Low levels of na+ (below the normal physiological levels) are correctly identified as

The body obtains sodium through food and drink and loses it primarily in sweat and urine. Healthy kidneys maintain a consistent level of sodium in the body by adjusting the amount excreted in the urine. When sodium consumption and loss are not in balance, the total amount of sodium in the body is affected. The amount (concentration) of sodium in the blood may be

The total amount of sodium in the body affects the amount of fluid in blood (blood volume) and around cells. The body continually monitors blood volume and sodium concentration. When either becomes too high, sensors in the heart, blood vessels, and kidneys detect the increases and stimulate the kidneys to increase sodium excretion, thus returning blood volume to normal.

When blood volume or sodium concentration becomes too low, the sensors trigger mechanisms to increase blood volume. These mechanisms include the following:

  • The pituitary gland secretes vasopressin (sometimes called antidiuretic hormone). Vasopressin causes the kidneys to conserve water.

As people age, the body is less able to maintain fluid and sodium balance for several reasons:

  • Decreased thirst: As people age, they sense thirst less quickly or less intensely and thus may not drink fluids when needed.

  • Changes in the kidneys: Aging kidneys may become less able to reclaim water and electrolytes from the urine (concentrate urine), and, as a result, more water may be excreted in urine.

  • Less fluid in the body: In older people, the body contains less fluid. Only 45% of body weight is fluid in older people, compared with 60% in younger people. This change means that a slight loss of fluid and sodium, as can result from a fever or from not eating and drinking enough (sometimes for only a day or two), can have more serious consequences in older people.

The above situations can result in losing fluid or not consuming enough fluid and thus can cause a high sodium level in blood (hypernatremia Hypernatremia (High Level of Sodium in the Blood) In hypernatremia, the level of sodium in blood is too high. Hypernatremia involves dehydration, which can have many causes, including not drinking enough fluids, diarrhea, kidney dysfunction... read more ) and/or dehydration Dehydration Dehydration is a deficiency of water in the body. Vomiting, diarrhea, excessive sweating, burns, kidney failure, and use of diuretics may cause dehydration. People feel thirsty, and as dehydration... read more . Because these situations are more common among older people, hypernatremia is also more common among them. Hypernatremia is poorly tolerated by older people and can result in confusion, coma, and death if severe.

A low sodium level in blood (hyponatremia Hyponatremia (Low Level of Sodium in the Blood) In hyponatremia, the level of sodium in blood is too low. A low sodium level has many causes, including consumption of too many fluids, kidney failure, heart failure, cirrhosis, and use of diuretics... read more ) is more common among older people. Hyponatremia usually results when the body retains too much fluid, as occurs in heart failure or liver disease. Hyponatremia also occurs in older people who take certain types of diuretics (thiazide diuretics such as hydrochlorothiazide), particularly if the kidneys are not functioning normally. Diuretics, which are sometimes called water pills, are drugs that help the body eliminate excess fluid. Using liquid nutritional supplements or receiving intravenous fluids that are low in sodium while in the hospital also may cause hyponatremia in older people.

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Low levels of na+ (below the normal physiological levels) are correctly identified as

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Low levels of na+ (below the normal physiological levels) are correctly identified as

Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and gastrointestinal or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with arterial blood gas (ABG) and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low.

Metabolic acidosis is acid accumulation due to

  • Increased acid production or acid ingestion

  • Decreased acid excretion

  • Gastrointestinal or renal HCO3− loss

Low levels of na+ (below the normal physiological levels) are correctly identified as

The most common causes of a high anion gap metabolic acidosis are

  • Ketoacidosis

  • Lactic acidosis

  • Renal failure

  • Toxic ingestions

Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis Diabetic Ketoacidosis (DKA) Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with... read more ), but it also occurs with chronic alcohol use disorder (see alcoholic ketoacidosis Alcoholic Ketoacidosis Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic... read more ), undernutrition Overview of Undernutrition Undernutrition is a form of malnutrition. (Malnutrition also includes overnutrition.) Undernutrition can result from inadequate ingestion of nutrients, malabsorption, impaired metabolism, loss... read more , and, to a lesser degree, fasting. In these conditions, the body converts from glucose metabolism to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and beta-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric acidemia Isovaleric acidemia Valine, leucine, and isoleucine are branched-chain amino acids; deficiency of enzymes involved in their metabolism leads to accumulation of organic acids with severe metabolic acidosis. There... read more or congenital methylmalonic acidemia Methylmalonic acidemia Valine, leucine, and isoleucine are branched-chain amino acids; deficiency of enzymes involved in their metabolism leads to accumulation of organic acids with severe metabolic acidosis. There... read more .

The most common causes of normal anion gap acidosis are

  • Gastrointestinal (GI) or renal HCO3− loss

  • Impaired renal acid excretion

Normal anion gap metabolic acidosis is also called hyperchloremic acidosis because the kidneys reabsorb chloride (Cl−) instead of reabsorbing HCO3−.

Many GI secretions are rich in HCO3− (eg, biliary, pancreatic, and intestinal fluids); loss due to diarrhea, tube drainage, or fistulas can cause acidosis. In ureterosigmoidostomy (insertion of ureters into the sigmoid colon after obstruction or cystectomy), the colon secretes and loses HCO3− in exchange for urinary chloride (Cl−) and absorbs urinary ammonium, which dissociates into ammonia (NH3+) and hydrogen ion (H+). Ion-exchange resin uncommonly causes HCO3− loss by binding HCO3−.

Symptoms and Signs

The most characteristic sign is hyperpnea (long, deep breaths at a normal rate), reflecting a compensatory increase in alveolar ventilation; this hyperpnea is not accompanied by a feeling of dyspnea.

Severe, acute acidemia predisposes to cardiac dysfunction with hypotension and shock Shock Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death. Mechanisms may involve decreased circulating volume, decreased cardiac output, and vasodilation, sometimes... read more , ventricular arrhythmias Overview of Arrhythmias The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial... read more

Low levels of na+ (below the normal physiological levels) are correctly identified as
, and coma. Chronic acidemia causes bone demineralization disorders (eg, rickets, osteomalacia Vitamin D Deficiency and Dependency Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more , osteopenia).

  • Arterial blood gas (ABG) and serum electrolyte measurement

  • Anion gap and delta gap calculated

  • Winters formula for calculating compensatory changes

  • Testing for cause

The cause of an elevated anion gap may be clinically obvious (eg, hypovolemic shock, missed hemodialysis), but if not, blood testing should include

  • BUN (blood urea nitrogen)

  • Creatinine

  • Glucose

  • Lactate

  • Possible toxins

Salicylate levels can be measured in most laboratories, but methanol and ethylene glycol frequently cannot; their presence may be suggested by presence of an osmolar gap.

Calculated serum osmolarity (2 [sodium] + [glucose]/18 + BUN/2.8 + blood alcohol/5, based on conventional units) is subtracted from measured osmolarity. A difference > 10 implies the presence of an osmotically active substance, which, in the case of a high anion gap acidosis, is methanol or ethylene glycol. Although ingestion of ethanol may cause an osmolar gap and a mild acidosis, it should never be considered the sole cause of a significant metabolic acidosis.

  • Cause treated

  • Sodium bicarbonate (NaHCO3) primarily for severe acidemia—give with caution

Treatment of acidemia with sodium bicarbonate (NaHCO3) is clearly indicated only in certain circumstances and is probably deleterious in others. When metabolic acidosis results from loss of HCO3− or accumulation of inorganic acids (ie, normal anion gap acidosis), bicarbonate therapy is generally safe and appropriate. However, when acidosis results from organic acid accumulation (ie, high anion gap acidosis), bicarbonate therapy is controversial; it does not clearly decrease mortality in these conditions, and there are several possible risks.

With treatment of the underlying condition, lactate and ketoacids are metabolized back to HCO3−; exogenous HCO3− loading may therefore cause an “overshoot” metabolic alkalosis. In any condition, sodium bicarbonate may also cause sodium and volume overload, hypokalemia, and, by inhibiting respiratory drive, hypercapnia. Furthermore, because HCO3− does not diffuse across cell membranes, intracellular acidosis is not corrected and may paradoxically worsen because some of the added HCO3− is converted to carbon dioxide (CO2), which does cross into the cell and is hydrolyzed to H+ and HCO3−.

Despite these and other controversies, most experts still recommend giving bicarbonate IV for severe metabolic acidosis (pH < 7.0).

Treatment requires 2 calculations (same for both conventional and SI units). The first is the level to which HCO3− must be raised, calculated by the Kassirer-Bleich equation, using a target value for [H+] of 79 nEq/L (79 nmol/L), which corresponds to a pH of 7.10:

79 = 24 × Pco2/HCO3−

or

Desired HCO3−= 0.30 × Pco2

The amount of sodium bicarbonate needed to achieve that level is

NaHCO3 required (mEq/mmol) = (desired [HCO3−] observed [HCO3−]) × 0.4 × body weight (kg)

For example, a 70-kg man has severe metabolic acidosis with a pH of 6.92, PCO2 40 mmHg and HCO3− of 8 mEq/L (8 mmol/L). The target bicarbonate level needed to achieve a pH of 7.10 is 0.30 × 40 = 12 mEq/L (12 mmol/L). This level is 4 mEq/L (4 mmol/L) more than his current bicarbonate level of 8. To increase bicarbonate by 4, multiply 4 by 0.4 times 70 (the body weight), giving a result of 112 mEq (112 mmol) of HCO3−. This amount of sodium bicarbonate is given over several hours. Blood pH and HCO3−levels can be checked 30 minutes to 1 hour after administration, which allows for equilibration with extravascular HCO3−.

Alternatives to sodium bicarbonate include

  • Lactate, either in the form of lactated Ringer's solution or sodium lactate (is metabolized mEq for mEq to bicarbonate when liver function is normal)

  • Sodium acetate (metabolized mEq for mEq to bicarbonate when liver function is normal)

  • Tromethamine, an amino alcohol that buffers both metabolic (H+) and respiratory (carbonic acid [H2CO3]) acid

  • Carbicarb, an equimolar mixture of sodium bicarbonate and carbonate (the latter consumes CO2 and generates HCO3−)

  • Dichloroacetate, which enhances oxidation of lactate

These alternatives do not offer a proven benefit over sodium bicarbonate alone and can cause complications of their own.

Potassium (K+) depletion, common in metabolic acidosis, should be identified through frequent serum K+ monitoring and treated as needed with oral or parenteral potassium chloride.

  • Metabolic acidosis can be caused by acid accumulation due to increased acid production or acid ingestion; decreased acid excretion; or gastrointestinal or renal bicarbonate (HCO3−) loss.

  • Metabolic acidoses are categorized based on whether the anion gap is high or normal.

  • High anion gap acidoses are most often due to ketoacidosis, lactic acidosis, chronic kidney disease, or certain toxic ingestions.

  • Normal anion gap acidoses are most often due to gastrointestinal or renal HCO3− loss.

  • Calculate delta gap to identify concomitant metabolic alkalosis, and apply Winters formula to see whether respiratory compensation is appropriate or reflects a 2nd acid-base disorder.

  • Treat the cause.

  • Intravenous sodium bicarbonate (NaHCO3) is indicated when acidosis is due to a change in HCO3− level (normal anion gap acidosis).

  • Intravenous sodium bicarbonate is controversial in high anion gap acidosis (but may be considered when pH < 7.00, with a target pH of ≥ 7.10).

Is hyponatremia acidosis or alkalosis?

Hyponatremia and metabolic acidosis are major symptoms of adrenocortical dysfunction such as occurs in Addison's disease. The hyponatremia is caused by insufficiency of both aldosterone and cortisol. Aldosterone insufficiency decreases sodium reabsorption in the collecting ducts of the kidney.

What are the signs of acidosis or alkalosis?

What are the symptoms of metabolic acidosis and alkalosis? If you have metabolic acidosis, you may have no symptoms. However, most people experience nausea, vomiting and fatigue (feeling tired and weak.) You may also start to breathe deeper and faster.

What is alkalosis and acidosis?

Acidosis is a condition in which there is too much acid in the body fluids. It is the opposite of alkalosis (a condition in which there is too much base in the body fluids).

How does metabolic alkalosis cause hyponatremia?

Severe vomiting also causes loss of potassium (hypokalemia) and sodium (hyponatremia). The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (sparing sodium/potassium pumps to prevent further loss of potassium), leading to metabolic alkalosis.