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{{Respiratory failure}}
{{Respiratory failure}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{MKA}}  
==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
Respiratory failure is the result of inadequate [[gas exchange]] in the [[pulmonary circulation]]. This could result from [[lung failure]] or [[pump failure]]. [[Lung failure]] which is failure of [[gas exchange]] results in [[hypoxemia]] (<PaO2) and [[pump failure]] which is [[Ventilation (physiology)|ventilatory]] failure would result in [[alveolar]] [[hypoventilation]] that causes [[hypercapnia]] (>PaCO2). Type I respiratory failure has a [[V/Q scan|V/Q]] mismatch that causes [[hypoxemia]]. Type II respiratory failure is caused by [[alveolar]] [[hypoventilation]] which results in [[hypercapnia]]. Type III respiratory failure occurs in the peri-operative period clinically progresses to Type I or Type II respiratory failure. Type IV respiratory failure results from an underlying [[Circulatory arrest|circulatory collapse]].


OR
==Pathophysiology==


It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
===Pathogenesis===
 
'''Mechanics of the respiratory system'''
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR


The progression to [disease name] usually involves the [molecular pathway].
The [[pathogenesis]] of respiratory failure is as follows:<ref name="pmid14621112">{{cite journal |vauthors=Roussos C, Koutsoukou A |title=Respiratory failure |journal=Eur Respir J Suppl |volume=47 |issue= |pages=3s–14s |date=November 2003 |pmid=14621112 |doi= |url=}}</ref>
*The [[respiratory system]] comprises of 2 parts:
**The gas exchanging organ, the [[lung]]
**The [[pump]] that ventilates the [[lungs]], the [[pump]] consists of:
***[[Chest wall]], the respiratory muscles
***The respiratory control system in the [[central nervous system]] ([[CNS]])
***The [[Spinal cord|spinal]] and [[Peripheral Nervous System|peripheral]] pathways that connect the [[CNS]] control system with the respiratory muscles
*The respiratory system has 2 main functions [[oxygenation]] of mixed [[venous]] [[blood]] and elimination of [[carbon dioxide]].
'''Respiratory failure'''
*Respiratory failure is a condition where there is loss of one or both of the functions of the respiratory system resulting in inadequate [[gas exchange]].
*Respiratory failure is defined as:
**[[Arterial]] [[oxygen]] tension ([[PaO2]]) < 60 mmHg
**[[Arterial]] [[carbon dioxide]] ([[PaCO2]]) > 45 mmHg
*Respiratory failure can be caused by [[lung failure]] or [[pump failure]].
*[[Lung failure]], which is [[gas exchange]] failure resulting in [[hypoxemia]] (<[[PaO2]]).
*[[Pump failure]], which is [[Ventilation (physiology)|ventilatory]] failure resulting in [[alveolar]] [[hypoventilation]] which in turn results in [[hypercapnia]] (>[[PaCO2]]).
*Hypercapnic respiratory failure can be caused by:
**Mechanical defects
**[[Central nervous system]] depression
**Imbalance of energy demands and supplies
**Adaptation of central controllers
**[[Neuromuscular transmission]] impairment
**Mechanical defect of the [[rib cage]]
**Fatigue of respiratory [[muscles]]
*Lung failure and [[pump failure]] can coexist in the same patient in cases of:
**[[Chronic obstructive pulmonary disease|Chronic obstructive pulmonary disease (COPD)]] with [[carbon dioxide]] retention
**Severe [[pulmonary edema]]
**[[Asthmatic]] crisis
*Acute respiratory failure can develop in minutes to hours
*Chronic respiratory failure takes days to develop
*The ph drops below 7.35 in acute [[Hypercapnia|hypercapnic]] respiratory failure
*In underlying chronic respiratory failure, the [[PaCO2]] rises unto 20mmHg above baseline
*Presentation of respiratory failure can be:
**Acute
**Chronic
**Acute on chronic ([[COPD]] exacerbation)
===Type I respiratory failure===
Characteristics of Type I respiratory failure include:<ref>{{cite book | last = Hall | first = Jesse | title = Principles of critical care | chapter = CHAPTER 43: The Pathophysiology and Differential Diagnosis of Acute Respiratory Failure  | publisher = McGraw-Hill Education | location = New York | year = 2015 | isbn = 0071738819 }}</ref><ref name="pmid16380593">{{cite journal |vauthors=Masip J, Roque M, Sánchez B, Fernández R, Subirana M, Expósito JA |title=Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis |journal=JAMA |volume=294 |issue=24 |pages=3124–30 |date=December 2005 |pmid=16380593 |doi=10.1001/jama.294.24.3124 |url=}}</ref>
*Severe oxygen-refractory [[hypoxemia]] (< PaO2)
*[[Ventilation]]/[[Perfusion]] (V/Q) mismatch
*A portion of total [[pulmonary]] blood flow is unable to pick [[oxygen]]
*[[Alveolar]] flooding (airspace filling)


OR
===Type II respiratory failure===
Characteristics of Type II respiratory failure include:<ref>{{cite book | last = Hall | first = Jesse | title = Principles of critical care | chapter = CHAPTER 43: The Pathophysiology and Differential Diagnosis of Acute Respiratory Failure  | publisher = McGraw-Hill Education | location = New York | year = 2015 | isbn = 0071738819 }}</ref><ref name="pmid10793162">{{cite journal |vauthors=Brower RG, Matthay MA, Morris A, Schoenfeld D, Thompson BT, Wheeler A |title=Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome |journal=N. Engl. J. Med. |volume=342 |issue=18 |pages=1301–8 |date=May 2000 |pmid=10793162 |doi=10.1056/NEJM200005043421801 |url=}}</ref><ref name="pmid26902369">{{cite journal |vauthors=Kreppein U, Litterst P, Westhoff M |title=[Hypercapnic respiratory failure. Pathophysiology, indications for mechanical ventilation and management] |language=German |journal=Med Klin Intensivmed Notfmed |volume=111 |issue=3 |pages=196–201 |date=April 2016 |pmid=26902369 |doi=10.1007/s00063-016-0143-2 |url=}}</ref><ref name="pmid1539142">{{cite journal |vauthors=Jeffrey AA, Warren PM, Flenley DC |title=Acute hypercapnic respiratory failure in patients with chronic obstructive lung disease: risk factors and use of guidelines for management |journal=Thorax |volume=47 |issue=1 |pages=34–40 |date=January 1992 |pmid=1539142 |pmc=463551 |doi= |url=}}</ref>
*[[Hypercapnia]] (Increased [[PaCO2]])
*[[Alveolar]] [[hypoventilation]]
*[[Alveolar]] [[minute ventilation]] (VA) is decreased
*Failure to adequately remove [[carbon dioxide]]
*[[Alveolar]] [[hypoventilation]] can be caused by:
**Loss of [[CNS]] drive
**Impaired [[neuromuscular]] competence
**Excessive [[dead space]]
**Increased mechanical load
*[[Hypoxemia]] can be present (corrected by supplemental [[oxygen]])


The pathophysiology of [disease/malignancy] depends on the histological subtype.
===Type III respiratory failure===
Characteristics of Type III respiratory failure include:<ref>{{cite book | last = Hall | first = Jesse | title = Principles of critical care | chapter = CHAPTER 43: The Pathophysiology and Differential Diagnosis of Acute Respiratory Failure  | publisher = McGraw-Hill Education | location = New York | year = 2015 | isbn = 0071738819 }}</ref><ref name="pmid5048300">{{cite journal |vauthors=Alexander JI, Horton PW, Millar WT, Parikh RK, Spence AA |title=The effect of upper abdominal surgery on the relationship of airway closing point to end tidal position |journal=Clin Sci |volume=43 |issue=2 |pages=137–41 |date=August 1972 |pmid=5048300 |doi= |url=}}</ref><ref name="pmid4606381">{{cite journal |vauthors=Ali J, Weisel RD, Layug AB, Kripke BJ, Hechtman HB |title=Consequences of postoperative alterations in respiratory mechanics |journal=Am. J. Surg. |volume=128 |issue=3 |pages=376–82 |date=September 1974 |pmid=4606381 |doi= |url=}}</ref>
*Progressive increased [[atelectasis]] due to a low [[functional residual capacity]] (FRC)
*Improper [[abdominal wall]] mechanics usually in the peri-operative or [[Post-operative complications|post-operative]] period
*Clinical progression is often either to Type I or Type II respiratory failure


==Pathophysiology==
===Type IV respiratory failure===
 
Characteristics of Type IV respiratory failure include:<ref>{{cite book | last = Hall | first = Jesse | title = Principles of critical care | chapter = CHAPTER 43: The Pathophysiology and Differential Diagnosis of Acute Respiratory Failure  | publisher = McGraw-Hill Education | location = New York | year = 2015 | isbn = 0071738819 }}</ref><ref name="pmid11794169">{{cite journal |vauthors=Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M |title=Early goal-directed therapy in the treatment of severe sepsis and septic shock |journal=N. Engl. J. Med. |volume=345 |issue=19 |pages=1368–77 |date=November 2001 |pmid=11794169 |doi=10.1056/NEJMoa010307 |url=}}</ref>
===Pathogenesis===
*Underlying cause is [[shock]] (inadequate [[oxygen]] delivery)
*The exact pathogenesis of [disease name] is not fully understood.
*Patients are often [[Mechanical ventilation|mechanically ventilated]] due to underlying [[shock]]
OR
*Resolves when the underlying [[shock]] or [[circulatory]] collapse is corrected
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*Poor [[prognosis]], if superimposed by Type I or Type II respiratory failure
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Genetics==
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*[[Genetic]] variants that can influence susceptibility to [[acute respiratory distress syndrome]] include:<ref name="pmid23048207">{{cite journal |vauthors=Tejera P, Meyer NJ, Chen F, Feng R, Zhao Y, O'Mahony DS, Li L, Sheu CC, Zhai R, Wang Z, Su L, Bajwa E, Ahasic AM, Clardy PF, Gong MN, Frank AJ, Lanken PN, Thompson BT, Christie JD, Wurfel MM, O'Keefe GE, Christiani DC |title=Distinct and replicable genetic risk factors for acute respiratory distress syndrome of pulmonary or extrapulmonary origin |journal=J. Med. Genet. |volume=49 |issue=11 |pages=671–80 |date=November 2012 |pmid=23048207 |pmc=3654537 |doi=10.1136/jmedgenet-2012-100972 |url=}}</ref>
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
**Functional [[single nucleotide polymorphism]] ([[SNP]]) in [[POPDC3]] [[gene]]
*The development of [disease name] is the result of multiple genetic mutations.
**Functional [[SNP]] in [[FAAH]] [[gene]]
*[[ARDS]] in severe [[sepsis]] is associated with the presence of [[allele]] D of the [[ACE]] [[gene]]<ref name="pmid23364437">{{cite journal |vauthors=Cardinal-Fernández P, Ferruelo A, El-Assar M, Santiago C, Gómez-Gallego F, Martín-Pellicer A, Frutos-Vivar F, Peñuelas O, Nin N, Esteban A, Lorente JA |title=Genetic predisposition to acute respiratory distress syndrome in patients with severe sepsis |journal=Shock |volume=39 |issue=3 |pages=255–60 |date=March 2013 |pmid=23364437 |doi=10.1097/SHK.0b013e3182866ff9 |url=}}</ref>


==Associated Conditions==
==Associated Conditions==
Conditions associated with respiratory failure include:<ref name="pmid16020801">{{cite journal |vauthors=Bernard GR |title=Acute respiratory distress syndrome: a historical perspective |journal=Am. J. Respir. Crit. Care Med. |volume=172 |issue=7 |pages=798–806 |date=October 2005 |pmid=16020801 |pmc=2718401 |doi=10.1164/rccm.200504-663OE |url=}}</ref><ref name="pmid19281077">{{cite journal |vauthors=Budweiser S, Jörres RA, Pfeifer M |title=Treatment of respiratory failure in COPD |journal=Int J Chron Obstruct Pulmon Dis |volume=3 |issue=4 |pages=605–18 |date=2008 |pmid=19281077 |pmc=2650592 |doi= |url=}}</ref><ref name="pmid27490597">{{cite journal |vauthors=Hornik C, Meliones J |title=Pulmonary Edema and Hypoxic Respiratory Failure |journal=Pediatr Crit Care Med |volume=17 |issue=8 Suppl 1 |pages=S178–81 |date=August 2016 |pmid=27490597 |doi=10.1097/PCC.0000000000000823 |url=}}</ref><ref name="pmid15296619">{{cite journal |vauthors=Wilson KC, Saukkonen JJ |title=Acute respiratory failure from abused substances |journal=J Intensive Care Med |volume=19 |issue=4 |pages=183–93 |date=2004 |pmid=15296619 |doi=10.1177/0885066604263918 |url=}}</ref><ref name="pmid630962">{{cite journal |vauthors=Neuhaus A, Bentz RR, Weg JG |title=Pulmonary embolism in respiratory failure |journal=Chest |volume=73 |issue=4 |pages=460–5 |date=April 1978 |pmid=630962 |doi= |url=}}</ref><ref name="pmid16912951">{{cite journal |vauthors=Bauer TT, Ewig S, Rodloff AC, Müller EE |title=Acute respiratory distress syndrome and pneumonia: a comprehensive review of clinical data |journal=Clin. Infect. Dis. |volume=43 |issue=6 |pages=748–56 |date=September 2006 |pmid=16912951 |doi=10.1086/506430 |url=}}</ref><ref name="pmid21471066">{{cite journal |vauthors=Raghu G, Collard HR, Egan JJ, Martinez FJ, Behr J, Brown KK, Colby TV, Cordier JF, Flaherty KR, Lasky JA, Lynch DA, Ryu JH, Swigris JJ, Wells AU, Ancochea J, Bouros D, Carvalho C, Costabel U, Ebina M, Hansell DM, Johkoh T, Kim DS, King TE, Kondoh Y, Myers J, Müller NL, Nicholson AG, Richeldi L, Selman M, Dudden RF, Griss BS, Protzko SL, Schünemann HJ |title=An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management |journal=Am. J. Respir. Crit. Care Med. |volume=183 |issue=6 |pages=788–824 |date=March 2011 |pmid=21471066 |pmc=5450933 |doi=10.1164/rccm.2009-040GL |url=}}</ref><ref name="pmid2382251">{{cite journal |vauthors=Mier A, Laroche C, Green M |title=Unsuspected myasthenia gravis presenting as respiratory failure |journal=Thorax |volume=45 |issue=5 |pages=422–3 |date=May 1990 |pmid=2382251 |pmc=462503 |doi= |url=}}</ref><ref name="pmid9742334">{{cite journal |vauthors=Massard G, Wihlm JM |title=Postoperative atelectasis |journal=Chest Surg. Clin. N. Am. |volume=8 |issue=3 |pages=503–28, viii |date=August 1998 |pmid=9742334 |doi= |url=}}</ref><ref name="pmid24171518">{{cite journal |vauthors=Vincent JL, De Backer D |title=Circulatory shock |journal=N. Engl. J. Med. |volume=369 |issue=18 |pages=1726–34 |date=October 2013 |pmid=24171518 |doi=10.1056/NEJMra1208943 |url=}}</ref><ref name="pmid16934165">{{cite journal |vauthors=Mehta S |title=Neuromuscular disease causing acute respiratory failure |journal=Respir Care |volume=51 |issue=9 |pages=1016–21; discussion 1021–3 |date=September 2006 |pmid=16934165 |doi= |url=}}</ref>
*[[Acute respiratory distress syndrome]] ([[Acute respiratory distress syndrome|ARDS]])
*[[Chronic obstructive pulmonary disease]] ([[COPD]])
*[[Opioid]] [[Toxicity]]
*[[Pulmonary edema]]
*[[Pulmonary embolism]]
*[[Pneumonia]]
*[[Idiopathic pulmonary fibrosis]]
*[[Asthma]]
*[[Myasthenia gravis]]
*[[Guillain-Barré syndrome]]
*Post-operative [[atelectasis]]
*[[Shock]]


==Gross Pathology==
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Respiratory failure is an end stage disease that has many underlying causes. The [[gross pathology]] may thus vary according to the underlying disease. To review all the causes of respiratory failure [[respiratory failure causes|click here.]]


==Microscopic Pathology==
==Microscopic Pathology==
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Respiratory failure is an end stage disease that has many underlying causes. The [[Microscopic examination|microscopic pathology]] may thus vary according to the underlying disease. To review all the causes of respiratory failure [[respiratory failure causes|click here.]]


==References==
==References==
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Latest revision as of 23:58, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M. Khurram Afzal, MD [2]

Overview

Respiratory failure is the result of inadequate gas exchange in the pulmonary circulation. This could result from lung failure or pump failure. Lung failure which is failure of gas exchange results in hypoxemia (<PaO2) and pump failure which is ventilatory failure would result in alveolar hypoventilation that causes hypercapnia (>PaCO2). Type I respiratory failure has a V/Q mismatch that causes hypoxemia. Type II respiratory failure is caused by alveolar hypoventilation which results in hypercapnia. Type III respiratory failure occurs in the peri-operative period clinically progresses to Type I or Type II respiratory failure. Type IV respiratory failure results from an underlying circulatory collapse.

Pathophysiology

Pathogenesis

Mechanics of the respiratory system

The pathogenesis of respiratory failure is as follows:[1]

Respiratory failure

Type I respiratory failure

Characteristics of Type I respiratory failure include:[2][3]

Type II respiratory failure

Characteristics of Type II respiratory failure include:[4][5][6][7]

Type III respiratory failure

Characteristics of Type III respiratory failure include:[8][9][10]

Type IV respiratory failure

Characteristics of Type IV respiratory failure include:[11][12]

Genetics

Associated Conditions

Conditions associated with respiratory failure include:[15][16][17][18][19][20][21][22][23][24][25]

Gross Pathology

Respiratory failure is an end stage disease that has many underlying causes. The gross pathology may thus vary according to the underlying disease. To review all the causes of respiratory failure click here.

Microscopic Pathology

Respiratory failure is an end stage disease that has many underlying causes. The microscopic pathology may thus vary according to the underlying disease. To review all the causes of respiratory failure click here.

References

  1. ↑ Roussos C, Koutsoukou A (November 2003). "Respiratory failure". Eur Respir J Suppl. 47: 3s–14s. PMID 14621112.
  2. ↑ Hall, Jesse (2015). "CHAPTER 43: The Pathophysiology and Differential Diagnosis of Acute Respiratory Failure". Principles of critical care. New York: McGraw-Hill Education. ISBN 0071738819.
  3. ↑ Masip J, Roque M, Sánchez B, Fernández R, Subirana M, Expósito JA (December 2005). "Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis". JAMA. 294 (24): 3124–30. doi:10.1001/jama.294.24.3124. PMID 16380593.
  4. ↑ Hall, Jesse (2015). "CHAPTER 43: The Pathophysiology and Differential Diagnosis of Acute Respiratory Failure". Principles of critical care. New York: McGraw-Hill Education. ISBN 0071738819.
  5. ↑ Brower RG, Matthay MA, Morris A, Schoenfeld D, Thompson BT, Wheeler A (May 2000). "Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome". N. Engl. J. Med. 342 (18): 1301–8. doi:10.1056/NEJM200005043421801. PMID 10793162.
  6. ↑ Kreppein U, Litterst P, Westhoff M (April 2016). "[Hypercapnic respiratory failure. Pathophysiology, indications for mechanical ventilation and management]". Med Klin Intensivmed Notfmed (in German). 111 (3): 196–201. doi:10.1007/s00063-016-0143-2. PMID 26902369.
  7. ↑ Jeffrey AA, Warren PM, Flenley DC (January 1992). "Acute hypercapnic respiratory failure in patients with chronic obstructive lung disease: risk factors and use of guidelines for management". Thorax. 47 (1): 34–40. PMC 463551. PMID 1539142.
  8. ↑ Hall, Jesse (2015). "CHAPTER 43: The Pathophysiology and Differential Diagnosis of Acute Respiratory Failure". Principles of critical care. New York: McGraw-Hill Education. ISBN 0071738819.
  9. ↑ Alexander JI, Horton PW, Millar WT, Parikh RK, Spence AA (August 1972). "The effect of upper abdominal surgery on the relationship of airway closing point to end tidal position". Clin Sci. 43 (2): 137–41. PMID 5048300.
  10. ↑ Ali J, Weisel RD, Layug AB, Kripke BJ, Hechtman HB (September 1974). "Consequences of postoperative alterations in respiratory mechanics". Am. J. Surg. 128 (3): 376–82. PMID 4606381.
  11. ↑ Hall, Jesse (2015). "CHAPTER 43: The Pathophysiology and Differential Diagnosis of Acute Respiratory Failure". Principles of critical care. New York: McGraw-Hill Education. ISBN 0071738819.
  12. ↑ Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M (November 2001). "Early goal-directed therapy in the treatment of severe sepsis and septic shock". N. Engl. J. Med. 345 (19): 1368–77. doi:10.1056/NEJMoa010307. PMID 11794169.
  13. ↑ Tejera P, Meyer NJ, Chen F, Feng R, Zhao Y, O'Mahony DS, Li L, Sheu CC, Zhai R, Wang Z, Su L, Bajwa E, Ahasic AM, Clardy PF, Gong MN, Frank AJ, Lanken PN, Thompson BT, Christie JD, Wurfel MM, O'Keefe GE, Christiani DC (November 2012). "Distinct and replicable genetic risk factors for acute respiratory distress syndrome of pulmonary or extrapulmonary origin". J. Med. Genet. 49 (11): 671–80. doi:10.1136/jmedgenet-2012-100972. PMC 3654537. PMID 23048207.
  14. ↑ Cardinal-Fernández P, Ferruelo A, El-Assar M, Santiago C, Gómez-Gallego F, Martín-Pellicer A, Frutos-Vivar F, Peñuelas O, Nin N, Esteban A, Lorente JA (March 2013). "Genetic predisposition to acute respiratory distress syndrome in patients with severe sepsis". Shock. 39 (3): 255–60. doi:10.1097/SHK.0b013e3182866ff9. PMID 23364437.
  15. ↑ Bernard GR (October 2005). "Acute respiratory distress syndrome: a historical perspective". Am. J. Respir. Crit. Care Med. 172 (7): 798–806. doi:10.1164/rccm.200504-663OE. PMC 2718401. PMID 16020801.
  16. ↑ Budweiser S, Jörres RA, Pfeifer M (2008). "Treatment of respiratory failure in COPD". Int J Chron Obstruct Pulmon Dis. 3 (4): 605–18. PMC 2650592. PMID 19281077.
  17. ↑ Hornik C, Meliones J (August 2016). "Pulmonary Edema and Hypoxic Respiratory Failure". Pediatr Crit Care Med. 17 (8 Suppl 1): S178–81. doi:10.1097/PCC.0000000000000823. PMID 27490597.
  18. ↑ Wilson KC, Saukkonen JJ (2004). "Acute respiratory failure from abused substances". J Intensive Care Med. 19 (4): 183–93. doi:10.1177/0885066604263918. PMID 15296619.
  19. ↑ Neuhaus A, Bentz RR, Weg JG (April 1978). "Pulmonary embolism in respiratory failure". Chest. 73 (4): 460–5. PMID 630962.
  20. ↑ Bauer TT, Ewig S, Rodloff AC, Müller EE (September 2006). "Acute respiratory distress syndrome and pneumonia: a comprehensive review of clinical data". Clin. Infect. Dis. 43 (6): 748–56. doi:10.1086/506430. PMID 16912951.
  21. ↑ Raghu G, Collard HR, Egan JJ, Martinez FJ, Behr J, Brown KK, Colby TV, Cordier JF, Flaherty KR, Lasky JA, Lynch DA, Ryu JH, Swigris JJ, Wells AU, Ancochea J, Bouros D, Carvalho C, Costabel U, Ebina M, Hansell DM, Johkoh T, Kim DS, King TE, Kondoh Y, Myers J, Müller NL, Nicholson AG, Richeldi L, Selman M, Dudden RF, Griss BS, Protzko SL, Schünemann HJ (March 2011). "An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management". Am. J. Respir. Crit. Care Med. 183 (6): 788–824. doi:10.1164/rccm.2009-040GL. PMC 5450933. PMID 21471066.
  22. ↑ Mier A, Laroche C, Green M (May 1990). "Unsuspected myasthenia gravis presenting as respiratory failure". Thorax. 45 (5): 422–3. PMC 462503. PMID 2382251.
  23. ↑ Massard G, Wihlm JM (August 1998). "Postoperative atelectasis". Chest Surg. Clin. N. Am. 8 (3): 503–28, viii. PMID 9742334.
  24. ↑ Vincent JL, De Backer D (October 2013). "Circulatory shock". N. Engl. J. Med. 369 (18): 1726–34. doi:10.1056/NEJMra1208943. PMID 24171518.
  25. ↑ Mehta S (September 2006). "Neuromuscular disease causing acute respiratory failure". Respir Care. 51 (9): 1016–21, discussion 1021–3. PMID 16934165.

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