chapter 11 electrolytes and acid-base balance

Chapter 11 Electrolytes and Acid-base

Balance

Tu Zhiguang

SODIUM, POTASSIUM, AND CHLORIDE-1

Normal Physiology And Homeostasis

The total body water constitutes 60% of the lean body mass and is distributed as intracellular fluid (ICF) and extracellular fluid (ECF).

The effective circulating volume (ECV) is the portion of the ECF that is actively perfusing tissues.

The ECF and ICF are in osmotic equilibrium, but the electrolyte composition of the two compartments differs.

Sodium ion (Na+) is the major cation in the ECF, whereas potassium ion (K+) predominates in the ICF. Sodium salts are thus the major component of the plasma osmolality.


The plasma Na+ and osmolality are regulated by water intake and renal water excretion.

Renal water excretion is regulated by pituitary antidiuretic hormone (ADH), which acts on the renal collecting tubules to enhance water

resorption.


K+ is the major intracellular ions. The normal plasma K+ is 3.2 to 5.0 mmol/L, whereas the normal concentration of ICF is approximately 150 mmol/L.

K+ balance is dependent on intake and renal excretion. K+ is filtered by the kidney and resorbed in the proximal tubule. However, the distal renal tubule is the major site for regulation of renal K+ excretion. Aldosterone promotes K+ excretion in the distal tubule.


Laboratory Measurement

flame photometry, ion-selective electrode method (ISE) and spectrophotometry.

Presently, ISE is the most common method for Na+, K+ and Cl- in clinical laboratory.

Plasma osmolality (Posm) is defined as the total amount of solute particles, including anions, cations and other solute, in 1 L water.


Posm can be measured directly by osmometry or estimated by the following formula:

Posm normally is 275~300 mOsm/kg.

9]urea[]glucose[][Na1.86(mOsmo/kg) Posmo


Interpretation Of Electrolyte Disorders-1

Hyponatremia

Plasma Na+ < 135 mmol/L. Usually hyponatremia is associated with hypoosmolality.

Hyponatremia may result from loss of Na+ or an increase in body water.

The kidney will excrete excess water to prevent hyponatremia, so most patients with hyponatremia exhibit abnormal water excretion as occurred in patients with ECV depletion, renal failure, inappropriate ADH secretion, and other causes.

Selective d

ifferential d

iagnosis an

d

laboratory ap

proach

to hyp

onatrem

ia

Selective differential diagnosis and laboratory approach to hypernatremia

Hypokalemia

Both of hypokalemia and hyperkalemia are very critical clinical conditions. Hypokalemia is defined as serum K+ <3.5 mmol/L.

An approach to the evaluation of hypokalemia and differential diagnosis is shown in Fig. 11-3.


Selective differential diagnosis and laboratory approach to hypokalemia

Hyperkalemia

Hyperkalemia can result from increased intake, redistribution, and decreased renal potassium excretion. Chronic hyperkalemia usually implies impaired urinary excretion.

Acidemia promotes the exchange of plasma H+ for cellular K+ and thus is a cause of hyperkalemia. The resulting hyperkalemia is greatest with hyperchloremic metabolic acidosis.


Selective differential diagnosis and laboratory approach to hyperkalemia

Hyperchloremia and hypochloremia

Chloride is quantitatively the most important extracellular anion, and so abnormalities in the serum chloride may occur in a variety of settings as a component of acid-base, fluid, or electrolyte disorders.

From a clinical perspective, the abnormality in the serum chloride itself is of little concern. Attention is focused on the underlying disorder causing the hyperchloremia or hypochloremia.


pH, PCO2 , AND BICARBONATE -1

Physiology Of Acid-Base Balance

An optimal pH is important for the functioning of cellular enzymes. The pH of the blood is normally maintained by a combination of the body’s buffering system and by renal and respiratory regulatory mechanisms.

As a general rule, acidemia below pH 6.8 or alkalemia above pH 7.8 is not compatible with life.

Acidemia is defined as arterial pH < 7.36 and alkalemia as a pH > 7.44.

Acid-base disorders affect a variety of metabolic processes, but the clinical signs and symptoms of acidosis and alkalosis are relatively nonspecific.

Therefore, the diagnosis requires laboratory confirmation by measurement of blood pH and gases.


CO2 is produced by cellular respiration and is the

most important substance to challenge the acid-base balance. Acid is produced by the association of CO2

with water, forming carbonic acid, which dissociates to H+ and HCO3

-. Almost all the CO2 produced

(volatile acid) is eliminated in the lungs.

Another acid load is created by the metabolism of proteins and the hydrolysis of phosphoester bonds, resulting in the production of nonvolatile acids.


Body Buffering Systems

The Henderson-Hasselbalch equation describes the relationship between pH and the acidic and basic forms of a buffer. The principal buffering system of plasma is the bicarbonate/carbonic acid system. Carbonic acid in plasma is in equilibrium with dissolved CO2 (dCO2).

)C

Clog(pK'pH

2

-

3

dCO

HCO


In plasma at 37℃ pK' is 6.1 ( expressed in mmol/L), and PCO2 is expressed in mmHg, the

Henderson-Hasselbalch equation for the bicarbonate/carbonic acid system is

Normally the ratio of bicarbonate to dCO2 is 20/1.

)0.03Pco

Clog(1.6pH

2

-3HCO


Changes in either the bicarbonate concentration or the PCO2 will affect the ratio and thus change the pH

of the blood.

Blood gas analyzers measure pH, PCO2, and PO2,

and the Henderson-Hasselbalch equation is used by the microprocessor built into the analyzer to calculate other quantities such as bicarbonate and total CO2

concentrations.


The rate of alveolar ventilation affects acid-base status through changes in the PCO2. The rate of

respiration is influenced by the arterial PO2 and pH.

Arterial pH is detected by chemoreceptors in the aortic arch and carotid bodies (peripheral) and in the brainstem (central).

This forms the basis of respiratory compensatory mechanism.

Respiration and Acid-Base Regulation-1

Conversely, a pathologic alteration in alveolar ventilation may itself be the cause of an acid-base

disorder by inducing CO2 retention (respiratory

acidosis) or excessive CO2 elimination (respiratory

alkalosis).


Renal Acid-Base Regulation

The kidney plays an important role in acid-base balance. The kidney regulates bicarbonate resorption and acid excretion, primarily in the form of NH4

+.

Plasma bicarbonate is filtered by the glomerulus and is resorbed to maintain acid-base balance. In alkalotic states, the kidney can also excrete bicarbonate to compensate for an elevated pH.


Normally the body produces a net excess of acid (50~100 mmol/day), only a small number of H+ can be excreted. Consequently, the kidney requires an alternate mechanism to excrete the normal daily acid load.

The two most important species are phosphate (HPO4

2-) and NH3, both of which can combine with

H+ secreted by renal tubular cells and are excreted in urine as H2PO4

- and NH4+.


MEASUREMENT OF pH, PCO2 AND PO2-1

Blood gas analyzers measure three quantities:

pH, PCO2 and PO2.

All other quantities of parameters including

bicarbonate, total CO2 (tCO2), dissolved CO2 (dCO2),

and base excess (BE) are calculated by the microprocessor in the instrument.

Specimens and Specimen Handling

The correctly collecting and handling specimen is very important for blood pH and gas analysis.

In the majority of blood gas testing, there is a need to evaluate the degree of oxygenation of the blood in addition to the acid-base status. A specimen of arterial blood is therefore required.


If it is not practical to obtain arterial blood, arterialized capillary blood may be used. The capillaries, usually of the foot or the fingertip, must be dilated by warming the skin so that the PO2 will

be close to the arterial level.

Despite this, the correlation of capillary PO2 to

arterial PO2 is not very good. However, The

correlation for PCO2 and pH is good.


Capillary specimens are collected in preheparinized glass capillary tubes. The blood must be well mixed in the tube to ensure homogeneity and dissolution of the anticoagulant.

If arterial PO2 is not a concern, the acid-base status

can be evaluated by analysis of venous blood for pH and PCO2 to avoid the discomfort and hazard of

arterial puncture.


Venous specimens may be collected in either syringes or evacuated tubes, but the latter must be completely filled.

Arterial specimens should be collected in a syringe.

Glass syringe is superior because plastic syringes can alter the PO2 (and, to a lesser extent, the

PCO2) of a blood specimen.


It is recommended that if plastic syringes are used, the blood not be chilled but that the analysis is completed within 20 min to reduce the probability of error owing to metabolic changes.

Conversely, if glass syringes are used, the specimens should be cooled in ice water so that metabolic changes will be insignificant


Anticoagulant

Sodium or lithium heparin is the anticoagulant to be used for blood pH and gas analysis. Both are available in dry and liquid forms.

If the liquid preparation is used, care must be taken not to use more volume than necessary because errors caused by sample dilution can be significant.


Measurement of blood pH, PCO2 and PO2

The routine measurements of pH, PCO2, and PO2

in clinical laboratory are all base on the electrochemical technology, in which some special electrodes are applied, respectively.


Temperature corrections

pH, PCO2, and PO2 are all temperature-

dependent quantities, and measurements are always made at 37.0℃.

If the patient temperature differs from37℃, then the question arises whether to adjust the measured values to the temperature of the patient. There has always been some controversy about the desirability of making this adjustment.


CALCULATIONS OF OTHER ACID-BASE BALANCE PARAMETERS -1

Although other parameters in acid-base balance such as concentration of bicarbonate ( ), tCO2

and BE could be directly determined, it is commonly to calculate them in conjunction with measurement of pH and PCO2 in whole blood.

The calculations are completed by microprocessor in the blood gas analyzer based on Henderson-Hasselbalch equation.

3HCO

C

Concentration of CHCO3- and total CO2

The relationship needed to calculate bicarbonate concentration is the Henderson-Hasselbalch equation, which may be written in the form

logP log'pKpHC log2

-3

COHCO


A close approximation of the total CO2 can be

made by adding the bicarbonate concentration and the concentration of dissolved CO2 (i.e., ignoring the

small amounts of carbonate ion and protein carbamates). This approximation is


Base Excess

When blood pH and PCO2 are abnormal, it is

often not immediately obvious whether the abnormality is purely respiratory in nature or whether a metabolic component is present.

Attempts have been made to define a quantity that can be readily calculated and that would reflect only the metabolic component of an acid-base imbalance.


Base excess (BE) of ECF is generally believed to be the most useful of these. BE represents the amount of buffering anions in plasma. A positive-BE indicates metabolic alkalosis or compensation to prolonged respiratory acidosis. A negative-BE indicates metabolic acidosis (e.g. lactic acidosis).

BE = [HCO3-] − 24.8 + 16.2 (pH − 7.40)


Interpretation of Acid-Base Disorders-1

Acid-base disorders are classified into four categories: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Each of these categories includes a number of possible causes.

The evaluation of an acid-base abnormality requires the correct classification, followed by a consideration of the differential diagnosis to obtain the specific etiology.

Respiratory acidosis

Respiratory acidosis results from any condition that impairs CO2 elimination and is characterized by

an increased PCO2 and a decreased pH.

In acute respiratory acidosis, the increase in PCO2 will stimulate the central respiratory center to

increase respiration. The HCO3- level and tCO2 are

normal.


Renal compensatory mechanisms require more time to show an effective response. When this occurs, the acid-base disorder is classified as chronic respiratory acidosis, characterized by an increased PCO2, a decreased pH, and an increase in the plasma

HCO3- and tCO2.


Respiratory alkalosis

Acute respiratory alkalosis is characterized by a low PCO2, a high pH, and a normal bicarbonate and

tCO2.

In chronic respiratory alkalosis the PCO2 is

low, the pH is high (but not as high as in acute condition), and the plasma HCO3

- and tCO2 are

decreased.


The two most common causes are acute anxiety and hyperventilation in response to hypoxemia.

A less obvious cause of respiratory alkalosis is the rapid correction of a metabolic acidosis, for example by bicarbonate infusion.


Metabolic Alkalosis

Metabolic alkalosis is characterized by increased pH, HCO3

-, and tCO2. The causes are often divided

into two categories, designated chloride-responsive and chloride-resistant types.

The laboratory distinction is made by measuring the urine Cl-; a level < 20 mmol/L is classified chloride responsive and > 20 mmol/L is chloride resistant.


Several causes of chloride-responsive metabolic alkalosis are associated with the loss of H+ from the gastrointestinal tract.

The major causes of chloride-resistant metabolic alkalosis are hyperaldosteronism, Cushing's syndrome, severe K+ depletion, and Bartter's syndrome.


Metabolic Acidosis

Metabolic acidosis is caused by an increased production of organic acids, decreased renal

hydrogen ion excretion, or loss of HCO3-. Any of

these mechanisms causes a decrease in the pH, the

HCO3-, and the total CO2.


Metabolic acidosis is usually classified based on whether the anion gap is increased. The anion gap (AG) is a calculated quantity that reflects the difference between the measured cations and the measured anions. The AG is usually defined as

AG = [Na+] − [Cl-] − [HCO3-].

The reference interval for the AG is 8 ~ 14 mmol/L. Its only clinical use is in the differential diagnosis of metabolic acidosis.


There are five conditions that may cause acidosis: renal failure, lactic acidosis, ketoacidosis, rhadbomyolysis, and some drugs and toxins.

(1) Renal Failure Renal failure can cause either a normal AG or a high-AG metabolic acidosis. Plasma pH and HCO3

- falls. Chloride replaces HCO3- in the

blood, resulting in a normal AG (hyperchloremic) acidosis. Conversely, severe renal failure is associated with renal retention of phosphate and sulfates (both unmeasured anions) and thus a high-AG acidosis.


(2) Lactic Acidosis: Lactic acidosis is a common cause of high-AG acidosis. Lactic acid is a product of anaerobic metabolism.

(3)Ketoacidosis: Ketoacidosis may occur in uncontrolled diabetes, starvation, or alcohol ingestion. Ketoacids (acetoacetic acid and β-hydroxybutyric acid) are overproduced by the liver, resulting in an increase in unmeasured anions and a high-AG acidosis.


(4) Rhabdomyolysis: Massive destruction of muscle tissue releases organic acids from damaged myocytes, leading to a high-AG metabolic acidosis.

(5) Drugs and Toxins.


Normal-AG metabolic acidosis (hyperchloremic acidosis)

A normal-AG acidosis can occur in several situations, including HCO3

- losses in the

gastrointestinal tract, infusion of acids, and after recovery from ketoacidosis.


chapter 11 electrolytes and acid-base balance

Documents

renal water excretion

renal excretion

renal potassium excretion

hyperkalemia hyperkalemia

water intake

abnormal water excretion

potassium ion

sodium ion na