hypoxemic resp. failure

7/28/2019 hypoxemic Resp. Failure

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Outline

1. Review of Pathophysiology

2. Clinical presentation and differential

diagnosis

3. ARDS

4. Reversible causes of ARDS Descriptionand Treatment


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Pathophysiology

Acute hypoxic respiratory failure (AHRF) is alsocalled Type I Respiratory Failure.

Marked by severe hypoxemia that isunresponsive to supplemental oxygen.

This results from widespread flooding andcollapse of alveoli that causes blood to flow pastunventilated alveoli (V/Q ratio of zero).

Also called shunt.


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As can be seen above, blood passing through theright alveoli does not pick up any oxygen while theleft is normal and fully saturated.

The reduced oxygen content from the right mixeswith the left and reduces the overall oxygen of the

blood returning to the heart.


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Pathophysiology

The intra-alveolar fluid and increased interstitialfluid decreases overall lung compliance.

This imposes a larger elastic work of breathingresulted in increased respiratory muscle oxygenconsumption.

A vicious cycle of increased O2 demand, muscle

fatigue and hypoxemia leads to respiratoryarrest and death if mechanical assistance is notinstituted.


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Differential Diagnosis of AHRF

1. Acute lung injury or ARDS

2. Acute cardiogenic pulmonary edema

3. Bilateral aspiration pneumonia4. Lobar atelectasis of both lower lobes

5. Severe unilateral lower lobe atelectasis,especially when the patient is receiving

vasodilators such as nitrates, calcium channelblockers, or nitroprusside that blunt hypoxicvasoconstriction.


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Differential Diagnosis of AHRF

6. Main stem bronchus obstruction from mucousplug or blood clot.

7. Bilateral or unilateral pneumothorax8. 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.


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Clinical Setting

Review of intravascular volume administrationwill often suggest an explanation for pulmonary

edema in patients with left ventricular or renaldysfunction.

ALI or ARDS commonly arises in a typical clinicalcontext with direct and indirect causes

(differential to be discussed soon).


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Clinical Setting

Echocardiography is helpful in distinguishingcardiogenic from noncardiogenic pulmonaryedema.

Echocardiography also helps identify leftventricular wall motion abnormalities, mitralvalve dysfunction, and ventricular dilation.

Early bronchoscopy is critical to identifyreversible causes and guide therapy.

Bronchoscopy can help diagnose some causes ofAHRF including diffuse alveolar hemorrhage,

pneumonia, and acute eosinophillic pneumonia.


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Acute Respiratory Distress

Syndrome (ARDS)Acute lung injury (ALI) and ARDS are

common causes of AHRF.

Both are defined by acute onset, bilateralpulmonary infiltrates on chest x-rayconsistent with pulmonary edema,

hypoxemia and the absence of evidence ofleft atrial hypertension.


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ARDS - Definition

The ratio of arterial oxygen (PaO2) to fraction ofinspired oxygen (FiO2), also called the P/F ratio,

reflects the degree of hypoxemia at differentlevels of FiO2.

The syndrome is called ALI when the ratio is 60%) which is toxic in itself. Higher levels of PEEP also prevents surfactant poor

alveoli from repeatedly opening and collapsing which isalso injurious to the lungs.


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ARDS/ALI Ventilation Goals

Conventional ventilation strategy usually requires a tidalvolume of 10-12 mL/kg in order to maintain minuteventilation and hence, normal PaCO2.

However, in an injured lung, that volume causes excessstretch 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 resultantelevated PaCO2 is tolerated as long as the pH is > 7.20. This is called permissive hypercapnia.


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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


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Reversible Causes of ARDS/ALI

Bacterial pneumonia

Viral pneumonia

Fungal pneumonia PJP

Diffuse alveolar hemorrhage

Eosinophillic pneumonia Lupus pneumonitis

Toxic drug reaction


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Community Acquired Pneumonia

There are more than 100 microbes (bacteria,viruses, fungi, and parasites) that can causeCAP.

Most cases of pneumonia are caused by 4 or 5microbes.

Bacteria are the most common cause of CAP andare divided into two groups:

Typical S. pneumoniae, H. influenzae, S. aureus,GAS, M. catarrhalis, anaerobes, and GNB. Atypical Legionella, Mycoplasma and Chlamydophila

pneumoniae.


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A microbiological diagnosis is confirmed in only20% of cases.

There are a few clinical clues that must beconsidered 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


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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 diseasessuch as COPD, diabetes, and alcohol abuse.


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Pseudomonas: Community acquired Pseudomonasoccurs mainly in immunocompromised patients orthose 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.


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Anaerobes: May be the cause of aspirationpneumonia and lung abscesses. Role is notclear since detection in routine cultures is not

possible. N. meningitidis: An uncommon cause of CAP

but is reportable to public health andprophylaxis must be given.

TB: Missed diagnosis is common and manypatients are initially treated for presumedCAP.


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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


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TreatmentAntibiotic recommendations for

hospitalized patients are divided between

ICU and non-ICU and whether the patientis admitted from a long term care facility.

When the etiology of CAP is identified,

treatment regimen must be simplified anddirected to that pathogen.


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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 2g q8h PLUS

Ciprofloxicin 400 mg q12h or levofloxicin 750 mg daily oraminoglycoside

Penicillin allergy use aztreonam, an aminoglycoside, andlevofloxicin

If initial gram strain suggests S. aureus then addvancomycin 15 mg/kg q12h


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Viral Pneumonia

Viruses are estimated to cause adult CAP in 10to 31% of cases.

Influenza A or B occurs in outbreaks and

epidemics. They can cause pneumonia althoughthey are more likely to cause a URTI and thenpredispose to a secondary pneumonia.

High risk patients include patients with heart

and lung disease, diabetes, renal diseases,immunosuppression, nursing home residentsand over 65.


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Viral Pneumonia

Parainfluenza are important in theimmunocompromised patients causing lifethreatening lower respiratory tract infections.

RSV is more common in children but can causeCAP in elderly.

Adenovirus presents with fever, cough, andperibronchial markings with patchy alveolar

infiltrates. Metapneumovirus is an emerging pathogen and

causes disease in young children and theelderly.


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Viral Pneumonia

SARS is a coronavirus that caused an outbreak after itjumped species in 2002. Currently quiescent.

Hantavirus is spread from the feces of infected mice.The illness is preceded by prodromal flu-like symptomsfollowed by ARDS. The virus does not cause pneumoniaand the ARDS is from the host response.

Avian influenza currently causes sporadic outbreaks butWHO and CDC consider it to be a potential source forthe next global pandemic.

Varicella pneumonia is the most frequent complication ofvaricella infection in healthy adults with a case fatalityrate of 10-30%.


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Fungal Pneumonia Fungal infections are an unusual cause of CAP inimmunocompetent 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 immunocompromisedpatients. Histoplasma proliferates in soil contaminated with

bird and bat droppings. Symptomatic patientspresent with flu-like illness and radiographic

abnormalities such as bronchopneumonia andinterstitial pneumonitis. Coccidioides typically presents with chest pain,

cough, and fever with a normal CXR in up to 50% ofpatients. It is endemic in the deserts ofsouthwestern North America.


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PJP Infection in HIV Patients

Most common opportunistic infection in patientswith HIV.

Frequently presents as the first manifestation of

HIV infection. 75% of the population are infected by age 4.

The primary infection is asymptomatic andremains latent throughout life unless the patient

becomes immunosuppressed. PJP does not occur until the CD4 count falls

below 200 cells/mL.


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PJP is generally gradual n onset and characterized byfever, cough, and progressive dyspnea andtachypnea.

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.


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Unlike CAP, establishing the diagnosisbefore starting therapy is important

PJP is less common and may have atypicalpresentation

Therapy may have complications such assteroids with undiagnosed TB

BAL is the procedure of choice fordiagnosis with a yield of 97 to 100%


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Diffuse Alveolar Hemorrhage

Hemoptysis is usually due from thebronchial circulation but DAH causes

alveolar bleeding from injury to thealveolar-capillary membrane.

Even severe DAH may not have

hemoptysis.


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One of three histological patterns may be seen:

Pulmonary capillaritis Neutrophillic infiltration of thealveolar septa then capillary necrosis

Bland alveolar hemorrhage Characterized byhemorrhage into the alveolar space withoutinflammation

Diffuse alveolar damage The underlying lesions ofARDS can occasionally cause 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 episodescan lead to fibrosis.

BAL demonstrates progressive hemorrhagicreturn and hemosiderin laden macrophages.


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Diffuse Alveolar Hemorrhage -Treatment

Steroids are the mainstay for DAH due tosystemic vasculitis, collagen vascular disease

and isolated pulmonary capillaritis. Start with Solu-medrol 500-2000 mg daily for 5

days followed by gradual tapering andmaintenance on an oral preparation.

Do not delay therapy, especially in the face ofrenal dysfunction, as the renal injury is morelikely to be irreversible than the lung disease.


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Diffuse Alveolar Hemorrhage -Treatment

Cyclophosphamide or azathioprine is addedbased on the response to steroids or ifWegeners disease is the etiology.

Start with a single dose of 0.75 gm/m2 andfollow the WBC Plasmapheresis is used in Goodpastures disease

although its role may expand in other vasculitis

syndromes Treatment for massive hemoptysis is covered in

a separate lecture


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Idiopathic Eosinophillic Pneumonia

Characterized by eosinophillic infiltration of thepulmonary parenchyma.

The cause remains unknown but thought to be

an acute hypersensitivity reaction to anunidentified inhaled antigen. Patients present with an acute febrile illness of

hypoxemic resp. failure

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