CARDIOVASCULAR

ANATOMY & PHYSIOLOGY

Departemen Anestesiogi
dan Intensive Care
 Ilustrasi kasus
 Psn 1 riwayat nyeri dada 6 mgg lalu, sulit dilokalisir
terkait aktivitas dan saat istirahat, bertambah sering dan
lama ( > 5-15 menit ), keringat, respon dengan nitrat SL,
terapi ca antagonis , beta bloker, aspilet, simvastatin .
EKG ; normal atau depresi segmen ST dan T inversi,
Enzim troponin T (+), CKMB -.
 Psn 2 dg trisomi 21, keluhan ; fatige, sesak, berkeringat,
sulit intake dan gagal tumbuh, sering batuk pilek . PF ;
sistolik murmur pada level ¾, spt bunyi tiupan, puncak di
mid sistolik, keras di daerah perbatasan sternum kiri
bawah dengan apex.
 Psn 3 dg keluhan sering berdebar, riw pingsan. PF ; TD
90/60 mmHg, pucat, takiaritmia. EKG ; P mitral, Atrial
Fibrilasi rapid response.
• Kesemuanya akan menjalani prosedur bedah dan
anestesi ???
 Diagnosis Penyulit
• Manifestasi Penyakit jantung koroner berupa ;
Angina pektoris stabil dan
Sindrom koroner akut.
• Sindrom koroner akut sesuai derajat
keparahannya terbagi 3 yaitu ;
1.Angina pektoris tidak stabil,
2.Miokar Infark non ST elevasi,
3.Miokard Infark ST elevasi.
Pedoman pengelolaan pasien jantung yang
menjalani operasi non jantung.
 ACC/AHA Guideline Update for Perioperative
Cardiovascular Evaluation for Noncardiac Surgery
The active cardiac conditions of increased perioperative
cardiovascular risk are ;
1.Recent unstable coronary syndrome such as acute MI
(documented MI less than 7 days previously),
2.Recent MI (more than 7 days but less than 1 month before
surgery), unstable or severe angina, evidence of a large
ischemic burden by clinical symptoms or noninvasive testing,
3.Decompensated HF,
4.Significant arrhythmias (highgrade AV block, symptomatic
arrhythmias in the presence of underlying heart disease, or
supraventricular arrhythmias with uncontrolled ventricular
rate),
5.Severe valvular disease
Kondisi yang mengganggu keseimbangan suplai
dan kebutuhan oksigen miokard.
 Tugas Kelompok
• Pada pasien dengan hipertensi yang akan
menjalankan operasi.
• Diagnosis dan severitas.
• Panduan pengelolaan perioperatif.
 CARDIOVASCULER SYSTEM &
HEART
• To transport oxygen, nutrients, endocrine
and exocrine hormones to the tissue and
to carry metabolic waste at rate
proportionate to body needs.

Explain the componen parts of the

cardiovasculer system and their
functions ???
 CARDIOVASCULER SYSTEM & HEART
1. Heart ;
Pump to force blood through the vasculer.
2. Arteries ;
as a delivery system to distributes CO, regulates
volume of flow delivered to each organ base on
metabolic need.
3. Capillaries ;
to exchange respiratorty gases, nutrient,
metabolits between plasma and body cells.
 CARDIOVASCULER SYSTEM & HEART
4. Veins ;
as a return system to bring deoxygenated blood
back, also a reservoir circulating blood through
venoconstriction and dilatation mechanism
5. Blood ;
Plasma is a liquid medium in which respiratory
gases, nutrient, metabolic waste & hormones
dissolved and formed elements of blood are
carried ( RBC, WBC).
Structure of the Heart ???
 HEART
Structure of the heart wall

1. Pericardium ; 2 layers sac to protect & covers

the heart, pericardial fluid, acting as a lubricant
the heart,
2. Myocardium ; the muscular middle layer of the
heart, has contractile properties as well as the
capacity to initiate and conduct electrical
stimuli for muscle contraction.
3. Endocardium ; serous membran that lines the
heart & extends out to form the heart valves .

Explain components of the heart at the

cellular level ???
 CELLULAR CARDIAC PHYSIOLOGY
Cellular Anatomy
• At the cellular level, the heart consists of
three major components:
1 Cardiac muscle tissue, bundles of myofibril
2 Conduction tissue (conducting cells), and
3 Extracellular connective tissue .
Otot jantung = miocytes di support cytoskeleton.
Miofibril dikelilingi oleh sarcolema, sarcolemik retikulum, di hubungkan oleh
intercalated disc.
Myofibril, actin, myosin, disk intercalated membentuk  Sincitium fungsional
Respon kontraksi “ALL OR NONE”, ditentukan oleh masuknya Ca+ ke dalam
troponin.
Sarcolema = tempat penyimpanan Ca+.
Kaya akan mitokondria & kapiler.
 Potensi elektrik jantung.
1. Excitability ; kemampuan aktivasi listrik dan kontraksi
akibat stimulus listrik, mekanik, kimia.
2. Automaticity ; kemampuan memulai impuls spontan dan
eksitasi mandiri baik ritme atau rate
3. Conduction ; kemampuan meneruskan impuls listrik dari
satu sel ke sel lain.
4. Kontraktilitas .
5. Relaksasi,
• Hantaran impuls listrik melalui ;
Depolarisasi aktif/ penyebaran potensial aksi.
Aktifasi elektrik pasif/ pengaruh elektriksitas.
 Potensial aksi sel otot jantung
• Aktifasi sel tunggal; selisih potensial transmembran
istirahat atrium & ventrikel 80-90 mV. Sel node SA & AV
50-70 mV. Intra sel lebih negatif dari ekstrasel. Saat
eksitasi terjadi lompatan muatan cepat.
Potensial aksi terdiri dari 4 fase.
Fase 0, fase awal Rapid Depolarisasi.
Fase 1, Repolarisasi cepat.
Fase 2, Plateu ; potensial aksi otot jantung jadi lebih panjang.
Fase 3, Repolarisasi; kembali ke potensial membran istirahat,
pembukaan kanal K & masuknya K. Terjadi gelombang T.
Fase 4, ekuilibrium potensial aksi, saat diastolik. Potensial aksi
istirahat fase 4 tergantung pada selisih konsentrasi K.
• Periode refraktory; kondisi dimana sel tidak dapat di
aktifasi & tidak respon terhadap stimulus dan tidak akan
terjadi efek tetani. Repolarisasi mengembalikan
potensial membran istirahat negatif & mampu menjalani
eksitasi kecuali di node SA dan AV memerlukan waktu
lebih.
 Pembentukan pulse normal
• Sumber impuls; node SA dan AV namun semua jaringan
otot jantung dapat mencetuskan impuls spontan.
• Node SA ; kumpulan sel di dinding atrium kanan posterior
perbatasan atrium kanan dan Vena Cava Superior
dikelilingi saraf simpatis dan parasimpatis. Pasokan darah
berasal dari cabang arteria coroner kanan.
• Node AV tertelak di septum interatrium sisi kanan
posterior triangle Koch dekat katup tricuspid. Suplai darah
pada Right dominan berasal dari cabang RCA, pada
infark dinding posterior-inferior akan terjadi blok akut node
AV.
 Elektrofisiologi pacemaker.
• Proses yang mendasari bentuk irama internal sel
pacemaker ; depolarisasi diastolik lambat.
• Potensial aksi transmembran node SA & AV memiliki
karakter sbb ;
1.Potensial istirahat rendah ( 60-40 mV),
2.Potensial istirahat tidak menetap dengan depolarisasi
lambat,
3.Peningkatan potensial aksi yang lambat,
4.Overshoot potensial aksi minimal.
5.Potensial membran istirahat dipengaruhi konsentrasi K.
Sistem konduksi ; Impuls Node SA di subendotel atrium.
menyebar melalui 3 jalur internodal ke node AV.
Node AV memiliki waktu refraktory panjang, terjadi
perlambatan konduksi impuls listrik di node AV.
 Eksitasi-kontraksi coupling.
• Respon kontraksi otot jantung setelah menerima impuls
listrik dengan proses perubahan konsentrasi Ca
interselluler.
• Depolarisasi miosit atrium & ventrikel, menimbulkan
pelepasan Ca terminal cisterna retikulum sarcoplasma.
• Proses amplifikasi membuat lebih banyak pelepasan Ca
hinga meningkat 1000 x dan mencetuskan kontraksi
melalui troponin.
Cardiac Chambers Atrium

• Function primarly as conduits to the ventricel,

but they also contract weakly to facilitate
movement of blood into ventricels & augment
ventricular filling.
• Both the right and left atria are thin-walled
muscular structures that receive blood from a
low-pressure venous system.

Pasien dg keluhan sering berdebar, riw pingsan. PF ;

TD 90/60 mmHg, pucat, takikardia. EKG ;
Supraventrikulartakikardia.
Cardiac Chambers Ventricles

• As power pumps to
supply the main force
that moves blood
through the systemic &
pulmonary circulatian.
• The left ventricel is 3
times thicker than the
right, which is consonant
with it’s greater
workload .
• Assesment of Systolic
function ?
 Pertanyaan
• Bayi lebih mudah mengalami gejolak penurunan curah
jantung di banding dewasa , kenapa ?
• Perbedaan struktur ventrikel pada neonatus dibanding
bayi.
• Bagaimana struktur dan fungsi myocardium berubah
akibat proses kronik atau kompensasi
• Noted : The Development of cardiovascular system
from fetus .
 Development of Myocardial contractility
• The fetal myocardium characterized by poorly organized
cellular arrangements, and fewer myofibrils, in contrast
to the parallel, well organized myofibrillar arrangement of
the adult myocardium.
• Calcium cycling and excitation contraction coupling ; with
poorly organized T-tubules and immature SR, leading to
more dependen on free ionized calcium for contractility.
• At birth the heart change from a parallel to a series
circulation, left ventricle must adapt to dramatically
increased preload from blood returning from the lungs,
and increased afterload as the placental circulation is
removed.
 Ilustrasi Kasus dg kelainan katup
• Pasien ke 3 dengan keluhan mudah lelah
bila aktivitas, berdebar, riwayat sesak bila
tidur.
• PF ; Takiaritmia, S 1 meningkat, Murmur
Diastolik di apek, rhonki basah minimal di
basal.
• EKG, P mitral, AF rapid respon.
• Working Diagnosis ??
Auscultation Areas
 Cardiac valves
• 4 heart valves normally permit only forward blood flow,
pressure gradients across valves are the major
determinants of whether they are open or closed.
• Semilunar valves & Atrioventriculer valves
AO
110-130/
70-80

15-25/ 4-12
8-15
0-8

110-130/
15-25/ 4-12
0-8
 RANGE OF NORMAL RESTING VALUES
PRESSURE

PARAMETER VALUES
Central venous (mean) 0–8 mm Hg
Right atrial (mean) 0–8 mm Hg
Right ventricular 15–25/ 0–8 mm Hg
(systolic/diastolic)
Pulmonary artery 15–25/ 8–15 mm Hg
(systolic/diastolic)
Left atrial (mean) 4–12 mm Hg
Left ventricular 100–150/ 4–12 mm Hg
(systolic/diastolic)
Aortic (systolic/diastolic 100–150/7 0–90 mm Hg
Semilunar valves The aortic & the pulmonary valve

• Three and half moon shaped cusps attach to a fibrous

ring located at the aorta & pulmonary artery. When
closed they resemble 3 small sacs filled with the blood &
ensure unidirectional flow by preventing blood from
flowing from the artery back into the ventricle.
Semilunar valves The aortic & the pulmonary valve

• Systole, when intraventricular exceed arterial

pressure, the leaflets open to allow flow into the
great arteries.
• Diastole, as ventricular falls bellow arterial
pressure, the leaflets close & prevent backflow
of blood into the ventricels.
Cardiac valves Atrioventriculer valves

• 2 leaflets shaped mitral valves & 3 leaflets

tricuspid valves are attached to a fibrous ring
located between atria & ventriculaer
• In systole, when intraventriculer pressure
exceed the atria, the leaflet spread out ( like
open parachute), approximate and occlude the
valves orificium, papilary contraction applies
tension to chordae & prevent backflow into the
atria.
• In diastole, when atrial pressure exceeds that of
the ventricle, the leaflet open passively form a
funnel like shape to allow ventricular filling.
Atrioventriculer valves
• The tricuspid and the mitral valve prohibit backward flow
during forceful contraction of the ventricles, and attached
to fibrous rings that encircle each valve annulus.
• The central regions of these valves attach via chordae
tendineae to papillary muscles that emerge from the
ventricular walls

Mitral Tricuspid
 Cardiac valves
• The predominant factor that determines valve opening
and closure is the pressure gradient.
• However, the papillary muscles contract synchronously
with the other heart muscles and maintaining proper
valve leaflet position, thus helping prevent regurgitant
flow during contraction.

B
A
 PHYSIOLOGY OF THE INTACT HEART
• To know the phases of the cardiac cycle and
determinants of ventricular function.
• Cardiac Cycle : the sequence of electrical and
mechanical events during the course of a single
heartbeat .
(1) The electrical events of a single cardiac cycle
represented by the ECG .
(2) The mechanical events of a single cardiac cycle represented by
left atrial and left ventricular pressure pulses correlated in time with
aortic flow and ventricular volume.
 Pertanyaan
• Frekuensi bradikardia pada neonatus lebih
sering karena respon terhadap stimulus (
vagal, obat vagotonik, dan kurang sensitif
terhadap simpatomimetik) ?
• Perkembangan Inervasi jantung.
 Innervation of the heart
• The sympathetic innervation and control of the
cardiovascular system is incomplete in the infant
compared to older children, and that the
parasympathetic innervation is intact.
• Studies demonstrated incomplete sympathetic
innervation in the neonatal heart compared to
the adult, but no differences in the number or
density of parasympathetic nerves.
Control heart rate
 CONTROL OF CARDIAC FUNCTION
Neural Regulation of Cardiac Function
• Simpatis & Para Simpatis mengatur ; HR, Kecepatan
hantaran listrik, kontraktilitas myocard.
• Simpatis berasal dari upper thoracis T1-T5  pelepasan
neurotransmiter epinep & nor-ep. mll stimulasi reseptor
saraf Beta dan Alpha di jaringan Kardiovaskuler.
• Simpatis dominan di ventrikel > atrium.
• Secara umum epi & nor-epi menghasilkan ;
1. Positive chronotropic (laju jantung),
2. Inotropic (kontraktilitas), and
3. Lusitropic (relaksasi).
 CONTROL OF CARDIAC FUNCTION
Beta Adrenergik Alpha Adrenergik
• Lokasi di myokardium, otot • Terutama di otot polos
polos pemb. darah & bronkus.
pembuluh darah ( tdk ada
• Stimulasi meningkatkan ; sinus
nodal, otomatisasi di myokardium) ,
kontraktilitas atrium & ventrikel, • Tdk memiliki efek
dilatasi ringan otot polos langsung myokardium.
arteriolar dan venula.
• Vasokontriksi pada
• Meningkatkan CO 2-3 x mll
peningkatan HR (200 x/menit) jaringan pembuluh
dan peningkatan kontraktilitas. koroner dan cerebral.
• Depresi SSS menurunkan 30
% CO.
 CONTROL OF CARDIAC FUNCTION
Neural Regulation of Cardiac Function
• Parasympathetic innervation of the heart is the
vagal nerve.
• Supraventricular (atrium) receives much greater
vagal innervation than the ventricles.
• The parasympathetic target neuroeffectors are
the muscarinic receptors through acetyl choline.
• Activation of muscarinic reduces pacemaker
activity, slows AV conduction, decreases the
atrial contractile, and exerts inhibitory
modulation of ventricular contractile.
 Neural Regulation vs Cardiac Reflexes
Neural Regulation Cardiac Reflexes

• At rest, the heart has a • Fast-acting reflex loops

tonic level of
parasympathetic cardiac
firing  the major
influence on the heart at
rest.
• During exercise or stress,
the sympathetic influence • Cardiac receptors can be
becomes more prominent
between heart and
central nervous system
that contribute the
regulation of cardiac
function and maintenance
of homeostasis.
found in the atria,
ventricles, pericardium,
and coronary arteries .
 The Heart's Conduction System
Basic components of conduction system
1.Sinoatrial node ;
1. Junction of the SVC with RA
2. 100-110/ minutes
3. Anterior, middle,posterior modal.
2.Inter-nodal fibre bundles
3.Atrioventricular node (AV node) ; Near the
ostium of coronary sinus.

4.Atrioventricular bundle/Bundle of His ;

Membranous interventricular to the apex of the septum
5.Right/ Left bundle branch ; Endocardium of the ventricle
6.Purkinje system.
Normal Cardiac Activation
 Cardiac conduction system
• The heart possesses its own conduction
system and can beat independently even
after being separated from its nerve
supply.
• The extrinsic (arising external to the heart)
nerve supply coming from the nervous
system serves to modify and control the
intrinsic (inherent to the heart itself)
beating established by the heart.
 Cardiac conduction system
• SA node :
• Spontaneus generation of action potencials & the
highest spontaneous depolarization rate
• The dominant cardiac pacemaker
• Vagal tone brings the resting heart rate down to 60-8O
beats/min.
• The normal range for SR is 60-100 beats/min.
• Control both rate & ventricular rhythm.
• SA node causing atrial contraction.
• The impulses travels into the ventricels via AV node.
 Normal Cardiac Activation
• Electrical activation of the heart depends on the
spread of a depolarizing from pacemaker cells
through cardiac muscle, as well as specialized
conducting tissues.
• This spreads throughout the right and left atria;
conducting tracts called Bachmann's bundle
speed the depolarizing wave front to the left
atrium.
• Electrical atrial activation triggers atrial muscular
contraction, which pumps blood through the
tricuspid and mitral valves.
 Cardiac conduction system
Atrioventricular (AV) node, where conduction delay is
physiologic, serves as the only electrical connection linking
the atria and ventricles; the AV valve rings are insulated.
 Normal Cardiac Activation
• The depolarizing wave front exits the AV node
into the bundle of His, a specialized conducting
tissue capable of rapid conduction.
• The bundle of His bifurcates into right and left
bundle branches; the left bundle branch divides
into the left anterior and left posterior fascicles.
• The bundle branches, as well as their more
distal ramifications of specialized conducting
tissue, the Purkinje system (the smallest
branches of the conduction system) .
 Normal Cardiac Activation
• From Purkinje system, the depolarizing wave
front enters into and then moves through
ventricular muscle (the individual ventricular
cardiomyocytes).
• Ventricular electrical activation begin muscular
contraction, which pumps blood through the
semilunar valves.
• After electrical activation, or depolarization, a
period of electrical recovery, or repolarization, is
necessary before repeated activation.
 Electrical Events and the ECG
• The action potential initiated at the SA node is
propagated to both atria by specialized
conduction tissue, and it leads to atrial systole
(contraction) and the P wave of the ECG .

The P wave represents atrial muscular

depolarization.
 Electrical Events and the ECG
• At the junction of the interatrial and interventricular
septa, atrial conduction tissue converges at the AV node,
which is connected distally to the His bundle .
• The PR interval which is the segment from the onset of
the P wave to the onset of the QRS complex can be
used to measure the delay between atrial and ventricular
contraction at the level of the AV node.
 Electrical Events and the ECG
• The spread of depolarization to the ventricular
myocardium manifested as the QRS complex
give information about the structure and function
of ventricular tissue.
• Followed by ventricular repolarization and
appearance of the T wave on the ECG.
 The Electrocardiographic Waves
• The ST segment and T wave (and U wave)
reflect ventricular repolarization, a process of
recovery that must take place before the
ventricle can be depolarized again.
• Atrial muscle also requires repolarization before
the next depolarizing wave front.
• The ventricular mass exceeds atrial mass, the
low-amplitude atrial repolarization wave is buried
underneath the QRS and is rarely manifested on
the ECG .
 Pertanyaan
• Gelombang P menggambarkan proses ?
• Gelombang Q menggambarkan proses ?
• Gelombang R menggambarkan proses ?
• Gelombang S menggambarkan proses ?
• Gelombang T menggambarkan proses ?
 ECG
• P = atrial depolarisation
• Q = depolarisation at the bundle of his.
• R = the main spread od the depolarisation, from
the inside out through the base of the ventricel.
• S = the subsequent depolarisation of the rest of
the ventricels upwards from the base of the
ventricels.
• T = repolarisation of the myocardium after
systole is complete.
 Cardiac blood flow & intrachambers
pressure

• The factors responsible for the forward

movement of blood through the heart are
Cyclic transchamber pressure gradients ;
Higher pressure in the delivering
chambers and
Lowers pressure in the receiving
chambers.
 RANGE OF NORMAL RESTING VALUES
PRESSURE

PARAMETER VALUES
Central venous (mean) 0–5 mm Hg
Right atrial (mean) 0–5 mm Hg
Right ventricular 20–30/0–5 mm Hg
(systolic/diastolic)
Pulmonary artery 20–30/8–12 mm Hg
(systolic/diastolic)
Left atrial (mean) 8–12 mm Hg
Left ventricular 100–150/8–12 mm
(systolic/diastolic) Hg
Aortic (systolic/diastolic): 100–150/70–90 mm
Hg
RANGE OF NORMAL RESTING VALUES
VOLUME

PARAMETER VALUES
Right ventricular end- 70–100 mL
diastolic volume:
Left ventricular end- 70–100 mL
diastolic volume:
Stroke volume: 40–70 mL

Cardiac index: 2.5–4. L/min/m2

Ejection fraction: 55–70%
RANGE OF NORMAL RESTING VALUES
RESISTANCE

PARAMETER VALUES

Systemic vascular 10–20 mm Hg·min/L

resistance:
Pulmonary vascular 0.5–1.5 mm Hg·min/L
resistance:
 PHYSIOLOGY OF THE INTACT HEART
• Cardiac Cycle : the sequence of electrical and
mechanical events during the course of a single
heartbeat ;
(1) The electrical events of a single cardiac cycle represented by the
ECG .
(2) The mechanical events of a single cardiac
cycle represented by left atrial and left ventricular
pressure pulses correlated in time with aortic flow
and ventricular volume.
 Siklus Cardiac
3 phases of 4 phases of ventricular
ventricular systole diastole
Isovolumic Isovolumic Pasive
contraction Rapid & relaksasi Filling
Rapid Sistolik
Slow
Filling Atrium
Ejection
 70 %
VOLUME

30 %
VOLUME
 Mechanical Events
• Cardiac cycle begin with return of the
blood to the right and left atria from the
systemic and pulmonary circulation .
• Atrial pressure increases until it exceeds
the pressure within the ventricle, and the
AV valve opens .
• Blood first flows passively into the
ventricular, and such flow accounts for
75% of total ventricular filling .
Central venous pressure waveform
 Mechanical Events
• The remainder of the blood flow is by active
atrial contraction or systole, as the atrial "kick.
• The onset of atrial systole is coincident with
depolarization of the sinus node and the P wave
• While the ventricles fill, the AV valves are
displaced upward and ventricular contraction
(systole) begins with closure of the tricuspid and
mitral valves, which corresponds to the end of
the R wave.
• The first part of ventricular systole is known as
isovolumic or isometric contraction
Cardiac cycle
Pressure-Volume loop for left ventricle
 Mechanical Events
• The electrical impulse tranverses the AV and
passes through the right and left bundle
branches into the Purkinje fibers, leads to
contraction of ventricular and a progressive
increase in intraventricular pressure.
• When intraventricular exceeds pulmonary artery
and aortic pressure, the pulmonic and aortic
valves open and ventricular ejection occurs,
which is the second part of ventricular systole.
 Mechanical Events
• Ventricular ejection separated into the rapid
ejection and the reduced ejection phase
• During the rapid ejection phase, forward flow is
maximal, and pulmonary artery and aortic
pressure is maximal.
• In the reduced ejection phase, flow and great
artery pressure taper with progression of systole.
• Pressure in both ventricular falls as blood is
ejected from the heart, and ventricular diastole
begins with closure of the pulmonic and aortic
valves.
 Mechanical Events
• The initial period of ventricular diastole consists
of the isovolumic relaxation /isometric relaxation
phase, concomitant with repolarization of the
ventricular and corresponds to the end of the T
wave.
• The final portion of ventricular diastole involves
a rapid decrease in intraventricular pressure
until it falls below that of the right and left atria,
at which point the AV valve reopens, ventricular
filling occurs, and the cycle repeats itself.
Cardiac cycle ; Ventricle volume, Ventricle pressure, Aortic pressure, Atrial
prssure
 Determinants of Cardiac Performance
• Primary measurements of cardiovascular
are ;
1. Arterial blood pressure and
2. Cardiac output (mean arterial blood flow).
• Those cardiac performance depend on
four factors:
1. Preload,
2. Afterload,
3. Ventricular contractility, and
4. Heart rate .
 Determinants of Cardiac Performance
Preload.

• Preload ; degree to which sarcomeres are

stretched just before the onset of systole,
is generally defined for the ventricle as
either end-diastolic pressure or end-
diastolic volume .
 Determinants of Cardiac Performance
Preload.
Factors affecting ventricular preload :
1. Venous Return .
2. Blood Volume.
3. Distribution of blood volume. :
a. Posture
b. Intrathoracic pressure
c. Venous tone.
4. Rhythm ( Atrial contraction )
5. Heart rate.
 Determinants of Cardiac Performance
Preload.

• Decrease in preload corresponds to a decrease

in both end-diastolic volume and pressure,
associated with decreases in peak pressure and
stroke volume .
• An increase in preload leads to an increase in
ventricular pressure and generation of flow, but
there are limits to how high preload pressures
can be increased ;
• LV end-diastolic pressures in excess of about 20 to 25
mm Hg typically cause exudation of fluid into the alveoli,
and the resulting pulmonary edema limits blood
oxygenation.
 Determinants of Cardiac Performance
Afterload

• Afterload ; the physical forces that must be

overcome for myocytes to shorten and for
the ventricle to eject blood.
• In the absence of LV outflow obstruction,
arterial pressure is an appropriate index
for quantifying myocyte afterload in vivo
 Determinants of Cardiac Performance

• Parameter that characterizes the

ventricular afterloading of the arterial
system is total peripheral resistance
(TPR), which predominantly relates to the
vasomotor tone of the resistance vessels .
 Determinants of Cardiac Performance

• Contractility ; the intrinsic strength of the cardiac

muscle (myocardial contractility) or the ventricle
(ventricular contractility), independent of external
conditions imposed by either preload or
afterload.
• Contractility is related to the rate of myocardial
muscle shortening, which in turn dependent on
the intracelluler calcium concentration during
systole.
Control Cardiac Output
Control Stroke Volume
 Cardiac Output
• Amount of blood pumped by the heart in a given
period of time.
• C.O. = Heart Rate X Stroke Volume
HR = beats per minute
SV = End Diastolic Volume - End Systolic
Volume. ( 120 cc- 50 cc = 70 cc ).
• Example.
• CO = 60 beats/min X 70 ml/beat = 4200 ml/min
(7.2 l/min)
The average 70 kg male has a CO of 5-6 l/min.
• CI=CO/BSA. Normal : 2,5-3,5 lt/min m2
 Contractility of the heart
• Contractility : Inotropic state independent of
changes in preload, afterload or heart rate.
• Compliance : Nonlinear change in ventricular
end diastolic volume/pressure.
 Blood Pressure
• MAP is the product of the CO & SVR.
• Arterial pressure varies with respiratory cycle :
Arteriole-Capilarry-Venule system
 Arteriole-Capilarry-Venule system
Arterioles Kapiler Venules
Otot polos
pembuluh darah
Filtrasi-resorpsi
 Venous system
• 60% of the systemic blood volume is in
small vessel and venules ( diam. 20 um 
2 mm).
• Venous return, the rate of flow blood from
the peripehry to the heart.
• CO is equal to venous return .
 Coronary Blood Flow: Metabolic and
Neurohormonal Regulation
• The myocardium relies on a continuous
supply of oxygen delivered via coronary
perfusion.
• The myocardium extracts 80 to 90% or
more of the oxygen delivered to it in blood,
even under basal resting conditions .
 The coronary circulation
• The main CA extend over the surface of the
heart & surround it like a crown. It is form these
arteries & their small penetrating branches that
the heart receives all of its blood supply.
 The coronary circulation
• The left main CA, divides into 2 main branches :
• LAD, branch contributes to perfusion of the RV
and vascularizes the anterior wall of the LV, &
the anterior 2/3 of the septum.
• Branches of LAD also perfuse conduction
tissues, such as the bundle branch of His, the
right & left bundle branches.
 The coronary circulation
• Circumflex, supplies blood to the lateral &
posterior walls of the LVand in small % of
the people to the sinus node & AV.
 The coronary circulation
• RCA, supplies to the sinus node, the AV node,
and the initial portion of the bundle of His in
majority. Also contributes to perfusion of the RV,
inferior wall of the LV, & posterior 3rd of the
ventricular septum.
• Most of the blood supplied by the coronary
arteries is returned to the right atrium by way of
the coronary sinus.
 Ilustrasi kasus
• Pasien 1 dengan keluhan,nyeri dada yg dalam,
sulit dilokalisir terkait aktivitas dan saat istirahat,
bertambah sering dan lama ( > 5-15 menit ),
keringat, respon dengan nitrat SL, terapi ca
antagonis , beta bloker, aspilet, simvastatin .
EKG ; normal atau depresi segmen ST dan T
inversi, Enzim +
 EKG changes in MI
Site of Changes seen Possible occlusion
infarction
1.Large anterior V1 – V6: ST segment Left main coronary
elevation artery
wall II, III, aVF: ST segment
depression
2.Anterior wall V2 – V4: ST segment Left anterior descending
elevation (LAD
II, III, aVF: ST segment
depression
3.Anteroseptal V1 – V4: ST segment LAD and branches
elevation supplying blood to the
II, III, aVF: ST segment septal wall .
depression
4.AnterolateralI aVL, V3 – V6: ST segment LAD and branches
elevation supplying blood to the
II, III, aVF: ST segment lateral wal .
depression
 EKG changes in MI
Site of Changes seen Possible
infarction occlusion
5.Lateral wall V5, V6, I, aVL: LCx and or LAD
Pathologic Q wave, ST
segment elevation,
inverted T wave
6.Inferior wall II, III, aVF: Pathologic Q RCA and/or LCx
wave, ST segment
elevation, inverted T
wave
7Posterior wall V1 – V3: ST segment Right coronary artery
depression, tall, upright, (RCA) and/or left
symmetrical R wave, and circumflex artery (LCx
tall, symmetrical T
wave.V7 – V9*: ST
segment elevation
8.Right ventricle V3R – V6R**: ST Proximal RCA .
segment elevation
 The coronary circulation
• Individual variations In CA.
• The left coronary circulation always provide flow
to the greates portion of the myocardium.
• The dominant circulation , as the CA that
perfuse the AV node & descends parallel to the
posterior intraventricular groove ( posterior
descending artery ) .
• The right coronary circulation is dominant in80%
population .
• The left coronary circulation is dominant in 20%
population .
 Coronary autoregulation
• Coronary perfusion constant at BP 50-120
mmHg.
• Coronary arteriole ( diam < 150 um)
dilatation.
• Oxygen demand alter autoregulation (
myocardial O2 tension )
• Most important regulator  metabolic
Coronary Blood Flow: Chamber Mechanical
Regulation
• The coronary arteries originate from the
aorta and spread over the outer surface of
the heart or epicardium .
• From this epicardial position the arteries
penetrate the myocardium from
epicardium to endocardium and form the
capillary network.
 Coronary Blood Flow
• The head of pressure at the origin of the
coronary artery and the pressure within the large
epicardial coronary arteries directly reflect
central aortic pressure.
• During diastole, resistance to blood flow from the
coronary arteries is largely from the tone of
resistance vessels.
• During systole, coronary perfusion pressure
(which equals aortic pressure) is determined by
LV intracavitary pressure. In turn, cavitary
pressure equals the pressure within the inner
myocardial wall.
 Coronary Blood Flow

• The endocardial coronary arteries are

compressed during systole.
• The systolic pressure within the thick LV
wall toward the epicardial surface is not
nearly as high as that in the endocardial
portion of the wall.
• Coronary blood flow during both systole
and diastole is directed toward the
epicardium but is essentially exclusively
limited to diastole in the subendocardium.
Coronary blood flow and Cardiac cycle
 Coronary Blood Flow

• The influence of heart rate on coronary blood

flow, to the subendocardium, is important.
• As the heart rate increases, the period of
diastole between beats becomes shorter.
• This limitation of coronary flow to the
subendocardium during tachycardia can have
profound effects  double effect.
• Coronary blood flow ; Continous or Intermitten ?
 Myocardial Oxygen Supply-Demand
Balance.
Supply :
1. Heart rate : diastolic time .
2. Coronary vessel diameter.
3. Arterial Oxygen content ;
1. Arterial Oxygen tension
2. Hemoglobin concentration
4. Coronary Perfusion Pressure ;
1. Aortic Diastolic Blood Pressure.
2. Ventricular end-diastolic pressure.
 Myocardial Oxygen Supply-Demand
Balance.
Demand :
1. Basal requirements.
2. Heart rate.
3. Total mechanical work performed by
the heart/ Wall Tension :
 Preload.
 Afterload.
4. Contractility
 Myocardial metabolism
• The heart relies exclusively on oxidation of fatty
acids and glucose as an immediate source of
energy.
• The heart normally extracts free fatty acids
preferentially from the coronary blood for
oxidative energy production.
• Under conditions of limited oxygen supply, this
preference is changed to glucose because
glucose metabolism generates a greater amount
of ATP for a given amount of oxygen consumed
 Myocardial metabolism
• In the heart, anaerobic metabolism (i.e.,
glycolysis) provides very limited energy, and
muscular contraction cannot be supported under
such conditions; as a result, the heart is
dependent on the availability of oxygen to
continue its function.
• When oxygen is unavailable (e.g., hypoxia,
ischemia,), heart function deteriorates
remarkably rapidly, essentially on a beat-to-beat
basis .
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