Clinical Aspects of Acid Base Control Flashcards
State the conversion rate between kPa and mmHg.
1kPa = 7.5mmHg
Identify the main buffers of the body. What is their main function ?
proteins
haemoglobin
carbonic acid / bicarbonate
Maintain pH in normal range
How does the body excrete acids ?
1) Lungs (volatile acid, i.e. CO2)
2) Kidneys (non-volatile acids)
State the normal pH, pO2, pCO2, and standard bicarbonate arterial, and veinous values.
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
Which of veinous or arterial normal values of pH, pO2, pCO2 and standard bicarbonate do we use ?
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.
Distinguish between actual and standard bicarbonate.
Actual bicarbonate is measured.
Standard bicarbonate is calculated from the actual bicarbonate but assuming 37 degrees Celcius and a paCO2 of 5.3kPa.
Which component of the following equation:
CO2+ H2O = H2CO3 = H+ + HCO3-
reflect the metabolic component ?
Standard Bicarbonate reflects the metabolic component of acid base balance.
Define base excess.
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).
Briefly describe the stepwise approach to the assessment of ABGs.
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 ?
Why do we need to assess pO2 and oxygenation before anything else in the assessment of ABGs ? How do we determine oxygenation ?
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
What is the main compensation if primary problem is respiratory ? if the main problem is metabolic ?
If main problem is respiratory: compensation is renal
If main problem is metabolic: compensation is respiratory
Define compensation.
Altering in function of the respiratory or renal system to change the secondary variable in an attempt to minimise an acid – base imbalance.
Will the body ever overcompensate ?
No, the body will never overcompensate
Based on the following equation, describe what happens in a metabolic acidemia.
pH ∝ HCO3/pCO2
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.
How do we know whether compensation is occurring ?
If pCO2 and bicarbonate are moving in the same direction compensation is likely to be occurring.
How do we know that a certain disorder is a mixed acid base disorder ?
If pCO2 and bicarbonate are moving in different directions suspect a mixed disorder.
Define anion gap.
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-])
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 ?
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”
What would a disturbed anion gap indicate ?
• 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).
Which of metabolic acidemias or alkalemias is more common ? Why ?
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)
What are the main causes of metabolic acidemias ?
Most commonly occurs from an overwhelming acid load:
- Body’s own production (endogenous)
- Ingestion (exogenous source)
- Failure of excretion/ regeneration bicarb by the kidneys
Explain how the body’s endogenous acid production can result in metabolic acidemia.
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)
Why doesn’t production of lactic acid in health result in lactic acidemia but does in hypoperfusion ?
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.
What are causes of endogenous (lactic acidemia) metabolic acidemia ?
-Hypoperfusion