Transcript Fisioterapi Kardiovaskuler Pulmonal 2 Pertemuan 1

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
•
•
•
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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.
• 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.
Ruang rugi
Proses pernafasan.
1. External Respirasi Anatomi:
Gas yanga
It has two phases: Ada pada
Jalan nafas
inspiration and
expiration.
150 CC
2. Internal Respirasi.
a. Tranportasi (sirkulasi).
b. Buffer
Inspirasi is an active
• Normal expiration is
process in which the
the passive process.
diaphragm and the
• The inspiratory muscle
external intercostal
muscles increase the
relax and the elastic
dimensions, and thus
tissue of the lungs
the volume, of the
recoils, returning the
thoracic cage.
thoracic cage to its
This decreases the
smaller, normal
pressure in the lungs
and draws air in.
dimensions.
Tekanan alveoli minus • This increases the
3 s/d 10 mmHg < dari
presure in the lungs
760 mmHg.
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 O2 in cells
a. Air to blood
b. Blood to cells
2.
Exchange CO2
1.
2.
3.
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
1
Pertahanan Respiratory
system
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:
Dalam paru Dipengaruhi:
respirasi
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.
2.
3.
4.
5.
6.
7.
Jalan nafas yang adeguat.
Fleksibilitan otot, fasia, kulit
sangkar thorax.
Perfusi O2 dan CO2
Volume, Hb, Ph, Plasma
darah
Keadan pleurae
Pusat kontrol fungsi
pernafasan
Fungsi bufer.
Pengaruh eksternal terhadap
kemampuan tubuh suply O2
1. Kadar
Oksigen
udara.
2. Posisi tubuh
3. Usia jenis
kelamin.
Factors Affecting Ventilation
1.
2.
3.
4.
5.
6.
Airway Resistance
Diameter
Mucous blockage
Bronchoconstriction
Bronchodilation
Alveolar compliance
1. Surfactants
2. Surface tension
7. Alveolar elasticity
Lung
volumes
,
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
1200 cc
1000
500
1900-3300
PRIA
WANITA
VCI
3,3
1,9
TV
0,5
0,5
VCE
1,0
0,7
VR
1,2
1,1
V TOTAL 6,0
4,2
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.
2.
3.
4.
5.
Glucose
N–wastes
Proteins
Antibodies
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
lymph vessels
Figure 15-18b: Fluid exchange at the capillary
PENDAHULUAN.
danArtery
jantungAnatomy
normal
TheAnatomi
Normalarteria
Heartcoronarria
- Coronary
Left Main CA
Layers of the Arterial Wall
Circumflex
Right CA
Left Anterior Descending Coronaria Arteri
Marginal Branch
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.
2.
3.
4.
sympathetic nerve activity (most influential)
catecholamines (epinephrine norepinephrine)
amount of contractile mass
drugs
Starlings Law of the Heart and Contractility
SV
u contractility
> 100
70-80 cc
< 60
left
ventricular
performance
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
Normal
Heart Failure
Gambaran
peningkatan saat
dan akhir tekanan
diastol
(lemah jantung)
0
Pada jantung normal SV= 60-80 CC
Jantung sakit SV = 40-50 CC
Jantung terlatih SV= 90-250 CC
Kemampuan kontraksi
dipengaruhi oleh
1.
2.
3.
4.
5.
6.
7.
Kekuatan otot jantung.
Fleksibilitas otot jantung.
Tahanan perifer (aorta, jaringan, vena
Peningkatan maks selisih preload dan
afterload (dP/dt from LV pressure curve)
Pengaruh Positive/negative iontropic.
Ejection fraction (EF = SV/EDV) used in
clinical practice
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:
predicted VO2max - attained VO2max
predicted VO2max
mild
moderate
marked
severe >
27% - 40%
41% - 54%
55% - 68%
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)
2.
blood viscosity (V)
3.
hydrostatic pressure (P)
4.
vessel radius (r)
TPR = ( 8 ) ( V ) ( L )
( p ) ( r4)
Kontrol fungsi jantung paru.
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
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
consumed = 5 kcal)
180
Heart
Rate
160
140
HR – VO2
100
1.0
2.0
3.0
Oxygen Uptake (L / min)
50
150
250
Workloads (Watts)
relationship is
linear until about
90% VO2max
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
(ml/beat
110
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
(ml/beat
110
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
 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
Saat exercise
RR rest
Saat exercise
TV rest
Exercise:
: 6 Liters/min
: 175 Liters/min
: 12-18/ min
: 45-60/ min
: 500 cc
: 2250 cc
Sirkulasi saat rest /exc
Daerah
Rest A-v
O2/100ml
light
Pencernaan
Ren
Cerebral
Coronaria
Otot kasar
Kulit
Lain-lain
4,1
1,3
6,3
14,0
8,4
1,0
-
1100
900
750
350
4500
1500
400
12%
10%
8%
4%
47%
15%
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 %
SV
Rest
EXC
Tak terlatih
Tak terlatih
HR
70/min
5000 ml/min
22000 ml/min 195/min
75 ml
113 ml
Terlatih
Terlatih
5000 ml/min
50/min
35000 ml/min 195/min
100ml
179 ml
COP
Acute Responses to Aerobic Exercise
•Volume Plasma
• Plasma darah meningkat
pada otot berkerja.
• Cairan tubuh turun 5%
• blood viscosity increases
Oxygen
Debt
and Deficit
DEBT
& Oxygen
DEFICIT
Oxygen Deficit Oxygen
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
Saat tidak aktivitas.
NC
VO2
=
HR
NC
SV
x
x
Seharusnya:
u time in diastole
Training Adaptations to
Chronic Endurance
Exercise
AVO2diff
Seharusnya:
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
note: a d in afterload (mentioned above)
accompanied by a d in HR response translates into
a d myocardial VO2 at rest or at any workload
Max Workload (measured at peak exercise)
NC
VO2
=
HR
x
SV
some studies show
a slight decrease
x
AVO2diff
Hubungan
Pengaruh dari
latihan terhadap
Komponen
menurut Fick
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 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
Turun//tak berubah Meningkatan
Meningkatan
Meningkatan
Turun
Turun
Meningkatan
Tak berubah
Kecil / tak
Ada
perubahan
Kecil / tak
Ada
perubahan
Kecil / tak
Ada
perubahan
Meningkatan
Tak berubah
Tak berubah
Turun
Turun
Turun
Tak berubah
Kesimpulan.
Cardiovascular/male/sesaat
Vareable
Pre training
Post training
Endurance
runner
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
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
59
183
80
140
4,7
25,6
820
5,1
130
205
76
80
36
174
125
200
4,5
34,8
1,200
6,0
120
210
65
65
Respirasi
Vareable
Pre
Post
Endurance
Runner
VE rest
VE max
TV rest
TV max
VC
RV
7 l/min
110 L
0,5 L
2,75 L
5,8 L
1,4 l
6
135
0,5
3,0
6,0
1,2
6
195
0,5
3,9
6,2
1,2
METABOLIC
Vareable
Pre
Post
Enduranc
e Runner
A-vO2 diff Rest
A-VO2 diff Max
VO2 Rest
VO2 Max
Blood lactate Rest
Blood lactate maX
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
6,0
15,0
3,5
49,8
1,0
8,5
6,0
16,0
3,5
76,7
1,0
9,0
Body composisi
Vareable
Pre
Weight Kg
79
Fat weight Kg
12,6
Fat-free weight Kg 66,4
Fat %
16,0
Post
Enduran
Runner
77
9,6
67,4
12,5
68
5,1
62,9
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
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