Weeks 7 & 8: Acute Respiratory Failure Flashcards
definition of acute respiratory failure
inadequate oxygenation OR ventilation which threatens function of vital organs
diagnostic criteria for acute respiratory failure
- hypoxemia: PaO2 < 60 mm Hg
and/or
- hypercapnia: PaCO2 > 50 mm Hg
what are the two types of acute respiratory failure
Type I ARF (hypoxic)
Type II ARF (hypoxic hypercarbic)
Description of Type I ARF (hypoxic)
- PaO2 < 60 mm Hg
- PA-PaO2 (A/a gradient) > 25 mm Hg
- increased shunt (PaO2/FiO2 ratio < 300)
- PaCO2 normal or < 50 mm Hg
Causes of Type I ARF (hypoxic)?
- V/Q mismatch
- alveolar hypoventilation
- diffusion defect
- R to L shunt
- low ambient oxygen
Description of Type II ARF (hypoxic hypercarbic).
- PaO2 < 60 mm Hg
- PaCO2 > 50 mm Hg
- acidosis
Causes of Type II ARF (hypoxic hypercarbic)
- alveolar hypoventilation
- increased airway resistance
- loss of lung surface area
- chest deformity
what is an intrapulmonary shunt
Percent of total veous blood that BYPASSES gas exchange (alveoli) and returns unoxygenated to systemic arterial system
what is a normal value for intrapulmonary shunt?
Normal 3-5% up to max of 10%
increased with each decade of life
Visual of intrapulmonary shunt
what do you need for a true shunt calculation?
mixed venous blood (from a Swan)
how do you estimate intrapulmonary shunt?
- 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
what do you need to do in order to be able to estimate shunt using a/A ratio?
must calculate Alveolar gas using standard equation
PAO2=[FiO2(Patm - PH2O)-(PaCO2/RQ)]
then divided PaO2/PAO2
what can you use to look at the diffusion defect?
A-a gradient = PAO2 - PaO2
what is a normal arterial - alveolar ratio
Normal > 0.8-0.9
is higher or lower a/A ratio make the shunt worse?
the lower the a/A ratio the worse the shunt
where do you obtain the PaCO2 & PaO2 values needed to calculate the diffusion defect/estimate the shunt?
ABG
what is normal PaO2/FiO2 ratio
550
what is the assumption for estimating shunt using PaO2 / FiO2 ratio?
that the patient is on 100% oxygen
what is the PaO2/FiO2 value for acute lung injury
<300
what is the PaO2 / FiO2 ratio value for ARDS
< 200
does a lower ratio for PaO2 / FiO2 ratio mean a larger or smaller shunt?
the lower the PaO2 / FiO2 ratio the larger the shunt
what is approximate shunt for PaO2 / FiO2 ratio for: 500, 300, 200?
500 - 5% shunt
300 - 15% shunt
200 - 20% shunt
clinical symptoms of ARF
dyspnea
orthopnea
anxiety
chest pain/stiffness
clinical signsof ARF
- 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
what is the most common cause of hypoxemic ARF?
a V/Q mismatch
what is a V/Q mismatch?
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
what are the most common causes of V/Q mismatch
PNA, aspiration, acute pulmonary edema, airway obstruction & severe stelectasis
what are less common causes of hypoexmic ARF?
- diffusion defect
- alveolar hypoventilation/inadequate minute ventilation
- high altitude
- low mixed venous oxygenation
definition of diffusion defect?
prevents O2 diffusion into blood
*
example of diffusion defect?
interstitial edema
inflammation
fibrosis
what do you do to fix diffusion defect?
treat causes: diuretics for cardiogenic pulmonary edema, corticosteroids for inflammatory disorder
examples of alveolar hypoventilation/inadequate minute ventilation?
anesthetic agents
opioid overdose
neuromusclar block/defect (myasthenia gravis)
how to treat alveolar hypoventilation/inadequate minute ventilation?
treat respiratory depression: stimulation, reversal getns, etc.
definition of high altitude hypoxemic ARF?
low inspired partial pressure of O2
definition of low mixed venous oxygenation?
extremely desaturation blood returning to lungs –> not adequately re-oxygenated
what is a potential cause of low mixed venous oxygenation, a less common cause of hypoxemic ARF?
low flow state could be causing extremely desaturated blood returning to lungs
what is V in V/Q mismatch?
v - ventilation: the air that reaches the alveoli
what is Q in V/Q mismatch
Q - perfusion: the blood that reaches the alveoli
Low V/Q?
limited ventilation relative to perfusion
Low PaO2
normal or low PaCO2
reasons for Low V/Q?
impaired gas exchange
venous admixture
cause of low PaO2 - should be corrected with O2
intrapulmonary shunt
examples of Low V/Q?
airway obstruction
atelectasis
consolidation
pulmonary edema
ARDS
basic definition of high V/Q?
better ventilation than perfusion
low PaO2, with high PaCO2
causes of high V/Q
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
example of high V/Q
pulmonary embolism
other caues of hypoxemic ARF
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
causes of hypercapnic ARF?
- 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
what should the evaluation of hypercapnic look like?
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
is a higher or lower NIF (negative inspiratory force) associated with a better prognosis?
the more negative the number the better they can take in a breath, the greater likelihood for successful extubation
what are these CXR findings assocaited with: clear with hypoxemia and normocapnia (initially)?
pulmonary embolus, R to L shunt, shock
what are these CXR findings assocaited with: clear with hypercapnia
COPD
asthma
overdose
neuromuscular weakness
what are these CXR findings assocaited with: diffusely white (opacified) with hypoxemia and normocapnia?
ARDS
NCPE (non-cardiogenic pulmonary edema)
CHF
pulmonary fibrosis
what are these CXR findings assocaited with: localized infiltrate
pneumonia
atelectasis
infarct
pros and cons to CXR?
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.
COPD related DDxs for acute on chronic respiratory failure
acute exacerbation COPD
bronchitis
PNA
LV failure (pulmonary edema)
pneumothorax
pulmonary embolus
drugs (beta blockers)
first phase of treatment of ARF?
- urgent resuscitation
- supplemetal oxygen
- supported repiration (Non-invasive vs invasive)
- ventilator management
- PEEP
- stabilization of circulation
- reverse sedatives
what are different things you can use to treat etiology that are tailored to the cause of ARF?
bronchodilators
steroids
antibiotics
diurese
inotropes
anticoagulation
treat metabolic / electrlyte
look for toxins
neuromusclar (CNS cause)
chest tube for PTX
drain effusion
ongoing care for treatment of ARF
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
indications for non-invasive positive ventialation?
it should be used early!
- COPD with hypercapneic acidosis PaCO2 > 45 or pH < 7.0
- cardiogenic pulmonary edema
- post estubation respiratory failure
what is good about Bi-level positive airway pressure (BPAP/BiPAP)
how are the settings written?
delivers inspiratory airway pressure and expiratory airway pressure
setting is written as I=15 E=10
what are contraindciations to non-invasive postive ventilation
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
what are traditional modes for mechanical ventialation?
Assist control (AC)
IMV/SIMV
pressure control/pressure support (PC/PS)
what are newer modes for mechanical ventilation
high frequency oscillation - delivers small tidal volume (TV) at 60-120 bpm
what are alternate modes of mechanical ventilation
pressure controlled inverse ratio ventilation
airway pressure release ventilation (APRV) and BiPhasic Airway Pressure
what are the benefits of PEEP
increase transpulmonary distending pressure, alveolar recruitment
decrease atelectasis
displace edema fluid into interstitium
decrease shunt
improved compliance
improved oxygenation
what are risks of PEEP
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
what is hospital acquired pneumonia (HAP)
episode of PNA not associated with mechanical ventialation acquired after 48 hours of admission to hospital
what are the main causes of hospital acquired pneumonia
GN bacilli such as Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, Acinetobacter species
symptoms/signs of HAP
fever (or hypothermia)
leukocytosis (or leukopenia)
increased tracheal secretions
poor oxygenation
what type of imaging supports HAP
alveolar shadowing on CXR or CT scan supports diagnosis
should you obtain a culture for HAP?
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
what kind of antibiotics should be used for patients with risk ractors for MDR pathogens?
broad specturm antimicrobials should be used initially for patients with risk factors for MDR pathogens
what is initial empiric antibiotics for HAP for those not at high risk of mortality and no factors increasing likelihood of MRSA?
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
what is initial empiric antibiotic therapy for individuals not at high risk of mortality but with factors increase the likelihood of MRSA?
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
what is initial empiric antibiotics for HAP for high risk of mortality or receipt of IV antibiotics during prior 90 days?
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
how much is spent on hospital acquired infections
$9.8 billion / year spent on treating hospital acquired infections
what is #2 HAI?
ventilator associated PNA (31.6%)
how much does HAI increase cost per case?
averaged $40,144
what are some general measures for infection control?
handwashing, alcohol based hand sanitizers
use of microbial surveillance
early removal of invasive devices (cental lines, foley catheters)
what is mortality risk for VAP?
10% (6-27%) = 30,000 VAP attributable deaths/year
what is #1 ICU infection?
VAP
25% of all ICU infections and 50% of ICU antibiotic use
how many cases of VAP are there a year?
300,000
in what percentage of ventilated patients does VAP produe complications?
8-28% of mechanically ventilated patients
does VAP increase ICU LOS?
yes, by 4-13 days, avergae increase is 6 days
what is the cost of VAP?
per case cost est. $40,000
= $112 billion in US/year
why is there such a wide range of estimates in VAP?
lack of universally accepted, reliable definition & diagnotic criteria
on what is the diagnosis of VAP based?
combination/variety of definitions
surveillance defition, clinical definition, microbiologically confirmed defintion
what is the OLD VAP definition
> 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
what is NEW VAP definition
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
are the current definitions of VAP adequate?
no, current standards of VAP definition are fraught with issues
what is the most accurate radiographic sign for PNA?
air bronchogram is most accurate radiographic sign for PNA
what is diagnostic accuracy for air bronchogram?
64%
what is the adequacy clinical signs/symptoms of VAP for definition?
2 of 3 clnical features of infection (fever, leukocytosis, purulent sputum) sensitivity & specificty ranged beteen 69-75%
is it difficult to distinguish between colonization & infection in VAP?
yes! difficult to distinguish between colonization & infection in VAP
what is the CDC ventilator assocaited events (VAE)?
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
what is Tier 1 of VAE?
>/= 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
tier 2 IVAC
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
tier 3 possible/probably VAP
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
benefits of CDC surveillance system
- 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
who is at risk for VAE/VAP
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
basic guidelines for VAE/VAP
if at all possible send sputum culture (BAL preferred) before starting antibiotics
start with broad spectrum and narrow once organisms speciate
what is the CPIS score?
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
what are other differential diagnosis to think of when acute respiratory failure?
CHF
pulmonary embolus
drug fever
ARDS
inflammatory disease (SLE, BOOP)
malignacy
Rx recommeatios for presumed VAP
- 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
pathogens causing VAP
- pseudomonas (24.4%)
- S aureus (20.4%, > 50% MRSA)
- enterobactericeae (14.1% - includes Klebsiella, E coli, Proteus, Enterobacter, Serratia, Citrobacter)
- Streptococcus (12.1%)
- Hemophilus (9.8%)
- Acinetobacter (7.9%)
- Neisseria (2.6%)
- Stenotrophomonas (1.7%)
- coagulae negative staphylococcus (1.4%)
- others (4.7% -Corynebacterium, Moraxella, Enterococcus, fungi)
what is the most common organism in healthy patients?
H. influenza & S. pneumo.
what are other common organisms for VAP
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
what type of infection should you consider for VAP in immunocompromised patients
fungal infections
facts about sensitivity of organinisms
- 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
what are risk factors for MDR VAP
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
risk factors for MDR HAP
prior IV antibiotics within 90 days
risk factors for MRSA/VAP/HAP
prior IV antibiotic use within 90 days
risk factors for MDR pseudomonas vap/hap
prior IV antibiotic use within 90 days
what are the 4 key managment strategies to prevent vap?
- subglottic suctioning endotracheal tubes
- oral care using chlorhexidine BID
- sedation vacation and spontaneous breathing trials
- 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)
what are some other treatment strategies for vented patients
closed in line endotracheal suctioning systems
humidification systems and ventilation circuit routine changes (every 5-7 days)
orotracheal route for intubation
what are non-VAP specific interventions
- 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
is sucralfate for VAP a prevention strategy?
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.
What do you use for VAP empiric therapy in ICU for MRSA and double anti-pseudomonal / Gram negative coverage
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
gram negative antibiotics with antipseudomonal activity (beta lactam)
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
gram negative antibiotics with antipseudomonal activity (non Beta lactam)
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
what is ARDS
a life threatening respiratory condition characterized by hypoxemia, and stiff lungs, without mechanical ventilation most patients would die
epidemilogy of ARL/ARDS
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?)
long term outcomes of ALI/ARDS
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
OLD criteria of ALI
severe hypoxemia
PaO2/FiO2 < 300 mm Hg
Old criteria of ARDS
acute severe hypoxemia
PaO2/FiO2 < 200 mmHg
ARDS/ALI old criteria
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
other questions regarding validity - reliability of old criteria
- 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
Berlin definition of ARDS?
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)
definition of mild ARDS?
PaO2/FiO2 between 200 - 300 mm Hg with PEEP/CPAP >/= 5 cm H2o
definition of moderate ARDS
PaO2/FiO2 between 100 - 200 mm Hg with PEEP/CPAP >/= 5 cm H2o
definition of severe ARDS
PaO2/FiO2 < 100 mmHg w/ PEEP >/= 5 cm H2O
How is Berlin definition different
- 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
ARDS direct injury triggers
PNA
aspiration of gastric contents
trauma with pulmonary contusion
drowning
reperfusion injury (transplant)
toxic inhalation (smoke, gas)
Sepsis & PNA account for 60% of cases
indirect injury triggers for ARDS
shock
sepsis
transufions
pancreatitis
Sepsis & PNA account for 60% of cases
what are ARDS predisposing conditions
intracranial HTN
blood products
catheter sepsis
drugs
PNA
pulmonary contusion
cardiopulmonary bypass
pancreatitis
translocation endotoxemia
urosepsis
amniotic fluid embolism
long bone fracture
pathophysiology of ARDS
damage to alveolar capillary membrane
increased capillary permeability
interstititial and alveolar exudate - surfactant damage, decreased FRC & diffusion defect & shunting)
what is the first stage of ARDS
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
2nd stage of ARDS?
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
3rd stage of ARDS?
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
clinical features of ARDS
- 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
radiologic features of ARDS
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
ARDS diagnostic differentials
- 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)
management of ARDS
- 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
what is the cornerstone of ARDS therapy?
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
ARDSnet protocol
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
when might a higher PEEP be beneficial?
ARDS with atelectasis, higher PEEP might be beneficial
NIH ARDS network low tidal volume protocol
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
ARDS ventilation management
- 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
daily wakening & wewaning trial
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
what is driving pressure
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
proning with SEVERE ARDS
improved survival in severe ARDS group
prone early in course (doing it earlier will make it better)
prone for > 16 hours /day
what is greatest risk of proning?
losing your airway
fluid management during ARDS
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
fluid management 2006 FACTT
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
sedation, analgesia, & paralytics
- 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
what is dexmedetomidine
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
neuromuscular blocade?
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
adjunctive therapies for ARDS
- 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
advanced ‘rescue’ therapies for ARDS
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
ARDS clinical course
continued mechanical ventilation
- improved oxygenation, but still hypoxic,
- poor lung compliance
complications of mechanical ventilation:
- barotrauma,
- infections,
- MODS
summary of ARDS
- 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
