Alkalosis

Alkalosis is the result of a process reducing hydrogen ion concentration of arterial blood plasma (alkalemia). In contrast to acidemia (serum pH 7.35 or lower), alkalemia occurs when the serum pH is higher than normal (7.45 or higher). Alkalosis is usually divided into the categories of respiratory alkalosis and metabolic alkalosis or a combined respiratory/metabolic alkalosis.[1]

Alkalosis

Signs and symptoms

Metabolic alkalosis is usually accompanied by low blood potassium concentration, causing, e.g., muscular weakness, muscle pain, and muscle cramps (from disturbed function of the skeletal muscles), and muscle spasms (from disturbed function of smooth muscles).

It may also cause low blood calcium concentration. As the blood pH increases, blood transport proteins, such as albumin, become more ionized into anions. This causes the free calcium present in blood to bind more strongly with albumin. If severe, it may cause tetany.

Causes

Respiratory alkalosis is caused by hyperventilation,[2] resulting in a loss of carbon dioxide. Compensatory mechanisms for this would include increased dissociation of the carbonic acid buffering intermediate into hydrogen ions, and the related excretion of bicarbonate, both of which lower blood pH. Hyperventilation-induced alkalosis can be seen in several deadly central nervous system diseases such as strokes or Rett syndrome.[2]

Metabolic alkalosis can be caused by repeated vomiting,[2] resulting in a loss of hydrochloric acid in the stomach contents. Severe dehydration, and the consumption of alkali are other causes. It can also be caused by administration of diuretics[2] and endocrine disorders such as Cushing's syndrome. Compensatory mechanism for metabolic alkalosis involve slowed breathing by the lungs to increase serum carbon dioxide,[2] a condition leaning toward respiratory acidosis. As respiratory acidosis often accompanies the compensation for metabolic alkalosis, and vice versa, a delicate balance is created between these two conditions.

Diagnosis

No diagnosis

See also

References

  1. ^ Mosby's Paramedic Textbook – Mick J. Sanders
  2. ^ a b c d e Yee AH, Rabinstein AA (February 2010). "Neurologic presentations of acid-base imbalance, electrolyte abnormalities, and endocrine emergencies". Neurol Clin. 28 (1): 1–16. doi:10.1016/j.ncl.2009.09.002. PMID 19932372.

External links

External resources
Acidosis

Acidosis is a process causing increased acidity in the blood and other body tissues (i.e., an increased hydrogen ion concentration). If not further qualified, it usually refers to acidity of the blood plasma.

The term acidemia describes the state of low blood pH, while acidosis is used to describe the processes leading to these states. Nevertheless, the terms are sometimes used interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, wherein the relative severity of both determines whether the result is a high, low, or normal pH.

Acidemia is said to occur when arterial pH falls below 7.35 (except in the fetus – see below), while its counterpart (alkalemia) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes.

The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g., healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage.

Acid–base homeostasis

Acid–base homeostasis is the homeostatic regulation of the pH of the body's extracellular fluid (ECF). The proper balance between the acids and bases (i.e. the pH) in the ECF is crucial for the normal physiology of the body, and cellular metabolism. The pH of the intracellular fluid and the extracellular fluid need to be maintained at a constant level.Many extracellular proteins such as the plasma proteins and membrane proteins of the body's cells are very sensitive for their three dimensional structures to the extracellular pH. Stringent mechanisms therefore exist to maintain the pH within very narrow limits. Outside the acceptable range of pH, proteins are denatured (i.e. their 3-D structure is disrupted), causing enzymes and ion channels (among others) to malfunction.

In humans and many other animals, acid–base homeostasis is maintained by multiple mechanisms involved in three lines of defence:

The first line of defence are the various chemical buffers which minimize pH changes that would otherwise occur in their absence. They do not correct pH deviations, but only serve to reduce the extent of the change that would otherwise occur. These buffers include the bicarbonate buffer system, the phosphate buffer system, and the protein buffer system.The second line of defence of the pH of the ECF consists of controlling of the carbonic acid concentration in the ECF. This is achieved by changes in the rate and depth of breathing (i.e. by hyperventilation or hypoventilation), which blows off or retains carbon dioxide (and thus carbonic acid) in the blood plasma.The third line of defence is the renal system, which can add or remove bicarbonate ions to or from the ECF. The bicarbonate is derived from metabolic carbon dioxide which is enzymatically converted to carbonic acid in the renal tubular cells. The carbonic acid spontaneously dissociates into hydrogen ions and bicarbonate ions. When the pH in the ECF tends to fall (i.e. become more acidic) the hydrogen ions are excreted into the urine, while the bicarbonate ions are secreted into the blood plasma, causing the plasma pH to rise (correcting the initial fall). The converse happens if the pH in the ECF tends to rise: the bicarbonate ions are then excreted into the urine and the hydrogen ions into the blood plasma.Physiological corrective measures make up the second and third lines of defence. This is because they operate by making changes to the buffers, each of which consists of two components: a weak acid and its conjugate base. It is the ratio concentration of the weak acid to its conjugate base that determines the pH of the solution. Thus, by manipulating firstly the concentration of the weak acid, and secondly that of its conjugate base, the pH of the extracellular fluid (ECF) can be adjusted very accurately to the correct value. The bicarbonate buffer, consisting of a mixture of carbonic acid (H2CO3) and a bicarbonate (HCO−3) salt in solution, is the most abundant buffer in the extracellular fluid, and it is also the buffer whose acid to base ratio can be changed very easily and rapidly.An acid–base imbalance is known as acidaemia when the acidity is high, or alkalaemia when the acidity is low.

Acid–base imbalance

Acid–base imbalance is an abnormality of the human body's normal balance of acids and bases that causes the plasma pH to deviate out of the normal range (7.35 to 7.45). In the fetus, the normal range differs based on which umbilical vessel is sampled (umbilical vein pH is normally 7.25 to 7.45; umbilical artery pH is normally 7.18 to 7.38). It can exist in varying levels of severity, some life-threatening.

Bartter syndrome

Bartter syndrome is a rare inherited defect in the thick ascending limb of the loop of Henle. It is characterized by low potassium levels (hypokalemia), increased blood pH (alkalosis), and normal to low blood pressure. There are two types of Bartter syndrome: neonatal and classic. A closely associated disorder, Gitelman syndrome, is milder than both subtypes of Bartter syndrome.

Base excess

In physiology, base excess and base deficit refer to an excess or deficit, respectively, in the amount of base present in the blood. The value is usually reported as a concentration in units of mEq/L, with positive numbers indicating an excess of base and negative a deficit. A typical reference range for base excess is −2 to +2 mEq/L.Comparison of the base excess with the reference range assists in determining whether an acid/base disturbance is caused by a respiratory, metabolic, or mixed metabolic/respiratory problem. While carbon dioxide defines the respiratory component of acid-base balance, base excess defines the metabolic component. Accordingly, measurement of base excess is defined, under a standardized pressure of carbon dioxide, by titrating back to a standardized blood pH of 7.40.

The predominant base contributing to base excess is bicarbonate. Thus, a deviation of serum bicarbonate from the reference range is ordinarily mirrored by a deviation in base excess. However, base excess is a more comprehensive measurement, encompassing all metabolic contributions.

Contraction alkalosis

Contraction alkalosis refers to the increase in blood pH that occurs as a result of fluid losses (volume contraction). The change in pH is especially pronounced with acidic fluid losses caused by problems like vomiting.

HUPRA syndrome

HUPRA syndrome is a rare syndrome that was first described in 2010 in two infants of Palestinian origin from the same village in the Jerusalem area. One of the two infants' parents were related. It was later described in a third infant from the same village, whose parents were not related.The acronym stands for Hyperuricemia, Pulmonary hypertension, Renal failure in infancy and Alkalosis. And it's due to mutations in the mitochondrial SARS enzyme. It's an autosomal recessive disease, that has a prevalence of less than one in a million. One in fifteen of the village's inhabitants were found to carry the genetic mutation.

Hyperaldosteronism

Hyperaldosteronism, also aldosteronism, is a medical condition wherein too much aldosterone is produced by the adrenal glands, which can lead to lowered levels of potassium in the blood (hypokalemia) and increased hydrogen ion excretion (alkalosis).

This cause of mineralocorticoid excess is primary hyperaldosteronism reflecting excess production of aldosterone by adrenal zona glomerulosa. Bilateral micronodular hyperplasia is more common than unilateral adrenal adenoma.

Hyperventilation

Hyperventilation occurs when the rate or tidal volume of breathing eliminates more carbon dioxide than the body can produce. This leads to hypocapnia, a reduced concentration of carbon dioxide dissolved in the blood. The body normally attempts to compensate for this homeostatically but if this fails or is overridden, the blood pH will rise, leading to respiratory alkalosis. The symptoms of respiratory alkalosis include: dizziness, tingling in the lips, hands or feet, headache, weakness, fainting and seizures. In extreme cases it may cause carpopedal spasms, a flapping and contraction of the hands and feet.Factors that may induce or sustain hyperventilation include: physiological stress, anxiety or panic disorder, high altitude, head injury, stroke, respiratory disorders such as asthma, pneumonia or hyperventilation syndrome, cardiovascular problems such as pulmonary embolisms, anemia, an incorrectly calibrated medical respirator and adverse reactions to certain drugs.

Hyperventilation can also be induced intentionally to achieve an altered state of consciousness such as in the choking game, or in an attempt to extend a breath-hold dive.

Hyperventilation syndrome

Hyperventilation syndrome (HVS); also chronic hyperventilation syndrome (CHVS) and dysfunctional breathing hyperventilation syndrome is a respiratory disorder, psychologically or physiologically based, involving breathing too deeply or too rapidly (hyperventilation). HVS may present with chest pain and a tingling sensation in the fingertips and around the mouth (paresthesia) and may accompany a panic attack.

People with HVS may feel that they cannot get enough air. In reality, they have about the same oxygenation in the arterial blood (normal values are about 98% for hemoglobin saturation) and too little carbon dioxide (hypocapnia) in their blood and other tissues. While oxygen is abundant in the bloodstream, HVS reduces effective delivery of that oxygen to vital organs due to low-CO2-induced vasoconstriction and the suppressed Bohr effect.

The hyperventilation is self-promulgating as rapid breathing causes carbon dioxide levels to fall below healthy levels, and respiratory alkalosis (high blood pH) develops. This makes the symptoms worse, which causes the person to breathe even faster, which then, further exacerbates the problem.

The respiratory alkalosis leads to changes in the way the nervous system fires and leads to the paresthesia, dizziness, and perceptual changes that often accompany this condition. Other mechanisms may also be at work, and some people are physiologically more susceptible to this phenomenon than others.

Hypochloremia

Hypochloremia (or Hypochloraemia) is an electrolyte disturbance in which there is an abnormally low level of the chloride ion in the blood. The normal serum range for chloride is 97 to 107 mEq/L.

It rarely occurs in the absence of other abnormalities. Its sometimes associated with hypoventilation. It can be associated with chronic respiratory acidosis. If it occurs together with metabolic alkalosis (decreased blood acidity) it is often due to vomiting. It is usually the result of hyponatremia or elevated bicarbonate concentration. It occurs in cystic fibrosis.

Hypophosphatemia

Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. Symptoms may include weakness, trouble breathing, and loss of appetite. Complications may include seizures, coma, rhabdomyolysis, or softening of the bones.Causes include alcoholism, refeeding in those with malnutrition, diabetic ketoacidosis, burns, hyperventilation, and certain medications. It may also occur in the setting of hyperparathyroidism, hypothyroidism, and Cushing syndrome. It is diagnosed based on a blood phosphate concentration of less than 0.81 mmol/L (2.5 mg/dL). When levels are below 0.32 mmol/L (1.0 mg/dL) it is deemed to be severe.Treatment depends on the underlying cause. Phosphate may be given by mouth or by injection into a vein. Hypophosphatemia occurs in about 2% of people within hospital and 70% of people in the intensive care unit (ICU).

Liddle's syndrome

Liddle's syndrome, also called Liddle syndrome is a genetic disorder inherited in an autosomal dominant manner that is characterized by early, and frequently severe, high blood pressure associated with low plasma renin activity, metabolic alkalosis, low blood potassium, and normal to low levels of aldosterone. Liddle syndrome involves abnormal kidney function, with excess reabsorption of sodium and loss of potassium from the renal tubule, and is treated with a combination of low sodium diet and potassium-sparing diuretics (e.g. amiloride). It is extremely rare, with fewer than 30 pedigrees or isolated cases having been reported worldwide as of 2008.

Metabolic alkalosis

Metabolic alkalosis is a metabolic condition in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations. The condition typically cannot last long if the kidneys are functioning properly.

Milk-alkali syndrome

In medicine, milk-alkali syndrome is characterized by high blood calcium and metabolic alkalosis caused by taking in too much calcium and absorbable alkali; common sources of calcium and alkali are dietary supplements taken to prevent osteoporosis and antacids. If untreated, milk-alkali syndrome may lead to kidney failure or death.It was most common in the early 20th century, but since the 1990s, there has been an increase in the number of cases reported, linked to the increased use of calcium supplements to address or prevent osteoporosis.

Renal compensation

Renal compensation is a mechanism by which the kidneys can regulate the plasma pH. It is slower than respiratory compensation, but has a greater ability to restore normal values.

In respiratory acidosis, the kidney produces and excretes ammonium (NH4+) and monophosphate, generating bicarbonate in the process while clearing acid.In respiratory alkalosis, less bicarbonate (HCO3−) is reabsorbed, thus lowering the pH.

Respiratory alkalosis

Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide. This condition is one of the four basic categories of disruption of acid–base homeostasis.

Respiratory compensation

Respiratory compensation is a mechanism of the respiratory center by which plasma pH can be altered by varying the respiratory rate. It is faster than renal compensation, but has less ability to restore normal values.

In respiratory alkalosis, chemoreceptors sense a deranged acid-base system, and there is increased breathing. The amount of respiratory compensation in metabolic acidosis can be estimated using Winters' formula.

In respiratory acidosis, the breathing rate is decreased.

Winters' formula

Winters' formula, named for Dr. R.W. Winters, is a formula used to evaluate respiratory compensation when analyzing acid–base disorders and a metabolic acidosis is present. It can be given as

,

where HCO3 is given in units of mEq/L and pCO2 will be in units of mmHg.

Winters' formula gives an expected value for the patient's PCO2; the patient's actual (measured) PCO2 is then compared to this:

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