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37 Cards in this Set
- Front
- Back
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*what is the base excess?
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mEq of acid or base needed to titrate 1 L of blood to pH 7.4 if PaCO2 constant at 40 mm Hg
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*formula for estimating sodium bicarb to be given
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NaHCO3 (in mEq) = base deficit (mEq/L) x ECF space (L) where ECF = 0.3x lean body mass in Kg
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formula for anion gap
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Na - (Cl + HCO3)
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what causes the normal anion gap?
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negative charges of plasma proteins
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causes of increased anion gap
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lactic acidosis or ketoacidosis, ingestion of organic anions (salicylate, methanol and ethylene glycol) renal retention of anions (sulfate, phosphate, urate)
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define A-a gradient
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difference between alveolar oxygen (PAO2) and oxygen in the blood (PaO2)
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normal A-a gradient
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10-15 torr
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significance of an increased A-a gradient
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increased difficulty in getting O2 from alveoli to blood
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*normal increase in A-a gradient
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advancing age (2.5 + 0.21 x age in years) and higher FiO2
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*abnormal increase in A-a gradient (etiologies)
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interstitial diseases (ILD, PNA, CHF), pulmo vasc disease (PE, shunts, pulmo HTN); V/Q mimatches
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*best use of A-a gradient
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determining severity of underlying disorder and whether there is a component of hypoventilation (if A-a gradient normal - ABG abnormality is all due to hypoventilation)
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3 main causes of increased A-a gradient
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ILD, V/Q mismatch, R-L shunts
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normal value for base deficit / excess
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-2 to +2
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two rules derived from HH equation
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change in PCO2 by 10 is associated with change in pH by 0.08; pH change of 0.15 is equivalent to base change of 10 mEq/L
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metab acidosis, expected PCO2 compensation
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PCO2 = (1.5 x [HCO3–])+8
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metabolic alkalosis expected PCO2 compensation
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inc in PCO2 = change in [HCO3–] x 0.6
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acute resp acidosis, expected HCO3 compensation
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inc in [HCO3–] = change PCO2/10
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chronic resp acidosis, expected HCO3 compensation
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inc in [HCO3–] = 4 x change in PCO2/10
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acute resp alkalosis, expected HCO3 compensation
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dec in [HCO3–] = 2 x change in PCO2/10
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chronic resp alkalosis, expected HCO3 compensation
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dec in [HCO3–] = 5 x change in PCO2/10
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steps in ABG analysis
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determine primary disorder, calculate expected compensatory response, calculate AG, if elevated, compare changes from normal between AG and HCO3
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how to interpret delta delta?
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change in AG / change in HCO3; if same, no metabo alkalosis or nongap metab acidosis; if >1, metab alkalosis present in addition to gap MA; if < 1, nongap MA present in addition to gap MA
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*causes of HAGMA (exogenous)
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salicylates, methanol, paraldhyde, ethylene glycol, hyperalimentation, ETOH ketoacidosis
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*causes of HAGMA (endogenous)
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lactic acidosis, ketoacidosis TA, CAI(DM, starvation), uremia
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causes of NAGMA renal
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RTA, carbonic anhydrase inhibitor, post hypocapnia
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causes of NAGMA gut
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diarrhea, fistula, ileal loop
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high anion gap
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>12
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normal AG
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8-12
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when to start bicarbonate therapy
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severe metabolic gap acidosis (pH <7.20)
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*formula for total replacement dose of HCO3
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HCO3 needed in mmol = base deficit (mmol) x Kg BW / 4; replace with 1/2 over 8-12 hours and reevaluate
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chloride resistant metabolic alkalosis
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excess mineralocorticoid (Cushing, hyperaldosteronism, exogenous steroids, Bartter syn)
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chloride responsive metabolic alkalosis
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renal loss (diuretics, post-hypercapnia) GI loss of H or Cl (NG suctioning, vomiting, chloride-wasting diarrhea)
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mechanism of metab alkalosis in chloride sensitive metabolic alkalosis
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loss of chloride (renal or GI) results in renal sodium conservation and reabsorption of HCO3 by kidney
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mechanism of metab alkalosis in chloride resistant metab alkalosis
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direct stimulation of kidneys to retain HCO3 irrespective of electrolyte intake and losses
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treatment of metabolic alkalosis
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chloride-responsive - replace volume with NaCl; if chloride-resistant, corect underlying problem
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DDx of respiratory acidosis
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NM abnormalities with vent failure, CNS (drugs, CVA, central sleep apnea, SCI); airway obstruction (COPD, asthma, OSA); thoracic pulmonary disorders (kyphoscoliosis, pneumothorax, severe pulmo edema, severe PNA, large pleural eff, scleroderma, marked obesity)
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salicylate overdose
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metab gap acidosis + resp alkalosis
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