Association of Early Hemodynamic Profile and the Development of Systolic Dysfunction Following Traumatic Brain Injury

Abstract

Background While systolic dysfunction has been observed following traumatic brain injury (TBI), the relationship between early hemodynamics and the development of systolic dysfunction has not been investigated. Our study aimed to determine the early hemodynamic profile that is associated with the development of systolic dysfunction after TBI. Methods We conducted a prospective cohort study among patients under 65 years old without cardiac comorbidities who sustained moderate-severe TBI. Transthoracic echocardiography was performed within the first day after TBI to assess for systolic dysfunction. Hourly systolic blood pressure (SBP), mean arterial pressure (MAP), heart rate, and confounding clinical variables (sedatives, fluid balance, vasopressors, and osmotherapy) were collected during the first 24 hours following admission. Multivariable linear mixed models assessed the early hemodynamic profile in patients who developed systolic dysfunction, compared to patients who did not develop systolic dysfunction. Results 32 patients were included, and 7 (22%) developed systolic dysfunction after TBI. Patients who developed systolic dysfunction experienced early elevation of SBP, MAP, and heart rate, compared to patients who did not develop systolic dysfunction (p<0.01 for all comparisons). Patients who developed systolic dysfunction experienced a greater rate of decrease in SBP [−10.2 mmHg (95% CI: −16.1, −4.2)] and MAP [−9.1 mmHg (95% CI: −13.9, −4.3)] over the first day of hospitalization, compared to patients who did not develop systolic dysfunction (p<0.01 for both comparisons). All sensitivity analyses revealed no substantial changes from the primary model. Conclusions Patients who develop systolic dysfunction following TBI have a distinctive hemodynamic profile, with early hypertension and tachycardia, followed by a decrease in blood pressure over the first day after TBI. This profile suggests an early maladaptive catecholamine-excess state as a potential underlying mechanism of TBI-induced systolic dysfunction.

Characterizing the relationship between systemic inflammatory response syndrome and early cardiac dysfunction in traumatic brain injury

“…A notable stress response phenomenon among critical illness paradigms is catecholamine excess, which has been widely described as the underlying mechanism of cardiac dysfunction following neurological injury (Bybee & Prasad, ; Masuda et al, ; Samuels, ). Recently, our group reported the distinct hemodynamic pattern in patients with moderate‐severe TBI who developed early systolic dysfunction and was suggestive of sympathetic hyperstimulation as one of the underlying mechanisms of cardiac dysfunction following TBI (Krishnamoorthy et al, ). However, the elevated catecholamine levels can also directly affect inflammatory cytokine expression during the acute‐phase response to injury (Elrifai, Bailes, Shih, Dianzumba, & Brillman, ; Severn, Rapson, Hunter, & Liew, ; Woiciechowsky et al, ).…”

“…This was a secondary analysis of a prospective cohort study of cardiac function conducted at Harborview Medical Center (Seattle, WA), a Level 1 trauma center for the states of Washington, Alaska, Montana, and Idaho and affiliated with the University of Washington (Krishnamoorthy et al, ). The study was approved by the Institutional Review Board at the University of Washington.…”

“…Details of transthoracic echocardiogram (TTE) methodology have been described previously (Krishnamoorthy et al, ). After informed consent was obtained from the patient's legally authorized representatives, a bedside TTE was performed within the first 24 hr after admission or on Hospital Day 2 if hemodynamically unstable or undergoing medical procedures.…”

“…Recently, cardiac dysfunction has been detected after TBI (Cheah et al, ; Prathep et al, ; Qian et al, ), which can contribute to cerebral hypoperfusion and secondary injury after TBI. While sympathetic overstimulation may play a role in the pathogenesis of TBI‐induced systolic dysfunction (Krishnamoorthy et al, ; Mazzeo, Micalizzi, Mascia, Scicolone, & Siracusano, ; Mierzewska‐Schmidt & Gawecka, ; Nguyen & Zaroff, ), other contributing pathophysiologic mechanisms remain unclear.…”

The authors reply

“…subarachnoid hemorrhage), namely a massive release of catecholamines. To illustrate this, recent work by our group has demonstrated that patients with TBI-induced cardiac dysfunction have a distinctive early hemodynamic profile that is likely secondary to a maladaptive catecholamine-excess state (3). …”