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THE CARDIOVASCULAR SYSTEM

MAJOR FUNCTION:
Transport
- O2 , nutrients, waste
- vital for homeostasis
I. HEART
II. BLOOD VESSELS

Serous fluid lubricating fluid


produced by the
pericardial membranes
- allows the heart to beat easily in a
frictionless
environment
Pericarditis inflammation of the
pericardium

HEART :

- often due to a decrease amount of


serous
fluid

- cone-shaped, hollow

Heart Walls/ Layers of the Heart:

- approximately the size of a persons


fist

A. Epicardium

- weighs less than a pound

B. Myocardium

- located within the bony thorax

- thick bundles of cardiac muscles

1. Apex pointed down

- arranged in a twisted & whorled


ringlike
arrangement

- 5th ICS Left Midclavicular line

Myocardium layer that contracts

2. Base postero-superior

- reinforced by dense fibrous CT

- broad, attached to several large


blood
vessels.

C. Endocardium

- 2nd ribs Right


Coverings of the Heart:
Pericardium double sac of serous
membrane
- covers the heart
a. Visceral
Pericardium/Epicardium

- outer layer

- thin sheet of endothelium that lines


the
heart chambers
- continuous with the lining of blood
vessels
that leave & enter the
heart
Chambers of the Heart :
4 hollow chambers/cavities
2 Atria

- thin sheet

2 Ventricles

- hugs the external surface of the


heart

Atria Receiving chambers

- continuous with the parietal


pericardium

- blood flows into the atria at low


pressures
from the veins of
the body

b. Parietal Pericardium

Ventricles Discharging chambers/


Pumps

- loosely attached to the heart


- reinforced by dense connective
tissue
- protects the heart & anchors it to the
surrounding structures

- superiorly located

- Contracts to propel blood out of the


heart
& into the circulation

Anteriorly the heart appears in a


twisted like position
Anterior- Right Ventricle

Apex Left Ventricle

- between the atria & ventricles

Interventricular Septum- divides


the ventricles into the right & left
ventricles

- prevents back flow of blood into the


atria when
the ventricles contract

Interatrial Septum- divides the atria


into right & left atrium

a. Bicuspid/Mitral Valve
- Left AV valve
- 2 cusps/flaps
b. Tricuspid Valve - Right AV valve

The heart works as a double pump


Right Side Pulmonary Circulation
- carry blood into the lungs for gas
exchange
(Oxygenation ) & then
returns it to the heart
Left Side Systemic Circulation
- supplies O2 rich & nutrient to all
body organs
Pulmonary Circulation :
Superior & Inferior Vena cava O2
poor blood

Chordae tendinae anchors the


cusps to the walls of
the ventricles
Relaxed heart- hangs limply
Contraction of the ventricles- tenses
2. Semilunar Valves- guards the
bases of the 2 large arteries that
leave the heart
- prevents blood from reentering the
heart
a. Pulmonary valve
b. Aortic valve
Ventricles contract valves open

Right Atrium

Ventricles relax valves close

Right ventricle

**The AV & Semilunar valves open at


different times

Pulmonary Trunk
Pulmonary Arteries
Right Pulmonary Artery
pulmonary Artery

Left

Pulmonary Veins O2 rich blood

AV Valves Open during heart


relaxation
Close during heart contraction

Left Atrium

Semilunar valves Closed during


hear relaxation

Systemic Circulation :

Open during heart contraction

Pulmonary Veins O2 rich blood

Incompetent Valve valves does not


close properly

Left Atrium

- backflow of blood occurs

Left Ventricle

- heart pumps & repumps the same


blood

Aorta
Body Organs/Tissues
Valves of the Heart :
4Valves allows blood to flow in one
direction
Atria
Ventricles

Ventricles
Arteries

1. Atrioventricular/ AV Valves

Valvular Stenosis valve flaps


become stiff
- due to infection

Cardiac Circulation:
Right & Left Coronary Arteries branch from the base of the Aorta

a. Anterior interventricular
Left
b. Circumflex artery

- Sets the pace for the whole heart


B. Atrioventricular Node (AV)
- junction of the atria and ventricles

c. Posterior interventricular
Right

Atria Contracts

d. marginal artery

C. Atrioventricular bundle (Bundle


of His)

Arteries are compressed when the


ventricles contract & fill when the
heart is relaxed
When the heart rate increases the
myocardium may receive inadequate
blood due to short relaxation periods
CARDIAC PHYSIOLOGY

D. Right & left Bundle branches


interventricular septum
E. Purkinje Fibers
spreads into the muscles of the
ventricles

- 6000 quarts of blood a day is


pumped by the heart
Conduction System of the Heart:
- Cardiac muscle cells can & do
contract
spontaneously & independently even if
its
nervous connections
are severed.
- These contraction occur in a regular
& continuous
way
- Different areas of the heart have
different rhythms
Atrial cells 60/min
Ventricular cells 20-49/min
Control System of the Heart:
1. Autonomic Nervous System
- increases or decreases the heart rate
2. Intrinsic Conduction System/
Nodal System
- built into the heart tissue
- causes heart depolarization in only
one
direction
Atria
Ventricles
- enforces a contraction rate of 75
beats/min
A.Sinoatrial Node(SA)
- Pacemaker of the heart
- Crescent shaped
- Located at the right atrium

Contraction of ventricles- begins at


the apex towards the atria
- ejects blood superiorly into the
large
arteries

Heart Block any damage to the AV


node which releases its control from
the SA node
- ventricles beat at their own rate
(slower)
Damage to the SA node Slow heart
rate
- Artificial pacemaker
Fibrillation rapid uncoordinated
shuddering of
the heart
muscle
- may be due to lack of adequate
blood
supply
- major cause of heart attacks in
adults
Tachycardia rapid heart rate;
greater than 100
beats/min
- prololnged tachycardia may lead to
fibrillation
Bradycardia slow heart rate; below
60 beats/min

Cardiac Cycle & Heart Sounds :

- closing of the semilunar valves

- In a healthy heart, the atria contract


simultaneously then as they relax the
ventricles contract.

- short & sharp

Systole Contraction ( Ventricles)


Diastole Relaxation (Ventricles)
Cardiac Cycle Events of one
complete heartbeat
- includes the time during which
both atria &
ventricles contract &
relax - 0.8 sec
A.Mid-to-late Diastole
- heart in complete relaxation
- low heart pressure

- AV valves open

- blood flows from the atria to the


ventricles passively

Murmurs abnormal or unusual heart


sounds
- due to turbulent flow of blood
- common in children / elderly
- may indicate heart valve problems
Incompetent valve
- valves does not close tightly
- swishing sound after valve closure
due
to backflow
Stenosis
- narrowed valves
Cardiac Output :

- atria contracts & forces the


remaining blood to the ventricles

- amount of blood pumped out by each


side of

B.Ventricular Systole

the heart in 1 minute.

- ventricles contract

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

- increase pressure in the ventricles


closes the
AV valves
- increase pressure in the ventricles
forces
open the semilunar
valves

= 5250 ml/min
Stroke volume

- blood rushes out of the ventricles

- volume of blood pumped out by a


ventricle with
each heart beat

- atria is relaxed & its chambers are


again
filling blood

* Stroke volume increases as the force


of ventricular contraction increases

C. Early Diastole

* The Cardiac Output varies with the


demands of the body

- ventricles relax
- semilunar valves snap shut
- ventricular pressure decreases
- AV valves open when atrial pressure
rises
Heart Sounds:
lub-dup
1st Heart sound lub

- increase CO if SV increases
increase CO if HR increases
increase CO if HR & SV increases
- decrease CO if SV, HR or both
decreases
Regulation of Stroke Volume :
- a healthy heart pumps out about
60% of the
blood that enters it

- closing of the AV valves


- longer & louder
2nd Heart sound dup

FRANK-STARLING LAW:

The critical factor controlling SV is how


much the cardiac muscle cells are
stretched just before they contract.
- the more they are stretched the
more stronger the contraction
* The most important in heart
stretching is

1. Autonomic Nervous system


Sympathetic NS

Increase HR

Parasympathetic NS
Decrease HR
2. Hormones
Epinephrine

Venous Return

increase HR

- the amount of blood entering the


heart
& distending the
ventricles

Thyroxine

- increase in volume of venous


return

Hypocalcemia decrease HR

increase stroke volume & force of


contraction

Hypokalemia abnormal rhythm

- slow heartbeat
return

5. Gender

increase venous

- exercise increase venous return


Severe blood loss decrease stroke
Extremely rapid heart rate & decrease
venous
return

3. Ions/ Electrolytes

Hypercalcemia increase HR

4. Age

Fetus increase HR
Females increase HR

6. Temperature
increase HR

Fever

Cold decrease HR
7. Exercise increase HR
Physiology of Circulation:
- Indication of efficiency of circulation
is obtained by taking the blood
pressure & arterial pulse.

Regulation of Heart rate:

Vital Signs ( PR, HR, BP, Temp,


RR )

When blood volume drops or heart is


weakened

Arterial Pulse:

Stroke volume decreases


Cardiac Output is maintained by an
increase in the heart rate
Factors that can affect the Heart
rate:
1. Autonomic Nervous System
2. Chemicals

4. Ions ( Electrolytes)
5. Physical factors

b. Gender

- Normally the PR=HR


- influenced by activity, postural
changes &
emotion.
Sites for taking the arterial pulse:

3. Hormones

a. age

- pressure wave generated by the


alternating
expansion & recoil of an
artery with each
beat of the left
ventricle.

c. Exercise
d. Body temp

Temporal
Facial

Radial
Femoral

Carotid

Popliteal

Brachial
Tibial

Posterior

Dorsalis pedis

Blood Pressure :
- pressure the blood exerts against the
inner wall of the blood vessels & it is
the force that
keeps blood
circulating continuously even
between heartbeats.
- When the ventricles contract they
force blood through the thick &
elastic arteries
- The high pressure in the arteries
forces the
blood to continually
move into areas where
the
pressure is lower
- Valves in veins, milking activity of
skel;etal
muscles & pressure
changes in the thorax
returns
blood into the heart.
Measuring Blood pressure:
Systolic pressure pressure in the
arteries at the peak of ventricular
contraction

Parasympathetic NS little or no effect


but
mostly decreases BP
Sympathetic NS
Vasoconstriction

causes

Increase BP
* No vasoconstriction occurs in the
Heart & Brain
B. Renal Factors: Kidneys
- by altering blood volume
* Increase BPIncrease excretion of
water
BP returns to normal
*Decrease BP/ blood volume
decrease
excretion of water
Increase in BP
Deccrease in BP

Diastolic pressure pressure when


the ventricles
are relaxing

Kidney release an enzyme called


Renin

Effects of Various factors on Blood


Pressure:

Renin converts Angiotensinogen to


Angiotensin I Angiotensin I is
converted

1. Cardiac Output

to Angiotensin II by Angiotensin

2. Peripheral Resistance

converting enzyme(ACE)

- Amount of friction encountered by


the blood as it flows through the blood
vessels
- influenced by the constriction or
narrowing of blood vessels
3. Blood Volume

Release of Aldosterone which


Reabsorbs water in the kidneys
Increase in the BP
C. Temperature
Cold Vasoconstriction
Warm Vasodilation

* Any factor that increases the above


may increase the blood pressure

D. Chemicals

Other factors that can alter the


blood pressure:

Epinephrine increases HR & BP

1. Age

4. Body position

Histamine Decrease BP

2.Weight

5. Emotional state

E. Diet

3. Time of day

6. Drugs

A. Neural Factors : Autonomic


Nervous System

Nicotine & Alcohol Increase BP

High salt diet increase BP

Blood Vessels :

Microscopic Anatomy of Blood Vessels:


Three Coats of Blood vessels:

Artery:

1. Tunica Intima

1. Thicker walls

- Lines the lumen/interior of blood


vessels

2. Heavier tunica media

- thin layer of endothelium


- slick surface which minimizes friction
2. Tunica Media
- bulky middle coat
- smooth muscle & elastic tissue
- controlled by the Sympathetic NS
3. Tunica Externa
- outermost coat
- fibrous connective tissue
- supports & protects blood vessels

- Walls must be able to expand &


recoil to take changes in blood
pressure
Veins:
1. Thinner walls
2. Larger lumen
3. Presence of valves prevents
backflow
Capillaries:
- 1 cell layer thick Tunica intima

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