Compensatory Responses to an acid-base imbalance week 2 Flashcards
What stimulates the respiratory comensation response in metabolic acidosis? What cells are stimulated?
What is the response of these cells after stimulation? Specifically, what are the changes in pH, CO2, and HCO3-?
What happens to buffering reactions during respiratory compensation?
The CO2 produced by CA buffering is lost as the blood passes through the lungs so that the arterial PCO2 is unchanged from normal, although the pH is low. The red line in the attached figure lies on the PCO2 = 40 isobar. This fall in pH stimulates compensation. The decrease in ECF pH stimulates the peripheral chemoreceptors. This increases ventilation, reduces arterial PCO2 below the normal value of 40 torr and increases pH towards normal. This is respiratory compensation. It follows a –11 sl trajectory (greeen line).
As respiratory compensation restores the pH toward normal, buffering reactions are reversed:
↓CO2 + H2O ← H2CO3 ← H+ + HCO3 -
HHb → H+ + Hb-
Note that all buffering rxns are reversed, not just Hb as shown.
What are the limitations of respiratory compensation?
Respiratory compensation for metabolic acidosis (HNC excess) produces systemic hypocapnia. So CO2 diffuses from the cerebral-spinal fluid (CSF) to the body, causing the CSF pH to increase. This reduces the central chemoreceptor-stimulated ventilation, partly offsetting the increased stimulation of the peripheral chemoreceptors caused by the low arterial pH. Thus, there are two competing effects: ventilatory stimulation (low arterial pH acting on peripheral receptors) and ventilatory inhibition (high CSF pH acting on the central chemoreceptor). As a consequence, respiratory compensation stops short of completely correcting the pH.
Central chemoreceptors stop peripheral chemoreceptors from driving CO2 to dangerously low levels.
Explain the RC (respiratory compensation) line on the Davenport nomogram.
The line labeled RC in FIGURE 11 (attached) shows the balance between these respiratory stimulating and inhibiting effects. It represents the maximum possible respiratory compensation (RC).
During respiratory compensation, pH and HCO3 – change by sliding up or down a line with slope –11 in the Davenport nomogram up to the RC line.
Can never get past RC line with respiratory compensation. are stuck at this point until renal compensation kicks in.
Explain how renal compensation restores pH back to normal in metabolic acidosis.
Explain how this looks on the Davenport nomogram.
In FIGURE 11 (attached), the point where the green arrow stops represents maximum respiratory compensation. However, it is possible for the body to completely restore pH to normal. This occurs as a result of H+ secretion into the urine by the kidneys and by renal ammonia production. For each H+ that is secreted into the urine (after all of the filtered HCO3 – has been reabsorbed), and during ammonia production, new HCO3 – enters the body. This added HCO3 – titrates excess H+ and over 3 to 4 days the added HCO3 – restores pH to 7.4. The trajectory is along the RC line because as HCO3 – is slowly added the pH changes, reducing the stimulation of the respiratory system. Ventilation decreases; PaCO2 moves closer to 40; and CSF PCO2 increases. Hence respiratory drive from central chemoreceptor increases, and maximum respiratory compensation is maintained.
In sum:
During renal (kidney) compensation of a metabolic acidosis/alkalosis:
- PCO2 changes back to normal (renal and respiratory compensation working at the same time) and
- pH and HCO3 – change back to normal by sliding up or down the RC line in the Davenport nomogram.
As respiratory compensation restores pH toward nromal, buffering rxns are reversed.
↓CO2 + H2O ← H2CO3 ← H+ + HCO3 -
HHb → H+ + Hb-
During this reaction, one buffer base (HCO3 - ) is lost for each one that is created (e.g., Hb- ).
Explain how this information can be used to calculate base excess and base deficit.
As respiratory compensation restores the pH toward normal, buffering reactions are reversed.
In this reaction one buffer base (HCO3 – ) is lost for each one that is created (e.g., Hb– ). This may be used to estimate the amount of NC acid that caused a metabolic acidosis. The amount of added NC acid is equal to the amount of base (a combination of HCO3 – , Hb– , and other NC bases) necessary to restore pH back to normal. Since respiratory compensation exchanges 1 HCO3 – for 1 NC base, we can estimate the amount of base needed to restore pH back to normal by hypothetically continuing respiratory compensation (pretending it could continue past the RC line).
This converts the unknown amount of NC buffers into only HCO3 – (which can be measured). Attached figure then represents the base deficit that was caused by the added acid. If HCO3 – had accumulated to produce an alkalosis, a similar process of extrapolating the respiratory compensation estimates the base excess (see slide 18 of notes). At the onset of respiratory acid/base problems, there is no base excess/deficit. PCO2 is changing and bound bases are exchanged, but total base is the same. However, when renal compensation occurs, bases are added or removed.
What may cause respiratory acidosis?
What increases in concentration in respiratory acidosis?
What is the role of respiratory compensation in respiratory acidosis?
Any problem that interferes with ventilation or pulmonary gas exchange causes CO2 to accumulate and produces a respiratory acidosis.
The excess H+ thus produced is first buffered by Hb. This shifts the CO2 reaction further to the right causing a measurable accumulation of HCO3 – .
↑CO2 + H2O → H2CO3 → H+ + HCO3 -
HHb ← H+ + Hb-
Get to a new pCO2 (new isobar). PCO2 will be constant until the respiratory problem is fixed.
- The condition is caused by a respiratory malfunction so respiratory compensation is not possible.
- PCO2 may not be normal, but it is constant.
Explain the role of renal compensation in respiratory acidosis.
What are the changes to PCO2, HCO3-, and pH?
Renal compensation adds HCO3 – to the plasma as the kidneys secrete H+ and produce ammonia. Some of the new HCO3 – reacts with some of the excess H+ bringing the pH closer to normal. Some of the new HCO3 – remains in the plasma raising [HCO3 –].
Arterial PCO2 does not change because the HCO3 – is added to the blood in the kidneys and the additional CO2 produced there is lost when the blood passes through the lungs before entering the arterial system.
Explain the limit of renal compensation in respiratory acidosis.
Explain the Davenport nomogram in this scenario.
There is a limit to renal compensation when plasma [HCO3 –] is high. This is shown by the MKC line in FIGURE 12 (attached). The initial step in urine formation is glomerular filtration. Each day 180 L of protein-free plasma filtrate is formed, containing about 24 meq/L HCO3 – , i.e. >4000 meq/day. Before the kidneys can add new HCO3 – to the body, all of the filtered HCO3 – must first be recovered. As the kidney makes more HCO3 – , plasma [HCO3 –] increases and the filtered load of HCO3 – to be reabsorbed also increases. The maximum rate of H+ secretion at each pH establishes a maximum value of plasma HCO3 – that can be achieved. This is shown by the MKC (maximum kidney compensation) line in FIGURE 12.
In sum:
During renal (kidney) compensation of a respiratory acidosis,
- PCO2 is constant
- pH and HCO3 – change back to normal by sliding up or down the (abnormal) PCO2 isobar in the Davenport nomogram to the MKC line.
Explain renal compensation in respiratory alkalosis.
What does the Davenport nomogram look like in this case?
During renal (kidney) compensation of a respiratory alkalosis,
- PCO2 is constant
- pH and HCO3 – change back to normal by sliding up or down the (abnormal) PCO2 isobar in the Davenport nomogram to the normal pH of 7.4.
In respiratory alkalosis, get back to normal pH because all the kidneys have to do is excrete bicarb. They do not have to produce anything that would increase their filtered load such as in respiratory acidosis. As a result, there is a chronically low HCO3- level. The body only cares about having a normal pH and not HCO3- level. However, this lower HCO3- level reduces buffering capacity.
Summary of compensatory responses
see reverse
T or F: • Respiratory compensation occurs in metabolic acid/base disorders only.
• Renal compensation occurs in all acid base disorders unless the problem is caused by kidney.
True.
During acidosis, part of the NCA buffering system is buffering of H+ by intracellular buffer.
What is required for H+ to move into cells?
- During acidosis [H+] is elevated. Part of the NC buffering system is buffering of H+ by intracellular buffer.
- H+ can enter a cell if the move is charge neutral
- • an anion must enter the cell with H+
- • or a cation must leave the cell.
What is the most common cation that moves in the opposite direction of H+ in cells?
In an acidosis, what is a possible consequence as it pertains to blood K+ levels?
- K+ is the most common cation that moves in the opposite direction of H+
- Therefore acid/base balance can affect K+ balance (and vice versa).
- In an acidosis, K+ leaving the cells can increase serum [K+] (hyperkalemia).
In an alkalosis, what is a possible consequence as it pertains to blood K+ levels?
What is the kidney’s role in this? Specifically, what part of the nephron?
- In an alkalosis, reduction of serum [H+] leads to dissociation of H+ from ICF buffers and H+ loss from cells.
- This is accompanied by transfer of K+ into the cells.
- If a large amount of K+ is transferred, serum [K+] will fall (hypokalemia).
- Kidney collecting duct (CD) cells participate in this process.
- In alkalosis, [H+] in CD cells decreases and [K+] increases.
- This facilitates the secretion of K+ and reduces the secretion of H+ into the CD fluid
- The excess excretion of K+ contributes to the hypokalemia.
What is the numerical relationship between pH and K+ levels?
A pH change of ±0.1 causes a change in [K+] p in the opposite direction, up to 0.7 mmol/L.
