Myocardial stunning after resuscitation from cardiac arrest following spinal anaesthesia.

Cardiac arrest associated with spinal anaesthesia has been well researched. Myocardial stunning after successful resuscitation from cardiac arrest is seen in up to 2/3(rd) of in-hospital cardiac arrests. Myocardial stunning after resuscitation from cardiac arrest associated with spinal anaesthesia has probably not been reported earlier. Our case, an ASA physical status I lady, posted for tubal reanastomosis surgery developed bradycardia followed by asystole, approximately 5 minutes after giving subarachnoid block. Return of spontaneous circulation (ROSC) was achieved within 2 minutes with cardiopulmonary resuscitation (CPR) and defibrillation for pulseless ventricular tachycardia. Patient developed delayed pulmonary oedema, which was probably due to myocardial stunning. In the present case, inadequate preloading could have precipitated bradycardia progressing to cardiac arrest which, after resuscitation led to reversible myocardial dysfunction. We conclude that early vasopressor infusion, titrated fluids and echocardiography should be considered in immediate post cardiac arrest phase following spinal anaesthesia.

INTRODUCTION

Cardiac arrest following spinal anaesthesia is well researched and argued. Different studies vary in results regarding incidence of cardiac arrest during spinal anaesthesia.[12345] Many have elaborated causes, mechanisms and ways to prevent cardiac arrest during spinal anaesthesia.[345] High mortality and neurological deficit in survivors of cardiac arrest associated with spinal anaesthesia have been reported.[46] Cardiac arrest-related myocardial stunning is a component of post cardiac arrest syndrome which manifests as reversible myocardial dysfunction due to global hypokinesis.[7] Myocardial dysfunction is reported in survivors of both in hospital (68%) and out of hospital cardiac arrests (49%).[89] Stunned myocardium after successful resuscitation from cardiac arrest associated with spinal anaesthesia has not been reported. We report such a case that developed myocardial stunning after successful resuscitation from cardiac arrest following spinal anaesthesia.

CASE REPORT

A 29-year-old female (55 Kg and 160 cm), American Society of Anaesthesiologists (ASA) physical status I, presented for tubal reanastomosis surgery. Patient had undergone previous two normal vaginal deliveries uneventfully. Clinical examination was unremarkable and all the investigations were within normal limits, including ECG and chest X-ray (CXR). On the day of surgery, 18 G IV cannula was established on right forearm and preloading started with ringer lactate. ECG was showing normal sinus rhythm with heart rate of 88/min, non invasive blood pressure (NIBP) was 110/70 mm Hg and oxygen saturation (SpO2) was 99% on room air.

Patient was premedicated with Inj. midazolam 1 mg and Inj. ondansetron 4 mg intravenously. Subarachnoid block was given in right lateral position at L3-L4 interspace with 15 mg of hyperbaric Bupivacaine. After turning patient to supine position, monitor showed HR of 70/min with sinus rhythm and BP of 90/60 mmHg. Patient was supplemented with oxygen through Hudson's mask at 5 lit/min. Five minutes later, after checking adequate sensory level (T6), surgeon was asked to proceed. Within a minute, before surgeon could start surgery, patient developed seizure like activity. Monitor showed bradycardia (35/min). Inj. Atropine 0.6 mg was given intravenously but patient developed asystole. Cardiopulmonary resuscitation was started with chest compression and mask ventilation. Inj. Adrenaline 1 mg was given intravenously. After two minutes, return of spontaneous circulation (ROSC) was noticed. ECG showed sinus rhythm with HR of 101/min. Next moment, patient developed ventricular tachycardia with HR of 160/min with no palpable pulse. Patient was successfully defibrillated with 150J (biphasic). Rhythm reverted back to sinus with HR of 160/min with SpO2 of 100% and BP of 90/60 mmHg. Breathing was assisted as patient started breathing spontaneously. Within few minutes, patient started obeying verbal commands, was vocalizing and was able to lift both upper limbs. Sensory level at this time was T4. By that time, patient had received 1000 ml of IV crystalloids. Surgery was cancelled and patient was kept on table for observation. 12 lead electrocardiogram was done, which showed sinus tachycardia.

Over the period of next 2 hours, patient was given another 1000 ml of crystalloids, 500 ml of colloid and intermittent intravenous boluses of Inj. ephedrine (total 24 mg) to manage hypotension secondary to sympathetic blockade due to spinal anaesthesia. Mean arterial pressure was maintained around 60 mm Hg and 200 ml of urine output was recorded. Approximately two and half hours after ROSC, patient started desaturating with signs of pulmonary oedema, SpO2 dropping to 92% on Hudson's mask. RR became 30/min, and bilateral crepitations were heard on auscultation. Patient was given continuous positive airway pressure (CPAP) with 100% oxygen on mask in post anaesthesia care unit (PACU). Titrated doses of Inj. morphine (10 mg total) and Inj. frusemide were administered. Sensory blockade level was below L1. Patient developed hypotension with worsening respiratory distress and hypoxia. Blood gas analysis showed PO2 of 50 mmHg, PCO2-45 mmHg, pH-7.31 with normal serum electrolytes. BP dropped to 60/40 mm Hg, and HR was130/min with sinus rhythm, SpO2 was 72%. Dopamine infusion was started at 5 mcg/kg/min along with fluid support. Patient was intubated and ventilated with 100% Oxygen and IPPV and shifted to intensive care unit. Right internal jugular vein was cannulated with 7.5 F catheter and patient was started on noradrenaline 2 mcg/min. 2 D Echocardiography (ECHO) was done in view of persistent hypotension and unresponsive pulmonary oedema. It showed ejection fraction (EF) of 35% with global hypokinesis. Diagnosis of probable post cardiac arrest myocardial stunning was made. Cardiac support was continued with inj. noradrenaline with addition of inj. dobutamine. Subsequent ECHO, 2 days later showed EF of 43% with global hypokinesia. Over the period of next one week, patient improved clinically. Patient was weaned off from vasopressor support and extubated.

DISCUSSION

Post cardiac arrest myocardial stunning is seen in many survivors of both in and out of hospital cardiac arrest with no previous cardiac pathology. Myocardial stunning is reversible myocardial dysfunction due to global hypokinesis, resulting in haemodynamic instability. Onset can be seen within minutes after cardiac arrest or can be delayed up to 4-7 hours after cardiac arrest and full recovery is usually seen in 72 hours.[789] However, more sustained depression of ejection fraction with continued recovery over weeks has also been reported.[8] Very few studies have investigated post resuscitation haemodynamic instability and myocardial dysfunction in human beings.[810] No reports of myocardial dysfunction after cardiac arrest associated with spinal anaesthesia were found by the author.

Myocardial dysfunction due to cardiac arrest results from global hypokinesia and reduced cardiac output. There can be persistent hypotension with dysrhythmia. Cardiac index can be low and left ventricular end diastolic pressure high. Management strategies include early haemodynamic optimization with IV fluids and ionotropes. Intra aortic balloon pump counter pulsation (IABP), left ventricular assist device (LVAD) and extra corporeal membrane oxygenation (ECMO) can be considered in patients who are not responding to ionotropes.[7] Angiography studies done in post cardiac arrest patients show that coronary blood flow is maintained which indicates true stunning of myocardium rather than infarction and hence myocardial dysfunction is transient with full recovery.[9]

In the present case, signs of myocardial dysfunction were noticed approximately 2 hours after cardiac arrest. During these 2 hours, intermittent fall in BP was treated with IV fluids and ephedrine, as it was thought to be due to sympathetic blockade of subarachnoid block. As per American Heart Association (AHA) guidelines on post resuscitation care, patient should have been started on some vasopressor support (dopamine, norepinephrine, epinephrine) in immediate post arrest phase.[11] Due to fluid resuscitation, mean arterial pressure was maintained and urine output was recorded. With regression of the subarachnoid block and return of sympathetic tone, the peripherally pooled intravascular volume probably caused an increase in the preload which the hypokinetic myocardium could not handle. This resulted in pulmonary congestion and oedema.

The most accepted aetiology for sudden cardiac arrest post subarachnoid blockade is vasodilatation with decrease in venous return and cardiac output with reflex bradycardia. Volume loading and aggressive vagolytic treatment for bradycardia have been recommended for prevention.[35] ASA physical status I, age < 50 yrs, sensory level above T6 are identified as risk factors for bradycardia; making patients susceptible to vagal predominance leading to circulatory collapse and asystole.[5] The seizure like activity noticed just before cardiac arrest probably represented cerebral hypoxia due to hypotension. Inadequate preload (250 ml) before subarachnoid block may have been an additional contributory factor in our case. Though anticholinergic was administered immediately when HR dropped to 35/min, there was asystole before it could act. Immediate CPR and adrenaline resulted in successful revival of patient without any neurologic injury. The almost immediate recovery of the patient with resuscitation makes drug allergy unlikely especially with no other supportive signs.

The other causes of cardiac arrest considered were a high or total spinal and electrolyte abnormalities. A high or total spinal were unlikely as the patient had a sensory level of T4 post resuscitation and electrolytes were within normal limits. Negative pressure pulmonary oedema as a cause for respiratory distress was unlikely in our case as patient's airway was maintained in the post resuscitation period with the patient vocalizing well. Moreover, the pulmonary congestion developed about 3 hours after the cardiac arrest.

Adrenaline given during resuscitation can potentiate post resuscitation myocardial dysfunction.[912] Cardioversion/defibrillation can cause post resuscitation myocardial dysfunction which could have been the cause in our case.[813] Delay in starting of vasopressor agents in immediate arrest period might have played role in delayed recovery from myocardial depression.

CONCLUSION

Vigilance, adequate preloading, escalation therapy with atropine, ephedrine and adrenaline to treat bradycardia can prevent cardiac arrest during spinal anaesthesia. Spinal vasodilatation makes successful resuscitation difficult in case of cardiac arrest. Early vasopressor infusion, titrated fluids and echocardiography should be considered in immediate post cardiac arrest phase following spinal anaesthesia.