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Respiratory Failure Workup

  • Author: Ata Murat Kaynar, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM  more...
 
Updated: Mar 31, 2015
 

Approach Considerations

Respiratory failure may be associated with a variety of clinical manifestations. However, these are nonspecific, and very significant respiratory failure may be present without dramatic signs or symptoms. This emphasizes the importance of measuring arterial blood gases in all patients who are seriously ill or in whom respiratory failure is suspected.

Chest radiography is essential. Echocardiography is not routinely done but is sometimes useful. Pulmonary functions tests (PFTs), if feasible, may be helpful. Electrocardiography (ECG) should be performed to evaluate the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmias resulting from severe hypoxemia or acidosis. Right-sided heart catheterization is controversial.

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Laboratory Studies

Once respiratory failure is suspected on clinical grounds, arterial blood gas analysis should be performed to confirm the diagnosis and to assist in the distinction between acute and chronic forms. This helps assess the severity of respiratory failure and helps guide management.

A complete blood count (CBC) may indicate anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure.

A chemistry panel may be helpful in the evaluation and management of a patient in respiratory failure. Abnormalities in renal and hepatic function may either provide clues to the etiology of respiratory failure or alert the clinician to complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ function.

Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure. An elevated creatine kinase level with a normal troponin I level may indicate myositis, which occasionally can cause respiratory failure.

In chronic hypercapnic respiratory failure, serum levels of thyroid-stimulating hormone (TSH) should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure.

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Radiography

Chest radiography is essential in the evaluation of respiratory failure because it frequently reveals the cause (see the images below). However, distinguishing between cardiogenic and noncardiogenic pulmonary edema is often difficult. Increased heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests acute respiratory distress syndrome (ARDS).

Bilateral airspace infiltrates on chest radiograph Bilateral airspace infiltrates on chest radiograph film secondary to acute respiratory distress syndrome that resulted in respiratory failure.
Extensive left-lung pneumonia caused respiratory f Extensive left-lung pneumonia caused respiratory failure; the mechanism of hypoxia is intrapulmonary shunting.
A 44-year-old woman developed acute respiratory fa A 44-year-old woman developed acute respiratory failure and diffuse bilateral infiltrates. She met the clinical criteria for the diagnosis of acute respiratory distress syndrome. In this case, the likely cause was urosepsis.
This patient developed acute respiratory failure t This patient developed acute respiratory failure that turned out to be the initial presentation of systemic lupus erythematosus. The lung pathology evidence of diffuse alveolar damage is the characteristic lesion of acute lupus pneumonitis.
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Echocardiography

Echocardiography need not be performed routinely in all patients with respiratory failure. However, it is a useful test when a cardiac cause of acute respiratory failure is suspected.

The findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema. A normal heart size and normal systolic and diastolic function in a patient with pulmonary edema would suggest ARDS.

Echocardiography provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure.

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Pulmonary Function Tests

Patients with acute respiratory failure generally are unable to perform PFTs; however, these tests are useful in the evaluation of chronic respiratory failure.

Normal values for forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) suggest a disturbance in respiratory control. A decrease in the FEV1 -to-FVC ratio (FEV1/FVC) indicates airflow obstruction, whereas a reduction in both FEV1 and FVC and maintenance of FEV1/FVC suggest restrictive lung disease.

Respiratory failure is uncommon in obstructive diseases when FEV1 is greater than 1 L and in restrictive diseases when FVC is greater than 1 L.

See Pulmonary Function Testing for further details.

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Right-Sided Heart Catheterization

Right-sided heart catheterization (also known as pulmonary artery catheterization or Swan-Ganz catheterization) remains a controversial issue in the management of critically ill patients. Invasive monitoring probably is not routinely needed in patients with acute hypoxemic respiratory failure, but when significant uncertainty about cardiac function, adequacy of volume resuscitation, and systemic oxygen delivery remain, right-sided heart catheterization should be considered.

Measurement of pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic edema. The pulmonary capillary wedge pressure should be interpreted in the context of serum oncotic pressure and cardiac function.

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Contributor Information and Disclosures
Author

Ata Murat Kaynar, MD Associate Professor, Departments of Critical Care Medicine and Anesthesiology, University of Pittsburgh School of Medicine

Ata Murat Kaynar, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Chest Physicians, American Society of Anesthesiologists, Society of Critical Care Medicine, Society of Critical Care Anesthesiologists

Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease, Clinical and Translational Science and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM is a member of the following medical societies: American College of Chest Physicians, Association of University Anesthetists, European Society of Intensive Care Medicine, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Shock Society, Society of Critical Care Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Masimo<br/>Received honoraria from LiDCO Ltd for consulting; Received intellectual property rights from iNTELOMED for board membership; Received honoraria from Edwards Lifesciences for consulting; Received honoraria from Masimo, Inc for board membership.

Acknowledgements

Cory Franklin, MD Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science; Director, Division of Critical Care Medicine, Cook County Hospital

Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Harold L Manning, MD Professor, Departments of Medicine, Anesthesiology and Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical School

Harold L Manning, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
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Bilateral airspace infiltrates on chest radiograph film secondary to acute respiratory distress syndrome that resulted in respiratory failure.
Extensive left-lung pneumonia caused respiratory failure; the mechanism of hypoxia is intrapulmonary shunting.
A 44-year-old woman developed acute respiratory failure and diffuse bilateral infiltrates. She met the clinical criteria for the diagnosis of acute respiratory distress syndrome. In this case, the likely cause was urosepsis.
This patient developed acute respiratory failure that turned out to be the initial presentation of systemic lupus erythematosus. The lung pathology evidence of diffuse alveolar damage is the characteristic lesion of acute lupus pneumonitis.
A Bilevel positive airway pressure support machine is shown here. This could be used in spontaneous mode or timed mode (backup rate could be set).
Headgear and full face mask commonly are used as the interface for noninvasive ventilatory support.
Bilevel positive airway pressure (BiPAP) and inspiratory positive airway pressure (IPAP) settings are shown. IPAP or expiratory positive airway pressure (EPAP) and frequency can be preset.
Noninvasive ventilation with bilevel positive airway pressure for acute respiratory failure secondary to exacerbation of chronic obstructive pulmonary disease.
Wave forms of a volume-targeted ventilator: Pressure, flow, and volume waveforms are shown with square-wave flow pattern. A is baseline, B is increase in tidal volume, C is reduced lung compliance, and D is increase in flow rate. All 3 settings lead to increase in peak airway pressures. Adapted from Spearman CB et al.
The cause of respiratory failure may be suggested by spirometry.
A 65-year-old man developed chronic respiratory failure secondary to usual interstitial pneumonitis. Loss of normal architecture is seen upon biopsy. Also seen are varying degrees of inflammation and fibrosis.
Lung biopsy from a 32-year-old woman who developed fever, diffuse infiltrates seen on chest radiograph, and acute respiratory failure. The lung biopsy shows acute eosinophilic pneumonitis; bronchoscopy with bronchoalveolar lavage also may have helped reveal the diagnosis.
Lung biopsy on this patient with acute respiratory failure and diffuse pulmonary infiltrates helped yield the diagnosis of pulmonary edema. Therefore, cardiogenic pulmonary edema should be excluded as the cause of respiratory failure prior to considering lung biopsy.
Pressure-volume curve of a patient with acute respiratory distress syndrome (ARDS) on mechanical ventilation can be constructed. The lower and the upper ends of the curve are flat, and the central portion is straight (where the lungs are most compliant). For optimal mechanical ventilation, patients with ARDS should be kept between the inflection and the deflection point.
Surgical lung biopsy was performed in the patient described in Image 3. The histology shows features of diffuse alveolar damage, including epithelial injury, hyperplastic type II pneumocytes, and hyaline membranes.
 
 
 
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