LAUSR

We describe a case of hypertension following high spinal anaesthesia in a parturient undergoing emergency lower segment caesarean section (LSCS). A 26-year-old primigravida without any comorbidities was brought for emergency LSCS in view of non-progression of labour. Her baseline vitals were as follows: heart rate (HR) 86/min; non-invasive blood pressure (NIBP) 116/72 mmHg; peripheral oxygen saturation (SpO2) 99% on room air. Subarachnoid block (SAB) was performed with 1.8 ml of hyperbaric bupivacaine (0.5%). Initial sensory level of blockade (checked with pin-prick) was T4. Immediately after administration of SAB, NIBP fell to 78/40 mmHg for which intravenous (IV) mephentermine 3 mg was administered and the rate of administration of IV fluids was increased. After a minute, NIBP increased to 106/56 mmHg. After 5 minutes of administration of the SAB, the patient complained of breathlessness, though the SpO2 was 98%, for which 100% oxygen was administered with a closed breathing circuit. It was observed that the patient was generating 40–60 ml of tidal volume (VT) and minute ventilation (MV) of 1.4 l/min−1 with respiratory rate (RR) of 35 min−1. There was almost no visible chest excursion, and she was using her accessory muscles of respiration. High spinal anaesthesia was suspected. A sensory level of blockade up to T1 was noted at that time along with good hand grip strength. Her vitals were: HR 106 min−1, NIBP 170/102 mmHg, RR 38 min−1, SpO2 98% with fraction of inspired oxygen concentration (FiO2) of 1.0 and end-tidal carbon dioxide (EtCO2) of 6–8 mmHg. Airway equipment and drugs were kept ready for intubation in case the need arose. However, assuming that diaphragmatic excursion may improve after delivery of the baby, intubation was not attempted immediately. Difficulty in breathing lasted for 3 minutes and by that time the baby was delivered. The patient started generating a VT of 160–200 ml which improved MV to 5.4 l/ min−1 with a RR of 30 min−1. The EtCO2 increased to 24–30 mmHg. Over the next 5 minutes, her VT improved to 400 ml and RR fell to 20 min−1. Here vitals were: HR 90 min−1, NIBP 130/72 mmHg and SpO2 99% with FiO2 of 0.4. The higher HR and BP despite the high level of spinal anaesthesia in this patient were probably due to hypercarbia leading to central sympathetic stimulation.