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Chapter 13 Outline
Functions
and Components of the Circulatory System Composition of Blood Structure of the Heart Cardiac Cycle and Heart Sounds Electrical Activity of the Heart and the ECG Blood Vessels Atherosclerosis and Cardiac Arrhythmias Lymphatic System
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roles in transportation of respiratory gases, delivery of nutrients and hormones, and waste removal And in temperature regulation, clotting, and immune function
13-4
cardiovascular and lymphatic systems Heart pumps blood thru cardiovascular system Blood vessels carry blood from heart to cells and back Includes arteries, arterioles, capillaries, venules, veins Lymphatic system picks up excess fluid filtered out in capillary beds and returns it to veins Its lymph nodes are part of immune system
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13-6
Composition of Blood
Consists
of formed elements (cells) suspended and carried in plasma (fluid part) When centrifuged, blood separates into heavier formed elements on bottom and plasma on top
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Composition of Blood
Total
blood volume is about 5L Plasma is straw-colored liquid consisting of H2O and dissolved solutes Includes ions, metabolites, hormones, antibodies Red blood cells (RBCs) comprise most of formed elements % of RBCs in centrifuged blood sample = hematocrit Hematocrit is 36-46% in women; 41-53% in men
13-8
Plasma Proteins
Constitute
7-9% of plasma 3 types of plasma proteins: albumins, globulins, and fibrinogen Albumin accounts for 60-80% Creates colloid osmotic pressure that draws H2O from interstitial fluid into capillaries to maintain blood volume and pressure Globulins carry lipids Gamma globulins are antibodies Fibrinogen serves as clotting factor Converted to fibrin Serum is fluid left when blood clots
13-9
Formed Elements
Are
erythrocytes (RBCs) and leukocytes (WBCs) RBCs are flattened biconcave discs Shape provides increased surface area for diffusion Lack nuclei and mitochondria Each RBC contains 280 million hemoglobin molecules About 300 billion RBCs are produced each day
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Leukocytes
Have
a nucleus, mitochondria, and amoeboid motion Can squeeze through capillary walls (diapedesis) Granular leukocytes help detoxify foreign substances and release heparin Include eosinophils, basophils, and neutrophils
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Leukocytes continued
Agranular
leukocytes are phagocytic and produce antibodies Include lymphocytes and monocytes
13-12
Platelets (thrombocytes)
Are
smallest of formed elements, lack nucleus, are not true cells Are fragments of megakaryocytes from bone marrow Constitute most of mass of blood clots Release serotonin to vasoconstrict and reduce blood flow to clot area Secrete growth factors to maintain integrity of blood vessel wall Survive 5-9 days
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Hematopoiesis
Is
formation of blood cells from stem cells in bone marrow (myeloid tissue) and lymphoid tissue Marrow produces about 500 billion blood cells/day In fetus occurs in liver
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Hematopoiesis continued
Erythropoiesis
is formation of RBCs Stimulated by erythropoietin from kidney Leukopoiesis is formation of WBCs Stimulated by variety of cytokines = autocrine regulators secreted by immune system
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Erythropoiesis
2.5
million RBCs are produced/sec Lifespan of 120 days Old RBCs removed from blood by phagocytic cells in liver, spleen, and bone marrow Iron recycled back into hemoglobin production
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present on RBC surface specify blood type Major antigen group is ABO system Type A blood has only A antigens Type B has only B antigens Type AB has both A and B antigens Type O has neither A or B antigens
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Transfusion Reactions
People
with Type A blood make antibodies to Type B RBCs, but not to Type A Type B blood has antibodies to Type A RBCs but not to Type B Type AB blood doesnt have antibodies to A or B Type O has antibodies to both Type A and B If incompatible blood types are mixed, antibodies will cause mixture to agglutinate
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blood types incompatible, recipients antibodies agglutinate donors RBCs Type O is universal donor because lacks A and B antigens Recipients antibodies wont agglutinate donors Type O RBCs Type AB is universal recipient because doesnt make anti-A or anti-B antibodies Wont agglutinate donors RBCs
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Rh Factor
Is
another type of antigen found on RBCs Rh+ has Rho(D) antigens; Rh- does not Can cause problems when Rh- mother has Rh+ babies At birth, mother may be exposed to Rh+ blood of fetus In later pregnancies mom produces Rh antibodies In Erythroblastosis fetalis, Rh antibodies from mom cross placenta and combine with Rh+antigens on fetal blood cells causing hemolysis of fetal RBCs
13-20
Hemostasis
Is
cessation of bleeding Promoted by reactions initiated by vessel injury: Vasoconstriction restricts blood flow to area Platelet plug forms Plug and surroundings are infiltrated by web of fibrin, forming clot
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Role of Platelets
Platelets
don't stick to intact endothelium because of presence of prostacyclin (PGI2-a prostaglandin) and NO Keep clots from forming and are vasodilators
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Role of Platelets
Damage
to endothelium allows platelets to bind to exposed collagen von Willebrand factor increases bond by binding to both collagen and platelets Platelets stick to collagen and release ADP, serotonin, and thromboxane A2 = platelet release reaction
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and thromboxane A2 stimulate vasoconstriction, reducing blood flow to wound ADP and thromboxane A2 cause other platelets to become sticky and attach and undergo platelet release reaction This continues until platelet plug is formed
13-24
Role of Fibrin
Platelet
plug becomes infiltrated by meshwork of fibrin Clot now contains platelets, fibrin and trapped RBCs Platelet plug undergoes plug contraction to form more compact plug
13-25
occur via 2 pathways: Intrinsic pathway clots damaged vessels and blood left in test tube Initiated by exposure of blood to negatively charged surface of glass or blood vessel collagen This activates factor XII (a protease) which initiates a series of clotting factors Ca2+ and phospholipids convert prothrombin to thrombin Thrombin converts fibrinogen to fibrin which polymerizes to form a mesh Damage outside blood vessels releases tissue thromboplastin that triggers a clotting shortcut (= extrinsic pathway)
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Dissolution of Clots
When
damage is repaired, activated factor XII causes activation of kallikrein Kallikrein converts plasminogen to plasmin Plasmin digests fibrin, dissolving clot
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Anticoagulants
can be prevented by Ca+2 chelators (e.g. sodium citrate or EDTA) or heparin which activates antithrombin III (blocks thrombin) Coumarin blocks clotting by inhibiting activation of Vit K Vit K works indirectly by reducing Ca+2 availability
Clotting
13-30
13-31
Structure of Heart
Heart
has 4 chambers 2 atria receive blood from venous system 2 ventricles pump blood to arteries 2 sides of heart are 2 pumps separated by muscular septum
13-32
atria and ventricles is layer of dense connective tissue called fibrous skeleton Which structurally and functionally separates the two Myocardial cells of atria attach to top of fibrous skeleton and form 1 unit (or myocardium) Cells from ventricles attach to bottom and form another unit Fibrous skeleton also forms rings, the annuli fibrosi, to hold heart valves
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coming from tissues enters superior and inferior vena cavae which empties into right atrium, then goes to right ventricle which pumps it through pulmonary arteries to lungs
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blood from lungs passes thru pulmonary veins to left atrium, then to left ventricle which pumps it through aorta to body
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circulation is path of blood from right ventricle through lungs and back to heart Systemic circulation is path of blood from left ventricle to body and back to heart Rate of flow through systemic circulation = flow rate thru pulmonary circuit
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in systemic circuit > pulmonary Work done by left ventricle pumping to systemic is 5-7X greater Makes left ventricle more muscular (and 3-4X thicker)
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Atrioventricular Valves
Blood
flows from atria into ventricles thru 1way atrioventricular (AV) valves Between right atrium and ventricle is tricuspid valve Between left atrium and ventricle is bicuspid or mitral valve
13-39
and closing of valves results from pressure differences High pressure of ventricular contraction is prevented from everting AV valves by contraction of papillary muscles which are connected to AVs by chorda tendinea
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Semilunar Valves
During
ventricular contraction blood is pumped through aortic and pulmonary semilunar valves Close during relaxation
13-41
Cardiac Cycle
13-42
Cardiac Cycle
Is
repeating pattern of contraction and relaxation of heart Systole refers to contraction phase Diastole refers to relaxation phase Both atria contract simultaneously; ventricles follow 0.1-0.2 sec later
13-43
Cardiac Cycle
End-diastolic
volume is volume of blood in ventricles at end of diastole Stroke volume is amount of blood ejected from ventricles during systole End-systolic volume is amount of blood left in ventricles at end of systole
13-44
ventricles contract, pressure rises, closing AV valves Called isovolumetric contraction because all valves are closed When pressure in ventricles exceeds that in aorta, semilunar valves open and ejection begins As pressure in ventricle falls below that in aorta, back pressure closes semilunars All valves are closed and ventricles undergo isovolumetric relaxation When pressure in ventricles falls below atria, AVs open and ventricles fill Atrial systole sends its blood into ventricles
13-45
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Heart Sounds
Closing
of AV and semilunar valves produces sounds that can be heard thru stethoscope Lub (1st sound) produced by closing of AV valves Dub (2nd sound) produced by closing of semilunars
13-47
Heart Murmurs
Are
abnormal sounds produced by abnormal patterns of blood flow in heart Many caused by defective heart valves Can be of congenital origin In rheumatic fever, damage can be from antibodies made in response to strep infection
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mitral stenosis, mitral valve becomes thickened and calcified, impairing blood flow from left atrium to left ventricle Accumulation of blood in left ventricle can cause pulmonary hypertension Valves are incompetent when don't close properly Can be from damage to papillary muscles
13-49
caused by septal defects are usually congenital Due to holes in septum between left and right sides of heart Pressure causes blood to pass from left to right
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cells are short, branched, and interconnected by gap junctions Entire muscle that forms a chamber is called a myocardium or functional syncytium Because action potentials originating in any cell are transmitted to all others Chambers separated by nonconductive tissue
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SA Node Pacemaker
In
normal heart, SA node functions as pacemaker Depolarizes spontaneously to threshold (= pacemaker potential)
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voltage begins at -60mV and gradually depolarizes to -40 threshold Spontaneous depolarization is caused by Na+ flowing through channel that opens when hyperpolarized (HCN channel) At threshold V-gated Ca2+ channels open, creating upstroke and contraction Repolarization is via opening of V-gated K+ channels
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Ectopic Pacemakers
Other
tissues in heart are spontaneously active But are slower than SA node Are stimulated to produce action potentials by SA node before spontaneously depolarize to threshold If action ptentials from SA node are prevented from reaching these, they will generate pacemaker potentials
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occurs as V-gated Na+ channels open MP rapidly declines to 15mV and stays there for 200-300 msec (plateau phase) Plateau results from balance between slow Ca2+ influx and K+ efflux Repolarization due to opening of extra K+ channels
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potentials from SA node spread through atrial myocardium via gap junctions But need special pathway to ventricles because of nonconducting fibrous tissue AV node at base of right atrium and bundle of His conduct Act. Pot. to ventricles
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septum of ventricles, bundle of His divides into right and left bundle branches Which give rise to Purkinje fibers in walls of ventricles These stimulate contraction of ventricles
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Pot. from SA node spread at rate of 0.8 -1 m/sec Time delay occurs as Act. Pot. pass through AV node Has slow conduction of 0.03 0.05 m/sec Act. Pot. speed increases in Purkinje fibers to 5 m/sec Ventricular contraction begins 0.10.2 sec after contraction of atria
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Excitation-Contraction Coupling
Depolarization
of myocardial cells opens V-gated Ca2+ channels in sarcolemma This depolarization opens V-gated and Ca2+ release channels in SR (calcium-induced-calcium-release) Ca2+ binds to troponin and stimulates contraction (as in skeletal muscle) During repolarization Ca2+ pumped out of cell and into SR
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Refractory Periods
Hearts
Act. Pot. lasts about 250 msec Has refractory periods almost as long as Act. Pot. Cannot be stimulated to contract again until has relaxed
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Electrocardiogram (ECG/EKG)
Is
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leads record voltage between electrodes placed on wrists and legs (right leg is ground) Lead I records between right arm and left arm Lead II: right arm and left leg Lead III: left arm and left leg
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leads record voltage between a single electrode placed on body and ground built into ECG machine Limb leads go on right arm (AVR), left arm (AVL), and left leg (AVF) The 6 chest leads, placed as shown, allow certain abnormalities to be detected
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ECG
3
distinct waves are produced during cardiac cycle P wave caused by atrial depolarization
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ECG
QRS
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heart sound (lub) comes immediately after QRS wave as AV valves close 2nd heart sound (dub) comes as T wave begins and semilunar valves close
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Blood Vessels
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layer of all vessels is the endothelium Capillaries are made of only endothelial cells Arteries and veins have 3 layers called tunica externa, media, and interna Externa is connective tissue Media is mostly smooth muscle Interna is made of endothelium, basement membrane, and elastin Although have same basic elements, arteries and veins are quite different
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Arteries
Large
arteries are muscular and elastic Contain lots of elastin Expand during systole and recoil during diastole Helps maintain smooth blood flow during diastole
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Arteries
Small
arteries and arterioles are muscular Provide most resistance in circulatory system Arterioles cause greatest pressure drop Mostly connect to capillary beds Some connect directly to veins to form arteriovenous anastomoses
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Capillaries
Provide
extensive surface area for exchange Blood flow through a capillary bed is determined by state of precapillary sphincters of arteriole supplying it
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Types of Capillaries
In
continuous capillaries, endothelial cells are tightly joined together Have narrow intercellular channels that permit exchange of molecules smaller than proteins Present in muscle, lungs, adipose tissue Fenestrated capillaries have wide intercellular pores Very permeable Present in kidneys, endocrine glands, intestines. Discontinuous capillaries have large gaps in endothelium Are large and leaky Present in liver, spleen, bone marrow
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Veins
Contain
majority of blood in circulatory system Very compliant (expand readily) Contain very low pressure (about 2mm Hg) Insufficient to return blood to heart
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Veins
Blood
is moved toward heart by contraction of surrounding skeletal muscles (skeletal muscle pump) And pressure drops in chest during breathing 1-way venous valves ensure blood moves only toward heart
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Atherosclerosis
Is
most common form of arteriosclerosis (hardening of arteries) Accounts for 50% of deaths in US Localized plaques (atheromas) reduce flow in an artery And act as sites for thrombus (blood clots)
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Atherosclerosis
Plaques
begin at sites of damage to endothelium e.g. from hypertension, smoking, high cholesterol, or diabetes
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Atherosclerosis
Plaques
begin at sites of damage to endothelium E.g. from hypertension, smoking, high cholesterol, or diabetes
13-81
blood cholesterol is associated with risk of atherosclerosis Lipids, including cholesterol, are carried in blood attached to LDLs (low-density lipoproteins) and HDLs (high-density lipoproteins)
13-82
and HDLs are produced in liver and taken into cells by receptor-mediated endocytosis In cells LDL is oxidized Oxidized LDL can injure endothelial cells facilitating plaque formation Arteries have receptors for LDL but not HDL Which is why HDL isn't atherosclerotic
13-83
most commonly due to atherosclerosis in coronary arteries Ischemia occurs when blood supply to tissue is deficient Causes increased lactic acid from anaerobic metabolism Often accompanied by angina pectoris (chest pain)
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infarction (MI) is a heart attack Usually caused by occlusion of a coronary artery Causing heart muscle to die Diagnosed by high levels of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) And presence of plasma troponin T and I from damaged muscle are now important for diagnosis of MI Dead cells are replaced by noncontractile scar tissue
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are abnormal heart rhythms Heart rate <60/min is bradycardia; >100/min is tachycardia
13-87
flutter, contraction rates can be 200-300/min In fibrillation, contraction of myocardial cells is uncoordinated and pumping ineffective Ventricular fibrillation is life-threatening Electrical defibrillation resynchronizes heart by depolarizing all cells at same time
13-88
node block occurs when node is damaged Firstdegree AV node block is when conduction through AV node > 0.2 sec Causes long P-R interval Second-degree AV node block is when only 1 out of 24 atrial Act. Pot. can pass to ventricles Causes P waves with no QRS In third-degree or complete AV node block no atrial activity passes to ventricles Ventricles are driven slowly by bundle of His or Purkinje fibers
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third-degree or complete AV node block, no atrial activity passes to ventricles Ventricles are driven slowly by bundle of His or Purkinjes
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Lymphatic System
13-93
Lymphatic System
Has
3 basic functions: Transports interstitial fluid (lymph) back to blood Transports absorbed fat from small intestine to blood Helps provide immunological defenses against pathogens
13-94
Lymphatic
capillaries are closed-end tubes that form vast networks in intercellular spaces Very porous, absorb proteins, microorganisms, fat
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Lymph
13-96
nodes filter lymph before returning it to R. & L. subclavian veins via thoracic duct or right lymphatic duct Nodes make lymphocytes and contain phagocytic cells that remove pathogens Lymphocytes also made in tonsils, spleen, thymus
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