Transcript Acute Hypoxic Respiratory Failure

Type I Respiratory Failure: Acute
Hypoxic Respiratory Failure
Division of Critical Care Medicine
University of Alberta
Outline
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Review of Pathophysiology
Clinical presentation and differential
diagnosis
ARDS
Reversible causes of ARDS – Description
and Treatment
Pathophysiology
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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.
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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
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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
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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.
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In this case, consider an error in the ABG, an intracardiac
shunt or AVM malformation.
Differential Diagnosis of AHRF
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Acute lung injury or ARDS
Acute cardiogenic pulmonary edema
Bilateral aspiration pneumonia
Lobar atelectasis of both lower lobes
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
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Main stem bronchus obstruction from mucous
plug or blood clot.
Bilateral or unilateral pneumothorax
Large unilateral or bilateral pleural effusions
Diffuse alveolar hemorrhage
Massive pulmonary embolus
Opening of patent foramen ovale with preexisting pulmonary hypertension.
Clinical Setting
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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
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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
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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 xray findings (i.e. lobar pneumonia, atelectasis,
effusion) and bilateral findings (i.e.. ARDS,
pulmonary edema, diffuse alveolar hemorrhage)
Clinical Setting
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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)
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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
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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
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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
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Aspiration of gastric contents
Bacterial pneumonia
Chest trauma with pulmonary contusion
Near drowning
PCP pneumonia
Toxic inhalations (i.e.. smoke, crack cocaine)
Viral pneumonia
ARDS – Indirect Precipitating
Causes
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Pancreatitis
Transfusion associated acute lung injury
(TRALI)
Post cardiopulmonary bypass
Primary graft failure of lung transplant
Severe sepsis and septic shock
Toxic ingestions (i.e.. ASA, TCA)
Trauma with multiple fractures and fat-emboli
syndrome
ARDS/ALI Pathology
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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
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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
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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
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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
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After the underlying cause is identified,
the focus is on ventilation goals:
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Maintain SaO2 < 88% and PaO2 < 55
Protect lung from further injury
Maintain lung recruitment
Maintain normal pH and PaCO2
ARDS/ALI – Ventilation Goals
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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 fluidfilled 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
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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
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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
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Bacterial pneumonia
Viral pneumonia
Fungal pneumonia
PJP
Diffuse alveolar hemorrhage
Eosinophillic pneumonia
Lupus pneumonitis
Toxic drug reaction
Community Acquired Pneumonia
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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:
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Typical – S. pneumoniae, H. influenzae, S. aureus,
GAS, M. catarrhalis, anaerobes, and GNB.
Atypical – Legionella, Mycoplasma and Chlamydophila
pneumoniae.
Community Acquired Pneumonia
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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
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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
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Bacteria are the most common cause of CAP.
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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
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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
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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
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The selection of specific antibiotics for
empiric therapy is based on a number of
principles:
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The most likely pathogen
Clinical trials proving efficacy
Risk factors for the presence of resistance
Presence of medical co-morbidities
Community Acquired Pneumonia Treatment
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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
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Not in the ICU
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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)
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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
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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
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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
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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
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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
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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
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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
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Unlike CAP, establishing the diagnosis
before starting therapy is important
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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
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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
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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
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One of three histological patterns may be seen:
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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
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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
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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 ChurgStrauss 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
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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
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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
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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
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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
ARDS/ALI is marked by inflammation and edema in the lungs.
ARDS is a syndrome diagnosis and, therefore, any reversible
underlying cause must be sought.
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Bacterial pneumonia
Viral pneumonia
Fungal pneumonia
PJP
Diffuse alveolar hemorrhage
Eosinophillic pneumonia
Lupus pneumonitis
Toxic drug reaction
Supportive therapy includes a low tidal volume, high PEEP lung
protection strategy.