ABG AND ELECTROLYTE ABNORMALITIES ALEX BUTTFIELD.

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Presentation transcript:

ABG AND ELECTROLYTE ABNORMALITIES ALEX BUTTFIELD

A DISCLAIMER

OUTLINE My approach to acid/base disturbances Multiple examples A few mnemonics Exam hints

MY APPROACH TO ABGs pH first (obviously) – Tailor approach to acidaemia vs alkalaemia and primary disturbance (respiratory vs metabolic)

MY APPROACH TO ABGs Metabolic acidosis: Anion gap – Na –(HCO3+Cl) – Raised if >12 – Normal 8-12 – Low <8 Expected CO2 (Winter’s formula  HCO3x ) Delta ratio (AG -12/24-HCO3) A-a gradient (not applicable if VBG or if FiO2 unknown) Electrolyte correction: – Na  Measured Na + (BSL/3 -10) – K  for every 0.1 pH below 7.4, subtract 0.5 from measured K Osmolality and osmolar gap (if applicable)

DIFFERENTIALS FOR HAGMA KETONES: – DKA – Starvation – Alcoholic ketoacidosis RENAL FAILURE LACTATE (type A and B) TOXINS (SEPTIC): – Salicylates – Ethylene glycol, methanol – Paraldehyde – Toluene – Iron, INH – Cyanide, Carbon monoxide

NON-ANION GAP METABOLIC ACIDOSIS U = Ureteric diversion S = Sigmoid fistula E = Excess saline D = Diarrhoea (or resolving DKA) C = Carbonic anhydrase inhibitors A = Addisons R = Renal Tubular Acidosis P = Pancreatic fistula

LOW ANION GAP In other words, excess unmeasured cations, or decreased anions: – Hypoalbuminaemia – Excess unmeasured cations (Mg, Ca, Li, myeloma)

Metabolic alkalosis: – Expected CO2 (0.7xHCO3 +20), can compensate to CO2 ~60 – Expected electrolyte disturbances (low K, Cl) – Good list of differentials

DIFFERENTIALS FOR METABOLIC ALKALOSIS C = Contraction L = Loop diuretics, licorice E = Endocrine (hyperaldosteronism, Bartter’s Conn’s, Cushings) V = Vomiting (including NG suction) E = Excess alkali (antacids, milk-alkali, dialysis) R = Refeeding R = Renal bicarbonate retention

Respiratory acidosis: – Expected HCO3: Acute = 24 + ([PCO2-40]/10) x 1 Chronic = 24 +([PCO2 -40]/10) x 4 – ?coexistent with other metabolic disturbance – Good list of differentials

RESPIRATORY ACIDOSIS ACUTE: – Airway obstruction (any cause) – Aspiration – Bronchospasm – CNS depression (drugs, CVA, bleed) – Muscle weakness (GBS, Duchenne’s) – Pulmonary disease CHRONIC: – Chronic lung disease – NM disorders – Obesity (obesity hypoventilation syndrome)

Respiratory alkalosis: – Expected HCO3: Acute (most common) = 24 – (40-PCO2/10) x 2 Chronic = 24 – (40-PCO2/10) x 5 – Put in context – Differentials  HYPERVENTILATION

RESPIRATORY ALKALOSIS CHAMPS – CNS disease (raised ICP) – Hypoxia (any cause) – Anxiety – Mechanical ventilation – Progesterone, pregnancy – Sepsis, salicylates (and other toxins)

CASE ONE 5 y.o. girl, previously well. Recent history of weight loss and 2-3 days of fever. Presented tachypnoeic, poor central perfusion, drowsy but easily rousable. – pH 6.89 – PCO2 26 – PO2 23 (VBG) – HCO3 5 – BE -28 – Lactate 1.92 – Na 136 – K 3.8 – Cl 97

CASE ONE Profound, life-threatening raised anion-gap metabolic acidosis with co-existent respiratory acidosis. Severe whole-body potassium depletion. Evidence of hypoperfusion. – Causes: DKA (first presentation) Toxins Renal failure Lactate (normal)

CASE TWO 21 y.o. female, unwell for one month with worsening cough/SOB. Brought in by partner as he “couldn’t wake her” – pH 6.94 – PO2 459 (FiO2 1) – PCO2 134 – HCO3 27 – BE -7 – Lactate 8.94 – K 5.2

CASE TWO Life-threatening type 2 respiratory failure with coexistent mild metabolic acidosis with markedly elevated lactate: – Likely bronchospasm Other causes – Causes elevated lactate: Type A Type B

CASE THREE 29 y.o. female with chronic LBP and analgesic abuse presents with 3 days of bilateral ankle and facial swelling after taking “lots of painkillers”. – pH 7.01 – PO2 33 (VBG) – PCO2 35 – HCO3 9 – BE -22 – Na 138 – K 3.8 – Cl 120 – BSL 4

CASE THREE Severe non-anion gap metabolic acidosis with severe whole-body depletion of potassium. – ?causes

CASE FOUR 61 y.o. female, BIBA with ?seizure. 5-6 days of vomiting, some diarrhoea. – pH 7.65 – PCO2 55 – PO2 80 – HCO3 60 – BE >+30 – K 2.3 – Cl 69 – Lactate 1.76

What about the seizure?

CASE FOUR Profound metabolic alkalosis with complete respiratory compensation – Likely due to vomiting illness ?underlying cause of vomiting Severe hypokalaemia with marked prolongation of QTc, risk of arrhythmia/sudden death

CASE FIVE 54 y.o. male. Unwell with flu-like illness for two weeks, has had back ache for one week, for which he has been using “a cream”. – pH 7.60 – PO2 181 (FiO2 40%) – PCO2 16 – HCO3 15 – BE -4 – Na 135 – K 2.9 – Cl 98 – Lactate 1.2

CASE FIVE Severe respiratory alkalosis with co-existent raised anion gap metabolic acidosis – Causes?

CASE FIVE Causes respiratory alkalosis  CHAMPS – CNS disease – Hypoxia of any cause – Anxiety – Mechanical over-ventilation – Progesterone/pregnancy – Sepsis, salicylates and other toxins (methylxanthines)

CASE SIX 43 y.o. male, three day history of epigastric pain and recurrent vomiting. Tachycardic (130), tachypnoeic (36) but normotensive. PMHx moderate daily alcohol intake. – pH 7.47 – PCO2 23 – PO2 28 (VBG) – BE -6 – HCO3 17 – Lactate 2.38 – Na 136 – K 2.9 – Cl 85 – BSL 7.2 – Ketones “HI”

CASE SIX Complex acid-base disturbance: – Raised anion gap acidosis – Intercurrent metabolic alkalosis (given delta ratio, hypochloraemia, hypokalaemia) – Coexistent respiratory alkalosis – Ketosis, euglycaemic – Any thoughts?