OXYGEN EQUILIBRIUM AND
TRANSPORT
CHAPTER 8
HOW DOES BLOOD CARRY OXYGEN?
• MIXED VENOUS BLOOD ENTERS THE PULMONARY
CAPILLARY WITH A PO2 OF ABOUT 40 mmHg AND IS
EXPOSED TO AN ALVEOLAR PO2 OF ABOUT 100
mmHg. OXYGEN DIFFUSES DOWN THIS PRESSURE
GRADIENT INTO THE BLOOD UNTIL EQUILIBRIUM IS
ESTABLISHED. LIQUID(PLASMA) AND CELLULAR
(ERYTHROCYTES) COMPONENTS OF BLOOD
CARRY OXYGEN. OXYEN IS DISSOLVED IN PLASMA
OR COMBINED WITH HEMOGLOBIN IN THE
ERYTHROCYTE.
OXYGEN DISSOLVED IN PLASMA
• THE RELATIONSHIP BETWEEN PARTIAL PRESSURE AND
DISSOLVED OXYGEN IS DIRECT AND LINEAR.
• IN NORMAL ARTERIAL BLOOD WITH PaO2 = 100mmHg, THERE
IS ABOUT 0.3 ml/dl OF DISSOLVED OXYGEN.
• IF AN INDIVIDUAL BREATHES PURE OXYGEN, THE PaO2
INCREASES TO APPROXIMATELY 670 mmHg, THE
DISSOLVED OXYGEN WILL INCREASE TO ABOUT 2.0 ml/dl
• SOMEONE BREATHING PURE OXYGEN IN A HYPERBARIC
CHAMBER AT 3 ATM WOULD CARRY NEARLY 6.5 ml /dl OF
DISSOLVED OXYGEN. THIS AMOUNT IS ENOUGH TO
SUPPLY MOST TISSUE NEEDS BY ITSELF.
• DISSOLVED PLASMA OXYGEN CONTENT AT ANY PO2 IS
CALCULATED AS FOLLOWS
DISSOLVED OXYGEN = PaO2 X 0.003 ( HENRY’S LAW)
OXYGEN COMBINED WITH HEMOGLOBIN
HEMOGLOBIN COMBINED WITH OXYGEN
• MOST OXYGEN IS TRANSPORTED IN CHEMICAL
COMBINATION WITH Hb IN THE ERYTRHROCYTES.
• WHEN Hb IS NOT CARRYING OXYGEN, THE FE2+
ION ATTACHED TO IT HAS FOUR UNPAIRED
ELECTRONS. IN THIS DEOXYGENATED STATE,THE
MOLECULE EXHIBITS THE CHARACTERISTICS OF A
WEAK ACID. AS SUCH DEOXYGENATED Hb SERVES
AS AN IMPORTANT BLOOD BUFFER FOR
HYDROGEN IONS, A FACTOR CRITICALLY
IMPORTANT IN CO2 TRANSPORT.
• WHEN Hb IS CARRYING OXYGEN, ALL THE
ELECTRONS OF THE IRON ION BECOME PAIRED
AND Hb IS CONVERTED INTO ITS OXYGENATED
STATE OXYHEMOGLOBIN.
OXYGEN COMBINED WITH HEMOGLOBIN
HEMOGLOBIN COMBINED WITH OXYGEN
• HEMOGLOBIN-OXYGEN CARRYING CAPACITY
- ONE GRAM OF Hb CAN CARRY ABOUT 1.34 ml
OF OXYGEN
- AVERAGE BLOOD HB CONTENT = 15 G/ DL
Hb CARRYING CAPACITY = 1.34 X 15 = 20.1 ml/dl
COMPARE WITH THE BLOOD’S ABILITY TO
CARRY DISSOLVED OXYGEN
DISSOLVED OXYGEN = 100 mmHg X 0.003 = 0.3 ml/dl
HEMOGLOBIN SATURATION AND OXYGEN PARTIAL
PRESSURE
SATURATION IS A MEASURE OF THE PROPORTION OF
AVAILABLE Hb THAT IS ACTUALLY CARRYING OXYGEN
Hb SATURATION WITH O2 VARIES WITH CHANGES IN PaO2.
UNLIKE DISSOLVED O2, Hb SATURATION IS NOT LINEARLY
RELATED TO PaO2. INSTEAD,THE RELATIONSHIP FORMS AN
S-SHAPED CURVE.
ARTERIAL O2 SATURATION(SaO2) IS ABOUT 97.5% AT A NORMAL
PO2 OF100 mmHg. ONLY 75%OF THE Hb IN MIXED VENOUS
BLOOD IS HBO2. MIXED VENOUS O2 SATURATION (SvO2) IS
THEREFORE NORMALLY 75%,CORRESPONDING WITH A PvO2 OF
ABOUT 40 mmHg. IF Hb CONCENTRATION IS LOW (AS IN
ANEMIA), THE BLOOD O2 CONTENT IS LOW, ALTHOUGH THE Hb
PRESENT IS 100% SATURATED WITH O2.
HEMOGLOBIN SATURATION AND OXYGEN PARTIAL
PRESSURE
LIKEWISE, LOW SATURATION DOES NOT AUTOMATICALLY MEAN
THAT THE BLOOD O2 CONTENT IS BELOW NORMAL, ALTHOUGH
THIS IS GENERALLY THE MEANING. FOR EXAMPLE, Hb
CONCENTRTION MAY BE ABNORMALLY HIGH (POLYCYTHEMIA)
IN INDIVIDUALS WHO HAVE CHRONIC HYPOXIA, THUS CAUSING
THE BLOOD O2 CONTENT TO BE NORMAL, ALTHOUGH THE Hb
SATURATION IS LOW.
HEMOGLOBIN CAPACITY FOR OXYGEN
• TOTAL OXYGEN CONTENT OF THE BLOOD
THE TOTAL OXYGEN CONTENT OF THE BLOOD EQUALS THE
SUM OF THAT DISSOLVED AND CHEMICALLY COMBINED WITH
HEMOGLOBIN.
CaO2 = ( 0.003 X PaO2 ) + ( Hb X 1.34 X SaO2)
OXYHEMOGLOBIN EQUILIBRIUM CURVE
PHYSIOLOGICAL ADVANTAGES OF THE HBO2
CURVE
• THE OXYHEMOGLOBIN DISSOCIATION CURVE
DEMONSTRATE THE EFFECTS OF OXYGEN
LOADING (ASSOCIATION) AND UNLOADING
(DISSOCIATION) IN THE LUNGS AND TISSUES.
• POINT A REPRESENTS FRESHLY ARTERIALIZED
BLOOD LEAVING THE LUNGS, WITH A PaO2 OF
APPROXIMATELY 100 mmHg AND SO2 OF
APPROXIMATELY 97%.
• POINT V REPRESENTS PERFUSION OF BLOOD OF
BODY TISSUES,OXYGEN UPTAKE CAUSES A FALL IN
BOTH PaO2 ( APPROXIMATELY 40 mmHg) AND SaO2
(APPROXIMATELY 73%)
Normal Loading and Unloading of Oxygen
PHYSIOLOGICAL ADVANTAGES OF THE HBO2
CURVE
• NORMAL LOADING AND UNLOADING OF
OXYGEN
• THE DIFFERENCE BETWEEN THE ARTERIAL AND
VENOUS OXYGEN CONTENTS IS NORMALLY ABOUT
5 ml/dl. THE C(a-v)O2 IS THE AMOUNT OF OXYGEN
GIVEN UP BY EVERY 100 ml OF BLOOD ON EACH
PASS THROUGH THE TISSUES. TISSUES EXTRACT
ABOUT 5 ml OF OXYGEN FROM EACH 100 ml OF
ARTERIAL BLOOD.
• THE C(a-v)O2 INDICATES OXYGEN EXTRACTION IN
PROPORTION TO BLOOD FLOW.
• THE PRINCIPLE RELATING C(a-v)O2 TO PERFUSION
IS USED TO MONITOR TISSUE OXYGENATION AT
THE BEDSIDE.
HbO2 CURVE SHIFTS
EFFECTS OF PCO2, pH, TEMPERATURE, AND
2,3 DPG
• THE DECREASED AFFINITY OF HEMOGLOBIN FOR OXYGEN,
OR THE RIGHT CURVE SHIFT CAUSED BY HIGH PCO2, IS
KNOWN AS THE BOHR EFFECT.
• CARBAMINOHEMOGLOBIN(CO2 COMBINED WITH Hb).
INCREASED CARBAMINOHEMOGLOBIN DECREASES Hb’S O2
AFFINITY, SHIFTING THE HbO2 CURVE TO THE RIGHT.
• IN HYPOTHERMIA THE HBO2 CURVE SHIFTS TO THE LEFT, AND
MORE O2 REMAINS ATTACHED TO Hb. AT 20ºC, Hb IS 100%
SATURATED AT A PO2 OF 60 mmHg. ALTHOUGH THIS GREATLY
REDUCES O2 RELEASE TO THE TISSUES, HYPOTHERMIC
TISSUES REQUIRE LESS O2.
CLINICAL SIGNIFICANCE OF CHANGES IN Hb’S
OXYGEN AFFINITY
•
EFFECT OF DECREASED Hb AFFINITY FOR O2 ON SaO2 AND PaO2 IN THE
TISSUES. TUBE A REPRESENT BLOOD IN SYSTEMIC CAPILLARIES AS IF pH
AND PCO2 DID NOT CHANGE. TUBE B SHOWS WHAT ACTUALLY ACCURS IN
SYSTEMIC CAPILLARIES (PCO2 RISES AND pH DECREASES) THUS Hb’S O2
AFFINITY DECREASES,RELEASING O2 INTO THE PLASMA. PO2 IN PLASMA
INCREASES AUGMENTING THE DIFFUSION GRADIENT INTO THE TISSUES.
OXYGEN DELIVERY TO THE TISSUES
• PaO2 AND SaO2 ALONE DO NOT PROVIDE AN ADEQUATE
ASSESSMENT OF THE PATIENT’S OXYGENATION. THE PaO2
CAN BE 100 mmHg AND THE SaO2 98%, AND YET THE ANEMIC
PATIENT WITH 5 g/dl OF Hb SUFFERS SERIOUS TISSUE
HYPOXIA.
• EVEN WITH A NORMAL Hb, PaO2 AND SaO2, A PERSON CAN
STILL SUFFER FROM INADEQUATE OXYGEN DELIVERY IF THE
BLOOD FLOW ( i.e. CARDIAC OUTPUT = Q) IS INADEQUATE.
THUS THE TENDENCY TO EVALUATE THE OXYGENATION
STATUS AS NORMAL JUST BECAUSE PaO2 AND SaO2 ARE
NORMAL MUST BE RESISTED.
• IN SUMMARY, FACTORS THAT AFFECT OXYGEN DELIVERY TO
THE TISSUES INCLUDE: 1- Hb CONCENTRATION 2- SaO2 3CARDIAC OUTPUT (SaO2 AND PaO2 DETERMINE CaO2.
OXYGEN DELIVERY DEPENDS ON CaO2 AND Q).
CYANOSIS
• WHEN THE Hb MOLECULE RELEASES O2 AND BECOMES
DEOXYHEMOGLOBIN(DESATURATED Hb ), IT CHANGES IT
SHAPE AND TURNS DEEP PURPLE. SEVERELLY HYPOXIC
PEOPLE MAY HAVE ENOUGH DESATURATED Hb IN THEIR
BLOOD THAT THE SKIN, NAILBEDS, LIPS, AND MUCOUS
MEMBRANES APPEAR BLUE OR BLUE-GRAY.
• MOST OBSERVERS DO NOT PERCEIVE CYANOSIS UNTIL THE
AVERAGE DESATURATED Hb CONCENTRATION IN THE
CAPILLARIES IS AT LEAST 5 g PER 100 ml ( 5 g/dl).
• TWO TYPES OF CYANOSIS EXIST: PERIPHERAL AND CENTRAL
CYANOSIS. PERIPHERAL IS CAUSED BY EXCESSIVELY LOW
SvO2 WHILE SaO2 MAY BE NORMAL.
• CYANOSIS DOES NOT ALWAYS ACCOMPANY SEVERE
HYPOXEMIA, AND CYANOSIS IS SOMETIMES PRESENT IN THE
ABSENCE OF HYPOXEMIA.
HEMOGLOBIN ABNORMALITIES
• CARBOXYHEMOGLOBIN
• THE Hb MOLECULE HAS AN AFFINITY FOR CARBON
MONOXIDE 210 TIMES GREATER THAN ITS AFFINITY FOR O2.
THIS MEANS THAT BREATHING AIR (21%O2) AND 0.1% CO
PUTS O2 AND CO ON EQUAL FOOTING IN COMPETING FOR Hb
BINDING SITES.
• CO NOT ONLYDECREASES THE AMOUNT OF Hb AVAILABLE
FOR O2 TRANSPORT, IT ALSO IMPAIRS Hb’S RELEASE OF O2 AT
THE TISSUES.
• FETAL HEMOGLOBIN
• METHEMOGLOBIN
• SICKLE CELL HEMOGLOBIN