wk 5. ch 15. arterial disorders

Artery wall layers

tunica intima,-- inner -- basement membrane, endothelia cells tunica media,-- middle -- smooth muscle tunica adventitia( extera) -- outter -- connective tissue

blood flow regulation

Blood flow inversely related to diameter of vessel •Flow from large diameter to small diameter reduces flow and increases pressure •Resistance affected by vessel diameter, vessel length, and blood viscosity Blood flow = blood pressure/resistance •Blood flow = CO (cardiac output) •Blood pressure = BP •Resistance = PVR (peripheral vascular resistance) Cardiac output (CO): Amount of blood from LV per minute •Blood pressure: measures force against walls of arteries •CO = BP/PVR •BP = CO × PVR •Factors can be adjusted independently To raise BP: •Increase CO •Increase PVR

Baroreceptors

Cells that are sensitive to blood pressure changes. §Short-term regulation of BP changes •Orthostatic hypotension §Located in walls of aorta and carotid arteries §Sense stretch of vessel wall §Send signal to cardioregulatory center •BP too low ‒Activate SNS: Increase HR, contractility, vasoconstriction •BP too high ‒Activate PNS (vagus nerve) : Decrease HR, contractility, vasoconstriction

laminar flow

Flows in parallel lines in a smooth progression

endothelial injury

Leads to arteriosclerosis and atherosclerosis Endothelial injury attracts WBC's •Initiates inflammation •vWF released increasing platelet aggregation •Foam cells (lipid-rich macrophages) form •NO release inhibited causing vasoconstriction •Plaque formation

turbulent flow

an irregular, mixing flow pattern •Rough flow perpendicular to vessel •Endothelial injury can lead to turbulent flow •"Whooshing" sound known as bruit Sluggish, stagnant, or turbulent blood flow increases risk of thrombus formation

blood pressure regulation

brain stem: medulla oblongata

hyperlipidemia

excessive fat in the blood §Elevated levels of lipids (cholesterols and triglycerides) in blood •Leads to atherosclerosis, CVD §Elevated lipid risk factors •Familial hypercholesterolemia (FH) •Diabetes mellitus •Hypothyroidism •Obesity, Sedentary lifestyle •Diet high in saturated fats •Medications: progestins, corticosteroids §Hyperlipidemia direct role in development of atherosclerosis 1.Injury of endothelium à inflammation, macrophages and platelets 2.Macrophages engulf/ingest LDLs ‒Lipid-filled WBC's (foam cells) 3.Foam cells deposit along vessel wall form fatty streaks à plaques §Overt signs and symptoms may be lacking §Review family history and look for risk factors for cardiovascular disease •Xanthoma: cholesterol deposits under skin •Xanthelasma: cholesterol deposits around eyes •Arcus senilis: yellow-white ring around cornea §Diagnosis •Blood sample to evaluate lipids •Rule out causes that may elevate lipids •hs-CRP; homocysteine levels §ASCVD Atherosclerotic Cardiovascular Disease Risk

Endothelial Factors

nitric oxide: stimulates vessel dilation endothelien: stimulates vessel vasoconstriction VEGF: vascular endothelial growth factor- stimulates new blood vessel growth Thromboxane A2: activates clots prostacyclin: inhibits clotting von Willebran factor: activates clotting

pressure relationships

§CO = BP/PVR or BP = CO × PVR §Flow, resistance, and pressure are all related §Factors can be changed •ANS affects PVR by changing vessel diameter •Changes in PVR affect BP ‒As PVR increases, BP and CO increase •Changes in BP affect CO •Changes in HR and SV affect CO

lipids

§Cholesterol: Used in cell membrane, hormone synthesis §Triglycerides §Lipoproteins •LDL: low-density lipoprotein ‒"Bad" cholesterol involved in plaque formation in arteries •HDL: high-density lipoprotein ‒"Good" cholesterol as it helps excrete cholesterol from body

hypertension treatment

§Diet: DASH (Dietary Approaches to Stop Hypertension) §Stress reduction and physical activity §Smoking cessation §Medications •Diuretics •ACE inhibitors •ARB's (angiotensin II receptor blockers) •Calcium channel blockers •Beta-adrenergic blockers

hypertension

§Elevated BP §General criteria: •2 or more BP readings of DBP >80 or SBP >130 mm Hg §5 Categories 1.Normal 2.Elevated BP 3.Stage 1 HTN 4.Stage 2 HTN 5.Hypertensive crisis §Controversy about recommended BP goals for different populations §Primary HTN: 95% •Etiology unknown §Secondary HTN •Due to underlying disease Box 15-2 §Risk factors •Age •African American ethnicity •Obesity •Family history •Diabetes mellitus •Tobacco use •Sedentary behavior •Stress •Excessive alcohol intake •Hypersensitivity to angiotensin II •High renin secretor

arterial wall tension

§Force opposing the distending pressure inside the vessel •Laplace's Law ‒Intraluminal pressure = tension/radius

antidiuretic hormone

§From posterior pituitary •AKA: vasopressin §Released in response to drop in BP and/or blood volume or increased blood osmolarity §Increases water reabsorption by kidneys •à Raises blood volume and blood pressure

athleroscletosis risk factors

§Gender §Age §Diabetes mellitus §Family history §Hypertension §Obesity §Lifestyle factors •Sedentary lifestyle •Diet high in saturated fats §Tobacco use

other factors affecting arterials

§Glucose •Injures endothelial cells à Inflammation and plaque formation may result §Free radicals •Damage cell membrane of endothelial cells, causing inflammation §Nicotine •Potent vasoconstrictor, especially coronary arteries; increase BP, SNS activation §Homocysteine •Damages endothelial linings (deficiencies in vit B12 or folic acid decrease homocysteine breakdown)

clinical manifestations of athlerosclerosis

§Gradual •often no symptoms until end organ dysfunction §Examine for CVD •Obesity, shortness of breath, cyanosis, elevated HR and BP, weak pulses in extremities, §Bruits §Arteriosclerotic changes to retina

Atherosclerosis

§Gradual process atherosclerotic plaques build up on arterial wall •Chronic, progressive, long asymptomatic phase §Contributes to CAD, cerebrovascular disease, peripheral arterial disease §Result of endothelial injury and inflammation •Lipids, elevated glucose levels, free radicals, shearing force of BP

Athlerosclerosis pathophysiology

§Injury to endothelium •Produce adhesion molecules that attract WBC's 1.WBC's differentiate into macrophages and engulf & ingest LDL's à foam cells § Foam cells store cholesterol until they undergo apoptosis and release lipids into tunica media layer •Inflammatory cytokines attract fibroblasts §Arterial wall becomes less elastic •Increase in vessel wall thickness •Diminished vasodilation ability 2.Fatty streaks form à plaques § Plaques protrude into vessel lumen, decreasing diameter §Plaque calcifies, covered with fibrous platelet cap •Vessel stiff and hardened ØPatient may begin to have symptoms ØEspecially during exertion 3.Plaque rupture causes bleeding §Plaque can break loose and travel to area and obstruct blood flow

RAAS

§Key role in BP regulation §Renin •From JG (juxtaglomerular) cells of kidneys in response to low pressure or perfusion •Converts angiotensinogen (from liver) to angiotensin I §Angiotensin I converted to angiotensin II •ACE (angiotensin-converting enzyme) in the lungs §Angiotension II •Potent vasoconstrictor •Activates aldosterone for adrenal cortex §Aldosterone stimulates sodium and water retention by kidneys to increase blood volume and pressure §Combination of vasoconstriction (angiotensin II) and fluid retention (aldosterone) serve to elevate BP

complications of hypertension

§LVH •May lead to MI or heart failure §Renal disease §Aneurysms §Cerebral hemorrhage §Hypertensive encephalopathy §Hypertensive retinopathy •Glomerular injury

diagnosis of athlerosclerosis

§Lipid profile •Cholesterol, TG's, LDL, HDL §Endothelial function assessment •Intracoronary Doppler technique •Ultrasound of brachial artery §C-reactive protein •hs-CRP (high sensitivity CRP): increased levels associated with elevated CVD risk §Homocysteine levels •High levels associated with endothelial injury §Calcium computerized tomography (CT) scan •detects calcified plaques §Cardiac angiography •Radiopaque dye study using cardiac catheterization to examine blocked vessel §Intravascular ultrasonography •Via catheterization provides cross-sectional image of coronary arteries

natriuresis

§Natriuretic peptides act at nephrons to release excess water into urine •Reduction in blood volume reduces blood pressure §ANP •Atrial natriuretic peptide •Released from atria when they are overstretched §BNP •B-type or brain natriuretic peptide •Released from ventricles

athlerosclerosis treatment

§Same as for hyperlipidemia §Coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) •angioplasty with stent placement, to reperfuse ischemic areas of heart

blood pressure regulation

§Systole - Cardiac contraction §Diastole - Cardiac relaxation §Pulse pressure: Difference between SBP and DBP •Ideal: approximately 40 mm Hg §Stroke volume (SV): Blood ejected per beat §CO = HR × SV •Approximately 5 L/min at rest •70 bpm × 70 ml/beat = 4.9 L/min

Hyperlipidemia treatment

§Table 15-1 AHA/ACA Cholesterol Management Guidelines §Lifestyle modifications §Medications •Statins (HMG-CoA reductase inhibitors) •Bile acid sequestrants •Fibrates •Monoclonal antibody medications

hypertension patholocial effects

§Two major pathological effects 1.High shearing stress on arterial walls ‒Causing injury and weakening ‒Injury to retina, kidneys, brain, lower extremities 2.Left Ventricular Hypertrophy (LVH) ‒High resistance places excessive workload on LV ‒Coronary blood supply unable to support additional ventricular tissue §Often no symptoms until organ dysfunction •Target organ damage may present with headaches, chest pain, dyspnea on exertion, vision disturbances, dizziness §BP measurement •Seated for 5 minutes •No caffeine, exercise, smoking within prior 30 minutes •2 measurements: use average •HTN: 2 separate measurements of elevated BP on separate days

compliance

•Distending capacity of a blood vessel

arteriosclerosis

•Hardening and narrowing of arteries

arteries

•Muscular-walled blood vessels with elastic fibers •Move blood away from heart ‒High pressure vessels

Atherosclerosis

•Plaque build up on arterial wall

hypertension

•Vessel walls hypertrophy (thicker), reducing tension and wall stress