Fisiologi Jantung

RUDIANTO JOTO
Tiga komponen utama sistem
sirkulasi:
• Jantung yang memompa darah
• Pembuluh darah yang mengalirkan darah.
• Darah yang merupakan medium transport, melayani
kebutuhan sel-sel tubuh.
– Sirkulasi pulmonal adalah sirkulasi antara jantung dan paru-paru.
– Sirkulasi sistemik adalah sirkulasi antara jantung dan sistem tubuh
lainnya.
 Lungs

Pulmonary
capillaries
Pulmonary
Pulmonary veins
circulation
Pulmonary
arteries

Right Left
side side Systemic
of of arteries
heart heart
Systemic Systemic
veins circulation

Systemic
= O2-rich blood
capillaries
Organ
systems
= O2-poor blood
 Jantung adalah organ
muskuler
– Berada dalam rongga thoraks, antara sternum dan
vertebrae Basis jantung berada di sebelah kanan
sternum. Apeks berada disebelah kiri sternum.
– Pada lokasi ini darah dapat dialirkan secara
manual dari jantung dengan CPR.
• Jantung adalah pompa ganda.
– Atrium. Menerima darah yang kembali ke jantung.
Mentransfer darah ke ventrikel.
– Ventrikel. Memompa darah dari jantung.
– Vena. Membawa darah dari jaringan ke jantung.
– Arteri. Membawa darah dari jantung ke jaringan.
Superior vena Aorta
cava (from head)
Left pulmonary
Right pulmonary artery
artery
Left pulmonary
Right vein
pulmonary vein

Left atrium
Pulmonary
semilunar valve
Left atrioventricular
Right atrium (AV) valve

Right atrioventricular Aortic semilunar

(AV) valve valve

Inferior vena cava Left ventricle

(from body)
Interventricular
Right ventricle
septum

Arrows indicate direction

of the blood flow. = O2-rich blood = O2-poor blood
 Venae cavae Pulmonary artery
Right Right
atrium ventricle

Other
Digestive Systemic Pulmonary
systemic Brain Kidneys Muscles Lungs
organs tract circulation circulation

Left Left
ventricle atrium Pulmonary veins
Aorta
The action of heart valves ensure that blood
flows in the proper direction.
• The AV valves are the tricuspid on the right and bicuspid on the left.
They allow blood to flow from the atria into the ventricles. This occurs
when atria pressure is greater than ventricular pressure, during
ventricular filling.
• During ventricular emptying, when ventricular pressure exceeds atrial
pressure, the AV valves close. This prevents the blood from flowing
backwards. The AV valves are anchored by chordae tendineae to
papillary muscles.
• The other pair of valves are the semilunar, pulmonary on the right and
aortic on the left. They are forced open when the ventricular pressures
exceed the pressures in the pulmonary arteries and aorta.
• The semilunar valves close when the pressure in the ventricles falls
below the pressures in these vessels. This prevents the blood from
flowing backwards.
• A fibrous skeleton separates the atria from the ventricles.
Right AV valve

Left AV valve

Aortic or pulmonary valve

 (Rear)

Fibrous
Right AV valve rings

Left AV valve

Aortic valve

Pulmonary semilunar
valve
Ventricular
myocardium

(Front)
The heart wall consists of
three layers.
– The endocardium is the inner layer of
epithelium.
– The myocardium is the middle layer of
cardiac muscle tissue.
– The epicardium is the external membrane.
– The heart in enclosed in a double-walled
pericardial sac (pericardial fluid;
pericarditis).
 Sel otot jantung
• Serat otot jantung dihubungkan dengan
diskus interkalaris.
• Membentuk sinsitium fungsional.
Plasma membranes of adjacent Desmosome
cardiac muscle fibers

Gap junction Action

potential
Intercalated disc
 Aktivitas elektris jantung
• 99% sel otot jantung bersifat kontraktil
• Kontraksi jantung berirama
• Irama jantung diatur oleh aktivitas
pacemaker
 Self-induced
action potential

Threshold
potential

Slow
depolarization
(pacemaker
potential)
 Potensial Pacemaker dan Potensial
aksi
• Potensial pacemaker adalah perubahan yang
lambat dari sebuah membran sel yang
berirama menjadi istirahat.
• Pergerakan ion pada pacemaker include:
– Pengurangan pengeluaran K+ dengan
pemasukan Na+ yang konstan ke dalam
membran sel.
– Peningkatan pemasukan Ca2+ .
• Transient Ca2+ channels
• Longer-lasting Ca2+ channel
 Sel-sel jantung khusus
• Sinoatrial node (SA node): normal pacemaker of
the heart – 70-80 action potentials per minute
• Atriventricular node (AV node): 40-60 action
potentials per minute
• The bundle of His (atrioventricular node): 20-40
action potentials per minute
• Purkinje fibers: 20-40 action potentials per minute
 Interatrial
Figure 9.11 pathway

Page 311
Atrioventricular
(AV) node
Sinoatrial
(SA) node

Right Left
atrium atrium

Internodal Left
pathway branch
of bundle
of His
Right Left
branch ventricle
of bundle
of His Right
ventricle Purkinje
fibers
 Aktivitas pacemaker yang
Abnormal
• Sel sel autoritmik yang bukan nodus disebut
latent pacemakers
• Complete heart block (Konduksi impuls
dari atrium ke ventrikel terhambat)
• Ectopic focus (e.g. depolarisasi Purkinje
fibers lebih cepat dari nodus SA node dan
menimbulkan premature beat –
extrasystole)
 Penyebaran eksitasi jantung
• Setiap ruang jantung berkontraksi sebagai sebuah
unit untuk dapat memompa secara efisien
• Atria and ventricles terkoordinasi secara
fungsional
• Eksitasi dan kontraksi Atrial telah selesai
sempurna sebelum kontraksi ventrikel
• Fibrillation adalah eksitasi dan kontraksi otot
jantung yang tidak terkoordinasi
• Ventricular fibrillation menyebabkan kematian
yang cepat
 Penyebaran eksitasi jantung
• Eksitasi Atrial
– Interatrial pathway: sebuah potensial aksi yang dimulai
dari nodus SA dan menyebar pertama-tama ke kedua
atrium
– Internodal pathway: Potensial aksi yang merangsang
nodus AV dalam 30 msec setelah nodus SA
melepaskan potensial aksi
• Eksitasi Ventricular
– Impuls menyebar dari nodus AV (AV node delay – 100
msec) ke bundle of His and Purkinje fibers
 Interatrial pathway
Right atrium Left atrium

SA node

AV node Internodal
pathway

Purkinje
fibers
Bundle
of His

Right ventricle Left ventricle

 Action potential in contractile
cardiac cells
• Contractile cardiac cells have a resting
membrane potential of ~ -90 mV
• Action potentail is generated by membrane
permeability and potential changes
• The action potential shows a characteristic
plateau
 Figure 9.15
Page 315
Plateau
phase of
action
potential

Threshold
potential
 Action potential
in cardiac
contractile cell

Travels down
T tubules

Release of large
Entry of small amount of Ca2+
amount of Ca2+ from sarcoplasmic
from ECF reticulum

Cytosolic
Ca2+

Troponin-tropomyosin complex
in thin filaments pulled aside

Cross-bridge cycling between

thick and thin filaments

Thin filaments slide inward

between thick filaments

Contraction
Refractory period in cardiac muscle

• Cardiac muscle has a prolonged refractory

period (250 msec) to prevent tetanic
contractions
• Normal cardiac muscle contraction lasts 300
msec
• This long refractory period is due to
inactivation of Na+ channels
 Electrocardiogram (ECG or EKG)

• The ECG is a recording of the electrical

activity induced in the body fluids by the
cardiac impulse that reaches the surface of
the body
• The electrocardiograph represents a
comparison in voltage detected by
electrodes at two different points on the
body surface, not the actual potential
 ECG components
• P wave represents atrial depolarization (recorded
when impulse spreads across the atria)
• QRS complex represents ventricular
depolarization
• T wave represents ventricular repolarization
• The heart and ECG remain at base line:
– During AV nodal delay – PR segment
– When ventricles are completely depolarized – ST
segment
– When the heart muscle is completely at rest – TP
interval
 R

T
P P

Q
S

PR ST TP interval
 Abnormal electrical patterns
• Abnormalities in rate:
– Tachycardia (>100 beats/minute)
– Bradycardia (<60 beats/minute)
• Abnormalities in rhythm (arrhythmia):
– Extrasystoles or premature beats (ectopic focus)
– Atrial flutter (200 to 300 beats/minute)
– Atrial fibrillation (rapid, irregular, uncoordinated depolarization)
– Ventricular fibrillation (uncoordinated, chaotic contractions)
– Heart block (defects in cardiac conducting system)
• Complete heart block (complete dissociation between atrial and
ventricular activity
• Cardiac myopathies:
– Myocardial ischemia; myocardial infarction
NORMAL RATE AND RHYTHM

ABNORMALITIES IN RATE
Tachycardia
ABNORMALITIES IN RHYTHM Extrasystole (premature beat)

Ventricular fibrillation

Complete heart block

CARDIAC MYOPATHIES

Myocardial infarction
 Cardiac cycle
• Systole – contraction and emptying
• Diastole – relaxation and filling
• Mechanical events of the cardiac cycle:
– Early ventricular diastole
– Late ventricular diastole
– End of ventricular diastole
– Ventricular excitation and onset of ventricular systole
– Isovolumetric ventricular contraction
– Ventricular ejection
– End of ventricular systole
– Ventricular repolarization and onset of ventricular diastole
– Isovolumetric ventricular relaxation
– Ventricular filling
 Passive filling during Atrial contraction
ventricular and atrial diastole

Left
atrium
Right
atrium

Right Left
ventricle ventricle

A B

Ventricular filling
Isovolumetric ventricular contraction

C
Ventricular ejection Isovolumetric ventricular relaxation

D E

Ventricular emptying
 Heart sounds
• The heart sounds are associated with valve
closures
• The first heart sound is associated with closure of
AV valves; it has a low-pitch and it is relatively
long. The first sound signals the onset of
ventricular systole.
• The second heart sound occurs when semilunar
valves close; it has a higher pitch and it is shorter.
This sound signals the onset of ventricular
diastole.
 Abnormal heart sounds
• Abnormal heart sounds (murmurs) are
generally associated with cardiac disease
• Blood flows in laminar manner (no sound is
produced)
• Turbulent blood flow produces sounds:
– Stenotic valve
– Insufficient valve
 Cardiac output
• Cardiac output is the volume pf blood
pumped by each ventricle per minute
• The heart rate and stroke volume determine
the cardiac output
• Average resting heart rate is 70
beats/minute
• Average resting stroke volume is 70 ml/beat
• Average cardiac output is about 5 l/minute
 Regulation of cardiac output
• Depends on the control of the heart rate and
stroke volume
• The heart is innervated by the ANS, both
parasympathetic and sympathetic nerves
• Under resting conditions, parasympathetic
control is dominant (vagus nerve)
 Parasympathetic stimulation
• Decreases the heart rate (influence on SA
node)
• Decreases the AV node excitability
• Shortens the action potentials in contractile
atrial cells (atrial contraction is weakened)
• Has little effect on ventricular contraction
(sparse parasympathetic innervation)
 Sympathetic stimulation
• Increases the rate (increase the rate of SA
node depolarization)
• Reduces AV nodal delay
• Speeds up the propagation of action
potential throughout conduction pathways
• Increase of contractile strength in both atria
and ventricles
 Threshold
potential

Threshold
potential

= Inherent SA node pacemaker activity

= SA node pacemaker activity on parasympathetic stimulation
= SA node pacemaker activity on sympathetic stimulation
 Heart rate

Sympathetic
Parasympathetic
activity
activity
(and epinephrine)
 Stroke volume
• Intrinsic control (end-diastolic volume - extent of
venous return; preload)
• Extrinsic control (sympathetic stimulation of the
heart)
• Frank-Starling law of the heart (the heart pumps
all the blood returned to it – increased venous
return increases the stroke volume)
• Length-tension relationship of cardiac muscle
 Stroke volume

Extrinsic
control Strength of
cardiac contraction

Intrinsic control

Sympathetic activity End-diastolic

(and epinephrine) volume

Intrinsic control

Venous return
End-diastolic volume
135 ml

Stroke volume
70 ml

End-systolic volume
65 ml
 End-diastolic volume
Figure 9.27 (2)
135 ml

Page 330
Stroke volume
100 ml

End-systolic volume
35 ml
End-diastolic volume
175 ml

Stroke volume
140 ml

End-systolic volume
35 ml
 Cardiac output

Heart rate Stroke volume

Extrinsic
control

Intrinsic control

Sympathetic End-diastolic
Parasympathetic
activity (and volume
activity
epinephrine)

Intrinsic control

Venous return
 Blood pressure and workload of the
heart
• The arterial blood pressure – afterload
• High blood pressure – ventricular pressure
increases
• Chronically elevated afterload leads to heart
failure (decrease heart contractility)
• Sympsthetic stimulation – compensatory
• Decompensated heart failure
 Coronary circulation
• Coronary arteries (from aorta)
• Coronary veins (empty in the right atrium)
• Coronary blood flow is adjusted in response
to changes in the heart’s O2 requirements
• Atherosclerotic coronary artery disease
Area of cardiac Area of cardiac
muscle deprived muscle deprived
of blood supply of blood supply
if coronary vessel if coronary vessel
is blocked at is blocked at
point point

Left
Right
coronary
coronary
artery
artery

Left
ventricle

Right
ventricle
Metabolic activity of cardiac muscle cells
( oxygen need)
Figure 9.32
Page 333
Adenosine

Vasodilation of coronary vessels

Blood flow to cardiac muscle cells

Oxygen available to meet oxygen need

 Collagen-rich
smooth muscle
cap of plaque Plaque
Normal blood
vessel wall

Lipid-rich core
of plaque

Endothelium
Blood flow Blood flow

Thrombus

Embolus