3
  • check plateau pressure
    • if <30 cm H20 - no change
    • > 30 cm H2O decreased tidal volume to 5 or 4 mL/kg
149
Q

daily wakening & wewaning trial

A

assess for weaning intolerance

RR> 35

SpO2 < 88% (< 5 minutes at 88% may be tolerated)

respiratory distress (2 of the following)

  • pulse > 120% of rate > 5 minutes
  • marked use of accessory muscles
  • abdominal paradox
150
Q

what is driving pressure

A

driving pressure = plateau pressure - PEEP

may be superior marker for lung injury

higher pressures correlate with increased mortality even with those receiving low volume lung protective strategies

151
Q

proning with SEVERE ARDS

A

improved survival in severe ARDS group

prone early in course (doing it earlier will make it better)

prone for > 16 hours /day

152
Q

what is greatest risk of proning?

A

losing your airway

153
Q

fluid management during ARDS

A

during acute phase of illness (sepsis, trauma, pancreatitis):

  • provide aggressive volume administration and pressors

once hemodynamically stable and off pressors (12 hours)

  • limit volume administration
  • target a CVP of 4 cm H2O & urine output > 0.5 mL/kg/hr
  • reduces time spent on mechanical ventilator and in the ICU

*CVP is easiest way to manage fluid resuscitation, trend is most accurate

bedside echo: can have better idea of the patient’s fluid status, non-invasive & a quick look. do a couple of times during a shift and you’ll get a good trend of volume status

154
Q

fluid management 2006 FACTT

A

liberal fluid for 1st 7 days

  • after acute shock keep CVP 10-14 or PAOP 14-18, cardiac inde <=/4.5 & FiO2
  • no difference in primary endpoint (mortality)
  • on average received 7L more fluid of 7 study days

conservative fluid for 1st 7 days

  • after acute shock-diuretics to keep CVP < 4 PAOP < 8
  • significant difference in oxygenation, increased vent-free days & shorter ICU days
  • did not worsen renal function, suggeting does not increase r/f AKI
    • near even fluid balance overall
155
Q

sedation, analgesia, & paralytics

A
  • thought process has changed dramatically over last 10 years: historically gave high doses of sedative infustions (esp. benzodiazepines)
  • 2000 Landmark study hypothesized that interruption in sedation might decrese both duration of mechanical ventilation & ICU stay, enabling better neurologic assessment
  • was replicated in multicenter Awaken and Breathing Controlled trial –> interruption of sedation was paired with daily spontaneous breathing trial
  • THIS LED TO…no benzo infusion (intermittent use only based on RAAS) and development of propofol & dexmeditomidine
156
Q

what is dexmedetomidine

A

a sedative - slective alpha 2 agonist

no repsiratory depression

safe and effective in ICU

may facilitate extubation in agitated patients

can shorten mechanical ventilation and length of ICU days

157
Q

neuromuscular blocade?

A

use cisatracurium within 48 hours of onset may improve outcomes–>lower 90 day mortality

  • evident 16-18 day post treatment in patients with severe ARDS (P/F ration <120)
  • unknown mechanism why
  • no difference in neuropathy between the treatment and control arms
158
Q

adjunctive therapies for ARDS

A
  • use of glucocorticoids, surfactants, antioxidants, protease inhibitors and recombinant human activated protein C –> no difference in mortality, ICU stay or vent days
  • inhaled b agonist albuterol: no difference vent free days or mortality
  • intravenous beta agonist salbuterol: increased mortality compared to untreated
  • 2 nutritionally focused trials: no difference in vent free days or mortality
    • lower volume vs. full volume enteral trophic feedings
    • use of Omega 3 fatty acids and antioxidant supplements
159
Q

advanced ‘rescue’ therapies for ARDS

A

non have shown mortality benefit

  • inhaled nitric oxide
  • inhaled prostacycline
  • prone positioning
  • high frequency oscillatory ventilation (HFOV), not really used anymore
  • ECMO (extracorporeal life support)

On the Horizon:

  • statins
  • inhaled heparin
  • adoptive cellular therapy with mesenchymal stem cells
160
Q

ARDS clinical course

A

continued mechanical ventilation

  • improved oxygenation, but still hypoxic,
  • poor lung compliance

complications of mechanical ventilation:

  • barotrauma,
  • infections,
  • MODS
161
Q

summary of ARDS

A
  • early recognition and treament can improve outcomes
  • early identification of abnormality allows for tailored therapy –> decrease mortality
    • better diagnosis for VAE/VAP and ARDS early appropriate empiric antibiotics for VAP
    • low tidal volumes for lung protection and improved outcomes in ARDS
    • fluid restriction after resuscitation for better ARDS outcomes
    • improved sedation and daily awakening and weaning trials
  • use bundles of care for multidisciplinary approach
    • prevention of VAE/VAP
    • ARDSnet protocol

Acute Care II - Summer 2017 (10 decks)

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