Diseases of Blood Circulation PDF

Diseases of Blood Circulation Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com. Learning Objectives Describe the four types of blood vessels and the pattern of blood flow. 2. List the four factors regulating the circulation of fluid between capil...

Diseases of Blood Circulation Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com. Learning Objectives Describe the four types of blood vessels and the pattern of blood flow. 2. List the four factors regulating the circulation of fluid between capillaries and interstitial tissue. 3. Describe the causes and types of circulatory disturbances. 4. Describe the causes and effects of venous thrombosis. 5. Explain the pathogenesis of pulmonary embolism. Describe the clinical manifestations and compare the techniques of diagnosis. 6. What factors predispose to thrombus formation in leg veins? What are the major complications of venous thrombi? 7. Explain the major clinical disturbances leading to edema. 8. Describe the factors leading to shock. 9. Describe the causes and effects of arterial thrombosis. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com 1. Learning Objectives 9. 10. Describe the natural history of atherosclerosis. 11. Explain the current concepts regarding risk factors for coronary heart disease. 12. Describe the adverse effects of hypertension on the cardiovascular system and the kidneys. 13. Differentiate between the pathogenesis and clinical manifestations of arteriosclerotic and dissecting aneurysms of the aorta. Explain the principles of treatment. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Describe the pathogenesis of the hypercoagulable state sometimes seen in patients with carcinoma. Blood Vessels Arterioles lack elasticity – use smooth muscle cells (contract/expand) to control blood flow to capillaries Capillaries: thin endothelium lines vessels that deliver nutrients/oxygen and remove waste products from cells Veins – return blood to heart under low pressure with assistance of one-way valves FIGURE 12-1 The composition and diameter of blood vessel walls vary with the type of blood vessel. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Arteries/arterioles: Conduct blood to tissues – maintain BP Factors Regulating Fluid Flow between Capillaries and Interstitial Tissue ▪ Capillary hydrostatic pressure: Force pushing fluid from capillaries into extracellular space ▪ Osmotic pressure: Water-attracting property of a solution; exerted by proteins in the blood (colloid osmotic pressure) that attract fluid from interstitial space back into the capillaries ▪ Higher pressure in artery tends to draw fluid into interstitial space ▪ Lower pressure in venous return capillaries will draw most fluid back into circulation ▪ Open lymphatic channels: Collect fluid forced out of the capillaries by the hydrostatic pressure and return fluid into circulation Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Capillary permeability: Determines ease of fluid flow through capillary endothelium Circulatory Disturbances Rare occurrence, commonly caused by partial/complete blockage of blood vessels Thrombus: An intravascular clot; can occur in any vessel or within the heart Arterial thrombi: related to development of atherosclerosis, formation of lipid plaques causing narrowing and hardening of arteries. Can become detached (embolus) and block downstream arterial circulation (embolism), blocking blood flow to the region (infarct) causing ischemia - necrosis Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Venous thrombosis: normally, blood does not clot within the vascular system but can be precipitated by and number of conditions “Virchow’s triad” ▪ Slowing or stasis of blood flow ▪ Blood vessel wall damage ▪ Increased coagulability of blood Diseases of the Veins Other factors that can interfere with circulation: ▪ Varices or varicosities: Excessive dilation and tortuosity (many twisting turns) ▪ Valves in veins prevent retrograde blood flow; varicose veins result if saphenous (large subcutaneous, superficial leg) veins become dilated and valves become incompetent ▪ Varicose veins in other locations: Hemorrhoids (lower rectum), varicocele (scrotum), esophageal varices ▪ Aneurysm :outpouching of arterial walls due to weakened area Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Phlebitis: Inflammation of vein (from stretching, or blockage) Venous Thrombosis Common presentation ▪ Leg swelling/pain from partial blockage of venous return in leg ▪ Risk of detachment and further injury causing pulmonary embolism ▪ Treat with anticoagulants – fibrinolytics (tpa – tissue plasminogen activator) and elevate leg Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Predisposing factors to clot formation in leg veins ▪ Prolonged bed rest, extended period of inactivity ▪ Cramped position for an extended period ▪ Varicose veins or any condition preventing normal emptying of veins ▪ Risk of clotting in post-op patients (increased clotting factors), confined to bed stasis- leads to increased risk Impaired milking action of leg musculature that normally promotes venous return, resulting in stasis of blood in veins Varicose Veins ▪ Result from incompetent valves ▪ Leads to poor nutrition of the tissues served by the veins ▪ Tends to run in families suggesting inherited genetic susceptibility ▪ Superficial veins are susceptible -poorly supported by muscle contractions ▪ If central veins are affected – can lead to poor nutrition and atrophy of limb, prone to rupture, thrombophlebitis Treatment – stocking, limb elevation, surgical removal/ligation in serious cases. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Dilated tortuous veins, usually in the leg resulting from poor blood return Pulmonary Embolism ▪ Large pulmonary emboli may completely block main pulmonary artery or major branches, obstructing blood flow to lungs – High risk of immediate fatality ▪ Lung not may not suffer complete infarct due to collateral blood flow from bronchial arteries (from descending aorta) that interconnect with pulmonary arteries via collateral channels ▪ With time – blood can find ways around clot and clot is dissolved… can also get worse as clot collects/traps debris and enlarges ▪ Cyanosis and shortness of breath due to inadequate oxygenation of blood Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Clinical manifestations depend on size of embolus and where it lodges in the pulmonary artery Large Pulmonary Emboli Complete block of pulmonary artery ▪ Pulmonary artery and right side of heart becomes overdistended with blood, causing increased pulmonary pressure ▪ Left ventricle unable to pump adequate blood to brain and vital organs ▪ Systemic blood pressure falls, and patient may go into shock Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Right side of heart becomes distended Small Pulmonary Emboli ▪ Raises pulmonary pressure and inadequate circulation to lung section ▪ Affected lung segment undergoes necrosis; wedge-shaped pulmonary infarct ▪ Can be mild if no infarct ▪ If infarct develops: Dyspnea, chest pain, cough, and expectoration of bloody sputum due to leakage of blood from infarcted lung tissue into bronchi Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Small emboli may pass through main pulmonary arteries, becoming impacted in peripheral arteries supplying lower lobes of the lungs Pulmonary Embolism Diagnosis ▪ D-dimer (byproduct of body breaking down fibrin clot) ▪ chest x-ray (poor sensitivity) ▪ ventilation/perfusion scan – if CTPA cannot be performed (allergy to dye/kidney problems) Uses radioactive tracer gas to measure air and blood flow in lungs – mismatch b/w ventilation and perfusion suggests pulmonary embolism Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Most important test is computerized tomography pulmonary angiography (CTPA), a specialized type of CT test in which a dye is injected into the vascular systems to allow visualization of the blood vessels in the lung. Pulmonary Embolism Treatment ▪ Supportive care – supplemental oxygen ▪ Allows embolus to slowly dissolve using natural hemostasis pathways of clot reduction ▪ If thrombus is large and life threatening – use of Thrombolytic drugs is indicated- tpa (tissue plasminogen activator) ▪ Angioplasty (balloon or stent to widen vein) ▪ Thrombectomy (clot extraction surgery) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Anticoagulants: Heparin initially – to block formation, followed by warfarin (coumadin) – to block clotting factor production (liver) Embolism Fat embolism ▪ Following severe bone fracture that disrupts fatty bone marrow and surrounding adipose tissue ▪ Emulsified fat globules sucked into veins and carried into lungs, obstructing pulmonary capillaries ▪ If it reaches systemic circulation, eventually blocks small vessels in brain and other organs Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com From blood clots, fat, air, amniotic fluid, and foreign particles Air Embolism ▪May be accidentally injected into circulation (IDU) ▪Air carried into right heart chambers and prevents filling of heart by returning venous blood ▪Heart unable to pump blood, and individual dies rapidly of circulatory failure Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪Large amount of air sucked into circulation from lung injury due to a chest wound Amniotic Fluid Embolism ▪Amniotic fluid enters maternal circulation through a tear in fetal membranes ▪Fetal cells, hair, fat, and amniotic debris fluid block maternal pulmonary capillaries, causing severe respiratory distress ▪Thromboplastic material in fluid activates coagulation mechanism leading to disseminated intravascular coagulation syndrome (DIC) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Devastating complication of pregnancy Foreign Particulate Matter Embolism ▪May be injected by substance users who crush and dissolve tablets and inject them. ▪Material injected intravenously and is trapped within small pulmonary blood vessels ▪Symptoms of severe respiratory distress Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪Various types of particulate material Circulatory disturbances - Edema ▪ Results from disturbance of extracellular fluid circulation between capillaries and interstitial tissues ▪ Pitting edema: extreme form of edema where a pit or indentation formed when edematous tissue is compressed with the fingertips ▪ Ascites: Fluid accumulates in peritoneal cavity (common with liver failure) ▪ Hydrothorax: Fluid accumulates in pleural cavity – most commonly from cardiac failure Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Refers to accumulation of fluid in interstitial tissues, most often noted in ankles and legs Pathogenesis of Edema 2. Low plasma proteins ▪ Excess protein loss (liver disease – albumin loss, kidney disease protein loss in urine) Causes reduced oncotic pressure in blood and loss of fluid to interstitial space and accumulation ▪ Inadequate synthesis (malnutrition due to starvation or GI disease, liver disease) 3. Increased hydrostatic pressure ▪ Heart failure ▪ Localized venous obstruction (blood clot, tumor) ▪ Inferior superior vena cava syndrome – fluid accumulation in lower/upper body due to blockage or compression of the vessel. 4. Lymphatic obstruction - Lymphatic drainage blocked Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com 1. Increased capillary permeability ▪ Causes swelling of tissues with acute inflammation ▪ Increase in capillary permeability from some systemic diseases Acute Pulmonary Edema Temporary reduction in output from left ventricle (forward failure) ; right heart pumps blood into lungs faster than left heart can deliver blood to peripheral tissues (reverse) Rapidly engorges lungs with blood causing ▪ Increased pulmonary capillary pressure ▪ Leakage of fluid in alveoli ▪ Shortness of breath from fluid accumulation in alveoli and impaired oxygenation Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Manifestation of acute heart failure from temporary disproportion in output of blood from ventricles Circulatory Disturbances - Shock Categories according to pathogenesis ▪ Hypovolemic shock: Low blood volume (blood loss, severe burns, diarrhea, dehydration) ▪ Cardiogenic shock: Reduced cardiac output (heart failure) ▪ Septic shock: Excessive vasodilatation secondary to release of microbial toxins and inflammatory mediators ▪ Anaphylactic shock: Excessive vasodilatation from release of inflammatory mediators Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Blood flow or blood pressure is too low to adequately supply body with blood; potentially life threatening; circulating blood volume is less than capacity of vascular system Shock ▪ Drugs that promote vasoconstriction (Epinephrine) ▪ Use of intravenous fluids or blood to restore blood volume secondary to fluid loss or hemorrhage ▪ Treat underlying cause Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Prognosis depends on early recognition and rapid, appropriate treatment Arterial Thrombosis Main cause: Injury to vessel wall from arteriosclerosis, causing ulceration, roughening of arterial wall with thrombi formation Blocks blood flow causing infarct ▪ Coronary artery: Myocardial infarction ▪ Major leg artery: Gangrene ▪ Cerebral artery: Stroke Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Stasis is not a factor due to rapid blood flow and high intravascular pressure Intracardiac Thrombosis May dislodge into systemic circulation and cause infarction of major organs: Spleen, kidneys, brain lung etc. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Clot formation ▪ Within atria: inappropriate contraction, atrial fibrillation ▪ Surfaces of damaged heart valves ▪ Wall of left ventricle (mural thrombi): on areas subject to myocardial infarction Thrombosis by Increased Coagulability Polycythemia Estrogen in contraceptive pills stimulates synthesis of clotting factors Hereditary gene mutations in clotting factors: ▪ Mutation of gene that codes for factor V results in abnormal factor V, more resistant to inactivation, prolonged activity, increased coagulability ▪ Mutation of gene regulating prothrombin synthesis, risk for venous thrombosis increases as prothrombin level rises Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Rise in coagulation factors following surgery or injury Thrombosis in Patients with Cancer ▪ Predisposes to both arterial and venous thromboses ▪ Hypercoagulability due to rapid release of thromboplastic materials into circulation from tumor: deposits/destruction/necrosis ▪ If widespread, platelets and coagulation factors consumed faster than can be replenished, leading to bleeding ▪ Large tumors release thromboplastic material slowly but continuously; production of coagulation factors exceeds destruction, leading to hypercoagulability DIC – Disseminated Intravascular Coagulation Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Thrombosis can occur in patients with cancer because of increased platelets and coagulation factors Arteriosclerosis/Atherosclerosis Arteriosclerosis :Chronic and progressive degenerative disease of large to mid sized arteries (thickening/ hardening due to aging) Pathogenesis: Endothelial injury causes cells to proliferate in vessel walls – leads to accumulation of inflammatory and immune cells (foamy Macrophages) ▪ Cholesterol and lipids accumulate in cytoplasm (unstable plaques) ▪ Cholesterol precipitates as crystals, causing cell necrosis ▪ Cholesterol crystals, debris, enzymes leak out ▪ Secondary fibrosis, calcification, degenerative changes in arterial wall ▪ Formation of atheroma (rough, ulcerated surface predisposed to clot formation) Atheroma – necrotic core rich in lipids with fibrous cap containing immune/inflammatory cells, smooth muscle cell and connective tissue. Gradual growth – decades, resulting in narrowing and eventual stenosis with turbulent flow increasing damage – potential of releasing thromboses/emboli Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Atherosclerosis: narrowing of arteries from lipid deposits (buildup of fat / cholesterol) from bloodstream Atheromatous Deposits FIGURE 12-14 Low-magnification photomicrograph of coronary artery in cross section illustrating several atheromatous plaques (arrows) surrounded by dense fibrous tissue. Atheromatous deposits reduce lumen of artery to a narrow slit (original magnification ×40). Courtesy of Leonard V. Crowley, MD, Century College. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Stable plaque Surrounded by fibrous tissue Causes permanent narrowing of vessel Atheromatous Deposits FIGURE 12-15 Advanced atherosclerosis of aorta. Many plaques are ulcerated and are covered by thrombus material (arrow). Courtesy of Leonard V. Crowley, MD, Century College. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Atheroma or atheromatous plaque Irregular mass of yellow, mushy debris encroaching on lumen of artery and extending into muscular and elastic tissues of arterial wall Risk Factors ▪Elevated blood lipids (most significant) ▪High BP ▪Smoking ▪Diabetes Genetic – not modifiable - largest impact (40-60%) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Modifiable risk factors: increased likelihood when combined Blood Lipids and Coronary Artery Disease ▪Trans fat and saturated fat: Atherogenic ▪Cholesterol: Synthesized in body and from diet Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪Neutral fat: Triglyceride (three molecules of fatty acid combined with glycerol) from ingested fat, sugar, and carbohydrates Blood Lipids and Coronary Artery Disease Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com High levels associated with premature atherosclerosis and increased cardiovascular disease risk; transported by lipoproteins ▪ Low-density lipoprotein (LDL): Bad cholesterol ▪ High-density lipoprotein (HDL): Good cholesterol; protective; increases with regular exercise, smoking cessation, modest alcohol intake Cardiovascular Risk Indicators ▪ C- Reactive Protein is produced in liver and released in response to inflammation. ▪ High CRP level predicts high cardiovascular disease risk ▪ Reflects accumulation of macrophages, lymphocytes, lipids, products of tissue injury in unstable plaques in coronary arteries Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com CRP (associated with inflammation) Cardiovascular Risk Indicators ▪ Elevated levels in homocystinuria marked by early onset of severe atherosclerosis ▪ High level is a risk factor for cardiovascular disease ▪ Metabolism requires vitamins B6, B12, and folic acid, and deficiency can cause increased homocysteine levels Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Homocysteine: Sulfur-containing amino acid formed from methionine that is abundant in animal protein Diagnosis and Treatment of CAD Treatment ▪ Angiogram – to detect artery obstruction Lifestyle changes (diet, exercise, stress) ▪ Echocardiogram – to evaluate blood flow, structural abnormalities Drugs: Anti anginal drugs (nitroglycerin), anti arrhythmic, statins (lower blood cholesterol) ▪ Stress tests – measure cardiac function (EEG) Surgical: bypass , angioplasty Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Diagnosis Hypertension Increased sympathetic stimulation can cause excessive vasoconstriction of small arterioles resulting in: ▪ Increased peripheral resistance; increased diastolic blood pressure ▪ Increased force of ventricular contraction ▪ Compensatory increase in systolic pressure Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Primary or essential hypertension (95% of cases): Unknown cause – multifactorial Hypertension Cardiac effects: Vascular effects: Increased pressure → premature wearing out of vessels; accelerates atherosclerosis; injury to arterioles → rupture and hemorrhage Renal effects: Narrowed renal arterioles → decreased blood supply to kidneys → injury and degenerative changes in glomeruli and tubules → renal failure Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Increased peripheral resistance → higher workload → heart enlarges → heart failure Hypertension Treatment Diuretics - to remove salt/water ACE inhibitors – reduce angiotensin II (potent vasoconstrictor) Calcium channel blockers (inhibit contraction of arteriolar smooth muscle cells) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Secondary hypertension: From a known disease (autoimmunity, chronic kidney disease, pituitary or adrenal tumor, hyperthyroidism) Hypertension and the Aorta ▪ Arteriosclerotic aneurysm ▪ Dissecting aneurysm of the aorta Diagnosis and treatment of coronary artery disease required Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Isolated systolic hypertension: Mild to moderate rise in systolic pressure, but low or normal diastolic pressure ▪ Increased rigidity of aorta with age ▪ Arteries have decreased ability to stretch and absorb force of ejected blood during ventricular contraction ▪ Diastolic pressure is normal because of absence of arteriolar vasoconstriction ▪ Same harmful effects as primary and secondary hypertension Aneurysms Dilatation or outpouching of portion of arterial wall ▪ Anastomoses - weak ▪ In aorta: Most common in distal part of aorta; may rupture, leading to massive and fatal hemorrhage Large arteriosclerotic aneurysm of renal arteries Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Causes: Arteriosclerosis (major cause); congenital ▪ Arteriosclerotic aneurysm: Arteriosclerosis causes narrowing, thrombosis, and weakening of vessel wall Aneurysms Dissecting aneurysm of aorta: ▪ Inner lining is subject to tear during separation (increased risk if high BP) ▪ Blood forced into aortic wall ▪ Occur most often in thoracic portion, but can also occur in abdominal aorta Symptoms: ▪ severe chest and back pain (similar to heart attack) ▪ tearing or ripping sensation, that spreads to the neck or down the back. ▪ Sudden severe abdominal pain – often fatal Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Degenerative changes over time can cause layers of aorta to separate Diseases of Blood Circulation Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com.