Thiamine deficiency, especially if child is dependent upon total parenteral nutrition without sufficient multivitamins. Ratio greater than 25 suggests tissue hypoxia, pyruvate decarboxylase deficiency, mitochondrial oxidative phosphorylation disorders.
Muscle biopsy — Useful in cases of suspected mitochondrial phosphorylation defects, looking for ragged red fibers. In cases of extreme acidosis pH less than 7. Rapid infusions of bicarbonate are not needed and may be deleterious in certain situations. Hypernatremia may result from overzealous bicarbonate administration. In DKA, the use of bicarbonate administration is not recommended except in cases of extreme acidosis as use may exacerbate CSF acidosis and contribute to the development of cerebral edema.
RTA 2 proximal will respond to exogenous alkali administration. Potassium supplementation is generally needed once alkali administration is begun due to enhanced urine potassium losses. Treatment with thiazide diuretics can enhance proximal reabsorption of bicarbonate but may have the secondary effect of potassium loss. The etiology of diarrhea should be investigated. If vomiting or gastric loses are present, the use of anti-emetics, H 2 blockers, or proton pump inhibitors PPI may be beneficial.
DKA — Factors associated with an increased risk of developing cerebral edema include: younger age, longer duration of symptoms, lower pCO 2 , severe acidosis, elevated BUN, failure of serum sodium to rise with therapy, treatment with bicarbonate and a higher volume of fluid resuscitation.
See chapter on diabetes mellitus for specifics. Acidosis and alkalosis are secondary findings of underlying diseases or medical conditions. Monitoring and follow up of the disease state are etiology specific. For example, children with RTA 2 can have growth retardation, rickets, osteomalacia and abnormal vitamin D metabolism but that is beyond the scope of this text ICU text.
If bicarbonate has been administered, a follow-up blood gas is recommended. If a ventilator adjustment has been made, then follow up monitoring by a blood gas or measurement of end-tidal CO 2 should be done. Acid-base balance is maintained by buffering of the acid load via intracellular and extracellular mechanisms, excretion of hydrogen ions in the urine, reabsorption of bicarbonate from the urine and alveolar ventilation.
Metabolism of dietary carbohydrates, fats, and proteins results in the addition of acids to the blood. Alveolar ventilation is a major contributor to extracellular buffering.
CO 2 , a product of fat and carbohydrate metabolism, is excreted by the lungs. Of note, urine cannot achieve a pH much less than 5. Phosphate and ammonia also act as buffers in the urine.
Additionally, as plasma pH decreases, the respiratory system attempts to compensate by increasing minute ventilation, which decreases PaCO 2. Therefore the respiratory system is a buffering system with limited gain as it cannot completely compensate for changes in pH due to metabolic disorders.
The respiratory system is an efficient mechanism to buffer in the short term until the kidneys can manifest chronic buffering. The kidneys have the capacity to control acid-base balance by excreting acidic or basic pH urine. Over time, the kidneys can completely correct for pH abnormalities.
The classification of the acid-base disorder depends upon determination of the presence of a base excess or base deficit, then eliciting the metabolic and respiratory impacts. Metabolic acidosis has many etiologies. In general it can be divided into gap acidoses and non-gap acidoses. Gap acidoses result from the accumulation of organic acids lactate, ketoacids, renal dysfunction or the effect of toxins methanol, ethylene glycol, salicylates, paraldehyde.
Inborn errors of metabolism, such as electron transport chain disorders, carbohydrate metabolism errors and some types of organic acidurias proprionic acidemia, methylmalonic acidemia. DKA — A state of relative or absolute deficiency of insulin observed in new or known diabetics.
Increases in counter-regulatory hormones including glucagon, cortisol, growth hormone and epinephrine occur, resulting in hepatic gluconeogenesis, glycogenolysis and lipolysis. Lipolysis yields an increase in free fatty acids, which are used as an alternative energy source and result in an increase of ketoacid metabolites, such as beta-hydroxybutyrate, acetoacetate and acetone.
Initially these ketoacids are buffered by various mechanisms, but once those mechanisms are overloaded, they spill into the urine, causing ketonuria. In the first year of life, an immature proximal tubule may result in symptoms and poor growth, which resolves with alkali administration for several years.
Metabolic alkalosis occurs due to gastrointestinal loss of HCl or as a result of renal issues. Diuretic-induced contraction alkalosis. Generally this is seen with use of loop diuretics and thiazides. Acute respiratory acidosis may be due to airway obstruction, central nervous system depression, neuromuscular disease and acute pulmonary disease.
No matter what the etiology of respiratory acidosis is, there is primary hypoventilation, which results in retention of carbon dioxide and acidosis. Buffering of the acidotic state occurs acutely via various cellular mechanisms, including renal retention of bicarbonate. Within a few days, renal mechanisms will maximally compensate for respiratory acidosis. Chronic respiratory acidosis is usually compensated via renal mechanisms.
Causes of chronic respiratory acidosis include chronic obstructive and restrictive lung disease, neuromuscular disease, and obesity-related hypoventilation. Respiratory alkalosis results from hyperventilation, which increases exhalation of CO 2. The increased alveolar ventilation pulls CO 2 from the circulation. The body produces excess acid in the advanced stages of shock Shock Shock is a life-threatening condition in which blood flow to the organs is low, decreasing delivery of oxygen and thus causing organ damage and sometimes death.
Blood pressure is usually low Symptoms of diabetic ketoacidosis include nausea, vomiting, abdominal pain, and a characteristic Even the production of normal amounts of acid may lead to acidosis when the kidneys are not functioning normally kidney failure Overview of Kidney Failure This chapter includes a new section on COVID and acute kidney injury AKI.
Kidney failure is the inability of the kidneys to adequately filter metabolic waste products from the blood. Metabolic acidosis also develops when the body loses too much base.
For example, bicarbonate can be lost through the digestive tract due to diarrhea or an ileostomy. Respiratory acidosis develops when the lungs do not expel carbon dioxide adequately inadequate ventilation , a problem that can occur in disorders that severely affect the lungs such as chronic obstructive pulmonary disease Chronic Obstructive Pulmonary Disease COPD Chronic obstructive pulmonary disease is persistent narrowing blocking, or obstruction of the airways occurring with emphysema, chronic obstructive bronchitis, or both disorders.
Pneumonia is one of the most common causes of death worldwide. Often, pneumonia is the final Coughing, wheezing, and shortness of breath that occur in response to specific triggers are With treatment, people As a result, the muscles stimulated by these nerves deteriorate, become In addition, people can develop respiratory acidosis when their breathing is slowed due to oversedation as a result of opioids narcotics , alcohol, or strong drugs that induce sleep sedatives.
As a result of the slowed breathing, the level of oxygen in the blood may be low. Sleep-disordered breathing for example, sleep apnea Sleep Apnea Sleep apnea is a serious disorder in which breathing repeatedly stops long enough to disrupt sleep and often temporarily decrease the amount of oxygen and increase the amount of carbon dioxide Breathing becomes deeper and slightly faster as the body tries to correct the acidosis by expelling more carbon dioxide. As the acidosis worsens, people begin to feel extremely weak and drowsy and may feel confused and increasingly nauseated.
Eventually, in severe cases, heart problems may develop and blood pressure can fall, leading to shock, coma, and death. Drowsiness may progress to stupor and coma as the oxygen in the blood becomes inadequate.
Stupor and coma can develop within moments if breathing stops or is severely impaired, or over hours if breathing is less dramatically impaired. The diagnosis of acidosis generally requires the measurement of blood pH and carbon dioxide in a sample of arterial blood, usually taken from the radial artery in the wrist. To learn more about the cause of the acidosis, doctors also measure the levels of bicarbonate in the blood.
Additional blood tests are then done to help determine the specific cause. Almost always, treatment of acidosis is directed at reversing the cause. Doctors rarely simply give alkaline drugs, such as bicarbonate, to reverse the acidosis. In metabolic acidosis, treatment depends primarily on the cause. Therefore, a basic understanding of how to interpret ABG results can be useful for pharmacists to help them clarify the clinical picture. The optimal physiological pH of extracellular fluid is 7.
The following equilibrium equation is crucial to understanding acid-base balance:. It is the renal and respiratory systems that are responsible for maintaining the pH of the blood. One way that the body controls the pH of extracellular fluid is by increasing or decreasing the rate and depth of respiration and thereby the amount of CO 2 expelled ie, slow, shallow breathing retains more CO2 than fast, deep breathing.
The body has three main buffers that minimise any changes in pH that occur when acids or bases are added, namely haemoglobin, HCO3 — and proteins. However, HCO3 — is the most important buffer in the blood and is the dominant buffer in the interstitial fluid. At an intracellular level buffering occurs instantly, but the effect is small.
The following are the commonly reported parameters of ABG results see Box 2 for the normal reference ranges :. Other parameters commonly found on ABG reports are: haemoglobin, glucose and electrolytes sodium, potassium, chloride and ionised calcium. The pH should be assessed first. A pH of less than 7. Having determined if the patient is acidotic or alkalotic, check the HCO3 — and the PaCO 2 to classify the results as follows:.
It is possible for patients to have a mixed respiratory and metabolic alkalosis or acidosis. This occurs when primary respiratory and primary metabolic disturbances exist simultaneously.
If the two processes oppose each other, pH derangement will be minimised see step 3. Check to see if the patient is compensating for his or her acid-base imbalance. This may create some apparently normal results amongst some deranged ones. When interpreting acid-base status, it is important always to take the clinical context into account.
0コメント