Highlights
Early Deterioration is Common
Approximately 27% of patients presenting with Society for Cardiovascular Angiography and Interventions (SCAI) Stage B cardiogenic shock experience clinical deterioration, including the need for higher-level care, stage escalation, or in-hospital mortality.
Potent Predictors of Decline
Acute kidney injury (AKI) and diuretic resistance are powerful independent predictors of clinical worsening. Specifically, diuretic resistance is associated with a nearly ten-fold increase in the odds of deterioration.
Phenotypic Differences Matter
Patients presenting with isolated hypotension in Stage B have significantly worse outcomes compared to those presenting with isolated hypoperfusion (elevated lactate), challenging the traditional prioritization of metabolic markers over physical vital signs.
The Evolution of Cardiogenic Shock Classification
Cardiogenic shock (CS) has historically been viewed as a binary state—either a patient is in shock or they are not. However, the introduction of the Society for Cardiovascular Angiography and Interventions (SCAI) staging system in 2019 (and its 2022 refinement) transformed this perspective into a continuum. Stage B, often referred to as “Beginning” or “Pre-shock,” represents a critical clinical window. These patients exhibit clinical signs of hemodynamic instability—such as hypotension or tachycardia—without yet manifesting the frank end-organ hypoperfusion seen in Stage C.
Despite the utility of this staging, data regarding the natural history and management of Stage B patients have remained sparse. Most clinical trials focus on Stage C or higher, where mechanical circulatory support (MCS) is often required. The recent study by Mehta et al. (2026) published in Circulation: Heart Failure provides much-needed clarity on the etiology and predictors of deterioration for this vulnerable “at-risk” population.
Study Design and Methodology
From 2017 to 2022, researchers conducted a retrospective evaluation across a six-hospital system, involving 500 adult patients. To ensure a pure cohort of Stage B shock, the study excluded patients who had already suffered cardiac arrest, those requiring immediate circulatory support, and those with non-cardiac etiologies for their instability.
SCAI Stage B was strictly defined as either hypotension (systolic blood pressure ≤90 mmHg or mean arterial pressure ≤65 mmHg) or mild hypoperfusion (lactate levels between 2 and 5 mEq/L). The primary composite endpoint was clinical deterioration, defined as a transfer to a higher level of care, escalation to a higher SCAI stage, or in-hospital death. This design allowed the investigators to pinpoint exactly which clinical features preceded the transition from “pre-shock” to overt shock.
Results: The Profile of SCAI Stage B
Among the 500 patients studied, the median age was 76 years, and the population was 56% male. The etiologies of Stage B shock were diverse, reflecting the complexity of modern cardiovascular care:
Heart Failure as the Primary Driver
Chronic heart failure exacerbation was the most common cause, accounting for 37% of cases. This was followed by arrhythmias (23%) and acute myocardial infarction (13%). This distribution suggests that Stage B shock is frequently an extension of chronic cardiac dysfunction rather than just acute ischemic events.
Hypoperfusion vs. Hypotension
Interestingly, the majority of the cohort (82%) presented with isolated hypoperfusion (lactate 2-5 mEq/L), while only 18% presented with isolated hypotension. This suggests that in clinical practice, Stage B is often identified by biochemical markers before a significant drop in blood pressure occurs.
The Downward Spiral: Predictors of Deterioration
One of the most significant findings of the study was that 27% of the cohort (135 patients) met the primary endpoint for clinical deterioration. When comparing this “deterioration cohort” to those who recovered, several key differences emerged in the 24 hours preceding their decline.
The Central Role of the Kidney
Acute kidney injury (AKI) was a dominant feature in those who worsened. In the deterioration cohort, 60% of patients experienced renal injury compared to only 33% in the recovery cohort. Multivariable analysis confirmed that AKI was independently associated with a 2.17-fold increase in the odds of clinical decline. This highlights the heart-kidney crosstalk, where early renal dysfunction serves as a sensitive barometer for failing cardiac output that may not yet be apparent in other vital signs.
Diuretic Resistance: The Strongest Warning Sign
Perhaps the most striking finding was the impact of diuretic resistance. Patients who failed to respond to diuretic therapy in the early stages of Stage B shock had an adjusted odds ratio of 9.55 for clinical deterioration. This suggests that the inability to achieve a negative fluid balance is not merely a symptom of shock but a primary driver of its progression. Patients who recovered had a significantly more negative fluid balance (-0.68 L) compared to those who deteriorated (-0.30 L).
Clinical Implications and Expert Commentary
These findings have profound implications for the management of patients in the intermediate care unit or the emergency department. The study suggests that clinicians must look beyond simple blood pressure readings and lactate levels to assess the risk of shock progression.
The Window of Opportunity
Stage B represents a “golden window” where aggressive management of volume status and early optimization of hemodynamics can prevent the need for invasive mechanical support. The high predictive value of diuretic resistance suggests that clinicians should have a low threshold for escalating diuretic doses or adding secondary agents (such as thiazides or SGLT2 inhibitors) at the first sign of poor urine output in a Stage B patient.
Reevaluating Hypotension
While lactate is a useful marker, the study found that isolated hypotension was actually associated with worse outcomes than isolated hypoperfusion. This serves as a reminder that a low blood pressure reading in a cardiac patient is never “benign” and warrants immediate attention, even if the patient appears clinically stable and has a normal lactate level.
Expert Perspectives on Pathophysiology
Mechanistically, the link between AKI, diuretic resistance, and shock progression is likely rooted in venous congestion. In many Stage B patients, the primary issue is not just a lack of forward flow, but an increase in backward pressure. This venous congestion leads to renal encapsulated pressure increases, reducing the glomerular filtration rate and causing resistance to loop diuretics. When these patients fail to achieve decongestion, the resulting fluid overload further stresses the right ventricle, leading to a vicious cycle of falling cardiac output and worsening shock.
Conclusion
The study by Mehta et al. provides a roadmap for managing the “beginning” of cardiogenic shock. By identifying AKI and diuretic resistance as early markers of failure, clinicians can more accurately triage Stage B patients who require intensive monitoring or early intervention. As we move toward a more personalized approach to shock management, these findings emphasize that the kidneys often tell the story of the heart’s future.
References
1. Mehta C, Has P, Mehta A, et al. Etiology, Management, and Outcomes of Society for Cardiovascular Angiography and Interventions Stage B Cardiogenic Shock. Circ Heart Fail. 2026;19:e013814. doi:10.1161/CIRCHEARTFAILURE.125.013814.
2. Schrage B, et al. The SCAI SHOCK Stage Classification: A Review of Current Evidence and Future Directions. J Am Coll Cardiol. 2023.
3. Vallabhajosyula S, et al. Standardized Staging for Cardiogenic Shock: The SCAI Classification. Current Cardiology Reports. 2022.
