Permissions and Reprints(opens in new window)

Cardiac complications occur in 40 to 50% of patients with traumatic brain injury (TBI) and are associated with increased morbidity and mortality.[1] [2] Although often reversible, the severity and duration of cardiac dysfunction can significantly influence clinical outcomes. Cardiac manifestations range from benign abnormalities to life-threatening arrhythmias including severe bradycardia, supraventricular tachycardia, QT interval prolongation, regional wall motion abnormalities, elevated cardiac biomarkers, myocardial stunning, and stress-induced cardiomyopathy (Takotsubo syndrome). Complete heart block (CHB), however, is rarely reported, and its true incidence remains poorly defined.[3] [4]

We report a case of severe TBI associated with CHB. A 51-year-old male presented to the emergency department within an hour of a road traffic accident, with loss of consciousness and epistaxis. On primary survey, Glasgow Coma Scale was E1V1M5. The airway was secured and mechanical ventilation was initiated. Postresuscitation vitals were stable, with baseline electrocardiography (ECG) showing normal sinus rhythm with heart rate of 80 beats per minute (bpm) ([Fig. 1B]) and mean arterial pressure (MAP) was 80 mm Hg.

Fig. 1 Axial computed tomography (CT) brain demonstrating a small left temporal hemorrhagic contusion (A). Baseline electrocardiography (ECG) showing normal sinus rhythm (B). ECG showing new-onset tri-fascicular block (C). ECG showing complete heart block (D).

Noncontrast computer tomography (NCCT) of the head revealed a small hemorrhagic contusion (1 × 1 × 1.5 cm) in the left temporal lobe associated with multiple facial and skull base fractures ([Fig. 1A]). There was no significant mass effect or midline shift, and the patient was admitted to the neurointensive care unit (NICU) for conservative management. A thorough history from the patient's family was unremarkable, with no cardiac or systemic comorbidities.

NICU monitoring included continuous five-lead ECG, oxygen saturation, noninvasive blood pressure, and temperature. Central venous and arterial lines were placed for advanced hemodynamic monitoring. On postinjury day 1, the patient developed hemodynamic instability (MAP < 50 mm Hg) requiring intravenous infusion of noradrenaline. ECG showed a trifascicular block ([Fig. 1C]). Serum electrolytes and arterial blood gases were within normal limits; troponin I card test showed positive. Within an hour, hemodynamic instability worsened, and the patient developed CHB with a heart rate of 30 to 35 bpm ([Fig. 1D]), unresponsive to atropine, adrenaline, or dopamine infusion. Temporary transcutaneous pacing was initiated, followed by placement of a temporary transvenous pacemaker (VVI mode, 100 bpm, 5 mA) by a cardiologist. Hemodynamics improved within an hour (MAP > 70 mm Hg) without inotropes.

After 24 hours, the CHB resolved spontaneously with an intrinsic heart rate of 120 to 130 bpm. The pacemaker threshold was gradually reduced, and the patient became pacemaker independent. The temporary pacemaker was removed on day 3, with no recurrence of atrioventricular (AV) blocks. The neurocritical care management included fentanyl infusion for analgesia and sedation, levetiracetam for seizure prophylaxis, paracetamol for analgesia and fever control, pantoprazole-ulcer prophylaxis, and hypertonic saline for intracranial pressure management as needed. Invasive intracranial pressure (ICP) monitoring was not performed, as the patient remained neurologically stable. Repeat NCCT brain did not demonstrate any radiological progression, new hemorrhage, or worsening cerebral edema compared with the initial scan. Therefore, clinical parameters, automated pupillometry, and optic nerve sheath diameter were used for indirect ICP assessment.

High-sensitivity troponin I was mildly elevated (37 pg/mL; reference < 26 pg/mL). However, the ECG showed no ischemic changes. Detailed two-dimensional echocardiography demonstrated a left ventricular ejection fraction of 60%, normal chamber sizes, no regional wall motion abnormalities, and no valvular or pericardial pathology. There was no evidence of blunt cardiac injury, coronary artery disease, pulmonary embolism, high cervical spinal cord injury, electrolyte imbalance, or AV-nodal blocking drug effects. The serial ECG revealed dynamic changes from normal sinus rhythm to trifascicular block and then to CHB and rapid recovery supporting a neurogenic mechanism secondary to TBI. CHB after isolated TBI is rarely reported. We could identify only a single case report describing transient high-grade AV block in a 63-year-old male with coronary artery disease following a skull fracture.[5] However, in our case there was no previous history of coronary disease.

Cardiac injury after TBI is mediated by brain–heart interactions. Acute brain injury triggers systemic inflammation and catecholamine surges, leading to the widespread release of neurotransmitters and proinflammatory cytokines. These mediators exert deleterious effects on both cerebral and peripheral organ function, creating a self-perpetuating cycle that exacerbates neuronal injury and precipitates cellular dysfunction.[4] Even small lesions can disrupt neural networks connected to autonomic centers. Temporal lobe injuries may indirectly influence the insular cortex, amygdala, and hypothalamus through limbic and cortical–subcortical pathways. Clinical studies have demonstrated that left-sided insular or temporal lesions are associated with increased parasympathetic activity, predisposing patients to bradyarrhythmia and AV conduction abnormalities.[6] Clinically, this phenomenon often manifests as electrocardiographic abnormalities, cardiac arrhythmias, elevated cardiac biomarkers, and left ventricular systolic dysfunction. As there was no prior history of cardiac disease and the patient demonstrated spontaneous recovery, the onset of CHB was most likely related to brain–heart interaction rather than any other systemic cause.

Even in isolated TBI without prior cardiac disease or chest trauma, clinicians should maintain vigilance for serious arrhythmias including CHB. Brain–heart interaction mediated conduction disturbances are typically transient. Supportive care and management of the primary brain injury remain mainstay. Acute hemodynamic instability can be ameliorated with temporary cardiac pacing, while permanent pacing is reserved for refractory cases. Early recognition, continuous ECG monitoring, and prompt intervention are essential.

Article published online:
10 April 2026

© 2026. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India