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: slamet.sumarno@gmail.com

• 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.

• 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.
• All living cells require to get oxygen from the fluid around them and to get rid of corbon dioxide to it.

1.
Exchange O
2
1.
Air to blood
2.
Blood to cells
2.
Exchange CO
2
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.
Proses pernafasan.
1. External Respirasi
It has two phases: inspiration and
Ruang rugi
Anatomi:
Gas yanga
Ada pada
Jalan nafas expiration.
2. Internal Respirasi.
150 CC a. Tranportasi (sirkulasi).
b. Buffer

Inspirasi is an active process in which the diaphragm and the external intercostal muscles increase the dimensions, and thus the volume, of the thoracic cage.
This decreases the pressure in the lungs and draws air in.
Tekanan alveoli minus
3 s/d 10 mmHg < dari
760 mmHg.
• Normal expiration is the passive process.
• The inspiratory muscle relax and the elastic tissue of the lungs recoils, returning the thoracic cage to its smaller, normal dimensions.
• This increases the presure in the lungs and forces air out.

 Forced or labored inspiration and expiration are active proceses, dependent on muscle actions.
 Aktif inspirasi dibantu otototot: Scalani, Sterno cledo mastoideus, pektoralis, membantu angkat sternum dan costae ke depan atas.
Tekanan alveoli turun sampai 100-80 mmHg.
 Aktif ekspirasi dibantu otototot : Abdominalis,
Latisimus dorsi Inspirasi. Ekspirasi

1.
Tranportasinya
Exchange O
2 a. Air to blood in cells b. Blood to cells
2.
Exchange CO
2
1.
Cells to blood
2.
Blood to air
3.
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

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

Eksteranal 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

2
2
• Kemampuan jantung (COP= HR
X Stroke volume).
• Tahanan perifer.
• Fleksibilitas pembuluh darah.
• Lumen.
• Vikositas.
• Hb.
• Saturasi darah dll.

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

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.

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

1.
Airway Resistance
2.
Diameter
3.
Mucous blockage
4.
Bronchoconstriction
5.
Bronchodilation
6.
Alveolar compliance
1.
Surfactants
2.
Surface tension
7.
Alveolar elasticity

1.
Volume paru a. RV b. ERV c. TV d. IRV
2. Capasitas paru a. Capasitas inspirasi b. Capasitas Ekspirasi c. Capasitas vital d. Capasitas total paru.
e. Kapasitas residual
VCI
TV
1200 cc
1000
500
1900-3300
PRIA
3,3
0,5
VCE 1,0
VR 1,2
V TOTAL 6,0
WANITA
1,9
0,5
0,7
1,1
4,2

Clinical Cardiovascular Anatomy & Physiology
Concepts, Definitions, & Principles
A.
LETAK.
B.
UKURAN.
C.
LAPISAN
JANTUNG .
D.
RONGGA .
E.
KATUP DAN
SEKAT.
F.
SYARAF
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.

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.

2
2
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: O
2
& CO
2
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.
O
2
& CO
2 transport
2.
White Blood Cells (WBC)
1.
Immune defense
2.
Phagocytosis
3.
Platelets: clotting

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

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 lymph vessels
Figure 15-18b: Fluid exchange at the capillary

Left Main CA
Circumflex
Layers of the Arterial Wall
Right CA
Left Anterior Descending Coronaria Arteri
Marginal Branch

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
> 100
70-80 cc
< 60 left ventricular performance u contractility normal contractility d contractility
(heart failure) 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
Heart Failure
Gambaran peningkatan saat dan akhir tekanan diastol
0
(lemah jantung)
Pada jantung normal SV= 60-80 CC Jantung terlatih SV= 90-250 CC
Jantung sakit SV = 40-50 CC

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 (AVO
2
D)
PENGUKURAN DALAM ml % - ml O
2
/ 100 ml blood
2. Oxygen Consumption (VO
2
) – 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: VO dan vena 2
= COP X Selisih O2 arteri
3.
Maximum Oxygen Consumption (VO
2max
) 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 VO
2 the heart muscle (myocardium)
"estimated" by RPP: HR X Sistole BP.
of
5. Functional Aerobic Impairment: predicted VO
2max
- attained VO
2max predicted VO
2max mild 27% - 40% moderate 41% - 54% marked 55% - 68% severe > 69%

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)
2.
blood viscosity (V)
3.
hydrostatic pressure (P)
TPR = ( 8 ) ( V ) ( L )
( p
) ( r 4 )
4.
vessel radius (r)

Cardiorespiratory Control
Exercise Systemic Blood Flow: Autonomic influences
Sympathetic outflow & circulating catecholamines
• a 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
• 500 ml/min d to kidneys
400 ml/min u to skin
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 (VO
2
)
Satuan ukur relative dan absolute :
• Relative: ml O
2
/kg/min Absolute: ml/min or L/min
• Rata-rata VO
2max usia 40 th- 37 th (laki) ml/kg/min
•
Resting metabolic equivalent = 1 MET = 3.5 ml/kg/min
•
Oxygen consumption linked to caloric expenditure (1 liter of O
2 consumed = 5 kcal)
180
Heart
Rate
160
140
100
1.0
2.0
3.0
Oxygen Uptake (L / min)
HR – VO
2 relationship is linear until about
90% VO
2max
50 150
Workloads (Watts)
250

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
Stroke
Volume
(ml/beat
120
110
70
25% 50% 75%
Percentage of VO
2 max

4. Stroke Volume
•
Meningkat sampai 1.5 kali istirahat bila exercise
•
Tahap peningkatan 40% - 50% VO
2 max
•
Venous return naik End Diastole Volume
(Starling mechanism)
•
End Systole Volume naik sesuai kemampuan kontraksi myocard.
•
Tahanan perifer 58% rest, max exercise: 83%
Stroke
Volume
(ml/beat
120
110
70
25% 50% 75%
Percentage of VO
2 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% O
2 arteri

Saat exercise 85% O
2 arterial
Acute Responses 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
 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
8. Aliran darah ke kulit.
Naik saat durasi rendah
Exercise
•
Turun saat latihan tinggi(krn peningkatan ke otot).
•
Naik selama exercise recovery percepatan penurunan suhu dan dan bufer.

• 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

Daerah
Pencernaan
Ren
Cerebral
Coronaria
Otot kasar
Kulit
Lain-lain
Rest A-v
O2/100ml
4,1
1,3
6,3
14,0
8,4
-
1,0 light
1100 12%
900 10%
750 8%
350 4%
4500 47%
1500 15%
400 4 %
Moderat max
600
600
750
750
12500
1900
500
300 1%
250 1%
750 3 %
1000 4 %
22.000 88%
600 2%
100 1 %
Rest
EXC
Tak terlatih
Tak terlatih
Terlatih
Terlatih
COP
5000 ml/min
22000 ml/min
5000 ml/min
35000 ml/min
HR
70/min
195/min
50/min
195/min
SV
75 ml
113 ml
100ml
179 ml

Acute Responses to Aerobic Exercise

Oxygen Deficit
“Steady State”
VO2
Oxygen Debt(EPEOC)
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.
NC
VO
2
Chronic Endurance
NC
= HR x SV x AVO
2 diff
Exercise
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
VO
2
= HR x SV x AVO
2 diff note: a d in afterload (mentioned above) accompanied by a d in HR response translates into a d myocardial VO
2 at rest or at any workload
Max Workload (measured at peak exercise)
NC
VO
2
= HR x SV x AVO
2 diff
Hubungan
Pengaruh dari latihan terhadap
Komponen menurut Fick 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 VO
2
• Pre-training: 50% VO
2 max
•Post-training: 80% VO
2 max max

Training Adaptations
• Mitochondria
• Jumalah naik, ukuran dan luas permukaan membrane
• Aerobic Enzymes in Exercising Muscle
• u Krebs cycle enzymes (succinate dehydrogenase)
• u b oxidation enzymes (carnitine acyltransferase)
• u electron transport enzymes (cytochrome oxydase)
• Fatty Acid & Glycogen Utilization
• u utilization of b 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
Meningkatan
Turun
Kecil / tak
Ada perubahan
Tak berubah
Turun
Turun//tak berubah
Meningkatan
Turun
Meningkatan
Meningkatan
Tak berubah
Kecil / tak
Ada perubahan
Kecil / tak
Ada perubahan
Tak berubah
Turun
Meningkatan
Turun
Tak berubah

sesaat
Vareable
HR Rest
HR Max
SV Rest
SV Max
Q rest
Q Max
Heart Volume
Blood Volume
Sys BPRest
Sys BP max
Dias BP rest
Dias BP Max
Pre training
71 beats/min
185 beats/min
65 ml/beat
120 ml/beat
4,6 l/min
22,2 l/min
750 ml
4,7 L
135 mmHg
210 mmHg
78 mmHg
82 mmHg
Post training Endurance runner
5,1
130
205
76
80
59
183
80
140
4,7
25,6
820
36
174
125
200
4,5
34,8
1,200
6,0
120
210
65
65

Vareable Pre Post
VE rest
VE max
TV rest
TV max
VC
RV
METABOLIC
7 l/min
110 L
0,5 L
2,75 L
5,8 L
1,4 l
Vareable Pre
A-vO2 diff Rest
A-VO2 diff Max
VO2 Rest
VO2 Max
Blood lactate Rest
Blood lactate maX
6
135
0,5
3,0
6,0
1,2
6,0 ml/100ml
14,5 ml/100ml
3,5 ml/kg/min
40,5 ml/kg/min
1,0 mmol/L
7,5 mmol/L
Post
6,0
15,0
3,5
49,8
1,0
8,5
Endurance
Runner
6
195
0,5
3,9
6,2
1,2
Enduranc e Runner
6,0
16,0
3,5
76,7
1,0
9,0

Vareable
Weight Kg
Fat weight Kg
Fat-free weight Kg
Fat %
Pre
79
12,6
66,4
16,0
Post
77
9,6
67,4
12,5
Enduran
Runner
68
5,1
62,9
7,5
Latihan Dilakukan pada atlit wanita dibandingkan dengan tidak latihan

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.