a&p 2 unit 5 cardiovascular physiology

8/6/2019 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



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G ranulocyte - BasophilNucleus lobed - U or S shapedCytoplasmic granules large & basic -(purplish/black)

Cause vasodilation by the release of histamines



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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 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



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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Prolon ged QTInterval =

Repolarizationabnormalitiesincrease chancesof ventriculararrhythmias.


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Elevated T wave :

H yperkalemia

C G fl i W


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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



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)



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.

a&p 2 unit 5 cardiovascular physiology

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