Alkalosis: what is it, causes, symptoms, treatment, prognosis

What is alkalosis?

Alkalosis Is an abnormal pathophysiological condition characterized by the accumulation of excess base or alkali in the body. This results in an abnormally high serum pH (arterial pH above 7.45) called alkalemia and forms one end of the acid-base spectrum. Usually there is a loss of hydrogen (H) ions or an excess of bicarbonate (OH) ions, and any of these can be caused by several factors. In general, alkalosis is less life threatening than acidosisbut severe electrolyte disturbances can accompany alkalosis due to transcellular shifts, which can lead to rare but severe clinical disturbances. Alkalosis can be of respiratory or metabolic origin, but metabolic alkalosis is much more common than respiratory.

Signs and symptoms

Alkalosis can present with a variety of signs and symptoms, depending on the etiology of the alkalosis (respiratory or metabolic) and the primary condition leading to the alkalosis.

Metabolic alkalosis can manifest in the central nervous system ranging from confusion to coma, peripheral neuropathic symptoms such as tremors, tingling and numbness, muscle weakness and twitching, and arrhythmias, particularly when associated with hypokalemia and hypocalcemia. Non-hypochloremic metabolic alkalosis is associated with hypertension and is usually the result of mineralocorticoid overproduction syndromes. They usually correlate with signs of hypertension and hypokalemia.

Respiratory alkalosis may be accompanied by fainting, tremors and signs of hyperventilation, as well as chest pain and dyspnea.

Causes

The causes of alkalosis are classified into metabolic and respiratory causes:

Metabolic:

1. Excessive loss of hydrogen ions - this is mainly due to gastric losses (prolonged and severe gastric aspiration, excessive vomiting of gastric contents, as in pylorus stenosis, congenital chloridorrhea).
2. Increased content of bicarbonate in the extracellular space - This is due to excessive enteral intake of bicarbonate or alkali (lactic alkaline syndrome) or increased parenteral intake of citrate or acetate. Increased renal reabsorption of bicarbonate can also cause metabolic alkalosis (severe hypokalemia, primary hyperaldosteronism, Cushing's syndrome, Bartter's syndrome, Gitelman's syndrome, the use of a toxic amount of licorice, excessive use of chloruretic diuretics).
3. Alkalosis, diuretic-induced - diuretics (loop and thiazide), which block the reabsorption of sodium and chloride, may cause increased absorption bicarbonate in the proximal tubule, resulting in an increase in serum bicarbonate concentration, also called contractile alkalosis.

Respiratory:

1. Low CO2 production - hypometabolic conditions such as severe coma, especially with mechanical ventilation.
2. Excessive CO2 loss in the lungs - this leads to alkalosis when the body's CO2 production is normal (psychogenic hyperventilation, iatrogenic hyperventilation in patients with assisted ventilation or extracorporeal membrane oxygenation, early stages of salicylate overdose due to overstimulation of the respiratory center).

Epidemiology

Among the various acid-base disorders, metabolic alkalosis is the most common disorder in hospitalized patients, with an incidence of 51% in this group. Respiratory alkalosis is also common in hospitalized patients. According to hospital studies in the United States, the prevalence ranges from 22.5% to 44.7%. An Italian study showed a prevalence of respiratory alkalosis of 24% at the time of admission.

The incidence of mixed respiratory and metabolic alkalosis is estimated to be approximately 29%.

There appears to be no significant gender distribution of alkalosis, except in the case of infantile pyloric stenosis, when there is a predominance of males.

Pathophysiology

The body has a robust buffer system that minimizes pH changes in the early stages of acid-base disruption. When these buffer systems are overloaded, alkalosis can occur.

The kidneys try to maintain a normal acid-base balance through dual mechanisms of reabsorption bicarbonate, mainly in the proximal tubule, and bicarbonate production in the distal nephron. The reabsorption of bicarbonate is mediated by the antiporter Na-H (sodium hydrogen), as well as H (+) - ATPase (adenosine triphosphatase). Effects on bicarbonate reabsorption include effective arterial blood volume, glomerular filtration rate, and serum chloride and potassium concentrations. In conditions leading to respiratory alkalosis, the kidneys reduce bicarbonate reabsorption and bicarbonate production as a compensatory mechanism. This process helps maintain pH in the extracellular space to neutralize the effect of low pCO2, which is a major disorder of respiratory alkalosis. However, the complex kidney buffering mechanisms may take several days to achieve the full effect, with the possible expected drop in bicarbonate by 4-5 mmol / L for every 10 mmHg. when pCO2 falls.

On the other hand, respiratory depression leading to an increase in PaCO2 occurs rapidly and predictably to buffer alkalemia, resulting from metabolic conditions (although this varies, it is expected that there will be a 0.5 mmHg increase in PaCO2). 1 mmol / L increase in HCO). Alkalemia also shifts the oxyhemoglobin dissociation curve to the left, thereby increasing the affinity of hemoglobin for oxygen and decreasing the release of oxygen to tissues.

When potassium intake is suboptimal, it may correlate with metabolic alkalosis due to intracellular sodium, as well as with an increase in the level of protons and, as a result, a decrease in the level aldosterone. When protons move into the cell compartment, metabolic alkalosis sets in; this is followed by depression of the respiratory center and, ultimately, cleansing of the kidney from bicarbonate.

Histopathology

There are no specific histopathological features pathognomonic for alkalosis. However, the primary cause of alkalosis can be determined by histopathological examination, especially if it is associated with kidney disease or adrenal glands.

Diagnostics

Analysis of blood gases, preferably arterial, is necessary to establish alkalosis and its metabolic or respiratory origin. Additional blood tests are needed; it is the chemical composition of serum with electrolytes, blood urea nitrogen and creatinine. Although a high concentration of bicarbonate may indicate the possibility of metabolic alkalosis, it is not confirmation, since both the concentration of carbon dioxide and the concentration of H + ions will affect the presence or no alkalosis. Therefore, an assessment of blood gases pH and pCO2 is also necessary. However, with mixed acid-base disturbances, complex calculations are required to establish multiple violations and determine whether they are primary and / or concomitant disorders or mechanisms of compensatory buffering.

It is necessary to identify concomitant electrolyte disturbances, including hypochloremia, hypokalemia and hypocalcemia. An EKG may be required to evaluate arrhythmias. A urinalysis is needed to assess the kidney response to alkalosis. With arterial hypertension, evaluation and other tests for hyperaldosteronism are required if indicated. Volume depletion also needs to be assessed as a concomitant condition.

Respiratory alkalosis associated with hypoxia or an increased alveolar-arterial (Aa) gradient, requires a search for the cause of hypoxia. but pulmonary embolism can cause respiratory alkalosis without associated hypoxia and should be ruled out before hyperventilation is associated with pain or anxiety.

Treatment

Appropriate treatment of alkalosis is based on rapid identification and subsequent treatment of the primary etiology of alkalosis and the type of alkalosis (metabolic, respiratory, or mixed). Specific etiologies, such as pyloric stenosis, require surgical correction, while excessive alkali intake responds to limiting excess intake. Alkalosis associated with aldosterone excess conditions may require hormonal adjustment or replacement along with the treatment of associated hypertension. Correction of chloride-sensitive alkalosis caused by volume depletion is possible by replenishing the extracellular volume. Electrolyte disturbances associated with alkalosis, such as hypokalemia and hypocalcemia, are major causes of clinical deterioration in the patient's condition and should be corrected before life-threatening complications.

Treatment of respiratory alkalosis is primarily aimed at correcting hyperventilation (primary or iatrogenic) and, in addition to treating anxiety and pain, sometimes it also requires adjustment of mechanical ventilation if deliberate hypercapnia.

Forecast

Alkalosis, respiratory or metabolic, is usually compensated for by the innate buffering mechanisms of the body in the acute and subacute phases. When alkalosis is persistent or chronic, buffering mechanisms can be overwhelmed and this can lead to poor prognosis. The prognosis depends on concomitant problems with volume depletion, electrolytes and hormonal imbalances, and varies with the primary etiology of alkalosis.

Patients with metabolic alkalosis were found to have an increased length of stay in the intensive care unit, more days on mechanical ventilation, and higher hospital mortality. A 5 mEq / L increase in serum bicarbonate above 30 mEq / L correlated with a 1.21 odds ratio for hospital mortality. The relationship between metabolic alkalosis and mortality is independent of the etiology of alkalosis.

Complications

Alkalosis can cause life-threatening arrhythmias (atrial and ventricular tachyarrhythmias), especially when associated with hypokalemia and hypocalcemia. These associated electrolyte disturbances can also cause wrist spasms, muscle weakness, and changes in mental status.