CARDIOVASCULAR SYSTEM

THE HEART

Cardiovascular System• series of tubes-blood vessels• filled with a fluid-blood• connected to a pump-heart• Arteries

– carry blood away from heart• Veins

– carry blood to heart• pressure generated in heart

pumps blood continuously through system

• Blood flow– movement of blood through

heart & around body to peripheral tissues

• Circulation

Circulation• right side of body-

Pulmonary Circuit– carries blood to & from

lungs for gas exchange• Systemic Circuit

– carries newly oxygenated blood from lungs to body & back to heart

• each circuit begins & ends at heart

Heart Anatomy• hollow, small organ• about size of clenched fist• weighs from 250-350 grams• located in middle of chest in

mediastinum• surrounded by pericardial cavity• lining of pericardial cavity is

pericardium– visceral & parietal part

• visceral pericardium -epicardium– superficial layer that covers

surface of heart• parietal pericardium

– lines inner surface of pericardial sac which surrounds heart

• between these two-pericardial cavity

• filled with pericardial fluid • to lubricate & reduce friction

Heart Wall• 3 layers

• Epicardium-visceral pericardium

– covers outer surface

• Myocardium

– muscular wall

• Endocardium

– simple squamous epithelium

Microscopic Anatomy• different from skeletal muscle

in several ways• cells are smaller• uninucleated• have branching

interconnections between have intercalated discs– location of gap junctions &

desmosomes– convey action potentials

from cell to cell – ensure cells contract

simultaneously

Heart Anatomy• top of heart-base• pointed, lower part-apex• 4 chambers

– 2 atria & 2 ventricles• coronary sulcus

(atrioventricular sulcus)

• anterior & posterior interventricular sulci– mark external

boundary of right & left ventricle

Coronary Sulcus

Heart Anatomy• each atrium has expandable

extensions- auricles– hold extra blood

• right atrium receives blood from systemic circuit via superior & inferior vena cavae & coronary sinus

• superior vena cava– returns blood from body areas

superior to diaphragm

• inferior vena cava– drains areas below diaphragm

• coronary sinus– delivers blood from myocardium

of heart

Internal Heart Anatomy• blood passes into right

ventricle via right AV (atrioventricular) valve or tricuspid valve– keeps blood flowing in one

direction from atrium to ventricle

– prevents backflow into atrium

• tiny, white collagen cords-chordae tendineae attach to each flap

• originate at papillary muscles– help to close valves

• chordae tendineae & papillary muscles anchor flaps in closed position

Internal Heart Anatomy• pectinate muscles-right

atrium• fossa ovalis also found here• muscular ridges- ventricles-

trabeculae carnae• moderator band extends

horizontally from right ventricle wall– coordinates contraction

of muscle cells– insures chordae tendinae

tense before ventricles contract

Internal Anatomy• from right ventricle blood is pumped to

pulmonary circuit• valves between ventricles & vessels-

semilunar valves– prevent back flow into ventricles

• each made of 3 pocket-like flaps shaped like crescent moons

• blood travels via pulmonary semilunar valve into pulmonary trunk– start of pulmonary circuit

• from pulmonary trunk, blood goes to left & right pulmonary arteries and to lungs for gas exchange

• after being oxygenated, blood reenters heart via 2 left & 2 right pulmonary veins-open into left atrium

• blood goes from left atrium to left ventricle via left AV valve

• bicuspid or mitral valve• from here blood is ejected through

aortic semi lunar valveinto aortic arch

Heart Anatomy• left ventricle

– discharging chamber• contractsblood propelled into

circulation• equal volumes are pumped to both

circuits• right pumps blood to pulmonary circuit

through pulmonary trunk– short path with low pressure

• left pumps blood through systemic circuit– long path-runs through entire body– 5X more resistance to flow – functional difference between left &

right ventricle is reflected in anatomy• left ventricle walls are 3X as thick as

right ventricle wall– allows left ventricle to generate more

pressure• pulmonary trunk is attached to aortic arch

by ligamentum arteriosum

Ligamentum arteriosum

Label Me

Valve Function • atrioventricular

& semilunar valves

• open & close in response to blood pressure differences

AV VALVES• relaxed heart• AV valve flaps hang

limply in ventricle– blood flows from atria

into ventricle

• when ventricles contract intraventricular pressure increases– forces blood superiorly

against flaps causing flap edges to meet & close valve

Semi-Lunar Valves• ventricles

contractintraventricular pressure rises

• blood pushes against valvesopen

• ventricles relax intraventricular pressure fallsblood flows back from arteriesfills cuspsvalve closes

Coronary Circulation• heart muscle must have its own

source of oxygenated blood• supplied by coronary arteries

– originate at base of ascending aorta

– blood pressure• right coronary artery follows coronary

sulcus & supplies right atrium, parts of both ventricles & parts of conducting system

• left coronary artery supplies: left ventricle, left atrium & interventricular septum

• great cardiac vein– begins anterior surface of

ventricles along interventriuclar sulcus

• curves around left side of heart in coronary sulcus

• empties into coronary sinus

Heart Beat• myocytes-autorhythmic

– depolarize spontaneously at regular time intervals

– initiate contraction without signals from brain

• each beat begins with action potential generated at SA node (sino-atrial)-pacemaker– generates impulses at regular

intervals• to ensure four chambers of heart are

coordinated electrical signals travel through cardiac conduction system

• sympathetic & parasympathetic connections to heart can modify heart beat– not involved in normal contractions

Conducting System• autorhythmic cells in SA

node (sinoatrial node)– right atrium

• AV-atrioventricular node– junction of atria &

ventricles• atrioventricular bundle

or bundle of his• right & left bundle

branches• purkinje fibers

Initiation of Contraction• action potentials are spontaneously initiated by

autorhythmic cells in SA node• possess leaky membranes

– have unstable resting potentials– exchange Na, K & Ca ions– causes changes in polarization– cells are continuously depolarized– drift slowly toward threshold

• spontaneously changing membrane potentials are pacemaker potentials

• initiate action potentials which spread throughout heart

Impulse Conduction• SA node contract 75X/minute• sets pace for heart beat

– no other area has faster depolarization rate

– pacemaker • action potential- conducted to AV node-

bottom of right atrium– conduction delayed about 0.1 sec– AV delay allows atria to respond & have

complete contraction before ventricles contract

• impulse travels to Bundle of His- atrioventricular bundle

• splits into right & left bundle branches• bundle branches go along interventricular

septum toward apex divide into purkinje fibersmoderator band papillary muscle of right ventricle contracts before rest of ventricleapplies tension on chordae tendineaebraces AV valvesprevents back flow into atria when ventricles contract

• contraction proceeds from bottom of ventricles

• blood is pushed toward base of heart

Label Parts of Conducting System

ECG-EKG-Electrocardiography• electrical currents can be detected by

placing electrodes (leads) on skin’s surface

• electrocardiograph amplifies signals• produces record-EKG, ECG or

electrocardiogram• measures rate & regularity of beats• measures size & position of heart

chambers• sum of all electrical potentials

generated by all cells of heart at any moment

• each component of EKG reflects depolarization and/or repolarization of a part of heart

• because depolarization is signal for contractionelectrical events shown as waves on EKG can be associated with contraction or relaxation of atria & ventricles

EKG Trace-Deflection Waves• P Wave

– represents depolarization of atria

• QRS complex – represents ventricular

depolarization– atrial repolarization

occurs during this time but is obscured by QRS complex

• T Wave – represents ventricular

repolarization

EKG Trace

• size, duration & timing of waves tend to be consistent

• any change may reflect damage to or problems with conduction system

Abnormal EKG Traces• lowered P

– AV block• enlarged R

– may indicate enlarged ventricle

• flattened T– cardiac ischemia

• prolonged Q– repolarization

problem

Contraction• purkinje fibers distribute action potential to

contractile cells of heart• action potentialsCa appears among

myofibrils binds to troponin cross bridges form contraction

• differences from skeletal muscle contraction• action potentials-30X longer, from 250-

300msec• source of Ca is different• duration of contraction longer

Action Potential• resting potential of ventricular

contractile cell is -90mV• action potential begins when

membrane of ventricular cell is brought to threshold

• depolarization travels from cell to cell by ions passing through gap junctions

• action potential proceeds in 3 steps

• rapid depolarization• plateau• repolarization

Action Potential• rapid depolarization• fast Na channels openNa rushes

indepolarization• plateau phase

– action potential flattens as membrane potential nears +30mV

– Na channels close & slow Ca channels open

• slow Ca channels remain open 175msec

– as long as Ca enters cellcell contracts

• repolarization– takes place as plateau phase ends– slow Ca channels close & slow K

channels open– K rushes out of the cell– restores resting potential

Muscle Tension• develops during plateau phase• peaks just after plateau ends• long plateau helps prevent

sustained contraction or tetanus

• refractory period– time when muscle is

inexcitable– in cardiac muscle lasts as

long as contraction• important since cardiac muscle

must relax between contractions so ventricles can fill with blood– would stop pumping action

Cardiac Cycle• time between start of one

heartbeat & start of next• includes one contraction & one

relaxation• for each chamber-cycle is

divided into 2 phases:• contraction or systole

– chamber contracts & pushes blood into adjacent chamber or arterial trunk

• relaxation or diastole– chamber fills with blood

• fluids flow from areas of higher to areas of lower pressures

• blood flows only if one chamber’s pressure is higher than another

Phases of Cardiac Cycle• beginning all chambers relaxed• atria & ventricle diastole• AV valves between atria &

ventricles are opened• semilunar valves areclosed• blood flows from veins into atria &

into ventricles-Passive Filling• -ventricles 70% filled with blood• atria contractatrial systole• complete ventricular filling• end of atrial systole-end of ventricular

diastole• ventricular volume is greatest at this time

– end-diastolic volume or EDV– maximum amount of blood ventricles can

hold

Phases of Cardiac Cycle• atria relax• atrial diastole continues until start of next cardiac

cycle• begins at same time as ventricular systole• ventricles contractpressure in ventricles rises

above pressure in atriaAV valves close– first heart sound-lubb

• both AV & semilunar valves are closed– blood has nowhere to goventricles continue

to contract• isometric contractionpressure increasestension• no change in ventricular volume

– isovolumetric contraction• once pressure in ventricles is greater than pressure

in arterial trunks, semilunar valve open blood flows into pulmonary & aortic trucks

• beginning of ventricular ejection• each ventricle ejects 70 ml of blood = stroke

volume-SV• as ventricle systole endsventricular pressure falls

rapidly• blood in aorta & pulmonary trunks flows towards

ventricles & fills cusps of semilunar valves causing them to close

– second heart sound-dupp

ventricular

Phases of Cardiac Cycle• amount of blood remaining in ventricles-

ESV or end systolic volume• Ventricular Diastole

– ventricles relax– all valves are closed

• ventricular pressure-still high• no change in ventricular volume• since all valves are closed this is

isovolumetric relaxation• ventricular pressure falls rapidly now• when ventricular pressure falls below

pressures in aortaatrial pressure forces AV valves openblood flows from atria to ventricles

• both atria & ventricles are in diastole• ventricular pressure continues to fall as

chambers fill passively• cycle repeats• when heart rate increasesall phases

shorten• greatest reduction in diastole

ventricular

Blood Pressure• Systolic blood

pressure– pressure in aorta– 120 mmHg

• Diastolic blood pressure – 80mmHg

• when semilunar valves close, aortic pressure rises as elastic arterial walls recoil

• small, temporary rise in pressure-dicrotic notch

Heart Sounds• Ausculation

– listening to heart using stethoscope

• several areas on chest where these are best heard

• Aortic Area• Pulmonic Area• Tricuspid Area• Mitral Area

Heart Sounds• S1

– AV valves close-lubb• S2

– semilunars close-dupp

• S3– ventriclular filling

• S4– atrial contraction

• third & forth are faint• seldom detected in

normal people

Cardiodynamics• need to review some terms• EDV

– amount of blood in ventricles at end of ventricular diastole

• ESV– amount of blood in each ventricle at end of

ventricular systole

• Stroke Volume– amount of blood pumped out of each ventricle

during one beat

• SV = EDV – ESV

Cardiodynamics• Stroke volume

– most important factor when examining single cardiac cycle– largest when EDV is as large as can be & ESV is as small as can be

• Cardiac Output– most important when looking at cardiac function over time– amount of blood pumped by each ventricle/minute

– represents blood flow through peripheral tissues or total blood flow through body

• CO (ml/min) = heart rate (beats/min) X SV (ml/beat)• CO = 75bpm X 70mL/beat = 5.250L/minute-average total blood volume• not constant

– varies with body’s state of activity• exercise increases CO

• CO precisely adjusted so peripheral tissues receive adequate supply of blood under variety of conditions

Control of Cardiac Output• adjusted by changing

SV or HR• changes generally

reflect change in both SV & HR

• HR can be adjusted with autonomic nervous system & hormones

• SV can be adjusted by changing EDV, ESV or both

Factors Affecting Stroke Volume

• Preload–degree of stretch on heart

before contraction• Contractility

–forcefulness of contraction• Afterload

–pressure that must be exceeded before ejection of blood can occur

Preload• indicates degree of stretch

prior to contraction– directly proportional to EDV

• greater EDVgreater preload

• the more the heart fills with blood during diastolethe greater force of contraction during systole

• relationship-Frank-Starling Law of the Heart

• greater EDVgreater SV due to stretch on muscle fibers

• SV is directly proportional to EDV

Factors Affecting EDV• Two key factors

determine EDV:• duration of

ventricular diastole

• venous return• volume of blood

returning to right atrium

Contractility• amount of force produced

during contraction at a given preload

• factors that increase contractility are positive inotropic agents

• those that reduce it-negative inotrophic agents

• positive ionotropic factors typically stimulate Ca entry into cells

• negative ionotropic factors function to block Ca

Afterload • blood pressure outside semilunar

valves• opposes opening of these valves

– amount of tension ventricles must produce to force semilunar valves open & eject blood

• increased afterload reduces stroke volume

• greater afterload longer isovolumetric contraction

• shorter time of ventricular ejection, and larger ESV

• as afterload increasesSV decreases

• afterload can be increased by any factor that restricts blood flow through arterial system– constriction of peripheral blood

vesselsdecreases BP & increases afterload

Regulation of Heart Rate• nervous system does not initiate

heart beat• modulates rhythm & force• sympathetic & parasympathetic

fibers innervate heart via cardiac plexus

• sympathetic & parasympathetic fibers SA & AV nodes & atrial muscle cells

• ventricles also innervated by sympathetic fibers

Tonic Control of Heart• both centers are involved• both fire at steady level• vagus nerve maintains constant background

firing rate– inhibits nodes

• if vagus is cutHR increases because SA node fires on its own at about 100X per minute

• vagus intact• keeps heart rate 75bpm

Cardiac Center• located in medulla

oblongata• has cardioacceleratory &

cardioinhibitory part• cardioacceleratory center

sends signals by sympathetic fibers to SA node, AV node & myocardium

• secrete norepinephrine– binds to beta-1 receptors

in heart– increases heart rate– Increases the entrance

of calcium– Increases contractility

Cardiac Center• cardioinhibitory centers• send signals via

parasympathetic fibers in vagus nerve to SA & AV nodes

• secretes acetylcholine• opens potassium channels

in nodal cells• as potassium leaves

cellsbecome hyperpolarizedfire less frequentlyheart rate slows

Receptors to Cardiac Centers• receive & integrate information from

many sources• sensory & emotional stimuli can act

by cerebral cortex, limbic system & hypothalamus to change heart rate

• Proprioceptors in muscles & joints report changes in physical activity

• Baroreceptors or pressure receptors in aorta & internal carotid arteries send continuous information to cardiac centers

• Chemoreceptors send information about Na, K, hydrogen ions and oxygen

Chemoreceptors• responses to fluctuations in blood chemistry are

called chemoreflexes • in aortic arch, carotid arteries & medulla

oblongata• monitor ph, carbon dioxide & oxygen levels in

blood• more important in respiratory rate-can function

to change HR• carbon dioxide accumulates in blood & cerebral

spinal fluidpH lowers acidosis• stimulates cardiac center to increase heart rate• oxygen deficiencyslows heart rate

Hormones• Catecholamines

–epinephrine & norepinephrine

–adrenal medulla–increase heart rate & contractility