The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In humans, the normal pH of arterial blood lies between 7. Blood pH values compatible with life in all mammals are limited to a pH range between 6.
Changes in the pH of arterial blood and therefore the extracellular fluid outside this range result in irreversible cell damage. Metabolic acidosis may result from increased production of metabolic acids or disturbances in the ability to excrete acid via the kidneys. Renal acidosis is associated with an accumulation of urea and creatinine as well as metabolic acid residues of protein catabolism.
Once oxygenation is restored, the acidosis clears quickly. Another example of increased production of acids occurs in starvation and diabetic acidosis. It is due to the accumulation of ketoacids ketosis and reflects a severe shift from glycolysis to lipolysis for energy needs. 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 for exhaustion leading to respiratory failure. The Henderson-Hasselbalch approximation is useful for calculating blood pH, because blood is a buffer solution. 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.
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, neutralizing the acidosis with infusions of bicarbonate may be required. Respiratory acidosis results from a build-up of CO 2 in the blood hypercapnia due to hypoventilation. It is most often caused by pulmonary problems, although head injuries, drugs especially anesthetics 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 CO 2 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. This is the practice adopted here. Many published articles refer to compensatory processes as though they were primary processes.
This lazy and incorrect use of these terms is extremely confusing so caution must be exercised and ultimately one should not be too pedantic in insisting on correct terminology in others as the practice is widespread in the clinical literature. For example: A patient with diabetic ketoacidosis and compensatory Kussmaul respirations should be described as having a 'metabolic acidosis with compensatory hyperventilation'.
It is possible that a patient such as this could have a mixed disorder with a respiratory acid-base disorder as well as the metabolic acidosis. The interpretation of these more complicated cases is discussed in Section 8. The clinical acid-base disorders are defined by their effects in the extracellular fluid or more specifically, in the arterial blood. The disorder may arise because of changes intracellularly eg excess lactate production but the effect extracellularly is what is able to be easily measured.
Despite the definitions of acidosis and alkalosis above, it is common to speak of an 'intracellular acidosis' or an 'intracellular alkalosis'. This use is not consistent with the definitions above but as there are no other satisfactory terms available so this common practice is followed here. Previous Index Top of page Next.
Acid-Base Physiology 3. Basic Definitions Acidosis - an abnormal process or condition which would lower arterial pH if there were no secondary changes in response to the primary aetiological factor. Alkalosis - an abnormal process or condition which would raise arterial pH if there were no secondary changes in response to the primary aetiological factor.
Simple Acid-Base Disorders 1 are those in which there is a single primary aetiological acid-base disorder. Mixed acid-Base Disorders 2,3 are those in which two or more primary aetiological disorders are present simultaneously.
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