Coursehero >> California >> Pasadena >> SPEECH 3

Course Hero has millions of student submitted documents similar to the one below including study guides, homework solutions, papers, exam answer keys and textbook solutions.

(prohormone Angiotensinogen produced by liver) Renin (kidney enzyme released by low BP) Angiotensin I ACE (angiotensin-converting enzyme in lungs) Angiotensin II very potent vasoconstrictor 20-1 Aldosterone ( BP) promotes Na+ and water retention by kidneys increases blood volume and pressure Atrial natriuretic factor ( BP) generalized vasodilation ADH ( BP) Antidiuretic hormone (water retention) Epinephrine and norepinephrine effects most blood vessels vasoconstriction binds to -adrenergic receptors, 20-2 skeletal and cardiac muscle blood vessels binds to -adrenergic receptors, vasodilation ACE inhibitors block the conversion of Angiotensin I to Angiotensin II (coughing?) (less effective in some people) Diuretics decrease total blood volume (K sparing or not) Beta-blockers (or alpha blockers) block the beta adrenergic receptors Angiotensin II receptor blockers ARBS (esp diabetics) Calcium channel blocker - Cause vasodilation Localized vasoconstriction pressure downstream drops, pressure upstream rises enables routing blood to different organs as needed Arterioles - most control over peripheral resistance located on proximal side of capillary beds most numerous more muscular by diameter 20-4 Arterioles shift blood flow with changing priorities 20-5 During exercise perfusion of lungs, myocardium and skeletal muscles perfusion of kidneys and digestive tract 20-6 Only occurs across capillary walls between blood and surrounding tissues 3 routes across endothelial cells intercellular clefts fenestrations through cytoplasm Mechanisms involved diffusion, transcytosis, filtration and reabsorption 20-7 Most important mechanism Lipid soluble substances steroid hormones, O2 and CO2 diffuse easily glucose and electrolytes must pass through channels, fenestrations or intercellular clefts Insoluble substances Large particles - proteins, held back 20-8 Pinocytosis - transport vesicles across cell exocytosis Important for fatty acids, albumin and some hormones (insulin) 20-9 Opposing forces blood (hydrostatic) pressure drives fluid out of capillary high on arterial end of capillary, low on venous end colloid osmotic pressure (COP) draws fluid into capillary results from plasma proteins (albumin)- more in blood oncotic pressure = net COP (blood COP - tissue COP) Hydrostatic pressure is defined as a physical force exerted against a surface 20-10 by a liquid. (BP is an example) Capillary filtration at arterial end Capillary reabsorption at venous end Variations by location (glomeruli vs. alveolus) 20-11 Capillary filtration ( capillary BP or permeability) poor venous return congestive heart failure - pulmonary edema insufficient muscular activity kidney failure (water retention, hypertension) histamine makes capillaries more permeable Capillary reabsorption hypoproteinemia (oncotic pressure blood albumin) cirrhosis, famine, burns, kidney disease Obstructed lymphatic drainage 20-12 Tissue necrosis oxygen delivery and waste removal impaired suffocation headaches, nausea, seizures and coma excess fluid in tissue spaces causes low blood volume and low BP Pulmonary edema Cerebral edema Circulatory shock 20-13 Pressure gradient 7-13 mm Hg venous pressure towards heart venules (12-18 mm Hg) to central venous pressure (~5 mm Hg) Gravity drains blood from head and neck thin Skeletal muscle pump in the limbs ea Br Thoracic pump g! inhalation - thoracic cavity expands (pressure ) abdominal pressure , forcing blood upward central venous pressure fluctuates 2mmHg- inhalation, 6mmHg-exhalation blood flows faster with inhalation 20-14 By the time the blood makes it through the capillary bed, blood pressure has dropped to almost zero. Blood returns to the heart through the veins largely the by action of your muscles in concert with the valves in your veins. Exercise venous return in many ways heart beats faster, harder vessels of skeletal muscles, lungs and heart dilate flow respiratory rate action of thoracic pump skeletal muscle pump Venous pooling occurs with inactivity venous pressure not enough force blood upward with prolonged standing, cardiac output may be low enough to cause dizziness or syncope prevented by tensing leg muscles, activate skeletal m. pump 20-16 jet pilots wear pressure suits Any state where cardiac output is insufficient to meet metabolic needs Cardiogenic shock - inadequate pumping of heart (MI) Hypovolemic shock (a form of low venous return shock) loss of blood volume: trauma, burns, dehydration Septic shock bacterial toxins trigger vasodilation and capillary permeability Anaphylactic shock 20-17 severe immune reaction to antigen, histamine release, generalized vasodilation, capillary permeability Compensated shock may be manageable Decompensated shock - bad 20-18 Homeostatic mechanisms bring about recovery BP triggers baroreflex and production of angiotensin II, both stimulate vasoconstriction If person faints and falls to horizontal position, gravity restores blood flow to brain; quicker if feet are raised 20-19 Life threatening positive feedback loops occur cardiac output myocardial ischemia and infarction cardiac output goes down even more slow circulation disseminated intravascular coagulation slow circulation ischemia and acidosis of brainstem vasomotor tone, vasodilation caridac output ischemia and acidosis of brainstem 20-20 Total perfusion kept constant seconds of deprivation causes loss of consciousness 4-5 minutes causes irreversible brain damage Responds to changes in blood pressure and chemistry cerebral arteries: dilate as BP , constrict as BP rises main chemical stimulus: pH CO2 + H2O H2 CO3 H+ + (HCO3) hypercapnia (CO2 ) in brain, pH , triggers vasodilation hypocapnia, pH, vasoconstriction occurs with hyperventilation, may lead to ischemia, dizziness and sometimes syncope 20-21 TIA s - transient ischemic attacks dizziness, loss of vision, weakness, paralysis, headache or aphasia lasts from a moment to a few hours, often early warning of impending stroke CVA - cerebral vascular accident (stroke) Two types brain infarction caused by ischemia atherosclerosis, thrombosis, ruptured aneurysm hemorrhagic stroke effects range from unnoticeable to fatal blindness, paralysis, loss of sensation, loss of speech common 20-22 recovery depends on CAUSE, surrounding neurons, collateral circulation, gender Highly variable flow OPPOSITE of brain At rest arterioles constrict, total flow about 1L/min During exercise arterioles dilate in response to epinephrine and sympathetic nerves precapillary sphincters dilate due to lactic acid, CO2 blood flow can increase 20 fold Muscular contraction impedes flow isometric contraction causes fatigue faster than isotonic 20-23 Low pulmonary blood pressure flow slower, more time for gas exchange capillary fluid absorption oncotic pressure overrides hydrostatic pressure Unique response to hypoxia pulmonary arteries constrict to redirect flow to better ventilated region 20-24 Pulmonary trunk to pulmonary arteries to lungs lobar branches for each lobe (3 right, 2 left) increased O2 and reduced CO2 levels Pulmonary veins return to left atrium 20-25 Basketlike capillary beds surround alveoli Exchange of gases with air at alveoli 20-26 19-27 Both ventricles must eject same amount of blood. They should have the same stroke volume. 19-28 Both ventricles must eject same amount of blood. They should have the same stroke volume.

Find millions of documents here - Study Guides, Homework Solutions, Papers, Exam Answer Keys and more. Course Hero has millions of course related materials that will enable you to learn better, faster and get an A in all your courses.
Below is a small sample set of documents: