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Introduction: Hydrogen ion concentration which is expressed as pH value is in human blood maintained in narrow physiological range (7.36-7.44 in arterial blood). This range is crucial for normal functioning of most biochemical reactions. Extreme acidosis with pH < 6.8 is incompatible with life, unless pathophysiologic process is rapidly reversed. Timely, standardized, and structured approach to assessment and management of extreme critical illness is essential to maximize the chances of patient's survival. Cases: We present a series of 3 critically ill patients admitted to Medical intensive care unit (MICU) diagnosed with extreme metabolic acidosis (pH ⩽ 6.8). Each patient was treated using C hecklist for E arly R ecognition and T reatment of A cute I llness and I N jury (CERTAIN) which is a standard decision support tool in our MICU. Causes of extreme metabolic acidosis included hemorrhagic shock, sepsis, and acute renal failure and diabetic ketoacidosis. Rapid assessment, prompt resuscitation (IV fluids, vasopressors, mechanical ventilation, and renal replacement), and application of specific causal treatment led to positive outcomes in all 3 patients. Discussion: Medical physiology textbooks set the lower limit of pH value at which life is possible to 6.8. However, examples from clinical practice show that if adequate resuscitation measures are taken early in the acute phase of the disease, the biochemical cascade of reactions that are considered irreversible (at pH ⩽ 6.8) may be reversed after all. Conclusion: Critical care approach to extreme metabolic acidosis is a prime example of applied clinical physiology where basic science and clinical practice connect. With these case series we show that timely and structured approach to critical illness shifts the boundaries of reversibility for some of the most severe physiologic derangements. [ABSTRACT FROM AUTHOR]

Ideal concentrations of inhaled oxygen with regard to lung protection during early traumatic hemorrhagic shock (THS) remain unknown especially in the era of targeted temperature management (TTM). We speculated that a significant increase in oxygen supply in early stage of THS would magnify the protecting role of hypothermia in acute lung injury. Forty male New Zealand rabbits were randomly divided into four groups (n = 10): sham group, control group, group 1, and group 2. Except for sham group, all other animals were submitted to 30 min of uncontrolled THS and received limited fluid resuscitation for 60 min. During resuscitation, in addition to 34°C of TTM, animals in group 1 inhaled 21% oxygen while animals in group 2 inhaled 50% oxygen. Animals in control group inhaled room air and were kept normothermia. Oxidative stress, inflammation, and apoptosis parameters in the lung tissues were determined. THS induced higher expression of malondialdehyde, surfactant protein A, nuclear factor kappa B, and caspase 3 as well as lower expression of Bcl-2 mRNA and superoxide dismutase activity. Compared with inhalation of 21% oxygen, inhalation of 50% oxygen during TTM significantly improves oxidative stress, inflammation, apoptosis, and acute lung injury. Oxygen supplement during TTM therapy alleviated acute lung injury in the early stage of THS. Further studies are required to explore the ideal combination forms of TTM and oxygen supplement with the purpose of maximizing therapeutic effect while minimizing adverse effects. [ABSTRACT FROM AUTHOR]