Transcript Slide 1
Angiotensinogen (prohormone produced by liver) Angiotensin I ACE (angiotensin-converting enzyme in lungs) Angiotensin II 20-1 Renin (kidney enzyme released by low BP) very potent vasoconstrictor 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 binds to -adrenergic receptors, vasoconstriction skeletal and cardiac muscle blood vessels binds to -adrenergic receptors, vasodilation 20-2 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 Nitroglycerin! for emergencies? Localized vasoconstriction Arterioles - most control over peripheral resistance 20-4 pressure downstream drops, pressure upstream rises enables routing blood to different organs as needed located on proximal side of capillary beds most numerous more muscular by diameter 20-5 Arterioles shift blood flow with changing priorities During exercise 20-6 perfusion of lungs, myocardium and skeletal muscles perfusion of kidneys and digestive tract Only occurs across capillary walls between blood and surrounding tissues 3 routes across endothelial cells intercellular clefts fenestrations through cytoplasm Mechanisms involved 20-7 diffusion, transcytosis, filtration and reabsorption Most important mechanism Lipid soluble substances Insoluble substances 20-8 steroid hormones, O2 and CO2 diffuse easily glucose and electrolytes must pass through channels, fenestrations or intercellular clefts Large particles - proteins, held back 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) 20-10 Hydrostatic pressure is defined as a physical force exerted against a surface by a liquid. (BP is an example) 20-11 Capillary filtration at arterial end Capillary reabsorption at venous end Variations by location (glomeruli vs. alveolus) Capillary filtration ( capillary BP or permeability) poor venous return congestive heart failure - pulmonary edema insufficient muscular activity Capillary reabsorption 20-12 kidney failure (water retention, hypertension) histamine makes capillaries more permeable hypoproteinemia (oncotic pressure blood albumin) cirrhosis, famine, burns, kidney disease Obstructed lymphatic drainage Tissue necrosis Pulmonary edema headaches, nausea, seizures and coma Circulatory shock 20-13 suffocation Cerebral edema oxygen delivery and waste removal impaired excess fluid in tissue spaces causes low blood volume and low BP 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 Skeletal muscle pump in the limbs Thoracic pump 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 Cardiac suction of expanding atrial space 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 by the 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) Septic shock bacterial toxins trigger vasodilation and ↑ capillary permeability Anaphylactic shock 20-17 loss of blood volume: trauma, burns, dehydration severe immune reaction to antigen, histamine release, generalized vasodilation, ↑ capillary permeability 20-18 Compensated shock – may be manageable Decompensated shock - bad 20-19 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 Life threatening positive feedback loops occur 20-20 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 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 During exercise arterioles constrict, total flow about 1L/min 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 20-23 isometric contraction causes fatigue faster than isotonic Low pulmonary blood pressure flow slower, more time for gas exchange capillary fluid absorption oncotic pressure overrides hydrostatic pressure Unique response to hypoxia 20-24 pulmonary arteries constrict to redirect flow to better ventilated region Pulmonary trunk to pulmonary arteries to lungs Pulmonary veins return to left atrium 20-25 lobar branches for each lobe (3 right, 2 left) increased O2 and reduced CO2 levels Basketlike capillary beds surround alveoli Exchange of gases with air at alveoli 20-26 Both ventricles must eject same amount of blood. They should have the same stroke volume. 19-27 Both ventricles must eject same amount of blood. They should have the same stroke volume. 19-28