08 cardiovascular system baru
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Cardiovascular SystemCardiovascular System
Overview of Anatomy & PhysiologyOverview of Anatomy & Physiology
Assessment of CV FunctionAssessment of CV Function
Ezra OktaliansyahEzra Oktaliansyah
e!artment of Anesthesiology & "eanimation #edical Faculty
Pad$ad$aran %niversity dr' (asan Sadikin )eneral (os!ital
*andung
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Function of the heart:
pump oxygenated (saturated) blood into the
arterial system, which carries it to the cells
pump deoxygenated (desaturated) blood
back to the lungs via the veins for
reoxygenation
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heart size depends on the size of the person
approximately the size of the fist
encased in a thin, fibrous sac called the
pericardial sac or pericardium (2 layers)
composed of three layers: inner layer endocardium middle layer myocardium
outer layer e!icardium
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!ardiac chambers:
"ight atrium receives deoxygenated blood
from the superior and inferior vena cava
(venous return)
"ight ventricle pumps blood against a low
resistance in the pulmonary artery (#$") on
the way to the lungs where oxygenationtakes place
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%eft atrium receives oxygenated blood
from the lungs via & pulmonary veins
%eft ventricle pumps blood to the systemic
circulation via the aorta against a high
resistance ('$")
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!ardiac valves:
ensure one way flow of blood
two types:
atriovenricular valves mitral (btw % * %$)
tricuspid (btw " * "$)
closed during $+ systole and therefore prevent
backflow of blood to the atria during ventricularcontraction (systole)
open during ventricular relaxation (diastole)
allowing for filling of the ventricles
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semilunar valves
pulmonic valve (btw "$ * pul+ artery)
aortic valve (btw %$ * aorta) closed during v+ diastole and prevent backflow
into the ventricles during relaxation (ventricular
diastole)
unlike the $ valves, they are open during
contraction of the ventricles (ventricular
systole) allowing for emptying of the ventricles
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!ardiac cycle
eart muscle contracts * relaxes
rhythmically to assure proper circulation
one cardiac cycle-. heart beat
two phases to the cardiac cycle: systole
diastole
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'ystole
ventricles contract
blood e/ected from the %$→aorta and from
the "$→ pulmonary artery
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0iastole
ventricles relax
pressure in the ventricle falls below that of
the atria
the $ valves open
blood which has been pooling in the atria
begins to flow into the ventricles
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as systole begins the $ valves (mitral *
tricuspid) close, '. (1lubb) produced
semilunar valves forced open, a silent event
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3hen ventricles are almost empty, pressure in
the ventricles drops, allowing the semilunar
valves (pulmonic and aortic) to close, '2(1dubb) produced
at this time atrial pressure higher, mitral *
tricuspid valves forced open, passively fillingthe ventricles up to a certain point (if rapid
filling of dilated ventricle, '4 possible)
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to ensure that the blood remaining in the
atria is e/ected, the atria contract (atrial
kick)
if there is any resistance to filling by the
ventricle, '& possible
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5lectrical activity
n electrical conduction system is
responsible for the se6uence of muscle
contractions that take place during thecardiac cycle
in essence an electrical current stimulates
each contraction under normal circumstances, this electrical
impulse originates in the ' node
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this property of the ' node to initiate an
impulse is known as +automaticity,
automaticity can be disturbed in 78 (d9thypoxia), electrolyte imbalance, acidbase
imbalance, drugs, etc+
onautomatic cell may become automaticand subse6uently cause dysrhythmias, (e+g+,
#!s, #;!s, #$!s, escape rhythms, etc+)
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ormal conduction pathway
SA node via internodal tracts to AV node to the
*undle of (is
the <undle of is then divides into the "ight*undle *ranch * the -eft *undle *ranch
each branch terminates to form the Purkinge
fi.ers located in the ventricular myocardium,where the ventricles, when stimulated, contract
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=wo electrical events
(recorded as waves on 5>?): de!olarization the spread of an electrical
impulse through the heart muscle
re!olarization the return of the heart muscleto a resting state
the corresponding mechanical events are
contraction and rela/ation, respectively =he ability of cardiac cells to respond to an
electrical impulse is called +e/cita.ility,
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=he se6uence of depolarization and
repolarization is called the cardiac action
!otential+ 8t results when ions (charged particles such
as a, >, * !a) shift across the cell
membrane+
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!onductivity
"efers to the ability of the heart muscle
fibers to transmit electrical impulses along
and across cell membranes can be enhanced or depressed by drugs,
ischemia, trauma
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!ontractility
"efers to the heart muscle fibers ability to
contract, or shorten, in response to an
electrical impulse (irrespective of volume) can be impaired in 78, electrolye
disturbances, drugs, hypoxemia
decreased contractility results in a drop in thestroke volume and ultimately leads to a drop
in cardiac output
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"efractoriness
"efers to the heart@s inability to respond to a
new stimulus while still in a state
depolarization from an earlier stimulus this prevents the possibility of tetanic
contractions that would be fatal
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5lectrical activity *
corresponding waves on 5>? # wave corresponds to the spread of the
impulse through the atria atrial
de!olarization #" interval conduction time through the
atria (+.2+2A sec+)
B"' complex corresponds to spread of theimpulse through the ventricles ventricular
de!olarization
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B"' interval conduction time through the
ventricles (+A&+.2sec+)
'= segment * = wave return of stimulated
ventricular muscle to a resting state
ventricular re!olarizationCC
B= interval time it takes for the ventriclesto depolarize * repolarize
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!oronary circulation
eart muscle itself re6uires a supply of
oxygenated blood to meet its own metabolic needs
supplied through the coronary arteries which branch off from the aorta /ust above the aortic
valve, encircle the heart, and penetrate the
myocardium
returned to right side of the heart via the coronary
veins
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"ight !oronary rtery ("!)
%eft 7ain !oronary rtery (%!): %eft anterior descending (%0)
!ircumflex artery
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!ollateral !irculation
=he presence of more than one artery
supplying a muscle (a capacity present at
birth but not functional) develops when the blood flow through an
artery progressively decreases and causes
ischemia to the muscle extra blood vessels develop to meet
metabolic needs of the muscle
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!ardiac Dutput
$olume of blood e/ected by the heart9min+
(E &%)
'troke volume G heart rate
cardiac index a calculation that helps to
determine if !D is ade6uate in relation to
body size !8-!D9<' (0ubois scale) in %9min9m2
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'troke volume
0etermined by: preload
afterload contractile state of the myocardium
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#reload
7yocardial fiber length of the ventricle at end
diastole
also known as amount of stretch 'tarling@s law (↑ stretch →↑ force of
contraction) C
stretch determined by volume of blood inventricle
#reload - $enous "eturn
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fterload
=he resistance against which the ventricle must
e/ect its volume
amount of pressure re6uired by the %$ to openthe aortic valve during systole and to e/ect
blood into the systemic circulation ('$")
afterload for right side of the heart (#$")
inversely related to stroke volume
related to <# ( systemic9pulmonary)
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!ontractile (inotropic) state
"efers to the vigor of contraction generated
by the myocardium regardless of its blood
volume (preload) increased by '' stimulation (epinephrine
endogenously or exogenously)
decreased by hypoxemia9acidosis
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"egulation of !$ system
involuntarily controlled by the '
the ' plays a role in regulating
heart rate (chronotropic effect) myocardial contractility (inotropic effect)
conduction velocity at the $ node
peripheral (systemic) vascular resistance
arteriole constriction and dilation
venous return
venule and vein constriction and dilation
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=he two subdivisions of the '
(sympathetic * parasympathetic) generally
exert opposing influences and balance theiractivities to promote cardiovascular
adaptation to internal and external demands
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#arasympathetic nervous system
7ediated via the vagus nerve
when stimulated, parasympathetic nerve
endings release the neurotransmitteracetylcholine, which produces inhibitory
effects
decreases the rate of ' node firing, thuslowering "
lessens atrial conductivity
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'ympathetic nervous system
7ediated by <eta receptors
when stimulated, the nerve endings release the
neurotransmitter norepinephrine and producethe following effects: increase in heart rate
increase in conduction speed through the $ node increased atrial and ventricular contractility
peripheral vasoconstriction (H result)
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ormonal * other influences on
!D 0
reninangiotensinaldosterone mechanism
exercise, anger, fear, pain, anxiety, excitementcan augment the '' effects
drugs
I2 adrenergic agonists stimulate '' (↑") I blockers <lock '' (↓")
cardioselective I blockers (block only I. receptors)
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<lood pressure
5xpressed as systolic blood pressure9diastolic
blood pressure
'<#peak pressure exerted against arterieswhen heart contracts (measure of contractile
function)
0<#residual pressure during relaxation ofthe heart (↑er in atherosclerosis)
<#-!Dx'$"
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8mportant receptors
!hanges in sympathetic and
parasympathetic activity occur in response
to messages sent from sensory receptors invarious parts of the body
for cardiovascular function, the important
receptors are: arterial baroreceptors, stretchsensitive cardiopulmonary receptors of the
atria and veins, and chemoreceptors
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<aroreceptors
'tretch sensitive nerve endings affected by changes
in art+ <#
located in the walls of the aortic arch and carotidsinuses
stimulated by an ↑in art+ <#, a vagal response
results in ↓in heart rate and art+ <#
with ↓ <#, less stretch, fewer impulses, see
sympathetic mediated ↑ in " and vasoconstriction
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!ardiopulmonary stretch
receptors located in vena cava * atria
respond to length changes, reflective of circulatory
volume status with ↓ in <# in vena cava and " due to
hypovolemia, stretch receptors send fewer impulses
than usual to the !'
result is a sympathetic response to kidney to
enhance a and water retention * release of 0
(hypervolemia produces the opposite)
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!hemoreceptors
Found in the aortic arch and carotid bodies
sensitive to ↑ !D2 and ↓arterial p
(acidemia) and secondarily sensitive tohypoxemia
when such changes occur, they send
impulses to the !' to increase "
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'ome factors affecting <#
cardiac output9blood volume
systemic vascular resistance
elasticity of blood vessels blood viscosity
age
weight
emotion
exercise
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ssessment of !$ function
istory
#hysical 5xamination inspection
palpation
percussion
auscultation
%ab * 0iagnostic =ests
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#resent istory
!hief complaint * symptom analysis
(#B"'=)
chest pain dyspnea (0D5, othopnea, #0)
cough (hemoptysis)
palpitations skipped beats
dizziness, fainting, syncope
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fatigue9weakness
weight gain
peripheral skin changes (e+g+, edema, #$0) leg pain
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#ast istory
ypertension
0iabetes
"heumatic fever9"heumatic heart disease
5levated homocysteine levels (homocysteine,
an amino acid produced in the body, is
considered to be a contributing risk factor andis associated with <.2, folic acid, and <J
deficiencies)
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%ifestyle
7ay constitute modifiable risk factors for
heart disease
smoking elevated cholesterol levels9high fat diet (esp+
saturated fats)
sedentary activity9physical inactivity obesity
stress
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#hysical 5xamination
8nspection color
presence of clubbing capillary refill
edema
vital signs peripheral pulses
level of consciousness (%D!)
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8nspection cont@d ;$#
urine output #78
xanthelasma
arcus senilus ear lobe creases
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#ercussion
#alpation thrill
heave9lift
abdomen
liver (including the hepato/ugular reflex)
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uscultation normal heart sounds ('., '2)
abnormal heart sounds ?allops ('4, '&)
pericardial friction rub
murmurs
bruit
lung sounds
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%ab * 0iagnostic =ests
!hest xray
5>? * cardiac monitoring
'tress test (5==)
5lectrophysiological studies
!ardiac catheterization
ngiography
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5chocardiogram
8ntraarterial pressure monitoring
emodynamic monitoring (!$#, # )