Key result
Moderate simulated hemorrhage (-30 mmHg lower-body negative pressure) significantly elevated the baroreflex arm (MAP→RR) of heart rate and blood pressure causal interaction compared to rest (p=0.004), whereas traditional markers like pulse pressure showed no change.
Why the study?
Does monitoring baroreflex causality (MAP→RR) detect simulated moderate hemorrhage earlier than traditional markers in healthy participants?
Observational (n=27)
No
Does monitoring baroreflex causality (MAP→RR) detect simulated moderate hemorrhage earlier than traditional markers in healthy participants?
Absolute Event Rate: 0.83% vs 0.77%
p-value: p=0.004
Monitoring baroreflex causality (MAP→RR) may serve as an early indicator of central hypovolemia before traditional markers like pulse pressure change.
May flag moderate hypovolemia earlier than pulse pressure; leaves open clinical utility pending patient validation.
Early detection of hemorrhage remains an open problem. In this regard, blood pressure has been an ineffective measure of blood loss due to numerous compensatory mechanisms sustaining arterial blood pressure homeostasis. Here, we investigate the feasibility of causality detection in the heart rate and blood pressure interaction, a closed-loop control system, for early detection of hemorrhage. The hemorrhage was simulated via graded lower-body negative pressure (LBNP) from 0 to -40 mmHg. The research hypothesis was that a significant elevation of causal control in the direction of blood pressure to heart rate (i.e., baroreflex response) is an early indicator of central hypovolemia. Five minutes of continuous blood pressure and electrocardiogram (ECG) signals were acquired simultaneously from young, healthy participants (27±1 years, N=27) during each LBNP stage, from which heart rate (represented by RR interval), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were derived. The heart rate and blood pressure causal interaction (RR↔SBP and RR↔MAP) was studied during the last 3 minutes of each LBNP stage. At supine rest, the non-baroreflex arm (RR→SBP and RR→MAP) showed a significantly (p<0.001) higher causal drive towards blood pressure regulation compared to the baroreflex arm (SBP→RR and MAP→RR). In response to moderate category hemorrhage (-30 mmHg LBNP), no change was observed in the traditional marker of blood loss i.e. pulse pressure (p=0.10) along with the RR→SBP (p=0.76), RR→MAP (p=0.60), and SBP→RR (p=0.07) causality compared to the resting stage. Contrarily, a significant elevation in the MAP→RR (p=0.004) causality was observed. In accordance with our hypothesis, the outcomes of the research underscored the potential of compensatory baroreflex arm (MAP→RR) of the heart rate and blood pressure interaction towards differentiating a simulated moderate category hemorrhage from the resting stage. Therefore, monitoring baroreflex causality can have a clinical utility in making triage decisions to impede hemorrhage progression.
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Verma et al. (2017) conducted an observational in Healthy (Simulated Hemorrhage) (n=27). Lower-body negative pressure (LBNP) vs. Supine rest (baseline) was evaluated on Baroreflex causality (MAP→RR) at -30 mmHg LBNP (p=0.004). Moderate simulated hemorrhage (-30 mmHg lower-body negative pressure) significantly elevated the baroreflex arm (MAP→RR) of heart rate and blood pressure causal interaction compared to rest (p=0.004), whereas traditional markers like pulse pressure showed no change.
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