Management of Post-CABG Cardiogenic Shock with Severe Metabolic Acidosis and Hyperglycemia
Immediate implementation of VA-ECMO is recommended for this patient with cardiogenic shock, severe metabolic acidosis, and hyperglycemia post-CABG as the current multiple vasopressor support and IABP are insufficient to maintain hemodynamic stability. 1, 2
Current Clinical Status Assessment
- The patient is in severe cardiogenic shock post-CABG for anterior wall STEMI with LAD/LMCA dissection, requiring multiple high-dose vasopressors (norepinephrine, adrenaline, vasopressin) and IABP support 1
- Severe metabolic acidosis with lactate of 9 indicates significant tissue hypoperfusion and end-organ damage 1
- VF arrest during surgery with 2-4 minutes of resuscitation suggests myocardial injury beyond the initial infarct 1
- Hyperglycemia (460 mg/dL) requires immediate management as it worsens outcomes in critically ill cardiac patients 1, 3
- Ongoing blood loss with high-dose antiplatelet therapy and heparin necessitates continued blood product replacement 1
Immediate Management Priorities
1. Mechanical Circulatory Support
- Escalate to VA-ECMO immediately as the patient shows signs of refractory cardiogenic shock despite maximal medical therapy and IABP 1, 2
- IABP alone has not shown mortality benefit in cardiogenic shock and should be used as a bridge to more definitive mechanical support 1
- Early implementation of VA-ECMO (within 1 hour of failing to maintain adequate perfusion) is associated with better outcomes than delayed implementation 1, 2
2. Metabolic Acidosis Management
- Initiate CRRT immediately rather than waiting for further deterioration of acidosis 1, 4
- Target parameters for CRRT:
- Avoid bicarbonate administration as it has not shown benefit in lactic acidosis and may worsen intracellular acidosis 4, 7
3. Blood Product Management
- Continue transfusion of the ordered 2 units PRBC to maintain hemoglobin >8 g/dL 1
- Consider additional blood products based on coagulation studies (PT, INR, APTT) 1
- Target platelet count >50,000/μL to minimize bleeding risk in this post-surgical setting 1
4. Glycemic Control
- Implement continuous intravenous insulin therapy to maintain blood glucose between 140-180 mg/dL 1
- Avoid hypoglycemia which can trigger arrhythmias and worsen outcomes 1
- Monitor glucose hourly until stable, then every 2-4 hours 3, 8
Ongoing Monitoring and Management
Hemodynamic Monitoring
- Maintain continuous invasive arterial pressure monitoring 1
- Consider pulmonary artery catheterization to guide therapy if hemodynamics remain unstable despite VA-ECMO 1
- Target mean arterial pressure >65 mmHg to ensure adequate organ perfusion 1
End-Organ Function Assessment
- Monitor urine output hourly (currently reported as "good") 1
- Serial lactate measurements every 2-4 hours to assess tissue perfusion improvement 1
- Regular assessment of liver function, coagulation parameters, and neurological status 1
Medication Adjustments
- Continue amiodarone infusion to prevent recurrent ventricular arrhythmias 1
- Titrate vasopressors based on hemodynamic parameters after VA-ECMO initiation, with goal to reduce doses 1
- Consider low-dose dobutamine or milrinone for inotropic support as they have less impact on mesenteric blood flow 1
Potential Complications and Prevention
- Mesenteric ischemia: High risk due to vasopressor use and poor perfusion; monitor for worsening metabolic acidosis and abdominal distension 1
- Acute kidney injury: Continue CRRT to support renal function and manage fluid balance 4, 5
- Bleeding: Careful balance between anticoagulation needed for ECMO and bleeding risk; consider reduced heparin dosing 2
- Limb ischemia with VA-ECMO: Ensure distal perfusion cannula if femoral artery access is used 2
Prognostic Considerations
Poor prognostic factors in this patient include:
- Severe metabolic acidosis with high lactate level 1, 2
- VF arrest during surgery 1
- Need for multiple high-dose vasopressors 1, 2
- Hyperglycemia 1, 3
Early implementation of VA-ECMO and CRRT offers the best chance for survival by supporting circulation and correcting metabolic derangements until myocardial recovery occurs 1, 2.