Clinical Aspects Of Acid-Base Control Flashcards
What is 1kPa in mmHg?
7.5mmHg
Steps of assessing 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?
PaO2/FiO2 ratio
P/F ratio > 50 = healthy
P/F ratio < 40 = acute lung injury
P/F ratio < 26.7 = ARDS
Compensation
Altering in function of the respiratory or renal system to change the secondary variable in an attempt to minimise an acid/base imbalance.
Body will never overcompensate.
Compensation is most likely occurring when…
pCO2 and bicarbonate are moving in the same direction - if going different directions suspect a mixed disorder.
Anion Gap
- Sum of routinely measured cations in venous blood minus routinely measured anions. ([Na+] + [K+]) - ([Cl-] + [HCO3-])
- Calculated from venous blood.
- Should be equal - normal anion gap is 16
- Increased anion gap signals the presence of a metabolic acidaemia, helps differentiate cause of it.
Lactic Acidaemia
Increased anaerobic metabolism with subsequent increased production of lactic acid.
Causes include any condition which causes hypoperfusion (shock, femoral artery embolism), severe acute hypoxia, severe convulsions, strenuous exercise/dehydration
Lactic Acidaemia
Increased anaerobic metabolism with subsequent increased production of lactic acid.
Causes include any condition which causes hypoperfusion (shock, femoral artery embolism), severe acute hypoxia, severe convulsions, strenuous exercise/dehydration.
Addition of lactic acid increases anion gap, HCO3- falls because it is used to buffer protons.
Lactate marker of concern
> 2mmol/L
Ketoacidosis
- increased anion gap
- decreased insulin and increased glucagon - uncontrolled diabetes mellitus, alcoholic ketoacidosis and starvation ketoacidosis
Ketone Blood Test Values
- Below 0.6mmol/l - normal
- 0.6 - 3mmol/L - follow sick day rules - ensure fluid intake adequate, additional short acting insulin, retest blood glucose and ketones in hour
- Over 3.0mmol/l - Risk of DKA
Exogenous Acid Load
- Accidental/deliberate ingestion will cause an increased anion gap.
- Methanol and Ethylene Glycol
Renal Causes of Metabolic Acidosis
- Renal failure (acute and chronic)
- Renal Tubular Acidosis
Normal Anion Gap Metabolic Acidosis
- Diarrhoea
- Renal Tubular Acidosis
GI Causes of Metabolic Acidosis (normal anion gap)
- much of gut below pylorus secretes bicarbonate into gut lumen
- for every bicarbonate ion into gut a H+ ion enters ECF
- diarrhoea this process increases
- and volume depletion, therefore renin/angiotensin/aldosterone axis stimulated retaining chloride
similar pathology - laxative abuse, ileostomy and colostomy
Metabolic Acidosis with Normal Anion Gap
Decrease in HCO3-, increase in Cl-.
To compensate for a metabolic alkalosis
pCO2 must increase therefore minute volume must fall
To compensate for a metabolic acidosis..
pCO2 must fall, therefore minute volume must increase. Kussmaul respiration - a laboured deep rapid pattern of breathing.
Maximal compensation can take up to 24hrs. Respiratory comp is limited. Can increase minute volume to 30l/min.
Compensation for metabolic acidaemia…..
- Is respiratory!!!!!
- Slow metabolic (renal) correction - secrete more acid (making new bicarbonate), plasma H+ decreases (pH rises) and plasma bicarbonate rises to normal. But only if: metabolic acidaemia is of non-renal origin and kidneys are fuctioning effectively.
Metabolic Alkalaemia
- Least common because the kidney is very good at excreting bicarbonate.
- 2 processes have to happen - initiating process and maintaining process.
- most common initiating process - loss of H+ ion from either gut (above pylorus) or from the kidney (due to furosemide and thiazide)
Maintenance of the Alkalosis
Processes which impair the kidneys ability to excrete bicarbonate:
- Hypokalaemia
- Aldosterone Excess
- Volume & chloride depletion group
Pyloric Stenosis
- In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
- Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
- Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
- Worsening volume depletion results in aldosterone secretion (RAAS)
- Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
Pyloric Stenosis
- In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
- Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
- Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
- Worsening volume depletion results in aldosterone secretion (RAAS)
- Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
Pyloric Stenosis
- In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
- Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
- Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
- Worsening volume depletion results in aldosterone secretion (RAAS)
- Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
Pyloric Stenosis
- In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
- Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
- Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
- Worsening volume depletion results in aldosterone secretion (RAAS)
- Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
Pyloric Stenosis
- In health parietal cell secrete H+ into lumen of the stomach. The bicarbonate is secreted into the ECF.
- Gastric fluid also contains Na+, water and K+ (5-10mmol/l)
- Initially excess bicarbonate is spilled in the urine but accompanied by a cation.
- Worsening volume depletion results in aldosterone secretion (RAAS)
- Sodium and water retained exacerbating hypokalaemia - losing K+ through vomiting and kidneys.
