1. First clarify whether this is truly DKA

• Diabetes or glucose ≥200 mg/dL
• Beta-hydroxybutyrate ≥3.0 mmol/L
• pH <7.30 and/or bicarbonate <18 mmol/L

• VBG or ABG: pH, bicarbonate, PaCO2
• Electrolytes, urea/creatinine, glucose, magnesium, phosphate
• Calculated anion gap and corrected sodium
• Serum beta-hydroxybutyrate trend
• Urine output and hourly fluid balance
• Bedside echo and lung ultrasound
• ECG and serial troponin as per ACS pathway
• Review for SGLT2 inhibitor use, prolonged fasting, vomiting, infection, missed insulin, or alcohol use

2. Fluid approach: do not use a standard DKA protocol

Practical fluid strategy

1. No maintenance crystalloid by default
   • Concentrate all infusions.
   • Account for heparin, vasopressor, insulin, antibiotic, and carrier volumes.
   • Restrict unnecessary IV intake and oral free water.
2. Only give a very small fluid challenge if there is objective evidence of fluid responsiveness or clear intravascular depletion
   • Examples: recent large GI loss, very low filling pressures on invasive monitoring, small/collapsible IVC interpreted in context, passive-leg-raise response with improved stroke volume.
   • If truly needed, use 250 mL balanced crystalloid or saline, then reassess immediately by blood pressure, urine output, lung ultrasound B-lines, oxygenation, echo stroke volume, and filling pressures.
   • Do not give repeated blind boluses.
3. Use invasive hemodynamic assessment early
   • Arterial line, central access if not already present.
   • Consider pulmonary-artery catheter or another validated advanced hemodynamic method in this mixed shock/metabolic situation, especially if deciding between diuresis, inotrope, vasopressor escalation, or mechanical circulatory support.
   • Determine whether the patient is “wet and cold,” and whether there is RV infarction or predominant RV failure. RV infarction is one important exception where cautious preload may be needed, but it must be echo/hemodynamically guided.
4. Continue active decongestion if congestion is present
   • IV loop diuretic infusion can be appropriate, with hourly urine output, creatinine, potassium, magnesium, and net balance monitored closely.
   • If diuretic-resistant with persistent severe pulmonary edema, worsening oxygenation, or renal failure, discuss ultrafiltration/CRRT with nephrology and cardiology. It can permit controlled net fluid removal while allowing insulin, dextrose, and electrolyte therapy.

3. Ketosis/DKA treatment without volume loading

Insulin

• Ensure K ≥3.5 mmol/L before initiating insulin.
• If true DKA, usual fixed-rate IV insulin is 0.1 units/kg/hour.
• If glucose falls below 200-250 mg/dL but ketonemia/anion gap persists, continue insulin to clear ketones and give concentrated dextrose rather than stopping insulin.
• In this fluid-restricted patient, use the minimum dextrose carrier volume feasible, for example D10 rather than D5 if local protocol and line access allow.
• Target glucose often around 150-200 mg/dL while clearing ketones, rather than rapidly normalizing glucose.

Potassium is the safety-critical issue

• Check potassium at baseline, then at least every 2-4 hours during IV insulin.
• K <3.5 mmol/L: replace potassium first and hold insulin.
• K 3.5-5.0 mmol/L: add potassium replacement as insulin is given, adjusted for renal function and urine output.
• K >5.0 mmol/L: do not give replacement initially, but recheck frequently because insulin can lower it quickly.

4. Cardiogenic pulmonary edema and shock

• Oxygen only for hypoxaemia. Use CPAP/BiPAP early if respiratory distress and the patient can protect the airway. Intubate if refractory hypoxaemia, exhaustion, altered sensorium, or inability to tolerate NIV. Avoid delayed intubation, and anticipate peri-intubation collapse in shock.
• Norepinephrine is an appropriate first vasopressor to maintain perfusion pressure, commonly targeting MAP ≥65 mmHg, individualized to chronic hypertension and organ perfusion.
• If MAP is adequate but there is persistent low output, cold extremities, oliguria, rising lactate, and low cardiac index, consider adding an inotrope such as dobutamine under echo/invasive hemodynamic guidance. Avoid making the patient more tachycardic or ischemic.
• Do not use nitrates while hypotensive/on vasopressor support. Consider vasodilators only after shock resolves and if blood pressure is robust with persistent hypertensive congestion.
• Evaluate urgently for mechanical complications of MI: acute MR, VSD, free-wall complication, and RV infarction.

5. Revascularization is central

• Clarify culprit vessel, coronary anatomy, TIMI flow, and whether urgent PCI has been performed or is pending.
• In cardiogenic shock with multivessel disease, the usual acute PCI strategy is culprit-lesion revascularization first, with non-culprit lesions considered later unless anatomy or ongoing ischemia dictates otherwise.
• Discuss early transfer to, or management in, a center with advanced shock support if escalating pressors/inotrope, persistent lactate rise, worsening renal function, refractory pulmonary edema, or persistent hypoperfusion.
• Mechanical circulatory support selection, such as IABP, Impella, or VA-ECMO, is case-specific and should be a shock-team decision. Routine IABP is not appropriate for all MI shock, but may have specific indications such as mechanical complications.

Bedside summary

• Serial acid-base, anion gap, glucose, ketone and potassium measurements
• IV insulin when indicated, with concentrated dextrose as required
• Minimal, reassessment-based 250 mL fluid challenges only if objectively fluid responsive
• Ongoing decongestion or controlled extracorporeal fluid removal if necessary
• Norepinephrine for perfusion pressure, add inotrope if low output persists after MAP support
• Urgent culprit-focused revascularization/shock-team assessment