Page 902 - Fundamentals of anatomy physiology
P. 902
Chapter 23 The Respiratory System 889
Clinical Note As diffusion takes place between fetal blood and maternal
blood, oxygen enters the fetal bloodstream until the PO2 reaches
Carbon Monoxide Poisoning The exhaust from auto- equilibrium at 30 mm Hg. At this PO2, the maternal hemoglo-
mobiles and other petroleum-burning engines, oil lamps, bin is less than 60 percent saturated, but the fetal hemoglobin
and fuel-fired space heaters contains carbon monoxide is over 80 percent saturated, as you can see on Figure 23–21. The
(CO). Each winter entire families die from carbon monoxide steep slope of the saturation curve for fetal hemoglobin means
poisoning. Carbon monoxide competes with oxygen mol- that when fetal RBCs reach peripheral tissues of the fetus, the
ecules for the binding sites on heme units. Unfortunately, Hb molecules release a large amount of oxygen in response to
the carbon monoxide usually wins the competition. The a very small change in PO2.
reason is that at very low partial pressures it has a much
stronger affinity for hemoglobin than does oxygen. The Carbon Dioxide Transport
bond formed between CO and heme is extremely durable.
As a result, the attachment of a CO molecule essentially Carbon dioxide is generated by aerobic metabolism in pe-
makes that heme unit inactive for respiratory purposes. ripheral tissues. Carbon dioxide travels in the bloodstream in
three different ways. After entering the blood, a CO2 molecule
If CO molecules make up just 0.1 percent of inhaled either (1) is converted to a molecule of carbonic acid, (2)
air, enough hemoglobin is affected that human survival binds to hemoglobin within red blood cells, or (3) dissolves
becomes impossible without medical assistance. Treatment in plasma. All three reactions are completely reversible, al-
includes (1) preventing further CO exposure; (2) admin- lowing carbon dioxide to be picked up from body tissues and
istering pure oxygen, because at sufficiently high partial then delivered to the alveoli. Let’s consider the events that take
pressures, the oxygen molecules gradually replace CO at place as blood enters peripheral tissues in which the PCO2 is
the hemoglobin molecules; and if necessary, (3) transfusing 45 mm Hg.
compatible red blood cells.
Carbonic Acid Formation
levels are low for an extended time, red blood cells generate more
BPG. These factors improve oxygen delivery to the tissues, because Roughly 70 percent of the carbon dioxide absorbed by blood
when BPG levels are elevated, hemoglobin releases about 10 per- is transported as molecules of carbonic acid. Carbon dioxide is
cent more oxygen at a given PO2 than it would do otherwise. converted to carbonic acid through the activity of the enzyme
carbonic anhydrase in RBCs. The carbonic acid molecules im-
The production of BPG decreases as RBCs age. For this rea- mediately dissociate into a hydrogen ion and a bicarbonate
son, the level of BPG can determine how long a blood bank can ion, as described earlier (p. 888). We can ignore the intermedi-
store fresh whole blood. When BPG levels get too low, hemoglo- ate steps in this sequence and summarize the reaction as
bin becomes firmly bound to the available oxygen. The blood is
then useless for transfusions, because the RBCs will no longer re- CO2 + H O ÷ Hcarbonic anhydrase + + HCO3−
lease oxygen to peripheral tissues, even at a disastrously low PO2. 2
Fetal Hemoglobin Figure 23–21 A Functional Comparison of Fetal 23
and Adult Hemoglobin.
The RBCs of a developing fetus contain fetal hemoglobin. The Oxyhemoglobin (% saturation)
structure of fetal hemoglobin differs from that of adult hemo- 100
globin, giving it a much higher affinity for oxygen. At the same 90
PO2, fetal hemoglobin binds more oxygen than does adult he- 80
moglobin (Figure 23–21). This trait is key to transferring oxygen 70 Fetal hemoglobin
across the placenta. 60
50 Adult hemoglobin
A fetus obtains oxygen from the maternal bloodstream. At 40
the placenta, maternal blood has a relatively low PO2, ranging 30
from 35 to 50 mm Hg. If maternal blood arrives at the placenta 20
with a PO2 of 40 mm Hg, hemoglobin saturation is roughly 75 10
percent. The fetal blood arriving at the placenta has a PO2 close 0 20 40 60 80 100 120
to 20 mm Hg. However, because fetal hemoglobin has a higher PO2 (mm Hg)
affinity for oxygen, it is still 58 percent saturated.
