Acid–base disorders | Alkalosis and Acidosis



what are the acid base disorders
Acid–base disorders are caused by disturbances in hydrogen ion (H+) homeostasis, which is ordinarily maintained by extracellular buffering, renal regulation of hydrogen ion and bicarbonate, and ventilatory regulation of carbon dioxide (CO2) elimination.

Buffering refers to the ability of a solution to resist change in pH after the addition of a strong acid or base. The body’s principal extracellular buffer system is the carbonic acid/bicarbonate (H2CO3/HCO3−) system.




Most of the body’s acid production is in the form of CO2 and is produced from
Catabolism of carbohydrates, proteins, and lipids.

There are four primary types of acid–base disturbances, which can occur independently or together as a compensatory response.

Metabolic acid–base disorders are caused by changes in plasma bicarbonate concentration
(HCO3−). Metabolic acidosis is characterized by decreased HCO3−, and metabolic alkalosis is characterized by increased HCO3−.

Respiratory acid–base disorders are caused by altered alveolar ventilation, producing changes in arterial carbon dioxide tension (Paco2). Respiratory acidosis is characterized by increased Paco2, whereas respiratory alkalosis is characterized by decreased Paco2.

Diagnosis

• Blood gases, serum electrolytes, medical history, and clinical condition are the primary tools for determining the cause of acid–base disorders and for designing therapy.

• Arterial blood gases (ABGs) are measured to determine oxygenation and acid–base status. Low pH values (greater than 7.45) indicate alkalemia. The Paco2 value helps determine whether there is a primary respiratory abnormality, whereas the HCO3− concentration helps determine whether there is a primary metabolic abnormality.

 
Metabolic acidosis- pathophysiology and treatment
 
Metabolic acidosis is characterized by decreased pH and serum HCO3− concentrations, which can result from adding organic acid to extracellular fluid (e.g., lactic acid and ketoacids), loss of HCO3− stores (e.g., diarrhea), or accumulation of endogenous acids due to impaired renal function (e.g., phosphates and sulfates).
Serum anion gap (SAG) can be used to elucidate the cause of metabolic acidosis. SAG is calculated as follows:
SAG = [Na+] − [Cl−] − [HCO3−]
The normal anion gap is approximately 9 mEq/L (9 mmol/L), with a range of 3 to 11
mEq/L (311 mmol/L). SAG is a relative rather than an absolute indication of the cause of metabolic acidosis.



The primary compensatory mechanism is to decrease Paco2 by increasing the respiratory rate.



Clinical presentation

• Relatively asymptomatic; major manifestations are bone demineralization with the development of rickets in children and osteomalacia and osteopenia in adults. 
Acute severe metabolic acidemia (pH below than7.2) involves the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. Respiratory compensation may occur as Kussmaul respirations (ie, deep, rapid respirations characteristic of diabetic ketoacidosis).
• Alkali therapy can be used to treat patients with acute severe metabolic acidosis due to hyperchloremic acidosis, but its role is controversial in patients with lactic acidosis.

Therapeutic options include sodium bicarbonate and tromethamine.

Sodium bicarbonate is recommended to raise arterial pH to 7.2. However, no controlled clinical studies have demonstrated reduced morbidity and mortality compared with general supportive care. If IV sodium bicarbonate is administered, the goal is to increase, not normalize, pH to 7.2 and HCO3− to 8 to 10 mEq/L (810mmol/L).

Tromethamine, a highly alkaline solution, is a sodium-free organic amine that acts as a proton acceptor to prevent or correct acidosis. However, no evidence exists that tromethamine is beneficial or more efficacious than sodium bicarbonate. The usual empiric dosage for tromethamine is 1 to 5 mmol/kg administered IV over 1 hour, and an individualized dose can be calculated as follows:
Dose of tromethamine (in mL) = 1.1 × body weight (in kg) × (normal [HCO3−] – current [HCO3−])
 
 
Metabolic alkalosis, pathophysiology, presentation and treatment
Metabolic alkalosis is initiated by increased pH and HCO3−, which can result from loss of H+ via the gastrointestinal (GI) tract (eg, nasogastric suctioning, vomiting) or kidneys (eg, diuretics, Cushing syndrome) or from gain of bicarbonate (eg, administration of bicarbonate, acetate, lactate, or citrate).
Metabolic alkalosis is maintained by abnormal renal function that prevents the kidneys from excreting excess bicarbonate.

The respiratory response is to increase Paco2 by hypoventilation.

Clinical presentation

• No unique signs or symptoms are associated with mild to moderate metabolic alkalosis.
Some patients complain of symptoms related to the underlying disorder (e.g., muscle weakness with hypokalemia or postural dizziness with volume depletion) or have a history of vomiting, gastric drainage, or diuretic use.

• Severe alkalemia (pH greater than 7.60) can be associated with cardiac arrhythmias and neuromuscular irritability.

Treatment

• Aim treatment at correcting the factor(s) responsible for maintaining the alkalosis and depends on whether the disorder is sodium chloride responsive or resistant.
 


Respiratory acidosis is characterized by an increase in Paco2 and a decrease in pH. Respiratory acidosis results from disorders that restrict ventilation or increase CO2 production, airway and pulmonary abnormalities, neuromuscular abnormalities, or mechanical ventilator problems.
Early compensatory response to acute respiratory acidosis is chemical buffering. If prolonged (above 1224 hours), proximal tubular HCO3 − reabsorption, ammoniagenesis, and distal tubular H+ secretion are enhanced, resulting in an increase in serum HCO3− concentration that raises pH to normal.


Clinical presentation




• Neuromuscular symptoms include altered mental status, abnormal behavior, seizures, stupor, and coma. Hypercapnia can mimic a stroke or CNS tumor by producing headache, papilledema, focal paresis, and abnormal reflexes. CNS symptoms are caused by increased cerebral blood flow and are variable, depending in part on the acuity of onset.

Treatment

• Provide adequate ventilation if CO2 excretion is acutely and severely impaired (Paco2 above 80 mmHg [above 10.6 kPa]) or if life-threatening hypoxia is present . Ventilation can include maintaining a patent airway (eg, emergency tracheostomy, bronchoscopy, or intubation), clearing excessive secretions, administering oxygen, and providing mechanical ventilation.

• Treat underlying cause aggressively (eg, administration of bronchodilators for bronchospasm or discontinuation of respiratory depressants such as narcotics and benzodiazepines). Bicarbonate administration is rarely necessary and is potentially harmful.

• Chronic respiratory acidosis (eg, chronic obstructive pulmonary disease [COPD]) is treated essentially the same as acute respiratory acidosis with a few important exceptions. Oxygen therapy should be initiated carefully and only if the Pao2 is less than 50 mm Hg, because the drive to breathe depends on hypoxemia rather than hypercarbia.
 
 
Respiratory alkalosis is characterized by a decrease in Paco2 that leads to an increase in pH. Paco2 decreases when ventilatory CO2 excretion exceeds metabolic CO2 production, usually because of hyperventilation.
Causes include increases in neurochemical stimulation via central or peripheral mechanisms, or physical increases in ventilation via voluntary or artificial means (e.g., mechanical ventilation). The earliest compensatory response is to chemically buffer excess bicarbonate by releasing hydrogen ions from intracellular proteins, phosphates, and hemoglobin. If prolonged (above 6 hours), the kidneys attempt to further compensate by increasing bicarbonate elimination.


Clinical presentation




• Although usually asymptomatic, respiratory alkalosis can cause adverse neuromuscular, cardiovascular, and GI effects.

• Light-headedness, confusion, decreased intellectual functioning, syncope, and seizures can be caused by decreased cerebral blood flow.

• Nausea and vomiting can occur, probably due to cerebral hypoxia.

• Serum electrolytes can be altered; serum chloride is usually increased; serum potassium, phosphorus, and ionized calcium are usually decreased.

Treatment

• Treatment is often unnecessary because most patients have few symptoms and only mild pH alterations 

• Direct measures (eg, treatment of pain, hypovolemia, fever, infection, or salicylate overdose) can be effective. A rebreathing device (eg, paper bag) can help control hyperventilation in patients with anxiety/hyperventilation syndrome.

• Correct respiratory alkalosis associated with mechanical ventilation by decreasing the number of mechanical breaths per minute, using a capnograph and spirometer to adjust ventilator settings more precisely, or increasing dead space in the ventilator circuit.

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