The intensive care unit (ICU) presents nephrologists with various acid-base disorders due to critical illnesses like sepsis, diabetes, kidney failure, and therapeutic interventions. Recognising and treating these disorders is crucial for patient care.

Approach to acid-base imbalance

Normal blood pH ranges from 7.36 to 7.44, with deviations indicating acidemia or alkalemia. However, multiple acid-base disorders can coexist, making diagnosis complex.

Acid-base disorders are categorised into:

• Metabolic acidosis
• Metabolic alkalosis
• Respiratory acidosis
• Respiratory alkalosis

The systematic approach to acid-base disorders outlined here provides a clear framework for evaluating patients in the ICU. Let's break down the key steps:

1. History and physical examination: Begin by gathering a thorough patient history and conducting a physical examination to identify clues pointing to an acid-base disturbance. This step is crucial for understanding the context of the disorder.
2. Measure pH and PCO2: Obtain a blood gas analysis to determine if there is acidemia or alkalemia and whether it is metabolic or respiratory. This helps in identifying the primary disturbance.
3. Assess compensation: Determine whether compensation occurs based on the expected changes in PCO2 and bicarbonate levels for various acid-base disorders. Compensation rarely restores pH to normal levels but can provide insights into the underlying condition.
4. Calculate Anion Gap (AG): Calculate the anion gap using the formula (Na+ - (Cl- + HCO3-)) + 2.5(4 - albumin). An elevated AG suggests the presence of unmeasured anions, often indicating metabolic acidosis.
5. Evaluate changes in Anion Gap and bicarbonate levels: Assess the relationship between changes in AG and bicarbonate levels. An increase in AG should be accompanied by a corresponding decrease in bicarbonate, assuming the proton and bicarbonate spaces are roughly equivalent.

The approach also emphasises the importance of considering the patient's clinical context and interpreting laboratory values in conjunction with clinical findings.

Metabolic acidosis

Metabolic acidosis is a disturbance characterised by a decrease in the serum bicarbonate concentration, resulting in an imbalance of acid-base homeostasis. Here are some key factors contributing to metabolic acidosis:

1. Increased acid production: Metabolic acidosis can occur due to an increase in endogenous acid production, leading to an excess of acid in the body. This can result from conditions such as diabetic ketoacidosis (DKA), where there is an accumulation of organic acids like ketones, or lactic acidosis, which occurs due to increased lactate production.
2. Decreased acid excretion: Impaired renal function can lead to decreased excretion of acids by the kidneys, contributing to metabolic acidosis. This can occur in conditions such as kidney failure, where the kidneys are unable to effectively eliminate acids from the body.
3. Increased loss of base: Metabolic acidosis can also result from increased loss of bicarbonate or base from the body. This can occur through gastrointestinal (GI) losses, such as diarrhoea, where bicarbonate is lost in excess, or through renal losses, as seen in renal tubular acidosis (RTA).

• RTA Type 1 and 4: Renal tubular acidosis Type 1 and Type 4 involve defects in the renal tubules that impair bicarbonate reabsorption or potassium secretion, leading to metabolic acidosis.
• Hypoaldosteronism: Conditions causing hypoaldosteronism, such as Addison's disease, can result in impaired acid secretion and potassium retention, contributing to metabolic acidosis.

Metabolic alkalosis

Metabolic alkalosis is indeed a complex acid-base disorder commonly encountered in critically ill patients. It often arises as a result of various factors, including therapeutic interventions and underlying physiological imbalances.

1. Aetiology: Metabolic alkalosis can result from the gain of base or the loss of acid. Factors contributing to its development include aggressive therapeutic interventions like diuretic use, nasogastric suction, administration of certain intravenous fluids (such as those containing base equivalents), and rebound alkalosis following correction of conditions like sepsis or diabetic ketoacidosis.
2. Pathophysiology: The development of metabolic alkalosis involves phases where there is either an addition of bicarbonate (HCO3) or a loss of hydrogen ions (acid). This is followed by a maintenance phase where the kidneys are unable to excrete the excess HCO3 efficiently. Hypokalemia often exacerbates metabolic alkalosis through various mechanisms.
3. Complications: Metabolic alkalosis is associated with increased morbidity and mortality, although the exact causal relationship is debated. It can lead to complications such as hypocalcemia, respiratory depression, and cardiac arrhythmias.
4. Treatment: Management of metabolic alkalosis depends on addressing the underlying cause. Strategies may include correcting hypokalemia, volume depletion, or acid-base imbalances. Specific interventions like proton pump inhibitors for reducing gastric acid secretion or acetazolamide for increasing renal bicarbonate excretion may be considered based on the aetiology.
5. Monitoring: Continuous assessment of acid-base status and electrolyte levels is crucial for guiding treatment decisions. Adjustments may be made based on patient response and changes in clinical parameters.

Respiratory alkalosis

Respiratory alkalosis, characterised by a decreased level of carbon dioxide (CO2) in the blood, is indeed a common occurrence in the intensive care unit (ICU) setting. Here are some key factors contributing to respiratory alkalosis in critically ill patients:

1. Sepsis: Sepsis, a severe immune response to infection, often manifests with an increase in respiratory rate as part of the body's attempt to compensate for the metabolic acidosis that can accompany septic shock.
2. Liver cirrhosis: Patients with cirrhosis may experience an increase in respiratory rate, likely due to elevated levels of progesterone, a hormone that affects respiratory drive. This respiratory alkalosis is presumed to be secondary to hormonal changes associated with liver dysfunction.
3. Hypoxia-induced hyperventilation: Conditions such as heart failure, acute asthma, pulmonary embolism, and interstitial lung disease can lead to hypoxia, stimulating an increase in respiratory drive and resulting in hyperventilation. This hyperventilation causes a decrease in CO2 levels, contributing to respiratory alkalosis.
4. Anxiety and stress: The stress and anxiety experienced by patients in the ICU environment can also lead to hyperventilation and subsequent respiratory alkalosis.
5. Inadequate sedation and pain control: Critically ill patients on mechanical ventilation may experience.

Mixed acid-base disorders

Disclaimer- The views and opinions expressed in this article are those of the author and do not necessarily reflect the official policy or position of M3 India.

About the author of this article: Dr Bhavin Mandowara is a practising nephrologist at Zydus Hospital, Ahmedabad.