Clinical Aspects of Acid Base Control

Question 1

State the conversion rate between kPa and mmHg.

Answer 1

1kPa = 7.5mmHg

Question 2

Identify the main buffers of the body. What is their main function ?

Answer 2

proteins
haemoglobin
carbonic acid / bicarbonate

Maintain pH in normal range

Question 3

How does the body excrete acids ?

Answer 3

1) Lungs (volatile acid, i.e. CO2)

2) Kidneys (non-volatile acids)

Question 4

State the normal pH, pO2, pCO2, and standard bicarbonate arterial, and veinous values.

Answer 4

ARTERIAL
pH: 7.35-7.45
pO2: 12-13 kPa
pCO2: 4.5-5.6 kPa
Bicarbonate (standard): 22-26 mmol/L

VEINOUS
pH: 7.32-7.45
pO2: 3.3-5.3 kPa
pCO2: 5.4-6.6 kPa
Bicarbonate (standard): 23-27 mmol/L

Question 5

Which of veinous or arterial normal values of pH, pO2, pCO2 and standard bicarbonate do we use ?

Answer 5

In metabolic disturbance, focus on pH and standard bicarbonate (which both mirror arterial values quite closely), so use veinous values (veinous sample easier to take, less harmful to the patient).

If need to look at pO2 and/or pCO2, use arterial values.

Question 6

Distinguish between actual and standard bicarbonate.

Answer 6

Actual bicarbonate is measured.

Standard bicarbonate is calculated from the actual bicarbonate but assuming 37 degrees Celcius and a paCO2 of 5.3kPa.

Question 7

Which component of the following equation:
CO2+ H2O = H2CO3 = H+ + HCO3-
reflect the metabolic component ?

Answer 7

Standard Bicarbonate reflects the metabolic component of acid base balance.

Question 8

Define base excess.

Answer 8

Value calculated from blood pH and pCO2. Defined as the amount of acid required to restore a litre of blood to its normal pH at a PCO2 of 5.3. Change in base excess mirrors change in standard bicarbonate. Normal range -2 - +2mmol/L. Becomes more negative in metabolic acidosis (because being used up to buffer that acid).

Question 9

Briefly describe the stepwise approach to the assessment of ABGs.

Answer 9

Step 1: assess pO2 and oxygenation
Step 2: assess pH: acidaemia or alkalaemia ?
Step 3: Determine the primary problem (think about
the patient)
Step 4: Is compensation occurring ?

Question 10

Why do we need to assess pO2 and oxygenation before anything else in the assessment of ABGs ? How do we determine oxygenation ?

Answer 10

Because hypoxia will kill you first.

We cannot only use PaO2 because may require additional oxygen to maintain PaO2 within that normal range. Hence, PaO2 / FiO2 ratio or the P/F ratio (kpa divided by inspired fraction of oxygen)

P/F ratio > 50 = healthy
P/F ratio < 40 = acute lung injury
P/F ratio <26.7 = ARDS

Question 11

What is the main compensation if primary problem is respiratory ? if the main problem is metabolic ?

Answer 11

If main problem is respiratory: compensation is renal

If main problem is metabolic: compensation is respiratory

Question 12

Define compensation.

Answer 12

Altering in function of the respiratory or renal system to change the secondary variable in an attempt to minimise an acid – base imbalance.

Question 13

Will the body ever overcompensate ?

Answer 13

No, the body will never overcompensate

Question 14

Based on the following equation, describe what happens in a metabolic acidemia.

pH ∝ HCO3/pCO2

Answer 14

In metabolic acidemia, protons getting dripped into bloodstream, so level of bicarbonate will decrease because being used up to buffer that acid (so will fall).
To minimise change in pH, that means pCO2 will decrease as well, so minute V must increase so respiratory rate and tidal V must increase.

Question 15

How do we know whether compensation is occurring ?

Answer 15

If pCO2 and bicarbonate are moving in the same direction compensation is likely to be occurring.

Question 16

How do we know that a certain disorder is a mixed acid base disorder ?

Answer 16

If pCO2 and bicarbonate are moving in different directions suspect a mixed disorder.

Question 17

Define anion gap.

Answer 17

Is the sum of routinely measured cations (Na+, K+) in venous blood minus
routinely measured anions (Cl-, HCO3-). This is calculated from veinous blood.

i.e. ([Na+] + [K+]) - ([Cl-] +[HCO3-])

Question 18

What is a normal anion gap ? Why is there an anion gap given that we should normally always be in balance in terms of positive vs negative ions ?

Answer 18

Normal anion gap = 16

In life we are in balance (positive charges must equal negative charges), but this anion gap only considers routinely measured anions, unmeasured anions would compensate for the anion “gap”

Question 19

What would a disturbed anion gap indicate ?

Answer 19

• An increased anion gap signals the presence of a metabolic acidaemia early.

• Anion gap also helps differentiate the cause of metabolic acidemia (Vast majority of metabolic acidemias will give you increased anion gap, but a
small number of less common pathologies will give you metabolic acidemia with normal anion gap).

Question 20

Which of metabolic acidemias or alkalemias is more common ? Why ?

Answer 20

Metabolic acidemias more common
Because the kidney is very good at excreting excess bicarbonate (If excess bicarboante in urinary tubule, there’s not enough phosphate or proton for it to bind to so just pours into urine)

Question 21

What are the main causes of metabolic acidemias ?

Answer 21

Most commonly occurs from an overwhelming acid load:

• Body’s own production (endogenous)
• Ingestion (exogenous source)
• Failure of excretion/ regeneration bicarb by the kidneys

Question 22

Explain how the body’s endogenous acid production can result in metabolic acidemia.

Answer 22

1) ANY CONDITION CAUSING HYPOPERFUSION (Increased anion gap)

– Of the whole body: shock (cardiogenic, septic, hypovolaemic, anaphylactic)
– Or part of the body: femoral artery embolism

… will result in increased anaerobic metabolism with subsequent increased production of lactic acid (i.e. lactic acidaemia)

• Severe acute hypoxia, severe convulsions (hypoxic + muscles working v hard), and strenous exercice (dehydration) will also all cause lactic acidemia

2) KETOACIDOSIS (Increased anion gap)

Due to situations of decreased insulin and increased glucagon

• Uncontrolled diabetes mellitus (severe, life threatening)
• Alcoholic ketoacidosis (common clinically)
• Starvation ketoacidosis (mild)

Question 23

Why doesn’t production of lactic acid in health result in lactic acidemia but does in hypoperfusion ?

Answer 23

Because lactic acid produced in health (in anaerobic metabolism) is metabolised in the liver, so no net production of acid.

However, this process needs oxygen so when O2 delivery falls (i.e. hypoperfusion), production increases and consumption of lactate by the liver falls.

Question 24

What are causes of endogenous (lactic acidemia) metabolic acidemia ?

Answer 24

-Hypoperfusion

Question 25

What instances may we test for amount of lactate ? What amount of lactate is a cause for concern ?

Answer 25

Test for amount of lactate in clinical suspicion of sepsis

Lactate >2mmol/L marker of concern (Indicates possible sepsis and possibly heading to metabolic acidemia)

Question 26

Draw a normal ionogram, and one with the addition of lactic acid, explaining your diagrams.

Answer 26

Refer to page 22 of lecture slides.

In the addition of lactic acid,
H+ ion combines with bicarbonate, which is used up in buffering that proton so bicarbonate ion falls.
Chloride stays the same.
Unmeasured ions increased due to addition of lactate (which is not routinely measured)

Overall increased in unmeasured anion (and therefore decrease in bicarbonate which IS routinely measured so increase in anion gap).

Question 27

Describe how to monitor response of ketones to treatment.

Answer 27

• Capillary blood ketones measurement (finger prick) (main point of care test)
• Venous blood should be used rather than arterial (because interested in pH and bicarbonate) (unless respiratory problems dictate otherwise) in blood gas analysers

(clinically, can also smell it, smells like nail varnish remover smell)

Question 28

What are normal and abnormal values for ketones ?

Answer 28

Below 1 mmol/L normal
Between 1 and 3 mmol/L, careful
Above 3 mmol/L, risk of DKA

Question 29

Explain how exogenous acid load can result in metabolic acidaemia.

Answer 29

ACCIDENTAL/DELIBERATE INGESTION (increased anion gap)

• Methanol (industrial solvent, windscreen wash)
• Ethylene glycol (anti-freeze)

Both metabolised in the liver to acids + Both directly toxic to kidneys (impairing renal ability to excrete acid load) + Methanol also toxic to optic nerve (can come in with impairment of vision)

Question 30

How may accidental ingestion of exogenous acid load occur ?

Answer 30

Some people trying to brew alcohol, may get unintended side products like methanol

Question 31

Identify renal causes of metabolic acidosis. Do these have normal, or increase anion gap ?

Answer 31

• Renal failure both acute and chronic (↑gap), get low eGFR so kidney loses ability to regenerate bicarbonate, resulting in metabolic acidemia
• Renal tubular acidosis (normal gap), kidney cannot reabsorb filtered bicarbonate

Question 32

Identify normal anion gap metabolic acidosis causes. How do these work ?

Answer 32

• Renal tubular acidosis, kidney cannot reabsorb filtered bicarbonate
• Diarrhoea (more common of the two) (also similar pathologies such as laxative abuse, ileostomy and colostomy which cause normal anion gap).
• Much of gut below pylorus secretes bicarbonate into gut lumen
• For every bicarb ion into gut a H+ ion enters ECF (i.e. bloodstream)
• In diarrhea, this process increases (so get marked loss of bicarbonate, sodium, and therefore water which will follow them)
• Hence, volume depletion means renin/angiotensin/aldosterone axis stimulated retaining chloride (reabsorbing Sodium which will be followed by water, and a negative ion must follow to keep ionic balance. Chloride therefore follows).

Question 33

Draw a normal ionogram, and a ionogram for metabolic acidosis with normal anion gap, explaining your diagrams.

Answer 33

• Bicarbonate falls (H+ secreted into bloodstream, bicarbonate used up to buffer this up).
• Kidney working to pull back sodium and water (to replace sodium and water lost in diarrhea), so sodium just getting replaced (stays at normal)
• Pulling back a negative ion with it, so chloride rises, so anion gap remains the same, no increase in unmeasured anions.

Question 34

How do ileostomies and colostomies cause normal anion gap metabolic acidemia ?

Answer 34

They cause loss of a lot of fluid. Rest of pathology is same as diarrhea.

Question 35

Is the compensation for metabolic problems respiratory or renal ? Explain.

Answer 35

Compensation for metabolic problems is RESPIRATORY, but there is also slow metabolic (renal) compensation correction (i.e. secrete more acid, therefore also make new bicarbonate, so plasma H+ decreases (pH rises) and plasma bicarbonate rises to normal).

Question 36

Does slow metabolic (renal) correction of metabolic problems always occur ? Explain.

Answer 36

No, it only occurs if:

1. The metabolic acidaemia is of non-renal origin
2. The kidneys are functioning effectively.

Otherwise kidneys unable to help correct the problem (e.g. lactic acidemia, impaired oxygen delivery to body, potentially including kidneys, in which case impaired functioning).

Question 37

Describe the compensation for a metabolic acidosis. How long does this compensation take ?

Answer 37

pH ∝ (HCO3 / pCO2)

If HCO3- falls because being used up to buffer increased protons, then pCO2 must fall, therefore minute V must increase. Hence, Kussmaul respiration takes place, a laboured deep, rapid pattern of breathing.

• Maximal compensation can take up to 24hrs

Question 38

What is the main issue of respiratory compensation of metabolic acidemia ?

Answer 38

• Respiratory compensation is limited by the work involved in breathing
• Can increase minute volume up to about 30l/min but difficult to maintain (can eventually get to respiratory arrest)

Question 39

Which of the acid base disturbances is the least common ?

Answer 39

Metabolic alkalaemia

Question 40

How does metabolic alkalaemia take place ?

Answer 40

For metabolic alkalaemia to take place, two processes have to happen:

• An initiating process:

a) usually associated with loss of H+ ions (can be from the gut or from the kidney)
- Pyloric stenosis is the most common initiating process, causing loss of H+ ions from gut above the pylorus through vomiting
- Furosemide and Thiazide can also cause loss of H+ ions from the kidney
b) gain of exogenous alkali much less common: clinical situation massive blood transfusion

• A maintaining process (a process which impairs the kidneys ability to excrete bicarbonate)
-Chloride depletion: in pyloric stenosis, body is volume depleted, so R/A/A system triggered, so sodium reabsorbed, and Cl- ions also reabsorbed to maintain positive/negative ion balance.
But actually, baby is chloride depleted because also lose Cl- ion through vomit.
Only other negative ion present in any substantial quantity in ECF is bicarbonate ion.
Instead of excreting excess bicarbonate, kidney starts reabsorbing more bicarbonate to maintain electrical neutrality.
-Potassium depletion

Question 41

Describe compensation for metabolic alkalosis. What is the problem with this ?

Answer 41

• pH ∝ HCO3/pCO2
• Since HCO3- levels increase, pCO2 must increase, so minute volume must fall (problematic because this usually occurs with pyloric stenotic babies, which are at risk of apnea (hence difficult to predict extent)