Adam suffers from severe emphysema. Gas exchange in his lungs is not adequate, and he requires supplemental oxygen. But even though his blood carbon dioxide levels are elevated, his blood pH is close to normal. Considering the urinary system, explain how this can occur.
3 answers
Dr Sarah can you respond to this?
This is a very complex process. Here is a good review for you.
"4.5.3 Chronic Respiratory Acidosis: Renal Bicarbonate Retention
With continuation of the acidosis, the kidneys respond by retaining bicarbonate.
If the respiratory acidosis persists then the plasma bicarbonate rises to an even higher level because of renal retention of bicarbonate.
Thus in a chronic respiratory acidosis there are TWO factors present which elevate the plasma bicarbonate:-
Firstly: The acute physicochemical change and consequent buffering esp by intracellular protein. (Immediate onset - as occurs with an acute respiratory acidosis.)
Secondly: The renal retention of bicarbonate as renal function is altered by the elevated arterial pCO2 and additional bicarbonate is added to the blood passing through the kidney. (Slow onset)
Studies have shown that an average 4 mmol/l increase in [HCO3-] occurs for every 10mmHg increase in pCO2 from the reference value of 40mmHg. For example, if arterial pCO2 has risen from 40mmHg to 60mmHg (due to decreased alveolar ventilaton) and remained elevated for several days, then this chronic rise of "2 tens" (i.e. 60-40=20mmHg rise = 2 rises of 10mmHg) results in a rise of plasma bicarbonate by 8 from its reference value of 24mmol/l up to 32 mmol/l. Consequently, we would predict that if this chronic respiratory acidosis was the only base disorder present, then plasma bicarbonate would be 32mmol/l.
The renal response in underway by 6 to 12 hours with a maximal effect reached by 3 to 4 days. This maximal effect is not sufficient to return plasma pH to normal, but because of the additional renal contribution, the pH is returned towards normal much more than occurs in an acute respiratory acidosis.
The response occurs because increased arterial pCO2 increases intracellular pCO2 in proximal tubular cells and this causes increased H+ secretion from the PCT cells into the tubular lumen. This results in:
1)increased HCO3 production which crosses the basolateral membrane and enters the circulation (so plasma [HCO3] increases.)
2)increased Na+ reabsorption in exchange for H+ and less in exchange for Cl- (so plasma [Cl-] falls)
3)increased 'NH3' production to 'buffer' the H+ in the tubular lumen (so urinary excretion of NH4Cl increases)"
"4.5.3 Chronic Respiratory Acidosis: Renal Bicarbonate Retention
With continuation of the acidosis, the kidneys respond by retaining bicarbonate.
If the respiratory acidosis persists then the plasma bicarbonate rises to an even higher level because of renal retention of bicarbonate.
Thus in a chronic respiratory acidosis there are TWO factors present which elevate the plasma bicarbonate:-
Firstly: The acute physicochemical change and consequent buffering esp by intracellular protein. (Immediate onset - as occurs with an acute respiratory acidosis.)
Secondly: The renal retention of bicarbonate as renal function is altered by the elevated arterial pCO2 and additional bicarbonate is added to the blood passing through the kidney. (Slow onset)
Studies have shown that an average 4 mmol/l increase in [HCO3-] occurs for every 10mmHg increase in pCO2 from the reference value of 40mmHg. For example, if arterial pCO2 has risen from 40mmHg to 60mmHg (due to decreased alveolar ventilaton) and remained elevated for several days, then this chronic rise of "2 tens" (i.e. 60-40=20mmHg rise = 2 rises of 10mmHg) results in a rise of plasma bicarbonate by 8 from its reference value of 24mmol/l up to 32 mmol/l. Consequently, we would predict that if this chronic respiratory acidosis was the only base disorder present, then plasma bicarbonate would be 32mmol/l.
The renal response in underway by 6 to 12 hours with a maximal effect reached by 3 to 4 days. This maximal effect is not sufficient to return plasma pH to normal, but because of the additional renal contribution, the pH is returned towards normal much more than occurs in an acute respiratory acidosis.
The response occurs because increased arterial pCO2 increases intracellular pCO2 in proximal tubular cells and this causes increased H+ secretion from the PCT cells into the tubular lumen. This results in:
1)increased HCO3 production which crosses the basolateral membrane and enters the circulation (so plasma [HCO3] increases.)
2)increased Na+ reabsorption in exchange for H+ and less in exchange for Cl- (so plasma [Cl-] falls)
3)increased 'NH3' production to 'buffer' the H+ in the tubular lumen (so urinary excretion of NH4Cl increases)"
if you need more, here is the source Dr Sarah, MD gave you : http://www.anaesthesiamcq.com/AcidBaseBook/ab4_5.php
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