Immediate Treatment for Acidosis and Shock
Begin immediate fluid resuscitation with at least 30 mL/kg of IV crystalloid within the first 3 hours, prioritize source control of bleeding or infection, and target a mean arterial pressure of 65 mmHg with vasopressors if needed after adequate fluid administration. 1, 2
Initial Resuscitation Protocol
Fluid Administration
- Administer 20-40 mL/kg of 0.9% saline or crystalloid solution as the initial bolus to correct hypovolemia and restore tissue perfusion 1
- Continue fluid resuscitation guided by frequent reassessment of hemodynamic status including heart rate, blood pressure, capillary refill time (target <2 seconds), urine output (target >1 mL/kg/hour), and mental status 1, 2
- Use dynamic variables rather than static measures to predict fluid responsiveness when available 1
- Stop fluid administration once signs of circulatory failure have reversed to avoid fluid overload complications 1, 3
Hemodynamic Targets
- Target mean arterial pressure ≥65 mmHg as the primary goal 1, 2
- Monitor urine output with a target of >0.5-1 mL/kg/hour as a marker of adequate renal perfusion 1
- Normalize lactate levels if initially elevated (repeat measurement within 6 hours) 1, 2
Source Control
Identify and control the underlying cause of shock immediately - whether hemorrhage, infection, or other etiology - as this takes priority over all other interventions 1, 2
For Hemorrhagic Shock
- Implement immediate bleeding control procedures unless initial resuscitation is successful 1
- Consider damage control surgery if patient presents with deep hemorrhagic shock, ongoing bleeding, coagulopathy, hypothermia, or severe acidosis 1
- Achieve surgical hemostasis before attempting definitive anatomical reconstruction 1
For Septic Shock
- Administer broad-spectrum IV antimicrobials within one hour of recognition 2, 3
- Obtain blood cultures before antibiotics if this does not delay administration beyond 45 minutes 2
- Remove infected foreign bodies or devices and drain abscesses as soon as medically practical 2
Vasopressor Support
- Initiate norepinephrine as the first-line vasopressor if hypotension persists despite adequate fluid resuscitation (typically after 40 mL/kg) 1, 2, 3
- Add epinephrine or consider dopamine as second-line agents if additional support is needed 3
- Place central venous access for ongoing vasopressor administration and hemodynamic monitoring in patients requiring >40 mL/kg fluid or persistent shock 1
Management of Acidosis
Addressing the Underlying Cause
The primary treatment of metabolic acidosis is correction of the shock state itself through restoration of tissue perfusion - buffering agents are secondary 4, 5
- Maximize oxygen delivery by increasing cardiac output while maintaining adequate hemoglobin concentration 4
- Ensure adequate ventilation to prevent respiratory acidosis from compounding metabolic acidosis 1
Bicarbonate Therapy Considerations
- Sodium bicarbonate is indicated only for severe metabolic acidosis with pH <7.15 in the context of shock, cardiac arrest, or severe primary lactic acidosis 6
- Do not routinely administer bicarbonate for hypoperfusion-induced lactic acidosis unless pH <7.15, as it has not been shown to improve outcomes and may worsen intracellular acidosis 1, 4
- Bicarbonate therapy should be superimposed on measures to control the basic cause of acidosis, not used as primary treatment 6
Ventilation Management
Critical Ventilation Principles in Shock
- Avoid excessive positive pressure ventilation rates as this impairs venous return and can precipitate cardiovascular collapse in hypovolemic patients 1
- When initiating mechanical ventilation in patients with severe acidosis, maintain their compensatory hyperventilation pattern initially to prevent rapid CO2 rise before acidosis is corrected 1
- Target protective ventilation with low tidal volumes (6-8 mL/kg) and moderate PEEP to prevent ventilator-induced lung injury 1
Oxygenation Goals
- Apply supplemental oxygen to achieve saturation >90% 2, 3
- Consider elective intubation for patients with persistent shock despite 40 mL/kg fluid, impaired consciousness (GCS ≤8), or respiratory failure 1
Special Considerations
The Lethal Triad
Recognize that hypothermia, acidosis, and coagulopathy form a synergistic lethal triad that dramatically worsens outcomes 1
- Hypothermia (core temperature <35°C) and acidosis (pH <7.2) together severely impair coagulation beyond either factor alone 1
- Prevent hypothermia by warming all IV fluids, maintaining ambient temperature, and using active warming devices 1
- Consider damage control approaches when this triad is present rather than pursuing definitive procedures 1
Timing Considerations
- Delay enteral nutrition if shock is uncontrolled and hemodynamic goals are not reached; initiate low-dose feeding only once shock is controlled 1
- For septic shock with perforation, source control surgery should occur within 6 hours of admission as delays beyond this eliminate survival 1
- Resuscitation should proceed rapidly but with frequent reassessment to avoid both under-resuscitation and fluid overload 1, 2
Monitoring Adequacy of Resuscitation
- Assess capillary refill time, skin mottling, peripheral pulses, mental status, and extremity temperature as markers of tissue perfusion 2
- Serial lactate measurements provide objective evidence of improving tissue perfusion 1, 2
- Base deficit >15 mmol/L indicates severe acidosis and predicts need for aggressive resuscitation 1
Common Pitfalls
- Do not delay source control (surgical bleeding control or infection drainage) while pursuing perfect hemodynamic parameters - source control takes priority 1, 2
- Avoid using Ringer's lactate in patients with severe head trauma due to hypotonic effects 1
- Do not administer bicarbonate routinely for lactic acidosis - it does not improve outcomes and may worsen intracellular acidosis 1, 4
- Recognize that standard coagulation assays run at 37°C underestimate the severity of coagulopathy in hypothermic patients 1
- In comatose patients with shock, use a more cautious fluid approach and consider human albumin solution over saline 1