Beyond 5Hs and 5Ts: a rare cause of cardiac arrest

Dear Sir,

A 59-year-old man who sustained a cardiac arrest with return of spontaneous circulation (ROSC) after two minutes of chest compressions was admitted to the accident and emergency department (A&E). The cardiac arrest occurred at a radiological facility while he was undergoing neck radiography due to a week's history of neck pain. The patient had no past medical history of trauma or drug overdose.

On arrival at the A&E, the patient was afebrile and had normal vital signs (heart rate [HR] 74 beats per minute, blood pressure [BP] 116/66, oxygen satuation [SpO₂] 97% on room air with spontaneous respirations). Cardiovascular examination was normal and per rectal examination did not reveal any bleeding or malaena. 12-lead electrocardiogram (ECG) did not show any obvious cardiac cause [Figure 1], and the blood gas test showed an absence of acidosis. A bedside ultrasonographic examination revealed normal cardiac contractility with no pericardial effusion, normal right ventricular size, absence of free intra-abdominal fluid, a normal-sized inferior vena cava, normal abdominal aortic size and normal lung sliding.

Figure 1.

ECG performed at 1520 hr shows sinus tachycardia of 108 bpm with no obvious cardiac cause for the collapse.

As the patient was unconscious (Glasgow Coma Score 3), intubation was done via rapid sequence intubation with intravenous ketamine and rocuronium. Shortly after intubation, he developed a hypotensive episode (BP 80/47, HR 117 beats per minute), which required peripheral adrenaline support. A central venous catheter was placed in the right internal jugular vein and a norepinephrine infusion was started, after which the patient stabilised.

The patient underwent computed tomography (CT) of the brain, which was negative for intracranial pathology. Post CT, he developed bradycardic pulseless electrical activity (PEA) and had ROSC after five minutes of resuscitation. He subsequently stabilised on adrenaline infusion, with ECG showing sinus arrhythmia [Figure 2]. The returned blood work revealed no abnormalities except for a phosphate level of 1.95 mmol/L and mild transaminitis (alanine transaminase 56 U/L and aspartate transaminase 109 U/L). Serum potassium was 5.3 mmol/L. No obvious reversible cause for PEA could be identified at that time.

Figure 2.

ECG performed at 1638 hr shows sinus arrhythmia of 78 bpm with no obvious cardiac cause for the collapse.

When the patient first presented to the A&E, his history of neck pain was considered nonspecific, as the pain had been present for a week with no history of trauma, red flag symptoms affecting gait or indication of any neurological deficits. The attending doctors did not consider a neck pathology as the cause of the cardiac arrest and felt that it could be worked up after the patient was stabilised; hence, CT of the cervical spine was not performed in the A&E and the patient was transferred to the medical intensive care unit (MICU). In the MICU, CT cervical spine and magnetic resonance imaging of the brain and cervical spine were performed, which revealed a large enhancing soft-tissue mass centred in the C2 vertebral body, causing a pathological fracture of the C2 vertebral body [Figures 3 and 4]. This was complicated by an acute infarction of the cervical cord and medulla oblongata with haemorrhagic conversion. The mass was also suspected to have encased the vertebral arteries and spread along the cord and medulla. The patient was reviewed by the inpatient spine team and deemed to have a poor prognosis for surgical intervention. A family conference was held and a decision was made for withdrawal of care and terminal extubation. The patient passed away on Day 4 of admission.

Figure 3.

Sagittal CT image of the cervical spine shows pathological fracture of the C2 vertebra (arrow).

Figure 4.

Sagittal non-enhanced T2-W MR image shows a large soft-tissue mass centred at the C2 vertebral level (arrow), with adjacent infarction of the cervical spinal cord (double-headed arrow shows the area of the cord with hyperintense signal).

The human heart rate is largely influenced by autonomic input. This is mainly controlled by the sympathetic and parasympathetic fibres from the medulla oblongata and the sympathetic fibres from the sympathetic chain that arises from the T1 to L2 spinal levels. Disruption of these fibres results in bradycardia and neurogenic shock. This is commonly seen in cases of traumatic spinal cord injury. However, a spinal cord tumour causing cord compression and cardiac arrest has not been reported.

The protocol and approach for cardiac arrest and PEA, based on the Advanced Cardiac Life Support algorithm, is well established. The '5Hs and 5Ts' is a mnemonic used to help in the recall of major contributing factors to pulseless arrest. They include hypovolaemia, hypoxia, hydrogen ion (acidosis), hyper-/hypokalaemia, hypothermia, toxins, tamponade (cardiac), tension pneumothorax, thrombosis (coronary) and thrombosis (pulmonary). These conditions were not found to be present in this patient, which makes this case a rare cause of cardiac arrest that is beyond the 5Hs and 5Ts.

Studies have shown that bradycardia is frequently seen in the acute period after cervical spinal cord injury.[1] The parasympathetic fibres, which control the heart, exit the central nervous system at the brain stem level, i.e., the vagal nerve (cranial nerve X). In contrast, the sympathetic control of the heart originates from the upper thoracic spinal cord segments (T1–T5). Trauma of the cervical region of the spinal cord will typically influence only the spinal sympathetic neutrons involved in heart regulation. Unopposed parasympathetic control is believed to cause episodes of marked bradycardia and asystole.

There has been a case report of a 36-year-old man with cervical schwannoma who experienced palpitations due to paroxysmal atrial fibrillation, with subsequent cessation of palpitations after exeresis of the tumour.[2] We also noted another case of a patient with a thoracic intramedullary space-occupying lesion having multiple preoperative ventricular premature beats, which reduced significantly after the tumour was completely resected, and the patient had remained free of arrhythmias in the postoperative period.[3]

Although cardiac arrhythmias following high spinal cord injury is well documented, the possibility of a cervical spinal cord lesion or mass affecting the autonomic regulation and causing arrhythmias and cardiac arrest is still underappreciated. There has been one reported case of acute tetraplegia, followed by cardiac arrest secondary to a high cervical cord compressive leptomeningeal metastatic mass, who had undergone prior resection of a supratentorial giant cell glioblastoma multiforme.[4]

In the present case, the patient presented after a period of cardiac arrest with a recent history of neck pain. Cervical or high spinal cord pathology should be considered as one of the causes after the usual 5Hs and 5Ts have been ruled out.

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