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CVT 109

Vascular Physiology. CVT 109. Introduction. The purpose of this portion of CVT 109 is to teach physiology relavant to non-invasive vascular technology. Major areas of interrogation Intracranial cerebrovascular Extracranial cerebrovascular Abdominal visceral vascular Peripheral arterial

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CVT 109

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  1. Vascular Physiology CVT 109

  2. Introduction • The purpose of this portion of CVT 109 is to teach physiology relavant to non-invasive vascular technology. • Major areas of interrogation • Intracranial cerebrovascular • Extracranial cerebrovascular • Abdominal visceral vascular • Peripheral arterial • Peripheral venous

  3. Normal Endothelial • This is about as normal as an adult aorta in America gets. The faint reddish staining is from hemoglobin that leaked from RBC's following death. The surface is quite smooth, with only occasional faint small yellow lipid streaks visible.

  4. Development and sequela of atherosclerosis. • A disease of the intima extending to the media of the arterial wall. • Abnormal build up of lipid and collegen cells. • Extends into and narrows the lumen of the artery. • Chronic in nature. • Content changes with age.

  5. Stages of development • Lipid deposits in the intima • subintimal collagen deposits • intrude into lumen, narrowing lumen • epithelial covering • fibrin accumulates • as more lipid accumulates the atheroma becomes larger. • Macrophages die, lipid is released and acts as an irritant.

  6. Development cont. / Calcium formation / hemorrhage in the atheroma- from vaso vasorm or into the lesion from the surface. / atheroma breakdown / endothelial rupture (plaque ulceration) / embolization - any of the constituants / occlusion - thrombosing / weakening of the arterial wall-aneurysm

  7. Sequela • Hemodynamic lesions • area and diameter stenosis • occlusion • flow reduction to distal vascular bed • embolization • portions of the plaque breaking off and obstructing flow distally. • Any material in the plaque can move.

  8. Areas of incidence of Atherosclerotic Lesions • Cerebral • Coronary • Aorta • Renal • Extremities • Mesenteric

  9. Cerebral • Stroke/TIA/Rind Thrombosis Embolic Hemorrhage

  10. Coronary • Angina • MI

  11. Aorta • Hemodynamic lesions • Dissection • Aneurysm

  12. Renal • Hemodynamic Lesions • Hypertension: decreased distal renal artery pressure activates renin-angiotensin system. Decreased renal function Atrophy of Kidney

  13. Mesenteric • Hemodynamic/Embolic lesions • Bowel arterial insufficiency • Intestinal angina • Intestinal gangrene

  14. Upper Extremities • Hemodynamic lesions • Highest incidence in subclavian region. • Causes “subclavian steal syndrome”. Neurological symptoms. • Rarely causes arm ischemia

  15. Upper extremity cont: • Radial and ulnar atherosclerotic lesions occur more frequently in diabetic patients and renal patients.

  16. Upper ext cont • Embolic ischemia of upper extremities can result from atherosclerosis in the following locations. Emboli from atherosclerotic lesions to upper ext is much less common than to lower extremities. Tends to affect digits. • Emoli to upper ext come from aorta, heart, and prox subclavian.

  17. Lower Extremity • Hemodynamic Lesions cause ischemia to lower legs and feet. • Claudication: Pain or tiredness of a muscle group, brought on by exercise and relieved by rest. • Ischemic rest pain: Pain in lower leg and foot brought on by rest and relieved by exercise.

  18. Lower extremity cont. • Emboli are a factor in lower extremity ischemia. Most likely sources include. • Heart • Aortic aneurysm • Iliac aneurysm • Poplital aneurysm

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