You are on page 1of 143

Physiology of

Cardiovascular System
 089622303075
 Line: dokterhardian
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
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
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 friction-
free environment
Pericardial Layers of the Heart

Figure 18.2
Heart Wall

 Epicardium – visceral layer of the serous

 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
 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

 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
 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
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
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

Microscopic Anatomy of Heart Muscle

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

 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
 General cardiac cell stuff:
 Intercalated discs
 Allow branching of the
 Gap Junctions (instead of
 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

 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
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
 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
 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
 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

 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
 Heart is inhibited by
the parasympathetic

Figure 18.15
 Electrical activity is recorded by electrocardiogram
 P wave corresponds to depolarization of SA node
 QRS complex corresponds to ventricular
 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

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
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
 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

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
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
and initiates a
cyclic AMP

Figure 18.22
Regulation of Heart Rate

 Positive chronotropic factors increase heart rate

 Negative chronotropic factors decrease heart rate
Regulation of the heart

Cardiac pressor reflex

 stretch receptors(baroreceptors)
 aortic baroreceptor- location aorta
 carotid baroreceptor -location common carotid
Cardiac pressor reflex


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

 afferent fibers - bring information to the

 sensory impulse from carotid baroreceptor
 travels up the Herring nerve
 joins the IX glossopharyngeal nerve
 goes to cardiac control center of the medulla
Homeostasis - carotid sinus reflex

 SENSORS- barorecptors found in the carotid

 INTEGRATOR- medulla oblongata
cardioregulatory center
 Stimulus -sudden raise in heart rate and or BP
 Result - Heart rate decreases, BP decreases
 sensors location- aortic arch
 afferent fibers
 aortic nerve joins the VAGUS nerve
 goes to cardiac control center
 integrator- medulla oblongata cardioregulatory
 efferent fibers
 VAGUS nerve goes to SA node
 also causes acetylcholine to be released

 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

 Starling’s 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

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

 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

Figure 18.23

 the greater the stretch of the heart (large

 the greater the strength of contraction
(within limits)

 arteriole runoff
 blood going from arteries to
 the greater the resistance the
less the runoff
 blood viscosity
 the more RBC and the more
protein the greater the
 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
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
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
 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
 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

 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

 skeletal muscle pump

 contraction and
relaxation pumps
blood upward
 note: both these
methods depend on
the presence of
functioning semilunar
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
What’s 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
 Vessel diameter has the most influence on blood
How velocity of blood flow is effected by cross-
sectional 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
 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 –
pressure wave
of blood
 Monitored at
points” where
pulse is easily
Figure 11.16
Blood Pressure

 Measurements by health professionals

are made on the pressure in large
 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
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
 Diet
Variations in Blood Pressure

 Human normal range is variable

 Normal
 140–110 mm Hg systolic
 80–75 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
 Right side fails = peripheral congestion and