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