Summary of “Association between mean hemodynamic variables during the first 24 h and outcomes in cardiogenic shock: identification of clinically relevant thresholds”
Abstract: This study investigated the association between mean hemodynamic variables within the first 24 hours and outcomes in patients with cardiogenic shock (CS). Using data from two prospective cohorts (OptimaCC and MicroShock), researchers aimed to identify clinically relevant thresholds in both macrocirculatory and tissue perfusion parameters that predict 30-day mortality. Among 118 patients, a 37% mortality rate was observed. Poor outcomes correlated with lower mean systolic and mean arterial pressure, cardiac output/index, and cardiac power index. Likewise, tissue perfusion indicators like elevated ΔPCO₂ and ΔPCO₂/C(a-v)O₂ were linked to higher mortality. Optimal thresholds were identified (e.g., MAP < 70 mmHg, CO < 3.5 L/min, ΔPCO₂ ≥ 9 mmHg), suggesting targets for early intervention in CS.
Key Points:
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Study Design and Population: This was a post hoc analysis of 118 CS patients pooled from two prospective studies (OptimaCC and MicroShock), focusing on the first 24 hours of ICU admission and involving longitudinal measurements of hemodynamic variables.
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Primary Outcome: 30-day mortality occurred in 37% of patients, with poorer outcomes significantly associated with impaired macrocirculatory and tissue perfusion variables measured over the first 24 hours.
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Macrocirculatory Thresholds Identified: Critical thresholds included MAP < 70 mmHg, SAP < 95 mmHg, CO < 3.5 L/min, CI ≤ 1.8 L/min/m², and CPI < 0.27 W/m², each correlating with significantly higher 30-day mortality.
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Tissue Perfusion Markers: ΔPCO₂ ≥ 9 mmHg and ΔPCO₂/C(a-v)O₂ ≥ 1.5 mmHg/mL were strong predictors of poor prognosis, emphasizing the role of tissue-level indicators in risk stratification.
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Loss of Hemodynamic Coherence: A notable dissociation was found between macro- and microcirculatory variables; correlations within each set were strong, but no significant relationship existed between them.
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MAP as a Target: A MAP below 70 mmHg was linked to increased mortality, supporting the need for consensus targets in managing CS, although current guidelines remain variable and under-validated.
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Cardiac Output and Index Relevance: While no established CI targets exist, this study showed a strong association between reduced CO/CI and mortality, particularly a CPI < 0.27 W/m².
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Importance of ΔPCO₂ and ΔPCO₂/C(a-v)O₂: These indicators of impaired microcirculatory flow offer additional prognostic insight and suggest the need to go beyond macro-hemodynamic metrics in managing CS.
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Clinical Implications: The findings support integrating both macrocirculatory and tissue perfusion variables in early hemodynamic monitoring, proposing specific thresholds that may help tailor resuscitative efforts.
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Limitations and Strengths: Despite a relatively small sample and cohort differences, this study provides a novel and dynamic assessment of CS patients’ physiology over the first 24 hours, encouraging a multimodal approach to monitoring.
Conclusion: This study identifies critical early hemodynamic thresholds associated with adverse outcomes in CS. By integrating macrocirculatory and tissue perfusion metrics, clinicians may better tailor interventions and resuscitation strategies to improve survival.
Watch the following video on “Session 1: Hemodynamics of Cardiogenic Shock” by Houston Shock Symposium
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