Physiology of Cardiac Muscle

and
Electrical Activity of the Heart
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Cardiac muscle

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Two Types of Cardiac Muscle Cells

Ordinary: make up 95%- 99% of all heart

muscle cells.
Also called worker cells or contractile cells
Biochemically similar to red skeletal muscle
Slow to fatigue
Specialized: make up remaining 1%-5%
Also called autorhythmic or automatic cells
Responsible for initiation and/or transportation of
electrical impulses through the heart
pacemaker potential

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 CONDUCTION SYSTEM

Sinoatrial
Node

Atrioventricular
Node

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 Electrical Conduction
SA node - 75 bpm
Sets the pace of the heartbeat
AV node - 50 bpm
Delays the transmission of action potentials
Purkinje fibers - 30 bpm
Can act as pacemakers under some conditions
 K

0
Membrane Potential (mV)

symphathetic
Threshold
Potential

-40
Ca (T-type)

-60 Na parasymphathetic

Spontaneous Time (msec)

Depolarization Denny Agustiningsih
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HEART RATE
Normally : 60-100 bpm
> 100 bpm : tachycardia
< 60 bpm : bradycardia

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 Resting heart rate is about 60-100
beats/min (lower in athletes because they
have large stroke volumes)
The HR can be increased about 3 times in
exercise
Above about 200 beats/min the heart
would not have time to fill properly
therefore nature limits the rate
Rate is controlled by the autonomic
nervous system

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 Extrinsic Influences
Autonomic nervous system
Hormonal influences
Ionic influences
Temperature influences

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Control of Heart by ANS
Sympathetic innervation-
+ heart rate
+ strength of contraction
+ conduction velocity
Parasympathetic innervation
- heart rate
- strength of contraction
- conduction velocity

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 Autonomic nervous system modulates the frequency of depolarization of
pacemaker
Sympathetic stimulation (neurotransmitter = NE ); binds to b1 receptors
on the SA nodal membranes
Parasympathetic stimulation (neurotransmitter = ACh ); binds to
muscarinic receptors on nodal membranes; increases conductivity of K+
and decreases conductivity of Ca2+
How do these neurotransmitters get these results?
Major Hormonal Influences
NE/E
Thyroid hormones
+ inotropic
+ chronotropic
also causes an increase in CO by BMR
Estrogen/ Testosteron

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Ionic influences
Effect of elevated [K+]ECF
dilation and flaccidity of cardiac muscle at
concentrations 2-3 X normal (8-12 meq/l)
Effect of elevated [Ca++] ECF
spastic contraction

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Effect of body temperature
Elevated body temperature
HR increases about 10 beats for every degree
F elevation in body temperature
Contractile strength will increase temporarily
but prolonged fever can decrease contractile
strength due to exhaustion of metabolic
systems
Decreased body temperature
decreased HR and strength

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Direct Stretch on SA node
Stretch on the SA node will increase
Ca++ and/or Na+ permeability which will
increase heart rate

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 Terminology

Chronotropic (+ increases) (- decreases)

Anything that affects heart rate
Dromotropic
Anything that affects conduction velocity
Inotropic
Anything that affects strength of contraction
eg. Caffeine would be a + chronotropic agent (increases
heart rate)

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 K out
+20 K out Ca in (L-Type)

plateau
0
Ca, K
mV

Na in

-90

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 AP of Contractile Cardiac cells

Action potentials of cardiac

contractile cells exhibit
prolonged positive phase
(plateau) accompanied by
prolonged period of
contraction
Ensures adequate ejection time
Plateau primarily due to
activation of slow L-type Ca2+
channels
Refractory period
 Action Potential

Skeletal

Cardiac
Mechanism of Cardiac Muscle Excitation, Contraction &
Relaxation

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 Relative
Refractory
period

1
+20 2

0
mV

3
Period of
Absolute Supranormal
Refractory excitability
4 period
-90 400
0 100 200 300

Time (msec)
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Modulation of Contraction

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RECORDING

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The Body as a Conductor

This is a graphical representation of the geometry and

electrical current flow in a model of the human thorax.
The model was created from MRI images taken of an
actual patient. Shown are segments of the body surface,
the heart, and lungs. The colored loops represent the
flow of electric current through the thorax for a single
instant of time, computed from voltages recorded from
the surface of the heart during open chest surgery.
The Modern ECG Machine
ECG examines how depolarization events occur in the heart

If a wavefront of depolarization
travels towards the electrode
attached to the + input terminal of
the ECG amplifier and away from
the electrode attached to the -
terminal, a positive deflection will
result.
If the waveform travels away from
the + terminal lead towards the -
terminal, a negative going
deflection will be seen.
If the waveform is travelling in a
direction perpendicular to the line
joining the sites where the two
leads are placed, no deflection or
a biphasic deflection will be
produced.
Serabut purkinje ventrikel
Nodus SA atrium
Atrium (ototnya lebih sedikit)
Klw siklusnya atrium - atrial cyte
Sirkulasi-peredaran darah
Siklus-kontraksi dan relaksasi
R

P T

Q
S

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 R

P T

Q
S

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 R 1 sec

P T

Q
S
0.5 Sec

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ECG Complexes
 Kontraksi sistol
Ventrike kaknan-memoma darah ke paru

ECG Complexes Ventrikel kiri-memompa darah keseluruh jantung

Pintu masuk katub yang menghubgungkan dengan
atrium (valam atrioventricualr)
Pintu keluar kiri - aorta
Pintu keluar kanan katub pulmu\onal
Tujuan awal kontraksi untuk membuka pintu keluar (aorta)
ECG Description
ECG description
amplitude (voltage)
recorded in mm
positive or negative or biphasic
width (duration)
ECG in Perspective
1. ECG recording of electrical activity not
the mechanical function
2. ECG does not depict abnormalities
3. ECG does not record all the hearts
electrical activity
Excitation-Contraction Coupling in Cardiac Contractile
Cells

Ca2+ entry through L-type channels in T tubules

triggers larger release of Ca2+ from sarcoplasmic
reticulum
Ca2+ induced Ca2+ release leads to cross-bridge cycling
and contraction
Frank-Starling Law
Preload, or degree of stretch, of cardiac muscle cells before
they contract is the critical factor controlling stroke volume
 Extrinsic Factors Influencing SV
Contractility is the increase in contractile strength,
independent of stretch and EDV
Increase in contractility comes from
Increased sympathetic stimuli
Hormones - epinephrine and thyroxine
Ca2+ and some drugs
Intra- and extracellular ion concentrations must be
maintained for normal heart function
Modulation of Cardiac Contractions

Figure 14-30
Reflex Control of Heart Rate
Regulation of Cardiac Output

Figure 18.23
 Depolarisasi mendahului kontraksi
Repolarisasi mendahului relaksasi
Kontraksi jantung tidak melalui otak
Listrik-otot atrium-kontraksi--ketika sampai di ventrikel-ventrike
berkontraksi
Gap junction
Kontraksi otot jantung-otot pekerja
Otot pekerja memiliki aktin & myosin
Mendapat rangsang sehingga ion
Repolarisasi = fase istrahat
Kontraksi & relaksasi-aktin & myosin
Sebagian kalsium pergi ke aktin & myosin untuk berikatan dengan
troponin C, sebagian ke retikulum sarkoplasma
Retikulum sarkoplasma-tempat penyimpanan ion calsium (ada pintu
yang disebut.........., hanya terbuka untuk kalsium)-masuk ke sitosol

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