Oxygen Transport

1
Oxygen Transport

• Chapter VI

2
Oxygen Transport

• An understanding of oxygen transport is essential
  to the study of pulmonary physiology and to the
  clinical interpretation of arterial and venous
  blood gases.

3
Normal Blood gas values

• Arterial blood
• pH7.35-7.45
• Pco235-45mmHg
• Po280-100mmHg
• HCO3-22-28mEq/L

• Venous Blood
• pH7.30-7.40
• 42-48 mmHg
• 35-45 mmHg
• 24-30 mEq/L

4
Oxygen Transport

• The transport of oxygen between the lungs and the
  cells of the body is a function of the blood and
  the heart.
• Oxygen is carried in the blood in two forms -
  as dissolved oxygen in the blood
  plasma - chemically bound to the
  hemoglobin (Hb) that is encased in the
  erythrocytes, or RBCs

5
O2 Dissolved in Plasma

• As O2 diffuses from the alveoli into the
  pulmonary capillary blood, it dissolves in the
  plasma of the blood.
• At normal body and temperature about 0.003 ml of
  O2 will dissolve in 100 ml of blood for every 1
  mm Hg of Po2
• Vol represents the amount of O2 in milliliters
  that is in 100 ml of blood.
• In terms of total oxygen transport, a relatively
  small percentage of O2 is transported in the form
  of dissolved O2.

6
Dissolved Oxygen

• Henrys Law states that the amount of gas that
  dissolves is proportional to its partial
  pressure.
• Dissolved Oxygen.003 mls x PAo2 .003 x
  100.3mls of dissolved O2

7
O2 Bound with Hemoglobin

• Most of the O2 that diffuses into the pulmonary
  capillary blood rapidly moves into the RBCs and
  chemically attaches to the hemoglobin.
• Each RBC contains about 280 million Hb molecules,
  which are highly specialized to transport O2 and
  CO2.
• The normal hemoglobin value for the adult male is
  14 to 16 g and female is 12 to 15 g.

8
The Hemoglobin Molecule

• Normal adult hemoglobin consists of -four hemo
  groups which are the pigmented, iron-containing
  non-protein portions -four amino chains
  that collectively constitute globin (a protein)
• At the center of each heme group, the iron
  molecule can combine with one O2 molecule for
  form oxyhemoglobin - Hb O2 ltgt Hbo2
• The amount of O2 bound to Hb is directly related
  to the partial pressure of O2.

9
Fetal Vs. Adult Hemoglobin

• The globin, or protein portion of each adult Hb
  molecule consists of two identical alpha chains
  and two identical beta chains.
• Normal fetal Hb (Hb F) has two alpha chains and
  two gamma chains.
• These gamma chains increase hemoglobins
  attraction to O2 and facilitates transfer of
  maternal O2 across the placenta.
• Fetal Hb is gradually replaced with adult Hb (Hb
  A) over the first year of postnatal life.

10
Quantity of O2 Bound to Hb

• Each g of Hb is capable of carrying
  approximately 1.34 ml of O2 thus - O2 bound to
  Hb 1.34 ml O2 x g Hb
• At a normal Pao2 of 100 MM Hg, hemoglobin
  saturation (Sao2) is about 97 because of normal
  physiologic shunts -thebesian veins
  (Coronary circ.) -bronchial venous
  drainage -V/Q mismatch

11
Total Oxygen Content

• To determine the total amount of O2 in 100 ml of
  blood, the dissolved O2 and the O2 bound to Hb
  must be added together.
• The total oxygen content of specific blood is
  calculated as follows - Cao2 (Hb x 1.34 x
  Sao2) (Pao2 x 0.003) - Cvo2 (Hb x 1.34
  x Svo2) (Pvo2 x 0.003) -Cco2 (Hb x
  1.34) (PAo2 x .003)

12
Oxygen Dissociation Curve

• The O2 dissociation curve graphically illustrated
  the percentage of Hb that is chemically bound to
  O2 at each O2 pressure.
• The curve is S-shaped with a steep slope between
  10 and 60 mm Hg and a flat portion between 70 and
  100 mm Hg.
• The flat and steep portions of the curve each
  have a distinct clinical significance.

13
Significance of the Flat Portion

• The flat portion of the curve shows that the P02
  can fall from 100 to 60 mmHg and the Hg will
  still be 90 saturated with 02
• At pressures above 60mm Hg, the standard
  dissociation curve is relatively flat. This
  means the oxygen content does not change
  significantly even with large changes in the
  partial pressure of oxygen.

14
Significance of Steep Portion

• PO2 reductions below 60 mm Hg produce a rapid
  decrease in the amount of O2 bound to hemoglobin.
• Clinically, when the PO2 falls below 60 mm Hg,
  the quantity of O2 delivered to the tissue cells
  may be significantly reduced.
• As oxygen partial pressures decrease in this
  steep area of the curve, the oxygen is unloaded
  to peripheral tissue readily as the hemoglobins
  affinity diminishes.

15
The P50

• A common point of reference on the oxygen
  dissociation curve is the P50.
• The P50 represents the partial pressure at which
  the hemoglobin is 50 saturated with oxygen,
  typically 26.6 mm Hg in adults.
• The P50 is a conventional measure of hemoglobin
  affinity for oxygen.

16
Shifts in the P50

• In the presence of disease or other conditions
  that change the hemoglobins oxygen affinity and,
  consequently, shift the curve to the right or
  left, the P50 changes accordingly.
• An increased P50 indicates a rightward shift of
  the standard curve, which means that a larger
  partial pressure is necessary to maintain a 50
  oxygen saturation, indicating a decreased
  affinity.
• Conversely, a lower P50 indicates a leftward
  shift and a higher affinity.

17
Factors that effect the 02 Dissociation

• pH- Change in the blood pH
• Temperature-temp increases the curve moves to the
  right
• 2,3 Diphosphoglycerate-Increases 2,3 DPG results
  in decreased affinity
• Carbon monoxide

18
Clinical Significance of Shifts

• Individuals with PaO2s within normal (80-100)
  limits are rarely afected by shift changes.
• However, when a patients PaO2 falls below 80, a
  shift to the right or left can have remarkable
  effects on the hemoglobins ability to pick up
  and release oxygen.

19
Right Shifts

• Right shift decrease the loading of oxygen onto
  Hb at the A-C membrane. -Decreased affinity
• The total oxygen delivery may be much lower than
  indicated by a particular Pao2 when the patient
  has some disease process that causes a right
  shift.
• Right shift curves enhance the unloading of
  oxygen at the tissue level.

20
Left shift

• Left shift curves enhance the loading capability
  of oxygen enhance the loading capability of
  oxygen a the A-C membrane.
• The total oxygen delivery may be higher than
  indicated by a particular Pao2 when the patient
  has some disease process that cause a left shift.
• Left shift curves decreases the unloading of
  oxygen at the tissue level.

21
Total Oxygen Delivery

• The total amount of oxygen delivered to the
  peripheral tissues is dependent on
• the bodys ability to oxygenate blood
• the hemoglobin concentration
• the cardiac output
• Total O2 delivery (DO2) is calculated
• DO2 QT x (CaO2 x 10)
• O2 delivery decreases when there is a decline in
  blood oxygenation, hemoglobin concentration, or
  cardiac output.

22
Arterial-Venous Difference

• The arterial-venous oxygen content difference,
  C(a-v)O2, is the difference between the CaO2 and
  the CvO2.
• The normal C(a-v)O2 is about 5 vol.
• Clinically, the C(a-v)O2 can provide useful
  information regarding the patients
  cardiopulmonary status.

23
Oxygenation Consumption

• The amount of oxygen extracted by the peripheral
  tissues during the period of one minute is called
  oxygen consumption or VO2.
• Oxygen consumption is calculated by
• VO2 QT C(a-v)O2 x 10
• O2 consumption is commonly indexed by the
  patients body surface area (BSA) and calculated
  by
• VO2 / BSA
• Normal VO2 index is between 125 - 165

24
Factors Affecting VO2

• Factors that increase O2 consumption
• exercise - seizures
• shivering - increased temp
• Factors that decrease O2 consumption
• skeletal relaxation
• peripheral shunting
• certain poisons
• decreased temperature

25
Oxygen Extraction Ratio

• The oxygen extraction ratio (O2ER) is the amount
  of oxygen extracted by the peripheral tissues
  divided by the amount of O2 delivered to the
  peripheral cells.
• O2ER CaO2 - CvO2 / CaO2
• normal O2ER is .25
• Under normal circumstances an individuals Hb
  returns to the alveoli approximately 75
  saturated with O2.

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Factors that affect O2ER

• Factors that increase O2ER
• decreased cardiac output
• increased oxygen consumption
• anemia
• decreased arterial oxygenation
• Factors that decrease O2ER
• increased cardiac output
• skeletal relaxation
• peripheral shunting
• hypothermia - increased Hb
• increased arterial oxygenation

27
Mixed Venous O2 Saturation

• Normally, the SvO2 is about 75, however,
  clinically an SvO2 of about 65 is acceptable.
• Factors that decrease the SvO2
• decreased CO
• increased O2 consumption
• Factors that increase the SvO2
• increased CO - peripheral shunting
• skeletal relaxation
• hypothermia

28
Mechanisms of Pulmonary Shunting

• Pulmonary shunting is defined as that portion of
  the cardiac output that enters the left side of
  the heart without exchanging gases with alveolar
  gases (true shunt) or as blood that does exchange
  gases with alveolar gases but does not obtain a
  PO2 that equals that of normal alveolus
  (shunt-like effect).
• Regardless of the type of shunt the physiologic
  effect is the same, hypoxemia.

29
True Shunt

• Clinical conditions that cause true shunt can be
  grouped under two major categories
• anatomic shunts
• congenital heart disease
• intrapulmonary fistula
• vascular lung tumors
• capillary shunts
• The sum of the anatomic and capillary shunts is
  referred to as true, or absolute shunt and
  refractory to O2.

30
Shunt-Like Effect

• When pulmonary capillary perfusion is in excess
  of alveolar ventilation, a shunt-like effect is
  said to exist.
• Common causes of this form of shunting are
• hypoventilation
• uneven distribution of ventilation
• alveolar-capillary diffusion defects
• Any of the previously mentioned phenomenon can be
  corrected by O2.

31
Venous Admixture

• The end result of pulmonary shunting is venous
  admixture.
• Venous admixture is the mixing of shunted,
  non-reoxygenated blood with reoxygenated blood
  distal to the alveoli.
• When venous admixture occurs, shunted and
  oxygenated blood mixes until the PO2 throughout
  all plasma of the newly mixed blood is in
  equilibrium and all the Hb molecules carry the
  same number of oxygen molecules.

32
Shunt Equation

• Pulmonary shunting and venous admixture are
  common complications in respiratory disorders,
  knowledge of the degree of shunting is often
  desirable when developing patient care plans.
• The amount of intrapulmonary shunting can be
  calculated by using the classic shunt equation
• QS/QT CcO2 - CaO2 / CcO2 - CvO2

33
Clinical Significance of Shunts

• Pulmonary shunting below 10 reflects normal lung
  status.
• A shunt between 10 and 20 is indicative of an
  intrapulmonary abnormality, but is seldom of
  clinical significance.
• Pulmonary shunting between 20 and 30 denotes
  significant intrapulmonary disease and may be
  life-threatening.
• Pulmonary shunting greater than 30 is a
  potentially life-threatening situation and
  aggressive support is needed.

34
Tissue Hypoxia

• Tissue hypoxia means that the amount of oxygen
  available for cellular metabolism is inadequate.
• There are four main types of hypoxia
• hypoxic hypoxia - circulatory hypoxia
• anemic hypoxia - histotoxic hypoxia
• Hypoxia leads to anaerobic mechanisms that
  eventually produces lactic acid and cause the
  blood pH to decrease.

35
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

36
Anemic Hypoxia

• Anemic hypoxia is when the oxygen tension in the
  arterial blood is normal, but the oxygen-carrying
  capacity of the blood is inadequate.
• This form of hypoxia can develop from
• a low amount of Hb in the blood
• a deficiency in the ability of Hb to carry O2
• Increased cardiac output is the main compensatory
  mechanism for anemic hypoxia.

37
Circulatory Hypoxia

• In circulatory hypoxia, the arterial blood that
  reaches the tissue cells may have a normal O2
  tension and content, but the amount of of
  blood--and therefore the amount of O2--is not
  adequate to meet tissue needs.
• The two main causes of circulating hypoxia are
• stagnant hypoxia
• arterial-venous shunting

38
Histotoxic Hypoxia

• Histotoxic hypoxia develops in any condition that
  impairs the ability of tissue cells to utilize
  oxygen.
• Clinically, the PaO2 and CaO2 in the blood are
  normal, but the tissue cells are extremely
  hypoxic.
• The PvO2, CvO2 and SvO2 are elevated because
  oxygen is not utilized.
• One cause of this type of hypoxia is cyanide
  poisoning.

39
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.

40
Polycythemia

• When pulmonary disorders produce chronic
  hypoxemia, the hormone erythropoietin responds by
  stimulating the bone marrow to increase RBC
  production.
• An increased level of RBCs is called
  polycythemia.
• The polycythemia that results from hypoxemia is
  an adaptive mechanism designed to increase the
  oxygen-carrying capacity of the blood.