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a&p II test 2

QuestionAnswer
what is the cardiovascular system composed of? a pump (heart), a conducting system(blood vessels), a fluid medium(blood),
functions of blood distribution, regulation, and protection
what does blood distribute O2 and nutrients to body cells, metabolic waste to lungs and kidneys, and hormones to endocrine organs
what does blood regulate? body temperature, pH, and fluid volume in the circulatory system
what does bllod protect against blood loss, and infection
what does whole blood contain plasma and the formed elements
what is plasma made of? 92% water, 7% plasma protiens, 1% other solutes
what are the formed elements erythrocytes (rbc) and leukocytes (wbc) and platelets
what is the cardiovascular system composed of? a pump (heart), a conducting system(blood vessels), a fluid medium(blood),
what are the physical characteristics of blood? opaque fluid, scarlet or dark red, pH 7.35-7.45, 38C, 8% of body weight average volume is 5-6L for men and 4-5L for females
functions of blood distribution, regulation, and protection
what are the plasma protiens? albumins 60%, globumins 35%, and fibrinogen 4%
what does blood distribute O2 and nutrients to body cells, metabolic waste to lungs and kidneys, and hormones to endocrine organs
what are albumins transport substances such as fatty acids, thyroid hormones, and steroid hormones
what does blood regulate? body temperature, pH, and fluid volume in the circulatory system
what are globumins antibodies, also called immunoglobumins. transport globumins: hormone binding protiens and steriod binding protiens
what does bllod protect against blood loss, and infection
what are fibrinogen molecules that form clots and produce long, insoluble strands of fibrin
what does whole blood contain plasma and the formed elements
what is serum? liquid part of blood sample, in which disolved fibrinogen has converted to solid fibrin
what is plasma made of? 92% water, 7% plasma protiens, 1% other solutes
what are the formed elements erythrocytes (rbc) and leukocytes (wbc) and platelets
what are the physical characteristics of blood? opaque fluid, scarlet or dark red, pH 7.35-7.45, 38C, 8% of body weight average volume is 5-6L for men and 4-5L for females
what are the plasma protiens? albumins 60%, globumins 35%, and fibrinogen 4%
what are albumins transport substances such as fatty acids, thyroid hormones, and steroid hormones
what are globumins antibodies, also called immunoglobumins. transport globumins: hormone binding protiens and steriod binding protiens
what are fibrinogen molecules that form clots and produce long, insoluble strands of fibrin
what is serum? liquid part of blood sample, in which disolved fibrinogen has converted to solid fibrin
what is hemoglobin the red pigment in whole blood hat gives it its color. binds and transports oxygen and carbon dioxide
what is the structure of RBC small highly specialized discs, thin in the middle and thick around the edges
what is the function of RBC dedicated to respiratory gas exchange
what are the important aspects of the structure high surface to volume ratio allows quick absorption and release of oxygen, discs can stack in roileaux to smooth the floow through narrow blood vessels, and the descis bend and flex so they can enter small capillaries
what is the lifespan of an RBC 120 days, they lack a nuclei, mitochondria and ribosomes so there is no repairs
what is the structure of hemoglobin? has two alpha and two beta chains each has a heme pigment bonded to it. each heme has an iron atom which can bind to one oxygen molecule so each hemoglobin molecule can transport four oxygen
what is the function of hemoglobin carries oxygen and transports carbon dioxide back to the lungs
how are RBCs recycled and broke down marcrophages of liver, spleen and bone marrow engulf RBC before it ruptures, hemoglobin is broke down by phagocytes into biliverdin, biliverdin is converted to bilirubin which is secreted by the liver
erythropoiesis occures in myeliod tissue (red bone marrow) in adults. stem cells mature to RBCs
the stages of maturation for RBCs is myeloid stem cell, proerythroblast, erythroblasts, reticulocyte, and mature RBC
regulation of erythropoiesis balance between too few and too many RBCs depends on hormone controls and supplies of amino acids, iron, and B vitamins
what arethe four types of blood a ,b, ab, o
the RH factor your blood can be RH+ or RH-
what happens in a cross reaction plasma antibodies meet specific surface antigen, blood agglutinates and hemolyze
white blood cells called leukocytes, do not have hemoglobin, have nuclei and other organelles
functions of WBCs defend against pathogens, remove toxins and waste, and attack abnormal cells
types of WBCs granulocytes (neutrophils,esoinophils, and basophils) monocytes, and lymphocytes
neutrophils 50-70% of circulating WBCs. first to attack bacteria, angulf and digest pathogense, release prostglandins and leukotrienes and form pus
esinophils 2-4% of WBCs, attack large paracites, excrete toxi compounds, sensitive to allergens, control inflammation
basophils less than 1% of WBCs , accumulate in damaged tissue, release histamine and heparin
monocytes 2-8 % of WBCs, larger than RBCs, migrate in and out of blood, ,ostly found in connective tissues and lymphoid organs, part of bodoies specific defence system
platelets cell fragments involved in human clotting system,circulate for 9-12 days, are removed by spleen, 2/3 are reserved for emergencys
functions of platelets release important clotting chemicals, temporarily patch damaged vessel walls, and reduce the size of break in vessel walls
platelet production occures in bone marrow (thrombocytopoiesis) megakaryocytes manufacture plateles from cytoplasma.
three stages of homeostasis vascular phase, platelet phase, and coagulation phase.
vascular phase a cut triggers vascular spams that last 30 minutes (3 stages)
stage one of vascular phase Endothelial cells contract and expose basement membrane to bloodstream
stage two of vascular phase Endothelial cells Release chemical factors ADP, tissue factor, and prostacyclin, Release local hormones, endothelins, Stimulate smooth muscle contraction and cell division
stage three of vascular phase Endothelial plasma membranes become “sticky” Seal off blood flow
platelet phase Begins within 15 seconds after injury: platelet adhesion and platelet aggregation
platelet adhesion To sticky endothelial surfaces, To basement membranes, To exposed collagen fibers
platelet aggregation Forms platelet plug which closes small breaks
factors that limit growth of platelet plug Prostacyclin, released by endothelial cells, inhibits platelet aggregation, Inhibitory compounds released by other WBCs, Circulating enzymes break down ADP, Negative (inhibitory) feedback from serotonin, Development of blood clot isolates area
coagulation phase Begins 30 seconds or more after the injury: Cascade reactions: Chain reactions of enzymes and proenzymes, Form three pathways, Convert circulating fibrinogen into insoluble fibrin
three coagulation pathways extrinsic pathway, intrinsic pathway, and common pathway
extrinsic pathway Begins in the vessel wall, Outside bloodstream, Damaged cells release tissue factor (TF), TF + other compounds = enzyme complex, Activates Factor X
intrinsic pathway Begins with circulating proenzymes, Within bloodstream, Activation of enzymes by collagen, Platelets release factors (e.g., PF-3), Series of reactions activates Factor X
common pathway Where intrinsic and extrinsic pathways converge, Forms enzyme prothrombinase, Converts prothrombin to thrombin, Thrombin converts fibrinogen to fibrin
clot reaction Pulls torn edges of vessel closer together Reducing residual bleeding and stabilizing injury site, Reduces size of damaged area Making it easier for fibrocytes, smooth muscle cells, and endothelial cells to complete repairs
fibrinolysis Slow process of dissolving clot: Thrombin and tissue plasminogen activator (t-PA), Activate plasminogen, Plasminogen produces plasmin and Digests fibrin strands
anticoagulants antithrombin-III, heparin, aspirin, protien C, and prostacyclin
what does the pulmonary circuit do? carries blood to and from gas exchange surfaces of lungs
what does the systemic circuit do? carries blood to and from the body
what are the three types of blood vessels? arteries, veins, and capillaries
arteries carry blood away from the heart
veins carry blood to the heart
capillaries form networks between arteries and veins. and carry blood to the cardiac muscles.
what are capillaries also called? exchange vessels because they exchange materials between blood and tissues
four chambers of the heart? right atrium, right ventricle, left atrium, and left ventricle.
right atrium collects blood from systemic surface
right ventricle pumps blood to pulmonary circuit
left atrium collects blood from pulmonary circuit
left ventricle pumps blood to systemic surface
the heart it is located slightly left of the midline. it is composed of great veins and arteries at the base, the pointed tip is called the apex, it is surrounded by a pericardial sac, and it sits between two pleural cavities in the mediastinum
the pericardium a double lining of the pericardial cavity, the two linings are visceral and parietal
the visceral pericardium inner layer of pericardium
the parietal pericardium outter layer of pericardium
pericardial cavity between the visceral and parietal layers and contains a pericardial fluid
paricaditis inflammation of the paricardial sac
atria thin walled, and has an expandable sac called an auricle
coronary sulcus divides the atria and ventricles
anterior and posterior interventricular sulcus separates left and right ventricles, contains blood vessels of cardiac muscles
what three layers makes up the heart wall? epicardium, myocardium, and endocardium
epicardium (outer layer) visceral pericardium, covers the heart
myocardium (middle layer) muscular wall of the heart, concentric layer of cardiac muscle tissue, atrial myocarium wraps around great vessels
endocardium (inner layer) simple squamous epithelium
intercalated disc interconnect cardiac muscle cells, secured by desmosomes, linked by gap junctions, convey force of contraction, and propogate action potentials
characteristics of cardiac muscle cells small size, single central nucleus, branching interconnections between cells, intercalated discs
interatrial septum separates atria
interventricular septum separates ventricles
atrioventricular (AV) valves connect atrium to ventricles, they are folds of fibrous tissue that extended into openings between atria and ventricles,blood presssure closes cusps during ventricular contraction permit blood flow in one dirrection
right atrium contains superior vena cava, inferior vena cava, coronary sinus, and foramen ovale, and pectinate muscles.
superior vena cava recieves blood flow from head, neck, upper limbs, and chest
inferior vena cava recieves blood from trunk, viscera, and lower limbs
coronary sinus cardiac veins return blood to coronary sinus, coronary sinus opens into right atrium
foramen ovale efore birth is an opening through interatrial septum, connects two atria. seals off at birth forming fossa ovalis
pectinate atrium contain prominent muscular ridges, located on atrial wall and inner surfaces of right auricle
right ventricle free edges attach to chordea tenineae from papillary muscles of ventricle, prevent valve from opening backward.
right atrioventricular (AV) valve also called tricuspid valve, opening from right atrium to right ventricle, has three cusps, prevents backflow
trabeculae carneae muscular ridges on internal surfaces of right and left ventricle, includes moderator band, ridge contains part of conducting system, coordinates contraction of cardiac muscle cells
pulmonary circuit superior end of right ventricle leads to pulmonary trunk, pulmonary trunk divides into left and right pulmonary arteries, blood flows from right ventricle to pulmonary trunk through pulmonary valve, pulmonary valve has three semilubar cusps
left atrium blood gathers into left and right pulmonary veins, pulmonary veins deliver to left atrium, blood from left atrium passes to left ventricle through left AV valve (bicuspid pr mitral valve)
left ventricle holds same volume as right ventricle, is larger, muscle is thicker and more powerful, similar internally to right ventricle bu no moderater band
systemic circulation blood leaves left ventricle through aortic valve into ascending aorta, acending aorta turns (aortic arch) and becomes descending aorta
semilunar valves pulmonary and aortic tricuspid valves, prevent backflow from pulmonary trunk aorta into ventricle, have no muscular support
aortic sinuses at base of ascending aorta, sacs that prevent valve cusps from sticking to aorta, origin of right and left coronary arteries
cardiac skeleton four bands around heart valves and bases of pulmonary trunk and aorta, stabilize valves, electrically insulate ventricular cells from atrial cells
coronary circulation cupplies blood to muscle tissue of heart, coronary arteries and cardiac veins
coronary arteries left and right, originate at aortic sinuses, high blood pressure, elastic rebound forces blood through coronary arteries between contractions
right coronary artery supplies blood to right atrium, portions of both ventricles, cells of SA and AV nodes, marginal arteries, and posterior interventricular artery
left coronary artery supplies blood to left ventricle, left atrium, and interventricular septum.
what are the two main branches of left coronary artery? circumflex artery, and anterior interventricular artery
cardiac veins great cardiac veins, anterior cardiac veins, posterior cardiac vein, middle cardiac vein, and small cardiac vein
great cardiac vein Drains blood from area of anterior interventricular artery into coronary sinus
anterior cardiac veins Empty into right atrium
posterior cardiac vein, middle cardiac vein, and small cardiac vein Empty into great cardiac vein or coronary sinus
coronary heart disease (CAD) Areas of partial or complete blockage of coronary circulation, Reduction in blood flow to heart muscle produces a corresponding reduction in cardiac performance
coronary ischemia reduced circulartory supply. results from partial or complete blockage of coronary artereis
causes of CAD formation of a fatty deposit (atherosclerotic plaque) in the wall of coronary vessel, The plaque or an associated thrombus then narrows the passageway and reduces blood flow, Spasms in smooth muscles of vessel wall can further decrease or stop blood flow
angina pectoris its most common form is a temporary ischemia which develops when the workload of the heart increases, can feel comforatble at reast but exertion or emotional stress can produce sensation of pressure
myocardial infarction (MI) (heart attack) Part of the coronary circulation becomes blocked, and cardiac muscle cells die from lack of oxygen, The death of affected tissue creates a nonfunctional area known as an infarct,most commonly result from severe coronary artery disease (CAD)
consequences of a MI near start of coronary artery: damage will be widespread and hear may stop beating, if involves one of smaller arterial branches: person may survive immediate crisis by may have complications like reduced contractility & cardiac arrythmias
treatment of CAD Stop smoking, High blood pressure treatment , Dietary modification to lower cholesterol and promote weight loss, Stress reduction, Increased physical activity (where appropriate)
drug treatment of CAD Drugs that reduce coagulation and therefore the risk of thrombosis, such as aspirin and coumadin, Drugs that block sympathetic stimulation, Drugs that cause vasodilation, such as nitroglycerin,
noninvasive surgery to treat CAD and MI atherectomy, balloon angioplasty, or coronary srtery bypass surgery
atherectomy Blockage by a single, soft plaque may be reduced with the aid of a long, slender catheter inserted into a coronary artery to the plaque
balloon angioplasty The tip of the catheter contains an inflatable balloon, Once in position, the balloon is inflated, pressing the plaque against the vessel walls Because plaques commonly redevelop after angioplasty,a stent may be inserted into the vessel, holding it open
coronary artery bypass surgery a small section is removed from either a small artery or a peripheral vein and is used to create a detour around the obstructed portion of a coronary artery,As many as four coronary arteries can be rerouted this way during a single operation
cardiac physiology conducting system control and coordinate heartbeat and contractile cells produce contractions that propel blood
cardiac cycle Begins with action potential at SA node: Transmitted through conducting system, Produces action potentials in cardiac muscle cells (contractile cells)
conducting system A system of specialized cardiac muscle cells Initiates and distributes electrical impulses that stimulate contraction
structures of the conducting system Sinoatrial (SA) node - wall of right atrium, Atrioventricular (AV) node - junction between atria and ventricles, Conducting cells - throughout myocardium
conducting cells Interconnect SA and AV nodes, Distribute stimulus through myocardium, In the atrium: Internodal pathways, In the ventricles: AV bundle and the bundle branches
prepotential Also called pacemaker potential, Resting potential of conducting cells Gradually depolarizes toward threshold, SA node depolarizes first, establishing heart rate
heart rate SA node generates 80–100 action potentials per minute, Parasympathetic stimulation slows heart rate, AV node generates 40–60 action potentials per minute
sinoatrial (SA) node In posterior wall of right atrium, Contains pacemaker cells, Connected to AV node by internodal pathways, Begins atrial activation (Step 1)
atrioventricular (AV) node In floor of right atrium, Receives impulse from SA node (Step 2), Delays impulse (Step 3), Atrial contraction begins
AV Bundle In the septum, Carries impulse to left and right bundle branches Which conduct to Purkinje fibers (Step 4), And to the moderator band Which conducts to papillary muscles
pukinje fibers Distribute impulse through ventricles (Step 5), Atrial contraction is completed, Ventricular contraction begins
abnormal pacemaker function bradycardia, tachycardia, etopic pacemaker
bradycardia abnormally slow heart rate
tachycardia abnormally fast heart rate
etopic pacemaker Abnormal cells , Generate high rate of action potentials, Bypass conducting system Disrupt ventricular contractions
electrocardiogram A recording of electrical events in the heart, Obtained by electrodes at specific body locations, Abnormal patterns diagnose damage
features of an ECG p wave, QRS complex, T wave
P Wave atria depolarize
QRS complex ventricle depolarize
T Wave ventricles repolarize
time intervals between ECG Waves P-R inerval, Q-T interval
P-R interval From start of atrial depolarization, To start of QRS complex
Q-T interval From ventricular depolarization, To ventricular repolarization
contractile cells Purkinje fibers distribute the stimulus to the contractile cells, which make up most of the muscle cells in the heart
refractory period Absolute refractory period: Long , Cardiac muscle cells cannot respond; Relative refractory period: Short, Response depends on degree of stimulus
role of calcium ions in cardiac contraction Contraction of a cardiac muscle cell Is produced by an increase in calcium ion concentration around myofibrils
stages of calcium ions in cardiac contractions Calcium ions enter plasma membrane during plateau phase, Arrival of extracellular Ca2+ Triggers release of calcium ion reserves from sarcoplasmic reticulum As slow calcium channels close Intracellular Ca2+ is absorbed by the SR Or pumped out of cell
cardiac cycle Is the period between the start of one heartbeat and the beginning of the next , Includes both contraction and relaxation
phases of cardiac cycle systole (contraction), diastole (relaxation) atrial systole, ventricular systole, atrial diastole, ventricular diastole
atrial systole atrial contraction begins and right and left AV valves are open, atria eject blood into ventricles filling them, atrial systole ends AV valves close, ventricles have max bloo volume. known as end-diastolic volume (EDV)
venticular systole ventricles contract and build pressure, pressure exceeds vessel pressure opening the semilunar valves allowing the blood to leave ventricle, amnt of blood ejected is called stroke volume (SV), pressure falls and semilunar valves close end systolic volume
ventricular diastole ventricular pressure is higher than atrial pressure, all heart valves are closed, ventricles relax, atrial pressure is higer than ventricular pressure, AV valves open, passice atrial filling, passive ventricular filling
blood pressure Rises during systole, Falls during diastole Blood flows from high to low pressure Controlled by timing of contractions and Directed by one-way valves
heart sounds S1: loud sounds produced by AV valves, S2: loud sounds produced by semilunar valves, S3 and S4: soft sounds produces by blood flow into ventricles and atrial contraction
heart murmur sounds produced by regurgitation through valves
cardiac output the volume pumped by left ventricle in one minute
factors effects cardiac output heart rate: adjusted by autonomic nervous system or hormones, stroke volume adjusted by changing EDV or ESV
effects on the SA node Membrane potential of pacemaker cells is Lower than other cardiac cells, Rate of spontaneous depolarization depends on: Resting membrane potential or Rate of depolarization
sympathetic and parasympathetic stimulation gratest at SA node (heart rate)
ACh slows heart rate
NE speeds heart rate
atrial reflex Also called Bainbridge reflex, Adjusts heart rate in response to venous return, Stretch receptors in right atrium Trigger increase in heart rate Through increased sympathetic activity
factors effecting the strok volume The EDV amount of blood a ventricle contains at the end of diastole, filling time, and venous return
the EDV and stroke volume at rest EDV is low, Myocardium stretches less, Stroke volume is low
EDV and stroke volume with exercise EDV increases, Myocardium stretches more, Stroke volume increases
Frank-Starling principle As EDV increases, stroke volume increases Physical Limits: Ventricular expansion is limited by: Myocardial connective tissue, The cardiac (fibrous) skeleton, The pericardial sac
end systolic volume Is the amount of blood that remains in the ventricle at the end of ventricular systole
three factors that effect ESV Preload: Ventricular stretching during diastole, Contractility: Force produced during contraction, at a given preload, Afterload: Tension the ventricle produces to open the semilunar valve and eject blood
Created by: jelizabeth10 on 2012-02-14



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