cardiovascular system the heart what is the cardiovascular ...€¦ · • internal features...

What is the Cardiovascular System?

Blood

circulated in

Arteries, veins, and capillaries

by the

Pumping action of the heart

Cardiovascular SystemThe Heart

Functions of the Heart

• Generating blood pressure sufficient to efficiently cause blood to flow from heart to veins

• Keeping oxygenated and low-oxygen blood separate

• Adjusting blood pressure as conditions change (maintain homeostasis)

– Changes in contraction rate and force match blood delivery to changing metabolic needs

Heart Anatomy

The Pulmonary and Systemic Circuits

• Heart is a transport system consisting of two side-by-side pumps

– Right side receives low-oxygen blood from tissues

• Moves blood to lungs to get rid of CO2, pick up O2, and return via pulmonary circuit

– Left side receives oxygenated blood from lungs

• Moves blood to body tissues via systemic circuit

Capillary bedsof lungs wheregas exchangeoccurs

Capillary bedsof all bodytissues where gasexchange occurs

Pulmonaryveins

Pulmonaryarteries

Systemic Circuit

Aorta and branches

Heart

Rightatrium Right

ventricle

Venaecavae

Leftatrium

Leftventricle

Pulmonary Circuit

Oxygen-rich,CO2-poor blood

Oxygen-poor,CO2-rich blood

Out to body tissues

and back –

oxygenate the

tissues, collect and

transport

To the lungs and

back – reoxygenate

the blood, transport

Location of the heart in the mediastinum.

Diaphragm

Sternum

2nd rib

Midsternal line

• Base (posterior surface) leans toward right shoulder

• Apex points toward left hip

• More of mass on left – lack of bilateral symmetry

• Fist-sized, 250-350 g

• Mediastinum = medial cavity of thorax

Chambers and Associated Great

Vessels

• Internal features

– Four chambers

• Two superior atria (singular atrium)

• Two inferior ventricles

– Interatrial septum: separates atria

• Fossa ovalis: remnant of foramen ovale of fetal heart

– Interventricular septum: separates ventricles

• ‘Walls’ consist of cardiac muscle, fibrous

connective tissue, others in lesser amounts

Brachiocephalic trunk

Superior vena cava

Right pulmonary artery

Ascending aorta

Pulmonary trunk

Right pulmonary veins

Right atrium

Right coronary artery(in coronary sulcus)

Anterior cardiac vein

Right ventricle

Right marginal artery

Small cardiac vein

Inferior vena cava

Anterior view

Left common carotidartery

Left subclavian artery

Aortic arch

Ligamentum arteriosum

Left pulmonary artery

Left pulmonary veins

Auricle ofleft atrium

Circumflex artery

Left coronary artery(in coronary sulcus)

Left ventricle

Great cardiac vein

Anterior interventricularartery (in anteriorinterventricular sulcus)

Apex

Aorta



Auricle of left atrium

Great cardiac vein

Posterior vein ofleft ventricle

Apex

Left atrium

Left ventricle

Posterior surface view

Superior vena cava

Right atrium



Inferior vena cava

Coronary sinus

Right coronary artery(in coronary sulcus)

Posterior interventricularartery (in posteriorinterventricular sulcus)

Middle cardiac vein

Right ventricle

Superior vena cava

Right atrium


Pulmonary trunk


Fossa ovalis

Pectinate muscles

Tricuspid valve

Right ventricle

Chordae tendineae

Trabeculae carneae

Inferior vena cava

Frontal section

Aorta


Left atrium


Mitral (bicuspid) valve

Aortic valve

Pulmonary valve

Left ventricle

Papillary muscle

Interventricular septum

Epicardium

Myocardium

Endocardium


Vessels (cont.)

Atria

• Auricle vs atrium

• Small, thin-walled– Receive blood from veins; Convey blood to

ventricles below

• Right atrium: receives low-oxygen blood from systemic veins– Superior & inferior vena cava, coronary sinus

• Left atrium: receives oxygenated blood from lungs– Four pulmonary veins


Vessels (cont.)

Ventricles

• Contain most of the volume of heart

• Primary pump– Thickness of ventricular myocardium reflects workload

• Right ventricle – Pumps blood into pulmonary trunk and pulmonary circulation

• Left ventricle– Pumps blood into aorta and systemic circulation

• Muscular appendages– Trabeculae carneae

• Prevent suction, aid papillary muscles

– Papillary muscles• Anchor chordae tendineae

The layers of the pericardium and of the heart wall.

Fibrous pericardium

Parietal layer of serous

pericardium

Pericardial cavity

Epicardium (visceral

layer of serous

pericardium)

Myocardium

Endocardium

Pulmonarytrunk

Heart chamber

Pericardium

Myocardium

Heart

wall

1. Superficial fibrous pericardium: functions to protect, anchor heart to surrounding structures, and prevent overfilling

2. Deep two-layered serous pericardium– Parietal layer lines internal surface of fibrous pericardium

– Visceral layer (epicardium) on external surface of heart

– Two layers separated by fluid-filled pericardial cavity (decreases friction)

Three Layers Of Heart Wall

1. Epicardium: visceral layer of serous pericardium

2. Myocardium: circular or spiral bundles of contractile cardiac muscle cells

– Cardiac skeleton: crisscrossing, interlacing layer of connective tissue

• Anchors cardiac muscle fibers

• Supports great vessels and valves

• Limits spread of action potentials to specific paths

3. Endocardium: innermost layer continuous with blood vessel endothelium– Lines heart chambers and covers cardiac skeleton

of valves

Heart valvesPulmonary valve

Aortic valve

Area of cutaway

Mitral valve

Tricuspid valve

Myocardium

Tricuspid(right atrioventricular) valve

Mitral(left atrioventricular)valve

Aorticvalve

Pulmonaryvalve

Cardiacskeleton Anterior

The function of the atrioventricular (AV) valves

Direction of

blood flow

Atrium

Ventricle

Cusp of

atrioventricular

valve (open)

Chordae

tendineae

Papillary

muscle

Atria contract, forcingadditional blood into ventricles.

As ventricles fill, AV valveflaps hang limply into ventricles.

Blood returning to theheart fills atria, pressingagainst the AV valves. Theincreased pressure forcesAV valves open.

3

2

1

AV valves open; atrial pressure greater than ventricular pressure

The function of the semilunar (SL) valves

Semilunar valves open

As ventricles contractand intraventricularpressure rises, bloodis pushed up againstsemilunar valves,forcing them open.

Pulmonarytrunk

Aorta

Semilunar valves closed

As ventricles relaxand intraventricularpressure falls, bloodflows back fromarteries, filling thecusps of semilunarvalves and forcingthem to close.

Pathway of Blood Through Heart and

Connected Vessels

• Equal volumes of blood are pumped through two circuits

• Pulmonary circuit – short, low-pressure

– ‘reoxygenation’

• Systemic circuit– long, high-friction

– ‘distribution’

• Anatomy of ventricles reflects differences– Left ventricle walls are much thicker than right

• Pumps with greater pressure

Right

atrium

Aorta

To body

To heart

To heart

To lungs

Mitralvalve

Leftventricle

Left

atrium

Pulmonary

veins

Pulmonary

arteries

Aorticsemilunarvalve

Tricuspid

valve

Tricuspid

valve

Pulmonary

trunk

Right

ventricle

Pulmonary

semilunar

valve

Pulmonary

semilunar valve

IVC

SVC

Mitralvalve

Aorticsemilunar valve

Coronary

sinus

Oxygen-poor blood is carriedin two pulmonary arteries tothe lungs (pulmonary circuit)to be oxygenated.

Oxygen-poor bloodreturns from the bodytissues back to the heart.

Oxygen-rich blood isdelivered to the bodytissues (systemic circuit).

Oxygen-rich bloodreturns to the heart viathe four pulmonary veins.

Pulmonarycapillaries

Systemic

capillaries

Superior vena cava (SVC)Inferior vena cava (IVC)

Coronary sinus

Rightatrium

Rightventricle

Pulmonarytrunk

LeftventricleAorta

Leftatrium

Four pulmonary

veins

Oxygen-poor blood

Oxygen-rich blood

Pathway of Blood Through Heart and Connected Vessels

Coronary Circulation• Coronary arteries and veins

• Functional blood supply to and from heart muscle– Living muscle tissue with limited anaerobic capabilities

– Delivered when heart is relaxed• myocardium contracted prevents blood flow

– Shortest circulation in body

• Left ventricle receives most of coronary blood supply; Heart receives 1/20th of body’s blood supply

• Arteries contain many anastomoses (junctions)– Provide additional routes for blood delivery but can’t completely

compensate for vessel occlusion

– Narrowing, closing, plugging leads to ischemia and/or infarction

• Branching of coronary arteries varies among individuals

Rightventricle

Aorta

Anastomosis(junction ofvessels)

Superiorvena cava

Left atrium

Pulmonarytrunk

Rightatrium

Rightcoronaryartery

Rightmarginalartery

Posteriorinterventricularartery

Anteriorinterventricularartery

Circumflexartery

Leftventricle

Leftcoronaryartery

Both left and right coronary arteries arise from

base of aorta and supply arterial blood to heart

© 2016 Pearson Education, Inc.

Superiorvena cava

Anteriorcardiacveins

Smallcardiac

vein

Middlecardiacvein

Coronarysinus

Greatcardiacvein

Microscopic anatomy of cardiac muscle fibers

Nucleus

Nucleus

I band

Cardiac muscle cell

A bandSarcolemma

Z disc

Mitochondrion

Mitochondrion

T tubule

Sarcoplasmic

reticulum

I band

Intercalated disc

Similarities with skeletal muscle

• Muscle contraction is preceded by depolarizing action potential

• Depolarization wave travels down T tubules; causes sarcoplasmic reticulum (SR) to release Ca2+

• Excitation-contraction coupling occurs – Ca binds to troponin causing filaments to slide

Desmosomes (keep

myocytes from pulling apart)

Gap junctions (electrically

connect myocytes)Nucleus

Intercalated

discs

Cardiac

muscle cell

Microscopic anatomy of cardiac muscle.

Pacemaker myocytes

Long absolute refraction

Differences in the Physiology of

Skeletal and Cardiac Muscle

• Heart contracts as a unit

– Cardiomyocytes form a functional syncytium for

effective pumping action

– Skeletal muscle fibers contract independently

• Influx of Ca2+ from extracellular fluid triggers

Ca2+ release from SR

– Depolarization opens slow Ca2+ channels in

sarcolemma, allowing Ca2+ to enter cell

– Extracellular Ca2+ then causes SR to release its

intracellular Ca2+

– Skeletal muscles do not use extracellular Ca2+

Differences in the Physiology of

Skeletal and Cardiac Muscle

Almost exclusively relying on aerobic respiration

• Cardiac muscle has more mitochondria than

skeletal muscle

• Skeletal muscle (depending on type) can go

through fermentation when oxygen not present

• Both types of tissues can use other fuel sources

– Cardiac is more adaptable to other fuels, including

lactic acid, but must have oxygen

Setting the Basic Rhythm: The Intrinsic Conduction System

Coordinated heartbeat is a function of:

1. Presence of gap junctions

2. Intrinsic cardiac conduction system

• Network of noncontractile (autorhythmic) cells

• Cardiac pacemaker cells have unstable resting membrane potentials called pacemaker potentials or prepotentials

• Initiate and distribute impulses to coordinate depolarization and contraction of heart

What is extrinsic control?

Action Potential Initiation By Pacemaker Cells

1. Pacemaker potential

2. Depolarization

3. Repolarization

Pacemaker and action potentials of typical cardiac pacemaker cells

Time (ms)

−70

Actionpotential

Threshold

Pacemakerpotential

−60

−40

−30

−20

−10

0

+10

−50

Mem

bra

ne p

ote

nti

al (m

V)

Pacemaker potential This slow

depolarization is due to both opening of Na+

channels and closing of K+ channels. Noticethat the membrane potential is never a flat line.

Depolarization The action potential

begins when the pacemaker potential reachesthreshold. Depolarization is due to Ca2+ influxthrough Ca2+ channels.

Repolarization is due to Ca2+ channels

inactivating and K+ channels opening. Thisallows K+ efflux, which brings the membranepotential back to its most negative voltage.

1

2

3

3

2

3

11

2

The Intrinsic Conduction System

1. Sinoatrial (SA) node– Primary pacemaker of heart in right atrial wall

• Spontaneously depolarizes faster than rest of myocardium

– Generates impulses about 75/minute• sinus rhythm

• Inherent rate of 100/minute tempered by extrinsic factors including parasympathetic inhibition

– Impulse spreads across atria cell to cell, reaching AV node


2. Atrioventricular (AV) node– In inferior interatrial septum

– Delays impulses approximately 0.1 second• Cause: fibers are smaller in diameter, have fewer gap

junctions

• Allows atrial contraction prior to initiation of ventricular contraction

– Inherent rate of 50/minute in absence of SA node input

– “ectopic focus” if it becomes primary pacesetter


3. Atrioventricular (AV) bundle (bundle of His)– In superior interventricular septum

– Only electrical connection between atria and ventricles

• Atria and ventricles not connected via gap junctions

– Carries AP through electrically-neutral cardiac skeleton

4. Right and left bundle branches– Two pathways in interventricular septum

– Carry impulses toward apex of heart


5. Subendocardial conducting network• Also referred to as Purkinje fibers

– Complete pathway through interventricular septum into apex and ventricular walls, then cell to cell

– AV bundle and subendocardial conducting network depolarize 30/minute in absence of AV node input “ectopic focus”

– Ventricular contraction initiates at apex toward atria

– Process from initiation at SA node to complete contraction takes ~0.22 seconds

Pacemaker potential

Plateau

Internodal pathway

Superiorvena cava Right atrium

Left atrium

Subendocardialconductingnetwork(Purkinje fibers)

Inter-ventricularseptum

Pacemakerpotential

Ventricularmuscle

AV node

Atrial muscle

SA node

0 200 400 600

Milliseconds

Comparison of action potential shape

at various locations

Anatomy of the intrinsic conduction system showing the sequence

of electrical excitation

The sinoatrial(SA) node (pacemaker)generates impulses.

The impulsespause (0.1 s) at theatrioventricular(AV) node.

Theatrioventricular(AV) bundle

connects the atriato the ventricles.

The bundle branches

conduct the impulses through the interventricular septum.

The subendocardialconducting network

depolarizes the contractilecells of both ventricles.

1

2

3

4

5

Autonomic (extrinsic)

innervation of the heart

Thoracic spinal cord

Cardioinhibitory

center

Cardioacceleratory

center Medulla oblongata

Sympathetictrunkganglion

Dorsal motor nucleus

of vagus

AVnode

SAnode

Parasympathetic neurons

Interneurons

Sympathetic neurons

Sympathetic trunk

Sympathetic cardiacnerves increase heart rateand force of contraction.

The vagus nerve(parasympathetic)decreases heart rate. Heartbeat modified by ANS

via cardiac centers in medulla oblongata• Cardioacceleratory center:

sends signals through sympathetic trunk to increase both rate and force

– Stimulates SA and AV nodes, heart muscle, and coronary arteries

• Cardioinhibitory center: parasympathetic signals via vagus nerve to decrease rate

– Inhibits SA and AV nodes via vagus nerve

• Remember: nervous stimulation is dependent on AP frequency, type of neurotransmitter, type of receptor

Action Potentials of Contractile Cardiac Muscle Cells

• Contractile muscle fibers make up bulk of heart and are responsible for pumping action

– Different from skeletal muscle contraction; cardiac muscle action potentials have plateau

• Steps involved in AP:

1. Depolarization opens fast voltage-gated Na+ channels; Na+ enters cell

Action Potentials of Contractile Cardiac Muscle Cells (cont.)

2. Depolarization by Na+ also opens slow Ca2+

channels

• At +30 mV, Na+ channels close, but slow Ca2+ channels remain open, prolonging depolarization

– Seen as a plateau

3. After about 200 ms, slow Ca2+ channels close, and voltage-gated K+ channels open

• Rapid efflux of K+ repolarizes cell to RMP

• Ca2+ is pumped both back into SR and out of cell into extracellular space

Action Potentials of Contractile Cardiac Muscle Cells (cont.)

• More differences between contractile muscle fiber and skeletal muscle fiber contractions– AP in skeletal muscle lasts 1–2 ms; in cardiac muscle it

lasts 200 ms

– Contraction in skeletal muscle lasts 15–100 ms; in cardiac contraction lasts over 200 ms

• Benefit of longer AP and contraction:– Sustained contraction ensures efficient ejection of

blood

– Longer refractory period prevents tetanic contractions

The action potential of contractile cardiac muscle cells.

−80

−60

−40

−20

0

20 Plateau

0 150 300

Plateau phase is due to Ca2+ influx

through slow Ca2+ channels. This keepsthe cell depolarized because most K+

channels are closed.

Time (ms)

Absoluterefractoryperiod

Tensiondevelopment(contraction)

Actionpotential

Ten

sio

n (

g)

Mem

bra

ne p

ote

nti

al (m

V)

Repolarization is due to Ca2+

channels inactivating and K+ channelsopening. This allows K+ efflux, whichbrings the membrane potential back toits resting voltage.

Depolarization is due to Na+ influx

through fast voltage-gated Na+ channels.A positive feedback cycle rapidly opensmany Na+ channels, reversing themembrane potential. Channel inactivationends this phase.

1

2

3

3

2

1

Mechanical Events

• Systole: period of heart contraction

• Diastole: period of heart relaxation

• Cardiac cycle:

– Atrial systole and diastole and ventricular systole and diastole

– Cycle represents series of pressure and blood volume changes leading to movement of blood in vessels

– Mechanical events follow electrical events seen on ECG

• Blood flows from area of high pressure to area of low pressure unless impeded (by things like valves)

Mechanical Events of Heart and Phases of the Cardiac Cycle

Ventricular filling1. Passive filling phase = atrial and ventricular diastole, all chambers filling2. Active filling phase = atrial systole but ventricles relaxed – ‘forced’

filling of ventricles• End diastolic volume (EDV): volume of blood in each ventricle at end

of ventricular diastoleVentricular systole3. Isovolumetric contraction phase: all valves are closed4. Ejection phase: ventricular pressure exceeds pressure in large arteries, forcing SL valves open

• Pressure in aorta around 120 mm Hg• End systolic volume (ESV): volume of blood remaining in each ventricle

after systole5. Isovolumetric relaxation phase: early ventricular diastole, atria

already in diastole and accepting venous blood

Heart Sounds• Two sounds (lub-dup)

• Associated with closing of heart valves

– First sound is closing of AV valves at beginning of ventricular systole

– Second sound is closing of SL valves at beginning of ventricular diastole

• Pause between lub-dups indicates heart relaxation

Electrocardiography

• Electrocardiograph can detect electrical currents generated by heart

• Electrocardiogram (ECG or EKG) is a graphic recording of electrical activity

– Composite of all action potentials at given time; not a tracing of a single AP

– Electrodes are placed at various points on body to measure voltage differences

• A diagnostic tool

An electrocardiogram (ECG) tracing.

Sinoatrialnode

QRS complex

Ventriculardepolarization

P-RInterval

0 0.2 0.4 0.6 0.8

Ventricularrepolarization

Atrialdepolarization

Atrioventricularnode

S-TSegment

Q-TInterval

Time (s)

S

Q

P T

R

Atrial depolarization, initiated by theSA node, causes the P wave.

P

R

T

QS

P

R

T

QS

P

R

T

QS

P

R

T

QS

P

R

T

QS

P

R

T

QS

SA node

AV node

With atrial depolarization complete,the impulse is delayed at the AV node.

Ventricular depolarization begins atapex, causing the QRS complex. Atrialrepolarization occurs.

Ventricular depolarization is complete.

Ventricular repolarization beginsat apex, causing the T wave.

3

2

1

4

6 Ventricular repolarization iscomplete.

Depolarization

Repolarization

5

Cardiac Output (CO)

• Volume of blood pumped by each ventricle in 1 minute

• Highly variable– CO changes (increases/decreases) if either or both SV or HR

is changed

• CO = heart rate (HR) stroke volume (SV)– HR = number of beats per minute– SV = volume of blood pumped out by one ventricle (left)

with each beat

• At rest:CO (ml/min) = HR (75 beats/min) SV (70 ml/beat)

= 5.25 L/min

Average Values

Cardiac Reserve

Difference between resting and maximal CO

• Maximal CO is 4–5 times resting CO in nonathletic people (20–25 L/min)

• Maximal CO may reach 35 L/min in trained athletes

Regulation of Cardiac OutputStroke Volume Mathematically: SV = EDV − ESV

• EDV is affected by length of ventricular diastole and venous pressure – 120 ml/beat

• ESV is affected by arterial BP and force of ventricular contraction – 50 ml/beat

• Normal SV = 120 ml − 50 ml = 70 ml/beat

• Three main factors that affect SV:– Preload– Contractility– Afterload

120

80

40

0

Left heart

P

1st 2nd

QRS

P

120

50

Atrial systole

Dicrotic notch

Left ventricle

Left atrium

EDV

SV

Aorta

Open OpenClosed

Closed ClosedOpen

ESV

Left atrium

Right atrium

Left ventricle

Right ventricle

Ventricular

filling

Atrial

contraction

Ventricular filling

(mid-to-late diastole)

Ventricular systole

(atria in diastole)

Isovolumetric

contraction phase

Ventricular

ejection phase

Early diastole

Isovolumetric

relaxation

Ventricular

filling

T

1 2a 2b 3

Atrioventricular valves

Aortic and pulmonary valves

Phase

Ve

ntr

icu

lar

vo

lum

e (

ml)

Pre

ssu

re (

mm

Hg

)

Heart sounds

Electrocardiogram

1 2a 2b 3 1

Putting it

all

together!

Regulation of Stroke Volume

Preload: degree of stretch of heart muscle just before systole• Stretch is directly proportional to volume of blood present in the

chamber

• Cardiac muscle exhibits a length-tension relationship– At rest, cardiac muscle cells are shorter than optimal length– Increases in EDV/blood volume stretch chamber walls & muscle cells

optimizing length-tension– a big increase in contractile force results as muscle cells shorten to

greater degree

• Most important factor in preload stretching of cardiac muscle is venous return—amount of blood returning to heart

Regulation of Stroke Volume (cont.)

Preload (cont.)• Increasing preload

– Slowed heart rate - more time for ventricles to fill – equilibrates in moments

– Exercise - increased venous return due to body movement

– Both stretch ventricles (chamber walls) and increase contraction force

• Frank-Starling law of the heart– “ability of the heart to change its force of contraction and therefore stroke

volume in response to changes in venous return”

Frank-Starling Law

ReturnVenous → EDV → SV → CO


Contractility

• Contractile strength at given muscle length– Independent of muscle stretch and EDV

• Increased contractility lowers ESV; caused by:– Sympathetic epinephrine release stimulates increased Ca2+

influx, leading to more cross bridge formations

– Positive inotropic agents increase contractility• Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca2+

• Decreased by negative inotropic agents– Acidosis (excess H+), increased extracellular K+, calcium

channel blockers

Norepinephrine

Adenylate

cyclase

ATPcAMP

GT P

G protein (Gs)

Active

protein

kinase

Phosphorylates

Sarcoplasmic

reticulum (SR)

Inactive

protein

kinase

Cardiac muscle

cytoplasm

Extracellular fluid

ATP is

converted

to cAMP

GTPGDP

Receptor

(1-adrenergic)

Ca2+ channels in the

plasma membrane

Ca2+ channels

in the SR

Ca2+

Ca2+ entry from

extracellular fluid

Ca2+ release

from SR

Ca2+ binding to troponin;

Cross bridge binding for contraction

Force of contraction


Afterload: back pressure exerted by arterial blood on semilunar valves

• ventricles must overcome afterload to eject blood

– Back pressure from arterial blood pushing on SL valves is major pressure

• Aortic pressure is around 80 mm Hg

• Pulmonary trunk pressure is around 10 mm Hg

• Hypertension increases afterload, resulting in increased ESV and reduced SV

Factors involved in determining cardiac output.

Exercise (bysympathetic activity,skeletal muscle andrespiratory pumps;

see Chapter 19)

Ventricularfilling time (due to heart rate)

Bloodborneepinephrine,

thyroxine,excess Ca2+

CNS output inresponse to exercise,

fright, anxiety, or blood pressure

Venousreturn

ContractilitySympathetic

activityParasympathetic

activity

EDV(preload)

ESV

Stroke volume (SV) Heart rate (HR)

Initial stimulus

Physiological response

ResultCardiac output (CO = SV HR)

cardiovascular system the heart what is the cardiovascular ...€¦ · • internal features...

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