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Acute Hypoxemic Respiratory Failure. Margaret J. Neff, MD MSc Assistant Professor of Medicine Pulmonary & Critical Care. “Your patient’s sat is 88%”. 55 y/o man with a history of mild COPD 3 days s/p elective surgery bilateral knee replacements

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Acute Hypoxemic Respiratory Failure

Margaret J. Neff, MD MSc

Assistant Professor of Medicine Pulmonary & Critical Care

your patient s sat is 88
“Your patient’s sat is 88%”
  • 55 y/o man with a history of mild COPD
  • 3 days s/p elective surgery
    • bilateral knee replacements
  • Uneventful post-operative course except for an ileus and ongoing complaints of pain
  • Had been on room air during the day
    • You’re called with this sat at 3 a.m.
he says he can t catch his breath
“He says he can’t catch his breath”
  • Repeat sat confirmed: 88%
  • CXR done in the a.m. had shown mild bibasilar atelectasis
    • possible RLL infiltrate
  • ABG: 7.45/32/60 on room air
  • On high flow oxygen, his PaO2 is 100
causes of hypoxemia
Causes of Hypoxemia
  • Decreased PiO2
  • Hypoventilation
  • Diffusion abnormality
  • Ventilation/Perfusion mismatch
    • Dead space (high V/Q)
    • Shunt (low V/Q)
decreased pio 2
Decreased PiO2
  • High altitude
  • Iatrogenic
    • i.e. wrong gas mixture
  • Unlikely to be an issue in clinical hypoxemia
  • Aa gradient normal
hypoventilation
Hypoventilation
  • Essentially alveolar hypoventilation
  • CNS drive depressed
  • Pain and splinting
  • Thoracic or abdominal restriction
  • Commonly seen clinically
    • May be manifest as bibasilar atelectasis
    • Hypoxemia reverses if take deep breath
  • Aa gradient normal
diffusion abnormality
Diffusion Abnormality
  • Acute or chronic disease which affects the ability for oxygen to transport from alveolus to capillary
  • Common in moderate to severe lung disease, vascular disease, etc
  • Unlikely to cause acute hypoxemia
  • Aa gradient increased
ventilation perfusion mismatch dead space
Ventilation/Perfusion MismatchDead Space
  • Areas with normal ventilation, reduced perfusion (high V/Q ratio)
  • Pulmonary embolus is a good example
  • Dead space and poor CO2 removal require increased minute ventilation
  • May or may not be hypoxemia
  • Aa gradient increased
ventilation perfusion mismatch shunt
Ventilation/Perfusion MismatchShunt
  • Areas with decreased ventilation and normal perfusion (low V/Q)
  • Consolidation from pneumonia
  • Can increase if lose ability for hypoxic pulmonary vasoconstriction
    • non-selective vasodilators: nitrates, nipride
  • Poorly oxygen responsive
  • Aa gradient increased
your patient is still sob
“Your patient is still SOB”
  • Unlikely a problem with PiO2 or diffusion
  • May be some degree of hypoventilation due to narcotic use
  • Sputum with lots of polys and GPC
  • Repeat CXR shows consolidated RLL
  • Other possibilities?
your next admit is here
“Your next admit is here”
  • 45 y/o man with diabetes and urosepsis
    • progressively hypotensive, tachypneic
  • Intubated for respiratory distress and hypoxemia: oxygen sat on high flow oxygen of 90%
effusion or edema
Effusion or Edema?
  • “Bilateral infiltrates consistent with pulmonary edema”
  • meets radiographic criteria for acute lung injury

CT reveals normal parenchyma but bilateral effusions

Courtesy of G. Rubenfeld

pleural effusion
Pleural Effusion

1 day later

After CT insertion

acute lung injury ali
Acute Lung Injury (ALI)
  • Clinical diagnosis (AECC definition)
  • CXR: bilateral infiltrates consistent with pulmonary edema
  • PaO2/FiO2 ratio < 300 (< 200 for ARDS)
  • No evidence of left atrial hypertension
    • PAWP < 18 if available

AJRCCM 1994

ali risk factors
ALI Risk Factors
  • Trauma
  • Sepsis
  • Aspiration
  • Multiple transfusions
  • Pancreatitis, overdose, near drowning
  • Still up to 20% of patients without a defined risk factor
    • in other words, don’t have to have a risk to have ALI/ARDS
ali pathophysiology
ALI Pathophysiology
  • Inflammatory process and increased vascular permeability
  • Bronchoalveolar lavage fluid: neutrophil predominant
    • those with persistent neutrophils in BAL tend to have a worse clinical course
ali clinical manifestations
ALI: clinical manifestations
  • Early in the course of ARDS, hypoxemia often dominant
  • Due primarily to intrapulmonary shunting
    • atelectasis and alveolar flooding
    • disruption of normally protective hypoxic pulmonary vasoconstriction
ali clinical manifestations1
ALI: clinical manifestations
  • After 3-7 days, poor compliance can become the major problem
    • fibroproliferative stage
  • Increasing dead space (can exceed 70%)
    • fibrosis, microthrombi in vessels
    • can lead to pulmonary hypertension and right heart dysfunction
ali management
ALI: Management
  • Lung protective ventilation
    • 22% reduction in mortality
    • Tidal volume 6 ml/kg (PBW)
    • Pst < 30 cmH2O
    • allowing pH down to 7.15 if necessary
    • confirms previous animal studies showing increased systemic inflammation with higher tidal volumes, precipitated by lung stretch

NEJM 2000

other potential therapies
Other Potential Therapies
  • Prone positioning?
  • Steroids?
  • Anti-inflammatory agents?
  • Surfactant?
  • Anti-oxidants?
  • Inhaled nitric oxide?

NONE PROVEN

corticosteroids
Corticosteroids
  • Hypothesized to be effective due to intense inflammatory response seen in ARDS patients
    • Bronchoalveolar lavage with >70% neutrophils (normally < 2%)
    • Plasma IL6 levels elevated
  • Previous studies using steroids early in ARDS have not proven beneficial1

1 Crit Care Med 23:1294-1303

steroids late in ards
Steroids Late in ARDS
  • After first 3-7 days, ARDS progresses in many patients to a fibrotic stage
    • Proliferation of alveolar type II cells
  • Several small studies of steroids at this phase1
    • Inconclusive, in part due to study design
    • Possibly due to the need for a balance of pro- and anti-inflammatory mediators

1 JAMA 280:159-165

recent steroid trial
Recent Steroid Trial
  • NIH sponsored ARDS network (“LaSRS”)
    • 10 sites nationally conducting ARDS studies
  • Enrolled patients at day 7-28 of ARDS
    • Receive steroids 2mg/kg/d (tapered over 2 weeks)
  • 180 patients enrolled
    • No difference in mortality (increased with steroids if given >14 days after ALI)
    • Steroids: more vent-free days, shock-free days; also more neuromuscular complications

NEJM 2006; 354(16):1671

factt study
FACTT Study
  • Liberal vs conservative fluid mgmt
    • No difference in mortality
    • Conservative strategy resulted in better lung fxn and shorter time on vent & in ICU
      • Fluid strategy initiated after shock resuscitation
  • PAC vs CVC
    • No difference in mortality
    • More complications in PAC

NEJM 2006; 354(21):2213-24 & NEJM 2006;354(24):2564-75

what else can we do for ards patients
What else can we do for ARDS patients?
  • Minimize ICU-related complications
    • HOB elevation
    • DVT prophylaxis
    • Stress gastritis prophylaxis
    • Optimizing nutrition
      • Early enteral feeding +/- TPN
  • Invasive diagnostic strategies for ventilator-associated pneumonia
  • Tight glucose control
  • Sedation management
rct of hob elevation
RCT of HOB Elevation
  • 1 year enrollment in MICU (Spain)
  • Randomized to HOB > 45° or supine
  • Excluded if recent abd or neurosurgery, refractory shock, re-intubation
  • Endpoint: clinically or microbiologically confirmed pneumonia
    • (not rigorously defined, though)
  • 86 patients enrolled
    • Mean age 65yr; 34% with COPD

Lancet 1999;354:1851-8

results
Results
  • Nosocomial pneumonia lower in semi-recumbent group
    • 8% vs 34% for clinically suspected
    • 5% vs 23% for micro proven
  • Supine position and enteral feeding were independent risk factors for VAP
    • Highest risk when both occurred together
ventilator associated pneumonia
Ventilator Associated Pneumonia
  • Often difficult diagnosis to make clinically
    • CXR in ALI patient is already abnormal
    • ET aspirates may just reflect colonization
    • May be on antibiotics for surgical procedures or other infections
vap diagnosis
VAP Diagnosis
  • RCT of 413 patients intubated for at least 48 hours1
    • Clinical suspicion of VAP
    • No antibiotic change for prior 72 hours
  • Bronchoscopy vs ET aspirate
  • Bronch: Reduced mortality at day 14, decreased antibiotic use, more antibiotic free days, more appropriate abx choices

1 Ann Intern Med 2000;132:621-30

tight glucose control in icu
Tight Glucose Control In ICU
  • Recognized hyperglycemia/insulin resistance in ICU patients
  • RCT of glucose control in SICU patients
    • 2/3 cardiac surgery patients
    • 13% with h/o diabetes
  • Glucose goals: 80-110 vs 180-200
  • Decreased mortality
    • (ICU) 4.6% vs 8%; (hospital) 10.9% vs 7.2%
  • Subsequent studies show benefit > 4yrs for CV surg patients; questions results in MICU

N Engl J Med 2001;3451359-67; Eur Heart J 2006 Apr 11 Epub; NEJM 2006 354(5):449-61

interruption of sedative infusions in the icu
Interruption of Sedative Infusions in the ICU
  • Prospective, randomized trial
    • 150 patients receiving continuous infusions
      • Targeted Ramsay 3-4
    • Randomized to daily interruption of infusion or standard care
    • The intervention was disruption of infusion, not controlling dosing or sedation targets
    • Once patient awake, investigator notified primary team and decision made regarding resuming infusion (not based on protocol)

Kress, et al. NEJM 2000; 342:1471-7

better outcomes with interruption of sedative analgesic infusion
Better Outcomes with Interruption of Sedative (& Analgesic) Infusion
  • 2 fewer days on ventilator (5 days vs 7)
  • 3.5 fewer days in the ICU (6.5 vs 10)
  • Fewer diagnostic tests to work up altered mental status (9% vs 27%)
  • No difference in complications
    • e.g. self-extubations (4% vs 7%)
does deep sedation predispose to ptsd
Does Deep Sedation Predispose to PTSD?
  • Factual memory protected against post-traumatic stress disorder symptoms
  • Delusional memory was a risk for PTSD
  • Implications:
    • Deep sedation and complete amnesia may not be beneficial to patients
    • Side effects of drugs (hallucinations, nightmares) may be harmful

Jones, et al. Crit Care Med 2001;29:573-80

ali outcomes
ALI: Outcomes
  • Improved mortality over the past 30 years
    • 60% mortality reduced to 30-40%
  • Most continue to improve lung function over the first year
    • often left with abnormal diffusion capacity
  • Evidence to suggest some loss in neuropsychiatric function/testing and neuromuscular function
respiratory failure
Respiratory Failure
  • Your 2 patients did well
    • Patient with pneumonia continued to improve and transferred to rehab
    • Patient with urosepsis was in the ICU for 7 days with ALI but was extubated and doing well.
acute respiratory failure
Acute Respiratory Failure
  • When faced with acute SOB, run through the list of possibilities while initiating diagnostic testing and applying oxygen
    • Think of the clinical scenario to help you trim the possibilities
    • See if interventions help
    • Diagnose and treat for the most life-threatening while you’re fine-tuning the diagnosis
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