OLEH:

Drs. SLAMET SUMARNO.M.Fis

Alamat: Jln. Masjid Almunir No. 6 Rt 011
Rw.03 Kel Makasar jak Timur.

TGL: 10 OKTOBER 2012.

Phone: 021 8098743
Hp. 0813 8213 9050
Email: [email protected]
 Kurikulum vite

• Drs.Slamet Sumarno,M.Fis.
• Wonogiri : 15-09-1950
• Akademi Fisioterapi Surakarta 1975
• Kardia Respirasi : Revalidasi
Centrum Ultreh Nedherland 198
• S1 1992 Unis Syeh Yusuf Tangerang
• S2 2010 UNUD BALI.
Pekerjaan.
• Dosen Akfis UPN 1983 – Sekarang
• Dosen Akfis Uki 1986 – Sekarang
• Dosen Fakultas Fisioterapi Esa Unggul
1998
• Dosen Fakultas Fisioterapi STIKES
Binawan 2004 – Sekarang.
• Dosen Akbid Sukawangi 2004 –
Sekarang
• Klinisi RSB Duren Tiga Jak Sel.
Agar peserta dapat memahami:
• Mekanisme pernafasan dan
sirkulasi normal.
• Fungsi kardiovakuler dan
respirasi.
• Kapasitas pernafasan dan
tranportasi oksigen normal.
• Mampu mengaplikasikan kordio
vaskuler respirasi dalam
penilaian klien/ pasien dengan
baik dan benar.
• Mampu menerapkan dalam
gangguan
kordivaskulerrespirasi
khususnya dan Neuromuskular
dan muskuloskeletal maupun
integumen.
• We cannot live
without oxygen.
• Anda tidak bisa hidup
tanpa oksigen
• All living cells
require to get
oxygen from the
fluid around
them and to get
rid of corbon
dioxide to it.
1. Exchange O2
1. Air to blood
2. Blood to cells
2. Exchange CO2
1. Cells to blood
2. Blood to air
3. Regulate blood
pH
4. Vocalizations
5. Protect alveoli External and cellular respiration
Oksigen = 20,93 %
Carbon diaksida= 0,03 %
Nitrogen = 79,04 %

TEKANAN
OKSIGEN

Di Daerah
SEA
LEVEL
Pulmonary ventilation
(breathing) is the proses by
which air is moved into and
out of the lungs.
It has two phases: inspiration
and expiration.
Ruang rugi
Proses pernafasan. Anatomi:
1. External Respirasi Gas yanga
Ada pada
a. Inspirasi.
Jalan nafas
b. Ekspirasi.
2. Internal Respirasi. 150 CC
a. Tranportasi (sirkulasi).
b. Buffer
Inspirasi is an active • Normal expiration is
process in which the the passive process.
diaphragm and the
external intercostal • The inspiratory muscle
muscles increase the relax and the elastic
dimensions, and thus tissue of the lungs
the volume, of the
thoracic cage. recoils, returning the
This decreases the thoracic cage to its
pressure in the lungs smaller, normal
and draws air in. dimensions.
Tekanan alveoli minus • This increases the
3 s/d 10 mmHg < dari
760 mmHg. presure in the lungs
and forces air out.
 Forced or labored
inspiration and expiration
are active proceses,
dependent on muscle
actions.
 Aktif inspirasi dibantu otot-
otot: Scalani, Sterno cledo
mastoideus, pektoralis,
membantu angkat sternum
dan costae ke depan atas.
Tekanan alveoli turun
sampai 100-80 mmHg.
 Aktif ekspirasi dibantu otot-
otot : Abdominalis,
Latisimus dorsi Inspirasi. Ekspirasi
1. Tranportasinya
Exchange O2 in cells
a. Air to blood
b. Blood to cells
2. Exchange CO2
• Cells to blood
• Blood to air
• Buffer
Ruang rugi Fisiologi:
Keterbatasan Ventilasi
Paru atau Raung residu
Yang tinggi
DAERAH
PERTUKARAN
O2 Dan CO2:
1. Brokus respiratoris
2. Ducctus
3. Succus dan
4. Alveoli
 Pertahanan Respiratory
system
1
Inhalasi melalui hidung
Mempunyai keuntungan
1.Udara disaring.
2.Udara dilembabkan.
3.Udara dihangatkan.
4.Cegah peradangan
jalan nafas bag atas.
2. Pembersih jalan nafas oleh cillia
dan fungsi menelan
Perfusi eksterna
Eksteranal respirasi:

respirasi Dalam paru Dipengaruhi:

1. Cairan surfaktan
2. Tebal membran.
3. Volume darah
4. Hb darah
5. Kecepatan sirkulasi.
6. Vicositas darah.
7. pH darah
Tranportasi O2 dan CO2
dalam darah
• Kemampuan
jantung (COP= HR
X Stroke volume).
• Tahanan perifer.
• Fleksibilitas
pembuluh darah.
• Lumen.
• Vikositas.
• Hb.
• Saturasi darah dll.
Ventilation: The Pumps
1. Inspiration
2. Expiration
3. Diaphragm
1. Low energy pump
2. Concavity – flattens
4. Thorax: ribs & muscles
5. Pleura: double membrane
1. Vacuum seal
2. Fluid-lubrication
Pengaruhi internal terhadap
kemampuan tubuh suply O2
1. Jalan nafas yang adeguat.
2. Fleksibilitan otot, fasia, kulit
sangkar thorax.
3. Perfusi O2 dan CO2
4. Volume, Hb, Ph, Plasma darah
5. Keadan pleurae
6. Pusat kontrol fungsi
pernafasan
7. Fungsi bufer.
Pengaruh eksternal terhadap
kemampuan tubuh suply O2

1. Kadar
Oksigen
udara.
2. Posisi tubuh
3. Usia jenis
kelamin.
 Factors Affecting Ventilation

1. Airway Resistance
2. Diameter
3. Mucous blockage
4. Bronchoconstriction
5. Bronchodilation
6. Alveolar compliance
1. Surfactants
2. Surface tension
7. Alveolar elasticity
 ,Lung volumes
1. Volume paru
a. RV 1200 cc
b. ERV
c. TV
1000
d. IRV
2. Capasitas paru 500
a. Capasitas inspirasi 1900-3300
b. Capasitas Ekspirasi
c. Capasitas vital PRIA WANITA
d. Capasitas total paru. VCI 3,3 1,9
e. Kapasitas residual TV 0,5 0,5
VCE 1,0 0,7
VR 1,2 1,1
V 6,0 4,2
TOTAL
 Jantung
Clinical Cardiovascular Anatomy & Physiology
Concepts, Definitions, & Principles

A. LETAK.
B. UKURAN.
C. LAPISAN
JANTUNG .
D. RONGGA .
E. KATUP DAN
SEKAT.
F. SYARAF
JANTUNG
 Pumpa jantung
Agar darah sampai pada sel
Tubuh harus dipompa jantung
Menuju jaringan, termasuk
Jaringan jantung sendiri.

Jumlah darah yang dipompa

jantung dipengaruhi:

Strooke vulume dan frekuensi

Denyut jantung per menit.

Makin tinggi strooke vulumee

Dan frekuensi makin tingg COP

Tetapi makin tinggi frekuensi

Jantung makin sedikit aliran
Koroner yang memberi nutresi
Jantung.
 Efisiensi kerja jantung.
Makin kuat dan fleksibel otot
Jantung , strooke volume
Makin besar dan makin
hemat energi kerja jantung

Sehingga frekuensi jantung

Permenit makin kecil.

Termasuk tahanan perifer

Sistem sirkulasi

Tahanan perifer meliputi:

1. Vulume pembuluh darah
2. Vikositas darah
3. Trammister
4. Jenis Kerja otot.
MICRO CIRKULASI
ANATOMI
Pusat
kontrol
cardio
vaskuler
respirasi
Conduction System of
the Heart
Tranportasi darah dan O2 CO2

1. Kemampuan
jantung (COP= HR
X Stroke volume).
2. Tahanan perifer.
3. Fleksibilitas
pembuluh darah.
4. Lumen.
5. Vikositas.
6. Hb.
7. Saturasi darah .
8. Sistem konduksi
Blood Components: Plasma Transports
Solutes
1. Water, ions, trace
elements
2. Gasses: O2 & CO2
3. Organic Molecules
1. Glucose
2. N–wastes
3. Proteins
4. Antibodies
5. Hormones
Blood
Components:
Plasma
Transports
Solutes
Blood
Compon
ents:
"Blood
Count" –
% of
Each
Compon
ent
Blood Components: Cells

1. Erythrocytes
1. Red Blood Cells (RBC)
2. O2 & CO2 transport

2. White Blood Cells (WBC)

1. Immune defense
2. Phagocytosis
3. Platelets: clotting
Vicositas darah
Lymphatic System: Structure and Roles
(overview)

1. Lymphatic structures
1. Capillaries with valves
2. Lymph vessels
3. Lymph nodes & organs
2. Immune defense:
lymphocytes
3. Transport of fats
4. Collects excess ECF
1. Returns to plasma
2. Edema
System
lymphe
 System Aliran Lymphe
Net Out Flow Into ECF
Hubungan antara kapiler dan pembuluh lymphe

Aliran air dan cairan

difilter keluar oleh
kapiler Ke atas oleh
pembuluh lymphe
dan masuk sirkulasi
• Net filtration –
net absorption
= net out flow
• About 2 L/day
collected by
Figure lymph vessels
15-18b: Fluid exchange at the capillary
 PENDAHULUAN.
TheAnatomi
Normalarteria
Heartcoronarria
- CoronarydanArtery
jantungAnatomy
normal

Left Main CA

Layers of the Arterial Wall

Circumflex

Right CA
Marginal Branch
Left Anterior Descending Coronaria Arteri
 Pengertian
1. Q=Cardiac Output (COP) = Heart Rate X Strooke Volumes
2. Cardiac Index = COP
body surface area
3. Preload: Volume darah yang masuk ventrikel saat diastole (End
Diastole Volume= reflects stretch of the cardiac muscle cells)
4. Afterload: Tahanan ventricular selama systole (Kemampuan
otot ventrikel untuk mendorong darah ke aorta)
5. Frank Starling Law of the Heart - Kemampuan kontraksi otot
ventrikel terbesar mulai pre load secara bertahap.
6. Myocardial Contractility – Kekuatan kontraksi otot jantung dan
perkembangannya sampai preload.
7. Regulated by:
1. sympathetic nerve activity (most influential)
2. catecholamines (epinephrine norepinephrine)
3. amount of contractile mass
4. drugs
 Starlings Law of the Heart and Contractility

SV
u contractility
> 100

70-80 cc normal
contractility
< 60
d contractility
(heart failure)
left
ventricular
performance
preload (venous return)
 Curves saat tekanan ventrikel
indikasi kemampuan kontraksi
Dan fungsi jantung.
Perubahan tekanan per tahap
dP/dt = change in pressure per unit of time

dP/dt dP/dt

120
Normal
Heart Failure
Gambaran
(lemah jantung)
peningkatan saat
dan akhir tekanan
diastol
0
Pada jantung normal SV= 60-80 CC Jantung terlatih SV= 90-250 CC
Jantung sakit SV = 40-50 CC
Kemampuan kontraksi
dipengaruhi oleh
1. Kekuatan otot jantung.
2. Fleksibilitas otot jantung.
3. Tahanan perifer (aorta, jaringan, vena
4. Peningkatan maks selisih preload dan afterload
(dP/dt from LV pressure curve)
5. Pengaruh Positive/negative iontropic.
6. Ejection fraction (EF = SV/EDV) used in clinical
practice
7. Hormonal (epineprin atau norepineprin) increase
contractility assumed with increase EF  with Ca,
NE, digitalis, exercise with [K]o, [Na]o
Contractility related to :
1. sympathetic adrenergic nerves
a. catecholamines: epinephrine
norepinephrine
b. Obat: digitalis
sympathomimetics
anesthetics, barbiturates
2. Hilangnya kemampuan kontraksi otot
misalnya MCI, cardiomyopathy.
 Definisi
1. Perbedaan tekanan oksigen antara darah arteri dan vena.
Arteriovenous Oxygen Difference (AVO2D)
PENGUKURAN DALAM ml % - ml O2 / 100 ml blood
2. Oxygen Consumption (VO2) – Jumlah oksigen yang
dibutuhkan darah untuk metabilism dalam menghasilkan
energi/
1. “absolute” measures: L / min , ml / min
2. “relative measures: ml / kg body wt. / min
3. Fick equation: VO2 = COP X Selisih O2 arteri
dan vena
3. Maximum Oxygen Consumption (VO2max) Jumlah oksigen
yang mampu disediakan secara maksimal per menit untuk
metabolism dalam menghasikan energi
1. Tak langsung 220-usia = 60-80 % VO2 maks.
2. Spirometri .
 Definisi

4. Myocardial Oxygen Consumption VO2 of

the heart muscle (myocardium)
"estimated" by RPP: HR X Sistole BP.

5. Functional Aerobic Impairment:

mild 27% - 40%
predicted VO2max - attained VO2max moderate 41% - 54%
predicted VO2max marked 55% - 68%
severe > 69%
 Definitions
1. Systolic Blood Pressure (SBP) pressure measured in brachial
artery during systole (ventricular emptying and ventricular
contraction period)
2. Diastolic Blood Pressure (DBP) pressure measured in brachial
artery during diastole (ventricular filling and ventricular
relaxation)
3. Mean Arterial Pressure (MAP) "average" pressure throughout
the cardiac cycle against the walls of the proximal systemic
arteries (aorta)
1. estimated as: .33(SBP - DBP) + DBP
4. Total Peripheral Resistance (TPR) - the sum of all forces that
oppose blood flow
1. length of vasculature (L)
TPR = ( 8 ) ( V ) ( L )
2. blood viscosity (V)
(  ) ( r4)
3. hydrostatic pressure (P)
4. vessel radius (r)
Kontrol fungsi jantung paru.
 Cardiorespiratory Control
Exercise Systemic Blood Flow: Autonomic influences
Sympathetic outflow & circulating catecholamines
•  activation r vasoconstriction in non - exercising tissue
• Approximate redistribution of blood flow during maximal exercise
• NC in brain blood flow 500 ml/min u to heart
• 11,300 ml/min u to muscle 400 ml/min u to skin
• 500 ml/min d to kidneys 800 ml/min d to viscera
• 200 ml/min d to various other parts of the body

REST KERJA
 Pengaruh langsung dari latihan aerobik
1. Heart Rate
Meningkat 3 kali lipat dari HR saa rest t
2. Oxygen Consumption (VO2)
Satuan ukur relative dan absolute :
• Relative: ml O2/kg/min Absolute: ml/min or L/min
• Rata-rata VO2max usia 40 th- 37th (laki) ml/kg/min
• Resting metabolic equivalent = 1 MET = 3.5 ml/kg/min
• Oxygen consumption linked to caloric expenditure (1 liter of O2
consumed180
= 5 kcal)
Heart 160
Rate
140
100 HR – VO2
1.0 2.0 3.0 relationship is
Oxygen Uptake (L / min) linear until about
50 150 250 90% VO2max

Workloads (Watts)
3 Cardiac Output (COP)
• Naik 4 x rest saat latihan
• COP meningkat akan meningkatkan sirkulasi vena
• Venous return dipengaruhi:
• sympathetic venoconstriction
• muscle pump
• Peningkatan inspirasi (thoracic pressure)
• Aliran darah ke jaringa meningkat
• Peningkatan inspirasi karena tekanan abdominal
• Kontraksi otot abdominal
• Pemerasan (squeezing) vena abdominal

120
Stroke
Volume 110
(ml/beat 70
25% 50% 75%
Percentage of VO2 max
4. Stroke Volume
• Meningkat sampai 1.5 kali istirahat bila exercise
• Tahap peningkatan 40% - 50% VO2 max
• Venous return naik End Diastole Volume
(Starling mechanism)
• End Systole Volume naik sesuai kemampuan
kontraksi myocard.
• Tahanan perifer 58% rest, max exercise: 83%
120
Stroke
Volume 110
(ml/beat 70
25% 50% 75%
Percentage of VO2 max
5. Perbedaan oksigen arteri dan vena
Tergambar pada oxyhemoglobin desaturation
curve
 up approximately 3 fold from rest to max exercise
 Saat rest antara 25% O2 arteri Acute Responses
 Saat exercise 85% O2 arterial to Aerobic
Exercise
6. Tekanan darah (B P) dan TPR
 SBP: up - failure to up signifies heart failure
 DBP: slight up or slight d or NC
 MAP: slight up
6. TPR: down - mainly due to vasodilation in exercising
muscle SBP= Sistole blood presure
DBP=Dyastole blood presure
MAP=Mean arterial presure
TPR=Total peripher resistance.
7. Coronary (Myocardial) Blood Flow
• 4.5% COP untuk myocardium saat rest dan
meningkat saat exercise
• Peningkatan ini karena meningkatnya Mean
Arteria Presure dan CA vasodilasi
Acute Responses
to Aerobic
Exercise
8. Aliran darah ke kulit.
• Naik saat durasi rendah
• Turun saat latihan tinggi(krn peningkatan ke
otot).
• Naik selama exercise recovery percepatan
penurunan suhu dan dan bufer.
 Acute Responses to
Aerobic Exercise
• Ventilasi semenit
• Saat rest : 6 Liters/min
• Saat exercise : 175 Liters/min
• RR rest : 12-18/ min
• Saat exercise : 45-60/ min
• TV rest : 500 cc
• Exercise: : 2250 cc
 Sirkulasi saat rest /exc
Rest A-v light max
Daerah O2/100ml
Moderat

Pencernaan 4,1 1100 12% 600 300 1%

Ren 1,3 900 10% 600 250 1%
Cerebral 6,3 750 8% 750 750 3 %
Coronaria 14,0 350 4% 750 1000 4 %
Otot kasar 8,4 4500 47% 12500 22.000 88%
Kulit 1,0 1500 15% 1900 600 2%
Lain-lain - 400 4% 500 100 1 %

Rest HR
EXC
COP SV
5000 ml/min 70/min 75 ml
Tak terlatih
Tak terlatih 22000 ml/min 195/min 113 ml
Terlatih 5000 ml/min 50/min 100ml
Terlatih 35000 ml/min 195/min 179 ml
 Acute Responses to Aerobic Exercise

•Volume Plasma
• Plasma darah meningkat
pada otot berkerja.
• Cairan tubuh turun 5%
• blood viscosity increases
 Oxygen
Oxygen Deficit Oxygen Debt
DEBT and Deficit
& Oxygen DEFICIT
Oxygen Debt(EPEOC)
“Steady State”
VO2

VO2 Untrained or people with

certain cardiorespiratory
diseases will have larger
DEBTS and DEFICITS
Rest

EXERCISE TIME
Onset Termination

Oxygen Deficit due to: delay in time for aerobic ATP production to
supply energy
Oxygen Debt due to:
• resynthesis of high energy pohosphates (CP, ATP)
• replace oxygen stores
• lactate conversion to glucose (gluconeogenesis)
• u HR, respiration, catecholamines, body temperature
 Training Adaptations to
Saat tidak aktivitas. Chronic Endurance
NC NC Exercise
VO2 = HR x SV x AVO2diff

Seharusnya: Seharusnya:
u time in diastole u preload
d afterload
u ventricle size
u blood volume

Submax Workload (measured at same pre-training workload)

NC NC
VO2 = HR x SV x AVO2diff
Hubungan
note: a d in afterload (mentioned above)
accompanied by a d in HR response translates into Pengaruh dari
a d myocardial VO2 at rest or at any workload latihan terhadap
Max Workload (measured at peak exercise) Komponen
NC menurut Fick
VO2 = HR x SV x AVO2diff

some studies show

a slight decrease
 Training Adaptations

1.Tekanan Arteria sedang

• NC Saat rest atau selama exercise
2.Systolic and Diastolic Blood Pressure
•usually NC at rest or during exercise
• Turun saat submaximal workload
• Mungkin turun terbatas saat rest
3. hypertensives
• Banyak studies mencatat rata-rata turun 9
mmHg
4.Total Peripheral Resistance and Afterload
• capillarization naik (more parallel circuits) r d TPR
• TPR turun r d Afterload (slight – not of major
significance)
 Training Adaptations

Respiratory Rate
• Rest: NC
• Submax exercise: Turun
• Max exercise: sedikit naik
• Tidal Volume
• Rest: NC
• Submax exercise: NC or slight u
• Max exercise: slight u
• Anaerobic Threshold (lebih tinggi) tidak peka
• Occurs at a higher percentage of VO2 max
• Pre-training: 50% VO2max
•Post-training: 80% VO2max
 Training Adaptations

• Mitochondria
• Jumalah naik, ukuran dan luas permukaan
membrane
• Aerobic Enzymes in Exercising Muscle
• u Krebs cycle enzymes (succinate dehydrogenase)
• u oxidation enzymes (carnitine acyltransferase)
• u electron transport enzymes (cytochrome oxydase)
• Fatty Acid & Glycogen Utilization
• u utilization of oxidative pathways to produce ATP
• Called the “glycogen sparring” effect
• d RER for any given submaximal workload
• u muscle glycogen stores (with high carbohydrate
diet)
 Training Adaptations

• d Platelet Aggregation
• u Fibrinolytic Activity
• d Circulating Catecholamines
• u vagal tone r d risk of arrhythmia
• No Appreciable Change in Resting Metabolic Rate
• Exception: training induced u in lean muscle mass
• Resistance to Pathological Events
• smaller infarct size and quicker recovery
• Less of a d in ventricular function during
ischemia
Tak berubah Turun//tak berubah Meningkatan
Meningkatan Meningkatan Meningkatan
Turun Turun Tak berubah

Kecil / tak Kecil / tak Kecil / tak

Ada Ada Ada
perubahan perubahan perubahan

Meningkatan

Tak berubah Tak berubah Turun

Turun Turun Tak berubah
Kesimpulan.
Cardiovascular/male/sesaat
Vareable Pre training Post training Endurance
runner
HR Rest 71 beats/min 59 36
HR Max 185 beats/min 183 174
SV Rest 65 ml/beat 80 125
SV Max 120 ml/beat 140 200
Q rest 4,6 l/min 4,7 4,5
Q Max 22,2 l/min 25,6 34,8
Heart Volume 750 ml 820 1,200
Blood Volume 4,7 L 5,1 6,0
Sys BPRest 135 mmHg 130 120
Sys BP max 210 mmHg 205 210
Dias BP rest 78 mmHg 76 65
Dias BP Max 82 mmHg 80 65
Respirasi
Vareable Pre Post Endurance
Runner
VE rest 7 l/min 6 6
VE max 110 L 135 195
TV rest 0,5 L 0,5 0,5
TV max 2,75 L 3,0 3,9
VC 5,8 L 6,0 6,2
RV 1,4 l 1,2 1,2
METABOLIC
Vareable Pre Post Endurance
Runner
A-vO2 diff Rest 6,0 ml/100ml 6,0 6,0
A-VO2 diff Max 14,5 ml/100ml 15,0 16,0
VO2 Rest 3,5 ml/kg/min 3,5 3,5
VO2 Max 40,5 ml/kg/min 49,8 76,7
Blood lactate Rest 1,0 mmol/L 1,0 1,0
Blood lactate maX 7,5 mmol/L 8,5 9,0
Body composisi
Vareable Pre Post Enduran
Runner
Weight Kg 79 77 68
Fat weight Kg 12,6 9,6 5,1
Fat-free weight Kg 66,4 67,4 62,9
Fat % 16,0 12,5 7,5

Latihan Dilakukan pada atlit wanita

dibandingkan dengan tidak latihan
Perpustakaan.

1. Brian J Sharkey; Physiology of

fitness; Human Kenetics
Publichers 1994
2. Per-olof Astrand, Kaare rodahl;
Textbook of Work Physiology
physiological Bases of
Exercise; Mc Graw-hill Book
Company,1998
3. Mc Ardle- Katch-Katch ; Exercise
Physiology, Lea&Febiger 1994.
4. Ann B Mc Naught, Robin
Callander ,Illustrated physiology, E&S
Livingstone ltd Edinburgh and London
1965.
5. Jack H Willmore/ David L costill,
Physiology of Sport and exercise, human
kenetic,1999
5. Stewart, j.v. basmajian: exercise in water,
edisi 3, williams&wilkins 1978.
6. W.F. Ganong, Review of Medical
Physiology, LMP, Los Altos, California,
1981.