Acidosis in Shock: Pathophysiological Mechanisms and Clinical Implications

Primary Mechanisms and Types of Acidosis

Lactic acidosis is a primary contributor to metabolic acidosis in shock, resulting from inadequate oxygen delivery to tissues and producing lactate as a byproduct, with the American College of Critical Care Medicine suggesting that lactate levels are a key indicator of tissue hypoperfusion 1
Metabolic acidosis is characterized by decreased blood pH (<7.35), reduced serum bicarbonate (<22 mmol/L), elevated blood lactate levels, and increased base deficit, according to the European Society of Intensive Care Medicine 2
The Society of Critical Care Medicine recommends monitoring of lactate, base deficit, and pH to assess shock severity and response to treatment, with elevated lactate levels (>2 mmol/L) indicating tissue hypoxia and correlating with mortality 1
Base deficit is an independent predictor of mortality in traumatic hemorrhagic shock, reflecting global tissue acidosis due to impaired perfusion, as stated by the American College of Surgeons 1
Respiratory compensation may be impaired in severe shock, leading to respiratory acidosis that compounds the metabolic acidosis, with the British Thoracic Society noting the importance of monitoring respiratory function in shock patients 2
Septic shock exhibits a complex metabolic acidosis with contributions from lactic acidosis, hyperchloremic acidosis, and increased strong ion gap, according to the Surviving Sepsis Campaign 1

The American College of Emergency Physicians suggests that serial measurements of lactate, base deficit, and pH provide valuable information about shock severity and response to treatment, and that prevention of complications such as hypothermia, hypocalcemia, and worsening acidosis is crucial during resuscitation 1
The European Society of Anaesthesiology recommends avoiding hypothermia, hypocalcemia, and worsening acidosis during resuscitation, as these can exacerbate coagulopathy and shock 3

The World Journal of Emergency Surgery recommends initiating aggressive fluid resuscitation with crystalloids and blood products to enhance visceral perfusion and correct hypovolemia, as well as implementing early hemodynamic monitoring to guide effective resuscitation and avoid both under-resuscitation and fluid overload 4
Target physiologic levels of oxygen delivery while monitoring lactate as an indicator of improvement, as recommended by the World Journal of Emergency Surgery 4
Correct electrolyte abnormalities immediately, particularly hyperkalemia and hypocalcemia, which commonly accompany severe metabolic acidosis, as recommended by the World Journal of Emergency Surgery 4
Administer broad-spectrum antibiotics immediately if sepsis or bowel ischemia is suspected, as the risk of infection outweighs concerns about antibiotic resistance, according to the World Journal of Emergency Surgery 4

Non-invasive ventilation (NIV) is only indicated for hypercapnic respiratory failure (pH <7.35 with PCO2 ≥6.5 kPa or 49 mmHg) after optimal medical therapy, as stated by Thorax 5, 6
NIV would be harmful by interfering with compensatory hyperventilation in patients with hypocapnia (PCO2 16 mmHg), not hypercapnia, as noted by Thorax 5, 7, 8

Repeat arterial blood gases every 1-2 hours initially to assess response to therapy and guide further management, as recommended by the World Journal of Emergency Surgery 4
Do not overlook life-threatening causes such as septic shock, mesenteric ischemia, or toxic ingestions that require immediate specific interventions, as recommended by the World Journal of Emergency Surgery 4
Do not delay surgical intervention if peritonitis or bowel infarction is suspected, as prompt laparotomy is indicated, according to the World Journal of Emergency Surgery 4