Metabolic Disorders

Melissa Davis, MSIV

Arterial Blood Gas

pH/PaCo2/PaO2/ HCO₃¯ /O2 Sat

7.4/40/95/24/98

• First determine if the patient is Oxygenating by determining the Pa02/FiO2

• PaFi >300 is normal

Primary Disorder

Normal pH

7.35-7.45

Normal HCO₃¯

21-27mEq/L

Start at HCO₃¯ HCO₃¯

Decreased

pH

Low

Metabolic Acidosis

High

Respiratory Alkalosis

Elevated

pH

Low

Respiratory Acidosis

High

Metabolic Alkalosis

Metabolic Acidosis

Normal Osmolal Gap <10

Normal Urine AG 30-50

Normal AG

12 ±2

Always Calculate Anion Gap

Anion Gap

Elevated

Osmolal gap

Elevated

Consider Ethylene Glycol

or Methanol

Normal

Consider Ketoacidosis, Lactic Acidosis, Renal Failure, ASA Toxicity

Normal

Urine Anion Gap

Negative

Extra Renal Cause

Positive

Renal Cause

Anion Gap

Cations

Na+

Anions

Unmeasured Anions

HCO₃¯

Cl-

Anion Gap= [Na+] – [Cl- + HCO₃¯ ]

Low Anion Gap

• Most unmeasured anions consist of albumin

– Hypoalbuminemia may cause a low AG

• Serum AG falling by 2.5meq/L for every 1 g/dL (10 g/L) reduction in the serum albumin concentration

• Increased Light Chains (Multiple Myeloma)is an unmeasured cation

– This results in a Low Anion Gap

MUDPILESMethanol

Uremia

Diabetic Ketoacidosis

Paraldehyde

Isoniazid or Iron tablets

Lactic Acidosis

Ethylene Glycol

Salicylate Toxicity

Osmolal Gap

Calculated Osmolality = 2 𝑁𝑎 + 𝑔𝑙𝑢𝑐𝑜𝑠𝑒18 + ( 𝐵𝑈𝑁

2.8)

Osmolal Gap = [Measured Osmolality] – [Calculated Osmolality]

Reasons for Increased Osmolal Gap: • The presence of an additional solute or solutes ( i.e. Ethanol,

Methanol, or Ethylene Glycol• The measured sodium concentration may be spuriously

reduced (called pseudohyponatremia) with marked hyperlipidemia or hyperproteinemia.

Normal Osmolality: 280 mosmol/kg

Urine Anion Gap

Indirect estimate of urinary ammonium (NH4+) excretion, which is not measured directly in clinical practice.

• Extrarenal causes have an increase in NH4+ excretion because they kidneys are responding appropriately to the acidosis and attempting to rid the body of H+.

• NH4+ is excreted in the form of NH4Cl thereby making the UAG negative.

Urine AG= ([UNa+] + [UK+]) – [UCl-]

Normal Urine AG: 30-50mEq/L

BloodRenal CellUrine

NH4+

NH4+ Cl-

NH4Cl

NH3 H+

Positive Urine Anion Gap

• Renal Causes

– Renal Tubular Acidosis

BloodRenal CellUrine

NH4+

NH4+ Cl-

NH4Cl

NH3 H+

RTA Type 2 (proximal)

RTA Type 1(distal)

RTA Type 4

H+

Mixed Disorders• Is there a compounding metabolic or respiratory disorder?• Determine what the HCO₃¯ would be if there were no Anion Gap by

calculating the Corrected [HCO₃¯ ].• Determine if the change is PCO2 is appropriate compensation for

the primary metabolic acidosis.

Corrected [HCO₃¯ ] = measured [HCO₃¯ ] + [AG – 12]

Expected Respiratory Compensation

Acute 𝐏𝐂𝐎𝟐 = 𝟏. 𝟓 × HCO₃¯ + 𝟖

Chronic 𝑃𝐶𝑂2 = HCO₃¯ + 15

Quick Check PCO2 value should approximate last 2 digits of pH

If PCO2 is not equal to expected compensatory value consider secondary respiratory disorder.

Metabolic Alkalosis

Urine Chloride

<20 mEq/L

Chloride Responsive

Gastrointestinal Loss

Renal LossAlkali

AdministrationContraction

Alkalosis

>20 mEq/L

Chloride Resistant

HyperaldosteronismZebras

Call Nephrology

Loss of H+ leads to an increase in HCO₃¯ , when renal excretion of HCO₃¯ is not equal to its production a metabolic alkalosis manifest.

Chloride Responsive Metabolic Alkalosis

• Delivery of NaCl to the distal tubule in the presence of Aldosterone results in H+ and K+ loss which maintains alkalosis.– GI Loss

• Vomiting, NG Tube

– Renal Loss• Diuretics

– Alkali Administration

– Contraction Alkalosis• Volume Loss leads to RAAS activation which causes a

metabolic alkalosis.

Mixed Disorders

Expected Respiratory Compensation for Metabolic Alkalosis

For every 1mEq/L increase in [HCO₃¯ ], PCO2 should increase 0.7 mm Hg

If PCO2 is not equal to expected compensatory value consider secondary respiratory disorder.

Respiratory Acidosis

Hypoventilation

CNS DepressionRespiratory

Muscle Weakness

Airway Obstruction

V/Q Mismatch

Causes of Respiratory Acidosis

• CNS Depression– Stroke– Opiates

• Respiratory Muscle Weakness– Myasthenia Gravis– Chest Wall Deformity

• Airway Obstruction– COPD

• V/Q Mismatch– Pulmonary Embolism

Mixed Disorders

Expected Renal Compensation for Respiratory Acidosis

Acute 1 mEq/L increase in [HCO₃¯ ] for each 10 mm Hg increase in PCO2

Chronic 3.5 mEq/L increase in [HCO₃¯ ] for each 10 mm Hg increase in PCO2

If [HCO₃¯ ] is not equal to expected compensatory value consider secondary metabolic disorder.

It is physically impossible to have a Respiratory Acidosis and Respiratory Alkalosis at the same time!

Respiratory Alkalosis

Respiratory Alkalosis

Pulmonary Vasculature

Disease

Pulmonary Parenchymal

DiseaseHyperventilation

Respiratory Alkalosis• Chronic Respiratory Alkalosis typically has

comorbid hyperchloremia– Due to retention of Cl- as HCO₃¯ is excreted in the

kidneys.

• Causes– Pulmonary Vasculature Disease

• Pulmonary HTN

– Pulmonary Parenchymal Disease• Pulmonary Fibrosis• Pneumonia

– Hyperventilation• Anxiety• Asprin Toxicity• Pregnancy

Mixed Disorders

Expected Renal Compensation for Respiratory Alkalosis

Acute 2 mEq/L decrease in [HCO₃¯ ] for each 10 mm Hg decrease in PCO2

Chronic 4-5 mEq/L decrease in [HCO₃¯ ] for each 10 mm Hg decrease in PCO2

If [HCO3-] is not equal to expected compensatory value consider secondary metabolic disorder.

It is physically impossible to have a Respiratory Acidosis and Respiratory Alkalosis at the same time!

References

• Internal Medicine ESSENTIALS for Students: A Companion to MKSAP® for Students 5 (2011)-American College of Physicians

• Step-Up to Medicine Second Edition (2008)- S. Agabegi & E. Agabegi

• Up to Date: Approach to the adult with metabolic acidosis; Methanol and ethylene glycol poisoning; Serum osmolal gap; Urine anion and osmolal gaps in metabolic acidosis; Pathogenesis of metabolic alkalosis