2022 SCAI SHOCK

Title:
Mechanical Circulatory Support in SCAI Stage B Cardiogenic Shock Complicating ST-Segment-Elevation Myocardial Infarction

Introduction:
The recent Society of Cardiovascular Angiography and Intervention (SCAI) classification classifies cardiogenic shock from stages A-E. In SCAI Stage C-E, there is clear hemodynamic compromise. However in SCAI stage B, there is ambiguity regarding optimal management especially in the setting of an ST-segment-elevation myocardial infarction (STEMI).

Clinical Case:
A 76-year-old male presented with severe substernal chest discomfort radiating across the precordium and left neck. He had a past medical history of hypertension, hyperlipidemia, tobacco abuse and prior coronary artery disease. Physical examination showed normal vital signs (heart rate 67 bpm, blood pressure 99/76 mmHg, respiratory rate 18, and SpO2 96%). Electrocardiogram demonstrated anterolateral STEMI with reciprocal inferior depressions. His initial laboratory parameters showed leukocytosis, elevated troponin and mildly elevated lactate (1.44 mmol/L).

Emergent coronary angiography demonstrated 100% proximal left anterior descending (LAD) artery occlusion with heavy thrombotic burden, and severe disease in the distal left main, ostial LAD and left circumflex vessels. Left ventriculogram demonstrated an ejection fraction of 30-35% with severe apical and anterolateral hypokinesis with an elevated left ventricular end-diastolic pressure of 41 mmHg. Despite normal vital signs, due to his tenuous ventricular function and concern for further deterioration, mechanical circulatory support was pursued. Percutaneous left ventricular assist device was placed and the distal left main and proximal LAD were treated using aspiration thrombectomy, high-pressure noncompliant balloon inflations and dedicated two stent bifurcation technique. Post intervention, he was transferred to the intensive care unit with Impella in situ to assist with post-procedure hemodynamic management.

In the intensive care unit, he developed persistent hypotension with increasing doses of norepinephrine and epinephrine support. He developed worsening multiorgan failure, severe lactic acidosis, acute kidney injury and acute liver failure. He was diagnosed with concomitant sepsis secondary to community-acquired pneumonia. Due to likely disseminated intravascular coagulopathy, he developed oozing from multiple intra-arterial intravenous sites including his percutaneous left ventricular assist device access site. Due to a mixed picture of cardiogenic, hypovolemic and septic shock, we performed a right heart catheterization that demonstrated mixed left ventricular failure and systemic vasodilatation.

Despite treatment with inotropes, vasopressors, judicious fluid boluses, invasive mechanical ventilation and continuous renal replacement therapy, he developed ventricular tachycardia and ventricular fibrillation arrest. This was presumed to be due to hyperkalemia secondary to his renal failure. Due to his poor prognosis and multiorgan failure, he was made comfort care by his family and he passed subsequently peacefully.

Discussion:
SCAI stage B cardiogenic shock constitutes a tenuous clinical entity that can rapidly escalate to stages C through E. Careful evaluation of hemodynamics, prompt optimization of hemodynamic insult, prevention of hemo-metabolic cascade of multiorgan failure and rapid reversal of inciting etiology (such as primary PCI for acute myocardial infarction) are important tenets in the management of such patients. Oftentimes, cardiogenic shock may be superimposed with septic and rarely hypovolemic shock which compounds the clinical assessment making therapeutic interventions challenging.