Respiratory failure pathophysiology: Difference between revisions
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*Acute respiratory failure can develop in minutes to hours | *Acute respiratory failure can develop in minutes to hours | ||
*Chronic respiratory failure takes days to develop | *Chronic respiratory failure takes days to develop | ||
*The ph drops below 7.35 in acute | *The ph drops below 7.35 in acute hypercapnic respiratory failure | ||
*In underlying chronic respiratory failure the PaCO2 rises unto 20mmHg above baseline | *In underlying chronic respiratory failure the [[PaCO2]] rises unto 20mmHg above baseline | ||
*Presentation of respiratory failure can be: | *Presentation of respiratory failure can be: | ||
**Acute | **Acute | ||
**Chronic | **Chronic | ||
**Acute on chronic (COPD exacerbation) | **Acute on chronic ([[COPD]] exacerbation) | ||
==Type I respiratory failure== | ==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> | 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) | *Severe oxygen-refractory [[hypoxemia]] (< PaO2) | ||
*Ventilation/Perfusion (V/Q) mismatch | *[[Ventilation]]/[[Perfusion]] (V/Q) mismatch | ||
*A portion of total pulmonary blood flow is unable to pick oxygen | *A portion of total [[pulmonary]] blood flow is unable to pick [[oxygen]] | ||
*Alveolar flooding (airspace filling) | *[[Alveolar]] flooding (airspace filling) | ||
==Type II respiratory failure== | ==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> | 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) | *[[Hypercapnia]] (Increased [[PaCO2]]) | ||
*Alveolar hypoventilation | *[[Alveolar]] [[hypoventilation]] | ||
*Alveolar minute ventilation (VA) is decreased | *[[Alveolar]] [[minute ventilation]] (VA) is decreased | ||
*Failure to adequately remove carbon dioxide | *Failure to adequately remove [[carbon dioxide]] | ||
*Alveolar hypoventilation can be caused by: | *[[Alveolar]] [[hypoventilation]] can be caused by: | ||
**Loss of CNS drive | **Loss of CNS drive | ||
**Impaired neuromuscular competence | **Impaired [[neuromuscular]] competence | ||
**Excessive dead space | **Excessive [[dead space]] | ||
**Increased mechanical load | **Increased mechanical load | ||
*Hypoxemia can be present (corrected by supplemental oxygen) | *[[Hypoxemia]] can be present (corrected by supplemental [[oxygen]]) | ||
==Type III respiratory failure== | ==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> | 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) | *Progressive increased [[atelectasis]] due to a low [[functional residual capacity]] (FRC) | ||
*Improper abdominal wall mechanics usually in the peri-operative or post-operative period | *Improper abdominal wall mechanics usually in the peri-operative or [[Post-operative complications|post-operative]] period | ||
*Clinical progression is often either Type I or Type II respiratory failure | *Clinical progression is often either to Type I or Type II respiratory failure | ||
==Type IV respiratory failure== | ==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> | 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> | ||
*Underlying cause is shock (inadequate oxygen delivery) | *Underlying cause is [[shock]] (inadequate [[oxygen]] delivery) | ||
*Patients are often mechanically ventilated due to underlying shock | *Patients are often mechanically ventilated due to underlying [[shock]] | ||
*Resolves when the underlying shock or circulatory collapse is corrected | *Resolves when the underlying [[shock]] or [[circulatory]] collapse is corrected | ||
*Poor prognosis if superimposed by Type I or Type II respiratory failure | *Poor prognosis if superimposed by Type I or Type II respiratory failure | ||
==Genetics== | ==Genetics== | ||
* | *[[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> | ||
**Functional single nucleotide polymorphism (SNP) in POPDC3 gene | **Functional [[single nucleotide polymorphism]] ([[SNP]]) in [[POPDC3]] [[gene]] | ||
**Functional SNP in FAAH gene | **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> | *[[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> | 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 (ARDS) | *[[Acute respiratory distress syndrome]] ([[Acute respiratory distress syndrome|ARDS]]) | ||
*Chronic obstructive pulmonary disease (COPD) | *[[Chronic obstructive pulmonary disease]] ([[COPD]]) | ||
*Opioid Toxicity | *[[Opioid]] [[Toxicity]] | ||
*Pulmonary edema | *[[Pulmonary edema]] | ||
*Pulmonary embolism | *[[Pulmonary embolism]] | ||
*Pneumonia | *[[Pneumonia]] | ||
*Idiopathic lung fibrosis | *Idiopathic lung fibrosis | ||
*Asthma | *[[Asthma]] | ||
*Myasthenia gravis | *[[Myasthenia gravis]] | ||
*Guillain-Barré syndrome | *[[Guillain-Barré syndrome]] | ||
*Post-operative atelectasis | *Post-operative [[atelectasis]] | ||
*Shock | *[[Shock]] | ||
==Gross Pathology== | ==Gross Pathology== | ||
Revision as of 17:44, 21 March 2018
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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
The exact pathogenesis of [disease name] is not fully understood.
OR
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].
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].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
The pathogenesis of respiratory failure is as follows:[1]
- The respiratory system is formed by 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 and 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 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:
- 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 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 (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 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:[2][3]
- 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)
Type II respiratory failure
Characteristics of Type II respiratory failure include:[4][5][6][7]
- 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)
Type III respiratory failure
Characteristics of Type III respiratory failure include:[8][9][10]
- Progressive increased atelectasis due to a low functional residual capacity (FRC)
- Improper abdominal wall mechanics usually in the peri-operative or post-operative period
- Clinical progression is often either to Type I or Type II respiratory failure
Type IV respiratory failure
Characteristics of Type IV respiratory failure include:[11][12]
- Underlying cause is shock (inadequate oxygen delivery)
- Patients are often mechanically ventilated due to underlying shock
- Resolves when the underlying shock or circulatory collapse is corrected
- Poor prognosis if superimposed by Type I or Type II respiratory failure
Genetics
- Genetic variants that can influence susceptibility to acute respiratory distress syndrome include:[13]
- ARDS in severe sepsis is associated with the presence of allele D of the ACE gene[14]
Associated Conditions
Conditions associated with respiratory failure include:[15][16][17][18][19][20][21][22][23][24][25]
- Acute respiratory distress syndrome (ARDS)
- Chronic obstructive pulmonary disease (COPD)
- Opioid Toxicity
- Pulmonary edema
- Pulmonary embolism
- Pneumonia
- Idiopathic lung fibrosis
- Asthma
- Myasthenia gravis
- Guillain-Barré syndrome
- Post-operative atelectasis
- Shock
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Roussos C, Koutsoukou A (November 2003). "Respiratory failure". Eur Respir J Suppl. 47: 3s–14s. PMID 14621112.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
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