Transportasi O2 dan CO2

pada
Sistem Pernafasan
Oxygen Transport

2
Total Body Oxygen Stores
 Oxygen in the Lung (~500 ml O2).

 Oxygen in the Blood (~850 ml O2).

 Oxygen in the Cells (very little except Mb-

bound).
4
 Physiology of respiration
Oxygen/Carbon dioxide interaction: Perfusion and Ventilation
Ventilation
O2 CO2
CO
CO 22 O2

Perfusion
 Physiology of respiration
Oxygen/Carbon dioxide interaction: Metabolism

Oxygen -> lungs -> alveoli -> blood

Oxygen

breath
CO2 produced by cellular metabolism
CO2 diffuses across the cell membrane into the
circulating blood. muscles + organs
lungs
5-10% carried in solution Oxygen
CO2 20-30% bound to haemoglobin
60-70% carried as bicarbonate in the red blood cell
cells
blood energy
Oxygen
+
Glucose
CO2
At the Lung Level
At the Tissue Level
9
 Oxygen Transport

 O2 is transported by the blood either,

◦ Combined with haemoglobin (Hb) in the red blood cells
(>98%) or,
◦ Dissolved in the blood plasma (<2%).
Oxygen Transport
 The resting body requires 250ml of O2
per minute.
 We have four to six billion haemoglobin
containing red blood cells.
 The haemoglobin allows nearly 70 times
more O2 than dissolved in plasma.
 Haemoglobin
Haemoglobin molecules can
transport up to four O2’s
Co-operative binding:
haemoglobin’s affinity for
O2 increases as its
saturation increases.

When 4 O2’s are bound to

Oxygen binding occurs in
haemoglobin, it is 100% saturated,
response to the high PO2 in the
with fewer O2’s it is partially
lungs
saturated.
 Oxygen Is Carried in Blood in 2
Forms

 Bound to hemoglobin in red blood cells.

 Dissolved in plasma. Normally insignificant.

Hemoglobin

 Each “heme” molecule is capable of binding with 1

O2 molecule and each “globin” molecule is
capable of binding with 1 CO2 molecule.
 So, each molecule of Hb can bind to either 4
molecules of O2 and 1 molecule of CO2
 100 ml of blood has about 15 gm of Hb, at Hct =
0.45

14
 Binding of O2 to 4 heme sites given by:
Hb  O2  HbO2
HbO2  O2  Hb (O2 ) 2
Hb (O2 ) 2  O2  Hb (O2 )3
Hb (O2 )3  O2  Hb (O2 ) 4

Equilibrium constants for different reactions

different
Binding of first O2 relatively low affinity
2nd, 3rd and 4th - much higher affinity

15
Oxygen as Oxyhemoglobin

 Each gram of Hb can store about 1.34 ml of

O2:
 1 L of blood (150 gm of Hb) can store about
208 ml of O2  Oxygen Capacity of Hb.
 With normal cardiac output, about 1040 ml of
O2 can be carried in blood per minute. (4 times
of the metabolic demands).

16
17
18
O2 Saturation.

 Units: percent.

 Fraction or percentage of all the

hemoglobin binding sites that are
currently occupied by oxygen.
Lets Now Look at Haemoglobin
Saturation
 Haemoglobin saturation is the
amount of oxygen bound by
each molecule of haemoglobin
 Each molecule of haemoglobin can carry four
molecules of O2.
 When oxygen binds to haemoglobin, it forms
OXYHAEMOGLOBIN;
 Haemoglobin that is not bound to oxygen is
referred to as DEOXYHAEMOGLOBIN.
Haemoglobin Saturation
 The binding of O2 to haemoglobin
depends on the PO2 in the blood and
the bonding strength, or affinity,
between haemoglobin and oxygen.
 The graph on the following page shows an
oxygen dissociation curve, which reveals
the amount of haemoglobin saturation at
different PO2 values.
The Oxygen Dissociation Curve

Reveals the amount of

haemoglobin saturation
at different PO2 values.
The Oxygen Disassociation Curve

In the lungs the partial

pressure is approximately
100mm Hg at this Partial
Pressure haemoglobin
has a high affinity to 02
and is 98% saturated.
 In the tissues of other
organs a typical PO2 is 40
mmHg here haemoglobin
has a lower affinity for O2
and releases some but
not all of its O2 to the
tissues. When
haemoglobin leaves the
tissues it is still 75%
saturated.
 Haemoglobin Saturation at High Values
Lungs at sea level:
PO2 of 100mmHg
haemoglobin is 98% Lungs at high
SATURATED elevations: PO2
of 80mmHg,
haemoglobin 95
% saturated
When the PO2 in the
lungs declines below
typical sea level values,
haemoglobin still has a Even though PO2
high affinity for O2 and differs by 20 mmHg
remains almost fully there is almost no
saturated. difference in
haemoglobin
saturation.
Haemoglobin Saturation at Low Values
Factors Altering Haemoglobin
Saturation
Factors Altering Haemoglobin
Saturation (Exercise)
Factors Affecting Haemoglobin
Saturation
 Blood acidity…
 Blood temperature…
 Carbon Dioxide concentration
Respiratory Response to Exercise

Factors affecting Disassociation

BLOOD TEMPERATURE
 increased blood temperature
 reduces haemoglobin affinity for O2
 hence more O2 is delivered to warmed-up
tissue

BLOOD Ph
• lowering of blood pH (making blood
more acidic)
• caused by presence of H+ ions from lactic
acid or carbonic acid
• reduces affinity of Hb for O2
• and more O2 is delivered to acidic sites
which are working harder

CARBON DIOXIDE CONCENTRATION

• the higher CO2 concentration in tissue
• the less the affinity of Hb for O2
• so the harder the tissue is working, the
more O2 is released
Oxygen Saturation of Hb
O 2 combined with Hb
SHbO2 (% saturation )   100
O 2 capacity of Hb

31
Four (5-6?) Things Change
Oxyhemoglobin Affinity

1. Hydrogen Ion Concentration, [H+]

 Carbon Dioxide Partial Pressure, PCO2
 Temperature
 [2,3-DPG]

 Special Case: Carbon Monoxide

 Hemoglobin variants
33
Factors Affecting Hb-O2 Affinity: Summary
 Hydrogen Ion:
◦ Increased H+ (decreased pH) increases H+ binding to Hb and
reduces O2 affinity (HbO2+H+HbH++O2).

 Carbon Dioxide (Bohr effect):

◦ Increased PCO2 increases CO2 binding to Hb and reduces O2
affinity (increased O2 delivery to tissue).
◦ Increased PCO2 increases H+ and reduces O2 affinity (fixed acid
Bohr effect).

 Temperature and 2,3-DPG (diphosphoglycerate):

◦ Increased temperature and 2,3-DPG reduces O2 affinity.
34
Exercise

 Increase temperature

 Increased PCO2 and

 Decreased pH (acidosis)
2,3-DPG

 2,3-DPG is a glycolytic intermediate

◦ accumulates to uniquely high levels in RBCs
-Increased 2,3-DPG right shift
-Decreased 2,3-DPG left shift

 Increased 2,3-DPG associated with hypoxia.

Conditions with Increased 2,3-DPG

 acclimatization to high altitudes.

 chronic lung disease; emphysema.
 anemia.
 hyperthyroidism.
 right to left shunt.
 congenital heart disease.
 pulmonary vascular disease.
Carbon Dioxide
Transport

39
At the Lung Level

40
At the Tissue Level

41
Carbon Dioxide Transport

 CO2 is transported in blood in dissolved form, as

bicarbonate ions, and as protein-bound carbamino
compound.

 Protein-bound CO2 (carbamino compounds):

 Amount of CO2 stored as carbamino compounds is

about 21 ml/L (4% of the total art CO2).

42
Carbon Dioxide Transport
 A majority amount of CO2 is transported in the
form of bicarbonate ions (HCO3-):
CO2  H2O 
CA
 H  HCO-3
 H2CO3 
 Amount of CO2 in HCO3- form at PCO2=40
mmHg is about 420 ml/L (90% of the total arterial
CO2).

43
Carbon Dioxide Transport

 Haldane Effect: Increasing O2-saturation reduces CO2

content and shifts the CO2 dissociation curve to
right.This is because, increasing PO2 leads to :
◦ Decrease in the formation of carbamino compound.
◦ Release of H+ ions from the hemoglobin and resulting in
dehydration of HCO3-.

44
45
46
Bicarbonate in RBCs.
 Carbonic anhydrase is present in RBCs
 CO2 forms carbonic acid which
dissociates to H+ and HCO3-
 H   HCO 3 
Carbonic Anhydrase
CO 2  H 2 O       
 H 2 CO 3 

 Released H+ is buffered by histidine

residues (imidazole group)

• Percent of the total PaCO2: 70%

Carbamino Compounds in RBCs.
 Approximately 30% of RBC contents is Hb

 CO2 forms carbamino hemoglobin

 Released H+ is buffered by histidine residues

(imidazole group)
• Percent of the total PaCO2: 23 %
 Tissue-Gas Exchange: Summary
 Gas exchange processes in the peripheral organs are
essentially opposite those in the lungs.
 O2 is released from the capillary blood to the tissues
and diffuses to the mitochondria where O2 is converted
to CO2 and energy (ATP) through cellular metabolism.
 CO2 diffuses from the tissues to the blood stream and is
transported to the lungs for elimination.
 The exchange of O2 and CO2 in the blood-tissue
exchange unit depends on PO2, PCO2, and also on O2 and
CO2 saturation curves.

50
Gas Transport in Cell

51
52
Pelepasan CO2

 Dilakukan oleh:
1. isositrat dehidrogenase
2. α-ketoglutarat dehidrogenase

 Pelepasan CO2 tidak mengkonsumsi

oksaloasetat.

53
 Siklus ATP/ADP

 Berperan untuk menghubungkan proses-proses

yg menghasilkan P-berenergi-tinggi dgn proses
yg menggunakan P-berenergi-tinggi.
 ATP dikonsumsi & dibentuk kembali secara
kontinu.
 Depot ATP/ADP sangat kecil, sehingga hanya
cukup untuk mempertahankan jaringan aktif
dlm waktu beberapa detik saja.

54
Siklus ATP/ADP

ATP
CO2

Pernapasan: Penggunaan energi:

pembentukan energi - biosintesis makro-
dari; - karbohidrat molekul
- lemak - kontraksi otot
- protein - transpor ion aktif
- termogenesis

O2
ADP + Pi

55
 Fosforilasi Oksidatif

 Adalah sistem dalam mitokondria yang

memasangkan respirasi dengan proses
pembentukan intermediat berenergi tinggi,ATP.

 Sistem ini memungkinkan organisme aerob

menangkap energi bebas dari substrat
respiratorik dalam jumlah lebih besar dibanding
organisme anaerob.

56
 Peran Rantai Respirasi

asam lemak
+ b-oksidasi
gliserol ATP
O2

glukosa Asetil KoA SAS 2H H2 O

rantai respirasi
Asam amino ADP

mitokondria

57
 Produk ATP pada Fosforilasi Oksidatif

Berdasarkan hipotesis kimiosmotik dari Mitchell

yaitu;
rantai bekerja --> proton dipompa keluar dari
membran dlm mitokondria --> pH antar
membran turun --> proton balik ke dalam
matrik lewat tonjolan ATP-sintase--> fosforilasi
ADP menjadi ATP.

58
 Produk ATP pada Fosforilasi Oksidatif

 Diperkirakan satu ATP disintesis setiap dua

proton melewati tonjolan tsb.
 Hasilnya ialah;
- 3 mol.ATP utk oksidasi 1 mol. NADH
- 2 mol.ATP utk oksidasi 1 mol. FADH2
 Laju fosforilasi oksidatif dikendalikan oleh;
NADH, oksigen,ADP

59
 Normal Blood gas values
 Arterial blood  Venous Blood

 pH=7.35-7.45  pH=7.30-7.40
 pCO2=35-45mmHg  42-48 mmHg
 pO2=80-100mmHg  35-45 mmHg
 HCO3-=22-28mEq/L  24-30 mEq/L

60
 Hypoxic Hypoxia

 Hypoxic hypoxia or hypoxemic hypoxia refers to

the condition in which the PaO2 and CaO2 are
abnormally low.
 This form of hypoxia is better known as
hypoxemia (low oxygen concentration in the
blood).
 This form of hypoxia can develop from:
◦ pulmonary shunting - low alveolar PO2
◦ diffusion impairment - V/Q mismatch

61
 Cyanosis

 When hypoxemia is severe, signs of cyanosis may

develop.
 Cyanosis is the term used to describe the blue-
gray or purplish discoloration seen on the
mucous membranes, fingertips, and toes
whenever the blood in these areas is hypoxemic.
 The recognition of cyanosis depends on the
acuity of the observer, on the lighting conditions,
and skin pigmentation.

62
 Polycythemia

 When pulmonary disorders produce chronic

hypoxemia, the hormone erythropoietin responds
by stimulating the bone marrow to increase RBC
production.
 An increased level of RBC’s is called
polycythemia.
 The polycythemia that results from hypoxemia is
an adaptive mechanism designed to increase the
oxygen-carrying capacity of the blood.

63
PULSEOXIMETRY
 Introduction

 The maintenance of optimal O2 delivery is the

core concern during anaesthesia

 “Oxygen lack not only stops the machine but

wrecks the machinery ”– J.S. Haldane.

 Monitoring of oxygenation using

pulseoximeter avoids many catastrophies
DEFINITION
 A NON INVASIVE TECHNOLGY TO
MONITOR OXYGEN SATURATION OF THE
HAEMOGLOBIN
HISTORY
 MATHEES- father of oximetry
 20 papers in1934 –1944
 HERTZMAN 1937 –use of photoelectric finger
plethsmography
 1975 –concept of pulse oximetry –Japan
 YELDERMAN &NEW -1983 –Nellcor pulse
oximeter
PRINCIPLES
 ABSORBTION SPECTRO PHOTOMETRY
 BEER LAMBERT LAW
 LAMBERT’S LAW states that when a light falls on a
homogenous substance,intensity of transmitted light
decreases as the distance through the substance
increase
 BEER’S LAW states that when a light is transmitted
through a clear substance with a dissolved solute ,the
intensity of transmitted light decreases as the
concentration of the solute increases
CONTD..
 Substances have a specific pattern of absorbing
specific wavelength –Extinction coefficient
Uses two lights of wavelengths
 660nm –deoxy Hb absorbs ten times as oxy hb
 940 nm – absorption of oxyHb is greater
 Lab oximeters use 4 wavelengths to measure 4
species of haemoglobin
 It =I o e –Ecd [Ecd –absorbance]
 DESIGN OF PULSEOXIMETER
 2 WAVELENGTHS-660nm [red] & 940nm[infra red]
The ratio of absorbencies at these two wavelengths
is calibrated empirically against direct measurements of
arterial blood oxygen saturation (SaO2) in volunteers, and
the resulting calibration algorithm is stored in a digital
microprocessor within the pulse oximeter.
 LED & PHOTODETECTOR
 Newer types of LED is based on aluminium gallium
arsenide system
 Signal processed in the micro processor
 Senses only the pulsatile flow
Oxygen desaturation
 Saturation is defined as ratio of O2
content to oxygen capacity of Hb
expressed as a percentage.
 Desaturation leads to Hypoxemia – a
relative deficiency of O2 in arterial blood.
PaO2 < 80mmHg – hypoxemia
CONTD…

 Oxygen saturation will not decrease until

PaO2 is below 85mmHg.
 At SaO2 of 90% PaO2 is already
60mmHg.
 Rough guide for PaO2 between saturation
of 90%-75% is PaO2 = SaO2 - 30.
 SaO2< than 76% is life threatening.
 Functional Saturation

 This is a measure of ratio between HbO2 and

sum of oxygenated and reduced Hb.

 Functional Saturation= HbO2

------------
HbO2 + Hb
 Types of Hypoxemia

1.Hypoxic hypoxemia
 PaO2  SaO2 – Normal Hb

2.Anaemic hypoxemia
Hb , Normal PaO2 & SaO2

3.Toxic hypoxemia
SaO2,Normal PaO2
 PaO2 [mmHg] SaO2 [%]

 Normal 97 to ≥80 97 to ≥95

 Hypoxia < 80 < 95
 Mild 60-79 90-94
 Moderate 40 – 59 75 – 89
 Severe <40 < 75
 Cardiovascular response to
hypoxemia
SPO2% HR BP Stroke SVR Response
volume

>80    No Reflex
chang
e
60-80   No  Direct
change
<60     Direct
 Uses of pulseoximetry
 Monitoring oxygenation During anaesthesiain ICU, PACU
during transport
 Monitoring oxygen therapy
 Assesment of perfusion
 Monitoring vascular volume
 Sleep studies -24-h ambulatory recordings of SpO2 is
useful for screening for daytime sleep sequelae
associated with the potential risk of this pathology in
OSAS during social activities.
 Advantages
 Simple to use

 Non-invasive

 Require no warm up time

 Especially in African &Asian patients

 Cost-effectiveness over ABG

Disadvantages
 Decrease in PAO2 before fall in SPO2

 Due to the shape of ODC

 SPO2 94% - PAO2 75%

Limitations

 Shivering patient -motion artefacts

 High intensity ambient light
 Perfusion of the patient
ear probe may be more reliable
 Abnormal pulses –erratic perfomance
 Penumbra effect
- light shunted directly to photo
dectector
Problems
 False positives and negatives
 Burn injury
 Pressure injuries
 Capnography
A powerful tool to objectively
monitor your patients ventilatory
status.
 Terminology: What is End Tidal
CO2?
O The non-invasive
measurement of CO2
exhaled at the airway at
the end of a breath
O Normal values are 33-42
mmHg
O (35-45 mmHg)

“capnos” = smoke
 Terminology

O Colorimetric
O Disposable
detector
O Litmus paper
O Color changes in
the presence of
CO2
 Terminology

O Capnogram
O Graphical tracing
or representation
of exhaled CO2 at
the airway
O Waveform
Terminology

O Capnograph
O Instrument
O Monitor that
provides a
number and a
waveform
O Capnography
The Gear
The Gear
 Physiology of Carbon Dioxide
• Oxygenation: The process of getting oxygen
into the body and to the tissues for metabolism,
is monitored with pulse oximetry.
• Ventilation: the process of eliminating CO2
from the body, is monitored with capnography.
 Physiology of Carbon Dioxide
• Capnography can provide information about the
profusion status.
• Example: Low cardiac output caused by
cardiogenic shock or hypovolemia wont carry as
much CO2 per minute back to the lungs.
ETCO2 will be reduced. Reduced perfusion to
lungs causes this phenomenon.
 Phases of Exhalation

O Beginning exhalation = no CO2 in breath

O Middle exhalation = Rapid rise in CO2

O End exhalation
O CO2 levels continue to gradually rise (alveolar
plateau)
O Peak just before inspiration (EtCO2)
Normal Waveform End of
Alveolar
Beginning of exhalation
plateau
exhalation

Beginning of
new breath
End of
inspiration

Clearing of anatomic dead space

What should you do with bagging?
What should you do with bagging?
What’s wrong with this waveform?
What does this indicate on intubated patient?
What’s happening with this non-intubated patient?
Is your bagging OK?
 Displaced Intubation
O The ETCO2 will respond much faster to the
displacement.
O ETCO2 is a monitor of ventilation, SPO2 is
oxygenation.

35 mmHg
 Non-Intubated Applications
O Bronchospastic Disease

O Hypoventilation States

O Shock States

O The list goes on…

The Head Injured Patient
Titration IS NOT hyperventilation. Intubating a head injured
patient and using capnography gives a means to closely
monitor CO2 levels.

Keep them between 30 and 35 mmHg

Titrate EtCO2