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Cardiovascular System

Dr. Anis Irmawati, drg., MKes

Physiology I

Dental Medicine Faculty


Universitas Airlangga
October, 2019
Anatomy

CVS consist of :
1. heart
2. blood vessel
3. blood

heart is the key organ of CVS


adult : weight = 350 g; L = 12 cm; W = 9 cm
lie : mediastinal cavity of the thorax
between lung
between 2nd & 5th intercostal space
Heart structure

1. three layers : epicardium, miocardium, endocardium

2. Two pace makers : sino atrial nodes (SA nodes = SAN)


atrio ventricular (AV nodes = AVN)

3. Four chambers : 2 atrium  RA & LA


2 ventricle  RV & LV
4. Four valves :
*atrioventricular  RA – RV : tricuspid
LA - LV : bicuspid (mitral)
*semilunar  RV – arteri pulmonalis : pulmonary
LV – aorta : aorta

5. Heart supply : coronaria blood vessel


Structure

heart is enclosed in a sac --> pericardium :


*protects and prevents it from over-expanding
*anchoring it inside the thorax
*attached to the diaphragm and inner surface of the sternum
*made up of :
**fibrous pericardium --> composed of a loosely fitting but
dense layer of connective tissue
**serous pericardium or epicardium --> composed of parietal
and visceral layers
**film of serous fluid :
between fibrous and serous pericardium --> allows them to
glide smoothly against each other
Structure

middle muscular layer --> myocardium --> made up of cardiac


muscle cells
inner lining --> endocardium
inside of the heart (heart cavity) --> divided into four chambers :
two atria and two ventricles --> separated by cardiac valves -->
regulate the passage of blood
Atria & ventricles

left atrium (LA) and left ventricle (LV) --> separated from right atria
(RA) and right ventricle (RV) by septum
RA receives deoxygenated blood :
*from the head and neck and from the rest of the body
*via the superior and inferior vena cava
RV then pumps blood into the lungs :
through right and left pulmonary arteries --> it is oxygenated
oxygenated blood is returned to the LA via the pulmonary veins -->
passes into the LV through the cardiac valves
from the LV --> blood delivered to the whole body --> via aorta
Atria & ventricles

RV does not need a huge amount of force :


to pump blood into the lungs --> compared with LV --> which has to
pump blood into the rest of the body
LV has a thicker wall and its cavity is circular (melingkar)
RV cavity is crescent-shaped (bulan sabit) with a thinner wall
Cardiac valves

deoxygenated blood : RA  RV : tricuspid valve


from RV  via pulmonary valve  pulmonary artery :
allowing deoxygenated blood to enter the lungs
pulmonary artery (change CO2 & O2)  oxygenated blood
oxygenated blood  pulmonary vein  into LA  via bicuspid
(mitral) valve  LV  via aorta valve  into aorta  all tissue
Conduction system

in the heart  electrical changes needed to generate a cardiac


impulse  regulated by its own conduction system  starts
with a sequence of excitation in a specialised area of cardiac
cells  sinoatrial node (SAN)  lie in the RA
SAN  heart’s natural pacemaker
SAN sets the heart rhythm (sinus rhythm)  initiates impulses
on the myocardium  stimulating cardiac contraction
cardiac impulse passes from SAN into the atria  starts to
contract  impulse is transmitted to another mass of specialised
cells : atrioventricular node (AVN)
Conduction system

AVN  lie in the inter-atrial septum


provides a pathway of conduction between atria and ventricles
there is a slight delay (of 0.1 seconds) of the impulse at the AVN
 because the fibres of the AVN are smaller  gives atria
time to contract and empty into the ventricles before ventricular
contraction occurs
impulse then travels down into specialised tissue  Bundle of His
 conducts with ventricles
Bundle of His subsequently splits into : right and left bundles
in the interventricular septum
Purkinje fibres  continue down to the inferior aspect of the heart,
before looping upwards and travelling in the lateral aspects of the
RV and LV
Coronary circulation

heart --> requires a richly oxygenated blood


delivered via the right and left coronary arteries --> lie on the
epicardium and penetrate the myocardium
right and left coronary arteries arise from vascular openings
at the base of the aorta --> called ‘coronary ostia’
left coronary artery runs towards the left side of the heart -->
divide into : left anterior descending artery and left circumflex
artery
right coronary artery  runs down the right side of the heart 
divide into marginal artery and posterior descending artery
Cardiac cycle

chambers of heart contract and relax in a coordinated fashion


contraction phase  called : systole
relaxation phase  heart fills up again  called : diastole
RA and LA synchronise during atrial systole and diastole
RV and LV synchronise during ventricular systole and diastole
one complete cycle of these events  called : cardiac cycle
during cardiac cycle  pressure in the cardiac chambers  or  
affecting valve opening or closure  regulating blood flow between
the chambers
pressures in the left side  5x higher than in the right side
blood flow through the chambers : depends on pressure changes
blood will always flow : from a high to a low-pressure area !!!
Atrial systole and ventricular filling

pressure in the heart is low --> blood from the circulation passively
--> fills the atria on both sides
this culminates : opening of the AV valves --> blood moving into
ventricles
 70% of ventricular filling occurs during this phase
after depolarisation of atria (P wave on ECG) --> atria contract -->
compressing blood in the atrial chambers --> also push residual
blood out into the ventricles
this signifies the last part of the ventricular resting phase (diastole)
--> the blood within the ventricles --> called : end diastolic volume
(EDV)
atria then relax --> then the electrical impulse is transmitted to
the ventricles --> which undergo depolarisation (QRS wave on ECG)
Ventricular systole

atria are relaxed --> ventricles begin to contract


contraction of the ventricles --> leads to an increase in ventricular
pressures within the cavity :
*open pulmonary valve --> blood enter pulmonary artery
*open aortic valve --> blood enter aorta --> distribute to all tissue
Isovolumetric relaxation

at this point --> ventricles relax --> any blood remaining in the
chamber --> called: end systolic volume (ESV)
ventricular pressure precipitously drops --> blood within aorta and
pulmonary trunk --> momentarily backflow --> the aortic and
pulmonary valves close
this backflow causes a brief rise (peningkatan singkat) --> in the
pressure of aorta --> giving a characteristic change --> in the
pressure of the cardiac cycle --> called : dicrotic notch
while the ventricles have been in systole --> atria are in diastole -->
fill again --> ready for the next cardiac cycle
Cardiac output and stroke volume

at this point --> ventricles relax and any blood remaining in the
chamber --> called : end systolic volume (ESV)
the ventricular pressure : referred to Cardiac output (CO)
CO : amount of blood pumped out by the heart in one minute
stroke volume (SV) : volume of blood pumped by the ventricles with
each heart beat
remember :
EDV = volume of blood left in the ventricles during diastole
ESV = volume of blood remaining in the ventricles after it has contracted
EDV = 120 ml
ESV = 50 ml, the SV will be:
SV = EDV - ESV = 120 ml – 50 ml = 70 ml/beat
CO = SV x heart rate
= 70 x 80 = 5600 ml/minute
Frank-Starling law

at this point, the ventricles relax and any blood remaining in the chambeA
physiological principle underpinning cardiac function is the Frank–Starling
law, which proposes that the critical factor affecting SV is the preload – that
is, the blood that goes from the returning circulation into the heart during its
filling.
The amount of preload determines the volume of blood that can leave the
heart (the CO) and influences the stretch and tension on the individual
muscle cells which make up the cardiac fibres. The SV increases in response
to preload. As a result of the filling, increased pressure in the ventricles
increases the stretching of the cardiac muscle fibres. This stretch culminates
in increased contractility of the heart and increased CO. Up to a certain
physiological limit, the preload and contractility of the heart are positively
correlated. This explains how exercise can improve cardiac performance.
ALHAMDULILLAH