When alveolar PO2 is decreased to as low as 60 mm Hg, what happens to the arterial hemoglobin saturation?
Explanation
This question uses a specific point on the oxygen-hemoglobin dissociation curve to illustrate the 'plateau' portion, which ensures near-normal oxygen loading in the lungs even when alveolar PO2 is significantly reduced.
Other questions
What is the normal average intracellular partial pressure of oxygen (PO2), as determined by direct measurement in experimental animals?
How many times more rapidly can carbon dioxide diffuse through tissues compared to oxygen?
What is the approximate partial pressure of carbon dioxide (PCO2) in the venous blood leaving the tissues under normal conditions?
What is the primary role of the Bohr effect in gas exchange?
Under normal conditions, what percentage of the total oxygen transported from the lungs to the tissues is carried in the dissolved state in the plasma and blood cells?
According to the oxygen-hemoglobin dissociation curve, what is the usual oxygen saturation of systemic arterial blood, which typically has a PO2 of about 95 mm Hg?
What is the average amount of oxygen released from hemoglobin to the tissues by each 100 ml of blood flow under normal, non-exercising conditions?
What is the normal value for the utilization coefficient, which represents the percentage of oxygenated hemoglobin that gives up its oxygen to the tissues as it passes through capillaries?
Which factor is known to shift the oxygen-hemoglobin dissociation curve to the left, indicating an increased affinity of hemoglobin for oxygen?
What is the primary limiting factor for the rate of oxygen usage by cells when the intracellular PO2 is above 1 mm Hg?
Carbon monoxide (CO) is particularly dangerous because it binds to hemoglobin with approximately how much more tenacity than oxygen?
What is the most prevalent form in which carbon dioxide is transported from the tissues to the lungs?
Which enzyme, found inside red blood cells, is crucial for the rapid conversion of CO2 and water into carbonic acid?
The phenomenon where the chloride content of venous red blood cells is greater than that of arterial red blood cells is known as what?
What is the primary mechanism of the Haldane effect?
What is the normal value for the respiratory exchange ratio (R) for a person on a normal diet consuming average amounts of carbohydrates, fats, and proteins?
What is the normal pressure differential that drives the diffusion of CO2 from intracellular fluid (PCO2 46 mm Hg) to interstitial fluid (PCO2 45 mm Hg)?
According to Figure 41-7, what is the effect on peripheral tissue PCO2 when blood flow is decreased to one-quarter of normal?
What is the primary function of hemoglobin's role as a 'tissue oxygen buffer' system?
During strenuous exercise, the utilization coefficient can increase from its normal value of 25 percent to as high as what range?
What happens to the oxygen-hemoglobin dissociation curve when the blood becomes slightly acidic, with the pH decreasing from a normal value of 7.4 to 7.2?
In hypoxic conditions lasting longer than a few hours, what substance in the blood increases, causing a rightward shift of the oxygen-hemoglobin dissociation curve?
How much oxygen is normally transported in the dissolved state to the tissues by each 100 ml of arterial blood flow?
A patient severely poisoned with carbon monoxide (CO) can be treated by administering pure O2. Why is this treatment effective?
What is the approximate percentage of total CO2 transported from the tissues to the lungs in the form of carbaminohemoglobin and in combination with plasma proteins?
According to the carbon dioxide dissociation curve in Figure 41-14, what is the normal concentration of CO2 in the blood in all its forms?
The Haldane effect approximately doubles the amount of CO2 released from the blood in the lungs. What is the additional amount of CO2 lost due to this effect, as shown in Figure 41-15?
What is the typical pH change that occurs in the blood as it passes from the arteries (pH 7.41) to the veins and acquires CO2?
Why does a person using fats exclusively for metabolic energy have a respiratory exchange ratio (R) of about 0.7?
What is the minimum O2 pressure normally required for full support of the chemical processes that use oxygen in the cell?
In the lungs, what is the pressure difference that causes all the required CO2 diffusion out of the pulmonary capillaries into the alveolar air?
What is the maximum amount of oxygen that can combine with the hemoglobin in 100 ml of blood from a normal person, if the hemoglobin is 100 percent saturated?
How does hemoglobin help maintain a nearly constant PO2 in the tissues, setting an upper limit on tissue PO2?
What is the approximate PCO2 of arterial blood entering the tissues?
During strenuous exercise, which combination of factors acts to shift the oxygen-hemoglobin dissociation curve to the right in muscle capillary blood?
What condition is described as 'diffusion-limited' oxygen usage by cells?
A carbon monoxide (CO) partial pressure of only 0.4 mm Hg in the alveoli can cause what percentage of hemoglobin to become bound with CO instead of O2?
Under normal resting conditions, what is the average amount of CO2 transported from the tissues to the lungs in each 100 ml of blood?
By what factor does the enzyme carbonic anhydrase accelerate the reaction rate between CO2 and water in red blood cells?
What is the primary reason why tissue PO2 is determined by a balance between the rate of O2 transport to tissues and the rate of O2 use by tissues?
When a carbonic anhydrase inhibitor like acetazolamide is administered, what is the potential effect on tissue PCO2?
The text states that CO2 can diffuse about 20 times as rapidly as O2. What is the main implication of this difference for gas transport?
What is the average blood pH of venous blood leaving the tissues?
When a person breathes air with an alveolar PO2 of 500 mm Hg, the maximum oxygen saturation of hemoglobin can never rise above what level?
The normal PCO2 in blood ranges from 40 mm Hg in arterial blood to 45 mm Hg in venous blood. How much CO2 (in volume percent) is exchanged during this normal transport?
What is the primary reason that carbon monoxide poisoning is especially dangerous and lacks obvious signs like cyanosis?
Which effect is described as being quantitatively far more important in promoting CO2 transport than the Bohr effect is in promoting O2 transport?
When the intracellular PO2 is below 1 mm Hg, what becomes the limiting factor for the rate of oxygen usage?
How does the Haldane effect contribute to the displacement of CO2 from the blood into the alveoli?