'Aliah's Cardiovascular System

8/9/2019 'Aliah's Cardiovascular System

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CARDIOVASCULAR

SYSTEM


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HISTOLOGICAL FEATURES OF HEART & BLOOD VESSELS

PROPERTIES DETAILS

HEART

HEARTWALL

1. Epicardium:

y Equal to tunica adventitia of blood vessels & also known as visceral pericardium.

y Located outer to it is pericardial cavity which is enclosed by fibrous sac of parietal pericardium.

y Divided into 2 layers:a. Outermost layer (free surface):

A single layer of flat epithelial cells (mesothelial layer). Secretes a small amount of serous fluid for lubrication . b. Sub-epicardial layer: Thin layer of connective tissue (fibroelastic layer) with broad layer of adipose tissue. Contain blood vessels (coronary blood vessels) & autonomic nerves.

2. Myocardium:

y E shape: long & elongated.

y E nucleus: 1 0r 2 in no with centrally located & barrel in shape.

y E muscle fibers branch & interdigitate, but each is a complete unit surrounded by a cell membrane.

y Intercalated disks r present which provide a strong union b/w fibers, maintaining cell to cell cohesion to transmitcontraction.

y Present of sacromere & T tubules (diad formation).

y Power of regeneration is absent.

y E cardiac muscle is thick & compact in ventricles but loose in atria.

y Papillary muscles: extension of myocardium to stabilize e valves. 3. Endocardium:

y Near to e chamber of e heart.

y Lined by a single layer of flat endothelial cells.

y Acts as e heart supporting tissue (sub -endocardial layer): a delicate layer of collagenous tissue.

y Also acts as fibro-elastic layer: because of this layer, e endothelium cannot be damaged while myoc ardium incontraction.

y May have a small amount of fat (may or may not).

HEARTVALVES

y Leaflets of collagenous tissue which r covered by a thin layer of endothelial layer which is continuous with that of eheart chambers & great vessels.

y E collagenous tissue is tough central fibrous sheet called lamina fibrosa which represents a merging of e fibroelasticsupporting layers beneath e endothelium.

y At e attached margins of each valve, e lamina fibrosa becomes condensed to form fibrous ring (valve annulus)& erings of e 4 valves together to form a central cardiac skeleton.

CONDUCTINGSYSTEM

1. AV & SANodes:

y Embedded in dense vascular connective tissue.

y Rich in ANS fibers.

y Small specialized myocardial fibers with electrochemical stimuli being transmitted via gap junction .2. Purkinje fibers:

y Modified cardiac muscle.

y Specialized conducting system for e contraction of e myocardium.

y Located subendocardially & r bundle in form .y E cells r larger, sometimes binucleate, & have an extensive cytoplasm.

y No T tubules system seen with electron microscope.

y Have fewer myofibrils which r distributed peripherally, leaving a perinuclear zone of comparatively clearsarcoplasm.

CLINICALCORRELATION

1. Cardiac muscles:a. Cardiac hypertrophy: no increase in myocardial fibers number but increase in size only. b. Heart damage: no regeneration of cardiac muscle tissue if damaged.Dead muscle cells r replaced by fibrous

connective tissue.c. Cardiac contraction: lack of calcium ions in e extracellular compartment leads to cessation of cardiac muscle

contraction within in one minute.d. Energy: total anerobic condition cannot sustain ventricular contraction (only up to 12% during hypoxia).

2. Endothelial cells: abnormal endothelial functions can cause hemorrhage, thrombosis, & exudation.

GENERAL FEATURES OF ARTERIES & VEINS

y Basically, arteries & veins have 3 layers of vascular walls from e lumen to outward:1. Tunica intima (consists of 3 layers) :

a. E endothelium:

Properties: Flat polygonal cells. Numerous pynocytic vesicles. Specialized membrane bound organelles called Weibel Palade bodies which store von Willebrand factor (VIII) in

coagulation cascade. Functions:

Acts as permeability barrier & basement membrane maintenance (collagen & proteoglycans). Promotes protective thrombus formation by secreting Willebrand factor (VIII). Produces vasoactive substances (for blood flow control such as protacyclin & N2O), growth factors for fibroblasts & platelets,

and stimulating factors for blood cells colony.b. E basal lamina of e endothelial cells.c. E subendothelial layer:

Consists of loose connective tissues occasionally with smooth muscle. Contains a sheet-like layer or lamella of fenestrated elastic material called internal elastic lamina (IEL). Fenestrations enable substances to diffuse readily through e layer & reach cells deep within e wal l of e vessel.


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Contains fibroblasts & myointimal cells which produce extra-cellular constituents.Lipid accumulation inside e myointimal cellswith increased age causes arthrosclerosis .

2. Tunica media: Consists of circumferentially arranged layers of smooth muscle cells which produce all of e extracellular components of e lay er. Variable amounts of elastin, reticular fibers, & proteoglycan r interposed b/w e smooth muscle cells of tunica media. There is external elastic lamina consists of elastin which separates tunica media from tunica adventitia.

3. Tunica adventitia: Composed of longitudinally arranged colagenous tissue & a few elastic fibers. Contains vasa vasorum that supply blood to e vascular walls as well as autonomic nerves called nervi vascularis that control e

contraction of e smooth muscle of e vessels.

ARTERIESPROPERTIES TUNICA

ADVENTITIATUNICAMEDIA TUNICAINTIMA EEL IEL EXAMPLES

ELASTICARTERIES

1.Connectivetissue.

2.Elastic fibers.3.Thinner than

tunica media.4.Vasa vasorum

Smooth muscle.

1.Endothelium.2.Connective

tissue.3.Smooth muscle.

Aorta & its major branches.

MUSCULARARTERIES

Smooth muscle (8 10) & collagen

fibers.

butlittle.

Baranches of elastic arteries &

distributing arteries.

ARTERIOLES Thin & ill-defined. Smooth muscle( loosely connective tissues in portal vein & compact connective tissue inother veins.

3. Tunica intima:

y Endothelium with small amount of connective tissue.

y Internal elastic lamina present but not well developed like in artery. 4. Examples: IVC, SVC, pulmonary trunk, & vena cava .

PROPERTIES TUNICAADVENTITIA TUNICAMEDIA TUNICAINTIMA EXAMPLES

MEDIUMSIZED VEINS

1. Connective tissue.2. Some elastic fibers.

3. Thicker thantunica media.

1.Smooth muscle (2 15 layers).

2.Collagen fibers.

1.Endothelium.2.Connective tissue.3.Smooth muscle.

Branches of large veins.

VENULES Smooth muscle (1 -2layers).

1.Endothelium.2.Pericytes.

Muscular & postcapillary veins.

CAPILLARIES

TYPES

y E smallest blood vessel with average diameter of 8 m (1/2 of e diameter ofRBC).

y Range of size 3 4 m to 30 40 m.

y Types of capillaries:1. Continuous capillaries: Found in muscles, lungs, & CNS. Numerous pinocytic vesicles underlie both e luminal & basal plasma membrane surfaces for e transportation of

materials b/w e lumen & e connective tissue. In some capillaries, pericytes (unspecialized cell s) may be associated with e endothelium .It can give rise to

smooth muscle cells during vessel growth. 2. Fenestrated capillaries:

Found in endocrine glands & sites of fluid & metabolite absorption such as gallbladder , kidney, & GIT. E fenestration provides channels across e capillary wall.It may have a thin, membranous diaphragm across its

opening with a central thickening.3. Sinusoidal capillaries:

Found in liver, spleen, & bone marrow . They r larger in diameter & > irregularly shaped than other capillaries. Eg: Kupffer cells & Ito cells in e liver occur in e association with e endothelial cells.

MICRO-

CIRCULATION

y Blood flow of microcirculation is d/t muscle contraction:1. Arterioles.2. Metarterioles: large diameter capillaries with discontinuous layer of smooth muscle cells.

3. Precapillary sphincter: a sphincter of smooth muscle which is located at their origin from either an arterioles ormetarterioles.It controls e amount of blood passing through e capil lary bed. 4. AV shunts: allow blood to bypass capillaries by providing direct routes b/w arteries & veins.Commonly found in skin.

y Controlled by: ANS, circulating hormones (adrenaline), O2 concentration, & metabolites (lactic acids).

CLINICAL CORRELATION

1. Endothelial cells with Weibel Palades bodies covered by glycoprotein:

y Contain von Willebrand factor which facilitates coagulation cascade.

y Manufactured by most of endothelial cells but it i s stored only in arteries.

y Persons with von Willebrand disease (inherited disorder) have prolonged coagulation times & excessive bleeding at an injury s ite.2. Weakened vessel wall d/t embryological disease or connective tissue disorders:

y Will cause balloon out at e affected site, forming an aneurysm.

y If ruptured can cause death.


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THE GROSS ANATOMY OF THE HEART

POINTS EXPLANATION

SURFACES1. Anterior (sternocostal) surface: mainly by Rt. ventricle.2. Diaphragmatic (inf. surface): mainly by Lt. ventricle, &

partly Rt. ventricle.

3. Lt.Pulmonary surface: mainly by Lt. ventricle (cardiac impressionofLt. lung).

4. Rt.Pulmonary surface: mainly by Rt. atrium.

BORDERS

1. Rt. border (slightly convex): b/w Rt. atrium whichextends b/w SVC & IVC.

2. Inf. border (oblique, nearly horizontal): mainly by Rt.ventricle, n slightly by Lt. ventricle.

3. Lt. border (nearly vertical): mainly by Lt. ventricle n slightly by Lt.auricle.

4. Sup. border: by Lt. n Rt. atria n auricle in ant.View & post. toaorta n pulmonary trunk n ant. to SVC, inf. to T. sinus.

APEX - Formed by inferolateral part ofLt. ventricle. - Remain motionless throughout cardiac cycle.- Lies post. to e Lt.5th interostal space n 9 cm from median pl. - Place where sound of mitral valve closure are maximal : apex beat

BASE

y Hearts post. aspect (opposite apex) which is f ormed mainly by Lt. atrium, lesser by Rt. atrium

y Faces post. towards e bodies of vertebrae T6 -T9 & is separated from them by pericardium, oblique sinus, esophagus, & aorta.

y Extends sup. to e bifurcation of pulmonary trunk n inf. to coronary groove.

y Receives pulmonary veins on Rt. n Lt. side ofLt. atrial n sup. n inf. venae cavae at sup. n inf. ends of its R t. atrial position.

FIBROUSSKELETON

y Properties: Complex framework of dense collagen

forming 4 fibrous rings. Surround e orifices of e valves, Rt. n Lt.

trigone, membranous part of interartrial &interventricular septa.

y Functions:1. Keep e AV orifices & semilunar valves patent n prevent them from

overly distended by blood volume.2. Provides attachment for leaflets & cups of valves as well as for

myocardium.3. Forms an electrical insulator by separating myenterically conducted

impulses of atria & ventricles.

LAYERS OFWALL

1. Endocardium: thin internal layer (endothelium n subendothelium) which is e lining membrane of e heart & its valves.2. Myocardium: thick, helical middle layer which composed of cardiac muscle. 3. Epicardium: thin external layer (mesothelium) which is formed by visceral layer of serous pericardium.

CHAMBERSRIGHT

ATRIUM

y Part: Receives venous blood from SVC, IVC, n coronary sinus. Rt. auricle: conical muscular pouch that projects from this chamber: Increasing

capacity of atrium as it overlaps e aorta. Has Rt.AV orifice where Rt. atrium discharges e blood to Rt. ventricle.

y Interior surface ofRt. atrium: Has smooth, thin walled, post, part (sinus venarum). Has rough, muscular ant. wall of musculi pectinati. Separated by ext: sallow vertical groove, sulcus terminalis, int: crista terminalis .

y Openings:1. SVC: into sup. part at 3 rd costal cartilage.2. IVC: into inf. part at 5 th costal cartilage.3. Coronary sinus: b/w Rt.AV orifice n IVC orifice. 4. Tricuspid O., Ant. carciad vein, n Venae cordis minimae.

y Others:1. Fossa ovalis: - Oval, thumbprint

depression ofIAseptum.(Surrounding ridge:Limbus FO).

2. SA node: at sup. end of sulcusterminalis, near junction with Rt.side ofSVC.

3. AV node: at IA septum, aboveattachment of septal cusp of3cuspid valve n to e Lt. ofopening of coronary sinus.

LEFTATRIUM

y Lt. auricle: Tubular, muscular, n its wall trabeculated with pectinate muscle (musculi pectinati). Form sup. part of heart, n overlaps root of pulmonary T. E remains ofLt. part of primodial atrium.

y Interior surface ofLt atrium: Larger, smooth-walled part: sinus venarum. Rough, muscular part: musculi pectinati ( ori.Auricular chamber of embryonic heart). Semilunar (oval thin) depression in IA setum: Fossa ovalis (surrounding ridge is valve of fossa ovalis).

y Others: A slightly thicker wall than that of e right atrium where e 4 pulmonary veins (2 sup. n 2 inf.) entering its smooth post. wal l. Has IA septum that slopes post. n to e right & e mitral V. replaces its ant. wall n leads to Lt. ventricle.

VENTRICLES Walls AVValves Papillary Muscle(PM)

Moderator Band (MB) Blood Pathway

RIGHT

VENTRICLE

1. Sup. - Conusarteriosus: an arterialcone which leads topulmonary trunk(infundibulum).

2.Int. - Trabeculaecarnae: Irregular

muscular elevations,3 pt.PM, CT, n MB.3.Supraventicular crest:

separates inflow(rough) pt. fromoutflow (smooth) pt.

4.Rt. ventricle less thickn lower in pressure.

y Guards AV orifice,AVO(4th-5thICS)

y Bases attached tofibrous ring which keepse caliber of orificeconstant .

y Chordae tendineae(CT) attached to cups

at free edges nventricular surfaces narises from e apices ofPM.

y Attachment to 2 cupsprevents theirseparation n inversionwhen tension is appliedto chordae tendinae.

1. Ant.PM: largest nmore prominent,from ant. wall,CT attaches toant. n post. cuspsof tricuspid valve.

2. Post.PM: smaller,consists of severalpt., from inf. wall,

CT attaches topost. n septalcusps of tricuspidvalve.

3. Septal PM: fromIV septum, CTattaches to ant. nseptal cusp oftricuspid valve.

A curved muscularbundle that traversesRt. ventricular chamberfrom inf. pt. ofIVS to e

base ofPM, carries pt ofRt. branch ofAVbundle.

yU-shaped pathway.

y Inflow of blood intoRt.

yVentricle enters post.

through AVO. Whenventricle contracts, eoutflow of blood intopulmonary T. leavessup. n to e Lt.


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LEFTVENTRICLE

y2 to 3 times as thickas of that Rt.ventricle.

yMostly covered withtrabeculae carnae:finer n > numerousthan Rt. ventricle.

yA conial cavity longerthan Rt. ventricle.

y Inflow (rough) pt.from outflow(smooth) pt.

y Double mitral valves,:post to sternum (4 thcostal cartilage), 2 cups:ant. & post.

y 3 PM n CT support MVto resists e pressureduring contraction ofLt.V.

y CTs become taut beforen during systole toprevent cusps into Lt.

atrium.y Ant. cup larger than

post. cusp: attached tofibrous ring.

Ant. & Post.PMs arelarger than Rt.ventricle.

Other - Aortic orifice:Lies in its Rt.posterosuperior pt. nsurrounded by fibrousring to which Rt., post.,n Lt. cusps of aorticvalve r attached-aorta

begins

yV-shaped pathway.

yAs blood traversesLt.ventricle, it undergoes2 Rt. angle turns,which result in 180ochange in direction.This reversal takesplace around ant.

cusp ofMV.

VALVES

1. Semilunar valve:a. Concave when viewed sup, n dont have CT to support them. b. Smaller in area than e cusps ofAV valves. c. Force exerted on them is less than half that exerted on AV valves. d. E cusps project into artery but are pressed toward its wall. e. E cups open up like pockets as they catch e reversed blood flow, coming together to completely close e orifice, supporting

each other n preventing any returning blood . f. E edge of each cusp is thickened (contact region) forming lunule. g. A sinus is a space at e origin of pulmonary T. n ascending aorta b/w dilated wall of vessel n each cusp of e semilunar valves. h. Rt. n Lt. aortic sinus: Rt. n Lt. coronary artery.No artery at pulmonary sinus.

2. Aortic valve:

y B/w Lt. ventricle n ascending aorta, post . to Lt. side of sternum at 3 rd ICS.

y Obliquely placed & has post., Rt., n Lt. cups.3. Pulmonary valve:

y At e apex of conus arteriosus at 3 rd costal cartilage.

y Has Ant., Rt., n Lt. cups.

CONDUCTINGSYSTEM

1. SA node (sinuatrial node) = Pace maker of the heart:

y Specialized type of cardiac muscle fibers.5mm at its widest part.

y Develops from e wall of the sinus venosus of e developing heart.

y Supplied by both divisions of e ANS.

y Regulates the heart to beat at 70 beats/min . & lies in the Right atrium just below the S.V.C. near e top of crista ter minalis.2. AV node(atrioventricular node): lies in e interatrial septum above and to e left of the opening of e coronary sinus.3. AVBundle = Atrio-ventricular bundle of (His) Purkinje bundle:

y Runs through the membranous part of e IVS which bridge between e atrial & e ventricular muscle tissue.

y Divided into Rt.And Lt. limbs at the junction b/w emembranous and muscular part ofIVS.

y Supply: anterior papillary muscle + ventricles walls.4. E conducting pathway:

y Impulse from SA node atrias muscles (contract) AV nodeAv bundle fibrous skeleton IV (membranous) inf.

border (lies inf. to septal cusp of 3cuspid valve Junction of membranous n muscular:a. Rt.Branches septomarginal band ant. papillary muscleant. wall of ventriclePurkinje fibre beneath

endocardium contraction of ventricular muscles. b. Lt. branches septal endocardium papillary muscle chordae tendinae drawing AV valves together

contraction of ventricular muscles.

CARDIACREFFERED

PAIN

y Pain originating at nociceptors at one site in e body (deep/visceral) is sensed as originating at another site (usually supercial).

y Referred to superficial regions sharing e same dorsal root as e deep/visceral site from which e pain actually orig inated.

y E pain of angina pectoris n myocardial infarction radiates from:1. Substernal region.2. Lt. pectoral region to Lt. shoulder .3. Medial aspect of e Lt. arm.

y E heart is insentitive to touch, cold, cutting, & heat.

y Ischaemia n accumulations of metabolic products stimulate pain endings in myocardium.

y CRP: Lt. side of chest n medial aspect ofLt. arm. Commissural neurons may make synaptic contacts with e Rt. side of ecomparable area of e cord.This why CRP may be referred to Rt. or both sides.

NERVESUPPLYOFTHEHEART

Cardiac Plexus ParasymphatheticSympathetic Supply

Presynaptic fibers- Cell bodies in intermediolateral

columns (IMLs) of sup. 5/6segments of spinal cord.

Postsynaptic fibers- Cell bodies in e cervical n sup.

thoracic paravebtebral gangliaof s m athetic trunk.

- Traversecardiopulmonary

splanchnic nerves ncardiac plexus toend in SA n AV

Increase:

1) Rate of polarization of SAnode.

2) Atrioventricular conduction.3) Atrial n ventricular

- From presynaptic fibers ofVagus nerves.

- Postsynaptic cell bodies inatrial wall n interatrial septumnear SA n AV nodes n along

coronary artery.

- Decrease:1) Heart rate

2) Force of contraction- Constrict coronary artery:

Saving energy b/w periods ofincreased demand.

SuperficialCardiac Plexus

- lies on aorticarch b/w

phrenic nvagus nerves

Deep CardiacPlexus

- lies to e Rt. ofligamentum

arteriosum, inf.n medial aortic

arch.

Vagus cardiacbranches:

- Sup. n inf. fromcervical region.

- Recurrentlaryngeal nerve.


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A

E

A

S

Y

E

EA

.

A E Y G SE S A AS SES

t. oronary Artery( A) Rt. aorticsinusFollowscoronary (A

) groov

b/w atria nv

ntricleRt. atriu

!, SAnA

nodes,n post. part of IVS

Circu!

flex n ant. IV branchesof Lt. coronaryA.

SA

odal RCAnear its origin(60%)

Ascendsto SAnodePulmonarytrunkn SA

node

t.

arginal RCA

Passesto inf. margin ofheartnapex

Rt. ventricle n apex IV branches

"ost.

nterventricular RCA (6

#

%) Runs post. IV groove to apexRt. n Lt. ventriclesn post.

thi

rd of IVS

Ant. IV branch of Lt. coronary

art

ery (at

apex)

A$ odal RCAnear origin ofpost. IV artery

Passesto AV node AV node

% t. oronary Artery(% A) Lt. aorticsinusRunsinAV groove n gives offant. IV ncircumflex branches

&ost of Lt. atrium n

ventricle, IVS,AV bundlesRCA

SA

odal Circumflex branch(40%)

Ascends on post. surface of Lt.atrium to SAnode

Lt. atrium n SAnode

Ant. nterventricular LCAPasses along ant. IV groove to

apexRt. n Lt. ventriclesn ant.

2 thirds of IVSPost. IV branch ofRCA (at

apex)

ircumflex LCAPassesto Lt. inAV groove nrunsto post. surface ofheart

Lt. atrium nventricle RCA

% t. arginal Circumflex branch Follows Lt. border ofheart Lt. ventricle IV branches

"ost.

nterventricular LCA

Runsin post. IV groove toapex

Rt. n Lt. ventriclesn post.third of IVS

Ant. IV branch of LCA (apex)

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Coronary Sinus

Great Cardiac Vein- Begins near e apex n ascends with e

ant. IV branch of LCA.- Its 2ndpart runs along Lt. side ofheart with e circumflex ofLCA to

coronary sinus.

- Drain most areas supplied by LCA

Middle Cardiac Vein- accompanies post. IV

artery branch- Post. interventricular

Post. Lt. ventricular veinAnt. Cardiac Vein- drains ant. aspect

of Rt. atrium nventricle beforecrossinf RCA to

Oblique vein of Lt. atriumSmall, merges with great cardiac

vein to form coronary sinus.

Small cardiac vein- Open directly to chambers of

heart(atria).


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Post. ) iew

0 1EPE

2 3 4A

2 5 3 6 7

PROPERTIES EX PLA8

ATION

PERICARDIUMy A fibro serous membrane thatcovers e heart at e beginning of its greatvessels.

y Aclosed saccomposed of 2 layers: ext. fibrous,int. serous.

y Influenced by e movement of e heartn greatvessels,sternum,n diaphragm.

FIBROUSLAYER(FP)

y Tough ext. layer.

y Continuousinf. withcentral tendon of diaphragm (pericardiophrenic ligament.

y Contin

uoussup. with

et

unic

a adventiti

a of great

vessels ent

erin

gn

leavin

gth

eh

eart

n

pret

rach

eal layer of deepc

ervic

al fasci

a.y Bound post. by loose connective tissue to structuresin post.mediastinum.

y Attached ant. to e post. surface of sternum bysternopericardial ligament.

y Protectsheart againstsudden overfilling (itsunyielding,closely related to greatvessels).

SEROUSLAYER(SP)

9

. Serous layer (general):Asingle layer of flattened mesothelium cells forming simple squamous ephitelium that lines bothint.surface of fibrous p. n ext. surf. ofheart.

2. Parietal layer:

y Lines with e int. surface of fibrous pericardium.

y Reflected onto heart at greatvessels: aorta, pulmonarytrunk, IVC.,nSVC.3. Visceral layer:

y Makesup e epicardium (outermost).

y Extend onto e beginning of greatvessels.

y Tranverse pericardial sinus: lies b/w group of aorta n pulmonarytrunkn group of SVC, IVC,n pulmonaryveinsn e reflectionof SP around them.

y Oblique pericardial sinus:Bounded laterally by pericardial reflectionsurrounding pulmonaryveinn IVC n post. bypericardium overlying e ant. aspect of esophagus. Its a blind sac.

y Its a wide pocket-like recessin pericardial cavity post. to e base ofheart, formed by Lt. atrium.

PERICARDIALCA

@ITY(PC)

y Is a potential space b/w parietal serous layer nvisceral serous layer.

y Contains a thin film of fluid that enables e heartto move n beatin a frictionless movement.

ARTERIALSUPPLY

A

. Branch of internal thoraciccavity: pericardiophrenic artery.2. Bronchial, esophageal,nsup. phrenic artery ofthoracic aorta.3. Musculophrenic artery: branch of internal thoracic artery.4. Coronary arteries.

VENOUSSUPPLY

B

. Pericardiophrenicveins:tributaries of barchiocephalicveins.2. Variable tributaries of e azygosvenoussystem.

NERVESUPPLY

C

. Phrenicnerves (C3-C5) (sensory fibres).2. Sympathetictrunks for vasomotor function.3. Vagusnerves.

Marginal a.

Ant.View

Right coronary a.

Anterior interventricular a.

CoronarySinus

Great Cardiac Vein

Inf.View

Lt atrium

BordersoftheHeart

Lt. SurfaceRt. Border

Lt. Border

Inf. Border

Ant. Border


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THE BODY FLUID

PROPERTIES EXPLANATION

OVERVIEW

y Definition: Body water n i ts dissolved substances. 60% of body weight is due to body fluid.In 70 kg man, 42 kg isdue to BF.

y Calculation: Total BF = Plasma Volume x 100 > Plasma Volume = 3500 mL.100 haematocrit > Haematocrit = e % of blood cells volume .

COMPARTMENTS

1. Intracellular Fluid (ICF)

y Fluid inside e cells. 40% of body weight (25L).

y Is measured using D2O, 3H20, n aminopyrine.

y Calculation: V= BF ECF.2. Extracellular Fluid (ECF)

y Fluid outside e cells. 20% of body weight (15L).

y Is measured using insulin, mannitol, n sucrose (difficult to measure because e limits of thin space are ill-defined).

y 2 divisions:a. Inside vascular system (25% of ECF n 3 L) :

i. Plasma measured using Evans Blue which bound to plasma proteins. ii. Blood cells measured by using tagged blood cells.

b. Outside vascular system (75% of ECF n 12 L). Known as interstitial fluid. Found in synovial joints, bathing cells, as well as ant. & post. sites of cells.

COMPOSITIONS

1. Mainly water (excellent solvent).

y Carries nutrients n waste products into n out of bodycells.

y Participate in chemical digestion.

y Acts as lubricant such as mucus in respiratory tract.

2. Electrolytes (ions) n non-electrolytes (urea,glucose, etc).

y Control osmosis of water b/w compartments.

y Maintain acid-base balance.

y Cellular excitability.

FACTORS

DETERMINEAMOUNT OF BF

1. Weight of e body (2/3 is due to BF).2. Sex: for male n female of e same body weight, male has greater fluid volume than female (amount of water in

adipose tissue is low compared to muscle).3. Age: infant is 75% is BF while adult is 60% is BF.

PRESSUREPROPERTIES

1. Hydrostatic pressure: pressure exerted by water (blood pressure) . 2. Oncotic pressure or colloid osmotic pressure: pressure exerted by plasma protein n colloids . 3. Osmotic pressure: pressure necessary to prevent solvent migration to e concentrated region . 4. Osmoles: concentration of osmotically active particles. 5. Osmolarity: no. of osmoles per liter of solvent.6. Osmolality: no. of osmoles per kg of solvent.

pH OF BF

y Definition: Negative logarithm of proton (H+) .

y pH of pure water at 25oC, in which H+ n OH- present in equal no. is 7.

y For each pH unit less than 7, e H+ concentration is increased 10 folds, n for each pH unit above 7, it is decreased 10folds.

BUFFERSYSTEM

y A buffer is a substance that has e ability to bind or releaseH + in solution, thus keeping e pH of e solution relativelyconstant despite e addition of considerable quantity of acid n base.

y Buffer system ofBF: carbonic acid, H2CO3 n plasma protein.

CHEMICALCONSTITUENTS& ELECTROLYTEDISTRIBUTION

y Electrolytes distribution in ECF n ICF is maintained by:

1. Selectively permeable membrane (fully, semi, n impermeable).2. Sodium-potassium pump maintains sodium n potassium ions concentration in ECF n ICF.

y Factors affecting e passage of molecules across e membrane:1. Molecular size (inversely proportionate).2. Solubility in lipids.

TONICITY

y Distribution of water inside n outside of cells is dependent on osmotic pressure.Normally, osmolarity inside n outsidee cells is equal: 290 300 mosm/L (ECF: 80% due to sodium n chloride ions, n ICF: > 50% due to potassium ions).

y Tonicity: term to describe e osmolarity of a solution relative to plasma. 1. Isotonitic: solution that has e same osmolarit y with plasma.2. Hypotonic: solution with lesser osmolarity than plasma.3. Hypertonic: solution with greater osmolarity than plasma.

APLLIEDPHYSIOLOGY

OEDEMA

y Definition: E abnormal collection of fluid in e interstitial spaces.

y 3 main causes:1. Increased capillary hydrostatic pressure due to obstruction of blood in venous system. Eg: failure ofRt.

ventricle.2. A decreased in e plasma colloid osmotic pressure. Eg: excessive loss of albumin in e urine (kidney disease). 3. Obstruction of lymph vessels accumulation of albumin in interstitial space.As a result: significant rise in colloid

osmotic pressure of e interstitial fluid n eventually becomes oedema.

Filtration Absor tion

Capillary: 25 mm Hg

VenD le: 10 mmArteriE le: 32 mm

Interstitial Fluid

MICROCIRCULATION

TISSUE FLUID EXCHANGE

1) Hydrostatic pressure is higher in capillaries than in tissue space n tends to drive fluid out ofcapillaries by filtration (outward).

2) Colloid pressure is higher in blood plasma than in interstitial fluid because plasma proteinsr retained inside it.This tends to draw water out of capillaries by osmosis (inward).

3) Colloid pressure is uniform throughout capillary length whi le hydrostatic pressure falls fromarteriolar to venular end.

4) Thus, at arteriolar end, water is mainly filtrated, while at venular end, water is reabsorbedback.This is important to maintain blood volume.

5) In lungs, capillary hydrostatic pressure is lesser than colloid osmotic pressure, thereforethere is no filtration to keep e alveoli wet .

6) In kidneys, hydrostatic pressure is higher than colloid osmotic pressure, therefore filtrationtakes place w/o absorption.

7) About 90% of fluid filt rated into interstitial space is goes back to circulation n 10% i sdrained via lymphatic vessels.


9/40

1= Depolarization (Na+ entry: Permeability to K+).

2 = Early rapid repolarization.

3 =Plateau phase (Ca2+ - Na+ open: Ca2+ influx).

4= Repolarization (Ca2+ - Na+ close: Ca2+ influx, Permeability

to K+ ).

5 = Base Line.

CONTRACTILE RESPONSE

ACTION POTENTIAL

ACTION POTENTIAL

Resting membrane potential = =90 mV

Electrical activity of pacemaker: stimulus

Membrane of a ventricular myocardial contractile is excited over -70 mV(threshold potential) generates action potential.

Explosive increase in membrane permeability to Na+ n a subsequent

massive Na+ influx (opening ofNa+ channels)

Rapid depolarization 2 msec (overshoot)

Early rapid repolarization (closure ofNa+ channels)

Subsequent prolonged plateau 250 msec (Opening ofCa2+ - Na+channels slow inward diffusion ofCa2+ n a marked decrease in K+

permeability).

Late rapid repolarization (inactivation ofCa2+ - Na+ channels diminishesslow n inward movement ofCa2+ n activation of K+ channels promotes

rapid outward movement of K+)

Inside of e cell: negativeOutside of e cell: positive

- Result in resting membrane potential = -90 mV

- Significance of plateau phase: Cardiac muscle cannot be excited againduring action potential.Thus, tetanus will not occur, which will ensure

safety supply of oxygen throughout e body.

THE CARDIOVASCULAR PHYSIOLOGY

PORTIONS EXPLANATION

FUNCTIONS

y Transportation of respiratory gases, nutrients, hormones, n enzymes to all cells of e body, as well as transportation ofwaste materials from cells to e lungs n kidneys for elimination.

y Body temperature regulation:1. Blood vessels constrict to retain body heat. 2. Blood vessels dilate to dissipate heat at skin surface.

y Body protection: Protect through immune system, blood cells, n etc.

HEART

y Separated into 4 chambers by a single fibrous skeleton which comprises of 4 interconnected rings of dense

connective tissue.y 4 chambers: Rt. n Lt. atria n Rt. n Lt. ventricles.

y 4 valves:1. Atrioventricular valves: Rt. Tricuspid, Lt. Mitral.2. Semilunar valves: Rt.Pulmonary, Lt. Aortic.

CARDIACMUSCLE

y 3 types:1. Atrial muscle.2. Ventricular muscle.3. Specialized conducting fibres.

y Microscopic appearance:1. Striated in appearance like skeletal muscle.2. Roughly quadrangular n usually have only a single centrally located nucleus.3. Muscle fibers branch n connected to each other by intercalated disk (provide a strong union b/w fibers,

maintaining cell-to-cell cohesion, so that e pull of 1 contractile unit can be transmitted along its axis to e next)which contain desmosomes n gap junction (provide low-resistance bridges for e spread of excitation from onefiber to another).

4. Close contact with large no. of elongated mitochondria.

PROPERTIES OFCARDIACMUSCLE

1. Autorhythmicity:

y E ability to generate electrical impulses spontaneously n rhythmically. y Under normal resting condition, cardiac muscle can contract n relax continuously n rhythmically w/o stopping.

y It contracts w/o extrinsive nerve or hormonal stimulation, but these reactions can cause increased or decreaseddischarge.

2. Conductivity:

y E ability of e heart muscle to conduct nerve impulses around its fibers.

y It is conducted by specialized conducting system.3. Excitability:

y E ability of heart muscle to respond to a stimulus.

y Cardiac muscle has extra-long rsting potential.4. Contractility: Cardiac muscle remains contracted (depolarized) longer than skeletal muscle due to prolonged

delivery of calcium ions from sarcoplasmic reticulum n ECF.

EFFECTS OF ECFIN CARDIACFUNCTION

y Decreased temperature of ECF: decreased cellular metabolism, lower heart rate, n strength of cardiac contraction.

y Variation in ECF electrolyte concentration has a direct effect on membrane potential of cardiac cells.

y Cardiac muscles are sensitive to ECF calcium concentration.

ABNORMALITIES

1. Hypercalcaemia: cardiac muscles become extremely excitable.Its contraction ism powerful n prolonged (can be

fatal, stop in systole).2. Hypocalcaemia: less excitable weak contraction weak heart beat.

1

2

3

+ 40

+ 20

0

- 20

- 40

- 60

- 70- 90

5

4

MembranePotential(mv)


10/40

THE CARDIAC OUTPUT


OVERVIEW

y Definition: Amount of blood ejected from Lt. or Rt. ventricles into e aorta or pulmonary trunk per minute respectively (i.e.amount of blood ejected by each ventricle, not e total amount pumped by both ventricles).

y Means that volume of blood flowing through pulmonary circulation is equivalent to e blood flowing through e systemic one.

EQUATION

y Cardiac Output, CO = Stroke Volume, SV x Heart Rate, HR

y At rest, SV = 70 mL, HR= 75 beats/min, so, CO = 70 x 75 = 5.25L/min.

y During exercise, CO can be increased 4-5 folds.

y Cardiac reserve = (Maximum volume of blood e heart is capable to pump) (CO at rest).

REGULATION

STROKE VOLUME

END DIASTOLIC VOLUME

y Frank-Starling Law of e heart: Energy of contraction is proportional to e initial length of e cardiac muscle fibers.

y E resting length of cardiac muscle < optimal length.y Thus, in initial cardiac muscle length (stretch), e contractile tension of e heart following systole .

y Cardiac muscle length increases with increasing EDV.y EDV cardiac muscle length Vigor (strength of cardiac muscle expulsion of greater blood volume into aorta

stroke volume cardiac output.

y Factors affecting EDV:1. Venous return (VR): VR, EDV.

Sympathetic stimulation produces venous vasoconstriction venous pressure venous filling capacity VR. Skeletal muscle pump: Muscular activities venous filling capacity venous pressure VR. Respiratory pump: Pressure different (Lower p ressure in chest wall, but higher in abdomen n limbs) squeezes

blood from lower to chest veins VR. During ventricular contraction, atrial cavities atrial pressure vein to atria pressure ratio VR total circulating blood volume VR.

2. Atrial contraction: e greater e atrial contraction, e greater will be e ventricular filling, e greater VR (but not that 70% ofventricular occurs passively before atrial contraction).

3. Distensibility of ventricles: pericardial temponade, myocardial infarction, n myocardial infiltrative disease all decreaseventricular distensibility, & reduce VR.

4. Duration of diastole: e longer e duration of diastole, e longer e blood filling into ventricles, e higher VR.

HEART CONTRACTION OR MYOCARDIAL ACTIVITYRelated to e extrinsic control by factors which are originating outside e heart, mainly e action of cardiac sympathetic nerve n

hormonal action.

SYMPATHETIC STIMULATION PARASYMPATHETIC STIMULATION

Sympathetic stimulation.

Release of ephinephrine, norephinephrine, n dopamine.

Increased Ca2+ influx into cytoplasm from sarcoplasmic reticulum nECF.

Cardiac muscles generate > contraction force through greater cross -bridge cycling.

> rapid n > forceful contraction of ventricles.

Increased stroke volume (Inotropic Effect).

Increased cardiac output.

Parasympathetic stimulation.

Release of acetylcholine.

Decreased Ca2+ influx into cytoplasm.

Reduced myocardial (atrial muscle) contraction.

Reduced stroke volume.

Reduced cardiac output.

HEART RATE

y Primarily determined by rate of spontaneous depolarization ofSA node.

y Determinants:1. ANS that innervate SA node. 3. Plasma electrolytes.2. Hormone thyroxine. 4. Body temperature.

y Sympathetic Effect: Sympathetic stimulation release of ephinephrine increased Ca2+ influx into cytoplasm increasedrate of spontaneous depolarization shorthened e time required for SA node to reach threshold SA node fires morefrequently increase heart rate (Chromotropic Effect).

y Parasympathetic Effect: Parasympathetic stimulation release of acetylcholine increased membranes permeabilitytowards K+ > K+ ions efflux decreased rate of spontaneous depolarization prolonged e time required for SA node toreach threshold SA node fires less frequently decreased heart rate.

CLINICALCORRELATION

1. Hypertension.

y A condition due to e chronic elevated atrial blood pressure.

y Heart need to generate more pressure in order to eject a normal cardiac output.

y Heart may be able to compensate for a sustained increase in afterload by enlarging (hyperthrophy).2. Heart failure.

y Refers to e inability of e cardiac output to keep pace with bodys demand for supplies n removal of wastes.

y Either 1 or both ventricles may progressively weaken n fail.

y When a failing ventricle is unable to pump blood out, e veins behind it wi ll be congested with blood.

y 2 most common reasons of heart failure:a. Damage to e heart muscle as a result of a heart attack or impaired circulation to e cardiac muscle.b. Prolonged pumping against a chronically increased afterload or sustained elevation in blood pressure.


11/40

THE CARDIAC CONDUCTING SYSTEM

F


OVERVIEW y Composed of modified cardiac muscle that is striated but has indistinct boundaries n fewer organelles n myofibrils. y It generates n distributes e electrical impulses that stimulate cardiac muscle fibers to contract.

COMPONENTS

1. Sinoatrial Node (SANode):

y Located at e junction of e sup. vena cava n e Rt. atrium.

y Characteristics: Able to spontaneously n rhythmically generate action potential

y Explanation: Cell membrane of sinus fibers r periodically very permeable to Na+ ions even in 1 resting state.Thus,

Na+ entry causes depolarization n action potential.This leakiness to Na+ ions does not cause e sinus nodal fibersto remain depolarized all e time because of e 2 events occur during e course of action potential, which r:a. Inactivation of Ca2+ - Na+ channels after openingb. Opening of K+ channel.

y Self-excitation, recovery from action potential, drift of e resting potential to firing level (this process continuesindefinitely throughout a persons life).

y SA nodes action potential per minute = 70 80.

y >> Prepotential/pacemaker potential r normally prominent only in SA n AV nodes.Atrial n ventricular musclefibers do not have prepotential, they discharge spontaneously only when injured or abnormal>>

2. Internodal Tracts:

y 3 bundles of atrial fibers which conduct impulses from SA node to AV node:a. E ant. internodal tract ofBachman.b. E middle internodal tract of Wenkebach.c. E post. internodal tract ofThorel.

3. Atroventricular Node (AVNode).

y Located in e Rt. post. portion of e interatrial septum near e mouth of e coronary sinus.

y E fibers of e internodal tracts converge n int erdigitate with e fibers in e AV node.

y AV node slows down e speed of electrical t ransmission.This delay permits enough time for e contracting atria to

empty their contents into e ventricle before ventricular contraction i s initiated. y AV node has a one-way conduction from atrium to ventricle.

y AV nodes action potential per minute = 40 60.

y Causes of slow conduction through AV node:a. Size ofAV node muscle tissues r smaller than atrial muscle fibres. b. Fewer gap junctions in AV node muscle results in greater resistance to conduction. c. Resting membrane potential > negative than atrial muscle tissues.

4. AVBundle / Bundle ofHis.

y Means a bundle of fibers from AV node running towards e interventricular septum.

y Gives off 2 branches at e top of e interventricular sept um:

y Lt. bundle branch which divides into ant. n post. fascicles/branches, n continues along inner side of e Lt. ventriclen gives rise to smaller Purkinje Fibers.

y ARt. bundle branch which is e continuation of e bundle, continue along e inner side of e Rt. ventricle, n gives riseto smaller Purkinje Fibers.

5. Purkinje System: e terminal ramifications of e conducting system which spreads to all parts of e ventricularmyocardium.

ABNORMALITIES

1. Abnormal heart rhythm (arrhythmias).

y May be caused by:a. SA node irregularities.b. AV node irregularities.c. By disturbance of conduction system.

2. Heart block.

y An interruption in conduction, i.e. some or all of e impulses fail to reach ventricles.

y 2 types:a. Incomplete heart block: Atria beat normally but conduction through AV node is slowed.b. Complete heart block: Conduction from AV node is severely hampers atria beat normally, but ventricles

beat independently at 20 40/min.3. Ectopic foci: in conduction defect, a site other than SA node may become excitable n initiate beat on its own but e

normal beat.

ELECTRICAL PATHWAY OF THE HEARTG

Action potential originates in SA node n 1st spreads through out both atria, from cell to cell via gap junction. Interatrial pathway: extends from SA node within Rt. atrium to Lt. atrium (A wave of excitation spreads across e gap junctions throughout e Lt.

atrium at e same time similar spread is being accomplished through out Rt. atrium. Internodal pathway: extends from SA none to AV node.This pathway directs e spread of action potential ori ginating at SA node to e AV node to

ensure sequential contraction of e ventricles following atrial contraction.

A slow transmission of action potential from atria to ventricles through AV node.This delayed time (0.1 sec) enables atria t o become completelydepolarized n to contract, emptying their contents into e ventricles, before ventricular depolarization n contraction occur.

Depolarization of ventricular muscle starts at e septum ofLt. ventricle n then spreads to Rt. across e midportion of e septu m .

Spread down e septum to e apex of e heart via Rt. n Lt. bundle branches.

Impulses enter Purkinje fibers n spread to entire endocardial surface of ventricular muscles.

Spreads to epicardial surface of ventricle n e last parts to be polarized are pos terobasal part ofLt. ventricle n Pulmonary conus.


12/40

THE SYSTEMIC ATRIAL BLOOD PRESSURE


OVERVIEW

y Pressure: e force per unit area.

y Blood pressure (BP): e force exerted by e contained blood on a u nit area of blood vessel wall, & e force is imported by econtraction of e heart (expressed in terms of displacement in mm Hg).

y Systolic blood pressure (SBP): e peak pressure in e atrial system during systole.

y Diastolic blood pressure (DBP): e minimum pressure in e atrial system during d iastole.

y Pulse pressure, PP = Systolic BP, SBP Diastolic BP, DBP.

y Mean atrial BP is e average pressure throughout e cardiac cycle (i t is slightly less than e value halfway b/w SBP n DBP

because systolic is shorter than diastolic). y Mean Pressure = DBP + 1 /3(Pulse Pressure)

= DBP + 1/3(SBP DBP)

NORMAL VALUE

y For resting young adult in e sitting n lying position, Branchial Atrial Blood Pressure:1. SBP = 90 130 mm Hg2. DBP = 60 90 mm Hg3. Pulse Pressure = 30 50 mm g

MEASUREMENT 1. Direct Measurement: cannula is inserted into an artery n connected to a mercury manometer or recording device. 2. Indirect Measurement or Clinically measured BP : e lateral or side-pressure exerted on e vessel wall by contained blood.

DETERMINANTS

y E amount of blood entering e arterial system which is determined by cardiac output.

y E amount of blood leaving arterial system through e arterioles which is determined by e resistance offered by e arterioles ofvarious vascular beds total peripheral resistance.

y Thus, Blood Pressure = Cardiac Output, CO x Total Peripheral Resistance, TPR.

PHYSIOLOGICALVARIATIONS

1. Age: SBP n DBP gradually rise with age.2. Circadian Rhythm: SBP of5-10 mm Hg rise in afternoon.3. Emotional Excitement: Transient rise.

4.Physical Exertion: Particularly isometric exercise rose BP.5.Eating (after meal): SBP rise due to increase in CO.6.Gravity.

REGULATIONS

y Reasons of regulation:1. It must be high enough to ensure sufficient driving pressure in order for e brain n other t issues to receive adequate

flow, no matter what local adjustments are made in e resistance of e arterioles supplying them. 2. E pressure must not be so high that it creates extra work for e heart n increases e risk of vascular damage n possible

rupture of small blood vessels.

SHORT TERM

y Within seconds.

y Adjustment is accomplished by alterations in cardiac output n total peripheral resistance, mediated by means ofANS influences on e heart, veins, & arterioles.1. Neural: E cardiovascular Reflex.

a. Baroreceptor Reflex: Includes a receptor, an afferent pathway, an integrating centre, an efferent pathway, n effector organs. Low pressure baroreceptors: atrial baroreceptor (volireceptor) n in pulmonary circulation. High pressure baroreceptor: systemic arterial baroreceptor (carotid sinus baroreceptor n aortic arch

baroreceptor) n Lt. ventricular baroreceptor). E integrating centre: e cardiovascular control centre located in e medulla within e brain stem. When BP rises: High pressure baroreceptors increase e rate of firing in their respective afferent neurons, n as a

result, cardiovascular control centre increases parasympathetic activity n decreases sympathetic activity. When BP falls: Low pressure barorecetors increase e rate of firing in their respective afferent neurons, n as aresult, cardiovascular centre increases sympathetic activity n decreases parasympathetic activity.

b. Chemoreceptor Feedback Control: Receptors located in e carotid n aortic arteries. Sensitive to low oxygen or high acid level in blood. Act by reflexly increasing BP by sending excitatory impulses to cardiovascular centre. Eg: Hypoxic,

hypercepnie, acidosis resultant from stagnation due to hypotension stimulates e receptors. Central Nervous System to Ischcaemic response. Compensating rise in e BP as a result of intense vasoconstriction. May be high enough to cause reflex bradycardia.

2. Hormonal Reflex. Noradrenaline: Adrenaline system increasesBP. Renin-angiotensin: Aldosterone system increasesBP. Antidiuretic hormones: Vasopressin system increasesBP.

LONG TERM

y Minutes to days.

y Control involves adjusting total blood volume by restoring normal salt n water balance through mechanisms that regulateurine output n thirst.

y Mediated by renal body fluid pressure control system.

OTHERS

y Lt. atrial volume receptors n hypothalamic osmoreceptors: important in water -salt n balance n affect BP by controllingplasma v.

y Cardiovascular responses associated with certain behaviors n emotions n r mediated through e cerebral cortex -hypothalamic pathway.Responses include e widespread changes in cardiovascular activity accompanying fight-to-flightresponse n etc n slightly increase BP.

y Hypothalamic control over cutaneous arterioles: results in cutaneous vasoconstriction which help maintain adequate TPR,n increases BP.


13/40

THEHEARTSOUND


OVERVIEH

y Normal heart produces 2 heartsounds whichcan be heard with a stethoscope during cardiaccycle.

y Esounds are caused byvibrationssetup within e walls of e ventriclesn major arteries during valvesclosure,not byvalvessnapping shut.

y Opening ofvalves doesnot produce anysound.

y Normal sound: lub-dup-lub-dup-lub-dup.

1STHEARTSOUND

y Low pitched,soft,n relatively long.

y Oftensaid to sound like LUB.

y Associated with e closure ofAV valves (tricuspid n mitral valves).y Signals e onset ofventricular systole.

y Duration ~ 0.I

5 secn frequency ~ 25 45 Hz.

y Softer whenheart rate is low because e ventricles are well filled with blood n e leaflets of e AV valves floattogether beforesystole.

2NDHEARTSOUND

y High-pitched,shorter nsharper.

y Oftensaid to sound like DUB.

y Associated with e closure ofsemilunar valves (pulmonaryn aorticvalves).

y Signals e onset ofventricular diastole.

y Duration ~ 0.P

2 sec & frequencies ~ 50 Hz.

y May become split during inspiration (physiological splitting) which due to e delayinclosure of pulmonaryvalve.

y Mechanism during inspiration: Intrathoracic pressure becomes > negativevenous returnstroke volume muscular

contraction of e heart ejectiontime (prolonged) pulmonaryvalve closes later thanusual.

3RDHEARTSOUND

y Softn low-pitched.

y Heard aboutQ

/3 of e waythrough diastole in manyyoung normal adult.

y Itcoincides with e period of rapid ventricular filling nis probably due to vibrationsetup by e inrush of blood.

y Durati

on

~ 0.

R

sec.

4THHEARTSOUND

y Cansometimes be heard immediately before eS

stsound when atrial pressure ishigh or e ventricle isstiff inconditionssuch asventricular hyperthrophy.

y Due to ventricular filling n rarelyheard innormal adult.

MURMUR

y Refersto abnormal heartsound.

y 2 types:T

. Pathologic:involving heart diseases.2. Non-pathologic:called functional murmur - > commoninyoung people.

y Caused byturbulent blood flow whichcreatesvibrationsin e surrounding structures.

y 2 types:U

. Systolic murmur:A murmur occurring b/wU

stn 2nd heartsounds (lub-murmur-dup).2. Diastolic murmur:A murmur occurring b/w 2nd n

U

stheartsounds (lub-dup-murmur).

y 2 characteristics:V

. Stenotic: Whistling murmur.2. Insufficient: Swishy murmur.

y 2 commoncauses:W

. Stenoticvalve:Astiff,narrowed valve that doesnot opencompletely. Blood must be forcedthrough e constricted opening

attreme

ndousvelo

city, resul

tingin

turbule

nceth

at

produces a

nab

normal w

histlin

g soun

d.2. Insufficient (leaky)valve: Valves whichcannotclose completely,usually because e valve edges are scarred n do not fittogether properly. Turbulence is produced when blood flows backward through e insufficientvalve ncollides with e bloodmoving in e opposite direction,creating a swishing or gurgling murmur.

THRILLS y Vibration whichcan be felt by e hand.

BRUITS y Heard over higher vascular region.


14/40

THE CARDIAC CYCLE


OVERVIEW

y Defined as e sequence of events associated with 1 heart beat.

y Consists of a systole n diastole of both atria n ventricles,

y Systole: Contraction phase (Occurs as a result of e spread of excitation across e heart).

y Diastole: Relaxation phase (Follows e subsequent repolarization of e cardiac musculature).

PROPERTIES OFCARDIAC CYCLE

1. Stroke Volume: E amount of blood pumped out / ejected by each ventricle with each contraction at rest. Normalvalue: 70 90 mL.

2. End-systolic Volume: E amount of blood remaining in e ventricle at e end of vent ricular systole when ejection IS

complete.Normal volume: 50 mL.3. End-diastolic volume: E volume of blood in e ventricle at e end of diastole. Normal value: 120 -1 30 mL.4. Ejection fraction = Stroke Volume - Normal value: 60% (valuable index of cardiac function).

End-diastolic volume

y Although Rt. n Lt. sides of heart have different atrial n ventricular pressure, they contract n relax at e same time n ejectan equal volume of blood simultaneously.

y During cardiac cycle, although events of e 2 sides of e heart are similar, they are somewhat asynchronous.

y E processes:1. Rt. atrial systole proceeds Lt. atrial systole (SA node located on Rt. atrium).2. Lt. ventricle systole proceeds Rt. ventricle systole (Depolarization starts on Lt. ventricle septum). 3. Rt. ventricle ejection before Lt. ventricle ejection (Resistance is low n pressure of pulmonary arter y > aortic

pressure).

VARIATION IN ELENGTH OFSYSTOLE NDIASTOLE

PORTIONS HEARTRATE (75 beats/min) HEARTRATE (200 beats/min)Duration of cardiac cycle 0.80 0.30

Duration of systole 0.27 0.16

Duration of diastole 0.53 0.14

PHYSIOLOGICALN CLINICAL

IMPLICATIONS

NORMALRANGE

y Normal cardiac cycle: 0.8 sec.

y Normal heart beat: 75 beat/min.y 1 heart beat = 60 sec = 0.8 sec.

75 beats

DURATIONOFSYSTOLE NDIASTOLE

y Duration of systole is much more fixed than diastole.

y When heart rate increased, diastolic period is shorthened.

y During diastole:1. Heart muscles rest.2. Ventricular filling occurs.3. Coronary blood flows to subendocardial portion of ventricles occurs.

y Heart rate period of diastole physiological needs of heart cannot be done adequately heart failure(prolonged).

y Example:1. Tachycardia >> High heart rate: > 100 beats/min .2. Bradycardia >> Low heart rate: < 60 beats/min.

1X

LATE DIASTOLEYATRIAL FILLING VENTRICLE FILLING

X

Both atria n ventricles r relaxed. As a consequence, pressure of both ventricles is lower

than that of aorta n pulmonary artery so that aortic npulmonary valves r closed.

Pressure in e atria is lower than that in e great veins, sothat blood flow into e atria n ventricles on each side(which r in continuity as e atrioventricular valves r

open).E rate of filling declines as e ventricle become distended(70% of blood flows passively from atria to ventricle).

2X

ATRIAL SYSTOLE

When SA node fires, atrial contraction occurs emptying30% of remaining blood from atria to ventricles.

Volume of blood in ventricles at e end of ventricles at eend of diastole is 120 130 mL (End-Diastole Volume).

3a

VENTRICLE SYSTOLE

Following atrial excitation, e impulse passes through e AV node n specialized conduction system to excite eventricle, n results in ventricles contraction.

Abrupt rise in ventricular pressure which causes AV valve to close (1st heart sound). Once e ventricular pressure exceeds aortic n pulmonary pressure, aortic n pulmonary valves open. Blood is forced from Lt. ventricle to aorta n Rt. ventricle to pulmonary arteries (Ventricular ejection).

When ventricular pressure becomes lesser than aortic pressure, semilunar valves close (2nd heart s ound) nventricular filling occur again. (Dicrotic notch: Disturbance or notch produced on e aortic curve pressure

during e closure of aortic valve).


15/40

THE ELECTROCARDIOGRAM


OVERVIEW

y Fluctuations in potential that represent e algebraic sum of e action potentials of myocardial fibers can be recordedextracellularly.

y This is because, e body fluids are good conductors (e body is a volume conductor).

y ECG: E record of these potential fluctuations during ca rdiac cycle.

MEASUREMENT

y Can be recorded by using an active or exploring electrode connected to an indifferent electrode at zero potential (unipolarrecording) or by using 2 active electrodes (bipolar recording).

y In a volume conductor, e sum of potentials at e points of an equilateral triangle with a current source in e centre is zero all

e time.y A triangle with e heart at e centre (Einthovens triangle) can be approximated by placing electrodes on both arms n e Lt.

leg called standard limb leads.If connected to a common terminal, an indi fferent electrode that stays near zero potential isobtained.

y Depolarization (positive) moves towards an active electrode n repolarization (negative) moves in opposite direction.

LEADS

1. Bipolar leads: these record e potential difference b/w 2 active electrodes.

Standard Limb Leads:Leads Positive Electrodes Negative Electrodes Results

I Lt.Arm (LA) Rt.Arm (RA) LA - RAII Lt.Foot (LF) Rt.Arm (RA) LF - RAIII Lt.Foot (LF) Lt.Arm (LA) LF - LA

2. Unipolar leads: these have an active (exploring) electrode placed or a chosen site linked with an indifferent elsctrode.1being zero, e potential difference b/w e 2 represents e actual local potential.They r called V leads because they recordvalues approaching meaningful voltages.Can also be placed at e tips of catheters n inserted into e esophagus or heart.

y Unipolar Limb Leads: aVR, aVL, as well as aVF for Rt. arm, Lt. arm, n Lt. foot respectively. (a = augmented, when eamplitude of deflection increased (These r recording b/w one limb n another 2).

y Unipolar Chest Leads (Precordial Leads). V1 4th ICS, Rt. sternal border. V2 4th ICS, Lt. sternal border.V3 Equidistance b/w V2 n V4.

V4 5th ICS, midclavicular line.

V5 5th ICS, ant. axillary line.V6 5th ICS, midaxillary line.

SEGMENTS

1. P Wave.

y Represents atrial depolarization.

y Begins as e impulse spread from SA node across e atria. E activity ofSA node itself cannot be detected in ECG.

y Duration: 0.1 sec indicates e time taken for e impulse to spread through atrial muscle.

y E magnitude ofP wave is some guide to e function of atria.

y Because e impulse spread from Rt. to Lt. n downward, e P wave is:

y Upright in leads I, II, aVF.

y Inverted in leads aVR, III, aVL, n V1.

2. PRInterval.

y Measured from onset ofP wave to e beginning of QRS complex. y It measures e AV conduction time which includes atrial depolarization, AV nodal delay, n conduction down e bundle of

His to e ventricular myocardium.

y Duration: 0.12 to 0.20 sec (normal adult with normal heart) .

3. QRSComplex.

y Represents ventricular depolarization.

y Q wave is a downward deflection preceeding an R wave which is an upward deflection of QRS.

y S wave is a downward deflection following an R wave.

y In e routine 12 leads ECG, e manifestation of atrial repolarization is submerged in QRS complex.

y Duration: 0.10 sec (upper limit for normal person).

4. STSegment n T Wave.

y Represents ventricular repolarization.

y ST segment is e part b/w e end of QRS complex n e beginning ofT wave.

y T wave is normally in e same direction as e largest part of QRS complex since repolarization takes place in e reversedirection from depolarization.

y Derivation from normal r commonly associated with myocardial ischaemic . y E hall mark of myocardial ischaemial infarction is ST segement elevation in leads overlying e area of infarction, n ST

segment depression in leads on e opposite side of e heart.At a later stage, ST segment elevation less pronounced as Twave inversion developed.

USES

1. Detection of heart rate (both atrial n ventricular).2. Rhythm (regular or irregular) for diagnosis of arrhytmias. 3. Conduction of cardiac impulse (delayed or block at e side of defect). 4. Change in myocardial perfusion (ischaemic), structure (infarction n hyperthrophy), n function (ventricular fibril lation or

cardiac arrest).5. Change in plasma electrolytes (potassium n calcium), eg: when blood potassium decreases, T wave decreases also. 6. To detect heart block, atrial extrosystoli, atrial tachycardiac, atrial flutation, atrial fibrillation, n myocardial infarct.

APEXLEADS


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THE CARDIOVASCULAR REFLEX

POINTS DETAILS

BARORECEPTORS

y Baroreceptors r stretch receptors in e wall of e heart & blood vessels.

y They r 2 types of baroreceptors:1. Low pressure baroreceptors:

a. Baroreceptors in pulmonary circulation. b. Atrial baroreceptors (volireceptor).

In atrialcaval & atriopulmonary vein junction . 2 types:

i. Type A receptors: discharge primarily during atrial systole.

ii. Type B receptors: discharge primarily during peak atrial filling. 2. High pressure baroreceptors:

a. Systemic arterial baroreceptors: 2 types of baroreceptors:

i. Carotid sinus baroreceptors: a small dilation of e internal carotid artery just above e bifurcation ofe common carotid.

ii. Aortic arch baroreceptors: found in e adventitia of e wall o f e aortic arch. These baroreceptors respond to changes in e wall stretch produced by:

i. Mean BP changes.ii. Changes in pulse pressure. iii. External pressure.

Increased baroreceptor discharge inhibits e tonic discharge of e vasoconstrictor nerves & excites e vagalinnervations of e heart, producing vasodilation, venodilation, a drop in BP, bradycardia, & a decreasein CO.

b. Left ventricular baroreceptors: maintenance of e vagal tone that keeps e heart rate low at rest.

BARORECEPTOR REFLEX

BARORECEPTORAFFERENT

y There r 2 baroreceptor afferents:

1. Carotid sinus (from neck): Glossopharyngeal nerve (IX craninal nerve). 2. Aortic arch (from thorax): Vagus nerve (X cranial nerve).

y E above cranial nerves r called buffer nerves because their roles in e baroreceptor reflex:1. Buffer e changes in e arterial BP.2. Maintain BP homeostaisis.

y Buffer nerves activities:1. Secrete glutamate which stimulates GABA-secreting inhibitory neurons.2. Discharge at a slow rate at normal BP. 3. E discharge increases when pressure in carotid sinus & aortic arch increase & vic e versa.

INTEGRATINGCENTRE

1. Vasomotor centre in medulla (CMV): increased baroreceptor discharge inhibits neuron ofVMC while decreaseddischarge stimulates e neuron.

2. Vagal nuclei in e medulla: impulses in e baroreceptor afferent excite vagal nuclei. 3. Vasopressin stretching neuron in e hypothalamus: increased baroreceptor discharge inhibits vasopressin secretion &

decreased discharge stimulates hormone secretion.

EFFECTORS

1. Heart: adjustment in CO.2. Arterioles: variation in total peripheral resistance.3. Veins: alteration in amount of blood stored in capacitance vessels. 4. Capillaries: fluid shift 2o to BP changes.

MECHANISM OFREFLEX

1. Fall in BP decreased baroreceptor discharge:a. Stimulate VMC sympathetic stimulation.b. Less stimulation of vagal nuclei decreased vagal tone.c. Less inhibition of vasopressin secretion secretion of vasopressin.

2. Rise in BP increased baroreceptor discharge:a. Inhibit VMC decreased sympathetic stimulation.b. More stimulation of vagal nuclei increased vagal tone.c. Inhibition of vasopressin secretion decreased secretion of vasopressin.

CHEMORECEPTOR REFLEX

y E CVS response to chemoreceptor stimulation consists of peripheral vasoconstriction & bradycardia .

y Hypoxia produces hyperpnea & increased cathecolamine secretion from e adrenal medulla which lead to tachycardia & increased CO.

y A rise in arterial PCO2 stimulates e vasomotor area but e direct effect of hypercapnia is vasodilation.

y Exposure to high concentration ofCO2 is associated with marked cutaneous & cerebral vasodilation but vasoconstriction occurs elsewhere &usually there is a slow rise in BP.

HORMONAL MECHANISM

1. Adrenal medullary (naroadrenaline adrenaline system): cathecolamines vasoconstriction.2. Renin angiotensin aldosteron system:3. Vasopressin: causes generalized vasoconstriction (particularly splanchnic vasculature) & water retention (anti -diuretic act).

OTHER CVS REFLEX

1. Renal body fluid control system:

y Is a long term mechanism.

y Rise in arterial BP greatly increases e rate at which e kidney excrete water and salt (pressure diuresis & pressure natriuresis ) loss of ECFvolume lower BP.

2. Coronary chemoreflex (Bezold-Jarisch Reflex): injection of certain chemical (e.g. serotonin) into coronary artery supplying e left ventricle resultsin hypotension, bradycardia & apnea followed by tachycardia .

3. Somato-sympathetic reflex: during muscular activity, proprioceptors & pain receptors r stimulated leading to increased sympathetic d ischarge4. Emotional stress reflex: limbic cortex VMS & vagal centre (anger excite ...). 5. Lung inflation reflex: lung inflation vagal afferent VMS inhibited BP decreases.6. Reflex from other pressure sensitive region : blow on abdomen & pressure on e eyeball lead to bradycardia & vasodilation.


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THE REGIONAL CIRCULATION

CIRCULATION DETAILS

CORONARYCIRCULATION

y At rest, e coronary blood flow is ~ 200 ml/min (4% ofCO).

y Rt. & Lt. coronary arteries arise from e root of e aorta.

y Factor influencing coronary blood flow:1. Haemodynamic determinants:

Pressure gradient b/w e aorta & e Lt. ventricle determines coronary blood flow. During systole there is less blood flow in e subendocardial portion of e Lt. ventricle because e contracting

muscle compresses e blood vessels but this force is dissipated in e more superficial portion of e Lt. ventriclemusculature to permit some flow in this region.

2. Chemical control (autoregulation): Metabolic theory of autoregulation: coronary blood flow is reduced accumulation of vasodilator

metabolites dilation of e coronary blood vessels restoration of e blood back to normal. Hypoxia increases coronary blood flow to 200 300% .

3. Neural regulation:

E coronary arterioles contain both & -noradrenagic receptors mediating vasoconstriction & vasodilatationrespectively.

-receptors r more sensitive to noradrenaline, thus e direct effect of noradrenergic sympathetic stimulation isvasoconstriction.

Noradrenaline increases cardiac rate & contraction as well as e work of e hear t which lead to accumulationofVDM & dilation of e coronary vessels.

This effect overrides e direct vasoconstriction effect via -receptors so that e overall effect of sympatheticnoradrenergic activity is coronary vasodilatation.

Increased vagal activity to e heart causes coronary vasodilatation & increased coronary flow .

SKELETALMUSCLE

CIRCULATION

1. Sympathetic nerves stimulation: causes vasoconstriction which is mediated by -adrenergic receptors in reflex responseto decreased arterial pressure.

2. Epinephrine causes vasodilatation when present in low concentration & vasoconcentration (via -adrenergic) whenpresent in high concentration.

3. Controlled by local metabolic factors during exercise.

SPLANCHNICCIRCULATION

y Involves GIT, spleen, pancreas, & liver which consists of 2 capillary beds which r in series with each other.

y Blood from e capillaries of GIT, spleen, & pancreas flow via portal vein to e liver which also receives a separate arterialblood supply.

y Sympathetic nerves cause vasoconstriction (-adrenergic) in reflex response to decreased arterial press ure & duringstress.Also, venous constriction causes displacement of a large volume of blood from e liver to e veins of e thorax.

y Increased blood flow occurs following ingestion of meal & is mediated by local metabolic factors hormones secreted bye GIT.

RENALCIRCULATION

y Flow autoregulation is a major factor.

y Sympathetic nerve causes vasoconstriction via Angiotensin II which is e major contrictor.

y This reflex conserves sodium & water.

CUTANEOUSCIRCULATION

y Controlled mainly by sympathetic nerves & mediated by -adrenergic receptors.

y Reflex vasoconstriction occurs in response to decreased arterial pressure & cold.

y Reflex vasodilatation occurs in response to threat.

y Substances released from e sweat glands & noradrenergic neurons also cause vasodilatation.

y Venous plexus contains large volumes of blood which contributes to skin.

PULMONARYCICULATION

y E circulation is in a very low resistance compared to systemic circulation.

y Controlled mainly by gravitational forces & passive physical forces within e lung.

y Constriction which is mediated by local factors occurs in low O 2 concentration, just opposite to that occurs in e systemiccirculation.

BRAINCIRCULATION

y E volume of blood & e extravascular fluid in e brain is relatively constant.

y Thus, changes in either of this fluid volume must be accompanied by a reciprocal change in other.

y In contrast to most other organs, e cerebral blood flow is held within a relatively narrow range which in human eaverage is 55 mL/min/ 100 g of brain.

y E brain is least tolerant organ to ischemia because if there is interruption of cerebral blood flow for as a little as 5seconds, loss of consciousness occurs.

y Ischemia lasts for just a few minutes (~ 5 mins) will result in irreversible tissue damage.

y E regulation of cerebral circulation is mainly under e direction e brain itself.

y Local regulatory mechanisms & reflexes that originate in e brain tend to maintain cerebral circulation relativelyconstant .

y This constancy prevails even in e preence of possible adverse extrinsic effects such as sympathetic vasomotor nerveactivity, circulating humoral vasoactive agents, & changes in arterial blood flow .

FETALCIRCULATION

y E fetal circulation differs from that of an adult by:1. Low pulmonary blood flow.2. High placental blood flow.3. Shunting of from Rt. atrium to e Lt. atrium through e foramen ovale & from e pulmonary artery to e aorta via e

ductus arteriosus.This shunts allow e blood to bypass e fetal lungs.

MICRO CIRCULATION

y Definition: e flow of blood in e system of linear blood vessels (50 m or less in diameter).

y It includes e capillary, precapillary arterioles, & postcapillary venules.

y Consists of5% of e circulatory blood volume.

y E functions:1. Exchange of respiratory gases. 2. Exchange of nutrients & metabolic waste products. 3. Exchange of water (formation of interstitial fluid & its regulation). 4. Exchange of other substance such as hormones. 5. Exchange of heat in thermoregulation.


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EDEMA

y Causes of edema:1. Increased filtration pressure: arteriolar dilatation & venular constriction . 2. Increased venous pressure d/t venous pressure & gravity . 3. Decreased oncotic pressure because of:

a. Diet: starvation or poor protein intake. b. Liver failure: failure to synthesis plasma protein as in cirrhosis. c. Kidney disease: loss of protein.

4. Increased capillary permeability d/t histamine, substanceP, or kinins. 5. Inadequate lymph flow d/t surgical removal of lymph nodes or obstruction of lymphatic vessels as in flariasis.

THE EFFECTS OF EXERCISE ON CVS

POINTS DETAILS

OVERVIEW

y Exercise is associated with very extensive alterations in e CVS.

y Mainly it is associated with increased oxygen consumption & e amount ofO2 required depends on intensity of exercise.

y Muscles convert about 20% of e energy ofATP to external work, e remaining energy appearing as heat.

y Consumption ofO2 by aerobic system takes time to develop & continues for some time after exercise stops.

y There are two types of exercises:1. Isotonic exercise (dynamic/rhythmic contraction).2. Isometric exercise (static/ sustained).

TYPES OF EXERCISE

ISOTONICEXERCISE

1. Blood flow to muscle increases during isotonic exercise as a result of:a. Vasodilatation in skeletal muscle blood vessels due to:

y Increased action of sympathetic cholinergic nerves to blood vessels in muscle.

y Catecholamine released from adrenal medulla (especially adrenali ne acts on F2 receptors in blood vessels ofskeletal muscle causing vasodilatation).

y Local factors: [PO2, PCO2, pH, K+ Vasodilatation] Increased in temperature also causes vasodilatation.

b. Shifting of blood from certain peripheral circulation (such as splanchnic & renal circulation) to exercising muscles as aresult of increased sympathetic stimulation causing vasoconstri ction.

2. Increased CO: d/t increased heart rate & stroke volume.3. Increased oxygen transfer or oxygen extraction d/t 2 things:

y Recruitment of previously closed capillaries.

y Increased in release ofO2 from haemoglobin due to local factors ( H+, temperature, & etc).

ISOMETRICEXERCISE

y E sequence isometric exercise: Sustained contraction of muscles Vasodilator metabolic accumulate in muscle Stimulation o f sensory nerves

Cardiovascular centre Increased sympathetic activity .

y E effects of isometric exercise:1. Increased heart rate d/t:

a. Increased sympathetic discharge .b. Decreased vagal discharge.

2. Increased DBP d/t increase in total peripheral resistance.

3. Increased SBP d/t increase incontractility of e heart .4. Mean arterial BP increases.

COMPARISONS

ISOTONIC EXERCISE PROPERTIES ISOMETRIC EXERCISE

Increase in CO mainly d/t heart rate not d/t strokevolume.

CO & HEART RATEHeart rate increased d/t:

1. Increase in sympathetic discharge.2.Decrease in vagal tone.

Net total peripheral resistance decreased/notchanged.

Tob c

l Pdripher

cl Resistan

ee Total peripheral resistance increased d/t increase in

sympathetic discharge.

1. Systolic BP increase d/t contractility.2. Diastolic BP decreases d/t decrease in net total

peripheral resistance.3. Mean BP slightly increases or stays e same.4. Pulse Pressure increases.

BP

1. Systolic BP increases.2. Diastolic BP decreases d/t increased total

peripheral resistance.3. Mean Arterial BP largely increases.4. Pulse Pressure only has a little change.

O2DEFICIT& DEBT

y If exercise is started abruptly & a constant moderate work output is maintained, e O2 uptake takes several minutes to reacha steady state.

y E oxygen deficit: e missing O2 that would have been consumed if e bodys response to e O2 demand of exercise wasimmediate.

y For mild to moderate exercise e O2 deficit is accounted for by:1. E lower content ofATP & creatinine phosphate in e active muscles. 2. E reduction in O2 content of myoglobin in e active muscle.

y E O2 debt or excess post-exercise O2 consumption represents repayment of e O2 deficit: When e exercise is vigorous or prolonged, e debt is considerably greater than e deficit. Following such exercise e ATP & cutreatinine phosphate stores & e O2 content of myoglobin & venous blood return to

normal within a min or two, but there i s a residual elevated O2 consumption that can last for min to hours. This depends on e intensity & duration of the exercise where e extra O2 consumption is attributed to:

1. E energy needed to dissipate heat & restore intracellular electrolyt es to normal concentrations2. E higher metabolic rate caused by e increase in body temperature & in e circulating levels of catecholamine &

thyroxine.

y Regeneration of intramuscular glycogen stores also produces a very small increase in O 2 consumption over a period of a dayor two following e exercise.


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RestExercise

Light Medium Heavy

Oxygen consumption (ml min-1) 250 1500 2800 3500

Oxygen consumption of muscles (ml min-1) 50 1250 2200 3150

Cardiac output (L min-1)5 13 16 21

Arterio venous oxygen difference (ml L-1)50

100 127 130

PvO2 (mmHg) 40 26 23 20

Heart rate (beats min-1)72 144 160 190

Diastolic filling time (ms) 500200 170 150

Stroke volume (ml)70 90 100 110

Mean blood pressure (mmHg)85

90 95 100

Pulse pressure (mmHg) 40 60 90 120

Systolic / diastolic pressure (mmHg) 110/70 130/70 155/65 180/60

Stroke Volume

(mL)

Heart Rate

(Beats / min.)

Resting

y Non-athlete

y Marathoner

Maximum:

y Non-athlete

y marathoner

75

105

110

162

75

50

195

185

1500

1000

500

0

2 4 6 8 10 12

Time (min.)

VO2

(mlmin-1)

O2deficit

O2debt

Work

COMPARISONOFCARDIACOUTPUTBETWEENMARATHONERANDNON-ATHLETE

Time-course ofO2 consumption (VO2) during moderate exercise, illustrating the O2 deficit and debt

Cardiorespiratory variables and indices at rest and during exercise .


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THEHYPERTENSION

POINTS DETAILS

OVERVIEf

y There r 2 types ofhypertension:g

. Essential hypertension: Also known as primaryhypertension. I.e. e hypertension whichiscaused by multiple factors & in mostinstances, e causes remainunknown.

2. Secondaryhypertension:hypertensionin which e cause isknown.

y Epidemiologic evidence pointto geneticinheritance, psychological stress, & environmental & dietary factorswhichperhaps maycontribute to e pathogenesis ofhypertension.

AETIOLO

GY& P

ATHO

GEN

ESIS

ABNORMALNEURAL

MECHANISM

y Eneural components which r importantin dealing with blood pressure:h

. Vasomotor center2. Dorsal motor nuclei of e vagusnerves.3. Nucleustractussolitaries.4. Hypothalamus.5. Parts ofcerebral cortex i.e. motor cortex.6. Anterior temporal lobe.7. Orbital areas of e frontal cortex.8. Cingulate gyrus, amygdala,septum,& hippocampus.

y Enormal physiological process:i

. E adrenergic junction: -adrenergicstimulation within CNS decreasesBP through aninhibitory effect on e vasomotor center. Increased Angiotensin II increasessympathetic outflow f rom e vasomotor center, resulting in anincrease in

BP. Pre-synaptic receptors:stimulation of pre-synapticreceptorsinhibitsNE release while stimulation of pre-

synaptic-receptorsincreasesNE release. Post-synaptic receptors: Stimulation of post-synaptic-receptors on arterioles & venulescauses

vasoconstriction. Stimulation ofp -receptorsin e heartcausesincrease in HR& contractility.

Stimulation of2-receptorsin arterioles & venulescausesvasodilatation.2. E baroreceptor reflex:they r responsible for rapid, moment-to-moment adjustmentsinBP,such asinchange

from a reclining to anupright posture.

y Ehypertensioncan be a result of any primary defectthatcan occur in any ofthese major components:q

. Central Nervous System.2. AutonomousNervous System.3. Adrenergic receptors.4. Baroreceptor-reflex.

y They r so physiologicallyinterrelated becausea defectin one component may disturb e normal functionin another& e combined abnormalities maythencause hypertension.

DEFECTSINPERIPHERAL

AUTOREGULATION

y The kidneyis mainly responsible for long-term BP control bycontrolling blood volume.

y E reflex mechanisms ofkidneyincontrolling BP:r

. Decrease in renal perfusion pressureintrarenal redistribution of flowincrease water & salt reabsorption.2. Decrease in renal perfusion pressureincrease Reninincrease Angiotensin IIincrease PVR & aldosterone increase sodium reabsortionincrease blood volumeincrease BP.

y Aninitial defectin e renal adaptive mechanism could lead to plasma volume expansion & blood flow to peripheral

tissue even whenBP isnormal.

y To offsetthisincreased blood flow,local tissue autoregulatory processes would induce arteriole vasoconstrictionwhichcan lead to increase peripheral vascular resistance,PVR. If thiscontinuesthenintime a thickening ofarteriolar wall may occur resulting in a sustained increase in PVR.

y Anincreased PVRis a commonunderlying problem in patients with essential hypertension.

DISTURBANCEINVASCULAR

ENDOTHELIALMECHANISM

y Vascular endothelium plays animportant role in regulating blood vessel tone.

y Endothelial cellssynthesize following vasoactive substances:s

. Prostacyclin.2. Bradykinin.3. Endothelium-derived-relaxing factor (EDRF NO).4. Angiotensin II.5. Endothelin I.

y Deficiencyinthe local synthesis ofvasodilator substancessuchasi,ii,iii or increase ine production ofvasoconstrictingsubstancessuch as Factor IV & V maycontribute to the pathogenesis ofhypertension.

INFLUENCEOFDIETARYSALT

y In general, populationstudiesindicate thathighsaltintake is associated with a high prevalence ofhypertension.

y Clinical studieshave shownthat restriction ofsaltintake ine diet lowers blood pressure inhypertensive patients.

CLINICALPRESENTATION

y Esymptoms:headaches, fatigue, & dizziness.y Ecomplication:MI, CHF,thrombotic & hemorrhagicstrokes,hypertensive encephalopathy, & renal failure.

y Physical findings:hypertensive retinopathy, retinal hemorrhage & exudates, & Lt. ventricular hypertrophy.


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Sequential steps by whi

t

h increased

extracellular fluid volume increasesthe BP.

Renin-angiotensin system mechanism for

BP control.

Hyperte u s v o u

Afterw oad

Systow v c

dysfunct v on

Heart fa v w ure

LVH

Diasto w icdysfunction

Myocardia w O2 dex and

COMPLICATION OF HYPERTENSION


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e. Lipid profile: adverse effect.f. Decrease Glucose tolerance .g. Crosses Placenta .

h. Appear in breast milk.

ANTIHYPERTENSIVE DRUGS

DRUGS DETAILS

DIURETICS

y They r antihypertensive when used alone & when used with other anti-hypertensive agents, they increase those agents efficacy. Initially: decrease EFV (15%) & CO. Later on: EFV remains reduced (5%), CO returns to pretreatment value , & PVR decreased.

y E mechanisms for reduction ofPVR by Diuretics :1. Decrease in EFV.2. Fall in smooth muscle Na+ concentration leading to reduced intracellular Ca2+ concentration, resulting in cells more resistant to contractile

stimuli.3. A change in affinity & response of cell surface receptors to vasoconstrictor hormones.

y 3 types ofDiuretics:1. Thiazide & related agents:

Among e drugs: hydrochlorothiazide & chlorthalidone. Mild antihypertensives & more effective in e elderly. E therapy:

a. Short-term therapy: used alone in low doses i.e.12.5 mg to 25 mg/day & 50 mg daily dose ifBP is not controlled by 3 or > drugs.b. Long-term therapy: used in combination with K-sparing agent such as amiloride (1 mg) + hydrochlorothiazide (10 mg).

Adverse effects of thiazides which mostly d/t fluid & electrolytes imbalance:a. Extra-cellular vol. depletion.b. Hypotension.c. Hypokalemia.d. Hyponatremia.e. Hypochloremia

Other adverse effects of thiazides:a. Sexual impotence.b. Gout.c. Muscle cramps.

d. Ventricular arrhythmias.2. Loop diuretics:

Among e drugs: furosemide & erhacrynic acid . Strong diuretic but weaker antihypertensive than thiazides. Dose: 20 to 80 mg daily in chronic renal failure & coexisting refractory CHF patients. E thiazide-type diuretics r more effective anti-hypertensive agents than r e loop diuretics in patients with normal renal functions.This

is most likely related to e short duration of action of loop diuretics as single daily dose does not cause a significant net loss ofNa+ foran entire 24 hours period.

3. Pot.-sparing diuretics: spironolactone, amiloride, & triamterene.

y Drugs interaction with diuretics:1. NSAIDs decrease e effectiveness of thiazide diuretics .2. Corticosteroids increase e risk of hypokalemia.3. Diminish e effects of insulin, sulfonylureas, & anticoagulants.4. Increase e effects of l ithium, cardiac glycosides, & anaesthetics.5. Contraindicated for who r hypersensitive to sulfonamides.

SYMPHATOLYTIC DRUGS

CENTRALLY ACTING

AGENTS

1. Clonidine:

yy

2- agonist which stimulates 2Asubtype of2- adrenergic receptors in e brainstem, resulting in a reductio n insympathetic outflow from e CNS.

y Imidazoline preferring binding sites in brain & peripheral t issues which may me

'Aliah's Cardiovascular System

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