Magnesium (normal range 1.5–2.4 mg/dL) is essential for enzyme function and plays a role in several physiological processes, including protein synthesis, heart rhythm regulation, and muscle and nerve function. Magnesium is primarily regu­lated by the kidneys but several factors can affect magnesium homeostasis, including the patient’s clinical condition, medications (e.g., loop diuretics, amphotericin B, regional anticoagulation with citrate), and alcohol use.

Severe hypomagnesemia (serum magnesium concentration of<1.0 mg/dL) can result in life-threatening conditions such as electrocardiographic changes, arrhyth­mias, seizures, and coma. Hypomagnesemia may cause concomitant refractory hypokalemia and hypocalcemia. Treatment is empirical and involves the adminis­tration of magnesium intravenously. Hypermagnesemia (>2.4 mg/dL) can cause symptoms such as nausea, vomiting, and loss of deep tendon reflexes, and in severe cases, respiratory paralysis, refractory hypotension, and even death. Treatment can involve magnesium restriction, diuretics, or hemodialysis. I.V. calcium should be administered to patients with severe symptomatic hypermagnesemia to reverse the cardiovascular and neuromuscular effects. The normal serum concentration of phosphorus is between 2.7 and 4.5 mg/dL and is essential for various physiological, metabolic, and homeostatic functions that re quire energy. It is particularly important for critically ill patients in the ICU, who may have higher phosphorus requirements due to hypermetabolism. Phosphorus and phosphate are necessary for glucose utilization, ATP synthesis, 2,3-diphosphoglycerate synthesis and function, neuro­muscular function, including the myocardium and diaphragm. If serum phosphorus levels are too low (hypophosphatemia), it can result in serious consequences such as respiratory failure, tissue hypoxia, paralysis, weakness, paresthesia, and seizures. Certain underlying conditions and treatments can cause hypophosphatemia in crit­ically ill patients, including malnutrition, alkalosis, and diabetic ketoacidosis. Treat­ment involves the administration of phosphate in oral form for the mild forms and intravenous for the severe and symptomatic ones. Hyperphosphatemia is defined as a serum phosphorus concentration greater than 4.5 mg/dL and is most caused by renal insufficiency in critically ill patients. It can also be caused by hemolysis, rhabdo­myolysis, hypoparathyroidism, and vitamin D toxicity. The most common clinical manifestation of hyperphosphatemia is hypocalcemia, which can lead to tetany and other symptoms of hypocalcemia. The risk of hypocalcemia increases when the serum calcium level multiplied by the serum phosphorus concentration exceeds 55–60 mg

Therefore, as the concentration of hydrogen ions increases,

the solution’sp decreases and vice versa. If we consider the narrow range of pH values compatible with life, we might think that biological tissues are extremely susceptible to varia­tions in H that a reduction in pH from 7.4 to 7 results in an increase in [H half times, which is significantly higher than the body can tolerate for variations in Na

There are extracellular buffer systems (ECB) and intracellular buffer systems (ICB). Although the latter are more relevant, both quantitatively and qualitatively, they are more difficult to measure. For this reason, extracellular buffers are used as a reference, particularly the bicarbonate buffer [HCO

From these definitions, the conditions of acidosis and alkalosis are not necessarily associated with an actual change in blood pH: the possibility of detecting a modi­fication of blood pH depends on the eventual development of a compensatory response and its degree. Therefore, in the absence of adequate compensation

(Table

in the second case, it is metabolic (Table 3.5).

If the pathological condition is characterized by the combination of two or more primary disturbances of the acid-base balance, it is defined as a mixed disorder. The treatment of a mixed disorder requires the management of the individual distur­bances present.

A disorder characterized by a primary reduction in [HCO

Increased acid presence is observed instead in cases of exogenous intoxication (methanol, ethylene glycol, formic acid, etc.) or due to an increase in endogenous acid components, such as in lactic acidosis (shock states, metformin intoxication, etc.), diabetic ketoacidosis, or even hyperuricemia.

To make a correct diagnosis of metabolic acidosis and determine the underlying cause, the concept of Anion Gap (AG) is particularly useful, representing the concentration of unmeasured anions in the plasma. Since every solution must respect the principle of electroneutrality, the sum of negative charges present in the plasma must be equal to those positive, and thus:

The Anion Gap (AG) includes proteins, phosphates, and sulfates, which is why AG must be corrected in case of hypoalbuminemia (for every g/dl reduction in albumin concentration compared to its reference value, AG is reduced by approxi­mately 2.5 mmol/L). Therefore, we will divide metabolic acidosis as follows:

Metabolic acidos

the Urinary Anion Gap (AGu).

and K

1. Inadequate alveolar ventilation due to depression of the respiratory centers at the

central level (neuroleptic intoxication, trauma, cerebral hemorrhage, etc.), inter­ruption of the transmission of the nerve impulse from the respiratory centers to the respiratory muscles (spinal cord lesions above T4, neuromuscular blockers, tetanus, botulism, Guillain-Barre syndrome, etc.), and lung diseases that reduce the ventilatory surface (COPD, ARDS, interstitial fibrosis, etc.).

without a

correspondingly rapid excretion of excess bicarbonates.

Under normal conditions, the kidney can rapidly correct a metabolic alkalosis, thanks to its ability to readily eliminate excess bicarbonate, especially when plasma levels exceed 24 mmol/l. For the development of metabolic alkalosis, the presence of factors that promote the onset of the disorder is necessary, generating an excess of bicarbonate (“initiating factors”), but also of factors that promote the renal conser­vation of the excess bicarbonate (“promoting factors”). The excess of bases can derive from exogenous administration of the same (repeated transfusions with an accumulation of citrate, excessive administration of lactate and gluconate), from the depletion of chloride due to hyperemesis, diuretics, or excessive fecal loss (the deficit of Cl reabsorb HCO mineralocorticoids, which in turn are capable of increasing the reabsorption of HCO

By embracing evidence-based practices and individualizing therapeutic approaches based on patient-specific needs, healthcare providers can mitigate the deleterious effects of fluid and electrolyte disturbances, fostering improved clinical trajectories and enhanced patient well-being. As our understanding of these phe­nomena continues to evolve, ongoing research endeavors and interdisciplinary collaboration will be essential in refining diagnostic modalities, therapeutic inter­ventions, and prognostic stratification strategies, ultimately advancing the standard of care for critically ill patients worldwide.