Two cases of asystolic cardiac arrests managed with therapeutic hypothermia

Poor neurological outcome is a common sequel of prolonged cardiac arrest. Although Therapeutic Hypothermia (TH) for neuroprotection has been a subject for research for over Half a century, its use has been limited because of many controversies and lack of clear guidelines. However for over two decades there has been a revival of interest in mild therapeutic hypothermia (32-34°C) for neuroprotection. However its use after primary asystolic cardiac arrest has been questioned.Herein presenting two cases of prolonged asystolic arrest (39 minutes and 25 minutes); where therapeutic hypothermia was successfully used in following prolonged cardio pulmonary resuscitation. On patients who were in deep coma after resuscitation, TH was applied for 24 hours as per institutional protocol with full neurological recovery in both the cases. Therapeutic hypothermia might have a potential role in even in non-shockable arrests and should be considered in every successful cardiopulmonary resuscitation with poor neurological status.     

Episodic asystole and apnoea as the presenting features of a diffuse glioma

A case of asystolic collapse and subsequent progression to apnoea as a presenting feature of cerebral glioma is presented. The pathophysiological mechanism is likely to have been a focal seizure within subcortical regions affecting autonomic function. This example and others in the literature illustrate that severe and life-threatening cardiorespiratory manifestations may be the presenting feature of neurological disease.     

Survival after hypocalcemia,hypomagnesemia, hypokalemia and cardiac arrest following mild hydrofluoric acid burn

Background.?Although hydrofluoric (HF) acid burns may cause extensive tissue damage, severe systemic toxicity is not common after mild dermal exposure. Case.?A 36-year-old worker suffered a first-degree burn of 3% of his total body surface area as a result of being splashed on the right thigh with 20% HF acid. Immediate irrigation and topical use of calcium gluconate gel prevented local injury. However, the patient developed hypocalcemia and hypomagnesemia, hypokalemia, bradycardia, and eventually had asystole at 16?h post-exposure, which were unusual findings. He was successfully resuscitated by administration of calcium, magnesium, and potassium. Conclusion.?This report highlights a late risk of HF acid dermal exposure.     

Late-onset periodic asystolia during vagus nerve stimulation

Cardiac changes may occasionally occur during vagus nerve stimulation (VNS) used in epileptic patients. As they can be potentially life-threatening, it is important to detect them, and this is why an intraoperative test is performed during the implantation. Few cases of asystole during this test have been described. Only one patient with late-onset bradyarrythmia caused by VNS has been reported. This patient had been implanted 2 years and 4 months before the episode. We present another case of late asystole in a patient whose VNS had been implanted 9 years before the arrhythmia onset. In our patient, each run of stimulation produced bradyarrhythmias and very often severe asystolia due to atrium-ventricular block.     

Transthoracic pacing in cardiac asystole

A total of 139 patients had transthoracic pacemakers introduced via a subxiphoid approach for asystole during advanced CPR in the emergency department of a large urban teaching hospital over a calendar year. Two groups were examined retrospectively, A) 34 patients who presented asystolic, and B) 99 patients who presented with ventricular fibrillation that became asystole. Age, sex, and etiologies for cardiac arrest were similar in both groups; there were no survivors. The mean duration of asystole before pacemaker insertion was 4 min (group A) to 7 min (group B). Temporary electrical capture was obtained in six patients from group B, but electrical-mechanical association could not be achieved in any of these patients.     

Treatment of presumed asystole during pre-hospital cardiac arrest: superiority of electrical countershock

Standard drug therapy for asystole during cardiac arrest includes epinephrine, atropine, and calcium chloride (CaCl). Recent studies have shown that ventricular fibrillation (VF) can appear to be asystole when recorded from the chest surface. To determine the efficacy of these drugs and electrical countershock for asystole, a group of 83 adult nontraumatic cardiac arrest victims (55 men, 28 women, mean age of 64 +/- 14 years) were studied. Asystole appeared at some time during arrest in 44 patients (53%) and was the initial rhythm in 24 (29%). The rate of survival to hospital discharge was significantly higher in patients whose initial rhythm was VF (46%) than in patients whose initial rhythm was asystole (0%). Epinephrine, CaCl and atropine infrequently changed the rhythm from asystole. Electrical countershock infrequently altered the rhythm from asystole when it appeared as the initial rhythm. However, countershock was significantly more effective than epinephrine (P less than 0.003), atropine (P less than 0.04), or CaCl (P less than 0.03) in altering the rhythm from asystole, which appeared later in resuscitation. Ventricular fibrillation was the most common rhythm appearing after countershock for asystole. Countershock appears to be superior to epinephrine, CaCl, and atropine for treating asystole during the course of resuscitation, suggesting that the rhythm diagnosed as asystole may actually be VF in many cases.     

Successful resuscitation of hypermagnesaemic asystolic cardiac arrest with the use of early transvenous cardiac pacemaker: a case report

A 63 year old woman presented to the emergency department (ED) with 1 week of progressive dyspnoea, constipation, and generalized weakness. She had undergone spinal fustion surgery 10 days previously, and had a history of chronic renal insufficiency. The patient had been using milk of magnesia and magnesium citrate in unknown amounts to alleviate her constipation over this time frame. During her ED stay she became progressively hypotensive and bradycardic, and despite aggressive resuscitative measures she suffered an asystolic arrest 1 hour into her ED course. She was resuscitated with conventional therapy, but her haemodynamic profile did not improve significantly until transvenous cardiac pacing was employed. Her magnesium level was 10.4 mmol/l. Treatment of magnesium overload has focused upon haemodialysis, forced diuresis, and the use of intravenous calcium salts. Case reports have previously documented survival of moderately to severely ill patients when these modalities have been used. Likewise, failure of resuscitation despite use of these methods has been previously noted. To our knowledge, this is the first reported case clearly demonstrating the efficacy of transvenous cardiac pacing to successfully resuscitate a patient upon whom multiple vasopressors, fluids, and calcium previously had no clear effect.