Acid-Base Disturbance

by Lamiess Osman, Qais Abuagla



  • Acid: a substance that is capable of donating a hydrogen ion to another substance
  • Base: the substance that is capable of receiving a hydrogen ion.
  • Acidemia is serum pH < 7.35.
  • Alkalemia is serum pH > 7.45.
  • Acidosis refers to physiologic processes that cause acid accumulation or alkali loss.
  • Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss.

Defense Mechanisms

The body has three defense mechanisms to maintain normal pH:

  1. The buffering system.
  2. The respiratory system.
  3. The renal system.

Among the three systems, the buffering is the fastest means of preventing disturbances in pH. It was likened to a ”sponge” that soaks up excessive hydrogen ions and releases them when there’s a deficient concentration. Several buffering agents bind hydrogen ions reversibly. These include bicarbonate, ammonia, hemoglobin and plasma proteins.

The respiratory system is a key player in acid-base regulation, albeit acting slightly slower than the buffer system. Central and peripheral chemoreceptors, when stimulated, increase the rate and depth of respiration when carbon dioxide (CO2) or hydrogen ions levels are elevated. This increases the rate of CO2 elimination from the lungs, resulting in less CO2 available to form carbonic acid.

The Renal system is a much slower process for dealing with hydrogen ion concentration change, taking hours to days. Therefore, it is more important for the long-term maintenance of acid-base balance. The kidneys can reabsorb bicarbonate and excrete hydrogen ions.

In clinical practice, the recognition of one acid-base disorder must prompt the search for other concurrent disorders. Due diligence must be exercised to complete the evaluation of the arterial blood gas (ABG) and manage it in the clinical context.

Case Presentation

A 15-year-old female presented with dyspnea, polyuria, and polydipsia for the last 3 days. She was slightly lethargic with dry oral mucosa. Vitals were BP 92/45mmHg, RR 27/bpm, HR119/bpm, Temp 37°C, SpO2 99% on INO2 1L/min. Physical examination revealed normal findings except there was a mild abdominal tenderness without guarding.

A bedside arterial blood gas revealed the following:

  • pH: 7.19
  • PaO2: 105mmHg
  • PaCO2: 19mmHg
  • HCO3: 7mmol/L
  • Na: 124mmol/L
  • K: 3.4mmol/L
  • Cl: 91mmol/L
  • Gluc: 310mg/dL
  • BUN: 13mmol/L

The patient was put under close monitoring, and intravenous fluids were initiated. Urine dipstick showed glucose 4+ with ketones. A diagnosis of diabetic ketoacidosis was made. The arterial blood gas (ABG) was evaluated at the end of the chapter for this case.

Critical Bedside Actions and General Approach

The emergency department is where you will first encounter sick patients having critical situations including acide-base disorders. Thetefore, you must have the ability to diagnose and manage acid-base derangement. However, every critically ill patient should be evaluated for airway, breathing and circulation in the initial assessment phase and necessary resuscitation effort should be applied. Many of the patients with acid-base problem require cardiac monitorization, IV lines, supplemental fluid and oxygen during the initial evaluation phase.

An acid-base derangement may contribute to the patient symptoms and in some cases signifies an immediate life threat.
The body produces acid as a byproduct of basal metabolism. Respiratory acids are made up of carbon dioxide; as an end product of the metabolism of carbohydrates and fats. Although CO2 is not an acid in itself, when combined with water it forms carbonic acid, which is capable of dissociating to hydrogen ions and bicarbonate ions. Lungs can excrete CO2 it is known as volatile acids. However, many acids are referred to as fixed acids such as ketoacidosis and lactic acid, and they depend on the kidneys for their excretion.

The body concentration of hydrogen ions must be maintained within a strict range for optimal cellular function, and even a small deviation can significantly affect the patient. This underscores the importance of being able to evaluate a blood gas for an acid-base disorder. Essentially, this is accomplished by these laboratory values: pH, PaCO2, and serum HCO3. Na and Cl are also required in the anion gap analysis.

5 Simple Steps to Solve an Acid-Base Problem


  • Metabolic Acidosis

    • Calculate the Anion Gap. AG = Na- (Cl + HCO3)
    • Normal anion gap is 8-16.
    • Causes of high anion gap metabolic acidosis (i.e., AG >16) can be remembered using mnemonic: “MUD PILES.”
      • Methanol
      • Uremia
      • DKA
      • Paraldehyde
      • Isoniazid
      • Lactic Acidosis
      • EtOH/Ethylene glycol
      • Salicylates
    • Causes of a normal anion gap metabolic acidosis (i.e., AG <16) can be remembered using the mnemonic: “HARDUPS”
      • Hyperalimentation/Hypoaldosteronism
      • Acetazolamide
      • Renal tubular acidosis
      • Diarrhea
      • Uretero-Pelvic shunt
      • Post hypocapnia
      • Spironolactone
  • Respiratory Acidosis

From a pathophysiological perspective, the two broad categories are V/Q mismatch with/out increased CO2 production, and alveolar hypoventilation due to either central causes or chest wall-neuromuscular disorders. Causes can also be classified according to its acuity.

  • Acute causes:
    • CNS depression (cerebrovascular accident/drugs)
    • Airway obstruction
    • Pneumonia
    • Pulmonary edema
    • Hemo/pneumothorax
    • Myopathy
  • Chronic cause:
    • Chronic obstructive pulmonary disease (COPD)
    • Restrictive lung disease
  • Metabolic Alkalosis

  • Obtain a urine Chloride level and remember the following mnemonic: “CLEVER PD”
    • Contraction (due to blood loss)
    • Licorice *
    • Endocrine (Conn’s/ Cushing’s/ Batter’s)*
    • Vomiting/nasogastric suction
    • Excess Alkali*
    • Refeeding Alkalosis*
    • Post-hypercapnia
    • Diuretics*
      (* associated with high urine Cl level)
  • Respiratory Alkalosis

This is secondary to excessive ventilation, i.e., excessive respiratory rate and/or depth from the following causes:

  • CNS disease
  • Hypoxia
  • Anxiety
  • Mechanical ventilation
  • Progesterone
  • Salicylates
  • Sepsis

Looking Back To Our Case

Step 1: Interpretation of pH
The pH <7.35 indicating acidosis

Step 2: Evaluate the primary process that accounts for the deranged pH.
The low HCO3 with a low PaCO2 indicates that the main primary disorder is metabolic acidosis.

Step 3: Evaluate for appropriate, over or under compensation: indicating the concurrent primary acid-base disorder in the compensating system.

Using the Winter’s formula {expected PaCO2 =1.5[HCO3]+ 8 (±2)}, the expected PaCO2 is 18.5. The patient’s actual PaCO2 (19mmHg) lies within this range. This means that the respiratory compensation is appropriate and there was no concurrent respiratory acid-based disorder.

Step 4: Calculate the Anion Gap, Anion Gap and delta HCO3
AG = Na – (HCO3 + Cl) ±4). The patient’s AG is 26±4 {i.e. 124 – (7 + 91 ) ±4}.
AG = AG-12. The patient’s AG is 14±4 {i.e.26-12(±4)}.

Delta HCO3 = 24-HCO3. The patient’s delta HCO3 is 17 {i.e. 24-7}
Since this drop in HCO3 (17) lies within the increased in AG (14±4), there is no second metabolic disorder.

In conclusion, the patient’s ABG is a pure High Anion Gap Metabolic Acidosis. As a Step 5, look for the causes of defined acid/base situation. In this case, use MUD PILES mnemonic to find specific problem.

References and Further Reading

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