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==Pathophysiology==
==Pathophysiology==
===Overview of Formation===
* Most pulmonary embolisms commonly originate in the [[iliofemoral vein]], deep within the vasculature of the lower extremity.
* Most pulmonary embolisms commonly originate in the [[iliofemoral vein]], deep within the vasculature of the lower extremity.
* Less commonly, a pulmonary embolism may also arise in the upper extremity veins, renal veins, or pelvic veins.
* Less commonly, a pulmonary embolism may also arise in the upper extremity veins, renal veins, or pelvic veins.
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:* The size of the embolus and the nature to which it occludes the vascular tree and its subsequent branches.
:* The size of the embolus and the nature to which it occludes the vascular tree and its subsequent branches.


Thrombus travels to the lung, and depending on its size, produce variable outcomes.
* After formation, a thrombus will travel from the site of origin and circulate through the [[inferior vena cava]] into the right ventricle where it will lodge.<ref name="McGill">McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.</ref>
*'''Large thrombus''': lodge at the bifurcation of the main [[pulmonary artery]] or lobar branches, and causes hemodynamic compromise.
* A pulmonary embolism can occur in singularity or in multiplicity depending on the patient. Size and physiologic impact will hinge largely on the individual patient and subsequent anatomy of the vasculature. <ref name="McGill">McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.</ref>
*'''Small thrombus''': travel distally and initiate an inflammatory response adjacent to the parietal pleura causing [[pleuritis]] and [[pleuritic chest pain]].


Chronic [[pulmonary hypertension]] may occur when the initial embolus fail to lyses and also in patients with recurrent thromboembolism.
===Physiologic Complications==
 
* Hemodynamic complication arise as a result of the obstruction of flow within the pulmonary arteries.
Gas exchange abnormalities, if present, happen due to a mix of the following factors:
*When there is a 50-60% reduction in perfusion, the following complications may arise:<ref name="McGill">McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.</ref>
*Mechanical obstruction of the vascular bed.
:*Increased resistence in the pulmonary vessels
*Alterations in the [[Ventilation/perfusion scan|ventilation to perfusion ratio]].
:*[[Pulmonary hypertension|Severe pulmonary hypertension]]
*Release of inflammatory mediators causing [[atelectasis]] and [[surfactant]] dysfunction.
:*[[Right ventricle|Right ventricular strain]]
:*[[Congestive heart failure|Cardiac heart failure]]
:*[[Vasoconstriction]]
*In 10% of all pulmonary embolism cases, the pulmonary embolism develops into [[pulmonary infarction]]. This is an exceedingly rare complication.<ref name="McGill">McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.</ref>
*Long term complications:<ref name="McGill">McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.</ref>
:*[[Pulmonary hypertension|Chronic obstructive pulmonary hypertension]]
:*[[Ventilation/perfusion ratio|Ventilation/perfusion ratio (V/Q ratio)]]


==Mechanism==
==Mechanism==
The following figure explains the pathophysiology and the cause of death in Pulmonary embolism.<ref name="pmid19041539">{{cite journal |author=Fengler BT, Brady WJ |title=Fibrinolytic therapy in pulmonary embolism: an evidence-based treatment algorithm |journal=Am J Emerg Med |volume=27 |issue=1 |pages=84–95 |year=2009 |month=January |pmid=19041539 |doi=10.1016/j.ajem.2007.10.021 |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-6757(07)00699-7 |accessdate=2011-12-21}}</ref>
*Current research suggests that a pulmonary embolism arises through the following progression of events.<ref name="pmid19041539">{{cite journal |author=Fengler BT, Brady WJ |title=Fibrinolytic therapy in pulmonary embolism: an evidence-based treatment algorithm |journal=Am J Emerg Med |volume=27 |issue=1 |pages=84–95 |year=2009 |month=January |pmid=19041539 |doi=10.1016/j.ajem.2007.10.021 |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-6757(07)00699-7 |accessdate=2011-12-21}}</ref>


[[File:PE.png|523x628px]]
[[File:PE.png|523x628px]]


 
===Comorbidites===
In conditions where more than 2/3rd of the [[pulmonary artery]] is occluded, in order to preserve pulmonary perfusion, the right ventricle is forced to: '''a).''' Generate a [[ systolic blood pressure|systolic pressure (SBP)]] in excess of 50 mmHg and '''b).''' Maintain a [[mean pulmonary artery pressure]] approximating 40 mmHg. Failure to do so would eventually lead to right heart failure.<ref name="pmid6488744">{{cite journal| author=Benotti JR, Dalen JE| title=The natural history of pulmonary embolism. | journal=Clin Chest Med | year= 1984 | volume= 5 | issue= 3 | pages= 403-10 | pmid=6488744 | doi= | pmc= | url= }} </ref>
*In circumstances where more than two-thirds of the [[pulmonary artery]] is occluded, in order to preserve pulmonary perfusion, the right ventricle adapts to:
 
:*Generate a [[systolic blood pressure|systolic pressure (SBP)]] in excess of 50 mmHg
Patients with underlying cardiopulmonary disease experience more substantial deterioration in [[cardiac output]] as compared with otherwise healthy individuals. Also, right ventricular failure following PE is more common in patients with coexisting [[coronary artery disease]].
:*Maintain a [[mean pulmonary artery pressure]] approximating 40 mmHg
 
*Without these adapations, a pulmonary embolism will lead to right heart failure.<ref name="pmid6488744">{{cite journal| author=Benotti JR, Dalen JE| title=The natural history of pulmonary embolism. | journal=Clin Chest Med | year= 1984 | volume= 5 | issue= 3 | pages= 403-10 | pmid=6488744 | doi= | pmc= | url= }}</ref>
'''The following video explains the pathophysiology of DVT and its most common complication, PE.'''
*In patients with underlying cardiopulmonary disease, the [[cardiac output]] suffers substantial deterioration in overall output as compared to otherwise healthy individuals.
{{#ev:youtube|gGrDAGN5pC0}}
*In patients with coexisting [[coronary artery disease|coronary artery disease (CAD)]], right ventricular failure is more common following a pulmonary embolism as compared to those without coexisting CAD.


==References==
==References==

Revision as of 19:36, 7 May 2012

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Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Pulmonary embolism occurs when there is an acute obstruction of the pulmonary artery or one of its branches. It is commonly caused by a venous thrombus that has dislodged from its site of formation and embolized to the arterial blood supply of one of the lungs. The process of this formation is termed thromboembolism.

Pathophysiology

Overview of Formation

  • Most pulmonary embolisms commonly originate in the iliofemoral vein, deep within the vasculature of the lower extremity.
  • Less commonly, a pulmonary embolism may also arise in the upper extremity veins, renal veins, or pelvic veins.
  • The nature of the clinical manifestation of a pulmonary embolism depends on a number of factors:[1]
  • The presence of any preexisting cardiopulmonary conditions.
  • The role of chemical vasoconstriction as it is insinuated by platelets releasing serotonin and thromboxane which adhere to the embolus.
  • The presence of pulmonary artery dilatation and subsequent reflex vasoconstriction.
  • The size of the embolus and the nature to which it occludes the vascular tree and its subsequent branches.
  • After formation, a thrombus will travel from the site of origin and circulate through the inferior vena cava into the right ventricle where it will lodge.[2]
  • A pulmonary embolism can occur in singularity or in multiplicity depending on the patient. Size and physiologic impact will hinge largely on the individual patient and subsequent anatomy of the vasculature. [2]

=Physiologic Complications

  • Hemodynamic complication arise as a result of the obstruction of flow within the pulmonary arteries.
  • When there is a 50-60% reduction in perfusion, the following complications may arise:[2]
  • In 10% of all pulmonary embolism cases, the pulmonary embolism develops into pulmonary infarction. This is an exceedingly rare complication.[2]
  • Long term complications:[2]

Mechanism

  • Current research suggests that a pulmonary embolism arises through the following progression of events.[3]

Comorbidites

  • In circumstances where more than two-thirds of the pulmonary artery is occluded, in order to preserve pulmonary perfusion, the right ventricle adapts to:
  • Without these adapations, a pulmonary embolism will lead to right heart failure.[4]
  • In patients with underlying cardiopulmonary disease, the cardiac output suffers substantial deterioration in overall output as compared to otherwise healthy individuals.
  • In patients with coexisting coronary artery disease (CAD), right ventricular failure is more common following a pulmonary embolism as compared to those without coexisting CAD.

References

  1. ↑ Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.
  3. ↑ Fengler BT, Brady WJ (2009). "Fibrinolytic therapy in pulmonary embolism: an evidence-based treatment algorithm". Am J Emerg Med. 27 (1): 84–95. doi:10.1016/j.ajem.2007.10.021. PMID 19041539. Retrieved 2011-12-21. Unknown parameter |month= ignored (help)
  4. ↑ Benotti JR, Dalen JE (1984). "The natural history of pulmonary embolism". Clin Chest Med. 5 (3): 403–10. PMID 6488744.

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