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CARDIOVASCULAR

PHYSIOLOGY
Departemen Fisiologi
Fakultas Kedokteran
Universitas Sumatera Utara

Dr. Poland Room 3-007, Sanger Hall, Phone: 828-9557


E-mail: poland@hsc.vcu.edu

?
m
e
t
Functions of the Cardio-Vascular
System
s
y
S
V
C
e
th
Delivery of O2, oGlucose
and other
f
n
o
i
t active tissues.
nutrients
to
c
n
u
F
y
r
Transport
a
of metabolites and other
m
i
Prsubstances to and from storage

s
n
a
r
T

t
r
o
p

sites.
Transport of hormones, antibodies
and other substances to site of
action.
Dr Peter K. McFawn Department of Physiology Queens University Botterell Hall 4 th floor
pkm@post.queensu.ca http://meds.queensu.ca/physiol/underg.html

The Heart

Four Chambered Organ


Circulates Blood to Lungs Unoxygenated
Circulates Blood to the Body
Oxygenated

Removal of CO2, Lactate


and other waste products
from active tissues.
The Lungs Relationship to the
CV System

Provides for exchange of


Oxygen and Carbon
Dioxide

Specialized Muscle Type Cardiac


Unique Vascular System Coronary
Arteries and Veins
Separate Nervous System
Beats (contracts) approximately 65-75
times/minute

The Circulatory System


2 main divisions
Pulmonary circulation (heart lungs)
Pulmonary artery: deoxygenated blood from the heart to the lungs
Pulmonary vein: oxygenated blood from the lungs to the heart

Systemic circulation: (Heart rest of the body)


Aorta: feeds oxygenated (arterial) blood to the body
Venae cavae: returns deoxygenated (venous) blood from the body

Series and
Parallel Vascular
Beds.

*The systemic and pulmonary


circulations are in Series with
each other.
*Systemic capillary beds are in
parallel with each other.
*The kidney and hepatic/gut
capillary beds are an
exception. The portal vein and
kidney efferent arteriole link
capillary systems in series.
PARALLEL SUBCIRCUITS
UNIDIRECTIONAL FLOW

PULMONARY
CIRCULATION
1. LOW RESISTANCE
2. LOW PRESSURE
(25/10 mmHg)

SYSTEMIC
CIRCULATION
1. HIGH RESISTANCE
2. HIGH PRESSURE
(120/80 mmHg)
PARALLEL
SUBCIRCUITS
UNIDIRECTIONAL
FLOW

CAPACITY VESSELS

THE SYSTEMIC
CIRCULATION
1. HIGH RESISTANCE
2. HIGH PRESSURE
(120/80 mmHg)

THE PULMONARY
CIRCULATION
1. LOW RESISTANCE
2. LOW PRESSURE
(25/10 mmHg)

NORMAL

PACEMAKER POTENTIAL

Fastest cells
located in SA node
(100/minute).
SA node sets
pace.
Bundle of His can
provide ectopic
pacemaker (2540/min)

Intrinsic Conducting
System

Sinoatrial node.

Electrical pace maker.

Atrioventricular node.
Receives impulses
originating from SA
node.

Bundle of His
Electrical link between
atria and ventricles.

Purkinje fibres.
Distribute impulses to
ventricles.

PACEMAKERS

(in order of
their inherent
rhythm)
Atrio-ventricular (AV) node

Sino-atrial (SA) node


Atrio-ventricular (AV) node
Bundle of His
Bundle branches
Purkinje fibers

Electrical Events

Autorhythmicity:heart contracts
without help of hormonal or neuronal
stimulation.
The conduction or nodal system of the
heart consists of the AV and SA nodes,
the AV bundle and bundle branches
and Purkinje fibers.
This system coordinates the
depolarization and ensures the heart
beats as one.
The SA acts as the hearts pacemaker
and sets the sinus rhythm.

Impulse pathway

SA node sends stimulus->reaches AV


node-->internodal pathways->atrial
contraction->IV septum->bundle
branches, Purkinje fibers, papillary
muscles->Purkinje relay to ventricular
myocardium->ventricular contraction>blood pushed to aortic and pulmonary
trunks.
Conduction deficit problems that
happen when the conducting pathways
are damaged. The rhythm of heart will
be disturbed.
Ectopic pacemaker:an abnormal cell
generates action potential which
overrides those of SA or AV nodes.
Disrupts timing of ventricular
contraction. Heart efficiency is reduced.

Properties of Cardiac Muscle


ELECTRICAL PROPERTIES
Resting Membrane & Action Potentials
The resting membrane potential of individual
mammalian cardiac muscle cells is about -90 mV
(interior negative to exterior).
Stimulation produces a propagated action potential
that is responsible for initiating contraction.

Depolarization lasts about 2 ms, but plateau phase


and repolarization last 200 ms or more.
Repolarization is therefore not complete until the
contraction is half over.

Autorhytmic cells begin depolarizing due to a slow continuous


influx of sodium and reduced efflux of potassium

When threshold is reached, the fast calcium channel open,


and calcium rushes in

Reversal of membrane potential triggers opening of potassium


channels, resulting in rapid efflux of potassium

Diagram of the membrane potential of


pacemaker tissue.

MECHANICAL PROPERTIES
Contractile Response
The contractile response of cardiac muscle begins
just after the start of depolarization and lasts about
1.5 times as long as the action potential

During its absolute


refractory period, cardiac
muscle cannot be excited
again
Therefore, tetanus of the
type seen in skeletal
muscle cannot occur.

Correlation Between Muscle Fiber


Length & Tension
Relation between
initial fiber length
and total tension in
cardiac muscle is
similar to that in
skeletal muscle;
there is a resting
length at which the
tension developed
upon stimulation is
maximal.

Frank StarlingS LAW


Kesanggupan intrinsik jantung untuk penyesuaian diri terhadap
beban yang berbeda
Dalam batas fisiologis jantung akan memompakan semua darah
yang masuk kedalam jantung tanpa menimbulkan penumpukan
darah berlebihan. Ini disebabkan oleh peregangan yang
ditimbulkan volume darah yang masuk menyebabkan kekuatan
kontraksi bertambah.
Dengan perkataan lain:

Kontraksi jantung sewaktu sistolis akan


bertambah kuat bila pengisian darah lebih banyak
pada masa diastolik.

Kurva Frank Starling


Pada kurva dapat dilihat
Bila pengisian ventrikel bertambah ,
Stroke volume

darah yang dipompakan >>


( EDVSTROKE VOLUME )

End Diastolic Volume

In the body, the initial length of the fibers


is determined by the degree of diastolic
filling of the heart, and the pressure
developed in the ventricle is proportionate
to the total tension developed (Starling's
law of the heart).
Developed tension increases as the
diastolic volume increases until it reaches
a maximum (ascending limb of Starling
curve), then tends to decrease
(descending limb of Starling curve).

Kurva Frank Starling


Stimulasi
Adrenergik

Stroke volume

Normal
Fungsi jantung
Syok
Kardiogenik

End Diastolic Volume

Stroke volume

Kurva Frank Starling

End Diastolic Volume


Total blood
volume
Atrial
contribution to
ventr.filling

Body
position

Intrathoracic
pressure

STRETCHING OF MYOCARD
Pumping action of
skletal muscle

Venous tone

Intrapericardial
pressure

The

force of contraction of cardiac muscle


is also increased by catecholamines, and
this increase occurs without a change in
muscle length.

The

increase, which is called the positively


inotropic effect of catecholamines, is
mediated via innervated 1-adrenergic
receptors and cyclic AMP.

When the cholinergic vagal fibers to nodal


tissue are stimulated, the membrane
becomes hyperpolarized and the slope of
the prepotentials is decreased because
the acetylcholine released at the nerve
endings increases the K+ conductance of
nodal tissue.

Spread of Cardiac Excitation


Depolarization initiated in the SA node
spreads radially through the atria, then
converges on the AV node.
Atrial depolarization is complete in about
0.1 s. Because conduction in the AV node is
slow, there is a delay of about 0.1 s (AV
nodal delay) before excitation spreads to
the ventricles.
This delay is shortened by stimulation of
the sympathetic nerves to the heart and
lengthened by stimulation of the vagi.

From

the top of the septum, the wave of


depolarization spreads in the rapidly
conducting Purkinje fibers to all parts of
the ventricles in the 0.08-0.1 s.
In humans, depolarization of the
ventricular muscle starts at the left side of
the interventricular septum and moves first
to the right across the midportion of the
septum.
The wave of depolarization then spreads
down the septum to the apex of the heart.

It

returns along the ventricular walls to


the AV groove, proceeding from the
endocardial to the epicardial surface.
The last parts of the heart to be
depolarized are the posterobasal portion of
the left ventricle, the pulmonary conus,
and the uppermost portion of the septum.

Normal spread of electrical activity in the heart.

Let it
beat!

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