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The Cardiovascular System: Blood
Chapter 14
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Function Transportation-hormones, gasses, nutrients, ions, heat
Regulation- pH, temperature, water balance in cells Protection- clotting, white cells interferons, complement
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Composition Connective tissue-Two parts
Plasma = soluble materials (~55%) Formed Elements = cells (~45%) Percent occupied by red blood cells (RBC) = hematocrit (Hct) White blood cells (WBC) ~1%
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Figure 14.1a
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Figure 14.1b
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Plasma ~91% water, 7% proteins, 1.5 % other solutes
Proteins: Albumin (54%)- osmosis and carriers; Globulins (38%)- antibodies Fibrinogen (7%)- clotting Other: Electrolytes , nutrients, gases, hormones, vitamins & waste products
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Formed Elements I. Red Blood Cells II. White blood cells III Platelets
A. granular Leukocytes Neutrophils Eosinophils Basophils B. Agranular leukocytes T & B lymphocytes & natural Killer cells monocytes III Platelets
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Formation of Blood Cells
Called hemopoiesis Just before birth and throughout life occurs in red bone marrow Contains pluripotent stem cells In response to specific hormones these develop through a series of changes to form all of the blood cells
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Figure 14.2a
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Figure 14.2b
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Erythrocytes (RBCs) Hemoglobin package- carries oxygen
Also carries some CO2 Male has ~ 5.4 million cells/µl; Female has ~4.8 million membrane, no nucleus, flexible structure use glucose for ATP production to maintain ionic composition No mitochondria Wear out fast- live ~120 days
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RBC Cycling cleared by macrophages (liver & Spleen)
Fe- recycled in bone marrow Carried in blood on transferrin Heme bilirubin and excreted (bile) Globin A.A. recycled.
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Figure 14.3
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RBC Synthesis called erythropoiesis From stem cells: hemocytoblasts
Released as reticulocytes Mature to erythrocytes in 1-2 days Production & destruction is balanced Low O2 delivery (hypoxia) erythropoietin release (EPO) from kidney Stimulates erythropoiesis
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Figure 14.4
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White Blood Cells Defenses: phagocytes, antibody production and antibacterial action Phagocytes: Neutrophil- first responders Monocytes macrophages (big eaters) Eosinophil- phagocitize antibody-antigen complexes Involved in suppressing allergic responses Basophil- intensify allergic reactions Immune response: T-cells, B-cells& natural killer (NK) cells
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WBC Life Span 5000-10,00 WBC /µl blood
Limited number of bacteria can be eaten Life span is a few days During active infection may be hours Leukocytosis= increased WBC numbers response to stresses Leukopenia = decreased WBC numbers
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Platelets Myeloid stem cells megakaryocytes fragments = platelets Plug damaged blood vessels Promote blood clotting Life span 5-9 days
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Hemostasis Hemostasis = stationary blood 1. Vascular reactions (spasm)
Response to damage Quick reduction of blood loss 2. platelet plug formation Become sticky when contact damaged vessel wall 3. blood clotting (coagulation) Series of chemical reactions involving clotting factors Clotting in unbroken vessel= thrombosis
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Coagulation Extrinsic pathway common steps
tissue factor(TF) from damaged cells 1 Intrinsic Pathway common steps Materials “intrinsic” to blood 1 1. prothrombinase which causes 2. prothrombin thrombin causes 3. fibrinogen fibrin clot
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Clot Retraction & Vessel Repair
Clot pugs ruptured area Gradually contracts (retraction) Pulls sides of wound together Fibroblasts replace connective tissue epithelial cells repair lining
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Control Mechanisms Fibrinolysis: dissolving of clot by activated plasmin enclosed in clot Clots can be triggered by roughness on vessel wall = thrombosis Loose clot = embolus and can block a small vessel = embolism
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Figure 14.5
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Blood Types Surface antigens- react with antibodies
Divided into groups based on antigens > 24 blood groups and > 100 different antigens We will deal with ABO and Rh groups
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ABO Group Two antigens = A & B If have only A –type A
If have only B –type B If neither then Type O Blood usually has antibodies that can react with antigens e.g. anti-A antibody or anti-B antibody You don’t react with your own antigens Thus: type A has anti-B and vice versa
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Figure 14.6
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Rh Blood Group Antigen discovered in rhesus monkey
If have antigen- Rh+ Normally don’t have antibodies antibodies develop after the first exposure from transfusion
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Transfusions If mismatched blood given antibodies bind to it and hemolyze cells Type AB has no AB antibodies so can receive any ABO type blood called Universal recipients Type O have neither antigen so can donate to any other ABO type called Universal donors Misleading because of many other blood groups that must be matched
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The Cardiovascular system: Heart
Chapter 15
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Location Thoracic cavity between two lungs surrounded by pericardium:
~2/3 to left of midline surrounded by pericardium: Fibrous pericardium- Inelastic and anchors heart in place Inside is serous pericardium- double layer around heart Parietal layer fused to fibrous pericardium Inner visceral layer adheres tightly to heart Filled with pericardial fluid- reduces friction during beat.
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Figure 15.1
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Heart Wall Epicardium- outer layer Myocardium- cardiac muscle
Two separate networks via gap junctions in intercalated discs- atrial & ventricular Networks- contract as a unit Endocardium- Squamous epithelium lines inside of myocardium
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Figure 15.2a
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Figure 15.2b
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Figure 15.2c
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Chambers 4 chambers 2 upper chambers= Atria
Between is interatrial septum Contains fossa ovalis- remnant of foramen ovalis 2 lower chambers = ventricles Between is interventricular septum Wall thickness depends on work load Atria thinnest Right ventricle pumps to lungs & thinner than left
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Great Vessels Of Heart- Right
Superior & inferior Vena Cavae Delivers deoxygenated blood to R. atrium from body Coronary sinus drains heart muscle veins R. Atrium R. Ventricle pumps through Pulmonary Trunk R & L pulmonary arteries lungs
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Great Vessels Of Heart-Left
Pulmonary Veins from lungs oxygenated blood L. atrium Left ventricle ascending aorta body Between pulmonary trunk & aortic arch is ligamentum arteriosum fetal ductus arteriosum remnant
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Figure 15.3a
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Figure 15.3b
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Figure 15.3c
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Valves Designed to prevent back flow in response to pressure changes
Atrioventricular (AV) valves Between atria and ventricles Right = tricuspid valve (3 cusps) Left = bicuspid or mitral valve Semilunar valves near origin of aorta & pulmonary trunk Aortic & pulmonary valves respectively
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Figure 15.4ab
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Figure 15.4c
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Figure 15.4d
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Figure 15.5a
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Figure 15.5b
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Blood Supply Of Heart Blood flow through vessels in myocardium = coronary circulation L. & Right coronary arteries branch from aorta branch to carry blood throughout muscle Deoxygenated blood collected by Coronary Sinus (posterior) Empties into R. Atrium
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Conduction System 1% of cardiac muscle generate action potentials= Pacemaker & Conduction system Normally begins at sinoatrial (SA) node Atria & atria contract AV node -slows AV bundle (Bundle of His) bundle branches Purkinje fibers apex and up- then ventricles contract
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Pacemaker Depolarize spontaneously sinoatrial node ~100times /min
also AV node ~40-60 times/min in ventricle ~20-35 /min Fastest one run runs the heart = pacemaker Normally the sinoatrial node
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Figure 15.6
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Electrocardiogram Recording of currents from cardiac conduction on skin = electrocardiogram (EKG or ECG) P wave= atrial depolarization Contraction begins right after peak Repolarization is masked in QRS QRS complex= Ventricular depolarization Contraction of ventricle T-wave = ventricular repolarization Just after ventricles relax
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Figure 15.7
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Cardiac Cycle after T-wave ventricular diastole
Ventricular pressure drops below atrial & AV valves open ventricular filling occurs After P-wave atrial systole Finishes filling ventricle (`25%) After QRS ventricular systole Pressure pushes AV valves closed Pushes semilunar valves open and ejection occurs Ejection until ventricle relaxes enough for arterial pressure to close semilunar valves
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Action Potential Review muscle Heart has addition of External Ca2+
creates a plateau prolonged depolarized period. Can not go into tetanus.
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Figure 15.8
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Flow Terms Cardiac Output (CO) = liters/min pumped
Heart Rate (HR) = beats/minute (bpm) Stroke volume (SV) = volume/beat CO = HR x SV
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Controls- Stroke Volume (S.V.)
Degree of stretch = Frank-Starling law Increase diastolic Volume increases strength of contraction increased S.V. Increased venous return increased S.V. increased sympathetic activity High back pressure in artery decreased S.V. Slows semilunar valve opening
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Controls- Heart Rate Pacemaker adjusted by nerves
Cardiovascular center in Medulla parasympathetic- ACh slows Via vagus nerve Sympathetic - norepinephrine speeds Sensory input for control: baroreceptors (aortic arch & carotid sinus)- B.P. Chemoreceptors- O2, CO2, pH
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Other Controls Hormones: Ions
Epinephrine & norepinephrine increase H.R. Thyroid hormones stimulate H.R. Called tachycardia Ions Increased Na+ or K+ decrease H.R. & contraction force Increased Ca2+ increases H.R. & contraction force
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Figure 15.9
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Exercise Aerobic exercise (longer than 20 min) strengthens cardiovascular system Well trained athlete doubles maximum C.O. Resting C.O. about the same but resting H.R. decreased
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Figure 15.10
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The Cardiovascular System: Blood Vessels and Circulation
Chapter 16
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Blood Vessels Arteries- from heart
Elastic => large Muscular => distribution to organs Arterioles => distribution to capillaries- mostly muscle Capillaries- thin walled for diffusion Veins- to heart Venules => from capillaries Veins from tissue to vena cavae to heart
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Figure 16.1ab
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Figure 16.1c
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Blood Vessel Structure
Three layers Arteries-> thicker tunica media Elastic tissue and/or muscle As they get smaller-> more muscle Arterioles-> very muscular- control Veins- bigger lumen and thinner walls Veins-> valves to prevent backflow Venules very thin, no valves
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Vessel Functions Muscular arteries & arterioles regulate flow
Sympathetic activity to smooth muscle vasoconstriction (narrowing) Decreased sympathetic activity or NO causes relaxation or dilation Arterioles adjust flow into capillaries Systemic veins & venules serve as blood reservoirs (~64% total blood volume)
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Capillary Details Capillaries only have endothelium
Very thin cells & cell nuclei protrude into lumen- easy diffusion Connected from arterioles to venules in networks Sometimes direct route from arteriole to venule Filling controlled by small arterioles & precapillary sphincters
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Figure 16.2a
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Figure 16.2b
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Capillary Exchange Slow flow through capillaries
Allows time for exchange through wall Blood pressure filtration of fluid out of capillary Mostly in first ½ of vessel length Osmosis (protein concentration) Reabsorption of fluid from outside to inside Mostly in last ½ of vessel length Balance determines fluid in circulation Excess fluid returned via lymphatic system Local signals can adjust capillary flow
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Figure 16.3
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Venous Return Blood enters veins at very low pressure.
Needs more pumping to get back to heart = action of heart; muscle pumps; respiratory pump Some pressure from heart action Not enough to overcome gravity
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Muscle & Respiratory Pumps
Contracting skeletal muscles squeeze veins emptying them Because of venous valves flow is toward heart Respiratory pump has similar action Inhalation decreased thoracic pressure & increased abdominal pressure Blood flows toward heart Exhalation allows refilling of abdominal veins
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Figure 16.4
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Blood Flow Resistance= opposition to flow
from high pressure area to lower pressure area, i.e. down pressure gradient Greater gradient greater flow Ventricular contraction blood pressure (BP) Highest in aorta and declines as flows through vessels mmHg in aorta ~16 mmHg at venules 0 at R. Atrium Resistance= opposition to flow depends on lumen diameter & length & blood viscosity Smaller lumen greater resistance Higher viscosity greater resistance viscosity of blood depends on Hct
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Resistance Depends on vessel lumen diameter And blood viscosity
Smaller lumen greater resistance And blood viscosity Higher viscosity greater resistance viscosity of blood depends on Hct And total vessel length Longer the length of flow the more friction with wall Total body resistance increases with growth and addition of tissue
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Anatomical Design Length and pressure
Design and local flow control- central pressure
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Pressure Gradients Adult anatomy gives constant length
If central blood pressure is controlled it is constant Only variable is radius of the arterioles Each tissue can do it separately Review design in picture below All tissues have the same pressure gradient
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Pressure Gradients (Cont.)
Note pulse in aorta & large arteries MAP pressure fall related to resistance Note role of arterioles Note low venous pressures can’t get back to the heart!
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Figure 16.5
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Regulation of Blood Pressure & Flow
Fast responses: e.g. standing up Slower responses: e.g. blood volume Distribution: e.g. to working muscles Balance of CO with flow to body Interacts with many other control systems Cardiovascular (CV) Center major regulator
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Inputs Higher centers: Sensory receptor input: cerebral cortex,
limbic system, hypothalamus HR increases before race; flow adjusted for body temperature Sensory receptor input: proprioceptors, baroreceptors chemoreceptors
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Inputs (Cont.) Proprioceptors: Baroreceptors: in aorta & carotid
Start HR change as activity starts Baroreceptors: in aorta & carotid pressure parasympathetic & sympathetic stimulation CO Chemoreceptors: in aorta & carotid Low O2, high H+, CO2 vasoconstriction BP
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Figure 16.6
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Output ANS to heart Vasomotor
Sympathetic HR & force of contraction Parasympathetic HR Vasomotor to arterioles vasomotor tone To veins move blood to heart BP
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Hormone regulation Renin-Angiotensin system
Angiotensin II vasoconstriction+ thirst aldosterone Na+ & water loss in urine on Epinephrine & Norepinephrine CO ADH = Vasopressin constriction BP Thirst & water retention in kidney BP ANP- from cells in atria Vasodilation & loss of salt & water in urine BP
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Figure 16.7
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Checking Circulation- Pulse
Pulse in arteries = HR Use radial artery at wrist, carotid artery, brachial artery Tachycardia = rapid rest rate (>100 bpm) Bradycardia= slow rest rate (<50 bpm)
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Blood Pressure Use sphygmomanometer Raise pressure above systolic-
Usually on brachial artery Raise pressure above systolic- stop flow Lower pressure in cuff until flow just starts first sound Systolic Pressure Lower until sound suddenly gets faint Diastolic pressure Normal values <120 mmHg for systolic & < 80 mmHg for diastolic
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Circulatory Routes Two parts: Systemic & Pulmonary
Systemic circulation- throughout body Oxygenated blood deoxygenated as it goes All systemic arteries branch from aorta All systemic veins empty into Superior Vena Cava, Inferior Vena Cava or the Coronary Sinus Carry deoxygenated blood to heart
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Figure 16.8
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Figure 16.9
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Figure 16.10a
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Figure 16.10b
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Figure 16.10c
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Figure 16.11
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Figure 16.12
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Figure 16.13
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Figure 16.14a
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Figure 16.14b
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Figure 16.14c
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Figure 16.15
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Pulmonary Circulation
From right ventricle pulmonary trunk R. & L. pulmonary arteries Carry deoxygenated blood R. & L. lungs Gas exchange occurs 2 R. & 2 L. pulmonary veins Carry oxygenated blood L. atrium
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Hepatic Petal Circulation
Portal vein transports blood from one capillary bed to another GI organs Splenic & superior mesenteric veins hepatic portal vein sinusoids in liver Mixes with oxygenated blood hepatic vein inferior Vena Cava
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Figure 16.16a
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Figure 16.16b
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Fetal Circulation Specialized for exchange of materials with maternal blood and bypass of lungs Exchange in placenta umbilical vein liver ductus venosus inferior vena cava R. atrium Mixes with deoxygenated blood from lower body foramen ovale L. Atrium Or R. Ventricle Pulmonary trunk ductus arteriosus aorta internal iliacs umbilical arteries Placenta
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Figure 16.17
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At Birth Umbilical arteries medial umbilical ligaments
Umbilical vein ligamentum teres Ductus venosus ligamentum venosum Placenta expelled Foramen ovalis closes fossa ovale Ductus arteriosus ligamentum arteriosum
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Aging Stiffening of aortae Loss of cardiac muscle strength
Reduced CO & increased systolic pressure Coronary artery disease Congestive heart failure atherosclerosis
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