Aneurysm pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The human [[aorta]] is a relatively low-resistance circuit for circulating blood. The lower extremities have higher arterial resistance, and the repeated trauma of a reflected arterial wave on the distal aorta may injure a weakened aortic wall and contribute to aneurysmal degeneration. Systemic hypertension compounds the injury, accelerates the expansion of known aneurysms, and may contribute to their formation. | The human [[aorta]] is a relatively low-resistance circuit for circulating blood. The lower extremities have higher arterial resistance, and the repeated trauma of a reflected arterial wave on the distal aorta may injure a weakened aortic wall and contribute to aneurysmal degeneration. Systemic hypertension compounds the injury, accelerates the expansion of known aneurysms, and may contribute to their formation. | ||
Aneurysm formation is probably the result of multiple factors affecting that arterial segment and its local environment. | Aneurysm formation is probably the result of multiple factors affecting that arterial segment and its local environment. Hemodynamically, the coupling of aneurysmal dilation and increased wall stress is approximated by the [[law of Laplace]]. Specifically, the Laplace law states that the (arterial) wall tension is proportional to the pressure times the radius of the arterial conduit (T = P X R). As diameter increases, wall tension increases, which contributes to increasing diameter. As tension increases, risk of rupture increases. Increased pressure (systemic hypertension) and increased aneurysm size aggravate wall tension and therefore increase the risk of rupture. | ||
Hemodynamically, the coupling of aneurysmal dilation and increased wall stress is approximated by the [[law of Laplace]]. Specifically, the Laplace law states that the (arterial) wall tension is proportional to the pressure times the radius of the arterial conduit (T = P X R). As diameter increases, wall tension increases, which contributes to increasing diameter. As tension increases, risk of rupture increases. Increased pressure (systemic hypertension) and increased aneurysm size aggravate wall tension and therefore increase the risk of rupture. | |||
In addition, the vessel wall is supplied by the blood within its lumen in humans. Therefore in a developing aneurysm, the most [[ischemic]] portion of the aneurysm is at the farthest end, resulting in weakening of the vessel wall there and aiding further expansion of the aneurysm. Thus eventually all aneurysms will, if left to complete their evolution, rupture without intervention. In dogs, collateral vessels supply the vessel and aneurysms are rare. | In addition, the vessel wall is supplied by the blood within its lumen in humans. Therefore in a developing aneurysm, the most [[ischemic]] portion of the aneurysm is at the farthest end, resulting in weakening of the vessel wall there and aiding further expansion of the aneurysm. Thus eventually all aneurysms will, if left to complete their evolution, rupture without intervention. In dogs, collateral vessels supply the vessel and aneurysms are rare. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[CME Category::Cardiology]] | |||
[[Category:Cardiology]] | |||
Latest revision as of 15:18, 12 July 2017
| https://https://www.youtube.com/watch?v=FgcHtmry3iA%7C350}} |
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Aneurysm Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Most frequent site of occurrence is in the anterior cerebral artery from the circle of Willis. The occurrence and expansion of an aneurysm in a given segment of the arterial tree involves local hemodynamic factors and factors intrinsic to the arterial segment itself.
Pathophysiology
The human aorta is a relatively low-resistance circuit for circulating blood. The lower extremities have higher arterial resistance, and the repeated trauma of a reflected arterial wave on the distal aorta may injure a weakened aortic wall and contribute to aneurysmal degeneration. Systemic hypertension compounds the injury, accelerates the expansion of known aneurysms, and may contribute to their formation.
Aneurysm formation is probably the result of multiple factors affecting that arterial segment and its local environment. Hemodynamically, the coupling of aneurysmal dilation and increased wall stress is approximated by the law of Laplace. Specifically, the Laplace law states that the (arterial) wall tension is proportional to the pressure times the radius of the arterial conduit (T = P X R). As diameter increases, wall tension increases, which contributes to increasing diameter. As tension increases, risk of rupture increases. Increased pressure (systemic hypertension) and increased aneurysm size aggravate wall tension and therefore increase the risk of rupture. In addition, the vessel wall is supplied by the blood within its lumen in humans. Therefore in a developing aneurysm, the most ischemic portion of the aneurysm is at the farthest end, resulting in weakening of the vessel wall there and aiding further expansion of the aneurysm. Thus eventually all aneurysms will, if left to complete their evolution, rupture without intervention. In dogs, collateral vessels supply the vessel and aneurysms are rare.