Regulation Of Hydrogen Ion H Concentration Biology Essay
Disclaimer: This work has been submitted by a student. This is not an example of the work written by our professional academic writers. You can view samples of our professional work here.
Any opinions, findings, conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of UK Essays.
Published: Mon, 5 Dec 2016
Regulation of hydrogen ion concentration in the body is a necessity for normal bodily functions. The concentration of H+ in all bodily fluids are maintained to keep pH ranges between narrow limits, this maintenance is known as acid-base balance (AB).Arterial blood pH is kept between 7.35-7.45, venous blood is kept close to 7.35. Most diseases/conditions disturb AB, AB changes can be more harmful than the original pathology. When the AB is affected, causing the pH to vary from its limits, it is called an acid-base imbalance (ABI). However, there are processes in place to make ABI less likely to occur. AB is maintained sequentially by several mechanisms: chemical buffers, the respiratory system and the renal system.
Acid-base imbalance is an irregularity in the body’s balance of acids and bases. These deviations cause blood pH to stray out of its normal range. The imbalances can become life-threatening. When an excess of acid causes pH to fall below 7.35 it results in acidosis. An excess in base, causing pH to rise above 7.45 is known as alkalosis. The imbalance is classified based on the origin of the disturbance (respiratory or metabolic) and the direction of change in pH (acidosis or alkalosis). Thus four processes can occur e.g. metabolic alkalosis (MK), metabolic acidosis (MA), respiratory alkalosis (RK) and respiratory acidosis (RA).
The general reasons for the build-up of acid are usually:
Poor carbon dioxide(CO2)excretion e.g. COPD
Excess H+ production from overproduction of organic acids
Excessive bicarbonate loss via excretion
Inadequate H+ production caused by Renal tubular acidosis
The typical sources of acid loss include:
Excessive reabsorption of bicarbonate due to gastrointestinal problems
Acid loss via prolonged vomiting
Excess CO2excretion via hyperventilation
Ingestion of alkalis
A buffer is a solution with the ability to maintain pH at its normal value, reacting to pH changes within seconds Buffers adjust the pH level of blood to lower pH if its level rises above 7.45, making the blood slightly more acidic. If blood pH falls below 7.35, buffers act to take up H+ thus decreasing the acidity of the blood. There are three different buffer systems working in the body.
Protein buffer system
Proteins are the most abundant buffers in the body fluid, it is an example of an intracellular buffer. Their functionality is mainly intracellular and includes haemoglobin (Hb). Hb is the protein that transports oxygen within the body. Plasma proteins also function as buffers but there are very few in comparison with the intracellular protein buffers. Protein buffers include basic and acidic groups that act as H+ acceptors or donors to maintain the pH level of bloodA.
Phosphate buffer system
The phosphate buffer system, another intracellular buffer is comprised of two ions: hydrogen phosphate and dihydrogen phosphate. Hydrogen phosphate ions accept all additional H+ ions to re-establish the equilibrium between the hydroxide and hydrogen ions in the blood. The dihydrogen phosphate ions release additional H+ to reinstate the pH level of the bloodB.
Bicarbonate suffer system
The most important buffer system is the bicarbonate buffer system, it is an extracellular buffer. Co2 is removed by the lungs and bicarbonate regenerated by the kidney. CO2can be shifted through carbonic acid to hydrogen ions and bicarbonateC .
As well as the buffer systems there are also the renal mechanisms of AB and respiratory regulation of H+. These systems form the physiological buffering systems that control pH by regulating the amount of acid/base in the body. They are slower than the chemical buffering systems, the lungs requiring minutes to hours to correct a change and the renal system needing hours to days to work efficiently. However, they’re much more powerful and effective than the chemical buffering systems.
CO2 is continually produced by body tissues due to metabolism, it is converted to bicarbonate ions for transportation C. Due to the equilibria of the reactions an increase in one of the chemical species will push the equilibrium in the opposite direction. The partial pressure of CO2 (pCO2) dissolved in blood gives a measurement of a person’s ventilation. The normal range is 35-45 mmHg. If the H+ concentration in the blood increases, usually resulting from metabolic processes, the respiratory centre is excited via peripheral chemoreceptors. Thus stimulating deeper and more rapid respiration. As ventilation increases, more CO2 is removed from the blood, pushing the reaction to the left and reducing the H+ concentration. When blood pH rises, the respiratory centre is depressed. As respiratory rate drops and respiration becomes shallower, CO2 accumulates; the equilibrium is pushed to the right, causing the H+ concentration to increase restoring normal blood pH.
Although the kidneys are slower to compensate, renal physiology has several powerful mechanisms to control pH by the excretion of excess acid/base.HCO3 is used as a measure of the metabolic component of AB. The normal range is 22-26 mEq/L, if levels are above 26 it is a result of metabolic alkalosis and a result of metabolic acidosis if the levels are below 22. In responses to acidosis, tubular cells reabsorb more bicarbonate from the tubular fluid C. The collecting duct cells can secrete more H+B. Bicarbonate can also be generated C and ammonium can be excreted, leading to increased formation of the NH3 buffer. In response to alkalosis, the kidney may excrete more bicarbonate by decreasing hydrogen ion secretion from the tubular epithelial cellsC , and lowering rates of glutamine metabolism and ammonia excretion.
Pneumonia is inflammation of the tissue in one or both lungs, usually caused by an infection affecting the microscopic air sacs known as alveoli. Typical symptoms include coughing, fever, muscle pain, and difficulty breathing in viral pneumonia. In bacterial pneumonia the symptoms include: Drowsiness, rapid breathing, chest pains and coughing.
Respiratory acidosis causes
One symptom of viral pneumonia is difficulty in breathing, this difficulty in breathing means that hypoventilation occurs – insufficient ventilation to meet body’s demand. Ventilation rate is very important in the balance of bodily fluid pH, if alveolar ventilation is halved there can be a 0.4 fall in pH. Specifically, the excretion of CO2 is inadequate, causing accumulation of CO2in the blood, hence pushing the pCO2 above the upper limit of 45mmHg. As the pCO2 rises it causes the blood pH to fall below 7.35, due to a decreased HCO3:pCO2 ratio. This is characteristic of RA.
Respiratory acidosis consequences
The physiological manifestations of RA are often those of the underlying disorder. Symptoms vary depending on the severity of the disorder and the rate of development of hypercapnia (excess Co2 in blood). Mild to moderate hypercapnia that develops slowly usually has minimal symptoms. Patients may be anxious and may complain of dyspnea (laboured or difficult breathing). Some patients may have disturbed sleep and daytime hypersomnolence. As the partial arterial pressure of carbon dioxide increases, the anxiety may progress to delirium, and patients become progressively more confused, drowsy, and obtunded.
Compensation of respiratory acidosis
When an ABI originates from the respiratory system, the compensation that occurs is dependent on whether or not the acidosis is acute or chronic. If acute, buffer systems will intervene, cellular buffering elevates plasma bicarbonate slightly, 1 mEq/L for each 10-mm Hg increase in pCO2.In the case of chronic RA, renal mechanisms are used to compensate for the ABI. New bicarbonate is generated via buffering of secreted H+ by monohydrogenphosphateE. Acid can also be excreted as NH4+. This occurs as part of glutamine metabolism and also generates new HCO3+ F. To further the compensation, bicarbonate can be reabsorbed from proximal convoluted tubule cells to Peri-tubular capillaryH. These renal mechanisms work to excrete H+ into the filtrate, in the tubule lumen, thus allowing acid to be excreted from the body. The loss of H+ alongside the regeneration and reabsorption of HCO3- returns the pH of the blood to its normal range.
Respiratory alkalosis causes
Rapid breathing is a symptom of bacterial pneumonia, this type of breathing is known as hyperventilation, where the ventilation exceeds metabolic demands. In this case pO2 is raised at the expense of over-excretion of CO2. The increase in pCO2 leads to an increased HCO3-:pCO2 ratio causing pCO2 to fall below the lower level of 35mmHg and blood pH to rise above 7.45. It is clear that RK is occurring in this case.
Respiratory alkalosis causes
Hyperventilation, the primary cause is also the primary symptom. Hyperventilation causes hypocapnia (deficiency of CO2in the blood).This symptom is accompanied by dizziness, light headedness, agitation and tingling. Muscle twitching, spasms and weakness may be noted in some patients. RK may disrupt calcium ion balance causing the symptoms of hypocalcaemia such as tetany and fainting.
Compensation of respiratory alkalosis
About 10 minutes after the onset of respiratory alkalosis, hydrogen ions move from the cells into the extracellular fluid, where they combine with HCO3 to form carbonic acid. The hydrogen ions are primarily derived from intracellular buffers such as haemoglobin, protein and phosphates. The reaction with bicarbonate ions leads to a mild reduction in plasma. In acute respiratory alkalosis, as a result of cell buffering, for every 10 mmHg decrease in the PCO2, there is a 2meq/L decrease in the plasma HCO3 concentration. In the circumstance of chronic RK, the kidney will respond by lowering hydrogen secretion, excretion of titratable acids, ammonium production and ammonium excretion. There will also be an increase in the amount of HCO3- excreted due to decreased reabsorption of filtered HCO3-
Gastroenteritis is an infection of the gastrointestinal tract (From the stomach to the intestines). Usually brought on by infection from viruses but contaminated or irritating foods have been known to also cause gastroenteritis. Its symptoms include various combinations of diarrhoea, vomiting, and abdominal pain and cramping.
Metabolic acidosis causes
Gastroenteritis can cause severe diarrhoea in those infected. This means that intestinal secretions that contain solutes which are normally reabsorbed are now rushing through the digestive tract. Bicarbonate is being lost at a rate greater than that of which new bicarbonate ions can be regenerated. The loss of HCO3 means that there will be a higher concentration of H+ in the body, causing pH to fall. The pH will fall below 7.35 and bicarbonate levels will decrease to at least the lower limit of 22mEq/L. This is metabolic acidosis.
Metabolic acidosis consequences
Aside from the symptoms of the underlying condition metabolic acidosis itself usually causes rapid breathing; confusion or lethargy may also occur. Severe metabolic acidosis can lead to shock or death. In some situations, metabolic acidosis can be a mild, chronic condition. The excess of H+ also means that potassium cannot be reabsorbed causing hypokalaemia.
Compensation of metabolic acidosis
The bicarbonate buffer system, works for metabolic acidosis as it does for respiratory acidosis by reabsorbing and regenerating bicarbonate. If the acidosis continues for a prolonged period, it’s detected by both peripheral and central chemoreceptors and the respiratory centre is stimulated. The subsequent increase in ventilation causes CO2 to be “blown off” thus a fall in arterial pCO2 occurs and carbonic acid levels fallC ridding the blood of excess acid.
Metabolic alkalosis causes
Although gastroenteritis may cause metabolic acidosis from diarrhoea, vomiting can lead to metabolic alkalosis. Vomiting leads to what is known as chloride-responsive metabolic alkalosis. This occurs when chloride is below 10mEq/L. Vomiting results in the loss of hydrochloric acid with the stomach contents. The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions. The loss of acid gives an increase in pH to 7.45 and the bicarbonate levels surpass the upper limit of their normal range of 26mEq/L, leading to metabolic alkalosis.
Metabolic alkalosis consequences
In cases of metabolic alkalosis, slowed breathing may be an initial symptom. The may also develop as a sign of inadequate oxygen intake. Other symptoms can include irritability, twitching, rapid heart rate, arrhythmia, and a drop in blood pressure. Severe cases can lead to convulsions and coma, it may also cause a loss of potassium (hypokalaemia) and sodium (hyponatraemia). Hypokalaemia occurs as H+ moves out of the cell thus potassium moves from the external cellular fluid to the internal cellular fluid. This causes hyperpolarisation of the resting membrane potential leading to decreased neuron excitability. Hyponatraemia occurs when the amount of sodium in fluids outside cells drops, water moves into the cells to balance the levels. This causes the cells to swell with too much water.
Compensation of metabolic alkalosis
Compensation for metabolic alkalosis occurs mainly in the lungs, which retain CO2 through slow, shallow breathing. CO2 is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH. Unlike renal compensation, respiratory compensation never returns the pH of the blood to the exact same range as before.
There are set parameters in place to help keep the human body functioning normally, blood pH, pCO2 and HCO3 levels. When the limits of these ranges are breached, alkalosis/acidosis can occur. Acidosis and alkalosis of both the renal and respiratory systems can be brought about by a variety of conditions.
Cite This Work
To export a reference to this article please select a referencing stye below: