cardiovascular physiology

CLEMENT TETTEY, PhD

Colosians 3:8
• Our ceaselessly beating heart has intrigued people for
centuries. The ancient Greeks believed the heart was the
seat of intelligence. Others thought it was the source of
emotions. While these ideas have proved false, we do
know that emotions affect heart rate. When your heart
pounds or skips a beat, you become acutely aware of how
much you depend on this dynamic organ for your very
life.
 COMPONENTS OF THE CVS
 Heart

 Blood vessels
 Arteries
 Veins
 Capillaries
 The heart is actually two pumps side by side
OVERVIEW OF CIRCULATORY SYSTEM
 Functions of the heart
 Generating blood pressure

 Routing blood
 Separating pulmonary and systemic circulation

 Ensuring one-way blood flow

 Valves prevent the backflow of blood

 Regulating blood supply

 Due to changes in heart rate
 Chambers and Associated Great
Vessels
The heart has four chambers
Two atria and
Two ventricles
• The atria are receiving chambers for blood
returning to the heart from the circulation
 The Right Side
• Deoxygenated Blood enters the right
atrium via three veins:

• ■ The superior vena cava returns

blood from body regions superior to
the diaphragm

• ■ The inferior vena cava returns

blood from body areas below the
diaphragm

• ■ The coronary sinus collects blood

draining from the myocardium
The Right Side
 The Right Side
 The right atrium contracts and pumps
the DB into the right ventricle

 The tricuspid valves closes as the right

ventricle contracts

 Blood is pumped into the pulmonary

trunk

 The pulmonary valve closes as the left

ventricle relaxes

 The DB moves through the pulmonary

arteries to the lungs
 (circulation animation)
 The Lungs
 carbon dioxide diffuses out of the
DB where as oxygen diffuses into
the Blood

 OB now leaves the lungs via the

pulmonary vein
 The Left Side
 OB coming from the lungs enters
the left atrium

 Four pulmonary veins enter the

left atrium
 The Left Side
 The bicuspid valve opens

 Left atrium pumps the OB into the

left ventricle

 Left ventricle relaxes

 Bicuspid valves closes

 Aortic valve opens

 Left ventricle pumps blood into

the aorta
 Left ventricle relaxes and aortic
valve closes
 The System
 OB from aorta passes through
arteries and then to arterioles
and capillaries

 Oxygen then diffuses via

capillaries into cells

 Cells take up oxygen and

return carbon dioxide via
capillaries to the blood

 Blood now becomes DB

 The System
 DB leaves the system and
goes back to the right atrium

 The DB enters the right

atrium via:

 The superior vena cava

 The inferior vena cava
 The coronary sinus

 The cycle continues

 Conducting System of the Heart
 What causes the muscles of the heart to contract?

 The heart itself is capable of generating electrical signals

 As these signals move across the chambers of the heart they

cause contraction

 The autonomic nervous system regulates the heartbeat

 But does not initiate the heartbeat
 Cardiac muscles are myogenic (they can generate their own
electrical signal)
 The heart is endowed with a special system for

 generating rhythmical electrical impulses to cause rhythmical

contraction of the heart muscle and

 conducting these impulses rapidly through the heart

 In the superior wall of the right
atrium, immediately below and
slightly lateral to the opening of the
superior vena cava

 Are specialized cells called

Sinoatrial (SA) node

 The cells of the SA node initiate

action potentials (impulses)

 The fibers of this node have almost

no contractile muscle filaments
 The sinus nodal fibers connect directly
with the atrial muscle fibers

 Hence any impulse that begins in the

sinus node spreads immediately into
the atrial muscle wall

 The sinus node ordinarily controls the

rate of beat of the entire heart

 Hence its called the pacemaker of the

heart
 The ends of the sinus nodal
fibers connect directly with
surrounding atrial muscle fibers

 Impulse from SA spreads

through the entire atrial muscle
mass

 Results in contraction of atria

 impulse then travel to A-V

node through internodal
pathways
 cardiac impulse does not travel
from the atria into the
ventricles too rapidly

 This delay allows time for the

atria to empty their blood into
the ventricles before ventricular
contraction begins

 The A-V node and its adjacent

conductive fibers delay this
transmission into the ventricles
 Impulses from the SA node travel
through the internodal pathways to the
A-V node in about 0.03 second

 there is a delay of 0.09 second in the

A-V node itself

 A final delay of 0.04 second occurs

mainly in the penetrating A-V bundle

 A total delay of 0.16 second occurs

before the excitatory signal finally
reaches the contracting muscle of the
ventricles
 slow conduction in A-V bundle fibers
caused by diminished numbers of gap
junctions between successive cells in
the conducting pathways

 Hence there is great resistance to

conduction of excitatory ions from one
conducting fiber to the next
 There are two major categories of cardiac muscle cells

 Autorhythmic cells
 Do not contract
 Specialized for initiating action potentials responsible for
contraction of working cells

 Contractile cells
 99% of cardiac muscle cells
 Do mechanical work of pumping
 Normally do not initiate own action potentials
 The action potentials generated by autorhythmic cells create
waves (impulses) of depolarization which spread to contractile
cells through gap junction

 Waves from autorhythmic cells stimulate contractile cells to

generate action potential

 This results in:

1. Depolarization (contraction)
2. Repolarization (relaxation) in contractile cells
 Initiation of Action potentials in
Autorhythmic Cells
 At rest, the outside of the membrane is positive whereas the
inside is negative
 The membrane potential is approximately -60 mV

 Hence membrane said to be polarized

 They begin depolarizing due to a slow influx of sodium

 when potential reaches apx. – 40 mV (threshold), calcium
rushes in through fast calcium channels

 Causes the rapidly rising phase of the action potential

 This makes the membrane potential positive
Action potentials in Autorhythmic
Cells
 Action potentials in Autorhythmic
Cells
 The high influx of calcium results
in a positive membrane potential

 This triggers the rapid efflux of

potassium via potassium channels
(repolarization)

 Bringing the membrane potential

back to its starting point
 Movement of Action potentials (Impulses) from
Autorhythmic Cells to Contractile Cells
 Authrhythmic cells are linked to
contractile cells by gap junctions

 Impulses from autorhythmic cells

move into contractile cells
through gap junctions
 Action potentials in Contractile Cells
 The movement of AP from the AR  This allows calcium into the cell
cells into contractile cells from the outside and the SR
stimulate depolarization
 At the same time Potassium starts
 This stimulate the opening of fast going out (video 10:01)
sodium channels in the contractile
cells  It is the calcium inside the cell
that brings about cell contraction
 Quick influx of sodium results in
depolarization (9:16 video)

 The inside of the cell becomes

positive
 Depolarization also stimulates the
opening of slow calcium channels
 The calcium channels then close
after a single contraction

 Potassium efflux is increased

(video 10:39)

 The rapid potassium efflux results

in repolarization (contraction)
 Electrocardiogram
 When the cardiac impulse passes through the heart, electrical
current spreads from heart into the adjacent tissues
surrounding the heart

 A small portion of the current spreads to the surface of the

body

 If electrodes are placed on the skin , electrical potentials

generated by the current can be recorded

 The recording is known as an electrocardiogram

 Electrocardiogram
 P-wave are the electrical activities that
occur on the body as a result of
depolarization in the atria (atrial
contraction)

 The QRS complex is the electrical

activity as detected on the surface of
the body that occur as a result of
depolarization in the ventricle
(ventricular contraction)

 The T- wave is the electrical activity

detected on the surface of the body
that occur as a result of ventricular
repolarization
 These electrical activities are
generated in the SA node
 The Cardiac Cycle

 The cardiac cycle includes all events associated with the blood flow through
the heart during one complete heartbeat—atrial systole and diastole followed
by ventricular systole and diastole

 The cardiac cycle is marked by a succession of pressure and blood volume

changes in the heart

 It consists of a period of relaxation called diastole, during which the heart fills
with blood, followed by a period of contraction called systole

 Blood flows continually from the great veins into the atria about 80 per cent
flows directly through the atria into the ventricles before the atria contract

 Atrial contraction usually causes an additional 20 per cent filling of the

ventricles
 The Cardiac Cycle
 During ventricular systole, large amounts of blood accumulate in the atria
 As soon as systole is over and the ventricles relax (diastole) blood flows
rapidly from the atria into t he ventricles
 This is called the period of rapid filling of the ventricles

 Emptying of the Ventricles During Systole

– period of isovolumic or isometric contraction
– Period of Ejection
The Cardiac Cycle
 Heart Sounds
 also known a lubb-dubb

 lubb occurs as the AV valves close when the ventricles

contract

 Dubb occurs as the aortic and pulmonary valves close when

the ventricles relax
 Control of Heart Rate
 Although the intrinsic conduction
system sets the basic heart rate, the
autonomic nervous system modifies
the rate

 The autonomic nervous system is

made up of:
 Sympathetic system
 Parasympathetic system

 The sympathetic nervous system (the

―accelerator‖) increases both the rate
and the force of heartbeat

 The parasympathetic activation (the

―brakes‖) slows the heart.
 The cardiac centers are located in the
medulla oblongata

 The cardioacceleratory center

projects to sympathetic neurons in the
spinal cord

 Then runs through the cervical and

upper thoracic sympathetic trunk

 Continuous through the cardiac plexus

to the heart where they innervate the:
 SA and AV nodes,
 heart muscle and
 coronary arteries
 The sympathetic stimulation increases
the overall activity of the heart

 The sympathetic stimulation:

 increases the rate of sinus nodal
discharge
 Increases the rate of conduction as well
as the level of excitability in all portions
of the heart

 Increases greatly the force of

contraction of all the cardiac
musculature, both atrial and ventricular

 Maximal sympathetic stimulation can

almost triple the frequency of heartbeat
as much as twofold
 The cardioinhibitory center sends
impulses to the parasympathetic dorsal
vagus nucleus in the medulla

 This sends inhibitory impulses to the

heart via branches of the vagus nerves

 Most parasympathetic motor neurons

in the heart wall project heavily to the
SA and AV nodes
 Weak to moderate parasympathetic
stimulation slows the rate of heart
pumping, often to as little as one half
normal

• strong parasympathetic can stop the

excitation by the sinus node
completely or block transmission of
the cardiac impulse from the atria into
the ventricles through the A-V mode
 DEFINITIONS
 Preload: Volume of blood returning to the right side of the
heart

 Starling`s law: the higher the volume of blood returning to the

heart, the greater the stretch of the heart chamber walls and
hence the greater the force of contraction

 Afterload: the pressure in the aorta that the left ventricle has to
overcome to pump blood into the system circulation
or
Afterload: Back Pressure Exerted by Arterial Blood
 DEFINITIONS
 Heart Rate (HR): number of times heart beats per minute

 Stroke volume (SV) : blood pumped out of the left ventricle

during each heartbeat

 Cardiac output (CO): amount of blood pumped by the heart

per minute

 CO = SV x HR
 BLOOD PRESSURES
 Systolic pressure: pressure in the aorta at maximum ventricular
contraction = 120 mmHg

 Pressure in the aorta at ventricular relaxation = 80 mmHg

 120 mmHg/ 80 mmHg= normal blood pressure= aortic

pressure
 BLOOD PRESSURE CONTROL
 Short term control
 Regulates Heart rate
 Regulates Heart contractility
 Regulates vessel diameter

 Long term control

 Regulate blood volume
 BLOOD PRESSURE CONTROL
 Rising blood pressure

 Stretching of arterial walls

 Stimulation of baroreceptors in aortic arc, carotid sinus and

other large arteries

 Increased impulse to brain

 SHORT TERM REGULATION OF
RISING BLOOD PRESSURE (V4:00)
 Rising blood pressure

 Stretching of baroreceptors
 Increased impulses to the brain

 Increased parasympathetic activity

 Decreased sympathetic activity

 Slowing of heart rate

 Increase arterial diameter

 Reduction of blood pressure

 SHORT TERM REGULATION OF
FALLING BLOOD PRESSURE (7:50)
 Falling blood pressure

 Baroreceptors inhibited

 Decreased impulses to brain

 Decreased parasympathetic activity

 Increase sympathetic activity

 Increase heart rate and contractility

 Increased vasoconstriction
 Release of epinephrine from adrenal gland(enhance heart
rate and vasoconstriction)
CONGESTIVE HEART FAILURE
 Usually starts from some kind of damage or weakening of the
heart muscles
 Clogged artery or increased afterload from chronic long-term
hypertension
 This weakening of the heart decreases stroke volume

 Decreased stroke volume results in lower cardiac output

 Heart compensates for lower cardiac output by;

 increasing heart rate (Price: less time to be filled with blood)
 Thickening of the ventricular walls (price: Less room for
filling)
CONGESTIVE HEART FAILURE
 Kidneys release:
 Renin

 Angiotensin

 Aldosterone
 Causes retention of sodium and water
 This resulting in increase blood volume
 Heart cant even pump the existing volume
 Now the volume has further been increased
CONGESTIVE HEART FAILURE
 If it is the left side that is failing;
 Blood will be waiting to enter the left side of the heart from
the lungs
 May start accumulating in the lungs
 May result in pulmonary edema

 If it is the right side that is failing;

 Blood hangs around in the periphery waiting to get into the
right side of the heart. This results in;
 Jugular vein distension
 Swollen ankles (peripheral edema)