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==Overview==
==Overview==
Pulmonary embolism (PE) occurs when there is an acute obstruction of the pulmonary artery (or one of its branches). Most often this is due to a venous thrombus (blood clot from a vein), which dislodges from its site of formation and embolizes to the arterial blood supply of one of the lungs. This process is termed thromboembolism.
Pulmonary embolism (PE) 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 clot formation and embolization is termed [[thromboembolism]]. PE results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the [[capillary]] by the [[embolism]], but also due to pulmonary vasoconstriction.  When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular [[afterload]] might lead to the dilatation of the right ventricular wall and subsequent [[right heart failure]].<ref name="pmid3916797">{{cite journal| author=Wiedemann HP, Matthay RA| title=Acute right heart failure. | journal=Crit Care Clin | year= 1985 | volume= 1 | issue= 3 | pages= 631-61 | pmid=3916797 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3916797  }} </ref><ref name="pmid7484782">{{cite journal| author=Lualdi JC, Goldhaber SZ| title=Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. | journal=Am Heart J | year= 1995 | volume= 130 | issue= 6 | pages= 1276-82 | pmid=7484782 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7484782  }} </ref>


==Pathophysiology==
== Pathophysiology ==
Iliofemoral veins are the source of most clinically recognized PE. It can cause death and significant disability.
=== Clot Formation ===
* Most PE commonly originate from a [[thrombus]] that has formed in the [[iliofemoral vein]], deep within the vasculature of the lower extremity.
* Less commonly, a PE may also arise from a [[thrombus]] in the upper extremity veins, renal veins, or pelvic veins.
* The development of thrombosis is classically due to a group of conditions referred to as [[Virchow's triad]]. Virchow's triad includes alterations in [[blood flow]], factors in the vessel wall, and factors affecting the properties of the [[blood]]. It is common for more than one risk factor to be present.  Shown below is an image depicting [[Virchow's triad]].


Thrombus travels to the lung, and depending on its size, produce variable outcomes.
[[File:VTE Pathophysisology Virchow's triad.JPG|300x400px]]
*'''Large thrombus''': lodge at the bifurcation of the main [[pulmonary artery]] or lobar branches, and causes hemodynamic compromise.
*'''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.
=== Embolization ===
* After its formation, a thrombus might dislodge from the site of origin and circulate through the [[inferior vena cava]], into the right ventricle, and into the pulmonary vasculature.<ref name="McGill">McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.</ref>


Gas exchange abnormalities, if present, happen due to a mix of the following factors:
=== Hemodynamic Consequences ===
*Mechanical obstruction of the vascular bed.
*Hemodynamic complications and the nature of the clinical manifestations of a PE depend on a number of factors:<ref name="Hellas">Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.</ref>
*Alterations in the [[Ventilation/perfusion scan|ventilation to perfusion ratio]].
** The size of the [[embolus]] and the degree to which it occludes the vascular tree and its subsequent branches 
*Release of inflammatory mediators causing [[atelectasis]] and [[surfactant]] dysfunction.
** The presence of any preexisting cardiopulmonary conditions
==Mechanism==
** The role of chemical [[vasoconstriction]] as it is insinuated by [[platelets]] releasing [[serotonin]] and [[thromboxane]] in addition to other vasoconstrictors
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>
** The presence of pulmonary artery dilatation and subsequent [[vasoconstriction|reflex vasoconstriction]]


[[File:Pulmonary embolism pathophysiology.jpeg|600x600px]]
* PE results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the [[capillary]] by the [[embolism]], but also due to pulmonary vasoconstriction.  Pulmonary vasoconstriction can be either biochemically mediated, hypoxia induced, or reflex-induced.<ref name="pmid1555481">{{cite journal| author=Elliott CG| title=Pulmonary physiology during pulmonary embolism. | journal=Chest | year= 1992 | volume= 101 | issue= 4 Suppl | pages= 163S-171S | pmid=1555481 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1555481  }} </ref><ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>


* Several mediators are involved the pulmonary [[vasoconstriction]] that occurs in the setting of acute PE, such as:
** [[Thromboxane A2]] (end product of [[arachidonic acid]] metabolism)<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
** [[Serotonin]] (vasoconstrictor in the pulmonary circulation and vasodilator in the systemic circulation)<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
** [[Endothelin 1]]<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
** [[Prostaglandin F2α]]<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
** [[Thrombin]]<ref name="pmid14656907">{{cite journal| author=Goldhaber SZ, Elliott CG| title=Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. | journal=Circulation | year= 2003 | volume= 108 | issue= 22 | pages= 2726-9 | pmid=14656907 | doi=10.1161/01.CIR.0000097829.89204.0C | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14656907  }} </ref>
** [[Histamine]]<ref name="pmid14656907">{{cite journal| author=Goldhaber SZ, Elliott CG| title=Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. | journal=Circulation | year= 2003 | volume= 108 | issue= 22 | pages= 2726-9 | pmid=14656907 | doi=10.1161/01.CIR.0000097829.89204.0C | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14656907  }} </ref>


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>
* While [[serotonin]] and [[thromboxane A2]] are mainly produced by activated [[platelets]], the vascular wall and pulmonary neuroendocrine cells might also be the source of some [[vasoconstrictor]]s.<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>


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]].
* [[Prostacyclin]] is a vasodilator produced by the [[endothelial cells]] in response to the hemodynamic changes induced by the acute PE.<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>


'''The following video explains the pathophysiology of DVT and its most common complication, PE.'''
* When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular [[afterload]] might lead to the dilatation of the right ventricular wall and subsequent [[right heart failure]]. In addition, the elevated pulmonary vascular resistance causes a decrease in the [[LV|left ventricular]] [[preload]] and consequently leads to systemic [[hypotension]].<ref name="pmid3916797">{{cite journal| author=Wiedemann HP, Matthay RA| title=Acute right heart failure. | journal=Crit Care Clin | year= 1985 | volume= 1 | issue= 3 | pages= 631-61 | pmid=3916797 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3916797  }} </ref><ref name="pmid7484782">{{cite journal| author=Lualdi JC, Goldhaber SZ| title=Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. | journal=Am Heart J | year= 1995 | volume= 130 | issue= 6 | pages= 1276-82 | pmid=7484782 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7484782  }} </ref> In patients with underlying cardiopulmonary disease, the [[cardiac output]] suffers substantial deterioration in overall output as compared to otherwise healthy individuals.
{{#ev:youtube|gGrDAGN5pC0}}
 
* [[Right heart failure]], as well as systemic [[hypotension]], can attenuate coronary perfusion and contribute to subsequent [[coronary ischemia]].<ref name="pmid3916797">{{cite journal| author=Wiedemann HP, Matthay RA| title=Acute right heart failure. | journal=Crit Care Clin | year= 1985 | volume= 1 | issue= 3 | pages= 631-61 | pmid=3916797 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3916797  }} </ref><ref name="pmid7484782">{{cite journal| author=Lualdi JC, Goldhaber SZ| title=Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. | journal=Am Heart J | year= 1995 | volume= 130 | issue= 6 | pages= 1276-82 | pmid=7484782 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7484782  }} </ref>
 
* In summary, the hemodynamic consequences of PE include:
**[[Pulmonary hypertension]]
**[[Right ventricular strain]]
**[[Right heart failure]]
**[[Systemic hypotension]]
 
===Abnormalities in Gas Exchange===
* In PE, [[hypoxemia]] occurs mainly due to the ventilation perfusion mismatch.<ref name="pmid14656907">{{cite journal| author=Goldhaber SZ, Elliott CG| title=Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. | journal=Circulation | year= 2003 | volume= 108 | issue= 22 | pages= 2726-9 | pmid=14656907 | doi=10.1161/01.CIR.0000097829.89204.0C | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14656907  }} </ref>  In fact, in the setting of an acute PE, the ventilation to perfusion ratio (V/Q) increases and the dead space enlarges.<ref name="pmid12468507">{{cite journal| author=Itti E, Nguyen S, Robin F, Desarnaud S, Rosso J, Harf A et al.| title=Distribution of ventilation/perfusion ratios in pulmonary embolism: an adjunct to the interpretation of ventilation/perfusion lung scans. | journal=J Nucl Med | year= 2002 | volume= 43 | issue= 12 | pages= 1596-602 | pmid=12468507 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12468507  }} </ref>
 
* In addition, the occurrence of [[right to left shunt]] also contributes to the [[hypoxemia]] among patients with PE. When [[right to left shunt]] occurs, the administration of oxygen to the patient fails to correct the [[hypoxemia]].<ref name="pmid14656907">{{cite journal| author=Goldhaber SZ, Elliott CG| title=Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. | journal=Circulation | year= 2003 | volume= 108 | issue= 22 | pages= 2726-9 | pmid=14656907 | doi=10.1161/01.CIR.0000097829.89204.0C | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14656907  }} </ref>
 
* [[Hypocapnia]] occurs among patients with PE secondary to a compensatory increase in the [[minute ventilation]].<ref name="pmid14656907">{{cite journal| author=Goldhaber SZ, Elliott CG| title=Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. | journal=Circulation | year= 2003 | volume= 108 | issue= 22 | pages= 2726-9 | pmid=14656907 | doi=10.1161/01.CIR.0000097829.89204.0C | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14656907  }} </ref>


==References==
==References==
{{reflist|2}}
{{Reflist|2}}


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Latest revision as of 18:08, 7 June 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] The APEX Trial Investigators; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Overview

Pulmonary embolism (PE) 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 clot formation and embolization is termed thromboembolism. PE results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the capillary by the embolism, but also due to pulmonary vasoconstriction. When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular afterload might lead to the dilatation of the right ventricular wall and subsequent right heart failure.[1][2]

Pathophysiology

Clot Formation

  • Most PE commonly originate from a thrombus that has formed in the iliofemoral vein, deep within the vasculature of the lower extremity.
  • Less commonly, a PE may also arise from a thrombus in the upper extremity veins, renal veins, or pelvic veins.
  • The development of thrombosis is classically due to a group of conditions referred to as Virchow's triad. Virchow's triad includes alterations in blood flow, factors in the vessel wall, and factors affecting the properties of the blood. It is common for more than one risk factor to be present. Shown below is an image depicting Virchow's triad.

Embolization

  • After its formation, a thrombus might dislodge from the site of origin and circulate through the inferior vena cava, into the right ventricle, and into the pulmonary vasculature.[3]

Hemodynamic Consequences

  • Hemodynamic complications and the nature of the clinical manifestations of a PE depend on a number of factors:[4]
    • The size of the embolus and the degree to which it occludes the vascular tree and its subsequent branches
    • The presence of any preexisting cardiopulmonary conditions
    • The role of chemical vasoconstriction as it is insinuated by platelets releasing serotonin and thromboxane in addition to other vasoconstrictors
    • The presence of pulmonary artery dilatation and subsequent reflex vasoconstriction
  • PE results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the capillary by the embolism, but also due to pulmonary vasoconstriction. Pulmonary vasoconstriction can be either biochemically mediated, hypoxia induced, or reflex-induced.[5][6]
  • When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular afterload might lead to the dilatation of the right ventricular wall and subsequent right heart failure. In addition, the elevated pulmonary vascular resistance causes a decrease in the left ventricular preload and consequently leads to systemic hypotension.[1][2] In patients with underlying cardiopulmonary disease, the cardiac output suffers substantial deterioration in overall output as compared to otherwise healthy individuals.

Abnormalities in Gas Exchange

  • In PE, hypoxemia occurs mainly due to the ventilation perfusion mismatch.[7] In fact, in the setting of an acute PE, the ventilation to perfusion ratio (V/Q) increases and the dead space enlarges.[8]

References

  1. ↑ 1.0 1.1 1.2 Wiedemann HP, Matthay RA (1985). "Acute right heart failure". Crit Care Clin. 1 (3): 631–61. PMID 3916797.
  2. ↑ 2.0 2.1 2.2 Lualdi JC, Goldhaber SZ (1995). "Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications". Am Heart J. 130 (6): 1276–82. PMID 7484782.
  3. ↑ McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.
  4. ↑ Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.
  5. ↑ Elliott CG (1992). "Pulmonary physiology during pulmonary embolism". Chest. 101 (4 Suppl): 163S–171S. PMID 1555481.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 Smulders YM (2000). "Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction". Cardiovasc Res. 48 (1): 23–33. PMID 11033105.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 Goldhaber SZ, Elliott CG (2003). "Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis". Circulation. 108 (22): 2726–9. doi:10.1161/01.CIR.0000097829.89204.0C. PMID 14656907.
  8. ↑ Itti E, Nguyen S, Robin F, Desarnaud S, Rosso J, Harf A; et al. (2002). "Distribution of ventilation/perfusion ratios in pulmonary embolism: an adjunct to the interpretation of ventilation/perfusion lung scans". J Nucl Med. 43 (12): 1596–602. PMID 12468507.

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