Definition, Etiology, Pathogenesis Top
Acute respiratory failure develops suddenly and is potentially reversible. This definition pertains to the timing of development rather than its cause, which may be due to any of the processes discussed in the chapter on respiratory failure.
Anatomical approach to acute hypoxemia:
1) Diffuse lung parenchymal disease:
a) Pulmonary edema caused by increased hydrostatic pressure in the pulmonary vessels (left ventricular failure, fluid overload), increased permeability of the alveolar-capillary barrier (acute respiratory distress syndrome [ARDS]), drowning, lung reperfusion [after lung transplant or arterial embolectomy]); of unclear or complex mechanism (decompression [eg, pneumothorax], postobstructive [following the elimination of the cause of atelectasis], neurogenic, following stroke, after tocolytic therapy).
b) Alveolar bleeding: Vasculitis and connective tissue diseases (including anti-glomerular basement membrane disease [formerly known as Goodpasture syndrome]), disorders of hemostasis (particularly disseminated intravascular coagulation).
2) Focal lung parenchymal disease: Severe pneumonia, atelectasis (resulting from airway obstruction by a foreign body, tumor, or exudate), pulmonary contusion.
3) Pleural disease: Pneumothorax (particularly tension or large pneumothorax), massive pleural effusions.
4) Reduced pulmonary perfusion: Pulmonary embolism, shock.
Clinical Features and Natural History Top
1. Symptoms: Dyspnea is a relatively uniform finding in acute respiratory failure. Depending on the cause, the following may also occur: cough, fever, chest pain, hemoptysis, and other symptoms.
2. Signs include signs of acute hypoxia (cyanosis, tachycardia, tachypnea) and acute hypercapnia (headache, altered mental status) as well as signs of the underlying condition. In more advanced states, the use of accessory respiratory muscles and paradoxical movements of the chest wall and abdomen may be observed. Pulsus paradoxus—for instance, in chronic obstructive pulmonary disease [COPD] or asthma—suggests that respiratory collapse is imminent. Untreated acute respiratory failure can be fatal.
1. Exclude other causes of dyspnea not related to respiratory failure (see Dyspnea).
2. Determine the cause of acute respiratory failure:
1) Assess the respiratory system: Inspect, palpate, and auscultate, looking for signs of upper airway obstruction, or parenchymal or pleural disease.
2) Assess the cardiovascular system: Assess for signs of cardiogenic pulmonary edema (Table. Initial differentiation between cardiogenic and...), pulmonary embolism, or anaphylaxis.
3) Exclude or confirm sepsis (see Sepsis and Septic Shock), and if confirmed, determine its cause.
1. Pulse oximetry: Low SpO2.
2. Blood tests:
1) Arterial blood gas analysis: Hypoxemia, hypercapnia (respiratory acidosis), and metabolic acidosis may be present in various combinations. Blood gas analysis provides measurement of blood pH, oxygen tension (PaO2), carbon dioxide tension (PaCO2), bicarbonate concentration, as well as the oxygen saturation of hemoglobin (SaO2), allowing interpretation of oxygenation, ventilation, and acid-base balance. While an arterial blood gas (ABG) sample accurately reflects oxygenation and pulmonary gas exchange, central venous blood is more accurate at detecting the acid-base status and hypercapnia at the tissue level if severe hypoperfusion is present (ie, circulatory failure).Evidence 1Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to data coming from a case series of 105 patients with consistent findings of acid-base status in patients with hemodynamic compromise. Adrogué HJ, Rashad MN, Gorin AB, Yacoub J, Madias NE. Assessing acid-base status in circulatory failure. Differences between arterial and central venous blood. N Engl J Med. 1989 May 18;320(20):1312-6. PubMed PMID: 2535633. Peripheral venous blood gas (VBG) analysis is a simpler, less painful, and more convenient alternative to ABG. While it is likely sufficient to estimate arterial pH, VBG may not be sufficient to estimate arterial pCO2, especially at highly abnormal values.Evidence 2Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to heterogeneity of findings in a systematic review of 20 eligible studies. Byrne AL, Bennett M, Chatterji R, Symons R, Pace NL, Thomas PS. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Respirology. 2014 Feb;19(2):168-75. doi: 10.1111/resp.12225. Epub 2014 Jan 3. PubMed PMID: 24383789. Byrne AL, Bennett MH, Pace NL, Thomas P. Peripheral venous blood gas analysis versus arterial blood gas analysis for the diagnosis of respiratory failure and metabolic disturbance in adults (Protocol). Cochrane Database of Systematic Reviews 2013, Issue 11. Art. No.: CD010841. DOI: 10.1002/14651858.CD010841. In the absence of circulatory failure or shock, venous pH, bicarbonate, and base excess have sufficient agreement with arterial values and, while the relationship between venous and arterial pCO2 remains unpredictable, it may still be of value as a screening test for arterial hypercapnia or to monitor changes in respiratory function.Evidence 3Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to imprecision. Kelly AM. Review article: Can venous blood gas analysis replace arterial in emergency medical care. Emerg Med Australas. 2010 Dec;22(6):493-8. doi: 10.1111/j.1742-6723.2010.01344.x. Review. PubMed PMID: 21143397. Bloom BM, Grundlingh J, Bestwick JP, Harris T. The role of venous blood gas in the emergency department: a systematic review and meta-analysis. Eur J Emerg Med. 2014 Apr;21(2):81-8. doi: 10.1097/MEJ.0b013e32836437cf. Review. PubMed PMID: 23903783.
2) Complete blood count and biochemical tests: Abnormalities may suggest specific etiologies (eg, leukocytosis, anemia, or eosinophilia; elevated serum brain natriuretic peptide or troponin, elevated D-dimers).
3. Microbiology: Because acute respiratory failure is frequently caused by infections, attempt to identify the etiologic agent (microbiological tests of respiratory secretions [eg, during flexible bronchoscopy], blood, or other clinically relevant material).
4. Imaging studies:
1) Plain chest radiography: Specific abnormalities may suggest the etiology (eg, various patterns of interstitial or air-space opacification in the lungs, volume loss, pneumothorax, pleural effusion).
2) Chest ultrasonography or computed tomography (CT) may further help in delineating the etiology of acute respiratory failure.
1. Clearing the upper airway, as the situation requires: Noninstrumental (see Cardiac Arrest, Head Injury); insertion of an oropharyngeal tube or other device; intubation (see Endotracheal Intubation); cricothyrotomy; tracheostomy (the procedure of choice in patients with massive laryngeal edema or prolonged mechanical ventilation). See also: management of aspiration.
4. Mechanical ventilation:
1) Noninvasive positive pressure ventilation should be an early consideration for patients with an acute exacerbation of COPDEvidence 4Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Evidence includes a systematic review of 16 randomized controlled trials within a clinical practice guideline. Trials showed large, precise reductions in the rate of endotracheal intubation as well as in the risk of mortality across a range of COPD populations. Keenan SP, Sinuff T, Burns KE, et al; Canadian Critical Care Trials Group/Canadian Critical Care Society Noninvasive Ventilation Guidelines Group. Clinical practice guidelines for the use of noninvasive positive-pressure ventilation and noninvasive continuous positive airway pressure in the acute care setting. CMAJ. 2011 Feb 22;183(3):E195-214. doi: 10.1503/cmaj.100071. Epub 2011 Feb 14. PubMed PMID: 21324867; PubMed Central PMCID: PMC3042478. or cardiogenic pulmonary edema (in the absence of shock or an acute coronary syndrome).Evidence 5Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Evidence includes a systematic review of 20 randomized controlled trials within a clinical practice guideline. Trials showed large and precise reductions in the rates of treatment failure and hospital mortality across a range of populations. Keenan SP, Sinuff T, Burns KE, et al; Canadian Critical Care Trials Group/Canadian Critical Care Society Noninvasive Ventilation Guidelines Group. Clinical practice guidelines for the use of noninvasive positive-pressure ventilation and noninvasive continuous positive airway pressure in the acute care setting. CMAJ. 2011 Feb 22;183(3):E195-214. doi: 10.1503/cmaj.100071. Epub 2011 Feb 14. PubMed PMID: 21324867; PubMed Central PMCID: PMC3042478. It may also be considered in other situations of acute respiratory failure.
2) Invasive mechanical ventilation may be required.
5. Respiratory physiotherapy, including postural drainage.
6. For nutrition support to prevent malnutrition, see chronic respiratory failure.
Consequences of hypoxemia and hypercapnia. More severe complications following intubation and mechanical ventilation: upper gastrointestinal tract bleeding—stress ulcers or hemorrhagic gastritis (prevention: see Acute Hemorrhagic/Erosive Gastropathy), venous thromboembolism (prevention: see Primary Prevention of Venous Thromboembolism).