VASCULATURE, HEMODYNAMICS AND THEIR PATHOPHYSIOLOGY

Blood Flow Blood vessels = arteries, veins Three tissue layers (inside to outside) –Intima Epithelium + connective tissue –Media Smooth muscle + elastic tissue –Externa Connective + elastic tissue

Arteries Thick to thin –Accommodate pressure changes Blood ejected as heart contracts –Contraction/relaxation of arteriolar smooth muscle Controls lumen size Controls fluid pressure inside lumen –REMEMBER: closed circuit of tubes Fluid pressing against the walls = fluid pressure If vessel clamped, inside opening now smaller, but contains same amount of fluid. What does this do to fluid pressure?

Veins Relatively thin, less elastic –Larger diameter –Some w/ valves –Flow toward heart assisted by skeletal muscle contraction

Systemic circulation controlled neurally Sympathetic only –NOTE: One of the few sites w/out dual innervation Cardiovascular control center Baroreceptors, chemoreceptors in arterial walls –Baroreceptors: blood pressure changes –Chemoreceptors: blood levels O 2, CO 2 and H+ Signal cardiovascular control center

Some characteristics Compliance = increase in volume vessel can accommodate w/ increased pressure –Depends on ratio elastic:muscle fibers in vessel walls Which types of vessels are most compliant? Why do they need to be? –Determines vessel's response to changes in pressures Blood pressure (use mean arterial pressure (MAP)) –Depends on compliance of arteries and mean blood vol in arterial system If patient had “hardening of the arteries”: would blood pressure be higher, lower or show no change? If patient had kidney problem and retains water: would blood pressure be higher, lower or show no change?

Lymphatic System Vascular system runs “parallel” to blood vasculature –Similar to blood vasculature (closed system of tubes filled with fluid) –Opens to blood vasculature at vena cava Lymph nodes –Lie along lymphatic vessels –Have cells, lymphocytes, wbc’s Filter lymph (fluid) Break down microbes/damaged cells/toxins

Lympatic system – cont’d Lymph – fluid filling lymphatic vessels. –Mostly water, proteins –“Begins” as ISF Drains to lymphatic capillaries  lymphatic vessels  lymph ducts  veins REVIEW FROM EARLIER TOPICS: –What is ISF? –What is it called when a disease or dysfunction  incr’d ISF? –What would happen to the ISF if the lymphatic vessels were blocked?

Diseases of the Veins Thrombus, embolism –Thrombus = blood “clot” attached to vessel wall –Embolism = obstruction of vessel by matter circulating in bloodstream Fat, air, infant’s cells (in pregnant women) –Thromboembolism = blood “clot” detached from the vessel wall that circulates

A coronary thrombosis is seen microscopically occluding the remaining small lumen of this coronary artery.

Venous Diseases – cont’d –Formation of thrombus Platelets adhere to vessel wall where irregularities –Hypertension may harm vessel wall over time Other platelets stick to the first  platelet aggregation and coagulation cascade Rbc’s/wbc’s also trapped where blood flow turbulent  layers of rbc’s, wbc’s and platelets

Venous Diseases – cont’d Thrombus, etc. –Causes Aging Immobilization –cells may deposit when vessels not compressed with muscle contraction Injury to vessel endothelium –Common in hypertension Increased clotting response

Venous Diseases – cont’d –Effects of thrombi Decreased venous emptying Increased venous pressures Edema Pain –Treatment Anticoagulants, fibrinolytics

Diseases of the Arteries Arterial occlusions –Arteriosclerosis Abnormal thickening, hardening of arterial vessel walls Smooth muscle and collagen stiffen vessel middle layer Lipids and cholesterol deposit on inner layer –Atherosclerosis -- affects larger vessels Fat, fibrin deposit on the inner vessel walls  atheroma Few symptoms unless >60% of the blood supply is blocked –NOTE: Atherosclerosis as sub-category of arteriosclerosis Arteries stiffen, harden, in response to chronic assault or dysfunction Atherosclerosis: atheroma (or deposits) form, enlarge, further complicating blood flow

This is a normal coronary artery with no atherosclerosis and a widely patent lumen that can carry as much blood as the myocardium requires.

The degree of atherosclerosis is much greater in this coronary artery, and the lumen is narrowed by half. A small area of calcification is seen in the plaque at the right.

Arterial Diseases – cont’d Arterial occulsions – cont’d –Progressive over years Fatty streaks of lipid material appear as yellow streaks, spots –Mainly in bends, branches of vessels –Common in most older than about 20 years Atheromas when fatty deposits complicated further with calcium, cell debris  Arterial wall degeneration –Due to Injury response aging Repeated deposits of blood elements

Here is occlusive coronary atherosclerosis. The coronary at the left is narrowed by 60 to 70%. The coronary at the right is even worse with evidence for previous thrombosis with organization of the thrombus and recanalization such that there are three small lumens remaining.

Arterial Diseases – cont’d Arterial occlusions – cont’d –Modifiable/nonmodifiable factors put some at risk –Modifiable risk factors 1. Hyperlipidemia = incr’d plasma lipoproteins –Caused by diet, disease, genetic defects –Lipoproteins -- carrier proteins for fats in bloodstream

Arterial Diseases – cont’d Arterial occlusions – cont’d –Modifiable risk factors – cont’d 2. Hypertension - may cause or exacerbate arteriosclerosis –Causes trauma to arterial walls 3. Cigarette smoking – STOP!! –  vascular damage: »Nicotine CNS effects  incr’d heart rate and incr’d vasoconstriction  incr’d blood pressure (=hypertension) »Platelet adhesiveness incr’d with tars, chemicals in cigarette smoke »Decr’d O 2 in arterial blood of smokers (CO replaces O 2 on Hb in rbc’s)

Arterial Diseases – cont’d Arterial occlusions – cont’d –Modifiable risk factors – cont’d 4. Diabetes (unrelieved; especially adult-onset) –  incr’d lipid levels, hypertension, obesity –Chronic hyperglycemia affects blood and vascular wall cells –Non-modifiable risk factors 1. Sex (males are at greater risk) 2. Age 3. Juvenile diabetes 4. Genetic predisposition

Arterial Diseases – cont’d Arterial occlusions – cont’d –Clinical Incr’d blood pressure Decr’d oxygen at tissues  pain, wasting, etc. –Treatment Reduce fat intake Drugs to decrease blood lipids Reduce risk factors (STOP SMOKING!!; treat hypertension, etc.)

Arterial Diseases – cont’d Other arterial problems –Aneurism - dilation arterial wall  Incr’d vessel wall tension/stress Layers of clot develop –Stagnant blood flow at region of “balloon” Asymptomatic until rupture (often); then  embolism; may   death Treatment by surgical repair

Arterial Diseases – cont’d Hypertension = consistent increase in arterial blood pressure. –  Damage of vessel walls –If arteries constrict over time and have incr’d pressure within  thickening of artery walls to withstand stress –  Narrowing of arterial lumen –  Inflammatory response

Arterial Diseases – cont’d –Primary hypertension No specific cause identified; Can happen with: –Retention of sodium and water  incr’d blood volume –Secondary hypertension Some systemic disease  incr’d cardiac output or incr’d vascular resistance –So heart pumps more blood w/ every beat or vessels resist pressure –Ex: kidney dysfunctions or some endocrine disorders About 5-10% of all hypertension

Arterial Diseases – cont’d –Complicated hypertension Sustained hypertension  pathology at other sites –Chronic pressures  edema and tissue damage –Most common organs effected: heart, kidney, eyes, brain –Treatment Modify lifestyle Drugs –NOTE: compliance difficult