Management of DKA in Cardiac Arrest
In DKA-related cardiac arrest, aggressive potassium repletion takes absolute priority before and during resuscitation, as hypokalemia is the most common lethal complication—delay insulin therapy if K+ <3.3 mEq/L and consider ECLS (extracorporeal life support) for prolonged arrest while correcting the underlying metabolic derangements. 1, 2, 3, 4
Critical Potassium Management During Arrest
The single most important intervention is preventing and treating hypokalemia-induced arrhythmias:
If K+ <3.3 mEq/L, DO NOT start insulin therapy—this is an absolute contraindication as insulin will drive potassium intracellularly and precipitate fatal arrhythmias including ventricular tachycardia and asystole 1, 5, 4
Aggressively replace potassium first until levels reach ≥3.3 mEq/L before initiating insulin to prevent life-threatening arrhythmias, cardiac arrest, and respiratory muscle weakness 1, 5
During active arrest or peri-arrest, rapid IV potassium boluses may be life-saving in refractory arrhythmias, though this requires extreme caution and continuous cardiac monitoring 4
Expect massive potassium requirements—patients may need >590 mEq over 36 hours, far exceeding typical replacement protocols 2
Target serum K+ of 4-5 mEq/L throughout resuscitation and DKA treatment 1, 5
Resuscitation Protocol
Immediate Actions During Arrest
Continue standard ACLS protocols while simultaneously correcting metabolic derangements 3
Initiate aggressive fluid resuscitation with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour to restore circulatory volume and tissue perfusion 1, 5
Consider ECLS (extracorporeal life support/ECVA) early if prolonged cardiac arrest is expected, as successful neurologically intact survival has been documented with this approach 3
Insulin Management in Arrest Setting
Hold insulin if K+ <3.3 mEq/L regardless of glucose or acidosis severity 1, 5
Once K+ ≥3.3 mEq/L, start continuous IV regular insulin at 0.1 units/kg/hour as this is the standard of care for critically ill DKA patients 5
Do NOT stop insulin when glucose falls—add 5% dextrose to IV fluids when glucose reaches 250 mg/dL to prevent hypoglycemia while continuing insulin to clear ketones 1, 5
Bicarbonate Controversy in Arrest
Bicarbonate is generally NOT recommended even in severe acidosis (pH >6.9-7.0):
Studies show no benefit in resolution time or outcomes, and bicarbonate may worsen ketosis, cause hypokalemia, and increase cerebral edema risk 1, 5
However, if pH remains <6.9 after initial fluid resuscitation, consider 100 mmol sodium bicarbonate in 400 mL sterile water at 200 mL/hour 1
The evidence is conflicting—some guidelines suggest bicarbonate may be beneficial at pH <6.9, but this carries Grade C evidence 1
Monitoring During and After Resuscitation
Check serum electrolytes, glucose, venous pH, and anion gap every 2-4 hours 1, 5
Monitor ECG continuously for arrhythmias related to electrolyte shifts, as DKA can cause pseudo-MI patterns and Brugada phenocopies that resolve with treatment 6
Check phosphate levels vigilantly—severe hypophosphatemia (<1.0 mg/dL) can cause respiratory failure and cardiac dysfunction requiring mechanical ventilation, especially in patients with cardiac dysfunction 1, 7
Add 20-30 mEq/L potassium (2/3 KCl and 1/3 KPO₄) to each liter of IV fluid once K+ is 3.3-5.5 mEq/L and adequate urine output is confirmed 1, 5
Common Pitfalls Leading to Arrest
Premature insulin administration with hypokalemia is the most common preventable cause of DKA-related cardiac arrest 2, 4
Bicarbonate therapy can worsen hypokalemia and precipitate arrhythmias—use with extreme caution 4
Cerebral edema treatments (mannitol, hypertonic saline) have kaliuretic effects that can worsen hypokalemia and require even more aggressive potassium repletion 2
Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA 5
Resolution Criteria
Continue aggressive treatment until DKA resolves:
When transitioning off IV insulin, administer basal insulin 2-4 hours BEFORE stopping the infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia 5