Respiratory failure pathophysiology: Difference between revisions
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*Clinical progression is often either Type I or Type II respiratory failure | *Clinical progression is often either 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> | 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 | *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 | ||
Revision as of 17:19, 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 hypercapnia 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]
- 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:[3]
- 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:[4]
- 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 Type I or Type II respiratory failure
Type IV respiratory failure
Characteristics of Type IV respiratory failure include:[5][6]
- 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
- Genes variants that can influence susceptibility to acute respiratory distress syndrome include:[7]
- Functional single nucleotide polymorphism (SNP) in POPDC3 gene
- Functional SNP in FAAH gene
- ARDS in severe sepsis is associated with the presence of allele D of the ACE gene[8]
Associated Conditions
Conditions associated with respiratory failure include:[9][10][11][12][13][14][15][16][17][18][19]
- 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Neuhaus A, Bentz RR, Weg JG (April 1978). "Pulmonary embolism in respiratory failure". Chest. 73 (4): 460–5. PMID 630962.
- ↑ 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.
- ↑ 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.
- ↑ Mier A, Laroche C, Green M (May 1990). "Unsuspected myasthenia gravis presenting as respiratory failure". Thorax. 45 (5): 422–3. PMC 462503. PMID 2382251.
- ↑ Massard G, Wihlm JM (August 1998). "Postoperative atelectasis". Chest Surg. Clin. N. Am. 8 (3): 503–28, viii. PMID 9742334.
- ↑ Vincent JL, De Backer D (October 2013). "Circulatory shock". N. Engl. J. Med. 369 (18): 1726–34. doi:10.1056/NEJMra1208943. PMID 24171518.
- ↑ Mehta S (September 2006). "Neuromuscular disease causing acute respiratory failure". Respir Care. 51 (9): 1016–21, discussion 1021–3. PMID 16934165.