Kp 1.3.2.1 Aktivitas Mekanik Jantung (2 Jam)

7/24/2019 Kp 1.3.2.1 Aktivitas Mekanik Jantung (2 Jam)

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AKTIVITAS MEKANIK

JANTUNG

Rahmatina B. Herman

Bagian FisiologiFakultas Kedokteran - Unand


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Position of Heart in Thoracic Cavity


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Structure of Heart


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Structure of Heart..


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Anatomy - Physiology of Heart

Two separate parts: left and rightRespectively:

- left atrium and ventricle

- right atrium and ventricle

Atrial function: primary pumps for ventricular

Ventricular function: pumping blood to all parts of

body and to the lungs

Ventricles pump more powerful than the atria

Atria contract prior to ventricles


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Anatomy - Physiology of Heart..


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Function of Valves and Papillary Muscles

The valves open and close passivelyAV valves (tricuspid and mitral):- Prevent backflow of blood from the ventricles into

atria during systole

Semilunar valves (aortic and pulmonary):- Prevent backflow of blood from aorta and pulmonary

arteries into ventricles during diastole

Papillary muscles:- Papillary muscles contract when the ventricular walls

contract

- They pull the vanes of valves inward toward the

ventricles to prevent their bulging too far backward

toward the atria during ventricular contraction


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AnatomyPhysiology of Cardiac Muscles

Myocardium:- Atrial muscles

- Ventricular muscles

- Specialized excitatory and conductive system

of the heart

Involuntary muscles

Similar manner to skeletal muscle contraction

Syncytium


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Structure of Cardiac Muscle Fibers

Sarcolemma

Myofibril

Filaments: - Actin

- Myosin

Sarcoplasma

Sarcoplasmic reticulum


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Structure of Cardiac Muscle Fibers..


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Intercalate Disc


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Electrical Activity of Cardiac Muscle Fibers

Polarization

Depolarization: - Plateau

- Rhythmicity

Repolarization

Conductivity

Refractory period


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Electrical Activity of Cardiac Muscle Fibers..


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Rhythmicity of Cardiac Action Potential


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Rhythmicity of Cardiac Action Potential..


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Refractory Period


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Conductivity of Cardiac Action Potential

Conduction velocity in atrial and ventricular musclefibers:

0,30,5 m/second

= 1/250 conduction velocity of action

potential in large nerve fibers

= 1/10 conduction velocity of action potential in

skeletal muscle fibers

Conduction velocity in Purkinye system

0,024 m/second depend on location


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Mechanism of Contraction


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Duration of Contraction

Duration of contraction = duration of action potential:- In atrial: 0,2 second

- In ventricular 0.3 second

Greatly influenced by frequency of heart rate (HR)

- The faster the frequency of HR, the shorter the

duration of contraction, especially diastolic period

- HR 72x/sec syst period : diast period = 40:60- HR increased 3x syst period : diast period = 65:35


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Oxygen Consumption By Heart

Basal O2 consumption is 2 ml/100g/minConsiderably higher than that of resting skeletal

muscle

O2 consumption by beating heart is 9 ml/100g/minat rest

Increases during exercise and in a number of different

states

Cardiac venous O2 tension is low, and little additional

O2 can be extracted from the blood in the coronaries

blood flow, so increases in O2 consumption require

increases in coronary blood flow


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SIKLUS JANTUNG

(CARDIAC CYCLE)


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The Cardiac Cycle

Definition:The cardiac events that occur from the beginning

of one heartbeat to the beginning of the next

The cardiac cycle consists of:

- Diastole : period of relaxation, during which the

heart fills with blood

- Systole : period of contraction, during whichthe heart ejects blood from its

chambers


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Conductive System of Heart

SA Node (sinoatrial node)/ sinus node :- located in the superior lateral wall of right atrium,immediately below and slightly lateral to theopening of the superior vena cava

Internodal pathways:- conductive system from SA node to AV node

AV node (atrioventricular node):- located in the posterior septal wall of right atrium,

immediately behind tricuspid valve and adjacent tothe opening of coronary sinus

AV bundle/ His bundle

Purkinje System


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Conductive System of Heart..


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Conductive System of Heart..


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Organization of AV node


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Transmission of Cardiac Impulse


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Events of Cardiac Cycle

Generating and transmission of cardiac impulses:1. Generating rhythmical impulses in SA node

2. Conducting the impulses rapidly throughout atria

atria contract3. Conducting impulses to AV node (delay 0,13 sec)

4. Conducting impulses through AV/ His bundle

5. Finally transmission impulses rapidly throughoutventricles through Purkinye systemventricle

contract


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Events of Cardiac Cycle..

Because of impulses generate in SA node and delay intransmission to ventricles atria contract (atrial

systole) prior to ventricles

Ventricles still in relaxation period (ventricular

diastole), called diastole

AV valves open and allow blood to flow into ventricles

filling of ventricles


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Filling of the ventricles during diastoleRapid filling:

- A-V nodes closed large amount of blood accumulate in

atria immediately push AV valves open blood flow

rapidly into ventricles; lasts for the first third of diastole

Diastasis:

- During the middle third of diastole, only a small amount

of blood that continues to empty into atria from veins and

passes directly into ventricles

Atrial systole:

- During the last third of diastole, atria contract and

give additional thrust to inflow of blood into ventricles



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Emptying of the ventricles during systolePeriod of isovolemic (isometric) contraction:- Ventricular contraction intraventricular pressures

AV valves close

- But not sufficient to push semilunar valves open noemptying of blood from ventricles

Period of ejection:- Semilunar valves opened blood pour out of ventricles

Period of isovolemic (isometric) relaxation:- Ventricular relaxation intraventricular pressures

semilunar valves close- But not sufficient to cause AV valves open no blood

flow into ventricles



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During ventricular contraction:- Period of ejection

- Ventricular pressure blood pour from ventricles

into arterial system (aorta and pulmonary trunks)

> cardiac output (volume / minute)

> stroke volume (volume/ contraction)

During atrial relaxation:

- Atrial pressure blood flow from veins into atria

venous return (volume/ minute)



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The greater venous return, the greater theheart muscle is stretched, the greater will be

the force of contraction and the greater stroke

volume

Within physiological limits, the heart pumps all

the blood that comes to it without allowingexcessive damming of blood in the veins


(Frank-Starling Law)


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Ventricular Volume

End diastolic volume (EDV): 110120 cc,- Can be increased to 150180 cc

Stroke volume (SV): 70 cc

- SV = EDVESV (110 cc40 cc)

Ejection fraction: 60 %

- SV/EDV x 100%

End systolic volume (ESV): 4050 cc,- Can be decreased to 1020 cc

- SV can be increased to 140 - 160 cc


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Relationship between left ventricular volume and intraventricular pressure duringdiastole and systole. The heavy red lines is volume-pressure diagram.

EW, net external work


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Concepts of Preload and Afterload

Preload:In assessing the contractile properties of muscle, it is

important to specify the degree of tension on muscle

when it begins to contract

After load:

To specify the load against which the muscle exerts

its contractile force


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Concepts of Preload and Afterload..

The importance of the concepts of preload andafterload:

Many abnormal function states of the heart or

circulation, the pressure during filling ofventricle (the preload), the arterial pressure

against which the ventricle must contract (the

afterload), or both are severely altered fromthe normal


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BUNYI JANTUNG

(HEART SOUNDS)

l d


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Normal Heart Sounds

Using a stethoscope, one hears a sound usuallydescribed as lub, dub, lub, dub

- The lub is 1stheart sound, associated with closure

of atrioventricular (A-V) valves at the beginning ofsystole

- The dub is 2ndheart sound, associated with closure

of semilunar (aortic and pulmonary) valves at theend of systole


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Normal Heart Sounds..

1stheart sound:- Duration: 0.14 seconds- Low pitch

2ndheart sound :- Duration: 0.11 detik seconds

- High pitch3rdheart sound :- heard at the beginning of the middle third of diastole- blood oscillation in ventricles initiated by inrushing blood from

atria- weak, rumbling- can often be recorded in the phonocardiogram

4thheart sound (atrial heart sound):- blood oscillation in ventricles when atria contract

- sometimes can be recorded in the phonocardiogram

l d


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Normal Heart Sounds..

Phonocardiogram from normal heart

C f H S d


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Causes of Heart Sounds

Vibration of the taut valves immediately after closure,along with vibration of adjacent walls of the heart andmajor vessels around the heart

Vibrating is caused by turbulencesin blood

1stheart sound:

Contraction of ventricles sudden backflow of bloodagainst A-V valves closing of valves and bulging towardatria vibrating turbulence in blood vibrations

2ndheart sound:Semilunar valves close rapidly at the end of systole bulge backward toward ventricles vibrating turbulencein blood vibrations

C f H S d


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Causes of Heart Sounds..

3rd

heart sound:Oscillation of blood back and forth between the walls of

ventricles initiated by inrushing from the atria

vibrations of the walls

This sound does not occur until the middle third ofdiastole because the ventricles are not filled sufficiently

to create elastic tension necessary for reverberation

4thheart sound (atrial heart sound):

Atria contract inrush of blood into ventricles vibrations


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Mitral and aortic valves (left ventricular valves)


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Chest areas from which sound from each valve is best heard


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CURAH JANTUNG

(CARDIAC OUTPUT)

D fi iti


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Definition

Cardiac output (COP):- is the quantity of blood pumped into the aorta each

minute by heart

- is also the quantity of blood that flows through circulation

The volume of cardiac output is equal with strokevolume (SV)multiplied by heart rate (HR) per minute

Venous return:- is the sum of all the local blood flows through all

individual tissue segments of peripheral circulation

COP = SV x HR

N l V l f C di O t t


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Normal Values for Cardiac Output

COP varies widely with the level of activity of body

Factors that directly affect COP:

1. Venous return (Frank-Starling Law)

2. Basic level of body metabolism

3. Body activity4. Age

5. Body size

Resting COP: the average 5 L/min for resting adult

- 5.6 L/min for young healthy men

- 4.9 L/min for young healthy women (10-20% lower)

With increasing age, body activity and metabolism

diminishes COP

C di I d


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Cardiac Index

Cardiac index is COP per square meter of bodysurface area (COP/surface area)

COP increases approximately in proportion to the

body surface area

The normal human being weighing 70 kg has body

surface area of 1,7 m2, COP 5 L/min.

cardiac index : 5 L/min/1,7 m2 = 3 L/min/m2of

body surface area


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Cardiac index for the human being

Cardiac Reser e


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Cardiac Reserve

Cardiac reserve is:- Ratio between maximum COP and resting COP

- Average: 4-5 times

- Athlete: may increase 7-8 times

- In severe heart disease: cardiac reserve 0

not be able to perform physical activity


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PENGATURAN

POMPA JANTUNG

(REGULATION

OF HEART PUMPING)

I Intrinsic Regulation


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I. Intrinsic Regulation

Intrinsic Regulation by Frank-Starlingmechanism

The amount of blood pumped by heart is

determined by the rate of blood flow into

the heart from veins (venous return)

Within physiology limits, heart pumps allblood that comes to it

II Control by Autonomic Nervous System


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II. Control by Autonomic Nervous System

Excitation of heart by sympathetic nerves:- Increasingheart rate (to 180200 bpm)

- Increasingthe force of myocardial contraction

stroke volume COP

Parasympathetic(vagal) stimulation:- DecreasingHR and force of contraction

- Vagal fibers are distributed mainly to atria, but not

much to ventricles- Strong vagal stimulation can stop heart beats, but

then usually escapes and beats at rate 20-40 bpm


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Cardiac sympathetic and parasympathetic nerves

The vagus nerves are parasympathetic nerves


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Control of Heart Rate


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Control of Heart Rate

Effects of strain on right atrial wallStrain on right atrial wall strain on SA

node increasing SA node rhythmicity

increasing heart rate

Strain on right atrial wall Bainbridge

reflect: increasing heart rate


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Kp 1.3.2.1 Aktivitas Mekanik Jantung (2 Jam)