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BIO 204 Exam 2

Cadiac Output, Blood Pressure Topic 2-3

QuestionAnswer
Stenosis *a narrowed valve *BC more pressure must eject blood thru valve--> 1. Increased residual bl. vol. in a chamber 2. Cardiac cell hypertrophy 3. Low PP *Usually assoc w/ calcification of valve
Incontinence *valve that does not close properly, can lead to—> 1. Backward blood flow 2. Increased bl. vol. in affected chamber 3. Low PP *Associated w/ valve leaflets "billowing" backwards
Heart Murmers turbulent blood flow, that can be caused by stenosis restricting opening of heart valve turbulent blood flow, that can be caused by stenosis restricting opening of heart valve
Cardiac Output *Volume of blood ejected by each ventricle per MINUTE *SV x HR *@ rest 5 L/min.
Stroke volume *Volume of blood ejected by each ventricle per BEAT *about 70 ml/beat *Diff. btw EDV and ESV
Heart Rate *# of times the heart beats/min. *ave. cardiac cycles/min. * about 75/min.
Cardiac Reserve *difference btw resting and maximal cardiac output
End Diastolic Volume *Volume of blood that fills a ventricle during diastole *about 120 ml.
End Systolic Volume *Volume of blood remaining in a ventricle after systole *about 50 ml.
SV SV= EDV-ESV
SV Factors 1. Preload 2. Contractility 3. Afterload
Remember Diastole= heart FILLING + Systole= heart EMPTYING
Ejection Fraction *Volume ejected * SV/EDV *average 70%, >50%= cardiac failure could occur, athletes=up to 90%
Preload *degree to which cardiac muscle fibers are stretched prior to contraction
Frank-Starling Law of Cardiac Muscle *If cardiac muscle sarcomeres are stretched w/in limits—> contract more forcibly *Recall length-tension relationship
Preload Factors *Factors that increase preload 1. Increased venous return 2. Increased time for filling (length of diastole) 3. increased muscle activity 4. increased inspiration 5. vasoconstriction
Contractility *any change in muscle contractile strength=independent of EDV & sarcomere length
Positive Ionotropic Effects *Increase Contractility 1. Autonomic Nerv. Sys.: SNS (Fight-or-Flight) 2. Chemicals: Epinephrine, Norepineprhine, Excess Ca2+, Glucagon, Thyroxine, Digitalis
Negative Ionotropic Effects *Decrease Contractility 1. Autonomic Nerv. Sys.: PNS 2. Chemicals: Acetylcholine Excess H+, Excess K+, Calcium channel blockers (like used in high blood pressure)
Afterload *Pressure that ventricles must overcome to eject blood into arteries *> arterial pressure= harder for ventricles to eject blood—> reduced SV
Corrective Response-Elevated Aortic&Carotid pressoreceptors stimulated—>afferent impulse across Glossopharyngeal/Vagus nerve to Medulla—>Cardiacinhibotory center activated/Cardioaccelatory Center inhibited—>Efferent message to SA node via Vagus nerve—>HR decreases, BP decreases
Corrective Response- Reduced Aortic/Carotid pressorecptors=NOT stimulated—>reduced messaged to medulla—>CAC activated/CIC inhibited—>Efferent messsage to SA node via cardiac sympathetic nerves—> HR/BP increases
Congestive Heart Failure heart's weak pumping action causes a buildup of fluid called congestion in lungs and other body tissues
Causes of CHF *High BP *Irregular heart beat *Heart valve disease *Cardiomyopathy * Congenital heart defects *Alcohol/drug use *Previous heart attacks *Coronary heart disease
Symptoms of CHF *Fatigue, weakness, swelling, edema of lung tissue, shortness of breath
Continuous Capillaries *endothelial cells joined by tight junctions-->maybe interrupted in some places by intercellular clefts
Fenestrated Capillaries *Like continuous cap. BUT endothelial cells have pores (fenestrations) covered by thin membranes-->more PERMEABLE than continuous cap.
Sinusoids *Leaky Cap. w/ large lumens & usually fenestrated *few tight jxns + intercellular clefts *Found: liver, bone marrow, lymphoid tissues, + some endocrine organs *Examples: spleen/liver sinusoids lined with macrophages = Kupffer Cells
Arteriosclerosis *Hardening/loss of elasticity of medium/large arteries *Cause: aging, hypertension, diabetes, smoking, hereditary factors, elevated cholesterol *Smooth muscle cells/collagen fibers migrate-->tunica MEDIA *Lumen-->narrowed
Atherosclerosis *Thickening of artery wall due to accumulation of fatty materials (cholesterol)
Varicose Veins *Damage to one or more valves in VEIN -->swollen, twisted veins due to abnormal collection of blood *Venous distention/pooling of blood-->become tangible/palpable/tortuous--> surrounding tissue may become--edematous
Aneurysm *Localized dilation/outpouching of blood vessel or cardiac chamber *Arterial walls= weakened, may rupture *Common sites: ab. aorta, renal arteries, cerebral arteries
Phlebitis *Inflammation of vein usually due to infection or trauma * May lead to pooled blood & edema
Thrombophlebitis *Inflammation of a vein associated with a blood clot *Redness, heat, swelling, pain in affected area--> clot may break off= embolus that blocks smaller vessels *Examples: occur after using intravenous line or trauma to vein
Blood Flow *Volume of blood following thru a vessel/organ/circulation in a given time pd. *Flow=cardiac output
Blood Flow Equation (Pressure in Arteries-Pressure in Veins) / Resistance
Mean Arterial Pressure *Blood pressure changes in elastic arteries (high systolic pressure, lower diastolic pressure) *Diastolic pressure + (Pulse Pressure/ 3)
Blood Pressure *Force per unit area exerted on a vessel wall by blood *Pressure diff. drives--> BLOOD FLOW
Pulse Pressure *The difference btw. systolic & diastolic pressure
Resistance *Opposition to blood flow *Opposition to blood flow *Systemic resistance= peripheral resistance *3 Factors 1: Blood Vessel Length 2. Viscosity 3. Vessel Radius ***RADIUS=BIGGEST DETERMINANT
Resistance Formula (Length x Viscosity) / radius^4
Systolic Arterial Pressure *Pressure in artery @ PEAK of ventricular SYSTOLE *about 120 mmHg
Pulse Pressure Factors *Pressure in artery @ END of ventricular DIASTOLE *Blood= moving from elastic arteries--> smaller vessels *Recoil of arterial wall *about 80 mmHg
Capillary Pressure 1. Dispensability of Artery: how well artery can expand to receive SV 2 2. Amount of SV *Strongest in arteries closest to heart + can be felt in any elastic artery positioned close to surface of bone and over firm tissue
Venous Pressure *Venous return= enhanced by respiratory movements and external pressure of contracting skeletal muscle *Normally 0-20 mmHg
MAP MAP= CO x R
Short-Term Controls of Bl. Volume & Resistance *Negative feedback 1. Vasomotor Center 2. Vasomotor Tone 3. Baroreceptors 4. Chemoreceptors 5.Higher brain centers 6. Chemicals + Hormones
Vasomotor Center *Sympathetic neurons in medulla oblongata that control resistance by stimulating vasoconstriction *works w/ cardiac center
Vasomotor Tone *State of partial arteriolar constriction that helps to maintain normal MAP
Baroreceptors *Blood pressure receptors in carotid sinuses + aortic arch *Activated by increased MAP * THINK BS-Barorecepoors in bodies
Chemoreceptors *Receptors (carotid + aortic bodies) in aortic arch + carotid sinuses that monitor blood pH, plasma O2, and CO2 concentrations *THINK CB-chemo in bodies
Higher Brain Centers The cerebral cortex + hypothalamus can modify mean arterial pressure by acting thru medulla oblongata
Velocity *Inversely related to Total Cross Sectional Area of blood vessels * Velocity= 1/ total cross sectional area
Autoregulation *automatic adjustment of blood flow to tissues based on their changing needs *Controlled by: 1. Local, NOT systemic factors (CO, Volume factors) 2. Altered by change in Arteriolar Diameter a & O opening/closing precapillary sphincters
Autoregulation Mechanisms 1. Myogenic Controls 2. Metabolic Controls 3. Angiogenisis (LT controls)
Myogenic Controls *Reduced Arteriolar PressureArteriolar Dilation *Increased Arteriolar PressureArteriolar Constriction
Metabolic Controls *Elevated MRarteriolar dilation & relaxation precapillary sphincters (blood flow increased) *Reduced MR arteriolar constriction & contraction of precapillary sphincters (blood flow decreased)
Reactive Hyperemia *Increased tissue blood flow in response to a period of ischemia
Active Hyperemia *Increased tissue blood in response to elevated MR
Vasomotion *the intermittent, slow flow of blood thru capillaries based on the opening/closing of precapillary sphincters
Angiogenesis *growth of new blood vessels into an area *stimulated by periods of hypoxia, or by growth factors, interleukins or colony stimulating factors (CSF’s)
Hydrostatic Pressure (HP) *Pressure exerted by a fluid in an enclosed space *Amount of pressure depends on amt. of fluid & size of space *Filtration OUT= HP
Osmotic Pressure (OP) * the “pulling pressure” that a hypertonic solution exerts on a hypotonic solution
Hydrostatic Capillary Pressure (HPc) *pressure that blood exerts on wall of capillary *Tends to favor fluid OUT of cap…diff. pressures on arterial vs. venous ends
Hydrostatic Fluid Reabsorption (HPif) *Hydrostatic pressure f interstitial fluid, ranges from slightly negative-slightly positive (0)
Capillary Osmotic Pressure (OPc) *Presence of large, nondiffusable proteins in blood plasma exerts osmotic pressure on tissue fluid *favors reabsorption *26 mmHg
Interstitial Fluid Osmotic Pressure (OPif) *Proteins in the interstitial fluid exert osmotic pressure on the plasma *Pulls things out, doesn’t change unless disease present *1 mmHg
Net Filtration Pressure (NFP) Net Pressure Out- Net Pressure In
Functions of Lymphatic System 1. Return protein w/ fluid interstitial fluid back to blood 2. Transport fat & fat soluble vitamins (D,A,K,E) from GIblood 3. Protect and defend body
Lymph *fluid that enters lymph cap. from interstitial fluid *similar to blood plasma with LESS PROTEIN
Lymph Capillary *Collects lymph from interstitial spaces and deliver to lymphatics *Made of: single layer of overlapping endothelial cells..NO basement membrane ..creates valve to allow lymph in not out
Lymphatic Collecting Vessels *Afferent: deliver lymph to lymph node *Efferent: carries lymph away from lymph node *Counterintuitive
Lymphocytes *arise in red bone marrow then migrate to other tissues to become immunocompetent
B-Lymphocytes *produce antibody secreting plasma cells
T-Lymphocytes *fight antigens directly and regulate the immune response
Macrophages Phagocytize foreign antigens and help to activate T-cells
Dendritic cells *Antigen presenting cells found in mucosal membranes and in the skin
Reticular Cells Connective tissue cells that produce reticular fibers for the stroma that supports other lymphoid cells in lymphoid organs
Lymphoid Tissue *Made of network of reticular fibers (STROMA) + lymphoid cells (macrophages + lymphocytes)
Diffuse Lymphatic Tissue Small areas of unencapsulated lymphatic tissue found in most organs + lamina propria of mucous membranes
Lymphoid Follicles *Greater density of fibers than diffuse lymphatic tissue * Lymph nodules: Peyer’s patches + appendix
Mechanisms of Lymph Movement 1. Contraction of skeletal muscles (near lymph. Vessels) 2. Pressure changes during ventilation 3. Presence of valves 4. Pulsations f large elastic arteries adj. to lymphatic vessels 5. Contraction of smooth muscle in walls of lym. Ducts/trunks
Lymph Nodes *Macrophages filter lymph + activate immune cells *Nodes scattered w/in connective tissue, assoc. w/ lymph. Vessels *Cluster in some areas (intuitive: inguinal, cervical, axxilary, mediastinal, mesenteric, etc.)
Spleen 1. Lymphocytes production 2. Fetal RBC production 3. Stores plateletls 4. Contains macrophagesdegrade RBCS + platelets 5. Stores iron
Spleen Pulps 1. White Pulp: lymphocytes attached to reticular fibers 2. Red Pulp: remaining tissue: venous sinuses & splenic cords (macrophages)
Thymus Gland * Thymic cells secrete Thymopoitin + thymosisntrigger differentiaon of lymphocytes into immunocomeptent T lymphocytes
Tonsils • Gather and remove pathogens from tissue fluid • Palentine, Lingual (tongue), Pharyngeal
Peyer’s Patches *Consists of nodules w/ germinal centers surrounded by lymphocytes *Located in intestinal wall * remove pathogens from absorbed material + site of antibody production
Non-Specific Systems (Innate) *Response Time: immediate * Targets: effective against range of targets *Examples: Barriers (skin, mucous membranes), chemical systems like salt in tears/lysosomes in saliva, cells (phag., NK)
Specific Systems (Adaptive) *Response Time: some delay *Targets: selective, adaptive response to each target *Examples: B + T lymphocytes, Antigen Presenting Cells
Non-Specific Resistance *Intact skin: 30-50 rows of stratified keratinized squamous epithelium, pH3-5 *NA+ +Cl- in sweat *Skin secretions: lysozymes and fatty acids *Normal flora *Mucous Membranes: acidic, may have cilia etc.
Phagocytes *Macrophages (monocytes), neutrophils, eosinophils, mast cells
Mechanisms of Phagocytosis
Other Phagocytosis Mechanisms
For Phagocytosis to Occur:
Natural Killer Cells
Perforins
Granzyme B
Antimicrobial Proteins
Interferons
Complement
Activation of Complements
Mechanism of Complements
Onsonizaton
C Reactive Protein
Inflammation
Symptoms of Inflammation
Mechanism of Inflammation
Vascular Changes
Vasodilation
Increased Capillary Permeability
Pain
Phagocyte Mobilization
Remember COLI
Diapedesis/ chemotaxis
Immune Response Characteristics
Two types of Cell Immunity
Humoral Immunity
Cell-Mediated Immunity
PLAN-OP
Neutralization
Agglutination
Precipiation
Cells of Adaptive Immune Responses
APCs
B Lymphocytes
T Lymphocytes
Immunogens (Antigens)
Incomplete Antigen (Hapten)
Antigenic Determinant (Epitopes)
Major Histocompatibility Antigens
MHC Class 1 Antigens
MHC Class II Antigens
MHC 1 Class Antigens can be Stimulated By:
Autoimmunity
Self Tolerance
Loss of Immunologic Tolerance
Immunodeficiency
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