Compensatory Response to an Acid/Base Imbalance

Question 1

What happens to CO2 in CA buffering?

Answer 1

It is unchanged! 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

Question 2

Explain chemoreceptors that respond to a decrease in ECF ph. How do they interact?

Answer 2

1. Intially peripheral chemoreceptors respond to increase ventilation thus reducing arterial PCO2
2. This increased ventilation causes hypocapnia— so the central chemoreceptor-stimulated ventilation, partly offsetting the
   increased stimulation of the peripheral chemoreceptors caused by the low arterial pH.

Ventiltoin stimulation by the low pH- peripheral chemorecetors

Ventilatory inhibition- by high CSF pH offsetting respiratory compensation

Question 3

What line does resp comp run on

Answer 3

On the -11 line (remember when CO2 is changing we aren’t on an isobar)

Question 4

What is the RC line?

Answer 4

The max possible resp compensation. It shows the balance between these respiratory stimulating and
inhibiting effects.

Remember that during resp comp we are sliding up or down a line with -11 slope.

Question 5

Resp comp can’t usually restore pH but renal can. What’s renal comp diong to restore pH

Answer 5

1. This occurs as a result of H+ secretion into the
   urine by the kidneys and by renal ammonia production.
2. Each time an H+ is secreted in urine a new HCO3- is made (assuming all the filterd bicarb has been reabsorbed)

This happens over 3-4 days.

Question 6

Why is renal comp of metabolic acidosis along the RC line

Answer 6

As we make more HCO3- we are slowly changin pH, reducing the stimulation of the resp system. As ventilation decrease, PCO2 moves closer to 40 and CSF PCO2 increases so we are still maxing out resp compensation

Question 7

Two main things that happen in metabolic acidosis/alaklosis

1. What happens to PCO2
2. pH and HCO2?

Answer 7

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.

Question 8

How can we hypothetically measure the base needed to restore pH?

Answer 8

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 tells us our base deficit

Question 9

What is happening at the onset of acid/base problems to the base deficit?

Answer 9

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.

Question 10

What happens in resp alkalosis/acidosis?

Answer 10

1. 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
   –.
2. there is no respiratory compensation because the underlying problem is respiratory.

Problem with pulmonary gas exchange or ventiatlion= resp alkalosis or acidosis.

Question 11

Explain what happens in resp acidosis in terms of renal comp

Answer 11

1. Kidneys secrete K+ and make ammonia– for each seretion a new HCO3- is made. This bicarb can react to H+ bringing the pH closer to normal.
2. Arterial PCO2 doesn’t hcange because the new HCO3- and the additional CO2 is lost when blood passes lungs.

Question 12

What are the limitations of renal comp?

Answer 12

1. WHen plasma HCO3 is high- because all the filtered HCO3 has to be reabsorbed before the kidneys make more HCO3-.
2. THe max rate of H+ secretion at each pH establishes a max value of plasma HCO3

Question 13

Impportant facts about renal comp during resp acidosis and resp alkalosis.

Answer 13

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.

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.

Question 14

Explain what happens in resp comp and renal comp for acidosis and alkalosis

Answer 14

Acidosis

1. Resp comp- increase ventilation which decrease PCO2 pushing the bicarb equation away from H+ + HCO3—> H20 + CO2
2. Renal Comp- Increase H+ excretation and increas bicarb production. Increase bicarb binds to H+ pushing quation towards water and carbon dioxide

Alkalosis

1. Resp comp- Decrease ventialtion and increase PCO2
2. Decrease H+ secretion and increase HCO3 excretaion

Question 15

When does resp comp occu?

Renal comp?

Answer 15

Respiratory compensation occurs in metabolic acid/base disorders only.

Renal compensation occurs in all acid/base disorders unless the problem is caused by kidney.

Question 16

Which line on davenport does Hb relate to?

Answer 16

Hb titration curve= (-11 sl line)

Question 17

What quadrants are you in for metabolic and respitatotry alkalosis and acidosis? What lines are you working to move towards?

Answer 17

1. Metabolic alkalosis- moves towards RC then down towards -11 (still on 40 isobar just need to move towards 7.4pH)
2. Respartory acidosis- moves towards MKC
3. MEtabolic Acidosis- towards RC line and up towards -11 (still on 40 isboar just needs to move up towards -11 line)
4. Respiratory alkalsis- down from -11 line– returns to pH but doesn’t reestablish buffering capabilites

Question 18

Explain what happens in K+ acid/base imbalacen

Answer 18

Consider acidosis

1. Part of buffering is buffering H+ by intracellular proteins so when H+ enters either A. Anion must enter wtih it B. a cation must leave (usually K+)

In acidosis- H+ enters to be buffered so K+ leaves making ECF hyperkalemic

In alkalosis- low serum H+ makes ICF buffers disscoiate and H+ loss from the cell, so K+ moves into the cell this causes hypokalemia.

Question 19

What happens with K+/acid/base in the CD and kidney cells that can be very dangerous?

Answer 19

When we have alkalosis, intracellular buffers unbind and go to ECF and K+ goes into the cell causes serum hypokalemia. (all cells)

in CD

1. When we have an increase in K+ intracellular, this facilitales K+ secretion and reduces H+ secretion. The resulting decrease of H+ excretion reduces bicarbonate reabsorption and
   compensates for the alkalosis. But, it also results in excess excretion of K+ and contributes to hypokalemia.

Question 20

What changes in K+ can induce secondary changes in acid base

Answer 20

inappropriate aldosterone secretion
• loss of body fluids high in K+ (e.g., sweat, vomit, diarrhea)
• insulin excess or deficiency