Fisiologi Otot dan

Katup Jantung

Saskia D Handari
 PERICARDIUM

A superficial fibrous

A deep two-layer serous

The parietal layer lines
The visceral layer

They are separated by the fluid-filled pericardial cavity

 HEART WALL
EPICARDIUM
Visceral layer of the serous
pericardium

MYOCARDIUM
Cardiac muscle layer forming
the bulk of the heart

ENDOCARDIUM
Endothelial layer of the inner
myocardial surface
Heart as a
pump
Cardiac
Muscle
GENERAL
PRINCIPLES
• Cardiac worker cells are similar to skeletal
muscle cells
 Need stimulation for contraction
Stimulation from conduction
system/electrical system of the heart
• The electrical activity always precede the
mechanical activity
 Mechanism of Cardiac Muscle
Excitation, Contraction &
Relaxation
STRENGTH OF CONTRACTION
 THE
CARDIAC
CYCLE
What is the cardiac cycle?
the sequence of events that occur when the heart beats.
Two Separate Pumps

Atria

Ventricle
s
Repetitive contraction (systole) and relaxation (diastole) of heart
chambers
Blood moves through circulatory system from areas of higher to
lower pressure.
 General Concepts of the Cardiac Cycle

• The events of the • Contraction and • Pressure changes

ECG precede relaxation of the drive fluid flow and
contraction of the myocardium cause the opening and
myocardium changes in pressure closing of the heart
• P wave before atrial and volume of the valves
contraction chambers • Closing the heart
• QRScomplex before valves makes heart
ventricular sounds
contraction
• T wave before
ventricular
relaxation
 • 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
Heart Sounds semilunar valves
at diastole,
lasts longer
Pumping
CARDI
AC
CYC
LE
 First heart sound

QRS complex
on ECG

Systolic Isovolumetric
 Increase
pressure in the
Phase contraction ventricle

 Highest
Ejection pressure of the
ventricle and aorta

Second heart
sound
Venou
sReturn
Muscle
Pump
 • Represents the
“load”
placed on the
muscle
fibers before they
contract
• Frank-Starling law
states
“Stroke volume
increase as EDV
(ending diastolic
volume) increases –
stretch  more
force”
• EDV is determine by
venous return
• Venous return is
affected by
• Skeletal muscle
Preload pump
• Respiratory
pump
 Second heart sound

T wave on ECG

Isovolumetric
relaxation
Diastolic
Phase Rapid filling
• Lowest pressure of
the ventricle

P wave on ECG

Atrial
contraction/systolic
 Ventricular Volumes

End Diastolic End Systolic Stroke volume Ejection

Volume-(EDV) Volume- (ESV) (EDV-ESV) fraction
volume in volume in % of EDV
volume
ventricles at ventricles at ejected =
ejected by
the end of the end of (SV/EDV X
ejection ventricle 100%)
filling
normally
> 50%
 Cardiac
Output?
The amount of blood the heart pumps in 1
minute
Controlled to maintain the proper amount
of flow to tissues
 Stroke Volume and Heart Rate
Determine Cardiac Output
CARDIAC OUTPUT

is a function of

Heart rate Stroke volume

determined by determined by

Rate of depolarization Force of contraction in

in auto-rhythmic cells ventricular myocardium

is influenced by

Decreases Increases increases

Contractility End-diastolic
volume
Sympathetic
Due to innervation and
parasympathetic which varies with
epinephrine
innervation
increases
Venous constriction Venous return

aided by

Skeletal muscle Respiratory

pump pump

Figure 14-31
 Contractility
• the intrinsic ability of cardiac muscle to
develop force for a given muscle length.
• Affected by inotropic agent

Factors Preload
Affecting • the muscle length prior to contractility

Stroke • dependent upon ventricular filling (or end

diastolic volume/EDV)
Volume Afterload
• the tension (or the arterial pressure)
against which the ventricle must contract.
• Depends on the diameter and elasticity of
the vessel’s wall
 • The difference between
resting and maximal CO
level

• Cardiac Output:
Example
Cardiac CO (ml/min) = HR (75
beats/min) x SV (70
ml/beat)
Reserve
*) CO = 5250 ml/min
(5.25 L/min)
Cardiac Output Distribution
Regulation of Cardiac
Output

Figure 18.23
VALVES
Function of normal Valves
Unidirectional blood flow, one-way flow of
blood from the atria to the ventricles to the
arteries.
Name of heart valves
• 1.Two atrioventricular valves:
Mitral valve: Left heart - “Bicuspid valve” .
Tricuspid valve: Right heart -“tricuspid”
• 2. Two semilunar valves:
Aortic valve: Left heart .
 Pulmonary valve: Right heart.
Valve competency depends on
1. Annulus
2. Leaflets
3. Cords
4. Papillary muscles
5. Ventricular wall layers
 The mitral valve The aortic valve

Bicuspid valve-thin delicate& leaflets Three thin and delicate cusps

Definition of Valvular stenosis ?
Stenosis is the failure of a valve to open completely, which obstructing forward flow.
Etiology  
• Almost caused by chronic primary cuspal abnormalities- (1)Calcification or
(2)Valve scarring.
• Stenosis of the mitral valve is a common complication of rheumatic fever.
Definition of Valvular Regurgitation ?
Insufficiency results from failure of a valve to close completely, thereby allowing
reversed flow.
Etiology
• (1) Intrinsic disease of the valve cusps= destruction.
• (2) Distortion of supporting structure (papillary M, cords,etc.)
 ETIOLOGY

1.Congenital heart valve disease -

e.g. Septal defect, Atresia, mal-position.
_______________________________________________
2. Acquired heart valve disease :- (most frequent)
A.Endocarditis– (MR & AR) most common is mitral valve.
B.Post-inflammatory healed scar (Rheumatic heart disease) MS+MR &
AS+AR
C.Senile calcific aortic stenosis- AS
D.Myxomatous - Mitral valve Prolapse- MR
E. Abnormalities of Leaflets and Commissures
F. Abnormalities of Tensor Apparatus.
G.Abnormalities of Left Ventricular Cavity and/or Annulus-
 VALVULAR STENOSIS
Pressure in upstream chamber IS HIGHER than
Pressure in downstream chamber during time of
flow (when valve is normally open).
Hemodynamic abnormality = "PRESSURE GRADIENT"
 
 
Upstream Down stream

High pressure
low pressure
 VALVULAR
REGURGITATION
Retrograde flow of blood "upstream" during time when
 
valve is normally
  closed.
Hemodynamic abnormality = "VOLUME OVERLOAD"
 

Upstream Down stream

Volume overload
Normal Cardiac Chamber Pressure
MITRAL STENOSIS
Elevated pulmanary
and right heart • In Mitral Stenosis (MS), there is
pressure obstruction to blood flow
LA : Pressure ↑ across the mitral , such that
volume ↑
emptying of the LA is impeded,
and there is an abnormal
pressure between LA and LV.

• High LA pressure  retrograde

to the pulmonary circulation 
pulmonary venous and
capillary pressure increase 
transudation of plasma into the
lung interstitium  DYSPNEA
 Atrial
Fibrillation
Chronic pressure overload of the LA  left
atrial enlargement  stretches the atrial
conduction fibers and disrupt the integrity of
the conduction system  Atrial fibrillation
(rapid irregular heart rhythm)

Relative stagnation of blood flow in the dilated

LA + Atrial Fibrillation  intra atrial thrombus
formation  thromboembolic to the brain and
other organ

REQUIRE AN
TI
COAGULANT
MITRAL REGURGITATION
ETIOLOG
Y
•Primary :
•due to structural defect of
•one or more of the valve
components

•Secondary:
•the valve structural
normal,
•but regurgitation results
from
•the left ventricular
enlargement
• Acute MR :
sudden damage to components of the valve apparatus
Ex: rupture of an infarcted papillary muscle due to
STEMI, sudden rupture of chorda tendinea result
from Infective endocarditis, blunt trauma to the chest,

• Chronic MR : rheumatic deformity of the valve, congenital valve

defects, myxomatoses degeneration of the valve, extensive
calcification of mitral annulus

• Acute MR: Normal LA size and compliance  high LA pressure 

High pulmonary venous pressure  pulmonary congestion and
edema

• Chronic MR : Increased LA size and compliance  relatively

normal LA and pulmonary venous pressure, but decreased
forward cardiac output
AORTIC STENOSIS
Aortic stenosis: failure of aortic valve to open
completely, which obstructing forward flow
across the aortic valve.
Normal aortic valve: 3 to 4 cm2

• ETIOLOGY
1. Degenerative calcification of a previously
normal trileaflet aortic valve
2. Calcification of a congenitally bicuspid aortic
valve
3. Rheumatic aortic valve disease
Three major
manifestations
occur in patients
with advanced AS:
1. Angina
2. Exertional
syncope
3. Heart Failure
AORTIC REGURGITATION
Aortic Regurgitation (AR) : Insufficiency results from
failure of aortic valve to close completely

Primary valvular cause:

1. Bicuspid aortic valve (in some patients AR
predominates over aortic stenosis
2. Infective endocarditis
3. Rheumatic heart disease

Primary aortic root disease

When the aortic annulus dilates sufficiently to cause
separation of the leaflets, preventing normal coaptation
in diastole.
Ex: age degeration, aortic aneurysms, aortic dissection
Acute AR:
LV is normal size 
volume load of regurgitation 
LV diastolic pressure to rise substantially 
The sudden high pressure is transmitted
to the LA and pulmonary circulation 
dyspnea and pulmonary edema

Chronic AR:
Adaptive LV and LA enlargement have occurred,
such that a greater volume regurgitation can be accommodated
with less of an increase in diastolic LV pressure,
so that pulmonary congestion is less likely Normal
TRICUSPID VALVE DISEASE
Tricuspid Stenosis (TS)
• Tricuspid stenosis is a narrowing of the tricuspid valve opening. TS
restricts blood flow between the upper and lower part of the right
side of the heart, or from the right atrium to the right ventricle
• TS is rare and is usually a long term consequence of rheumatic fever
• Patients may develop abdominal distention and hepatomegaly
owing to passive venous congestion

Tricuspid regurgitation (TR)

• TR is a disorder in which tricuspid valve does not close tight
enough. It causes blood to flow backward into the right atrium
when the right ventricle contracts.
• TR is usually functional (results from right ventricular
enlargement) rather than structural in nature.
• Among patients with rheumatic mitral stenosis, 20% also have
significant TR (80% have functional TR because of pulmonary HT
with Right ventricular enlargement, 20% resulting from rheumatic
involvement of the tricuspid valve)
PULMONIC VALVE DISEASE
Pulmonic Stenosis (PS)
• Pulmonic stenosis , is a dynamic or fixed obstruction
of flow from the right ventricle of the heart to
pulmonary artery
• PS is rare and its cause is almost always congenital
deformity of the valve.

Pulmonic regurgitation (PR)

• PR is a leaky pulmonary valve. It allows blood to flow
back into the heart chamber before it gets to the
lungs for oxygen.
• PR most commonly develops in the setting of severe
pulmonary hypertension and results from dilatation
of the valve ring by the enlarged pulmonary artery
Text Book Refference
Leonard S. Lily. 2016. Pathophysiology of Heart
Disease

Mann, Douglas,, et al. 2022. Braunwald’s Heart

Disease. A textbook of cardiovascular Medicine,
Single Volume 12th Edition.
THANK YOU