Cardiogenic shock (CS) is a state of decreased cardiac output resulting in end-organ hypoperfusion in the absence of intravascular hypovolemia with Acute Myocardial Infarction (AMI) and Decompensated Heart Failure (DHF) remaining the most common etiologies. Though the management of this complex condition has improved, in-hospital and early month mortality remain elevated up to 50%.1, 2, 3

Various risk stratification tools have been developed to predict outcomes and guide the management of such patients, including the APACHE-II, SAPS-II, APACHE-III, and GRACE with the newly Society for Cardiovascular Angiography and Interventions (SCAI) classification to be on the rise. It stratifies the patients in 5 stages, ranging from at-risk of CS (stage A) to the highest severity requiring intervention (stage E) by encompassing physical examination findings, biochemical markers, and most notably hemodynamic assessment.4

Even though hemodynamic status evaluation in patients with DHF used to be done exclusively via RHC by pulmonary artery catheterization (PAC) in the 70s, the rise of Doppler echocardiographic hemodynamic parameter measuring proved to be on par and more applicable due to being less invasive.5 Moreover, the debate concerning the non-selective usage of RHC was put on an end after the ESCAPE trial showed no benefit in routine use of PAC in chronic DHF without shock.6 Thus, nowadays, the American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) and European Society of Cardiology (ESC) guidelines for the management of heart failure recommend the usage of PAC in selected complex cases in which there is diagnostic or therapeutic ambiguity or in patients that do not improve with initial treatment. However, the same does not apply in patients with DHF and CS.

In addition, emerging data from prospective and retrospective studies have demonstrated a mortality benefit and in-hospital cardiac arrest in CS patients with PAC usage as compared to those without PAC. Moreover, in the management of DHF with CS, alongside with vasoactive medications, mechanical support devices (MCS) are utilized for hemodynamic support in CS and their use has significantly increased in recent times with inconsistent results.7 Early on, the IABP-SHOCK-II trial demonstrated that IABPs did not benefit mortality in CS secondary to AMI when coupled with revascularization.3 However, contemporary data from the Catheter-based Ventricular Assist Device Registry analysis indicated that early MCS implantation before starting vasoactive medications and PCI was independently associated with improved survival rates.8

Unlike the lack of concrete data on MCS devices, the most notable and evidence-based treatment in CS in the setting of AMI is early revascularization of the culprit vessel with PCI or CABG.9, 10, 11 The SHOCK trial illustrated that early revascularization improved the 6-12 months mortality rate despite not influencing the 30-day mortality.1 Overall, a deeper understanding of the heterogeneous nature of CS and the validation of a proper risk stratification tool, possibly with the SCAI stages, will strengthen evidence-based practices of CS. As such, the timing of intervention greatly depends on the current hemodynamic and metabolic state of a patient.12 Our current fund of knowledge lacks understanding about the specific medications or MCS utilized in CS in regards to their timing and escalation as it relates to a patient's clinical severity.13,14 With the use of the SCAI staging tool to stratify illness severity, we sought to advance our understanding of the therapies utilized in the management of CS, specifically examining the timing of initiation of vasoactive medications and MCS devices for the unique CS severity levels.