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NUR 344 Chapter 26: Disorders of Blood Flow and Blood Pressure
Regulation STUDY GUIDE 2023
Blood flow requires a system of patent blood vessels and adequate perfusion pressure. Structural disorders of arteries and arterioles decrease blood flow to the tissues, causing impaired delivery of oxygen and nutrients and accumulation of waste. Venous structural disorders interfere with blood outflow from capillary beds, trapping fluid, and cellular waste products in the tissues. A critical decrease in blood flow (hypotension) can produce an immediate threat to life, continuous elevation (hypertension) contributes to premature death and disability because of damage to blood vessels. Blood Vessel Structure and Function The walls of all blood vessels, except the capillaries, are composed of a tunica externa, tunica media, and tunica intima. Thin capillaries consist of a single layer of endothelial cells surrounded intermittently by pericytes. Pericytes share some characteristics with smooth muscle cells. Endothelium Endothelium- specialized squamous epithelial cells that form a continuous, semipermeable lining for the vascular system. Homeostatic functions such as: ● transfer across the vascular wall, ● platelet adhesion, ● blood clotting, ● modulation of blood flow and vascular resistance, ● metabolism of hormones, ● regulation of immune and inflammatory reactions, and ● elaboration of factors that influence cell growth
Endothelial Dysfunction- potentially reversible changes in endothelial function that occur in response to environmental stimuli This can be caused by: ● inflammation, ● hemodynamic stress, ● certain lipid molecules, ● and hypoxia. Vascular Smooth Muscle Cells Vascular SMC s in the tunica media constrict and dilate blood vessels in response to ● hormonal and neural stimulation (particularly in response to the sympathetic branch of the autonomic nervous system [ANS]). ● Norepinephrine(vasoconstriction: increased blood pressure) diffuses into the tunica media. ● Action potentials are then propagated along SMCs through gap junctions, causing contraction of the muscle layer and reducing lumen radius, which increases the resistance to flow through the vessel. ● No local regulation ● Vascular SMCs also synthesize biologic molecules such as collagen, elastin, growth factors, and cytokines. When injured, SMCs migrate into the tunica intima and proliferate. SMCs are important in normal vascular repair and in pathologic processes such as atherosclerosis. Regulation of Systemic Arterial Blood Pressure Blood pressure rises during systole (as the left ventricle contracts) and falls as the heart relaxes during diastole. The end of systole is marked by a brief downward deflection and the dicrotic notch: the point at which ventricular pressure falls below aortic pressure and triggers sudden closure of the aortic valve. mean arterial pressure = diastolic pressure + pulse pressure/ The pressure at the height of the pressure pulse (systolic pressure) ideally is less than 120 mm Hg in adults, with the lowest pressure (diastolic pressure) less than 80 mm Hg. The difference between pressures (40 mm Hg in healthy adults) is the pulse pressure. Two major factors affect the magnitude of pulse pressure—volume of blood ejected from the left ventricle during a beat (stroke volume or SV) and the degree of distensibility within the arterial tree (reflecting the ability of arterial vasculature to accept ejected blood). Arterial distensibility is
Chemoreceptors are in close contact with arterial blood, and although their main function is to regulate ventilation, they
also communicate with brain stem cardiovascular centers for widespread vasoconstriction. When arterial blood pressure drops, chemoreceptors are stimulated because of diminished oxygen and a buildup of carbon dioxide and hydrogen ions. In chronic lung disease, systemic and pulmonary hypertension may develop in response to hypoxemia. People with sleep apnea may also experience increased blood pressure due to hypoxemia during apneic periods Humoral Mechanisms Humoral mechanisms that contribute to blood pressure regulation include the renin–angiotensin– aldosterone system, vasopressin, and epinephrine/norepinephrine. ● Norepinephrine/epinephrine (catecholamines) from adrenal gland modifies blood pressure by increasing HR by vasoconstriction and cardiac contractility ● Renin release occurs with increased SNS activity or decreased blood pressure, extracellular fluid volume, or extracellular sodium concentration. Most renin leaves the kidney. In the bloodstream, it converts an inactive circulating plasma protein, angiotensinogen, to angiotensin I. Angiotensin I is converted to angiotensin II while blood is flowing through the lungs, catalyzed by angiotensin-converting enzyme(ACE) produced in the endothelium of lung blood vessels. ● Angiotensin II is a vasoconstrictor of arterioles and, to a lesser extent, veins. Arteriole constriction increases PVR, contributing to short-term regulation of blood pressure. ○ reduces sodium excretion by increasing sodium reabsorption by kidney proximal tubules ○ stimulates adrenal gland aldosterone secretion, which contributes to long-term regulation of blood pressure by increasing kidney salt and water retention ● Vasopressin (or antidiuretic hormone, ADH ) is released from the posterior pituitary gland in response to decreased blood volume or blood pressure ○ It has a direct vasoconstrictor effect, particularly on vessels of splanchnic circulation that supply abdominal viscera, but long- term increases cannot maintain increased blood pressure Long-Term Regulation ● Extracellular fluid volume and arterial blood pressure are regulated near an equilibrium point. Arterial pressure rises when increased water and salt intake increase extracellular fluid. This increases the rate of kidney water
diuresis(increased or excessive production or urine) and natriuresis(excretion of sodium in urine) occur. ● Increased fluid volume can elevate blood pressure through (a) a direct effect on the preload component of CO and (b) an indirect effect on PVR through mechanisms that autoregulate blood flow. Autoregulatory mechanisms distribute blood flow to body tissues according to metabolic needs. When blood flow is excessive, local vessels constrict, and when flow is deficient, local vessels dilate (autoregulation of blood flow). Circadian Variations in Blood Pressure Acute and chronic mechanisms regulate blood pressure around a set point. This set point varies in a circadian pattern: nocturnal blood pressure declines 10% to 20%. Decreased nocturnal dipping of blood pressure is a useful predictor of adverse cardiovascular events and has been noted in people with repetitively shortened sleep periods Disorders of Systemic Arterial Blood Flow Ischemia is the reduction in arterial flow to a level that is insufficient to meet the oxygen demands of the tissues. Infarction refers to an area of ischemic necrosis in an organ produced by occlusion of its arterial blood supply or venous drainage. Dyslipidemia Dyslipidemia is a condition of imbalance of the lipid components (triglycerides, phospholipids, and cholesterol) of the blood. Triglycerides are used in energy metabolism Phospholipids contain a phosphate group and are important structural constituents of lipoproteins, blood-clotting components, the myelin sheath, and cell membranes. Cholesterol has a steroid nucleus synthesized from fatty acids, and its chemical and physical activities are similar to that of other lipid substances Classification of Lipoproteins ● Chylomicrons ● Very–low-density lipoprotein (VLDL) ○ Carries large amounts of triglycerides ● Intermediate-density lipoprotein (IDL)
● Low-density lipoprotein (LDL) ○ Main carrier of cholesterol ● High-density lipoprotein (HDL) ○ 50% protein The small intestine and liver are the sites of lipoprotein synthesis. LDL is the primary transport molecule for cholesterol. Uptake of LDL by macrophages in the arterial wall can lead to atherosclerosis. HDL facilitates reverse transport of cholesterol (carrying cholesterol from peripheral tissues back to the liver, where it is secreted into the bile). Exercise, moderate alcohol consumption, and certain lipid medications increase HDL levels, whereas smoking, the metabolic syndrome, and excess alcohol consumption are associated with decreased levels of HDL. Etiology and Pathogenesis of Dyslipidemia ● Primary dyslipidemia is abnormalities in lipid and cholesterol levels developing independent of other health problems or behaviors, ● Secondary dyslipidemia is associated with other health problems and behaviors. ● Dyslipidemia is characterized by increased triglycerides, increased total blood cholesterol, increased LDL cholesterol, and decreased HDL cholesterol Primary Dyslipidemia Primary dyslipidemia may have a genetic basis. There may be a defective synthesis of apoproteins, a lack of receptors for lipids, defective lipid receptors, or genetically determined defects in the handling of cholesterol by cells. Familial Hypercholesterolemia (Primary) The LDL receptor is deficient or defective in familial hypercholesterolemia , an autosomal dominant disorder that causes a mutation in a gene that codes for an LDL receptor. ● Because most circulating cholesterol is removed through receptor- dependent mechanisms, cholesterol levels are elevated in people with this disorder. ● 240 mg/dL or greater ○ with a mean of 350 mg/dL ● They often develop xanthomas (cholesterol deposits) along the tendons and
Secondary Dyslipidemia The causes of secondary dyslipidemia include dietary factors, obesity, and the metabolic changes associated with type 2 diabetes mellitus. Decrease salt Recommendations are to adopt a diet high in fruits, vegetables, whole grains, dairy products, chicken, fish, legumes, and nuts. Intake of sweets and red meat should be minimized. These recommendations are consistent with the DASH diet (D ietary A pproaches to S top H ypertension) or a Mediterranean approach. Type 2 diabetes mellitus is characterized by the development of a state of insulin resistance along with a collection of metabolic alterations, including dyslipidemia, called the metabolic syndrome. Defined as the presence of 3 or more of these things: ● Elevated fasting blood glucose (or current treatment for diabetes) ● Elevated blood pressure (or current treatment for hypertension) ● Elevated waist circumference (country-specific norms) and increased abdominal fat deposits ● Dyslipidemia reflected by increased blood triglycerides and/or decreased HDL cholesterol in the blood (or receiving current treatment for dyslipidemia). Other systemic disorders that can elevate lipids include hypothyroidism, nephrotic syndrome, and obstructive liver disease. Medications such as beta-blockers, estrogens, and protease inhibitors (used in the treatment of HIV infection) can also increase lipid levels. Atherosclerosis Atherosclerosis is the hardening of the arteries characterized by the formation of fatty lesions in the intimal(intima) lining of large- and medium-sized arteries that protrude and eventually obstruct blood flow Complications: Stroke, Ischemic heart disease, peripheral vascular disease Etiology and Risk Factors ● The major risk factor for atherosclerosis is hypercholesterolemia and elevations in LDL cholesterol levels. ● Hypercholesterolemia is one of several risk factors for atherosclerosis that can be modified by dietary and lifestyle changes and medications.
● Cigarette smoking, obesity and visceral fat, hypertension, and diabetes mellitus are also risk factors for atherosclerosis. Toxins that enter the bloodstream with cigarette smoking can damage endothelial tissue.
formation. Complicated Lesion - Contains hemorrhage, ulceration, and scar tissue deposits
Development of Atherosclerosis
1. Endothelial Cell Injury. a. Smoking, elevated LDL levels, immune mechanisms, and mechanical stress associated with hypertension share the potential for causing endothelial injury with adhesion of monocytes and platelets. 2. Migration of Inflammatory Cells. a. After monocytes adhere to the endothelium, they migrate between the endothelial cells to localize in the intima of the vascular wall. Monocytes then transform into macrophages, which engulf lipoproteins, particularly LDL. Activated macrophages become foam cells when they release toxic oxygen species that oxidize the engulfed LDL. 3. Lipid Accumulation and Smooth Muscle Cell Proliferation. a. The recruitment of monocytes and their transformation into foam cells is protective because it removes excess lipids from circulation. However, accumulation of foam cells in the vessel wall eventually leads to lesion progression. Ultimately, foam cell macrophages die, depositing necrotic cellular debris and lipids within the vascular wall. 4. Plaque Structure. a. Atherosclerotic plaques consist of SMCs, macrophages, and other leukocytes; ECM, including collagen and elastic fibers; and intracellular and extracellular lipids. b. Rupture, ulceration, or erosion of a vulnerable fibrous cap may lead to hemorrhage into the plaque or thrombotic occlusion of the vessel lumen. Thrombosis( blood clot) is the most important complication of atherosclerosis. The thrombus may cause occlusion of small vessels in the heart and brain. Aneurysms (Buldge in blood vessel) may develop in arteries weakened by extensive plaque formation. Special Arterial Involvement in Atherosclerosis ● In larger vessels, the important complications are those of thrombus
● In medium-sized arteries, ischemia and infarction due to vessel occlusion are more common. ● Arteries supplying the heart, brain, kidneys, lower extremities, and small intestine are most frequently involved. Vasculitis The vasculitides are a group of vascular disorders that cause inflammatory injury and necrosis of the blood vessel wall (i.e., vasculitis). Because they may affect veins and capillaries, vasculitis, angiitis, and arteritis are often used interchangeably. Clinical manifestations often include fever, myalgia, arthralgia, and malaise. Vasculitis may result from direct injury to the vessel, infectious agents, or immune processes, or they may be secondary to other disease states such as systemic lupus erythematosus. Classification of Vasculitides (by professor) ● Group I ○ Systemic necrotizing vasculitides ● Group II ○ Hypersensitivity vasculitides ● Group III ○ Giant cell arteritis ● Group IV ○ Miscellaneous Classification of Vasculitides(in textbook)
develop during childbirth.
A thrombus is a blood clot on the wall of a vessel that continues to grow until obstructing blood flow. Thrombi often arise from erosion or rupture of the fibrous cap of an arteriosclerotic plaque. Clinical Manifestations Emboli often lodge in bifurcations of major arteries, including the aorta and iliac, femoral, and popliteal arteries. Presentation is often described by the seven “Ps”:
- pistol shot (acute onset),
- pallor,
- polar (cold),
- pulselessness,
- pain,
- Paresthesia (a burning or pricking sensation)
- paralysis. Occlusion in an extremity causes sudden onset of acute pain with numbness, tingling, weakness, pallor, and coldness. There is often a line between the oxygenated tissue above and the ischemic tissue below the obstruction. Pulses are absent below the level of the occlusion. This is followed rapidly by cyanosis, mottling, and loss of sensory, reflex, and motor function. Tissue death occurs unless blood flow is restored Diagnosis and Treatment Diagnosis of acute arterial occlusion uses visual assessment, palpation of pulses, and methods to assess blood flow. Treatment is aimed at restoring blood flow. An embolectomy , surgical removal of the embolus, is the optimal therapy when a large artery is occluded Thrombolytic therapy (i.e., streptokinase or tissue plasminogen activator) may dissolve the clot. Anticoagulant therapy (i.e., heparin) is usually given to prevent extension of the embolus and to prevent progression of the original thrombus. Cold should be avoided, and the extremity should be protected from injury caused by hard surfaces and overlying bedclothes.
