A Case Report of Elderly Woman with Supraventricular Tachycardia associated with Intracranial Bleeding

Background The neurogenic cardiac injury is related to brain injury-induced catecholamine and neuro-inflammatory responses and is more likely in those with the most severe neurological insult. Case Report A 78 years-old female presented to the emergency department after being found lying on the floor with a laceration on the head. On physical examination GCS 3, BP 140/90 mmHg, HR 190 bpm, respiratory rate 25x/minute. PMH of hypertension and diabetes were denied. ECG showed supraventricular tachycardia of 186 bpm. Laboratory exams showed hyponatremia, hypokalemia, and leukocytosis. CT scan revealed subarachnoid hemorrhage, intracerebral hematomas, chronic subdural hematoma, midline shift and subfalcine herniation. The systemic catecholamine ‘storm’ driven by the central neuroendocrine axis massively increases sympathetic outflow, activates the adrenal gland and may lead to arrhythmia. Increased ICP, Midline shift, and subsequent physical compression of the brainstem and hypothalamic autonomic centers can trigger catecholamine responses that could instigate an arrhythmia. Suboptimal cardiac output and cerebral perfusion worsen secondary brain injury leading to a worse prognosis. Since cardioversion failed, amiodarone was administered. Cardioversions failed to convert to sinus rhythm and amiodarone was administered. Therapy to reduce intracranial pressure was also administered. The patient passed away 4 hours after admission. Conclusion Arrhythmia related to brain injury may lead to suboptimal cerebral perfusion and leads to further autonomic derangements leading to a vicious cycle of cerebral and cardiovascular injuries. This condition should be accounted for swiftly to prevent secondary brain injuries and myocardial ischemia.


Introduction
Cardiovascular complications are common after brain injury with a consequent increase in morbidity and mortality, although most patients who die do so because of their brain injury. 1,2Abnormalities includes hypertension, hypotension, electrocardiography (ECG) changes, cardiac arrhythmias, the release of biomarkers of cardiac injury, and left ventricular dysfunction.Neurogenic cardiac injury is related to brain intracranial pressure.However, despite these measures, her condition deteriorated and she passed away 1 hours after admission.
injury-induced catecholamine and neuroinflammatory responses and is more likely in those with the most severe neurological insult. 1

Case Report
A 78 years-old female presented to the emergency department after being found lying on the floor with a laceration on the head.Her medical and family history was unremarkable.On admission, physical examination revealed Glasgow comatose scale E1V1M1 3, BP 140/90 mmHg, HR 190 bpm, respiratory rate 27x/minute.The cardiorespiratory examination was within normal limits.ECG showed supraventricular tachycardia (SVT) of 186 bpm.Laboratory exams showed hyponatremia 129 mmol/L, hypokalemia 2.9 mmol/L, and leukocytosis 22.700 x 10^3 u/L.Chest X-Ray revealed elongated aorta.Computed Tomography scan of the head revealed subarachnoid hemorrhage, intracerebral hematomas, chronic subdural hematoma, midline shift and subfalcine herniation.Synchronized cardioversions of 50 and 100 joules failed to convert the patient to sinus rhythm and amiodarone was administered.Therapy to reduce intracranial pressure was also administered.Correction of hyponatremia and hypokalemia was also done.Mannitol was administered to reduce   driven by the central neuroendocrine axis massively increases sympathetic outflow, activates the adrenal gland and may lead to arrhythmia. 1 Damage to the insular and hypothalamus resulted in complex cascade of events, including activation followed by dysfunction of the autonomic nervous systems and an intense inflammatory response, which have major adverse effects on the heart. 1 It may also cause direct injury to myocardium. 3 Hemorrhages, increased intracranial pressure (ICP), midline shift, and subsequent physical compression of the brainstem and hypothalamic autonomic centers can trigger catecholamine responses that could instigate arrhythmia in this patient. 2his means that the arrhythmia in this patient is most probably caused by enhanced automaticity due to systemic catecholamine storm is driven by central neuroendocrine axis.Due to high circulating catecholamine for up to 10 days cardiac dysfunction may persist for a protracted period.Suboptimal cardiac output and cerebral perfusion may worsen secondary brain injury leading to a dismal prognosis. 4In patients with increased intracranial pressure (ICP), the higher mean arterial pressure is needed to maintain cerebral perfusion pressure (CPP).SVT may jeopardize this by limiting cardiac output especially if condition deteriorates further and affect blood pressure.The basis for cardioversion in this patient is to prevent secondary brain injury rather than blood pressure, signs of heart failure or loss of consciousness.Loss of consciousness in this patient was predominantly caused by intracranial hemorrhage.Even though the cerebral perfusion is not usually impaired in SVT without structural heart disease, the presence of high ICP is our consideration to optimize the cardiac output before further cardiac deterioration (due to any cause but especially secondary brain injury) compromise perfusion leading to more severe cardiac and cerebral injury.12-lead ECG should be repeated at 24 h intervals until any abnormalities have resolved.There is no specific treatment for brain injury induced cardiac arrhythmia, correction of electrolyte disturbances and management of the underlying intracranial pathology is the most effective way to prevent and treat the arrhythmia. 1 Hence correction of hyponatremia, hypokalemia and reducing intracranial pressure are integral to the treatment of this patient.This highlights the importance of mannitol administration to reduce intracranial pressure and the necessity of neurosurgical consult.To maintain optimal CPP in this patient ICP monitor is necessary for precise calculation. 5Since cardioversion failed, the antiarrhythmic drug amiodarone was administered in an attempt to convert SVT to sinus rhythm.This is understandable because the mechanism of arrhythmia in this patient was most likely due to enhanced automaticity due to catecholamine storm which is rather difficult to terminate using electrical cardioversion.Another option that may be effective in this patient is to use AV nodal blocking agent which may act rapidly and maintained for a longer period of time.The prognosis was bleak and the patient passed away despite maximum effort.

Conclusion
Arrhythmia related to brain injury may lead to suboptimal cerebral perfusion and leads to further autonomic derangements leading to a vicious cycle of cerebral and cardiovascular injuries.This condition should be accounted for swiftly to prevent secondary brain injuries and myocardial ischemia.

Figure 3 .
Figure 3. Patient's CT-Scan of the head