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Acute Hypoxic Respiratory Failure

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					Type I Respiratory Failure: Acute
   Hypoxic Respiratory Failure

   Division of Critical Care Medicine
          University of Alberta
                  Outline

1.   Review of Pathophysiology
2.   Clinical presentation and differential
     diagnosis
3.   ARDS
4.   Reversible causes of ARDS – Description
     and Treatment
               Pathophysiology
   Acute hypoxic respiratory failure (AHRF) is also
    called Type I Respiratory Failure.
   Marked by severe hypoxemia that is
    unresponsive to supplemental oxygen.
   This results from widespread flooding and
    collapse of alveoli that causes blood to flow past
    unventilated alveoli (V/Q ratio of zero).
   Also called shunt.
   As can be seen above, blood passing through the
    right alveoli does not pick up any oxygen while the
    left is normal and fully saturated.
   The reduced oxygen content from the right mixes
    with the left and reduces the overall oxygen of the
    blood returning to the heart.
               Pathophysiology
   The intra-alveolar fluid and increased interstitial
    fluid decreases overall lung compliance.
   This imposes a larger elastic work of breathing
    resulted in increased respiratory muscle oxygen
    consumption.
   A vicious cycle of increased O2 demand, muscle
    fatigue and hypoxemia leads to respiratory
    arrest and death if mechanical assistance is not
    instituted.
             Clinical Presentation
   There are many causes of AHRF, however, the
    clinical presentation is remarkably similar.
   Almost all patients are tachypneic and dyspneic.
   Initial room air ABG show a PaO2 of 30-35 and SaO2
    < 85%.
   If supplemental oxygen by mask or cannula is given
    and the SaO2 rises to >95%then a large
    intrapulmonary shunt is unlikely.
   The chest x-ray will provide further clues into the
    cause of the hypoxemia and only rarely will it be
    normal.
       In this case, consider an error in the ABG, an intracardiac
        shunt or AVM malformation.
     Differential Diagnosis of AHRF

1.   Acute lung injury or ARDS
2.   Acute cardiogenic pulmonary edema
3.   Bilateral aspiration pneumonia
4.   Lobar atelectasis of both lower lobes
5.   Severe unilateral lower lobe atelectasis,
     especially when the patient is receiving
     vasodilators such as nitrates, calcium channel
     blockers, or nitroprusside that blunt hypoxic
     vasoconstriction.
      Differential Diagnosis of AHRF

6.    Main stem bronchus obstruction from mucous
      plug or blood clot.
7.    Bilateral or unilateral pneumothorax
8.    Large unilateral or bilateral pleural effusions
9.    Diffuse alveolar hemorrhage
10.   Massive pulmonary embolus
11.   Opening of patent foramen ovale with pre-
      existing pulmonary hypertension.
                Clinical Setting
   Given the extensive differential for AHRF, the
    clinical setting and further investigations are
    invaluable in establishing the cause.
   Cardiogenic edema is usually accompanied by
    systolic left ventricular or valvular dysfunction
    and abnormal heart sounds or murmurs should
    be sought.
   ECG and biochemical evidence of ischemia
    should be considered as an obvious cause of
    cardiogenic edema.
                Clinical Setting
   Review of intravascular volume administration
    will often suggest an explanation for pulmonary
    edema in patients with left ventricular or renal
    dysfunction.
   ALI or ARDS commonly arises in a typical clinical
    context with direct and indirect causes
    (differential to be discussed soon).
               Clinical Setting
   The chest x-ray is not very accurate for
    distinguishing cardiogenic from non-cardiogenic
    causes.
   However, it can help sort out the other causes of
    AHRF.
   Essentially, the differential can be broken down
    into those causes that present with unilateral x-
    ray findings (i.e. lobar pneumonia, atelectasis,
    effusion) and bilateral findings (i.e.. ARDS,
    pulmonary edema, diffuse alveolar hemorrhage)
               Clinical Setting
   Echocardiography is helpful in distinguishing
    cardiogenic from noncardiogenic pulmonary
    edema.
   Echocardiography also helps identify left
    ventricular wall motion abnormalities, mitral
    valve dysfunction, and ventricular dilation.
   Early bronchoscopy is critical to identify
    reversible causes and guide therapy.
   Bronchoscopy can help diagnose some causes of
    AHRF including diffuse alveolar hemorrhage,
    pneumonia, and acute eosinophillic pneumonia.
        Acute Respiratory Distress
            Syndrome (ARDS)
   Acute lung injury (ALI) and ARDS are
    common causes of AHRF.
   Both are defined by acute onset, bilateral
    pulmonary infiltrates on chest x-ray
    consistent with pulmonary edema,
    hypoxemia and the absence of evidence of
    left atrial hypertension.
              ARDS - Definition
   The ratio of arterial oxygen (PaO2) to fraction of
    inspired oxygen (FiO2), also called the P/F ratio,
    reflects the degree of hypoxemia at different
    levels of FiO2.
   The syndrome is called ALI when the ratio is <
    300 and ARDS when < 200.
   ALI was coined to identify those patients who
    are early in the course of their ARDS or have a
    form of AHRF that is milder than ARDS.
     ARDS – Precipitating Causes

   ALI/ARDS is a syndrome diagnosis and
    should be considered a final common
    pathway reaction of the lung to a large
    variety of insults.
   Precipitating causes can be broken down
    into direct (pulmonary) and indirect
    (systemic).
 ARDS – Direct Precipitating Causes

1.   Aspiration of gastric contents
2.   Bacterial pneumonia
3.   Chest trauma with pulmonary contusion
4.   Near drowning
5.   PCP pneumonia
6.   Toxic inhalations (i.e.. smoke, crack cocaine)
7.   Viral pneumonia
      ARDS – Indirect Precipitating
               Causes
1.   Pancreatitis
2.   Transfusion associated acute lung injury
     (TRALI)
3.   Post cardiopulmonary bypass
4.   Primary graft failure of lung transplant
5.   Severe sepsis and septic shock
6.   Toxic ingestions (i.e.. ASA, TCA)
7.   Trauma with multiple fractures and fat-emboli
     syndrome
           ARDS/ALI Pathology
   Early in the development, interstitial and
    alveolar edema, capillary congestion, and intra-
    alveolar hemorrhage with minimal evidence of
    cellular injury appears.
   This is the early exudative phase of diffuse
    alveolar damage with inflammatory cell
    infiltration in the lung interstitium.
   Also during this phase, the pulmonary capillaries
    sequester neutrophils contributing further to the
    inflammation.
          ARDS/ALI Pathology
   Over the next days, hyaline membranes
    form in the alveolar spaces.
   These membranes contain condensed
    fibrin and plasma protein.
   Inflammatory cells become more
    numerous in the interstitium and there is
    extensive necrosis of type I alveolar cells.
             ARDS/ALI Pathology
   The late phase is dominated by disordered healing and
    begins to occur 7 to 10 days after initial injury.
   This is the fibroproliferative phase and is marked by
    increasing type II alveolar cells, fibroblasts and
    myofibroblast.
   Patients in this stage are typically left with a large dead
    space fraction, high minute ventilation requirement,
    progressive pulmonary hypertension, slightly improved
    pulmonary shunt, and reduction in lung compliance.
           ARDS/ALI Treatment
   A key step in treating patients with ARDS/ALI is
    to identify and treat the underlying cause.
   The ventilatory and other support of ALI is
    doomed to failure if the precipitant is not dealt
    with.
   ARDS/ALI is a syndrome diagnosis based on
    nonspecific criteria only, therefore, making the
    diagnosis of ALI/ARDS is not equivalent to
    diagnosing the patient’s underlying problem.
         ARDS/ALI – Ventilation Goals

    After the underlying cause is identified,
     the focus is on ventilation goals:
    1.   Maintain SaO2 < 88% and PaO2 < 55
    2.   Protect lung from further injury
    3.   Maintain lung recruitment
    4.   Maintain normal pH and PaCO2
       ARDS/ALI – Ventilation Goals
   The primary problem in ARDS is that there is a large
    intrapulmonary shunt that is resistant to oxygen therapy.
   In order to meet oxygenation goals, sufficient PEEP
    needs to be given.
   PEEP works by recruiting collapsed and partially fluid-
    filled alveoli and therefore increasing FRC.
   It also redistributes alveolar fluid into the interstitium.
   By this approach, the patient should be able to avoid
    high levels of FiO2 (> 60%) which is toxic in itself.
   Higher levels of PEEP also prevents surfactant poor
    alveoli from repeatedly opening and collapsing which is
    also injurious to the lungs.
       ARDS/ALI – Ventilation Goals
   Conventional ventilation strategy usually requires a tidal
    volume of 10-12 mL/kg in order to maintain minute
    ventilation and hence, normal PaCO2.
   However, in an injured lung, that volume causes excess
    stretch and perpetuates the injury.
   Therefore, the current goal is a low tidal volume strategy
    of 6 mL/kg.
   If this tidal volume is insufficient for minute ventilation
    (even at a higher respiratory rate) then the resultant
    elevated PaCO2 is tolerated as long as the pH is > 7.20.
   This is called permissive hypercapnia.
        ARDS/ALI – Other Adjuvant
               Measures
   Prone Position – Increases FRC, redistributes perfusion
    and better secretion clearance.
   Recruitment Maneuvers – Open partially collapsed alveoli
    which is then kept inflated by a high level of PEEP.
   Other savage measures:
      NO
      Steroids during fibroproliferative stage
      High frequency oscillation
      EMCO
      Partial liquid ventilation
      Surfactant
     Reversible Causes of ARDS/ALI

   Bacterial pneumonia
   Viral pneumonia
   Fungal pneumonia
   PJP
   Diffuse alveolar hemorrhage
   Eosinophillic pneumonia
   Lupus pneumonitis
   Toxic drug reaction
    Community Acquired Pneumonia

   There are more than 100 microbes (bacteria,
    viruses, fungi, and parasites) that can cause
    CAP.
   Most cases of pneumonia are caused by 4 or 5
    microbes.
   Bacteria are the most common cause of CAP and
    are divided into two groups:
       Typical – S. pneumoniae, H. influenzae, S. aureus,
        GAS, M. catarrhalis, anaerobes, and GNB.
       Atypical – Legionella, Mycoplasma and Chlamydophila
        pneumoniae.
    Community Acquired Pneumonia

   A microbiological diagnosis is confirmed in only
    20% of cases.
   There are a few clinical clues that must be
    considered for the etiology of CAP
       Know your local epidemiology
       Be aware of outbreaks
       Never forget TB and PJP
       MRSA is an increasingly recognized cause of severe,
        necrotizing CAP
Community Acquired Pneumonia
   Bacteria are the most common cause of CAP.
       S. pneumoniae: Most common cause overall
       H. influenzae: Important in the elderly, COPD and
        CF.
       M. pneumoniae: The most common cause of
        atypical pneumonias.
       C. pneumoniae: Accounts for 5-10% of cases.
        Most common in the elderly.
       Legionella: Causes 2-8% of cases either
        sporadically or outbreaks.
       Klebsiella: Should be considered as a cause in
        patients who have significant underlying diseases
        such as COPD, diabetes, and alcohol abuse.
Community Acquired Pneumonia
    Pseudomonas: Community acquired Pseudomonas
     occurs mainly in immunocompromised patients or
     those with structural lung abnormalities such as
     CF or bronchiectasis.
    Acinetobacter: Typically seen in hospitalized
     patients but starting to emerge in the community.
    S. aureus: Usually seen in the elderly and young
     who are recovering from influenza.
    GAS: Can cause a fulminant pneumonia with early
     empyema formation even in healthy patients.
Community Acquired Pneumonia

   Anaerobes: May be the cause of aspiration
    pneumonia and lung abscesses. Role is not
    clear since detection in routine cultures is not
    possible.
   N. meningitidis: An uncommon cause of CAP
    but is reportable to public health and
    prophylaxis must be given.
   TB: Missed diagnosis is common and many
    patients are initially treated for presumed
    CAP.
    Community Acquired Pneumonia -
              Treatment
   The selection of specific antibiotics for
    empiric therapy is based on a number of
    principles:
       The most likely pathogen
       Clinical trials proving efficacy
       Risk factors for the presence of resistance
       Presence of medical co-morbidities
    Community Acquired Pneumonia -
              Treatment
   Antibiotic recommendations for
    hospitalized patients are divided between
    ICU and non-ICU and whether the patient
    is admitted from a long term care facility.
   When the etiology of CAP is identified,
    treatment regimen must be simplified and
    directed to that pathogen.
Community Acquired Pneumonia -
          Treatment
   Not in the ICU
       Cefotaxime 1 g q8h and azithromycin 500 mg daily
       Levofloxicin 750 mg daily or moxifloxacin 400 mg daily
   Admitted to ICU (high risk for resistant organisms)
       Pipericillin/tazobactum 4.5 g q6h or imipenem 500 mg q6h
        or meropenem 1 g q8h or cefepime 2 g q8h or ceftazidime 2
        g q8h PLUS
       Ciprofloxicin 400 mg q12h or levofloxicin 750 mg daily or
        aminoglycoside
       Penicillin allergy use aztreonam, an aminoglycoside, and
        levofloxicin
       If initial gram strain suggests S. aureus then add
        vancomycin 15 mg/kg q12h
              Viral Pneumonia
   Viruses are estimated to cause adult CAP in 10
    to 31% of cases.
   Influenza A or B occurs in outbreaks and
    epidemics. They can cause pneumonia although
    they are more likely to cause a URTI and then
    predispose to a secondary pneumonia.
   High risk patients include patients with heart
    and lung disease, diabetes, renal diseases,
    immunosuppression, nursing home residents
    and over 65.
              Viral Pneumonia
   Parainfluenza are important in the
    immunocompromised patients causing life
    threatening lower respiratory tract infections.
   RSV is more common in children but can cause
    CAP in elderly.
   Adenovirus presents with fever, cough, and
    peribronchial markings with patchy alveolar
    infiltrates.
   Metapneumovirus is an emerging pathogen and
    causes disease in young children and the
    elderly.
                Viral Pneumonia
   SARS is a coronavirus that caused an outbreak after it
    jumped species in 2002. Currently quiescent.
   Hantavirus is spread from the feces of infected mice.
    The illness is preceded by prodromal flu-like symptoms
    followed by ARDS. The virus does not cause pneumonia
    and the ARDS is from the host response.
   Avian influenza currently causes sporadic outbreaks but
    WHO and CDC consider it to be a potential source for
    the next global pandemic.
   Varicella pneumonia is the most frequent complication of
    varicella infection in healthy adults with a case fatality
    rate of 10-30%.
            Fungal Pneumonia
   Fungal infections are an unusual cause of CAP in
    immunocompetent patients but should be considered
    in those with neutropenia, organ transplant, and HIV.
   Cyptococcus is mostly asymptomatic and usually
    discovered incidentally on CXR in normal patients. It
    is usually symptomatic in immunocompromised
    patients.
   Histoplasma proliferates in soil contaminated with
    bird and bat droppings. Symptomatic patients
    present with flu-like illness and radiographic
    abnormalities such as bronchopneumonia and
    interstitial pneumonitis.
   Coccidioides typically presents with chest pain,
    cough, and fever with a normal CXR in up to 50% of
    patients. It is endemic in the deserts of
    southwestern North America.
     PJP Infection in HIV Patients
   Most common opportunistic infection in patients
    with HIV.
   Frequently presents as the first manifestation of
    HIV infection.
   75% of the population are infected by age 4.
    The primary infection is asymptomatic and
    remains latent throughout life unless the patient
    becomes immunosuppressed.
   PJP does not occur until the CD4 count falls
    below 200 cells/mL.
    PJP Infection in HIV Patients
   PJP is generally gradual n onset and characterized by
    fever, cough, and progressive dyspnea and
    tachypnea.
   The most common radiographic abnormalities are
    diffuse, bilateral interstitial or alveolar infiltrates.
   Other less common presentations include:
      Pneumothoraces

      Lobar infiltrates

      Cysts

      Nodules

      Pleural effusions

   Infection is also associated with a high LDH.
    PJP Infection in HIV Patients

   Unlike CAP, establishing the diagnosis
    before starting therapy is important
       PJP is less common and may have atypical
        presentation
       Therapy may have complications such as
        steroids with undiagnosed TB
   BAL is the procedure of choice for
    diagnosis with a yield of 97 to 100%
    PJP Infection in HIV Patients
   Patients with a PaO2 < 70 or a-A gradient > 35
    should receive prednisone 40 mg twice daily for
    5 days, then 40 mg daily for 5 days, then 20 mg
    daily for 11 days.
   TMP/SMX is the preferred treatment, 2 DS
    tablets q8h but convert to IV if respiratory
    failure occurs.
   Continue treatment for 21 days.
   Start HAART therapy after therapy completion,
    patients already on treatment should be
    continued.
      Diffuse Alveolar Hemorrhage

   Hemoptysis is usually due from the
    bronchial circulation but DAH causes
    alveolar bleeding from injury to the
    alveolar-capillary membrane.
   Even severe DAH may not have
    hemoptysis.
        Diffuse Alveolar Hemorrhage

   One of three histological patterns may be seen:
       Pulmonary capillaritis – Neutrophillic infiltration of the
        alveolar septa then capillary necrosis
       Bland alveolar hemorrhage – Characterized by
        hemorrhage into the alveolar space without
        inflammation
       Diffuse alveolar damage – The underlying lesions of
        ARDS can occasionally cause hemorrhage.
      Diffuse Alveolar Hemorrhage

   The onset of DAH is often abrupt.
   Hemoptysis can be absent at presentation in a
    third of DAH cases.
   The CXR commonly demonstrates new patchy or
    diffuse alveolar opacities. Recurrent episodes
    can lead to fibrosis.
   BAL demonstrates progressive hemorrhagic
    return and hemosiderin laden macrophages.
     Diffuse Alveolar Hemorrhage –
           Clues to the Cause
   Exposure history to drugs and chemicals
   History of BMT and cytotoxic drugs
   History of systemic vasculitis, collagen vascular disease,
    or mitral valve disease
   C-ANCA positive = Wegener’s Disease
   P-ANCA positive = Microscopic Polyarteritis or Churg-
    Strauss syndrome
   Anti-GBM = Goodpasture’s syndrome
   Hypocomplementemia, ANA+, or anti-DNA+ = SLE
   Idiopathic pulmonary hemosiderosis is a diagnosis of
    exclusion and is established by lung biopsy
     Diffuse Alveolar Hemorrhage -
               Treatment
   Steroids are the mainstay for DAH due to
    systemic vasculitis, collagen vascular disease
    and isolated pulmonary capillaritis.
   Start with Solu-medrol 500-2000 mg daily for 5
    days followed by gradual tapering and
    maintenance on an oral preparation.
   Do not delay therapy, especially in the face of
    renal dysfunction, as the renal injury is more
    likely to be irreversible than the lung disease.
     Diffuse Alveolar Hemorrhage -
               Treatment
   Cyclophosphamide or azathioprine is added
    based on the response to steroids or if
    Wegener’s disease is the etiology.
   Start with a single dose of 0.75 gm/m2 and
    follow the WBC
   Plasmapheresis is used in Goodpasture’s disease
    although its role may expand in other vasculitis
    syndromes
   Treatment for massive hemoptysis is covered in
    a separate lecture
Idiopathic Eosinophillic Pneumonia

   Characterized by eosinophillic infiltration of the
    pulmonary parenchyma.
   The cause remains unknown but thought to be
    an acute hypersensitivity reaction to an
    unidentified inhaled antigen.
   Patients present with an acute febrile illness of <
    3 weeks, tachypnea, and inspiratory crackles.
   63% develop respiratory failure and need
    mechanical ventilation.
Idiopathic Eosinophillic Pneumonia

   The WBC is elevated with a high eosinophil
    fraction.
   If measured, the IgE level is high.
   In addition, eosinophils are found in the pleural
    fluid and BAL.
   CT scan demonstrates bilateral, random, and
    patchy ground glass or reticular opacities.
   Treatment is with steroids only and usually there
    is a dramatic (12 to 48 hours) response with no
    relapse.
                             Summary
1.       ARDS/ALI is marked by inflammation and edema in the lungs.
2.       ARDS is a syndrome diagnosis and, therefore, any reversible
         underlying cause must be sought.
           Bacterial pneumonia
           Viral pneumonia
           Fungal pneumonia
           PJP
           Diffuse alveolar hemorrhage
           Eosinophillic pneumonia
           Lupus pneumonitis
           Toxic drug reaction
3.       Supportive therapy includes a low tidal volume, high PEEP lung
         protection strategy.

				
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