#Low carbon dioxide in blood free

A small amount of dissolved CO 2 produces a small rise in hydrogen ions which is capable of altering the blood pH. The conversion of carbonic acid (H 2CO 3) to a hydrogen and bicarbonate ion (H + + HCO 3 -) is almost instantaneous. Fig 1 - The reaction that produces bicarbonate within the body.įigure 1 shows how CO 2 dissolves in the blood. It is important to identify it as it can be mistaken for intoxication. Symptoms of acidosis include rapid breathing (to blow off CO 2), confusion, fatigue and headache. However, the main correction must be accomplished by the kidneys which can both increase hydrogen excretion to reduce the acidity of the blood and increase bicarbonate reabsorption to allow increased buffering of blood acidity. This allows one to “blow off” some CO 2 reducing the acidity of the blood. In such cases, the respiratory system attempts to compensate by increasing respiration rate ( hyperventilating). However, a disorder of the kidneys themselves such as chronic kidney disease may reduce HCO 3 – production. Conditions such as diabetic ketoacidosis can increase acid production. Metabolic acidosis can result from an excess of H + production or a reduction in the HCO 3 – buffer. It can be broadly classified as metabolic or respiratory acidosis. Thus the high O 2 concentrations reduce the CO 2 carrying capacity of blood, in accordance with the Haldane effect.Īcidosis occurs when the pH of the blood falls below 7.35.

#Low carbon dioxide in blood free

These hydrogen ions become free to react with bicarbonate ions to produce CO 2 and H 2O, where the CO 2 is exhaled. When the red blood cells reach the lungs, oxygen binds to the haemoglobin and promotes the R state, allowing the release of H + ions. It also prevents hydrogen entering the blood to lower pH, stabilising the pH. This contributes to the Bohr effect as O 2 release from haemoglobin is promoted in active tissues where H + concentration is higher. The H + created by the carbonic anhydrase reaction in the red blood cell binds to haemoglobin to produce deoxyhaemoglobin. The HCO 3 – can now act as a buffer against any hydrogen in the blood plasma. This HCO 3 – is transported back into the blood via a chloride-bicarbonate exchanger (aka anion exchanger/AE). CO 2 diffuses into the red blood cells and is converted to H + and HCO 3 – by an enzyme called carbonic anhydrase. This is explained in the diagram below (Figure 2). HCO 3 – ionsĦ0% of all CO 2 is transported through production of HCO 3 – ions in the red blood cell. This allows more O 2 to be picked up and transported in the blood. This stabilises the R state, which promotes the release of CO 2 (Haldane effect). When the blood cell reaches areas of high O 2 concentrations again (such as the lungs), it preferentially binds O 2. Bohr effect – it stabilises the T state of haemoglobin, promoting the release of O 2 from the other subunits of haemoglobin into the tissues that are most active, undergoing the most respiration and producing the most CO 2.Stabilising pH – CO 2 is unable to leave the blood cell to contribute to changes in pH.This is because release of O 2 from Hb promotes binding of CO 2.įormation of carbamino compounds achieves 2 goals: This occurs where O 2 concentration is lower (as in the active peripheries where O 2 is being consumed) and causes the CO 2 carrying capacity of the blood to increase. The Haldane effect also contributes to the formation of carbamino compounds. Carbamino formation is most effective at the periphery where CO 2 production is high due to cellular respiration. At high concentrations carbon dioxide directly binds to amino acids and the amine groups of haemoglobin to create carbaminohaemoglobin.

CO 2 is transported in the blood in 3 ways:Ībout 30% of all CO 2 is transported as carbamino compounds.