12 Acid Base Disturbance

Question 1

Q: Compare oxygen levels in post alveolar venules and systemic arterial circulation to the venous side and pre alveolar arterioles.

Answer 1

A: much more to much less

Arterial pH = 7.4
Venous pH = 7.36

Question 2

Q: Define acidaemia.

Define alkalaemia.

What does -aemia describe?

Answer 2

A: Refers to lower-than-normal pH of blood

Refers to high-than-normal pH of blood

at a point in time, the condition of the blood

Question 3

Q: Define acidosis.

Define alkalosis.

What does -osis describe?

Answer 3

A: Describes circumstances that will increase [H+] and decrease pH

Describes circumstances that will decrease [H+] and increase pH

describes things causing change

Question 4

Q: What’s an acid? What must be regulated? why? What is a base? Relationship?

Answer 4

A: molecule that has a loosely bound H+ ion (proton) that it can donate

The acidity of the blood must be tightly regulated, marked changes will alter the 3D structure of proteins (enzymes, hormones, protein channels)

anionic (negatively charged ion) molecule capable of reversibly binding protons (to reduce the amount that are ‘free’)

dissociation eqm:

(conjugated) H+A- H+ and A-
- > concentration of acid determines where eqm lies

Question 5

Q: Application version of the dissociation eqm eqn. How can it be adjusted?

Answer 5

A: H2O + CO2 H2CO3 H+ + HCO3-

for inhalation of CO2 and movement of HCO3- around body (CO2 is considered an acid as it makes HCO3-)

(Increasing something on one side will push the equation in the opposite direction)

Question 6

Q: What capacity does the blood have? can?

Answer 6

A: The blood has an ENORMOUS buffering capacity that can react almost IMMEDIATELY to imbalances

Question 7

Q: What is pH related to? Unit? What’s wrong with this? Solution? (2) Summary eqn.

Answer 7

A: power of hydrogen/ concentration of H+ in blood

since it refers to charges-> use Eq/L (equivalence per L) (not mmol)

Eq system counts the charges

concentration of H+ in blood is actually so small= almost unmanageable -> [H+] = 0.00000004 Eq/L

solution= Sørensen scaled the data using a log10 transformation = much more manageable but negative -> easily fixed by applying a minus sign to the equation
-> -log10[H+] = 7.4

(inversa function of log) [H+] = 10^-pH

Question 8

Q: What are the 2 sources of acid for the body? Ratio? Where is most coming from?

Answer 8

A: respiratory acid eg CO2 as it makes HCO3-

metabolic acid eg pyrvate, lactic acid

~99:1 (most is coming from CO2 as part of NRG production in cells)

Question 9

Q: What does the Sørensen eqn allow? what is it? What does the Henderson eqn allow? what is it?

Answer 9

A: To calculate pH from proton concentration (or vice versa)
pH = - log10 [H+]

To calculate the dissociation constant (Ka) (compares how much was in the free form vs conjugated)
……..[H+][HCO3-]
K = ——————-
…………..[CO2]

Question 10

Q: What does the Henderson-Hasselbalch equation allow? What is the eqn?

Answer 10

A: allows us to take into consideration the dissociation constant (ie how strong of an acid it is) when calculating pH

combines sorenson and henderson eqn
…………………………….[HCO3-]
pH= pK + log10 —————
………………………………[CO2]

Question 11

Q: Estimate the volume of respiratory acid (i.e. CO2) produced in a typical adult over a 24-hour period. Explain.

Answer 11

A: ANS:
4 mL/dL (x50) = 200 mL/min (x60) = 1200 mL/h (x24) = 288 L/day = volume of CO2 produced everyday

WORKING:

CO2 flux is 4 mL/dL/min = for every 100 mL (1 dL) of blood that goes through the systemic capillaries, 4 mL of CO2 is added, on top of the CO2 already in there

Using this 4 mL value, we can extrapolate to a 5 L cardiac output (there are 50 decilitres (100 mLs) in 5 L of blood) by multiplying by 50. This gives us a CO2 production rate of 200 mL every minute

Question 12

Q: Arterial blood gas (ABG).

H+ 35.2 nmol/L
pCO2 4.56 kPa
pO2 7.09 kPa
BE (B) 0.3 mmol/L

What does this patient have?

Answer 12

A: from H+ calculate pH -> in this case pH is high

PaCO2 assesses the respiratory component and in this case is low

PO2 is low

BE (B) is assessing the metabolic component and is normal (base excess= calculated variable that uses measured bicarbonate and compares it to estimated bicarbonate-> able to do so since CO2 and bicarb. are in eqm)

Uncompensated respiratory alkalosis with moderate hypoxaemia

Question 13

Q: Basic guidelines for PaO2. What is normal? Mild hypoxaema? moderate hypoxaemia? severe hypoxaemia?

Threshold for BE (B)? higher than this? pH relation?

Answer 13

A: >10 kPa is normal
8-10 kPa is mild hypoxaemia
6-8 is moderate hypoxaemia
<6 kPa is severe hypoxaemia

-2 to 2 (over 2= more bicarbonate than there should be-> more protons bound-> pH will decrease)

Question 14

Q: If there’s an issue with the lungs to change pH, what fixes it and how fast? What does hyperventilation do?

Answer 14

A: (resp problem)

slow compensatory response by kidneys by changing HCO3- and H+ retention/secretion

hyperventilation-> lose CO2-> lose acid-> increase pH (cause alkalosis)

Question 15

Q: If there’s an issue with the kidneys to change pH, what fixes it and how fast?

Answer 15

A: (metabolic problem)

rapid compensatory response by lung to change CO2 elimination and therefore alter pH

Question 16

Q: Draw graph between acidosis and alkalosis. Relationship? (2) Describe graph (4).

Answer 16

A: REFER

An acidosis will need an alkalosis to correct
An alkalosis will need an acidosis to correct

first points= normal
second= uncompensated disorders (situation is bad and compensatory mechanisms haven’t kicked in)
third= partially compensated response
forth= provided the stimulus is still there-> fully compensated disorder

Question 17

Q: What would indicate uncompensated respiratory acidosis? (3) What needs to be done? how? Phases? (2) Result? Now called?

Answer 17

A: -high CO2 (possibly caused by low ventilation) causes

• increases H+ concentration
• BE (B) is normal as level of bicarb is normal for CO2
• reduce [H+]
• increasing bicarbonate to bind to some excess H+

1. acute phase- CO2 moving into erythrocytes combines with H2O in presence of carbonic anhydrase to form bicarbonate -> moves out of cell via AE1 transporter

increased plasma bicarbonate concentration pushes eqm backwards so that more conjugated carbonic acid forms -> increases pH

2. chronic phase- increase amount of bicarbonate reabsorbed in kidneys -> provides longer term mechanism to stabilise pH

• once corrective mechanisms are in action-> blood gases still show that pH is low (but closer to normal)
• pCO2 is still high if breathing has not changed
• BE (B) is now high

=> partially compensated resp acidosis

Question 18

Q: What can indicate partially compensated resp acidosis? (3) Eventually? What does this look like? (3) Now called?

Answer 18

A: -blood gases still show that pH is low (but closer to normal)

• pCO2 is still high if breathing has not changed
• BE (B) is now high

eventually compensation is enough to return pH to normal range

• normal pH
• high BE (B)
• high pCO2

fully compensated resp acidosis

Question 19

Q: What’s the interpretation procedure of an ABG? (4)

Answer 19

A: Type of imbalance?
Acidosis (or acidaemia) / Alkalosis (or alkalaemia) / Normal

Aetiology of imbalance?
Respiratory (acidosis or alkalaemia) / Metabolic (acidosis or alkalosis) / Mixed (respiratory and metabolic) / Normal

Any homeostatic compensation?
Uncompensated / Partially compensated / Fully compensated

Oxygenation?
Hypoxaemia / Normoxaemia / Hyperoxaemia

Question 20

Q: Uncompensated (3). Uncompensated mixed.

Answer 20

A: -either have normal CO2 or normal BE

• normal BE but abnormal CO2= resp
• normal CO2 but abnormal BE= met

both lungs and kidneys are making it acidic or alk

Question 21

Q: pH___CO2__BE

low\_\_\_high\_\_--
high\_\_low\_\_\_-- 
low\_\_\_--\_\_\_\_low 
high\_\_\_--\_\_\_high
low\_\_\_high\_\_low
high\_\_low\_\_\_high
low\_\_\_low\_\_low
high\_\_low\_\_\_low
--\_\_\_\_low\_\_\_low
--\_\_\_high\_\_\_high
--\_\_\_--\_\_\_\_--

Answer 21

A: pH___CO2__BE

low\_\_\_high\_\_-- \_\_\_\_\_\_\_\_U resp acid
high\_\_low\_\_\_-- \_\_\_\_\_\_\_\_U resp alk
low\_\_\_--\_\_\_\_low \_\_\_\_\_\_\_U met acid
high\_\_\_--\_\_\_high\_\_\_\_\_\_\_U met alk
low\_\_\_high\_\_low\_\_\_\_\_\_\_U mix acid
high\_\_low\_\_\_high \_\_\_\_\_\_U mix alk
low\_\_\_low\_\_\_low\_\_\_\_\_\_\_PC met acid
high\_\_low\_\_\_low \_\_\_\_\_\_\_PC resp alk
--\_\_\_\_low\_\_\_low \_\_\_\_\_\_\_FC resp alk/ met acid
--\_\_\_high\_\_\_high\_\_\_\_\_\_\_FC met alk/ resp acid
normal

Question 22

Q: Phases to fix uncompensated resp alkalosis. Result? (3) Next? Result? (3)

Answer 22

A: no acute phase, just chronic

decreases amount of bicarb reabsorbed in kidneys

-still high pH
-still low pCO2
-low BE (B) (was normal before)
=> partially compensated resp alk

eventually bicarb excretion and increase in dissociation to produce H+ will decrease pH

-normal pH
-low pCO2
-low BE (B)
=> fully compensated resp alk

Question 23

Q: What can diarrhoea result in? 3 readings. What changes as you fix it?

Answer 23

Q: Excess secretion of HCO3- which means increase dissociation and therefore increase H+

-low pH
-normal pCO2
-low BE (B)
=>uncompensated metabolic acidosis

low pCO2