Pulmonary embolism pathophysiology: Difference between revisions
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=== Hemodynamic Consequences === | === Hemodynamic Consequences === | ||
*Hemodynamic complications and the nature of the clinical manifestations of a pulmonary embolism 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> | *Hemodynamic complications and the nature of the clinical manifestations of a pulmonary embolism 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> | ||
** The size of the embolus and the degree to which it occludes the vascular tree and its subsequent branches | ** 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 presence of any preexisting cardiopulmonary conditions | ||
** The role of chemical [[vasoconstriction]] as it is insinuated by platelets releasing [[serotonin]] and [[thromboxane]] | ** 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 [[vasoconstriction|reflex vasoconstriction]] | ** The presence of pulmonary artery dilatation and subsequent [[vasoconstriction|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.<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: | * 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> | ** [[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> | ** [[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> | ** [[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 | ** [[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> | ** [[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> | ** [[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> | ||
* While serotonin and thromboxane A2 are mainly produced by activated platelets, the vascular wall and pulmonary | * While [[serotonin]] and [[thromboxane A2]] are mainly produced by activated [[platelets]], the vascular wall and pulmonary neuroendocrine cells might also be the source of vasoconstrictors.<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> | ||
* When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular afterload leads to the dilatation of the | * When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular [[afterload]] leads 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. | ||
* Right heart failure, as well as systemic hypotension, can | * [[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: | * In summary, the hemodynamic consequences of PE include: | ||
Revision as of 19:47, 7 July 2014
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Editor(s)-In-Chief: C. Michael Gibson, M.S., M.D. [1], The APEX Trial Investigators; Associate Editor(s)-in-Chief:
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 clot formation and embolization is termed thromboembolism.
Pathophysiology
Clot Formation
- Most pulmonary emboli 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 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 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.[1]
Hemodynamic Consequences
- Hemodynamic complications and the nature of the clinical manifestations of a pulmonary embolism depend on a number of factors:[2]
- 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.[3][4]
- 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)[4]
- Serotonin (vasoconstrictor in the pulmonary circulation and vasodilator in the systemic circulation)[4]
- Endothelin 1[4]
- Prostaglandin F2α[4]
- Thrombin[5]
- Histamine[5]
- While serotonin and thromboxane A2 are mainly produced by activated platelets, the vascular wall and pulmonary neuroendocrine cells might also be the source of vasoconstrictors.[4]
- When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular afterload leads 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.[6][7] In patients with underlying cardiopulmonary disease, the cardiac output suffers substantial deterioration in overall output as compared to otherwise healthy individuals.
- Right heart failure, as well as systemic hypotension, can attenuate coronary perfusion and contribute to subsequent coronary ischemia.[6][7]
- In summary, the hemodynamic consequences of PE include:
Adaptive Mechanisms
- Prostacyclin is a vasodilator produced by the endothelial cells in response to the hemodynamic changes induced by the acute PE.[4]
- Changes in the the right ventricle occur as an adaptative mechanism of the right ventricle to preserve pulmonary perfusion. Without these adaptations, a PE can lead to right heart failure.[8] These adaptations aim to:
- Generate a systolic blood pressure in excess of 50 mmHg
- Maintain an average pulmonary artery pressure of approximately 40 mmHg
Abnormalities in Gas Exchange
- In PE, hypoxemia occurs mainly due to the ventilation perfusion mismatch.[5] In fact, in the setting of an acute PE, the ventilation to perfusion ratio (V/Q) increases and the dead space enlarges.[9]
- 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 he hypoxemia.[5]
- Hypocapnea occurs secondary to a compensatory increase in the minute ventilation.[5]
Mechanism
The diagram below summarizes the sequence of pathophysiologic events in pulmonary embolism:[10]
References
- ↑ McGill University. (2004, June 24). Pulmonary Embolism. Retrieved May 7, 2012, from McGill Virtual Stethoscope Pathophysiology.
- ↑ Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.
- ↑ Elliott CG (1992). "Pulmonary physiology during pulmonary embolism". Chest. 101 (4 Suppl): 163S–171S. PMID 1555481.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 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.
- ↑ 5.0 5.1 5.2 5.3 5.4 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.
- ↑ 6.0 6.1 Wiedemann HP, Matthay RA (1985). "Acute right heart failure". Crit Care Clin. 1 (3): 631–61. PMID 3916797.
- ↑ 7.0 7.1 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.
- ↑ Benotti JR, Dalen JE (1984). "The natural history of pulmonary embolism". Clin Chest Med. 5 (3): 403–10. PMID 6488744.
- ↑ 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.
- ↑ 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
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