Acid-Base Disturbances

Initial Approach

1. What is the primary derangement and is it metabolic or respiratory?

   • Acidosis = pH < 7.35

     • Respiratory: pCO2 > 40

     • Metabolic: pCO2 < 40

   • Alkalosis = pH > 7.45

     • Respiratory: pCO2 < 40

     • Metabolic: pCO2 > 40

2. Is the primary derangement acute/chronic and adequately compensated?

   • Clinical assessment and a blood gas (arterial or venous) are needed to determine etiology and degree of compensation

   • Respiratory acidosis

     • Acute

       • Δ PaCO2 of 1 → Δ pH 0.01

       • For every ↑ 10 mEq PaCO2 = ↑ 1 mEq HCO3

     • Chronic: For every ↑ 10 mEq PaCO2 = ↑ 3-5 mEq HCO3

   • Metabolic acidosis: Expected PaCO2 = (1.5 x HCO3) + 8 +/- 2

     • If measured PaCO2 is higher than expected, then respiratory compensation is inadequate, i.e. respiratory acidosis.

     • If measured PaCO2 is lower than expected, it implies underlying respiratory alkalosis.

   • Metabolic alkalosis: Expected PaCO2 = (0.7 x HCO3) + 21 +/- 2

     • If measured PaCO2 is higher than expected, it implies acute respiratory acidosis, i.e. inadequate respiratory compensation.

     • If measured PaCO2 is lower than expected, it implies underlying respiratory alkalosis.

Respiratory Acidosis Etiology

• Central nervous system depression

  • Acute: Trauma, intoxication, encephalitis

  • Chronic: Neuromuscular disease, e.g. muscular dystrophy

• Lung disease

  • Asthma/COPD exacerbation

  • Pneumonia

  • Pleural effusion

Metabolic Acidosis Etiology

Anion gap

• [Na+] - ([Cl-] + [HCO3-])

• Normal anion gap ≈ 12

High Anion Gap Metabolic Acidosis (HAGMA): MUDPILES

• Methanol

• Uremia

• DKA

• Paraldehyde

• Iron, INH toxicity

• Lactic acidosis

• Ethanol, ethylene glycol

• Seizure, starvation, salicylates (aspirin)

Normal Gap Metabolic Acidosis: USED CAR

• Urinary-colonic fistula

• Saline

• Endocrine disorders of aldosterone, e.g. Addison’s disease

• Diarrhea

• Carbonic anhydrase inhibitor, e.g. acetazolamide

• Alimentary (total parenteral nutrition)

• Renal tubular acidosis

Etiology per Pathophysiology

• HAGMA due to increased acid ingestion/production

  • Lactic acidosis

    • Hypoxia including hypovolemic, cardiogenic, and distributive (septic) shock

    • Systemic disease, e.g. cirrhosis, malignancy

  • Ketoacidosis: Starvation, Alcohol, DM (ketoacidosis = SAD)

  • Acid ingestion: Methanol, ethylene glycol, salicylic acid (aspirin)

• Normal anion gap metabolic acidosis: HCO3 versus H+

  • Bicarbonate: Decreased production or increased elimination

    • Diarrhea

    • Carbonic anhydrase inhibitors

    • Type 2 (proximal) renal tubular acidosis

  • Decreased renal acid excretion

    • Chronic kidney disease

    • Renal tubular acidosis types 1 and 4

Additional Calculations

• Osmolar gap = Measured serum OSM - [2(Na+) + (glucose/18) + (BUN/2.8)]

  • Normal ≈ 10 to 15

  • Used to help further differentiate HAGMA etiology in cases of toxic ingestion

    • > 10 to 15 but < 25 indicates alcohol toxicity, e.g. methanol, ethanol, ethylene glycol, propylene glycol, isopropyl alcohol

    • > 25 indicates methanol or ethylene glycol

• Urine anion gap = [(urine Na)+(urine K)] - urine Cl

  • Normal ≈ 0

  • Negative balance indicates gut losses

  • Significantly elevated balance indicates chronic kidney disease or renal tubular acidosis

Acidosis Management

Metabolic

• Treat underlying etiology: DKA, lactic acidosis (shock/cirrhosis/malignancy), diarrhea, CKD, toxic ingestion

• Severe acidosis (pH < 7.1)

  • Transfer patient to ICU and assess for intubation

  • Initiate sodium bicarbonate at 50 to 100 mEq per day and titrate to pH > 7.3

Respiratory (hypercapnia)

• Treat underlying etiology

  • Common: Asthma, COPD, PNA

  • Additional considerations: Trauma (e.g. tension pneumothorax), toxic ingestion (e.g. opioids), pleural effusion

• Hypercarbia/CO2 narcosis in patient with altered mental status, RR > 25, and/or pH < 7.3:

  • Initial evaluation

    • Consider contributing etiologies (see above)

    • Note: Altered conscious does not usually occur until PaCO2 > 75 mmHg

  • Start BiPaP 12/5 at 30% FiO2

    • Increase FiO2 by 5% every 10 minutes to achieve to SPO2 90-93%, i.e. FiO2 30% → 25% → 40% → etc.

    • If pt cannot tolerate BiPaP, transfer to ICU for sedation and monitoring

  • Provided continued hemodynamic stability, recheck ABG after 1 hour if significant clinical improvement is noted

  • Intubate for any of the following

    • Development of hemodynamic instability

    • No significant improvement of clinical status and ABG values after 1 hour

• Intubate for pH < 7.2

Alkalosis

Common Etiologies

• Metabolic

  • Diuretic therapy

  • Gastric secretion loss (vomiting)

• Respiratory

  • Acute: Hyperventilation (multiple respiratory etiologies)

  • Chronic: Pregnancy, heart failure, hepatic failure, hyperthyroidism

• Treatment

  • Address underlying etiology, e.g. stop diuretics, control nausea, etc.

  • Consider administration of one of the following:

    • Potassium chloride if hypokalemia is present

    • Acetazolamide (carbonic anhydrase inhibitor) 500 mg IV x 1 dose