a&p 2 unit 5 cardiovascular physiology
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Blood Functions - Distribution Supplies Oxygen from lungs to cells S
upplies nutrients from digestive system tocells Transports metabolic wastes from cells todisposal sites
Transports hormones to targettissues/organs
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Blood Functions - Regulation
R egulates body temperature R egulates the pH of body fluids R egulates blood volume to support efficientcirculation to cells, tissues, organs &systems
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Blood Functions - Protection
Prevents blood lossPrevents infection through the activity of white blood cells, complement & antibodies
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Plasma
L iquid part of blood Contains:
Water
Proteins Hormones Nutrients
Electrolytes R espiratory Gases Wastes
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Plasma Proteins
Include:Albumin (60%)Globulins (36%)
(Antibodies &transport proteins)
C lotting Proteins
(4%)Enzymes &Hormones
Plasma
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S erum
Albumin (60%)Globulins (36%)(Antibodies &transport proteins)
C lotting Proteins(4%)Enzymes &Hormones
Plasma
Liquid part of blood without clotting proteins
S erum
X Clot
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H ematocritPercent of formed elements
H ematocrit
Normal H ematocrit is around 45%,
depending on gender
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Formed Elements -Cells/Components
Erythrocytes ( R BC s)
Platelets
Leucocytes (WB C s)
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2 50,000-
500,000/mm3
4 - 6 million/mm 3
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G ranulocyte - Neutrophil
Nucleus with 3 to 6 lobes
Phagocytize bacteria & some fungi
Produced in bone marrow by myeloblasts
Cytoplasmic granules fine, both basic & acidic
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G ranulocyte - EosinophilNucleus bilobedCytoplasmic granules coarse & acidic(red/orange)
Destroy parasitic worms & immune complexes
Produced in bone marrow by myeloblasts
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G ranulocyte - BasophilNucleus lobed - U or S shapedCytoplasmic granules large & basic -(purplish/black)
Cause vasodilation by the release of histamines
Produced in bone marrow by myeloblasts
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Agranulocyte - LymphocyteNucleus spherical-fills half or more of cell
B lymphocytes - H umoral Immunity (antibodies)T lymphocytes - Cellular Immunity
Produced in lymphatic tissues
No visible granules in cytoplasm
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Agranulocyte - MonocyteNucleus U or kidney shaped -fills half or more
of cell
Differentiate into macrophages in tissues.
Provide defense against viruses & intracellularbacteria in chronic infections.Activate lymphocytes
Produced by monoblasts in lymphatic tissues.
No visible cytoplasmic granules
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Blood C lotting ProcessPlatelets - Form temporary plug &release platelet factors which catalyzeclot formation
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Platelet factors - React with Calcium (Ca 2+ )& other clotting factors in the plasma to
initiate clot formation.
Thromboplastin - a lipid (Tissue Factor) released from injured cellmembranes which accelerates the clotting process.
Lipids released from damaged cell membranes such as
thromboplastin having a localized effect are called Prostaglandins.
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Platelet factors, Ca2+
& other clotting factors inplasma initiate clot formation
A plasma protein ( Prothrombin ) is converted by
prothrombin activator into an enzyme Thrombin .
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Thrombin converts the plasma proteinFibrinogen into the insoluble protein Fibrin.
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Fibrin forms a mesh which glues the platelets
& RBCs together to form the clot.
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Factors Affecting Clot Formation
Vitamin K - Required by liver to produceprothrombin & several other clottingfactors.
Calcium - Necessary for prothrombinconversion into thrombin & fibrinogenconversion into fibrin.
Thromboplastin - S peeds up clotformation from 3 - 6 minutes to 15seconds.
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Factors Affecting Clot FormationH eparin - A natural anticoagulant whichprevents clot formation by inhibitingthrombin formation.S odium Citrate - An agent used onglassware & instruments to preventcoagulation by tying up Calcium.
Plasmin (Fibrinolysin) - Breaks downclots by dissolving the fibrin after the clotis no longer needed.
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ABO & Rh Blood G roups
(Types)Based on the presence of specific antigens(proteins) on the outer surface of cells.
M any other antigens exist on cellmembranes besides A, B, AB, O & R h.Because A, B, AB, O & R h antigens can
cause severe transfusion reactions, bloodtyping is always done for these prior totransfusions.Other types are of medical or legal interest.
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ABO Blood Types
Type A
Type B
Type AB
Type O
Type A Antigen on cells
Type B Antigen on cells
Type A & B Antigens
Neither A nor B Antigens
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ABO Antibodies In Plasma
Type A blood
Type B blood
Type AB blood
Type O blood
Anti-B Antibodies
Anti-A Antibodies
No Anti-A orAnti-B Antibodies
Both Anti-A & Anti-BAntibodies
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Rh (Rhesus) FactorUp to 8 genes determine if a person is Rhpositive.The most common of these are the C, D& E genes which determine if a personhas C, D and/or E antigens on the walls
of the cells.People who do not have Rh antigens ontheir cell membranes are Rh negative .
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Rh Blood G roups
Rh -
Rh +
No Rh Antigens oncell membranes
Type Rh Antigenson cell membranes
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Rh Antibodies in Plasma
Rh -
Rh +
No Anti-Rh antibodies inplasma until sensitized to Rhantigens
No Anti-Rh antibodiesin plasma
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Antibody/Antigen R eactionsW
hen antibodies in plasma react withantigens on cell membranes, they bind tothe cells causing the cells to clump.The clumping of cells due toantigen/antibody reactions is calledagglutination .
Agglutinated cells block the flow of blooddisrupting circulation and the distribution of
O 2 , gases and nutrients.
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Transfusion Considerations
Type A blood
Type B blood
Type AB blood
Type O blood
Anti-B Antibodies
Anti-A Antibodies
No Anti-A orAnti-B Antibodies
Both Anti-A & Anti-BAntibodies
No A or B antigens
Type O - Theoretical Universal Donor
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Transfusion Considerations
Type A blood
Type B blood
Type AB blood
Type O blood
Anti-B Antibodies
Anti-A Antibodies
No Anti-A orAnti-B Antibodies
Both Anti-A & Anti-BAntibodies
Type AB - Theoretical Universal Recipient
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Inappropriate PhysiologicalApplications
ABO & Rh blood antigens representonly a few of many blood cell antigens.Estimates vary from more than a 100 to
millions.Even though ABO & Rh blood typing isdone, the possibility exists that persons
receiving more than one transfusioncould have a reaction to less common orcurrently unknown blood types.Cross matching may avoid reactions.
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Erythroblastosis Fetalis
No problem with first pregnancy. M aternal & fetal blood dont mix. D uring delivery if mother becomes
sensitized to R h + blood, she will begin to produce anti- R h antibodies. This may also occur due to placentalabnormalities, prior tubal
pregnancies, miscarriage, abortions or amniocentesis in which R h + fetal
blood may sensitize the R h - mother.
R H -
Rh +
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Erythroblastosis FetalisIn subsequent pregnancies with an R h +fetus, mothers anti- R h antibodies willcross the placenta causing fetal bloodcells to agglutinate & be destroyed.
Effects on fetus may range from jaundice, to brain damage (anoxia), to possible death.
R hoGA M shots at 28 weeks and after delivery may prevent sensitization.
R hoGam offers no protection after a
woman is sensititized.
R H -
Rh +
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Anemia - reduced O 2 carrying
capacity of the blood Insufficient number of RBCs :
H emorrhagic - due to blood loss associated with an injury,undiagnosed bleeding ulcer, etc.
H emolytic - due to blood loss due to transfusion reactions &certain bacterial and parasite infections.
Aplastic - due to destruction or inhibition of red marrow bydrugs, ionizing radiation or certain bacterial toxins.
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Anemia - reduced O 2 carrying
capacity of the blood Insufficient hemoglobin content in RBCs :
Iron Deficiency - inadequate intake or absorption of iron.
Pernicious - dietary deficiency of Vitamin B 12 or inadequate
production of intrinsic factor for absorption of Vitamin B 12 .
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Anemia - reduced O 2 carryingcapacity of the blood
A bnormal hemoglobin in RBCs :S ickle Cell - one amino acid in the 2 87 forming the betachains is wrong.
In low O 2 conditions the beta chains form stiff rods whichcause RBCs to sickle blocking small vessels.
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Other Blood Related Disturbances
Polycythemia - abnormally high number of RBCs (8 - 11 million/mm 3). Increases bloodviscosity & blood pressure.Cause - most often the result of bonemarrow cancer.
Lecuopenia - abnormally low number of W BCs (less than 5,000/mm 3).Cause - drugs, steroids & anti-canceragents.
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Other Blood Related Disturbances
Leukemia - abnormally high numbers of immature W BCs that are mitotic &unspecialized.Named according to abnormal W BC typeinvolved Myelocytic - derived from myeloblasts
(chronic) Lymphocytic - involves lymphocytes (acute)
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Other Blood Related DisturbancesThrombus - a clot that forms & isstationary in an unbroken blood vessel.If sufficiently large, it may block the flow of blood downstream causing death of thosetissues.Embolus - an abnormal object movingthrough a blood vessel, ie. Clot, air bubble,
lipid droplet, etc.Embolism - a blockage of blood vessels causedby an embolus. May cause a stroke or heart
attack depending on tissues affected.
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Intrinsic Cardiac Conduction S ystemApproximately 1% of cardiac muscle cells are
autorhythmic rather than contractile
75/min
40-60/min
30/min
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Intrinsic Conduction S ystemFunction: initiate & distribute impulses so
heart depolarizes & contracts in orderlymanner from atria to ventricles.
SA node
AV node
Bundle of H is
Bundle Branches
Purkinje fibers
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EC G Deflection W aves
(Pacemaker) Atrial repolarization
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EC G Deflection W aves
1st Degree H eartBlock = P-Q intervallonger than 0. 2 seconds.
60 seconds 0.8 seconds = resting heart rate of 75 beats/minute
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EC G Deflection W aveIrregularities
Enlarg ed QR S =
H ypertrophy of
ventricles
G f
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EC G Deflection W aveIrregularities
Prolon ged QTInterval =
Repolarizationabnormalitiesincrease chancesof ventriculararrhythmias.
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EC G Deflection W aveIrregularities
Elevated T wave :
H yperkalemia
C G fl i W
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EC G Deflection W aveIrregularities
Flat T w ave :
H ypokalemia
or ischemia
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H eart Blocks
Normal EC G
3rd Degree Block
No P waves. Ratedetermined byautorhythmic cellsin ventricles
2 nd Degree Block Not a QR S foreach P wave
P
QR S
T
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Cardiac Cycle
All events associated with a single heart beat including atrial systole & diastolefollowed by ventricular systole & diastole.
(V. S ystole) (V. Diastole)
S ystolic BP
Diastolic BP
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EC G Deflection W aves60 seconds 0.8 seconds = resting heart rate of 75 beats/minute
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Frank S tarling Law of the H eart
The more cardiac muscle is stretched within physiological limits, the more forcibly it willcontract.
R ubber band analogyIncreasing volumes of blood in ventriclesincrease the stretch & thus the force
generated by ventricular wall contraction.Greater stretch means more blood volume is
pumped out, up to physical limits.
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Frank S tarling Law of the H eart
Increased blood volume =increased stretch of myocardium
=
Increased force to pump bloodout.
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Terms, Definitions & UnitsBlood Pressure - force generated againstarterial walls per unit of area in mm H g.S ystolic Pressure - peak arterial pressure .Averages about 1 2 0 mm H g in healthyadults.Diastolic Pressure - lowest arterialpressure . Averages between 70 - 80 mm
H g in healthy adults.Blood Volume - quantity of blood incardiovascular system . Varies from 4-5 L.
in females to 5-6 L. in males.
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Terms, Definitions & Units
Cardiac Output - the amount of bloodpumped by a ventricle per minute . Unitsmay be in milliliters or Liters per minute.H eart Rate - number of cardiac cycles perminute . Average for males = 64-7 2 /min.Average for females = 7 2 -80/min.
S troke Volume - amount of blood pumpedout of a ventricle each beat . Averageresting stroke volume = 70 ml.
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Blood volume increases due to increasedwater retention from increased AD H production, IVs or transfusions = BP
Blood volume loss due to injuries,hemorrhages, use of diuretics, etc. = BP
Blood Pressure = Blood Volume Peripheral Resistance
Factors influencing blood pressure
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Cardiac Output = circulating blood volume
Blood Pressure = Blood Volume Peripheral Resistance
Factors influencing blood pressure
Cardiac Output = H eart Rate S troke Volume
Increased heart rate caused by the release of epinephrine into blood by the adrenal glands =increased cardiac output, which increasescirculating blood volume, to increase blood
pressure.
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Vasodilation = diameter = resistance = BP
Peripheral Resistance affected by:
blood viscosity (thickness)
diameter of vessels (vasoconstriction/vasodilation)
Blood Pressure = Blood Volume Peripheral Resistance
Factors influencing blood pressure
Vasoconstriction = diameter = resistance = BP
Elastic Arterial W alls = BP
(Polycythemia)
elasticity of arterial walls
H l d
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BP - S timulates Cardioinhibitory center toheart rate & Vasomotor center to diameter.
H omeostatic Blood PressureRegulation Mechanisms
Medullary Reflex Centers: Cardioacceleratory - increases heart rate Cardioinhibitory - decreases heart rate Vasomotor - changes diameter of vessels
BP - S timulates Cardioacceleratory center toheart rate & Vasomotor center to diameter.
Baroreceptors in aortic arch & carotid sinuses: sensitive to changes in blood pressure.
H i l d
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in CO 2 or in O 2 stimulates Vasomotor
center to diameter (vasoconstrict) of vessels toBP.
H omeostatic Blood PressureRegulation Mechanisms
Medullary Reflex Centers: Cardioacceleratory - increases heart rate Cardioinhibitory - decreases heart rate Vasomotor - changes diameter of vessels
in CO 2 stimulates Vasomotor center to
diameter (vasodilate) of vessels to BP.
Chemoreceptors in aortic bodies & carotid bodies: sensitive to changes in CO 2 & O 2 in blood.
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Aneurysm
W eakness of the wall of an artery causingan abnormal enlargment or bulge.The aorta or the arteries that supply the
heart, brain, legs or kindeys are mostcommonly affected.
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Angina Pectoris
M edical term for chest pain due to coronaryheart disease.It occurs when the myocardium doesnt getas much blood (Oxygen) as it needs.Insufficient blood supply is called ischemia .
M ay initially occur during physicalexercise, stress, or extreme temperatures.It is a sign of increased risk of heart attack.
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H ypertension
High blood pressure. Sustained arterial blood pressure of 140/90mm Hg or above.
R ising diastolic pressure generallyindicative of progressive hardening of arteries.
Since the heart must work harder to pump blood against higher pressures, there isincreased risk of a cardiovascular accident.
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Hypotension
Abnormally low blood pressure. Sustained systolic blood pressure of below100 mm Hg.Generally associated with lower risk of cardiovascular accidents & long life
providing that the tissues are adequately perfused..
Ci l t S h k
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Circulatory S hock Blood vessels inadequately filled to
enable normal circulation & supply of O 2& nutrients.May result in death of cells & damage to
organs.Common Types:H ypovolemic - severe blood loss
Cardiogenic - heart (pump) failureVascular - excessive vasodilationS epticemic - vasodilation due to bacterial
toxins produced during an infection.
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Atherosclerosis (Arteriosclerosis) Narrowing and hardening of arteries andimpairment of blood flow due to thedeposition of fatty materials and calcium in
their walls. R isk factors include:
smoking
inactivity diabetes high blood cholesterol personal or family history of heart disease
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Arteriosclerosis (Atherosclerosis):
All images copyright C amera M .D . S tudios. S pecial thanks to
GregoryC
urfman,M
.D
..
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AcknowledgementsMost of the figures used in this presentation came from the Benjamin Cummings Digital Library
Version 2 .0 for H uman Anatomy & Physiology, Fifth Edition. Other figures came from publicdomain internet sources and software in the possession of the author.
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