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Interpreting Arterial Blood Gases in Trauma Patients
Published in Kajal Jain, Nidhi Bhatia, Acute Trauma Care in Developing Countries, 2023
Once diagnosis of metabolic acidosis is established, look for respiratory compensation for it. There will be a decrease in the CO2 level as per the value of HCO3–. Whenever compensation is complete, then the pH will be in normal range; and if incomplete, then the pH will not be fully corrected. The following formula can be used to calculate the expected level of CO2 for respiratory compensation with metabolic acidosis:
Acid–base disturbances
Published in Sherif Gonem, Ian Pavord, Diagnosis in Acute Medicine, 2017
Similarly, a primary metabolic acid–base disturbance will be accompanied by respiratory compensation that tends to return the pH towards normal. Specifically, a metabolic acidosis will cause compensatory hyperventilation, thus reducing the pCO2, whereas a metabolic alkalosis may result in a degree of hypoventilation, thus increasing the pCO2. Maximal compensation may take a number of hours.
Assessment of acid–base balance
Published in Jonathan Dakin, Mark Mottershaw, Elena Kourteli, Making Sense of Lung Function Tests, 2017
Jonathan Dakin, Mark Mottershaw, Elena Kourteli
There is a limit to the scope for respiratory compensation. Even under conditions of severe metabolic acidosis (e.g. serum concentration <6 mmol/L), the Pco2 is constrained to remain above 1.5 kPa. To achieve such drastic reduction in Pco2, the minute volume of ventilation may be increased by up to 30 L/min. The duration that such compensation can be maintained is limited by respiratory muscle fatigue.
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.
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.
The role of exercise hemodynamics in assessing patients with chronic heart failure and left ventricular assist devices
Published in Expert Review of Medical Devices, 2019
Aaron Koshy, Thomas Green, Anet Toms, Sophie Cassidy, Stephan Schueler, Djordje Jakovljevic, Guy A MacGowan
Patients with CHF increase mean arterial pressure (MAP), HR, VO2, PAWP, right atrial pressure, and cardiac index with a drop in SVR from rest to peak during dynamic exercises [4,13], a similar relationship to healthy controls. Interestingly, our team [14] have found that supplementary oxygen (28% and 40%) is associated with a greater exercise time and slight decrease in mean HR without a corresponding change to BP, suggesting that hypoxia may also play a role in exercise intolerance in CHF. Patients failing to reach their anaerobic threshold and respiratory compensation point (onset of hyperventilation during exercise) in itself are the poor prognostic sign [15]. However, few direct comparisons between CHF patients and the healthy population have been made. Barrett-O’Keefe et al [16] compared CHF patients and controls when performing both a handgrip and knee extension exercise. Interestingly during both static exercises, both groups increased their MAP in a similar fashion during which CHF patients had a higher HR (94 ± 4 bpm vs 78 ± 2 bpm, p < 0.05 during knee raise) and controls had a higher blood flow to the arms and legs. In this study, heart failure patients increased SVR (with weaker vasodilation of both upper and lower limbs) during static exercise more so than their control counterparts with an associated reduced exercise capacity. In general, CHF patients increase MAP, SV, and CO less in response to exercise compared to matched controls [17].