According to Henry's law, the amount of oxygen dissolved in blood is directly proportional to the PO2 of the blood
O2 bound to hemoglobin is 98.5% while O2 dissolved in plasma is 1.5%
Hemoglobin is a protein that consists of 4 copies of the globin protein all bound together in a quaternary structure with heme groups in each protein; iron is in each of these groups. Can be oxygenated or deoxygenated
Hemoglobin saturation = O2 bound to Hb/Max capacity of Hb to bind O2 * 100
Factors that determine Hb saturation include:
Blood PO2
Amount of hemoglobin in blood
Anemia is diagnosed when a blood test shows a hemoglobin value of <13.5 g/dL in males and <12.0 g/dL in females
As PO2 increases, hemoglobin saturation increases until it reaches 60 mmHg
A) Unloaded O2
B) systemic venous
C) systemic arterial
The more oxygen binds to hemoglobin, the higher oxygen affinity becomes
During the slope of the PO2 vs saturation graph, blood passes through the pulmonary arteries to get oxygenated and then passes through the systemic arteries where oxygen then goes to the tissue
ideal unloading of oxygen to tissue is between 20-60 mmHg
O2 bound to Hb doesn't contribute to the partial pressure of O2 in the blood. It is the plasma that contributes
Pulse oximeter measures oxygen saturation
O2 binds to globin in hemoglobin
Most oxygen from alveoli is moved into the hemoglobin so PO2 remains lower in the blood (<2% dissolved) to facilitate simple diffusion
AS you move into the tissue, plasma PO2 is lower than RBC PO2 and at its lowest in mitochondria PO2 so, with the help of the diffusion gradient, oxygen moves from the RBC, to the plasma, and finally into the mitochondria
In most tissue, hemoglobin is still 75% oxygenated when the oxygen leaves to the mitochondria
Active hyperemia is when there is less oxygen in the blood leading to vasodilation to occur to get more oxygen in the blood
O2 is lowest in the mitochondria because it is needed for aerobic respiration
If the saturation curve shifts to the right, then it has a less affinity for oxygen making Hb saturated slower
If the saturation curve shifts to the right, then there is a greater affinity for oxygen making Hb getting saturated faster
If a higher temperature is present, this allows for more metabolization to take place, so we would need more O2 causing the saturation curve to shift to the right. Vice versa for cold
2,3 - DPG is made from glycolysis and allows for allosteric binding of hemoglobin causing a decreased affinity for oxygen. This causes the curve to shift to the right allowing for more O2 release
At a higher altitude, less O2 is present so DPG increases so that the hemoglobin affinity for O2 lowers allowing for more O2 release
When acidosis occurs, blood pH is lower allowing for more H+ ions to bind to hemoglobin causing a lower O2 affinity
Carbon monoxie distorts Hb so less O2 binds to it' it has a higher affinity for hemoglobin and can look saturated
Fetal hemogobin has a higher affinity for O2 than adult hemoglobin; prenatal steals O2 from mom
CO2 production is toxic because it generates H+. If rising H+ is not buffered, then changes in pH will take place making it more acidic
At rest, the body makes about 200 mL CO2/min diffusing into the blood. CO2 is more soluble in water than O2
Carbonic anydrase breaks down CO2 and water to form carbonic acid which can also turn into bicarbonate and H+
CO2 comes from cellular expiration, tissues, and breaking down sugar
CO2 moves using a high to low diffusion gradient from the cells to the capillaries where Hb is to the alveoli where it is expired
10% of CO2 goes into the plasma where it will allow HCO3- to buffer by binding to H+ and prevent blood from becoming acidic
Chloride shift prevents charge change from happening in the RBCs by moving Cl- ions in while HCO3- moves out
The venous side of the capillaries has the highest H+ concentration because CO2 is released in this area
H+ binds to deoxygenated Hb
Only a small amoutn of H+ generated in blood remains free. When released, H+ becomes a part of the buffer system
Total-blood carbon dioxide level = dissolved Co2 + HCO3- + CO2 in carbaminohemoglobin
dorsal respiratory group is controlled by inspiratory motor neurons and activate external intercostal muscles as well as the diaphragm
the ventral respiratory group is controlled by expiratory motor neurons and activate internal intercostal muscles
action potential signaling causes skeletal muscles, like the diaphragm, to contract