Regulation of hydrogen ion concentration in the body is a necessity for normal bodily functions.1 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)2.Arterial blood pH is kept between 7.35-7.45, venous blood is kept close to 7.352. 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)2. 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 system3.
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ABI 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 acidosis1. An excess in base, causing pH to rise above 7.45 is known as alkalosis1. The imbalance is classified based on the origin of the disturbance (respiratory or metabolic) and the direction of change in pH (acidosis or alkalosis)2. Thus four processes can occur e.g. metabolic alkalosis (MK), metabolic acidosis (MA), respiratory alkalosis (RK) and respiratory acidosis (RA)2.
The general reasons for the build-up of acid are usually4:
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 include4:
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 that maintains pH at its normal value5. They lower pH if it 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 body1.
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. The intracellular buffers comprise basic and acidic groups that act as H+ acceptors or donors to maintain the pH level of bloodA.1
Phosphate buffer system
The phosphate buffer system, another intracellular buffer is comprised of two ions: hydrogen phosphate and dihydrogen phosphate. Hydrogen phosphate ions accept additional H+ ions to re-establish the equilibria between the hydroxide and H+ in the blood. The dihydrogen phosphate ions release additional H+ to reinstate the pH level of the bloodB.1
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. CO2 can be shifted through carbonic acid to hydrogen ions and bicarbonateC .1
As well as the buffer systems there are also the renal mechanisms and respiratory regulation of AB. These systems form the physiological buffering systems that control pH by regulating the amount of acid/base in the body6. They are slower than chemical buffering, the lungs require minutes to hours and the renal system need hours to days to correct a change. However, they are more powerful7.
CO2 is continually produced by body tissues due to metabolism, it is converted to HCO3- for transportation C.3 Due to the equilibria of the reactions an increase in one of the chemical species pushes the equilibrium in the opposite direction2. The partial pressure of CO2 (pCO2) dissolved in blood gives a measurement of a person’s ventilation8. The normal range is 35-45 mmHg9. If the H+ concentration in the blood increases, the respiratory centre is excited via peripheral chemoreceptors, stimulating deeper and more rapid respiration8. As ventilation increases, more CO2 is removed from the blood, pushing the reaction to the left and reducing the H+ concentration10. When blood pH rises, the respiratory centre is depressed7. 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 pH10.
Although the renal system is slower to compensate, it is much more powerful when it comes to compensation4. HCO3 is used as a measure of the metabolic component of AB9. The normal range is 22-26 mEq/L, if levels are above 26 it is a result of MK and a result of MA if the levels are below 229. In responses to acidosis, tubular cells reabsorb more bicarbonate from the tubular fluid C.10 The collecting duct cells can secrete more H+B.10 Bicarbonate can also be generated C and ammonium can be excreted, leading to increased formation of the NH3 buffer.10 If alkalosis is presented, the kidney will excrete more HCO3- by decreasing H+ secretion from the tubular epithelial cellsC , lowering rates of glutamine metabolism and ammonia excretion10.
Pneumonia is the inflammation of lung tissue, usually caused by an infection affecting the 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 coughing11.
Respiratory acidosis causes
One symptom of viral pneumonia is difficulty in breathing, this difficulty in breathing means that hypoventilation occurs. The excretion of CO2 is inadequate, causing accumulation of CO2 in the blood, hence pushing the pCO2 above the upper limit of 45mmHg9. As the pCO2 rises it causes the blood pH to fall below 7.35, due to a decreased HCO3:pCO2 ratio9. This is characteristic of RA10.
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. Patients can become anxious and complain of dyspnea8. Sometimes disturbed sleep can be an issue. As the pCO2 rises, the anxiety could progress to delirium and the patient becomes progressively more confused, drowsy, and obtunded8.
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 pCO210. 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.2 Acid can also be excreted as NH4+.2 This occurs as part of glutamine metabolism and also generates new HCO3+ F.2 To further the compensation, bicarbonate can be reabsorbed from proximal convoluted tubule cells to Peri-tubular capillaryH.2 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 CO2.3 The decrease 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, a clear indication of RK9.
Respiratory alkalosis causes
Hyperventilation, the primary cause, is also the primary symptom. Hyperventilation causes hypocapnia.7 This symptom is accompanied by dizziness, light headedness, agitation and tingling.7 Muscle twitching, spasms and weakness may be noted in some patients.7 RK may disrupt calcium ion balance causing the symptoms of hypocalcaemia such as tetany and fainting.8
Compensation of respiratory alkalosis
Within minutes of RK occurring, H+ move from inside cells to the extracellular fluid, there they combine with HCO3 to form carbonic acid.6 H+ is mostly derived from haemoglobin, protein and phosphate buffers. By reacting with bicarbonate ions a mild reduction in plasma pH is possible. In acute RK, due to cell buffering, there is a 2meq/L decrease in the plasma HCO3 concentration for every 10 mmHg decrease in the pCO2.10 In chronic RK, the renal system responds by decreasing hydrogen, titratable acid and ammonium excretion as well as ammonium production.6 The amount of HCO3- excreted will increase due to reduced reabsorption of filtered HCO3-.6
Gastroenteritis is an infection of the gastrointestinal tract. Usually brought on by infection from viruses but contaminated or irritating foods are also known causes. Its symptoms include various combinations of diarrhoea, vomiting, abdominal pain and cramping12.
Metabolic acidosis causes
Gastroenteritis can cause severe diarrhoea, meaning that intestinal secretions containing solutes which are normally reabsorbed are now rushing through the digestive tract.2 Bicarbonate is being lost faster than it can be regenerated and will decrease at least to the lower limit of 22mEq/L.13 The loss of HCO3 means that there will be a higher concentration of H+ in the body, causing pH to fall below 7.35, which is characteristic of MA13.
Metabolic acidosis consequences
Aside from the symptoms of the underlying condition MA usually causes rapid breathing; confusion or lethargy could also present13. Severe MA can result in shock or death. The excess of H+ also means that potassium cannot be reabsorbed causing hypokalaemia13.
Compensation of metabolic acidosis
The bicarbonate buffer system, works 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 stimulated8. 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 acid13.
Metabolic alkalosis causes
Gastroenteritis can also lead to MK, via another of its symptoms12. Vomiting leads to what is known as chloride-responsive MK. This occurs when chloride is below 10mEq/L14. Vomiting results in the loss of hydrochloric acid with the stomach contents2. The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions2. 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/L10.
Metabolic alkalosis consequences
Slowed breathing is an initial symptom of MK14. Cyanosis would also develop as a symptom of poor oxygen intake14. Other symptoms can include irritability, twitching, rapid heart rate, arrhythmia, and a drop in blood pressure14. Severe cases can lead to convulsions and coma, it may also cause hypokalaemia and hyponatraemia14. Hypokalaemia occurs as H+ moves out of the cell thus potassium moves from the external cellular fluid to the internal cellular fluid3. This causes hyperpolarisation of the resting membrane potential leading to decreased neuron excitability3. Hyponatraemia occurs when the concentration of sodium in the extracellular fluid drops. Water then moves into the cells via osmosis and can cause cells to swell3.
Compensation of metabolic alkalosis
Compensation for MK occurs mainly in the lungs, which retain CO2 through slow, shallow breathing14. CO2 is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH14. Unlike renal compensation, respiratory compensation never returns the pH of the blood to the exact same range as before1.
There are set parameters in place to help keep the human body functioning normally, blood pH, pCO2 and HCO3 levels. The balance and movement of electrolytes and hydrogen ions also needs to be controlled. When the normal ranges are breached, or balances are upset, alkalosis/acidosis can occur. Acidosis and alkalosis of both the renal and respiratory systems can be brought about by a variety of conditions such as pneumonia or gastroenteritis. Chemical buffers are key in maintaining the acid base balance of the body and when they are not enough the renal and respiratory systems are there to take over.
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