Arterial Blood Gases Flashcards
Pre-analytical factors of analysis
Adequate mixing (or else may clot; use balanced heparin syringe) Anaerobic collection (don't expose sample to air and expel any bubbles before capping) Placed on ice (slow down cellular metabolism) Reach lab without delay (<30 min)
Venous blood gas
pH, HCO3, pCO2 comparable with ABG and changes in parallel
BUT
O2 levels correlate poorly
Reference ranges
pH: 7.35-7.45
pO2: 80-110 mmHg
pCO2: 35-45 mmHg
HCO3: 23-33 mmol/L
1 mmHg = 0.133 kPa
1 kPa = 7.5 mmHg
Respiratory failure
Type 1 Hypoxaemic respiratory failure
- failure of lungs to maintain adequate oxygenation
- PaO2 <60 mmHg in room air
Type 2 Hypoxaemic and Hypercapnic respiratory failure
- failure of lungs to maintain adequate ventilation
- PaCO2 >50 mmHg
Effects of acidemia and alkalemia
Acidemia (<7.35)
- CNS depression, disorientation, coma, death (<6.8)
Alkalemia (>7.45)
- CNS over-stimulation, convulsion, death (>7.8)
- due to increased binding of Ca to albumin –> reduced ionised Ca (as H+ released to buffer alkaline conditions)
Buffers - why do we need them, examples in body
Mixture of weak acid and salt of its conjugate base
- minimise changes in pH when strong acid or base is added
Regulation of
- enzyme functions
- cellular uptake and use of metabolites
- conformation of biological structural components
- uptake and release of oxygen
Buffers in our body
- **plasma bicarbonate/carbonic acid
- plasma RBC and urine phosphate
- plasma proteins
- RBC haemoglobin
Acid production in our body
Metabolism of proteins (100 mmol/day)
Incomplete metabolism of fats or carbohydrates (keto/lactic)
Produced in metabolism (usually completely consumed)
Henderson-Hasselbalch equation
pH = pKa + log [X-]/[HX]
- in the body, H2CO3 and HCO3-
- H2CO3 = 0.03 pCO2 (in mmHg)
- pKa = 6.1
- ratio of base:acid is 20:1 to maintain pH 7.4
([H+][HCO3-]/pCO2 = 24 – for checking validity of data)
Respiratory and Renal regulation of acid-base
CO2 + H2O – H2CO3 – H+ + HCO3-
- shifting of equilibrium in response to changes in H and HCO3
Respiratory acidosis = retention of CO2 (hypoventilation)
Metabolic acidosis = loss of HCO3 or accumulation of acids
Respiratory alkalosis = hyperventilation
Metabolic alkalosis = retention of HCO3 or loss of H
Compensation
Unaffected organ produces a change to oppose the primary acid-base disorder
Typically incomplete compensation (except in chronic respiratory alkalosis e.g. living in high altitudes)
Respiratory compensation starts immediately and is rapid (max in 12-24 hrs)
Metabolic compensation is slow and takes several days (there is acute minor change due to buffer initially)
Compensating parameter always changes in the same direction as primary parameter
Approach to acid-base disturbances
- Acidosis vs Alkalosis
- Metabolic or Respiratory (assess CO2 and HCO3)
- Compensation
- present or absent
- if present, complete or partial
- appropriate degree of compensation? (calculations) to determine if there is 2nd acid base disorder
- overcompensation never occurs!!
- if absent, consider mixed acid-base disturbance
- if pH normal but parameters abnormal (change in opposite directions), consider mixed acid-base
- always check anion gap (may be only clue to metabolic acidosis)
Mixed acid base disturbances
Remember respiratory acidosis and alkalosis can’t occur at the same time!
(anything with diuretic therapy causes metabolic alkalosis)
Metabolic alkalosis and Respiratory alkalosis e.g. diuretic therapy and pneumonia/ hepatic failure
Metabolic alkalosis and respiratory acidosis e.g. **diuretic therapy and COPD or vomiting and COPD
Metabolic acidosis and respiratory alkalosis e.g. **aspirin overdose (accumulates in blood as excess anion - HAGMA; stimulates resp centre - alkalosis)
Metabolic alkalosis and metabolic acidosis e.g. diuretic therapy and ketoacidosis
Metabolic Acidosis: Anion Gap
HAGMA vs NAGMA
Anion Gap = (Na + K) - (Cl + HCO3) –> 7-17 mmol/L
- normal for non-volatile acids with measured anion e.g. HCl
- normal for loss of bicarbonate (equal loss of Na)
- increased in non-volatile acids with unmeasured anion e.g. lactic acid
HAGMA a/w normal [Cl]
NAGMA a/w high [Cl]
HAGMA causes, investigations
Causes: MUDPILES
- Methanol, Uraemia (late), DKA (and alcoholic/starvation ketoacidosis), Paraldehyde, Isoniazid, Lactic acidosis (tissue hypoxic of metformin poisoning), Ethylene glycol, Salicylate (rmb also causes respiratory alkalosis)
- rhabdomyolysis
Investigations of HAGMA
- plasma glucose
- plasma beta-hydroxybutyrate (if glucose elevated) – urine ketone only detects acetoacetate
- renal function tests (metabolic acidosis occurs when Cr around 350 micromol/L in CKD)
- plasma lactate
- serum osmolality (OG >10 in alcohol poisoning)
- urine toxicology screen
- serum toxicology if suspicious (salicylate, iron, paracetamol)
- serum CK
Pathogenic mechanisms of ketoacidosis and lactic acidosis
DKA
- decreased insulin: glycogen ratio –> inhibition of glycolysis + less inhibition of carnitine acyltransferase –> increased lipolysis, FA transport to liver and FA oxidation in liver –> increase acetyl Co-A
- acetyl Co-A channeled to ketogenesis
Starvation: use fat as fuel
Alcoholism
- starvation and increased NADH:NAD+ inhibits gluconeogenic enzymes
- use fat as energy source
Lactic acidosis
- anaerobic conditions = glucose –> pyruvate by glycolysis and then pyruvate –> lactate
Treatment of DKA
- Insulin
- Rehydration (dehydrated due to osmotic diuresis from DKA)
- K replacement
- usually hyperK due to insulin deficiency, hypertonicity and decreased GFR (not acidosis!)
- however osmotic diuresis means patient is actually K depleted
- -> K shifts intracellularly upon treatment with insulin leading to dangerously low [K] if not replaced
NAGMA
Determine K+ level
Hyperkalemia
- early uraemic acidosis
- mineralocorticoid deficiency/ resistance (Type 4 RTA)
- Ingestion of acids e.g. ammonium chloride, HCl (H+ load excreted in exchange for K)
Hypokalemia
- diarrhoea
- RTA Type 1 and 2
- Carbonic anhydrase inhibitors e.g. acetezolamide
- Ureterosigmoidostomy
Patients with chronic metabolic acidosis can have high ALP
Ca dissolves in acid –> increase bone resorption so patients as risk of osteoporosis and osteopenia
Metabolic alkalosis
Commonly a/w hypokalaemia (either can cause the other)
Saline responsive
- secondary hyperaldosteronism due to volume contraction e.g. vomiting, previous use of diuretics
- -> kaliuresis and secretion of H
- maximal reabsorption of Na and Cl at renal tubules due to volume depletion –> U[Cl] <20
- treatment: fluid replacement and potassium replacement
Non-saline responsive (U[Cl] >20)
- current use of diuretics (loop/ thiazide)
- primary hyperaldosteronism
- Bartter and Gitelman syndromes
- severe hypoK
- milk alkali syndrome
Recall mechanism of vomiting induced metabolic alkalosis
Loss of HCl causes hypochloremic metabolic alkalosis
Kidney compensates by increasing bicarbonate excretion with Na, urine is alkaline
As patient becomes more volume depleted, secondary hyperaldosteronism sets in –> kaliuresis and paradoxical aciduria
Bartter and Gitelman syndromes
Bartter syndrome
- mimics loop diuretics
- defects in Na-K-Cl cotransport in the TAL
Gitelman syndrome
- mimic thiazide diuretics
- defects in Na-Cl transport at DCT
==> increase Na reabsorption at collecting ducts –> increase K/H secretion –> hypoK and alkalosis
Respiratory acidosis
CNS depression e.g. head injury, opioids, coma
Airway obstruction e.g. tumour, foreign body
Chest wall disease e.g. resp muscle fatigue in prolonged/severe asthma, MG
Respiratory alkalosis
Hyperventilation e.g. anxiety, asthma (initially), artificial ventilation
Stimulation of respiratory centre e.g. PE, high altitude, salicylate
