Management of Severe Acidosis in Cardiac Arrest

Initial Management of Cardiac Arrest with Acidosis

The American Heart Association recommends administering 1-2 ampules of 50 mL of sodium bicarbonate (44.6-100 mEq) in a rapid initial IV bolus, followed by 50 mL (44.6-50 mEq) every 5-10 minutes as needed, guided by arterial gasometry and pH 1
Sodium bicarbonate is indicated in cardiac arrest when deep acidosis is present, especially if pH <7.15, as severe acidosis causes resistance to catecholamine receptors, reducing the effectiveness of vasopressors 1, 2
The initial dose is 1-2 ampules of 50 mL (44.6-100 mEq) in a rapid IV bolus, which can be repeated every 5-10 minutes during resuscitation 1
Basic life support with adequate oxygenation and ventilation should be continued throughout the administration of bicarbonate 1
The British Medical Journal suggests that the risks of acidosis outweigh the risks of hypernatremia during cardiac arrest, justifying the aggressive use of hypertonic bicarbonate solutions 1
The cateter should be flushed with normal saline solution before infusing other medications after bicarbonate to avoid incompatibilities 1

The American College of Critical Care Medicine recommends administering a bolus of 20 mL/kg of lactated Ringer's solution over 15-30 minutes as the initial crystalloid 3, 4
Normal saline solution should be avoided as it will worsen metabolic acidosis through hyperchloremic mechanisms 3, 4
Repeat boluses up to a total of 60 mL/kg until perfusion improves, unless pulmonary edema develops 3

If hypotension persists after 40-60 mL/kg of volume resuscitation, norepinephrine should be started as the first-line vasopressor 3, 2
Norepinephrine is more effective than dopamine and causes fewer tachyarrhythmias 3
In severe refractory acidosis (pH <7.1), consider vasopressin as an adjunct or alternative, as it works through non-adrenergic mechanisms that are not attenuated by acidosis 2
Consider dobutamine if myocardial dysfunction is present 3

Use mild hyperventilation to partially compensate for metabolic acidosis, but avoid excessive hyperventilation 4
Avoid excessive PEEP in severely hypovolemic patients, as it will further compromise venous return and cardiac output 4
If intubation is necessary, use ketamine with atropine instead of propofol or etomidate to maintain cardiovascular stability 4

Check potassium, magnesium, calcium, and phosphorus immediately 3, 4
Monitor hyperkalemia as acidosis is corrected with resuscitation, as potassium will return to the intracellular space 3, 4
Replace magnesium if <0.75 mmol/L, as hypomagnesemia impairs other electrolyte corrections 3, 4

Acidosis, hypothermia, and coagulopathy form the "lethal triad" that should be rapidly interrupted 5
Severe acidosis decreases the activity of the coagulation cascade and increases fibrinolysis 5
There is a synergistic effect on compromising coagulation when acidosis is present with hypothermia 5

Correct coagulopathy with fresh frozen plasma if PT/PTT is elevated, but avoid rapid infusion due to hypotensive effects 4
Consider tranexamic acid 10-15 mg/kg followed by an infusion of 1-5 mg/kg/hour if bleeding is related to trauma 4
Aggressively prevent hypothermia, as it worsens coagulopathy and acidosis 5, 4
Use forced-air warming devices and warm all IV fluids and blood products 4