Chapter 15 Arterial Disorders Class Notes (1) PDF

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Summary

These notes summarize Chapter 15, Arterial Disorders, focusing on concepts like arteries, arteriosclerosis, atherosclerosis, and blood pressure regulation. They detail the composition of the arterial wall and the function of the endothelium, including details on factors leading to blood pressure regulation, including the role of the Renin-Angiotensin-Aldosterone system.

Full Transcript

**Chapter 15 Arterial Disorders: General Principles** Basic Concepts - Arteries - Muscular-walled blood vessels - Move blood away from heart - High pressure vessels - Higher the pressure, the greater the resistance the heart must work against - Arte...

**Chapter 15 Arterial Disorders: General Principles** Basic Concepts - Arteries - Muscular-walled blood vessels - Move blood away from heart - High pressure vessels - Higher the pressure, the greater the resistance the heart must work against - Arteriosclerosis - Hardening and narrowing of arteries - Atherosclerosis - Plaque build-up on arterial wall Arterial Wall Composition - Tunica intima - Inner lining of endothelial cells - Damage may lead to arteriosclerosis and atherosclerosis - Tunica media - Smooth muscle - Regulate blood flow - Alpha-adrenergic nerve fibers: vasoconstriction - Beta-adrenergic nerve fibers: vasodilation - Tunica externa (adventitia) - Outer covering Endothelium Function - Fluid filtration, maintain blood vessel tone, semipermeable barrier, neutrophil chemotaxis - Vessel dilation - Nitric oxide (NO) - Vessel constriction - Endothelin - Angiogenesis - VEGF - Diuresis - C-type natriuretic peptide - Clot prevention - Prostacyclin - Clot formation - Thromboxane A2 Endothelial Injury - Leads to arteriosclerosis and atherosclerosis - Attracts WBC's - Initiates inflammation - vWF released increasing platelet aggregation - Foam cells (lipid-rich macrophages) form - NO release inhibited causing vasoconstriction - Plaque formation 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 - CO = BP/PVR - BP = CO × PVR - Factors can be adjusted independently - To raise BP: - Increase CO - Increase PVR Turbulent vs Laminar Flow - Laminar - Smooth flow parallel to vessel - Turbulent - Rough flow perpendicular to vessel - Endothelial injury (atherosclerosis) can lead to turbulent flow - "Whooshing" sound known as *bruit* - Sluggish, stagnant, or turbulent blood flow increases risk of thrombus formation Arterial Wall Tension and Distension - Arterial wall tension - Force opposing the distending pressure inside the vessel (smaller vessel, need greater pressure) - Laplace's Law - Intraluminal pressure = tension in wall vessel/radius - Tension=pressure x radius - Hypertension (HTN) - Vessel walls hypertrophy, reducing tension and wall stress - Tension=(pressure x radius)/wall thickness - Compliance - Distending capacity of a blood vessel Blood Pressure Regulation - Systole - Cardiac contraction (left ventricle) - Diastole - Cardiac relaxation - SBP/DBP: 120/80 mm Hg - Pulse pressure - Difference between SBP and DBP - Ideal: approximately 40 mm Hg Cardiac Factors - Stroke volume (SV) - Amount of blood ejected per beat - CO = HR × SV - 4.9 L/min=70 bpm × 70 ml/beat - Approximately 5 L/min at rest Pressure Relationships - CO = BP/PVR or BP = CO × PVR - Flow, resistance, and pressure are all related - Factors can be changed - ANS innervation affects PVR by changing vessel diameter - Changes in PVR affect BP - Changes in BP affect CO - Changes in HR and SV can affect CO and BP Baroreceptors: Neural Regulation of BP - Short-term regulation of BP changes - *Example:* lying down to standing - Located in walls of aorta and carotid arteries - Sense stretch of vessel wall - Send signal to cardioregulatory center - Medulla oblongata and pons - BP too high - Activate PNS - Decrease HR, contractility, vasoconstriction - BP too low - Activate SNS - Increase HR, contractility, vasoconstriction Orthostatic Hypotension - Drop in BP when changing position from lying down to standing - Decreased cerebral perfusion - Dizziness - Possible causes - certain medications (e.g. alpha blockers)  - autonomic neuropathy  - decreased blood volume - age-related blood-vessel stiffness. Renin-Angiotensin-Aldosterone System (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 Antidiuretic Hormone (ADH) - 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 - Raises blood volume and blood pressure Blood Pressure Regulation (image) Natriuresis - Increased urine output when blood volume is elevated - 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 - C-type discussed earlier from endothelium **Chapter 15 Arterial Disorders: Modifiable Risk Factors for Atherosclerosis** Effect of Glucose on Arteries - Glucose injures endothelial cells - Glycoslation (aka: glycation) - Forms AGE's (advanced glycosylation end products) - Inflammation and plaque formation may result - AGE's increase endothelin release leading to vasoconstriction - Reason for diabetes mellitus being a risk factor for CAD Other Factors Affecting the Arteries - 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 vitamin B~12~ or folic acid decrease homocysteine breakdown) Lipids - Cholesterol - Ingested from diet; made by liver - Used in cell membrane, hormone synthesis - Triglycerides - Ingested in diet - LDL: low-density lipoprotein (L for lousy) - "Bad" cholesterol as involved in plaque formation in arteries - HDL: high-density lipoprotein (H for happy or healthy) - "Good" cholesterol as it helps excrete cholesterol from body ("reverse cholesterol transport") Dyslipidemia - Associated with cardiovascular disease (CVD) - Associated with elevated LDL - Low levels HDL - Low levels HDL and high triglycerides - Causes of dyslipidemia - Familial hypercholesterolemia (FH) - Diabetes mellitus - Obesity - Hypothyroidism - Sedentary lifestyle - Diet high in sat. fats, alcohol, or excessive simple carbs - Medications: progestins, corticosteroids - Plaque formation along vessel walls - Lipid-filled WBC's (foam cells) - 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 - *Example:* hypothyroidism - Also: hs-CRP; homocysteine levels - ASCVD= Atherosclerotic Cardiovascular Disease Dyslipidemia---Treatment - Lifestyle modifications - Dietary cholesterol less than 300 mg/day - Limit saturated fats - Regular physical activity - Medications - Statins (HMG-CoA reductase inhibitors) - Decrease liver cholesterol synthesis and may also reduce plaque - Bile acid sequestrants - Lower LDL by blocking reabsorption of bile acid in the gut - Cholesterol is key component of bile - Niacin - Lower triglycerides and raise HDL - Risk of increasing insulin resistance in DM - Fibrates - Lower triglycerides and raise HDL Cholesterol Management Guidelines: Risk Calculator: https://tools.acc.org/ASCVD-Risk-Estimator-Plus/\#!/calculate/estimate/ Hypertension - Elevated BP - "Silent killer" - General criteria: - 2 or more BP readings of DBP greater than 80 or SBP greater than 130 mm Hg - Primary HTN: 95% - Etiology unknown - Secondary HTN - Due to underlying disease - *Example:* Cushing's disease - Hypertension Guidelines - Controversy about recommended BP goals for different populations - \~1 in 3 adults in U.S. - Risk factors - Age - African American ethnicity - Obesity - Family history - Diabetes mellitus - Tobacco use - Stress - Excessive alcohol intake - Excess Na+ in diet - Insufficient K+ in diet - Two major pathological effects - High shearing stress on arterial walls - Injury to retina, kidneys, brain, lower extremities - LV hypertrophy (LVH) - Coronary blood supply unable to support additional ventricular tissue - Often no symptoms - Target organ damage may present with headaches, chest pain, vision disturbances, dizziness - Check for disorders and medications known to elevate BP - 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 - Ambulatory BP monitoring may be used Hypertension Assessment - Fundoscopic exam to examine retinas - Chest - Alteration in PMI (point of maximal impact) - Bruits- renal artery stenosis - Peripheral arteries of lower extremities - Temperature, sensation, pulses - Diagnosis - Rule out underlying diseases that may elevate BP, 12-lead ECG, urinalysis (checking for protein in urine which may occur with HTN damage of kidneys), CBC Hypertension---Treatment - Stress reduction and physical activity - Smoking cessation - Medications - Diuretics - ACE inhibitors - ARB's (angiotensin II receptor blockers) - Calcium channel blockers - Beta-adrenergic blockers - Diet: DASH (Dietary Approaches to Stop Hypertension) Limit sodium in diet \< 1500 mg per day - Cheese leading contributor of Na+ in the diet - UPF industry is huge contributor to Na+ intake (3/4 salt is from UPF) - Chicken has high salt level (up to 840 mg per serving of chx breast) - \# 1 source of Na+ for kids is pizza, age 20-50 chicken, over 50 years bread Complications of Hypertension - LVH - May lead to MI or heart failure - Aneurysms - Bulge in weakened area of arterial wall - Cerebral hemorrhage - Hypertensive encephalopathy - Hypertensive retinopathy - Arteriovenous nicking - Renal disease - Glomerular injury **Chapter 15 Arterial Disorders: Atherosclerosis** Atherosclerosis - Result of endothelial injury and inflammation - Lipids, elevated glucose levels, free radicals, shearing force of BP - Gradual process by which atherosclerotic plaques build up on arterial wall - Contributes to CAD, cerebrovascular disease, peripheral arterial disease Atherosclerosis Risk Factors - Gender - Age - Diabetes mellitus - Family history - Tobacco use - Hypertension - Obesity - Lifestyle factors - Sedentary lifestyle - Diet high in saturated fats Atherosclerosis Pathophysiology - Injury to endothelium - Produce adhesion molecules that attract WBC's - Vascular cell adhesion molecule 1 and chemoattractant protein-1 - WBC's differentiate into macrophages and fill with LDL's - Become foam cells - Foam cells store cholesterol until they undergo apoptosis and release lipids into tunica media layer - Inflammatory cytokines attract fibroblasts - Fatty streaks form leading to plaques - Arterial wall becomes less elastic - Plaques calcify and are covered with fibrous platelet cap - Plaque rupture causes bleeding - Plaque can break loose and travel to area and obstruct blood flow - hs-CRP: high sensitivity CRP - Measures CRP levels - CRP associated with inflammation and increased plaque formation Clinical Manifestations of Atherosclerosis - Gradual, so may have no symptoms until end organ dysfunction - Examine for CVD - Obesity, shortness of breath, cyanosis, rapid pulse, elevated BP, weak pulses in extremities, etc. - Bruits - Arteriosclerotic changes to retina Diagnosis of Atherosclerosis - Lipid profile - Cholesterol, TG's, LDL, HDL - Endothelial function assessment - Intracoronary Doppler technique - Ultrasound of brachial artery - C-reactive protein - CRP acute phase protein from liver: inflammation - hs-CRP (high sensitivity CRP): increased levels associated with elevated CVD risk - Homocysteine levels - High levels associated with endothelial injury - Calcium computerized tomography scan - 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 Cardiac Catheterization and Coronary Angiography Atherosclerosis Treatment - Lifestyle Modification - Health diet - Stress reduction - Physical activity - Social connectedness - Specific tx for where atherosclerosis is located but commonly includes stenting or bypass surgery Peripheral Arterial Disease---PAD - Arteriosclerosis and atherosclerosis outside coronary arteries - Most common site: femoral artery above knee - Same risk factors as atherosclerosis - Diabetes mellitus accelerates process - Peripheral neuropathy may be present - Gradual onset - Usually symptoms don't present until 70% occlusion - Intermittent claudication: primary sign - Pain with exertion, relieved by rest - Occlusion decreases oxygenation of tissue, leading to ADP and lactic acid formation - Reducing activity enables oxygen levels to meet metabolic demand, eliminating pain - Metabolic changes in muscle occur with ischemia and reperfusion cycles - Assessment - Examine for signs of arteriosclerosis and atherosclerosis - HTN, hyperlipidemia, diabetes, CAD, MI - Assessment of patient symptoms: pain and numbness with exertion alleviated by rest, etc. - Clinical Manifestations - Examine for diminished or absent pulses (bilateral comparison), palpable coolness, paresthesia, pallor, sensation distal to proximal - Diagnosis - Ankle-brachial index (ABI): compare upper and lower extremity BP - Normal: 1 or slightly greater - Less than 1 indicates PAD - Serum labs: CBC, ESR, CRP, lipids - Arterial plethysmography, conventional angiography, arteriogram, CT scan, MRI, capillary refill time (normal refill less than 2 seconds) - Treatment - Lifestyle modification - Exercise stimulates collateral circulation - Medications - Cholesterol lowering, anti-hypertensive, platelet inhibitors, vasodilators - Thrombolytic agents may be used - Peripheral arterial revascularization (angioplasty and stenting) procedures help restore circulation - Open surgical vascular bypass grafting - Peripheral Arterial Disease Stent with angioplasty image Aneurysm - Weakening of arterial wall causing bulging or dilation - Locations - Cerebral arteries - Sometimes called "berry aneurysms" - Aorta (thoracic or abdominal) - Most common: abdominal aortic aneurysm (AAA) - Commonly caused by arteriosclerotic damage - Also genetic predisposition, infection, vascular disease - Risk factors for rupture - Atherosclerosis, smoking, HTN - Classified by size, shape, location - Aneurysm - Involves all 3 layers of vessel wall - Fusiform shape - All layers of vessel wall dilate equally - Saccular shape - Weakness on one side of vessel - Presentation depends on size, location, and integrity - May be missed until rupture occurs - AAA: may present with abdominal or back pain - May compress organs causing nausea and vomiting - In thin patient, may see pulsatile mass - Deep palpation should not be performed - Bruit may be present - Cerebral aneurysms are normally silent - If rupture: subarachnoid hemorrhage - Diagnosis - Found incidentally - Ultrasonography - Treatment - Lifestyle modifications - Smoking cessation, BP regulation - AAA: periodic follow up (until increases to a certain size) - Surgical treatment may be necessary - Endovascular/endoluminal graft (like a stent) - Open repair Aortic Dissection - Tear in lining between tunica intima and media of aorta leading to a splitting of layers - Blood flows between layers - Potentially lethal - Symptom onset is sudden - Patient hears "ripping" or "tearing" sound - Pallor, tachycardia, BP presentation may be variable depending on dissection location - Signs may include bounding pulse, wide pulse pressure, diastolic murmur, and signs of heart failure - Cardiac tamponade may occur - 20% of cases present with neurological deficit, such as syncope - Diagnosis - ECG, chest CT scan or MRI, transesophageal echocardiogram - Treatment - Surgery Arterial Ulcers - Ischemic skin wounds due to lack of blood flow - Pale, diminished pulses in extremities with delayed capillary refill - Ulcers usually located distally at tips of toes, heel, lateral malleolus - Antibiotics may be needed to prevent infection - Preventive measures to lessen further injury to skin

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