Anatomi-Fisiologi

Sistem
Kardiovaskuler
M. Saifur Rohman, dr SpJP(K),
PhD
Dept. of Cardiology and Vascular Medicine
Faculty of Medicine, Brawijaya University

Outline

Cardiovascular /Circulatory System

Heart and Blood Vessel Anatomy
Cardiovascular System Physiology
Basic Electrophysiology : ECG

Circulatory System
Three basic components
Heart
Serves as pump that establishes the pressure
gradient needed for blood to flow to tissues

Blood vessels
Passageways through which blood is distributed
from heart to all parts of body and back to heart

Blood
Transport medium within which materials being
transported are dissolved or suspended

Circulatory System
Pulmonary circulation
Closed loop of vessels
carrying blood between
heart and lungs

Systemic circulation
Circuit of vessels
carrying blood between
heart and other body
systems

Systemic and Pulmonary

Circulation
Oxygen
Electrolite
Hormone
Glucose
Free fatty acid
Amino acids

Functions of the Heart

Generating blood pressure
Routing blood
Heart separates pulmonary
and systemic circulations
Ensuring one-way blood flow

Regulating blood supply

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

Functions of the Heart

Regulates blood supply
Changes in contraction rate and force
match blood delivery to changing
metabolic needs
Most healthy people can increase
cardiac output by 300500%
Heart failure is the inability of the heart
to provide enough blood flow to
maintain normal metabolism
HODS - November 2006

Blood Flow Through and Pump Action of

the Heart

Blood Flow Through Heart

The Heart : General

Information
Long axis of the heart is directed:

Obliquely
Leftward
Downward
Forward

Heart is 12 cm long from base to

LV
apex.
Base of heart:
LA & small part of RA & RV
Parallel to the right edge of the
sternum.

Apex of heart:
Junction of ventricles & ventricular
septum
Found at left of MCL @ 5th ICS.

Surfaces of the Heart

Anterior
Formed by the RV &
parts of the RA & LV.
Small portion of LV
extends anteriorly;
forms a blunt tip.
Forward tilt of heart.
Movement of apex
forms the PMI.

Surfaces of the Heart

Inferior
Diaphragmatic
surface of the heart.
Comprised chiefly of
LV.
Portion of inferior
surface is RV.

Surfaces of the Heart

Posterior
Thoracic aorta,
esophagus & vertebrae

Lateral
Lateral right heart
border: RA.
Lateral wall of LV &
small part of LA form
most of left heart border.

Major components

Muscle; contractile apparatus

Nerve; conducting system and innervation
Vessel; Supporting oxygen from the blood
Extra cellular matrix
Endocardium; valves
Pericardium
Etc.

Type of Cells in The Heart

Pacemaker cells
5 10 um in length;
Sinoatrial and atrioventricular nodes
Spontaneous depolarization
Action Potential
Electrical conducting cells
Long thin cells
Atrial conducting system
Ventricular conducting system
Myocardial cells
Contractile units in the heart, most are
myocardial cells
Calcium is responsible for contractile process
after
initiation of action potential

Endocardium

Cardiac Wall

Inner membranous surface of heart.

Lines chambers & valves.

Myocardium
Muscular portion.
Composed of cardiac muscle cells.
Contractile portion.

Epicardium
Visceral layer of serous pericardium.
Completely encloses external surface of
the heart.

Pericardium of the Heart

Pericardium
Parietal
Visceral

Pericardium
Pericardium: Fibroserous membranous sac
that encloses the heart & root of the great
vessels.
Pericardial space contains 10-20 ml of fluid.
Two Layers:
1. Fibrous pericardium
Outermost layer
2. Serous pericardium
Parietal
Visceral

Pericardium Functions
Protects heart from friction.
Lubricates moving surfaces of the
heart.
Helps hold heart in position.
Forms a protective barrier against
infection & neoplasia
Trauma to chest results in damage
to the RV.

Myocardium

Cardiac Myocyte
Myofiber: is a group of myocytes held together by
surrounding collagen connective tissue
Excess collagen, may cause LV diastolic dysfunction
(e.g. left ventricular hypertrophy)
10-20 m in diameter
50-100 m long
single central nucleus
the cell is branched, attached to adjacent cells in
an end-to-end fashion (intercalated disc)
desmosomes (proteoglycan glue)
gap junction (region of close apposition)

Cardiac Chambers: Atria

Thin walled; low pressure (0-5 mmHg)
Left & right separated by septum
Act as reservoirs of blood for ventricles
70% passive flow
RA blood supply
Receives venous blood

LA blood supply
Receives O2 blood

Lower Chambers:
Ventricles
Major pumps
Right Ventricle
Contraction propels deoxygenated blood into
pulmonary circulation via PA.
Functions in a low pressure system (20-30/0-5)
Left Ventricle
Ejects blood into systemic circulation via aorta during
ventricular systole.
Functions in a high pressure system (100-140/60-80)

Valves

Cardiac Valves:
Atrioventricular Valves
Located between atria &
ventricles
Mitral Valve
2 cusps
Located between LA &
LV
Tricupsid Valve
3 cusps
Located between RA &
RV

Atrio-Ventricular Valves
Allow unidirectional blood to flow from
atria to
ventricles during ventricular diastole
Prevent retrograde flow during systole.
Diastole: Papillary muscles relax &
valve leaflets
open.
Systole: Valve leaflets close
AV valve closure produces a sound that
constitutes the first heart sound (S1).

Semi-Lunar Valves
Location
Pulmonary valve
Between RV & PA
3 cusps or semilunar cups
Aortic valve
Located between
LV & aorta
3 cusps

Semi-Lunar Valves
Permits unidirectional blood flows from ventricle to
artery during ventricular systole
Valve opens when ventricle contracts
Pressure greater in ventricle than arterial
outflow tract and valve opens.
Prevents retrograde blood flow during ventricular
diastole.
Pressure in arterial outflow tract exceeds
pressure in ventricle & causes valve to close.
Valve closure produces sound that is S2

Papillary Muscle
Papillary Muscle
Arise from
endocardial &
myocardial surface
of ventricles.
Attach to tendinae.
Blood supply from
coronary arteries.

Chordae Tendinae
Chordae Tendinae
Tendinous attachments to
tricuspid & mitral valves
Prevent eversion of
valves into atria during
systole.
String-like in appearance
and are sometimes
referred to as "heart
strings."

Heart Sounds
First heart sound or lubb
AV valves close and surrounding fluid
vibrations at systole
Second heart sound or dupp
Results from closure
of aortic and pulmonary
semilunar valves at
diastole, lasts longer

Cardiac Blood Vessels

Coronary arteries branch off at base of aorta &
supply blood to the electrical conduction system
& myocardium.
3 main arteries:
RCA
LCA
Circumflex

Cardiac Blood Vessels

Coronary Arteries

Coronary Arteries
Originates from the
aorta just beyond the
aortic valve
Coronary blood flow to
the myocardium occurs
primarily during diastole
* To maintain adequate
blood flow through the
coronaries, mean
arterial pressure
(MAP) must be at least
60 mmHg

Coronary Arteries
Left main coronary artery
(LCA)
- Left anterior descending
artery (LAD)
>descends toward the
anterior wall & apex of LV
> supplies LV, ventricular
septum, chordae, papillary
muscle & RV
- Left circumflex artery (LCX)
> descends toward the
lateral wall of LV & apex
> supplies LA, lateral &
posterior LV surfaces
*45% supplies SA node

Coronary Arteries
Right main
coronary artery
(RCA)
- descends
toward the apex
of RV
- supplies the
RA, RV, & inferior
portions of LV
.

Coronary Arteries
RCA Supplies
SA node in 55% of hearts
AV node in 90% hearts
RA & RV heart muscle
Inferior wall of LV
Posterior 1/3 of intraventricular
septum
In 85% of hearts, RCA provides the
posterior descending branch.

Coronary Arteries
LCA
Branches into LAD & L Circumflex
Left Anterior Descending
Anterior wall of LV & anterior 2/3 septum
RBB & part of LBB
LA
Circumflex Supplies
AV node in 10% hearts
SA node in 45% hearts
Posterior surface of LV

Cardiac Veins
Return deoxygenated blood back to the
heart
Coronary Sinus: Drains into RA
Great cardiac vein
Small cardiac vein
Thesbesian Veins
Numerous small veins, present
mostly in RA & RV
Empty into chambers

Electricity

Electrical Activity of Heart

Heart beats rhythmically as result of action
potentials it generates by itself
(autorhythmicity)
Two specialized types of cardiac muscle cells
Contractile cells
99% of cardiac muscle cells
Do mechanical work of pumping
Normally do not initiate own action potentials

Autorhythmic cells
Do not contract
Specialized for initiating and conducting action potentials
responsible for contraction of working cells

Intrinsic Cardiac Conduction

System

Approximately 1% of cardiac muscle cells are autorhythmic rather than contractile

70-80/min
40-60/min

20-40/min

Sinoatrial (SA) Node

Normal cardiac impulse originates
here
Natural pacemaker
Inherent rate: 60-100 bpm
Atrial depolarization occurs cell to
cell
Four conduction pathways
transmit impulse to AV node:
Bachmans Bundle and 3
internodal pathways (anterior,
middle & posterior tracts).
Spreads impulse throughout
the atrium

Atriovenous (AV) Node

Located inferiorly in RA
All impulses initiated in atria
will be conducted to
ventricles via AV node alone.
Impulse slows here to allow
diastolic filling time
Inherent rate: 40-60 bpm
Conduction delay at AV node
so that ventricular filling from
atrial contraction

Bundle of HIS
Electrical impulses conducted
to ventricles via Bundle of HIS
& purkinjie fibers
Divides into bundle branches
Right
Left
Anterior Fascicle
Posterior Fascicle

Purkinje Fibers
Impulse stimulates
ventricular myocardial cells
Inherent rate: 20-40
bpm

Physiology of the Heart

Electrophysiologic properties (regulates heart rate &
rhythm)
- Automaticity ability of all cardiac cells to initiate an
impulse spontaneously & repetitively
- Excitability ability of cardiac cells to respond to
stimulus by initiating an impulse (depolarization)
- Conductivity cardiac cells transmit the electrical
impulses they receive
- Contractility cardiac cells contract in response to
an impulse
- Refractoriness cardiac cells are unable to respond
to a stimulus until theyve recovered (repolarized)

Action potential in
autorhythmic cells

Action Potential in
contractile cells

Action Potential in contractile cells and ECG

Depolarization of atrium and ventricle

Electrical to mechanical
response
Excitation-contraction coupling

During phase 2 of the action potential Ca enter

through L Type Ca Channel in the sarcolemma and T
tubule
Ca triggers release much greater Ca from SR via
Ryanodine receptor into cytosol result in an
increased Ca in the cytosol
Ca bind to Trop C and the activity of Trop I is inhibited
and induce conformational change of tropomyosin
result in unblock the active site between actin and
myosin
Myosin head bind to actin causing interdigitating
thick and thin filament in ATP dependent reaction

Electrical Conduction in Heart

Atria contract as single unit followed after brief delay b

a synchronized ventricular contraction
1
1
SA node
AV node

2
1 SA node depolarizes.

THE CONDUCTING SYSTEM

OF THE HEART

SA node

Internodal
pathways

2 Electrical activity goes

rapidly to AV node via
internodal pathways.
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.

AV node
A-V bundle
Bundle branchesPurkinje
fibers
5

4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
5 Depolarization wave
spreads upward from
the apex.

Purple shading in steps 25 represents depolariz

Excitation-Contraction Coupling in
Cardiac Contractile Cells

Ca2+ entry through L-type channels in T

tubules triggers larger release of Ca2+ from
sarcoplasmic reticulum
Ca2+ induced Ca2+ release leads to crossbridge cycling and contraction

Electrocardiogram (ECG)
Record of overall spread of electrical activity through heart
Represents
Recording part of electrical activity induced in body
fluids by cardiac impulse that reaches body surface
Not direct recording of actual electrical activity of heart
Recording of overall spread of activity throughout heart
during depolarization and repolarization
Not a recording of a single action potential in a single
cell at a single point in time
Comparisons in voltage detected by electrodes at two
different points on body surface, not the actual potential
Does not record potential at all when ventricular muscle
is either completely depolarized or completely
repolarized

Electrocardiogram (ECG)
Different parts of ECG record can be
correlated to specific cardiac events

Heart Excitation Related to

ECG
START

P wave: atrial
depolarization
P

The end
R

PQ or PR segment:
conduction through
AV node and A-V
bundle

QS

Atria contract.
T wave:
ventricular
Repolarization

R
T

ELECTRICAL
Repolarization
EVENTS
OF THE
CARDIAC CYCLE

QS
P Q wave
Q

ST segment
R

R wave
R

P
QS
P

Ventricles contract.

Q
P

S wave
QS

ECG Information Gained

(Non-invasive)
Heart Rate
Signal conduction
Heart tissue
Conditions

Cardiac Cycle: Contraction

Electroactivity of the heart produces muscle
contraction
Isovolumeteric Ventricular Contraction
First phase of ventricular depolarization
In response to ventricular depolarization,
tension in the ventricles increases.
Rise in pressure in ventricles leads to closure
of the mitral & tricupsid valves.
Pulmonic & aortic valves stay closed during
the entire phase.
Pressure increases, but no blood enters or
leaves the ventricles

Cardiac Cycle: Contraction

Ventricular Ejection or Systole (contraction)
Ventricular pressure exceeds aortic & pulmonic
arterial pressure
Aortic & pulmonic valves are forced open.
Ventricles eject blood to the pulmonary circuit &
aorta.

Cardiac Cycle: Relaxation

Isovolumetric Relaxation or Atrial Diastole

Ventricular pressure falls below pressure in

the aorta & PA.
Aortic & pulmonic valves close
Atrial diastole occurs as blood fills the atria

Cardiac Cycle: Relaxation

Ventricular Filling or Diastole (relaxation)
Atrial pressure exceeds ventricular
pressure
Mitral & tricupsid valves are
forced
open
Blood enters ventricles passively
Accounts for 70% of ventricular
filling

Cardiac Cycle: Atrial Kick

Atrial Systole (contraction)
Occurs in response to SA
node impulse
Propels blood into
ventricles
Known as atrial kick
Supplies 25-30%
blood for each heart
beat

Cardiac Cycle - Filling of Heart

Chambers

Heart is two pumps that work together, right and

left half
Repetitive contraction (systole) and relaxation
(diastole) of heart chambers
Blood moves through circulatory system from
areas of higher to lower pressure.
Contraction of heart produces the pressure

Cardiac Cycle - Mechanical Events

1
START

Isovolumic ventricular
5 relaxation: as ventricles
relax, pressure in ventricles
falls, blood flows back into
cups of semilunar valves
and snaps them closed.

Ventricular ejection:
4 as ventricular pressure
rises and exceeds
pressure in the arteries,
the semilunar valves
open and blood is
ejected.

Late diastole: both sets of

chambers are relaxed and
ventricles fill passively.

Atrial systole: atrial contraction

forces a small amount of
additional blood into ventricles.

Isovolumic ventricular
contraction: first phase of
ventricular contraction pushes
AV valves closed but does not
create enough pressure to open
semilunar valves.

Figure 14-25: Mechanical events of the cardiac cycle

Wiggers Diagram
0
Electrocardiogram
(ECG)

Time (msec)
200 300 400

100

QRS
complex

500

600

700

800
QRS
complex

Cardiac cycle
T

120

Pressure
(mm Hg)

90

Aorta

Dicrotic
notch
Left
ventricular
pressure

60
Left atrial
30 pressure

Heart
sounds
Left
ventricular
volume
(mL)

S1

EDV

135
ESV
65
Atrial
systole

Atrial systole

S2

Isovolumic
ventricular

Ventricular
systole

Ventricular
systole

Ventricular
diastole

Early
ventricular

Atrial
systole

Late
ventricular

Atrial
systole

ATRIAL SYSTOLE
The end of
diastole

ATRIAL SYSTOLE - Heart

Prior to atrial systole, blood

has been flowing passively
from the atrium into the
ventricle through the open AV
valve.
During atrial systole the
atrium contracts and tops off
the volume in the ventricle
with only a small amount of
blood. Atrial contraction is
complete before the ventricle
begins to contract.

ATRIAL SYSTOLE
Pressures & Volumes
The "a" wave occurs when the
atrium contracts, increasing atrial
pressure (yellow).
Blood arriving at the heart cannot
enter the atrium so it flows back
up the jugular vein, causing the
first discernible wave in the
jugular venous pulse.
Atrial pressure drops when the
atria stop contracting.
During atrial systole the atrium
contracts and tops off the volume
in the ventricle with only a small
amount of blood.
Atrial contraction is complete
before the ventricle begins to
contract.

ATRIAL SYSTOLE
ECG

An impulse arising from the SA node results in depolarization

and contraction of the atria (the right atrium contracts slightly
before the left atrium).
The P wave is due to this atrial depolarization.
The PR segment is electrically quiet as the depolarization
proceeds to the AV node.
This brief pause before contraction allows the ventricles to fill
completely with blood.

ISOVOLUMETRIC
CONTRACTION
The Beginning
of systole

ISOVOLUMETRIC
CONTRACTION
Heart
The atrioventricular (AV) valves
close at the beginning of this
phase.
Electrically, ventricular systole
is defined as the interval
between the QRS complex and
the end of the T wave (the Q-T
interval).
Mechanically, ventricular
systole is defined as the
interval between the closing of
the AV valves and the opening
of the semilunar valves (aortic
and pulmonary valves).

ISOVOLUMETRIC
CONTRACTION
Pressures & Volumes

The AV valves close when the

pressure in the ventricles
(red) exceeds the pressure in
the atria (yellow).
As the ventricles contract
isovolumetrically -- their
volume does not change
(white) -- the pressure inside
increases, approaching the
pressure in the aorta and
pulmonary arteries (green).

ISOVOLUMETRIC
CONTRACTION
ECG

The electrical impulse propagates from the AV node through

the His bundle and Purkinje system to allow the ventricles to
contract from the apex of the heart towards the base.
The QRS complex is due to ventricular depolarization, and it
marks the beginning of ventricular systole. It is so large that
it masks the underlying atrial repolarization signal. the
ventricles to fill completely with blood.

RAPID EJECTION

RAPID EJECTION
Heart

The semilunar (aortic and

pulmonary) valves open at
the beginning of this phase.

RAPID EJECTION
Pressures & Volumes

While the ventricles continue

contracting, the pressure in the
ventricles (red) exceeds the pressure
in the aorta and pulmonary arteries
(green); the semilunar valves open,
blood exits the ventricles, and the
volume in the ventricles decreases
rapidly (white).
As more blood enters the arteries,
pressure there builds until the flow of
blood reaches a peak.
The "c" wave of atrial pressure is not
normally discernible in the jugular
venous pulse. Right ventricular
contraction pushes the tricuspid valve
into the atrium and increases atrial
pressure, creating a small wave into
the jugular vein. It is normally
simultaneous with the carotid pulse.

RAPID EJECTION
ECG

No Deflections

REDUCED EJECTION
The end of
systole

REDUCED EJECTION
Heart

At the end of this phase the

semilunar (aortic and
pulmonary) valves close.

REDUCED EJECTION
Pressures & Volumes
After the peak in ventricular and
arterial pressures (red and
green), blood flow out of the
ventricles decreases and
ventricular volume decreases
more slowly (white).
When the pressure in the
ventricles falls below the
pressure in the arteries, blood in
the arteries begins to flow back
toward the ventricles and
causes the semilunar valves to
close. This marks the end of
ventricular systole mechanically.

REDUCED EJECTION
ECG

The T wave is due to ventricular repolarization. The end

of the T wave marks the end of ventricular systole
electrically.

ISOVOLUMETRIC
RELAXATION
The
beginning of Diastole

ISOVOLUMETRIC RELAXATION
Heart

At the beginning of this

phase the AV valves are
closed.

ISOVOLUMETRIC RELAXATION
Pressures & Volumes
Throughout this and the previous
two phases, the atrium in
diastole has been filling with
blood on top of the closed AV
valve, causing atrial pressure to
rise gradually (yellow).
The "v" wave is due to the back
flow of blood after it hits the
closed AV valve. It is the second
discernible wave of the jugular
venous pulse.
The pressure in the ventricles
(red) continues to drop.
Ventricular volume (white) is at a
minimum and is ready to be
filled again with blood.

ISOVOLUMETRIC RELAXATION
ECG

No Deflections

RAPID VENTRICULAR
FILLING

RAPID VENTRICULAR FILLING

Heart

Once the AV valves open,

blood that has accumulated
in the atria flows rapidly into
the ventricles.

RAPID VENTRICULAR FILLING

Pressures & Volumes

Ventricular volume (white)

increases rapidly as blood
flows from the atria into the
ventricles.

RAPID VENTRICULAR FILLING

ECG

No Deflections

REDUCED VENTRICULAR
FILLING
(Diastasis)

REDUCED VENTRICULAR
FILLING
Heart

Rest of blood that has

accumulated in the atria
flows slowly into the
ventricles.

REDUCED VENTRICULAR
FILLING Pressures & Volumes

Ventricular volume (white)

increases more slowly now.
The ventricles continue to fill
with blood until they are
nearly full.

REDUCED VENTRICULAR
FILLING
ECG

No Deflections

Mechanical Properties of the

Heart
Cardiac output
- volume of blood (liters) ejected by the heart each
minute
- 4 7 L/min
- heart rate x stroke volume
Heart rate
- number of times the ventricles contract each minute
- 60 100 beats/min
- controlled by the ANS via the vagus nerve
Stroke volume
- amount of blood ejected by the LV during each
systole

Cardiac Output = Heart Rate X

Stroke Volume
Around 5L :
(70 beats/m 70 ml/beat = 4900 ml)
Rate: beats per minute
Volume: ml per beat
SV = EDV - ESV
Residual (about 50%)

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

Factors Affecting Cardiac

Output
Cardiac Output = Heart Rate X Stroke Volume
Heart rate
Autonomic innervation
Hormones - Epinephrine (E),
norepinephrine(NE), and thyroid hormone (T3)
Cardiac reflexes
Stroke volume
Starlings law
Venous return
Cardiac reflexes

Factors Influencing Cardiac Output

Intrinsic: results from normal functional
characteristics of heart - contractility, HR, preload
stretch
Extrinsic: involves neural and hormonal control
Autonomic Nervous system

Regulation of Cardiac
Output

Figure 18.23

Stroke Volume (SV)

Amount of blood ejected from the ventricles
during one contraction (Measured in mL).

Determined by extent of venous

return and by sympathetic activity
Influenced by two types of controls
Intrinsic control
Extrinsic control
Both controls increase stroke volume by
increasing strength of heart contraction

Intrinsic Factors Affecting SV

Contractility cardiac cell
contractile force due to
factors other than EDV
Preload amount ventricles
are stretched by contained
blood - EDV
Venous return - skeletal,
respiratory pumping
Afterload back pressure
exerted by blood in the
large arteries leaving the
heart

Stroke volume

Strength of
cardiac contractio

End-diastolic
volume

Venous return

Mechanical Properties of the

Heart
Preload
- degree of myocardial stretch at the end
of diastole & just before contraction
- determined by the amount of blood
returning to the heart from the venous
& pulmonary system (L) LVED
*Starlings law the more the heart is filled
during diastole, the more forcefully it
contracts

Mechanical Properties of the

Heart
Afterload
- pressure or resistance that the ventricles must
overcome to eject blood through the semilunar
valves & into the peripheral blood vessels
- directly proportional to the BP & diameter of
blood vessels
Impedance (peripheral component of afterload)
- pressure that the heart must overcome to
open the aortic valve
- depends on aortic compliance, blood viscosity
& arteriolar constriction

Mechanical Properties of the

Heart
Myocardial contractility
- force of cardiac contraction
independent of preload
- increased by sympathetic nervous
stimulation, calcium release &
positive inotropic drugs
- decreased by hypoxemia &
acidemia

Pre-Load
The stretch or volume
Measured by CVP & PA pressures
Increase in pre-load has following effects:
the volume of blood returning to ventricles
Stretches myocardial fibers, causing a more
forceful subsequent ventricular contraction
SV and thus CO
Ventricular work
Myocardial oxygen consumption

After Load
Amount of resistance to blood flow out
of the ventricles into the aorta
The initial resistance that the
ventricles must overcome in order to
open the semi-lunar valves & propel
blood into the systemic and pulmonary
circulatory systems

Systemic blood pressure

Contractility
The ability of a muscle
fiber to shorten
Hearts ability to
squeeze blood out &
change shape from full to
empty

Extrinsic Factors Influencing

SV
Contractility is the increase in contractile
strength, independent of stretch and EDV
Increase in contractility comes from

Increased sympathetic stimuli

Hormones - epinephrine and thyroxine
Ca2+ and some drugs
Intra- and extracellular ion concentrations must
be maintained for normal heart function

Medulla Oblongata Centers

Affect Autonomic Innervation
Cardio-acceleratory
center activates
sympathetic neurons
Cardio-inhibitory
center controls
parasympathetic
neurons
Receives input from
higher centers,
monitoring blood
pressure and
dissolved gas
concentrations

Neurologic Control of
Heart
Autonomic Nervous System
Influences
Contractility
Depolarization &
repolarization
Rate of conductivity
Sympathetic Nervous
System
Alpha
Beta
Dopaminergic

Autonomic Nervous System:

(Sympathetic Nervous System)
Beta-adrenergic (Beating of heart & Breathing)
Beta 1: Increases HR & force of contraction
Chronotropic Effect (increases HR)
Inotropic Effect (increases contractility)
Beta 2: Dilates smooth muscle in
bronchioles, GI, & uterus
Dopaminergic
Renal & mesenteric dilation

Autonomic Nervous System:

(Parasympathetic Nervous System)

Causes release of acetylcholine

Decrease rate of SA node discharge; slow
HR
Slows conduction through AV node
Effects include vasodilatation

Neurologic Control of
Heart
Chemoreceptors
Sensitive to changes in pO2/pCO2/pH
Cause changes in HR & RR
Baroreceptors
Stretch receptors in aortic arch &
heart
Respond to pressure & volume
changes

Reflex Control of Heart Rate

Regulating Cardiac Output

CO = Heart Rate x Stroke Volume
Heart Rate = Beats/minute
Stroke Volume = L/ventricular
contraction
Effects of:
sympathetic stimulation
parasympathetic stimulation
adrenal stimulation

Systemic Vasculature
Major Function
Supply tissues with blood, nutrients
& hormones
Remove metabolic wastes
Blood flow to tissues
Controlled via chemical reactions &
nerves that dilate or constrict
vessels

Vascular System
Provide conduits for blood to travel
from the heart to nourish the body
Carry cellular wastes to the excretory
organs
Allow lymphatic flow to drain tissue
fluid back to the circulation
Return blood to the heart for
recirculation

Major Components
Arteries
Strong, compliant, elastic-walled vessels that
carry blood AWAY from the heart & distribute
to capillary beds.
High pressure circuit
Stretch during systole & recoil during diastole.
3 layers
Intima
Media
Adventita

Arterial
System
Delivers blood to
various tissues
for nourishment
Transport of
cellular wastes
Contribute to
thermal
regulation

Arterial System
Blood pressure
- force of blood exerted against the vessel
walls
= CO x peripheral vascular resistance
- regulated by:
> autonomic nervous system (ANS)
> kidneys (renin-angiotensin-aldosterone)
> endocrine system (catecholamines,
kinins, serotonin, histamine)

Arterioles
Contain smooth muscle
Major vessels which control arterial pressure
Innervated by sympathetic nerve fibers
Stimulation causes vascular constriction

adrenergic discharge causes vasodilation

Lead directly into capillaries
A decrease in pressure within the arterioles
results in vasodilation.

Blood Pressure
Systolic:
- amount of pressure/force generated by LV to
distribute blood into the aorta w/ each contraction
of the heart
- 90 135 mmHg (120)
- affected by CO and arterial distention
Diastolic:
- amount of pressure/force sustained by the
arteries during the relaxation phase of the heart
- ability of the heart to rest while filling with blood
- affected by peripheral vascular resistance
- 60 85 mmHg (80)

Regulation of BP
Autonomic Nervous System
- Baroreceptors (arch of aorta & origin of
internal carotid arteries)
> stimulated when arterial walls are
stretched by increased BP
> inhibit vasomotor center (pons &
medulla
or brainstem)
- Chemoreceptors (bifurcation of carotid
arteries & aortic arch)
> sensitive to hypoxemia, hypercapnia

Venous System
Stores 60% total volume of blood in the circulatory
system.
Venules
Receive blood from capillaries
Serve as storage vessels
Veins
Storage vessels
Conduct blood back to heart in a low pressure
system
Venous pump (valves)

Venous
System

Series of veins
located adjacent to
arterial system
Veins collect blood
from the capillaries
& terminal arterioles
Acts as reservoir for
blood
Low-pressure,
collapsible system
that work against
effects of gravity

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

Capillaries
Diffusion & exchange
Oxygen/CO2/solutes:
blood & tissues
Fluid: plasma &
interstitium
Lack smooth muscle
Lumen diameter
passively controlled
by changes in pre &
post-capillary
resistance

Capillaries
Capillary wall is permeable to all substances in
plasma & tissue fluid, except plasma proteins
Plasma proteins cause colloid osmotic pressure.
Fluid movement due to hydrostatic pressure.
Hydrostatic pressure pushes fluid out of the
capillaries. Oncotic pressure balances this by
maintaining fluid inside the capillaries.

Terima Kasih