Acid Base Handling Flashcards
What are the normal ranges for CO2 (kPa)?
4.7 – 6
What is the normal range for arterial pO2?
10 – 13kPa
What is the normal range for bicarbonate on ABG?
22-30mmol/L
What are the most commonly measured Cations and Anions in the blood?
What other, usually not measured cations and anions are there?
Routinely measured
Cations: sodium (and potassium).
Anions: Chloride and Bicarbonate
Therefore
Anion gap is calculated = Na+K-Cl-HCO3 (14-18 range)
Unmeasured
1. Cations: calcium and magnesium.
2. Anions: phosphate, sulfate, organic acids (both endogenous and exogenous), and most proteins (e.g., albumin).
How is the Anion Gap Calculated?
What does it usually signify?
Calculated: (Na+K)-(Cl-HCO3) (14-18 range)
The physiological anion gap is almost entireyl attributed to albumin (Proteins)
If there is is high Anion Gap: there are some other substances in the blood that are not usually there (e.g. ketones, lactate)
What are some of the causes for a elevated anion gap metabolic acidosis?
KULT
Ketoacidosis (DKA, alcoholic, starvation)
Uraemia (renal failure)
Lactic Acidosis (shock, ischaemia, sepsis)
Toxins (ethylene glycol, methanol, paraldehyde, salicylate)
What are some of the causes for normal Anion gap metabolic acidosis?
(FUSEDCARS):
Most common: GI loss (loss of HCO3 in GI system)
Cases mainly
1. Addison’s disease
2. Bicarbonate loss (diarrhoea, laxative abuse, Renal Tubular Acidosis)
3. Chloride gain (Sodium Chloride 0.9% infusion)
4. Drugs (acetazolamide)
Increase in H+/ acidic components–> usually increase in anion gap
Decreased renal H+ excretion
* Renal tubular acidosis
* Addisons (causing hyperkalaemic tubular necrosis), hyperparathyroidism
Bicarbonate loss
* Fistula (biliary, pancreatic)
* Diarrhea
Others
* Saline administration (acidotic)
* Ammonium chloride ingestion (who knows)
What would the expected HCO3 levels be in
- Metabolic vs. resp acidosis
- Metabolic vs resp alkalosis
Generally: acutely in resp acid-base disturbances HCO3 expected to be unchanged (long-term compensation can cause change in HCO3),
think of HCO3 as a base
- In Acidosis: Resp: late compensatory increase, metabolic: HCO3 decrease (often cause for the Acidosisor due to buffering)
- In alkalosis: Resp: late compensatory decrease, in metabolic: increase
What are the causes of metabolic alkalosis?
H+ loss
* Vomiting
* Conn’s (hyperaldesteronism –> increased H+ renal excretion
HCO3- increase
* increased renal absorbtion –> e.g. due to fluid depletion like Loop or thiazide diuretics
* Hypokalaemia –> increased renal absorption (e.g. due to GI loss or renal loss of K+)
* Alcalotic drugs: **antacids –> bicarbonates **
hypokalaemia causes activation of RAAS –> increased HCO3 resorption of kidneys as well as increased H+ exresion therefore can lead to metabolic alcalosis
BUT: renal K+/H+ exchange can also contribute to hypokalaemia –>renal H+ reabsorption might demand K+ excretion
Explain the relationship between K+ and H+ levels.
NB: H+ and Potassium are intimately linked as one moves into cells one moves out
This is because of the hydrogen-potassium co-transporter. A rise is potassium means the body compensates by pumping potassium into cells, along with hydrogen ions too (and vice-versa) For every drop in pH of 0.1 there is an increase in K+ of 0.7
What is Renal tubular acidosis?
Group of disorders, characterised by a failure to acidify the urine (due to defects in H+/ HCO3- transport), leading to acidosis
Usually presents with normal anion gap metabolic acidosis
What are the different types of Renal tubular acidosis?
Usually classified via site of malfunction
- Type 1: Distal tubule
- Type 2: Proximal tubule
- Type 3: nieche
- Type 4: Hyperkalaemia (aldosterone resistance/ lack)
What is the most common form of Renal tubular acidosis?
What are the aetiologies?
Type 4: Hyperkalaemic
Due to
1. Hypoaldosteronism (e.g. Addison’s, diabetic nephropathy, drugs)
2. Aldosteorone resistance (e.g. drugs or chronic interstitial)
What is the pathophysiology of Type 4 renal tubular acidosis?
Type 4 =RTA due to aldosterone deficiency/ resistance
Aldosterone deficiency and/or resistance in the collecting duct and distal convoluted tubule cause hyperkalemia, which inhibits ammonia synthesis in the proximal convoluted tubule and decreases urinary ammonium excretion.
–> Hyperkalaemia
What is the pathophysiology of Type 1 and 2 Renal tubular acidosis?
