Transcript Sample slide - 5 NE Competency Wiki
Acute Hypoxemic Respiratory Failure
Margaret J. Neff, MD MSc Assistant Professor of Medicine Pulmonary & Critical Care
“Your patient’s sat is 88%”
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55 y/o man with a history of mild COPD 3 days s/p elective surgery
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bilateral knee replacements
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Uneventful post-operative course except for an ileus and ongoing complaints of pain
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Had been on room air during the day
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You’re called with this sat at 3 a.m.
“He says he can’t catch his breath”
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Repeat sat confirmed: 88% CXR done in the a.m. had shown mild bibasilar atelectasis
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possible RLL infiltrate ABG: 7.45/32/60 on room air On high flow oxygen, his PaO 2 is 100
Causes of Hypoxemia
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Decreased PiO 2 Hypoventilation Diffusion abnormality Ventilation/Perfusion mismatch
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Dead space (high V/Q) Shunt (low V/Q)
Decreased PiO
2
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High altitude Iatrogenic
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i.e. wrong gas mixture
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Unlikely to be an issue in clinical hypoxemia
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Aa gradient normal
Hypoventilation
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Essentially alveolar hypoventilation CNS drive depressed Pain and splinting Thoracic or abdominal restriction Commonly seen clinically
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May be manifest as bibasilar atelectasis Hypoxemia reverses if take deep breath
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Aa gradient normal
Diffusion Abnormality
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Acute or chronic disease which affects the ability for oxygen to transport from alveolus to capillary
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Common in moderate to severe lung disease, vascular disease, etc
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Unlikely to cause acute hypoxemia
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Aa gradient increased
Ventilation/Perfusion Mismatch Dead Space
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Areas with normal ventilation, reduced perfusion (high V/Q ratio) Pulmonary embolus is a good example Dead space and poor CO 2 removal require increased minute ventilation May or may not be hypoxemia
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Aa gradient increased
Ventilation/Perfusion Mismatch Shunt
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Areas with decreased ventilation and normal perfusion (low V/Q)
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Consolidation from pneumonia Can increase if lose ability for hypoxic pulmonary vasoconstriction
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non-selective vasodilators: nitrates, nipride
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Poorly oxygen responsive
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Aa gradient increased
“Your patient is still SOB”
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Unlikely a problem with PiO 2 or diffusion May be some degree of hypoventilation due to narcotic use
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Sputum with lots of polys and GPC Repeat CXR shows consolidated RLL Other possibilities?
“Your next admit is here”
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45 y/o man with diabetes and urosepsis
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progressively hypotensive, tachypneic Intubated for respiratory distress and hypoxemia: oxygen sat on high flow oxygen of 90%
Effusion or Edema?
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“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 1 day later After CT insertion
Acute Lung Injury (ALI)
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Clinical diagnosis (AECC definition) CXR: bilateral infiltrates consistent with pulmonary edema PaO2/FiO2 ratio < 300 (< 200 for ARDS) No evidence of left atrial hypertension
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PAWP < 18 if available
AJRCCM 1994
ALI Risk Factors
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Trauma Sepsis Aspiration Multiple transfusions Pancreatitis, overdose, near drowning Still up to 20% of patients without a defined risk factor
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in other words, don’t have to have a risk to have ALI/ARDS
ALI Pathophysiology
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Inflammatory process and increased vascular permeability
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Bronchoalveolar lavage fluid: neutrophil predominant
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those with persistent neutrophils in BAL tend to have a worse clinical course
ALI: clinical manifestations
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Early in the course of ARDS, hypoxemia often dominant Due primarily to intrapulmonary shunting
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atelectasis and alveolar flooding disruption of normally protective hypoxic pulmonary vasoconstriction
ALI: clinical manifestations
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After 3-7 days, poor compliance can become the major problem
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fibroproliferative stage
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Increasing dead space (can exceed 70%)
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fibrosis, microthrombi in vessels
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can lead to pulmonary hypertension and right heart dysfunction
ALI: Management
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Lung protective ventilation
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22% reduction in mortality
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Tidal volume 6 ml/kg (PBW) Pst < 30 cmH2O
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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
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Prone positioning?
Steroids?
Anti-inflammatory agents?
Surfactant?
Anti-oxidants?
Inhaled nitric oxide?
NONE PROVEN
Corticosteroids
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Hypothesized to be effective due to intense inflammatory response seen in ARDS patients
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Bronchoalveolar lavage with >70% neutrophils (normally < 2%)
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Plasma IL6 levels elevated
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Previous studies using steroids early in ARDS have not proven beneficial 1
1 Crit Care Med 23:1294-1303
Steroids Late in ARDS
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After first 3-7 days, ARDS progresses in many patients to a fibrotic stage
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Proliferation of alveolar type II cells
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Several small studies of steroids at this phase 1
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Inconclusive, in part due to study design
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Possibly due to the need for a balance of pro and anti-inflammatory mediators
1 JAMA 280:159-165
Recent Steroid Trial
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NIH sponsored ARDS network (“LaSRS”)
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10 sites nationally conducting ARDS studies Enrolled patients at day 7-28 of ARDS
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Receive steroids 2mg/kg/d (tapered over 2 weeks) 180 patients enrolled
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No difference in mortality (increased with steroids if given >14 days after ALI)
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Steroids: more vent-free days, shock-free days; also more neuromuscular complications
NEJM 2006; 354(16):1671
FACTT Study
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Liberal vs conservative fluid mgmt
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No difference in mortality
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Conservative strategy resulted in better lung fxn and shorter time on vent & in ICU
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Fluid strategy initiated after shock resuscitation PAC vs CVC
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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?
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Minimize ICU-related complications
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HOB elevation DVT prophylaxis Stress gastritis prophylaxis Optimizing nutrition
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Early enteral feeding +/- TPN Invasive diagnostic strategies for ventilator associated pneumonia Tight glucose control Sedation management
Pneumothorax
RCT of HOB Elevation
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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
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(not rigorously defined, though) 86 patients enrolled
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Mean age 65yr; 34% with COPD
Lancet 1999;354:1851-8
Results
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Nosocomial pneumonia lower in semi recumbent group
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8% vs 34% for clinically suspected 5% vs 23% for micro proven
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Supine position and enteral feeding were independent risk factors for VAP
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Highest risk when both occurred together
Ventilator Associated Pneumonia
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Often difficult diagnosis to make clinically
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CXR in ALI patient is already abnormal ET aspirates may just reflect colonization
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May be on antibiotics for surgical procedures or other infections
VAP Diagnosis
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RCT of 413 patients intubated for at least 48 hours 1
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Clinical suspicion of VAP
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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
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Recognized hyperglycemia/insulin resistance in ICU patients RCT of glucose control in SICU patients
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2/3 cardiac surgery patients 13% with h/o diabetes Glucose goals: 80-110 vs 180-200 Decreased mortality
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(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
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Interruption of Sedative Infusions in the ICU
Prospective, randomized trial
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150 patients receiving continuous infusions
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Targeted Ramsay 3-4
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Randomized to daily interruption of infusion or standard care
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The intervention was disruption of infusion, not controlling dosing or sedation targets
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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
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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%)
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No difference in complications
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e.g. self-extubations (4% vs 7%)
Does Deep Sedation Predispose to PTSD?
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Factual memory protected against post traumatic stress disorder symptoms Delusional memory was a risk for PTSD Implications:
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Deep sedation and complete amnesia may not be beneficial to patients
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Side effects of drugs (hallucinations, nightmares) may be harmful
Jones, et al. Crit Care Med 2001;29:573-80
ALI: Outcomes
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Improved mortality over the past 30 years
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60% mortality reduced to 30-40% Most continue to improve lung function over the first year
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often left with abnormal diffusion capacity Evidence to suggest some loss in neuropsychiatric function/testing and neuromuscular function
Respiratory Failure
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Your 2 patients did well
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Patient with pneumonia continued to improve and transferred to rehab
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Patient with urosepsis was in the ICU for 7 days with ALI but was extubated and doing well.
Acute Respiratory Failure
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When faced with acute SOB, run through the list of possibilities while initiating diagnostic testing and applying oxygen
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Think of the clinical scenario to help you trim the possibilities
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See if interventions help Diagnose and treat for the most life threatening while you’re fine-tuning the diagnosis