Bezold Jarisch reflex and acute cardiovascular collapse during craniotomy.

Sir,

Bradycardia and hypotension during craniotomy can have deleterious consequences to the vulnerable brain. Usually, bradycardia is associated with hypertension (trigeminocardiac reflex [TCR] or Cushing's reflex) and tachycardia with hypotension (acute blood loss). In this report, we describe simultaneous occurrence of severe bradycardia and acute hypotension immediately after craniotomy.

A 35-year-old man presented with insidious onset headache of 1 month duration and weakness of left upper and lower limbs. Computed tomography and magnetic resonance imaging of the brain demonstrated a large right parasagittal meningioma with oedema, mass effect on the ventricles and subfalcine herniation [Figure 1a]. He was initiated on anti-oedema measures before his scheduled surgery. The pre-operative investigations including an electrocardiogram were normal. The baseline heart rate was 72/min and blood pressure 130/90 mmHg. Standard anaesthetic induction and maintenance were performed. The patient received mannitol 20 g at the beginning of burr-hole placement. Twenty minutes later, as the bone flap was removed, sudden bradycardia (lowest heart rate of 30/min) and hypotension (arterial blood pressure of 70/30 mmHg) was noted [Figure 1b]. The end-tidal carbon dioxide (ETCO2) decreased from 31 to 28 mmHg, but oxygen saturation remained at 100%. At this point, the patient had received 1200 ml of crystalloids, and the urine output was 500 ml with blood loss of 300 ml. The surgeon was notified immediately who stopped the surgery, but cardiovascular changes persisted. Atropine 0.6 mg was administered intravenously, and 500 ml of crystalloid was rapidly infused following which heart rate and blood pressure improved to 82/min and 151/97 mmHg, respectively. Thereafter, haemodynamics remained stable throughout the surgery, and recovery was uneventful.

Figure 1

(a) Computed tomography scan (axial sequences) demonstrating a large parasagittal lesion with oedema, mass effect and subfalcine herniation. (b) Numerical trend from the multi-parameter monitor showing acute event of bradycardia and hypotension

Simultaneous occurrence of bradycardia and hypotension is rare, compared to other cardiovascular changes during craniotomy. Our initial suspicion was venous air embolism (VAE), in view of head-end elevation and the proximity of lesion to superior sagittal sinus which can inadvertently open during craniotomy (especially in infiltrating meningioma). However, an intact duramater and venous sinus, and minimal change in ETCO2 ruled out its occurrence. Therefore, we considered Bezold-Jarisch reflex (BZR) as a possible cause for this acute event. BZR occurs from peripheral venous pooling causing hypercontractility of the myocardium. This leads to reflex arterial vasodilatation and cardiac parasympathetic activation resulting in hypotension and bradycardia.[1] In our patient, mannitol-induced diuresis possibly caused intravascular volume reduction, and the upright position (45°) produced peripheral venous pooling, both reducing the venous return to the heart. In addition, the sudden fall in the elevated intracranial pressure (ICP) following bone flap removal decreased the systemic vascular resistance aggravating the reduction in intracardiac volume, a phenomenon well-documented in literature.[2] Thus, decreased cardiac filling stimulated pressure receptors in the under-filled ventricular wall and triggered activation of the afferent c-fibres (BZR). The atrioventricular block responded to atropine, restoring heart rate and blood pressure.

The other possibilities mimicking similar clinical presentation are TCR, anaphylaxis, VAE and sudden decrease in ICP after craniotomy. The TCR presents mostly with bradycardia and hypertension and occurs due to stimulation of the 5th cranial nerve. This was ruled out as there was no hypertension and no stimulation of 5th nerve preceding the haemodynamic change in our patient. Anaphylaxis to the drug(s) administered requires temporal relationship to its occurrence. Again, no pharmacological agent or blood was administered before this episode. We did consider and excluded VAE as a cause for this acute haemodynamic presentation for reasons explained above. Finally, sudden decrease in ICP as a cause for abrupt decrease in blood pressure is likely when raised ICP is present as in our patient. However, this is accompanied by an increase in heart rate, unlike bradycardia which was observed in our patient.

To the best of our knowledge, there is only one recent report describing BZR-induced cardiovascular changes during neurosurgery.[3] Others have mainly observed it after spinal anaesthesia, shoulder surgery in sitting position under interscalene block and after post-operative head-end elevation.[145] The focus should be on preventing its occurrence by optimising intravascular volume during anaesthesia, especially during periods of head end elevation, mannitol administration and during craniotomy for raised ICP. Simultaneous occurrence of bradycardia and hypotension should alert clinicians to the possibility of BZR. Once BZR occurs, aggressive fluid resuscitation and administration of vagolytic such as atropine and if unresponsive, use of vasopressors should be considered.

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