Acid–Base Balance
Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod in The Primary FRCA Structured Oral Examination Study Guide 1, 2017
Correction occurs when all three variables (pH, HCO3− and PaCO2) are restored to normal levels. Initial compensation is by intracellular buffering (carbonic acid–bicarbonate buffer system and haemoglobin) and occurs within 2 hours.Respiratory compensation reaches its maximum by 24 hours and is by: Hyperventilation in the presence of a metabolic acidosis.Hypoventilation in the presence of a metabolic alkalosis.Renal compensation is by: Increased acid (H+) secretion andretention (reabsorption and regeneration) in the presence of a respiratory (and metabolic) acidosis.Decreased acid (H+) secretion andretention (reabsorption and regeneration) in the presence of a respiratory (and metabolic) alkalosis.
Acid–base physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
In metabolic alkalosis, there is an increase in plasma [] concentration and the respiratory drive is decreased, resulting in a rise in PaCO2. Thus, respiratory compensation to acid–base disturbances controls the excretion of CO2 to restore the []/PaCO2 ratio closer to normal. The capacity of the respiratory system to buffer acid–base disturbances is approximately twice the buffering capacity of the chemical buffers in ECF. The other important feature of the respiratory control of acid–base balance is that it responds rapidly and hence prevents large acute changes in plasma [H+].
Compensatory Mechanisms in Acid–Base Disorders
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
In metabolic alkalosis, there is an increase in plasma concentration and the respiratory drive is decreased, resulting in a rise in . Thus, respiratory compensation to acid–base disturbances controls the excretion of CO2 to restore the ratio closer to normal. The capacity of the respiratory system to buffer acid–base disturbances is approximately twice the buffering capacity of the chemical buffers in ECF. The other important feature of the respiratory control of acid–base balance is that it responds rapidly and, hence, prevents large acute changes in plasma [H+].
Calcium and pH value might predict persistent renal failure in acute pancreatitis in the early phase
Published in Current Medical Research and Opinion, 2022
Xuanfu Chen, Meng Jin, Yi Li, Yamin Lai, Xiaoyin Bai, Hong Yang, Hong Lv, Jiaming Qian
The two parameters were simple, quantitative and easy to obtain. However, their mechanisms of predicting renal injury are likely multifactorial. With respect to pH, on the one hand, some AP patients lost intravascular blood volume due to severe response to pancreatic injury, which led to a decrease of the renal perfusion and then caused renal failure. On the other hand, a complex inflammatory network combined with (peri)pancreatic necrosis influenced the severity of the renal failure, and the latter exacerbated the development of pancreatitis3. The acid–base balance was maintained by pulmonary excretion of carbon dioxide, metabolic utilization of organic acids and renal excretion of nonvolatile acids. Respiratory compensation in metabolic acidosis or alkalosis was a rapid response. For instance, the reaction of metabolic acidosis began within 30 min14 and was completed within 12–24 h. If the respiratory disorder persisted for more than minutes to hours, the kidneys responded by producing more significant changes in serum HCO3. As it always took hours for patients to reach the hospital, the pH was regulated by renal compensation. So we could conclude that a lower pH level on admission indicated impaired renal compensatory function and was more likely to be associated with PRF. Previous research has found that lower arterial pH on admission could better predict an adverse outcome in patients with AP15. Meanwhile, lower blood pH suggests higher mortality, elevated severity scores and longer hospital stay in AP patients, which is similar to our results16.
Cobalamin and folic acid deficiencies presenting with features of a thrombotic microangiopathy: a case series
Published in Acta Clinica Belgica, 2022
Britt Ceuleers, Sofie Stappers, Jan Lemmens, Lynn Rutsaert
Our initial physical examination revealed a very pale, tachypneic but euvolemic woman appearing older than her stated age. There were no abnormal neurological or gastrointestinal findings. Vital signs were as follows: oxygen saturation 98%, heart rate 133/min, a blood pressure of 154/81 mmHg and a temperature of 37.3°C. A complete blood count (Table 1) revealed a severe macrocytic anemia with thrombocytopenia. Reticulocyte count was normal. An additional hemolytic workup showed elevated LDH, decreased haptoglobin, hyperkalemia, indirect hyperbilirubinemia and a negative Direct Coombs test. Laboratory findings also showed normal kidney function (creatinine 1.02 mg/dl), hypovitaminosis B12 (<148 ng/L) with hyperhomocysteinemia and normal folic acid levels (9.4 µg/L). By means of an arterial blood gas analysis, we established a high anion gap metabolic acidosis with partial respiratory compensation, assumedly as a consequence of high lactate levels in the blood. A peripheral blood smear revealed schistocytes.
The serum glycolate concentration: its prognostic value and its correlation to surrogate markers in ethylene glycol exposures
Published in Clinical Toxicology, 2022
Darren M. Roberts, Robert S. Hoffman, Jeffrey Brent, Valéry Lavergne, Knut Erik Hovda, William H. Porter, Kenneth E. McMartin, Marc Ghannoum
Because glycolate assays are rarely available rapidly enough to influence clinical decisions, surrogate markers for the glycolate concentration are valuable to guide management. This systematic review, like others [4,6,28,40,46], demonstrates that the anion gap is the surrogate measure that best correlates with the glycolate concentration and outperforms other acid-base markers such as pH, base excess, and HCO3−. The poorer correlation of other surrogates is unsurprising as they can be influenced by other physiological factors, such as inadequate respiratory compensation, exogenous bicarbonate administration, mechanical ventilation, and other coingestants [4].
Related Knowledge Centers
- Breathing
- Carbon Dioxide
- Chemoreceptor
- Metabolic Acidosis
- Metabolic Alkalosis
- Ph
- Renal Compensation
- Hypoventilation
- Respiratory Center
- Acid–Base Homeostasis