Physiology of

Cardiovascular System

Heart Anatomy

Approximately the size of your fist

Location
Superior surface of diaphragm
Left of the midline
Anterior to the vertebral column, posterior to the
sternum

Heart Anatomy

Figure 18.1

Coverings of the Heart: Anatomy

Pericardium a double-walled sac around the heart

composed of:
A superficial fibrous pericardium
A deep two-layer serous pericardium
The parietal layer lines the internal surface of the
fibrous pericardium
The visceral layer or epicardium lines the surface
of the heart
They are separated by the fluid-filled pericardial
cavity

Coverings of the Heart: Physiology

The pericardium:
Protects and anchors the heart
Prevents overfilling of the heart with blood
Allows for the heart to work in a relatively frictionfree environment

Pericardial Layers of the Heart

Figure 18.2

Heart Wall

Epicardium visceral layer of the serous

pericardium
Myocardium cardiac muscle layer forming the
bulk of the heart
Fibrous skeleton of the heart crisscrossing,
interlacing layer of connective tissue
Endocardium endothelial layer of the inner
myocardial surface

External Heart: Major Vessels of the Heart

(Anterior View)

Vessels returning blood to the heart include:

Superior and inferior venae cavae
Right and left pulmonary veins

Vessels conveying blood away from the heart

include:
Pulmonary trunk, which splits into right and left
pulmonary arteries
Ascending aorta (three branches) brachiocephalic,
left common carotid, and subclavian arteries

External Heart: Vessels that Supply/Drain the

Heart (Anterior View)

Arteries right and left coronary (in atrioventricular

groove), marginal, circumflex, and anterior
interventricular arteries
Veins small cardiac, anterior cardiac, and great
cardiac veins

External Heart: Anterior View

Figure 18.4b

External Heart: Major Vessels of the Heart

(Posterior View)

Vessels returning blood to the heart include:

Right and left pulmonary veins
Superior and inferior venae cavae

Vessels conveying blood away from the heart

include:
Aorta
Right and left pulmonary arteries

External Heart: Vessels that Supply/Drain the

Heart (Posterior View)

Arteries right coronary artery (in atrioventricular

groove) and the posterior interventricular artery (in
interventricular groove)
Veins great cardiac vein, posterior vein to left
ventricle, coronary sinus, and middle cardiac vein

External Heart: Posterior View

Figure 18.4d

Gross Anatomy of Heart: Frontal Section

Figure 18.4e

Circulation Reviewed

Heart "four chambered"

Right atrium & ventricle

Pulmonary circuit

Left atrium & ventricle

Systemic circuit

Atria of the Heart

Atria are the receiving chambers of the heart

Each atrium has a protruding auricle
Pectinate muscles mark atrial walls
Blood enters right atria from superior and inferior
venae cavae and coronary sinus
Blood enters left atria from pulmonary veins

Ventricles of the Heart

Ventricles are the discharging chambers of the heart

Papillary muscles and trabeculae carneae muscles
mark ventricular walls
Right ventricle pumps blood into the pulmonary
trunk
Left ventricle pumps blood into the aorta

Circulation review

Blood Vessels "closed circulation"

Arteries from heart
Capillaries cell exchange
Veins to heart

Pathway of Blood Through the Heart and Lungs

Right atrium tricuspid valve right ventricle

Right ventricle pulmonary semilunar valve
pulmonary arteries lungs
Lungs pulmonary veins left atrium
Left atrium bicuspid valve left ventricle
Left ventricle aortic semilunar valve aorta
Aorta systemic circulation

Circulation Reviewed

Figure 14-1: Overview of circulatory system anatomy

Pathway of Blood Through the Heart and Lungs

Figure 18.5

Coronary Circulation

Coronary circulation is the functional blood supply

to the heart muscle itself
Collateral routes ensure blood delivery to heart even
if major vessels are occluded

Coronary Circulation: Arterial Supply

Figure 18.7a

Coronary Circulation: Venous Supply

Figure 18.7b

Heart Valves

Heart valves ensure unidirectional blood flow

through the heart
Atrioventricular (AV) valves lie between the atria
and the ventricles
AV valves prevent backflow into the atria when
ventricles contract
Chordae tendineae anchor AV valves to papillary
muscles

Heart Valves

Aortic semilunar valve lies between the left ventricle

and the aorta
Pulmonary semilunar valve lies between the right
ventricle and pulmonary trunk
Semilunar valves prevent backflow of blood into the
ventricles

Heart Valves

Figure 18.8a, b

Heart Valves

Figure 18.8c, d

Atrioventricular Valve Function

Figure 18.9

Semilunar Valve Function

Figure 18.10

Heart Sounds

Heart sounds (lub-dup) are associated with closing

of heart valves
First sound occurs as AV valves close and signifies
beginning of systole
Second sound occurs when SL valves close at the
beginning of ventricular diastole

Heart Sounds

32

Microscopic Anatomy of Heart Muscle

Cardiac muscle is striated, short, fat, branched, and

interconnected
The connective tissue endomysium acts as both
tendon and insertion
Intercalated discs anchor cardiac cells together and
allow free passage of ions
Heart muscle behaves as a functional syncytium

Microscopic Anatomy of Heart Muscle

Figure 18.11

Cardiac Muscle Cells:

Myocardial Autorhythmic Cells
Membrane potential never
rests pacemaker potential.
Myocardial Contractile Cells
Have a different looking action
potential due to calcium
channels.
General cardiac cell stuff:
Intercalated discs
Allow branching of the
myocardium
Gap Junctions (instead of
synapses)
Fast Cell to cell signals
Many mitochondria
Large T tubes
: Cardiac muscle

Coordinating the Pump: Electrical Signal Flow

Figure 14-18: Electrical conduction in myocardial cells

Mechanism of Cardiac Contractile Cell Muscle

Excitation, Contraction & Relaxation

Excitation-contraction coupling and relaxation in cardiac muscle

The heart; why is the left side of the heart

hypertrophied compared to the right side?

Modulation of Contraction

Graded Contraction: proportional to crossbridges

formed
More [Ca++]: crossbridges, more force & speed
Under catecholemine control:
Norepinephrine
Epinephrine

Modulation of Contraction- what is the key ion?

Modulation of cardiac contraction by catecholamines

Action potential of a cardiac contractile cell

Refractory period

Autorhythmic Cells: Initiation of Signals

Pacemaker membrane potential
I-f channels Na+ influx
Ca++ channels influx, to AP
Slow K+ open repolarization

Funny current (or funny channel, or If, or IKf, or pacemaker

current) refers to a specific current in the heart. The funny current
is highly expressed in spontaneously active cardiac regions, such
as the sinoatrial node (SAN, the natural pacemaker region), the
atrio-ventricular node (AVN) and the Purkinje fibres of conduction
tissue.

Action potentials of Autorhythmic Cells:

Pacemaker potential

Depolarization due to calcium NOT sodium!

Action potentials in cardiac autorhythmic cells

Pacemaker and Action Potentials of the Heart

Figure 18.13

Sympathetic and Parasympathetic

Sympathetic speeds heart rate by Ca++ & I-f channel flow
Parasympathetic slows rate by K+ efflux & Ca++ influx

Figure 14-17: Modulation of heart rate by the nervous system

Coordinating the Pump: Electrical Signal Flow

Figure 14-19a: Electrical

conduction in the heart

Cardiac Muscle Contraction

Heart muscle:
Is stimulated by nerves and is self-excitable
(automaticity)
Contracts as a unit
Has a long (250 ms) absolute refractory period

Cardiac muscle contraction is similar to skeletal

muscle contraction

Heart Physiology: Intrinsic Conduction System

Autorhythmic cells:
Initiate action potentials
Have unstable resting potentials called pacemaker
potentials
Use calcium influx (rather than sodium) for rising
phase of the action potential

The Heart: Conduction System

Intrinsic conduction system

(nodal system)
Heart muscle cells contract, without nerve
impulses, in a regular, continuous way

The Heart: Conduction System

Special tissue sets the pace
Sinoatrial node (right
atrium)
Pacemaker
Atrioventricular node
(junction of r&l atria
and ventricles)
Atrioventricular bundle
(Bundle of His)
Bundle branches (right
and left)
Purkinje fibers

Heart Physiology: Sequence of Excitation

Sinoatrial (SA) node generates impulses about 75

times/minute
Atrioventricular (AV) node delays the impulse
approximately 0.1 second
Impulse passes from atria to ventricles via the
atrioventricular bundle (bundle of His)

Heart Physiology: Sequence of Excitation

AV bundle splits into two pathways in the

interventricular septum (bundle branches)
Bundle branches carry the impulse toward the apex
of the heart
Purkinje fibers carry the impulse to the heart apex
and ventricular walls

Heart Physiology: Sequence of Excitation

Figure 18.14a

Heart Excitation Related to ECG

Figure 18.17

Extrinsic Innervation of the Heart

Heart is stimulated
by the sympathetic
cardioacceleratory
center
Heart is inhibited by
the parasympathetic
cardioinhibitory
center
Figure 18.15

Electrocardiography

Electrical activity is recorded by electrocardiogram

(ECG)
P wave corresponds to depolarization of SA node
QRS complex corresponds to ventricular
depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger
QRS complex

Electrocardiograms (EKG/ECG)

Three formations
P wave: impulse across atria
QRS complex: spread of impulse down septum,
around ventricles in Purkinje fibers
T wave: end of electrical activity in ventricles

The electrocardiogram

Cardiac muscle polarization & ECG

SA node
AV node

Electrocardiography

Figure 18.16

Electrocardiograms (EKG/ECG)

Figure 8.15B, C

Cardiac Cycle

Cardiac cycle refers to all events associated with

blood flow through the heart
Systole contraction of heart muscle
Diastole relaxation of heart muscle

The Heart: Cardiac Cycle

Atria contract simultaneously

Atria relax, then ventricles contract
Systole = contraction
Diastole = relaxation

Phases of the Cardiac Cycle

Isovolumetric relaxation early diastole

Ventricles relax
Backflow of blood in aorta and pulmonary trunk
closes semilunar valves

Dicrotic notch brief rise in aortic pressure caused

by backflow of blood rebounding off semilunar
valves

Phases of the Cardiac Cycle

Ventricular filling mid-to-late diastole

Heart blood pressure is low as blood enters atria
and flows into ventricles
AV valves are open, then atrial systole occurs

Phases of the Cardiac Cycle

Ventricular systole
Atria relax
Rising ventricular pressure results in closing of AV
valves
Isovolumetric contraction phase
Ventricular ejection phase opens semilunar valves

Filling of Heart Chambers

Figure 11.6

Phases of the Cardiac Cycle

Figure 18.20

Phases of the Cardiac Cycle

Figure 18.20

Summary

The Wiggers diagram

Cardiac Output (CO) and Reserve

CO is the amount of blood pumped by each ventricle

in one minute
CO is the product of heart rate (HR) and stroke
volume (SV)
HR is the number of heart beats per minute
SV is the amount of blood pumped out by a ventricle
with each beat
Cardiac reserve is the difference between resting and
maximal CO

Cardiac Output: Example

CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)

CO = 5250 ml/min (5.25 L/min)

Regulation of Stroke Volume

SV = end diastolic volume (EDV) minus end

systolic volume (ESV)
EDV = amount of blood collected in a ventricle
during diastole
ESV = amount of blood remaining in a ventricle
after contraction

Factors Affecting Stroke Volume

Preload amount ventricles are stretched by

contained blood
Contractility cardiac cell contractile force due to
factors other than EDV
Afterload back pressure exerted by blood in the
large arteries leaving the heart

Frank-Starling Law of the Heart

Preload, or degree of stretch, of cardiac muscle cells

before they contract is the critical factor controlling
stroke volume
Slow heartbeat and exercise increase venous return
to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease
SV

Preload and Afterload

Figure 18.21

Extrinsic Factors Influencing Stroke Volume

Contractility is the increase in contractile strength,

independent of stretch and EDV
Increase in contractility comes from:
Increased sympathetic stimuli
Certain hormones
Ca2+ and some drugs

Extrinsic Factors Influencing Stroke Volume

Agents/factors that decrease contractility include:

Acidosis
Increased extracellular K+
Calcium channel blockers

Contractility and Norepinephrine

Sympathetic
stimulation
releases
norepinephrine
and initiates a
cyclic AMP
secondmessenger
system
Figure 18.22

Regulation of Heart Rate

Positive chronotropic factors increase heart rate

Negative chronotropic factors decrease heart rate

Regulation of the heart

86

Cardiac pressor reflex

stretch receptors(baroreceptors)
aortic baroreceptor- location aorta
carotid baroreceptor -location common carotid

Cardiac pressor reflex

CAROTID SINUS REFLEX

Sensor- baroreceptors found in the carotid
sinus
carotid sinus found at beginning of the internal
carotid
and under sternocleidomastoid muscle

Cardiac pressor reflex

afferent fibers - bring information to the

integrator
sensory impulse from carotid baroreceptor
travels up the Herring nerve
joins the IX glossopharyngeal nerve
goes to cardiac control center of the medulla
oblongata

Homeostasis - carotid sinus reflex

SENSORS- baroreceptors found in the carotid sinus

INTEGRATOR- medulla oblongata cardioregulatory
center
EFFECTOR- SA node
Stimulus -sudden raise in heart rate and or BP
Result - Heart rate decreases, BP decreases

AORTIC REFLEX
sensors location- aortic arch

afferent fibers
aortic nerve joins the VAGUS nerve
goes to cardiac control center
integrator- medulla oblongata cardioregulatory center
efferent fibers

VAGUS nerve goes to SA node

also causes acetylcholine to be released

AORTIC REFLEX, cont.

effector- SA node
stimulus for reflex- Sudden raise in heart rate and or BP
Result of stimulation- Heart rate decreases, blood
pressure decreases
cellular mechanism
when K+ ion leave hyperpolarized cardiac muscle cells
heart rate decreases

The Heart: Regulation of Heart Rate

Stroke volume usually remains relatively

constant
Starlings law of the heart the more that the
cardiac muscle is stretched, the stronger the
contraction

Changing heart rate is the most common

way to change cardiac output

Regulation of Heart Rate: Autonomic Nervous

System

Sympathetic nervous system (SNS) stimulation is

activated by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation
is mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing
heart rate and causing vagal tone

Regulation of Heart Rate

Increased heart rate
Sympathetic nervous system
Crisis
Low blood pressure
Hormones
Epinephrine
Thyroxine
Exercise
Decreased blood volume

The Heart: Regulation of Heart Rate

Decreased heart rate
Parasympathetic nervous system
High blood pressure or blood volume
Dereased venous return
In Congestive Heart Failure the heart is worn
out and pumps weakly. Digitalis works to
provide a slow, steady, but stronger beat.

Atrial (Bainbridge) Reflex

Atrial (Bainbridge) reflex a sympathetic reflex

initiated by increased blood in the atria
Causes stimulation of the SA node
Stimulates baroreceptors in the atria, causing
increased SNS stimulation

Chemical Regulation of the Heart

The hormones epinephrine and thyroxine increase

heart rate
Intra- and extracellular ion concentrations must be
maintained for normal heart function

The Heart: Cardiac Output

Cardiac output (CO)
Amount of blood pumped by each side of the
heart in one minute
CO = (heart rate [HR]) x (stroke volume [SV])

Stroke volume
Volume of blood pumped by each ventricle in
one contraction

Comparisons

increases in heart rate tend to make cardiac out

put increase
increases in stroke volume tend to make cardiac
out put increase
increases in cardiac out and peripheral resistance
tend to make blood pressure higher

Cardiac output
CO = HR x SV
5250 ml/min = 75 beats/min x 70 mls/beat
Norm = 5000 ml/min
Entire blood supply passes through body
once per minute.
CO varies with demands of the body.

Cardiac Output Regulation

Figure 11.7

Factors Involved in Regulation of Cardiac

Output

Figure 18.23

STARLING LAW OF THE HEART

the greater the stretch of the heart (large

volume)
the greater the strength of contraction
(within limits)

PERIPHERAL RESISTANCE
arteriole runoff
blood going from arteries to
arterioles
the greater the resistance the
less the runoff
blood viscosity
the more RBC and the more
protein the greater the
resistance
the greater the viscosity the
higher the resistance

vasomotor control mechanism

vasomotor control center - medulla oblongata
efferent nerves go to smooth muscle layer of
vessels in blood reservoirs
blood reservoirs- venous plexuses
spleen, liver, skin
changes in arterial oxygen or carbon dioxide
levels triggers reflexes

Vasomotor pressoreceptor reflexes

STIMULUS- a sudden increase in blood

pressure
sensors- carotid and aortic baroreceptor
inhibits vasoconstrictor centers, stimulates
vasodilation centers
vasodilation occurs and less blood is returned
to heart

Vasomotor pressoreceptor reflexes

integrator
activation of vasomotor center
causes a decrease in stroke volume
decrease cardiac output which leads to
reduced BP
END RESULT- blood pressure returns to
normal

Vasomotor pressoreceptor reflexes

sensor- baroreceptors in carotid and aorta

integrator- vasomotor centers- stimulation of
vasodilation center
effector- precapillary sphincter muscles in
blood reservoirs capillaries

Vasomotor pressoreceptor reflexes

STIMULUS-a sudden drop in blood pressure

carotid & aortic baroreceptors are activated

stimulates vasoconstrictor centers, inhibits

vasodilation center
venous blood volume to the heart increases
blood volume to the heart increases
cardiac output increases, blood pressure
increases

vasomotor pressoreceptor reflexes

End Result- Blood pressure returns to normal

sensor- baroreceptors in carotid and aorta
integrator- vasomotor centers- stimulation of
vasoconstrictor centers
effectors- precapillary sphincter muscles in blood
reservoirs capillaries

note :this mechanism is active during exercise

Vasomotor chemoreceptor reflexes

stimulus- hypercapnia (high CO2 in blood)
some reaction to low O2 in blood

hypoxia or decreased arterial pH

impulses to vasoconstrictor center of medulla
increases
venous blood volume to the heart increases
increases pulmonary circulation

Vasomotor chemoreceptor reflexes

Result :oxygen levels raise and carbon dioxide

levels decrease
sensor chemoreceptors found in aorta and
carotid sinus
integrator- vasoconstriction center of medulla
effector- more blood flow to the lungs

Medullary ischemic reflex

emergency mechanism
active when oxygen is low to brain stem
Sensors- osmotic receptors in the medulla
integrator- vasomotor center
effector- lungs- increase blood flow to the lung

VENOUS RETURN TO HEART

Respiratory pump
decreased thoracic pressure (during inspiration)

pulls blood into central veins

increasing thoracic pressure (during
expiration)
pushes blood in central veins into heart
deeper respirations increase venous return to
heart

VENOUS RETURN TO HEART

skeletal muscle
pump
contraction and
relaxation pumps
blood upward
note: both these
methods depend on
the presence of
functioning
semilunar valves

Blood Vessels: The Vascular System

Taking blood to the tissues and back

Arteries
Arterioles
Capillaries
Venules
Veins

The Vascular System

Figure 11.8b

Blood Vessels: Anatomy

Three layers (tunics)

Tunic intima
Endothelium
Tunic media
Smooth muscle
Controlled by sympathetic nervous
system
Tunic externa
Mostly fibrous connective tissue

Differences Between Blood Vessel Types

Walls of arteries are the thickest

Lumens of veins are larger
Skeletal muscle milks blood in veins
toward the heart
Walls of capillaries are only one cell
layer thick to allow for exchanges
between blood and tissue

Whats this mean?

Pressure Gradient

What cardiovascular structure

generates this pressure gradient?

Blood Flow: Pressure Changes

Figure 14-2 : Pressure gradient in the blood vessels

Some Physics of Fluid Movement: Blood Flow

Flow rate: (L/min)

Flow velocity
= rate/C-S area of vessel
Resistance slows flow
Vessel diameter (radius)
Blood viscosity
Tube length
Which 2 above are
relatively constant?
Figure 14-4 c: Pressure differences of static and flowing fluid

 2 factors effecting blood flow: 1. Pressure gradient

and 2. Resistance (VESSEL DIAMETER, tube
length, blood viscosity)
Blood viscosity and tube length are basically
constant.
Vessel diameter has the most influence on blood
flow.

How velocity of blood flow is effected by crosssectional area (A)

Figure 14-6: Flow rate versus velocity of flow

Movement of Blood Through Vessels

Most arterial blood is

pumped by the heart
Veins use the milking
action of muscles to
help move blood
Figure 11.9

Capillary Beds

Capillary beds
consist of two
types of vessels
Vascular shunt
directly connects an
arteriole to a venule

Figure 11.10

Capillary Beds
True capillaries
exchange vessels
Oxygen and
nutrients cross to
cells
Carbon dioxide
and metabolic
waste products
cross into blood
Figure 11.10

Diffusion at Capillary Beds

Figure 11.20

Vital Signs

Arterial pulse
Blood pressure
Repiratory Rate
Body Temperature
All indicate the efficiency of the system

Pulse

Pulse
pressure wave
of blood
Monitored at
pressure
points where
pulse is easily
palpated
Figure 11.16

Blood Pressure
Measurements by health professionals
are made on the pressure in large
arteries
Systolic pressure at the peak of
ventricular contraction
Diastolic pressure when ventricles relax

Pressure in blood vessels decreases as

the distance away from the heart
increases

Blood Pressure = COP X peripheral resistance

COP= Stroke volume X heart rate
Stroke volume affected by:
- Negative pressure in thorax cavity
- Muscle pump
- Vein valve
- Intra abdominal pressure

Measuring Arterial Blood Pressure

Figure 11.18

Blood Pressure: Effects of Factors

Neural factors
Autonomic nervous system adjustments
(sympathetic division)

Renal factors
Regulation by altering blood volume
Renin hormonal control

Blood Pressure: Effects of Factors

Temperature
Heat has a vasodilation effect
Cold has a vasoconstricting effect

Chemicals
Various substances can cause increases or
decreases

Diet

Variations in Blood Pressure

Human normal range is variable
Normal
140110 mm Hg systolic
8075 mm Hg diastolic
Hypotension
Low systolic (below 110 mm HG)
Often associated with illness
Hypertension
High systolic (above 140 mm HG)
Can be dangerous if it is chronic

The Seventh Report of the Joint National Committee on

Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure

Pathology of the Heart

Damage to AV node = release of ventricles

from control = slower heart beat
Slower heart beat can lead to fibrillation
Fibrillation = lack of blood flow to the heart
Tachycardia = more than 100 beats/min
Bradychardia = less than 60 beats/min

Congestive Heart Failure (CHF)

Decline in pumping efficiency of heart

Inadequate circulation
Progressive, also coronary atherosclerosis, high
blood pressure and history of multiple Myocardial
Infarctions
Left side fails = pulmonary congestion and
suffocation
Right side fails = peripheral congestion and edema