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Acid-Base Balance

by 5m Editor
1 January 2008, at 12:00am

Acid-base balance, dietary electrolytes and dietary electrolyte balances (DEB) for broilers are explained, together with the impact of ionophore anticoccidials in <em>Tech Info 10</em> from the Canadian Poultry Industry Council.

Electrolytes

Electrolytes are compounds capable of dissolving and dissociating into positively and negatively charged ions. These ions are the means by which the body maintains normal acid-base balance. There are many environmental, and nutritional factors that can challenge the acid-base balance of an animal. However, the animal’s body has many and varied, homeostatic mechanisms which it calls on when necessary, to maintain an acid-base balance environment conducive to good health and optimum performance.

Physiological Considerations

Hydrogen ion (H+) is constantly being produced in the body. It’s concentration in extra cellular fluid (ECF) is kept within a very close range by various homeostatic mechanisms, in order to maintain normal enzymatic and physiological functions including cell membrane conductance. While there are a number of buffer systems that play a role in maintaining normal H+ concentration in the ECF, by far the most important of these is the one involving carbonic acid (H2CO3) and bicarbonate ion (HCO3).

The Role of H+, CO2 and HCO-3

H+, CO2 and HCO-3 are produced directly or indirectly by cellular metabolism (other cations and anions are ingested). The end products of body metabolism are H2O and CO2, and energy.

Hydrogen Ion

H+ results from:

  1. oxidation of sulphur amino acids (methionine and cystine) and phosphorus containing proteins to sulphuric and phosphoric acid.
  2. Incomplete oxidation of fats and carbohydrates to organic acids (eg. acetic, pyruvic, etc.).
  3. Anaerobic glycolysis, which yields lactic acid.
  4. From breakdown of the carbonic acid (H2CO3) formed from CO2 and H2O.

Carbon Dioxide

CO2 is produced during cellular decarboxylation reactions (removing the carboxyl group (COON) from various organic acids). Most of the above CO2 is transported in the blood in 3 forms:

  1. free CO2 (7%)
  2. that associated with plasma proteins (23%)
  3. that associated with HCO-3 (70%) formed in the red blood cells through the carbonic-anhydrase stimulated reaction:
    CO2 + H2O →H2CO3H+ + HCO-3

In the lungs, the reverse reaction occurs from that which occurs intracellularly thus releasing CO2 for exhalation.

Bicarbonate Ion

Besides the red blood cells, HCO3 is produced in numerous tissues (eg. kidney tubules, digestive glands, etc.) where it is required to maintain normal acid-base balance. Renal re-absorption of Na+ and H+ occurs in association with HCO-3 formation.

Excretion and Re-absorption

Most H+ that is excreted is eliminated through the conversion of HCO-3 to carbonic acid and subsequently to CO2 and H2O. H+ is also eliminated by secretion in the renal tubules in exchange for Na+. H+ is also eliminated by secretions in association with Cl- in the gastric mucosa. HCO-3 is excreted via conversion to H2O and CO2 as well as being present in many secretions such as saliva, bile, etc.

Regulation of H+, HCO-3 and CO2

Regulation of H+, HCO-3 and CO2 in the blood are controlled by the respiratory centre, the kidneys, and by various buffer systems. Respiration controls CO2 and thus H2CO3 levels. Increased CO2 expulsion lowers H2CO3 and thus ultimately H+ concentration in ECF, while decreased CO2 expulsion increases H2CO3 and thus H+ concentration in ECF.

Buffering Systems

Acids in the body are mainly neutralized by sodium bicarbonate (NaHCO3) in the short term and by other buffering systems in the long term. The general reaction is:
H+ + A- + NaHCO3 NaA- + H2CO3.

Re-absorption:

H+ that is derived from H2CO3 is eliminated via the kidneys by several mechanisms, all of which result in Na+ re-absorption and the return of HCO-3 to the ECF. When excess HCO-3 is present it is excreted in the urine. Plasma proteins can also be H+ and thus act as an extra cellular buffer.

Metabolic Acidosis

Definition

Metabolic acidosis occurs with an increased production or ingestion of organic acids, or excessive loss of HCO-3. Reduced efficiency of the kidneys to excrete H+ or to re-absorb HCO-3 can also result in acidosis.

Conditions

Several common metabolic conditions can lead to metabolic acidosis, one of these is starvation. This is often referred to as ketosis and results from the incomplete metabolism of fatty acids that are mobilized by the body because of the lack of available glucose as an immediate source of energy for the cells. Another is lactic acidosis, caused by low oxygen uptake by the lungs or excessive oxygen demands by the body (eg. fever, seizures). Decreased hepatic blood flow, as experienced with cold exposure, can also result in decreased lactic acid metabolism and thus lactic acidosis. Diarrhea can result in HCO-3 loss and thus trigger metabolic acidosis. Diuretics that act as carbonic anhydrase inhibitors and ingestion of acidifying salts like ammonium chloride, can also cause the condition.

From the above it is obvious that metabolic acidosis can be caused by excessive acid or a loss of bicarbonate in the body.

Hyperkalemia:

In metabolic acidosis hyperkalemia can occur since H+ moves intracellularly replacing K+. If the replaced K+ cannot be effectively excreted, plasma K+ levels increase and hence renal excretion is increased. Acidosis can also lead to increased urinary calcium excretion by decreasing renal tubular re-absorption of Ca++, thus increasing Ca++ release from bone.

Metabolic Alkalosis

Definition

Metabolic alkalosis occurs due to loss of acid, excessive ingestion of a base or when hypokalemia persists resulting from H+ entering the cell in exchange for K+. Primarily hypokalemia results in a net renal retention of Na+ and HCO-3 leading to an acidosis condition. Metabolic acidosis can lead to hypopnea (shallow breathing).

Respiratory Acidosis

This condition develops when CO2 elimination is impaired which results in increased blood CO2 and H2CO3 plasma levels. Any condition that reduces lung alveolar ventilation ultimately leads to respiratory acidosis. Cyanosis and unconsciousness can result.

Respiratory Alkalosis

This condition is induced by hyperventilation leading to increase loss of CO2 via the lungs. While acidosis can lead to hyperventilation, other factors can include fear, pain, hypothermia, etc.

Dietary Electrolyte Balance (DEB)

Definition

In animal nutrition, electrolytes in the past have primarily referred to sodium, potassium and chloride. Thus, DEB, expressed as Na+K-Cl, in meg/kg of diet, has been shown to have a direct effect on acid-base balance within the bird, and thus an effect on flock performance. While Na, K and Cl are the main electrolytes that are monitored in animal nutrition, recent work would suggest, that with the use of certain dietary ingredients and under various environmental conditions, DEB should be expanded to consider the following equation when expressing dietary meg: Na+K+Ca+Mg-Cl-S-P.

Clinical Observations

Excessive Cl can negatively affect feed intake, increase the incidence of leg problems and partially inhibit carbonic anhydrase, a very important enzyme which functions in egg shell formation.

Increased intakes of Na and K have been shown to increase water intake and thus negatively affect litter quality. However, during periods of heat stress, the use of electrolytes to increase water intake and thus result in a cooling affect on the bird, can have a positive effect on feed intake and hence performance.

Dietary Electrolyte Balance

While maintaining optimum DEB is important the required levels of electrolytes is not static but can vary depending on dietary intake, health status and environmental conditions. The lysine, arginine, potassium interaction that has been extensively studied, demonstrates that increased dietary K+ levels can alter the utilization of these two amino acids, especially if their balance is not ideal. This demonstrates, in part, the importance of acid-base balance in enhancing feed utilization.

Ionophores

Definition and Mode of Action

Ionophores are antiprotozoal agents with the ability to form complexes with various ions, especially K+, Na+ and Ca++. They form lipid-soluble complexes and selectively help and modify the transport of these cations through cell membranes. Such a process can obviously alter cellular functions which depend on ion transport. Both extracellular and intracellular stages of a parasite are affected by the ionophores. In the case of most of the common ionophores used in coccidiosis therapy, they cause cations to accumulate within the intra cellular sporozites (a parasitic protozoa – in this case coccidia). Water then enters the sporozoite by osmosis until the coccidia swell and rupture. The ionophores, in effect, act as chelates with varying affinities for cations.

Possible Side Effects

Most of the ionophores cause some alteration in growth, feed intake and/or water consumption. They have also been implemented in the “knockdown” condition sometimes seen with broilers and turkeys. While the direct involvement of the ionophores in this apparent “toxicity” condition has not been verified, it has been suggested that the marked increase in intracellular Ca++ brought about by the ionophores, may exceed the ability of cellular components to cope with such changes. The Ca++ overloaded cells eventually develop membrane damage which can lead to acute or chronic alterations in acid-base balance. Various responses induced by different ionophores is undoubtedly related to their individual characteristics regarding cation transport.

Efficiency Enhancement

The ability to respond to an acute or chronic acid-base balance induced condition will depend on the factor(s) initiating the condition, as well as environmental factors such as temperature, stress and health status as well as DEB.

Sodium bicarbonate has been designated by some workers as the “privileged” ingredient. Not only does it provide Na+ which favorably affects blood pH and acid-base balance, but it also supplies HCO-3 which plays a critical role in maintaining metabolic equilibrium. Hence, in many conditions that negatively affect acid-base balance of the animal, dietary Na HCO-3 supplementation has been shown to result in a positive effect on performance.

Na HCO-3 has also been reported to enhance the response of ionophores. Reduced coccidia lesions and improved liveability, weight gain and feed conversion have been credited to its’ use along with certain ionophores. By supplementing up to ¼ of the supplemental Na+ in a diet with Na HCO-3 it is possible to reduce the level of Cl- added via NaCl. Reduced dietary Cl- can, depending on diet composition, result in drier litter as well as favorably alter DEB.

Future Considerations

Metabolic disease problems such as ascites, sudden death, spiking mortality, leg problems, etc., continue to contribute to a higher percentage of total flock mortality and condemnations and trim at the processing plant. Thus, it is time that more attention be paid to DEB and its’ subsequent effect on acid-base balance of the bird, as the industry strives to improve the economics of production in the coming years.


November 2008