Acidosis

Last updated

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

Contents

Acidemia

The term acidemia describes the state of low blood pH, when arterial pH falls below 7.35 (except in the fetus – see below) while acidosis is used to describe the processes leading to these states. Nevertheless, the terms are sometimes used interchangeably. The distinction is 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.

(alkalemia) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes. In certain situations the main cause is clear. For instance, a diabetic with ketoacidosis is a recognizable case where the main cause of acidemia is essentially obvious.

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).

Signs and symptoms

General symptoms of acidosis. These usually accompany symptoms of another primary defect (respiratory or metabolic). Symptoms of acidosis.png
General symptoms of acidosis. These usually accompany symptoms of another primary defect (respiratory or metabolic).

Nervous system involvement may be seen with acidosis and occurs more often with respiratory acidosis than with metabolic acidosis. Signs and symptoms that may be seen in acidosis include headaches, confusion, feeling tired, tremors, sleepiness, flapping tremor, and dysfunction of the cerebrum of the brain which may progress to coma if there is no intervention. [1]

Metabolic acidosis

Metabolic acidosis may result from either increased production of metabolic acids, such as lactic acid, or disturbances in the ability to excrete acid via the kidneys, such as either renal tubular acidosis or the acidosis of kidney failure, which is associated with an accumulation of urea and creatinine as well as metabolic acid residues of protein catabolism.

An increase in the production of other acids may also produce metabolic acidosis. For example, lactic acidosis may occur from:

  1. severe (PaO2 <36mm Hg) hypoxemia causing a fall in the rate of oxygen diffusion from arterial blood to tissues.
  2. hypoperfusion (e.g., hypovolemic shock) causing an inadequate blood delivery of oxygen to tissues.

A rise in lactate out of proportion to the level of pyruvate, e.g., in mixed venous blood, is termed "excess lactate", and may also be an indicator of fermentation due to anaerobic metabolism occurring in muscle cells, as seen during strenuous exercise. Once oxygenation is restored, the acidosis clears quickly. Another example of increased production of acids occurs in starvation and diabetic ketoacidosis. It is due to the accumulation of ketoacids (via excessive ketosis) and reflects a severe shift from glycolysis to lipolysis for energy needs.

Acid consumption from poisoning such as methanol ingestion, elevated levels of iron in the blood, and chronically decreased production of bicarbonate may also produce metabolic acidosis.

Metabolic acidosis is compensated for in the lungs, as increased exhalation of carbon dioxide promptly shifts the buffering equation to reduce metabolic acid. This is a result of stimulation to chemoreceptors, which increases alveolar ventilation, leading to respiratory compensation, otherwise known as Kussmaul breathing (a specific type of hyperventilation). Should this situation persist, the patient is at risk of exhaustion leading to respiratory failure.

Mutations to the V-ATPase 'a4' or 'B1' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineural deafness.

Arterial blood gases will indicate low pH, low blood HCO3, and normal or low PaCO2. In addition to arterial blood gas, an anion gap can also differentiate between possible causes.

The Henderson-Hasselbalch equation is useful for calculating blood pH, because blood is a buffer solution. In the clinical setting, this equation is usually used to calculate HCO3 from measurements of pH and PaCO2 in arterial blood gases. The amount of metabolic acid accumulating can also be quantitated by using buffer base deviation, a derivative estimate of the metabolic as opposed to the respiratory component. In hypovolemic shock for example, approximately 50% of the metabolic acid accumulation is lactic acid, which disappears as blood flow and oxygen debt are corrected.

Treatment

Treatment of uncompensated metabolic acidosis is focused upon correcting the underlying problem. When metabolic acidosis is severe and can no longer be compensated for adequately by the lungs or kidneys, neutralizing the acidosis with infusions of bicarbonate may be required.

Fetal metabolic acidemia

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). [2] Fetal metabolic acidemia is defined as an umbilical vessel pH of less than 7.20 and a base excess of less than −8. [3]

Respiratory acidosis

Respiratory acidosis results from a build-up of carbon dioxide in the blood (hypercapnia) due to hypoventilation. It is most often caused by pulmonary problems, although head injuries, drugs (especially anaesthetics and sedatives), and brain tumors can cause this acidemia. Pneumothorax, emphysema, chronic bronchitis, asthma, severe pneumonia, and aspiration are among the most frequent causes. It can also occur as a compensatory response to chronic metabolic alkalosis.

One key to distinguish between respiratory and metabolic acidosis is that in respiratory acidosis, the CO2 is increased while the bicarbonate is either normal (uncompensated) or increased (compensated). Compensation occurs if respiratory acidosis is present, and a chronic phase is entered with partial buffering of the acidosis through renal bicarbonate retention.

However, in cases where chronic illnesses that compromise pulmonary function persist, such as late-stage emphysema and certain types of muscular dystrophy, compensatory mechanisms will be unable to reverse this acidotic condition. As metabolic bicarbonate production becomes exhausted, and extraneous bicarbonate infusion can no longer reverse the extreme buildup of carbon dioxide associated with uncompensated respiratory acidosis, mechanical ventilation will usually be applied. [4] [5]

Fetal respiratory acidemia

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 7.20 to 7.38). [2] In the fetus, the lungs are not used for ventilation. Instead, the placenta performs ventilatory functions (gas exchange). Fetal respiratory acidemia is defined as an umbilical vessel pH of less than 7.20 and an umbilical artery PCO2 of 66 or higher or umbilical vein PCO2 of 50 or higher. [3]

See also

Related Research Articles

<span class="mw-page-title-main">Lactic acidosis</span> Metabolic medical condition

Lactic acidosis is a medical condition characterized by a build-up of lactate in the body, with formation of an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's oxidative metabolism.

<span class="mw-page-title-main">Arterial blood gas test</span> A test of blood taken from an artery that measures the amounts of certain dissolved gases

An arterial blood gas (ABG) test, or arterial blood gas analysis (ABGA) measures the amounts of arterial gases, such as oxygen and carbon dioxide. An ABG test requires that a small volume of blood be drawn from the radial artery with a syringe and a thin needle, but sometimes the femoral artery in the groin or another site is used. The blood can also be drawn from an arterial catheter.

A blood gas test or blood gas analysis tests blood to measure blood gas tension values, it also measures blood pH, and the level and base excess of bicarbonate. The source of the blood is reflected in the name of each test; arterial blood gases come from arteries, venous blood gases come from veins and capillary blood gases come from capillaries. The blood gas tension levels of partial pressures can be used as indicators of ventilation, respiration and oxygenation. Analysis of paired arterial and venous specimens can give insights into the aetiology of acidosis in the newborn.

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

The control of ventilation is the physiological mechanisms involved in the control of breathing, which is the movement of air into and out of the lungs. Ventilation facilitates respiration. Respiration refers to the utilization of oxygen and balancing of carbon dioxide by the body as a whole, or by individual cells in cellular respiration.

<span class="mw-page-title-main">Metabolic acidosis</span> Medical condition

Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. Metabolic acidosis can lead to acidemia, which is defined as arterial blood pH that is lower than 7.35. Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low to high.

<span class="mw-page-title-main">Respiratory acidosis</span> Medical condition

Respiratory acidosis is a state in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH.

<span class="mw-page-title-main">Respiratory alkalosis</span> Medical condition

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 primary disturbance of acid–base homeostasis.

The anion gap is a value calculated from the results of multiple individual medical lab tests. It may be reported with the results of an electrolyte panel, which is often performed as part of a comprehensive metabolic panel.

<span class="mw-page-title-main">Metabolic alkalosis</span> Medical condition

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.

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 (mmol/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.

Carbaminohemoglobin (carbaminohaemoglobin BrE) (CO2Hb, also known as carbhemoglobin and carbohemoglobin) is a compound of hemoglobin and carbon dioxide, and is one of the forms in which carbon dioxide exists in the blood. Twenty-three percent of carbon dioxide is carried in blood this way (70% is converted into bicarbonate by carbonic anhydrase and then carried in plasma, 7% carried as free CO2, dissolved in plasma).

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 in the ECF is crucial for the normal physiology of the body—and for cellular metabolism. The pH of the intracellular fluid and the extracellular fluid need to be maintained at a constant level.

In acid base physiology, the Davenport diagram is a graphical tool, developed by Horace W. Davenport, that allows a clinician or investigator to describe blood bicarbonate concentrations and blood pH following a respiratory and/or metabolic acid-base disturbance. The diagram depicts a three-dimensional surface describing all possible states of chemical equilibria between gaseous carbon dioxide, aqueous bicarbonate and aqueous protons at the physiologically complex interface of the alveoli of the lungs and the alveolar capillaries. Although the surface represented in the diagram is experimentally determined, the Davenport diagram is rarely used in the clinical setting, but allows the investigator to envision the effects of physiological changes on blood acid-base chemistry. For clinical use there are two recent innovations: an Acid-Base Diagram which provides Text Descriptions for the abnormalities and a High Altitude Version that provides text descriptions appropriate for the altitude.

<span class="mw-page-title-main">Acid–base disorder</span> Medical condition

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. In the fetus, the normal range differs based on which umbilical vessel is sampled. It can exist in varying levels of severity, some life-threatening.

<span class="mw-page-title-main">High anion gap metabolic acidosis</span> Medical condition

High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap. Metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing enough acid from the body. Several types of metabolic acidosis occur, grouped by their influence on the anion gap.

Winters' formula, named after Dr. R.W. Winters, is a formula used to evaluate respiratory compensation when analyzing acid-base disorders in the presence of metabolic acidosis. It can be given as:

Fetal scalp blood testing is a technique used in obstetrics during active labor to confirm whether a fetus is receiving enough oxygen. This is a supplementary procedure used to determine if fetal acidemia has occurred following fetal cardiac distress. While continuous fetal heart rate monitoring is the primary method for assessing fetal wellbeing during labor, a change in fetal heart rate is not indicative of fetal acidemia. Some of the signs and symptoms of oxygen deprivation are pH in the umbilical cord, abnormal fetal heartbeat and abnormal coloration of amniotic fluid. This correlation can only be concluded by sampling fetal scalp blood and measuring acid status. Therefore, fetal scalp blood testing could be used to reduce the number of unnecessary emergency caesarean sections made on the decision of fetal heart rate alone.

Blood gas tension refers to the partial pressure of gases in blood. There are several significant purposes for measuring gas tension. The most common gas tensions measured are oxygen tension (PxO2), carbon dioxide tension (PxCO2) and carbon monoxide tension (PxCO). The subscript x in each symbol represents the source of the gas being measured: "a" meaning arterial, "A" being alveolar, "v" being venous, and "c" being capillary. Blood gas tests (such as arterial blood gas tests) measure these partial pressures.

Delta ratio, or "delta-delta", is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether a mixed acid–base disorder is present. The anion gap (AG) without potassium is calculated first and if a metabolic acidosis is present, results in either a high anion gap metabolic acidosis (HAGMA) or a normal anion gap acidosis (NAGMA). A low anion gap is usually an oddity of measurement, rather than a clinical concern.

References

  1. 1 2 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.
  2. 1 2 Yeomans, ER; Hauth, JC; Gilstrap, LC III; Strickland DM (1985). "Umbilical cord pH, PCO2, and bicarbonate following uncomplicated term vaginal deliveries (146 infants)". Am J Obstet Gynecol. 151 (6): 798–800. doi:10.1016/0002-9378(85)90523-x. PMID   3919587.
  3. 1 2 Pomerance, Jeffrey (2004). Interpreting Umbilical Cord Gases: For Clinicians Caring for the Fetus or Newborn. Pasadena, CA: BNMG. ISBN   978-0-9752621-0-8.
  4. "MedlinePlus Medical Encyclopedia: Respiratory acidosis". Archived from the original on 11 December 2008. Retrieved 2008-12-06.
  5. "eMedicine - Respiratory Acidosis : Article by Jackie A Hayes". Archived from the original on October 29, 2008. Retrieved 2008-12-06.
Notes