Asystole on induction

Chen

Taiwanese Journal of Obstetrics and Gynecology

2006

Vasovagal syncope refers to a reflex cardiovascular depression that gives rise to loss of consciousness with bradycardia and profound vasodilatation. This response commonly occurs during regional anesthesia, hemorrhage or supine inferior vena cava compression in pregnancy. The changes in circulatory response from the normal maintenance of arterial pressure to parasympathetic activation and sympathetic inhibition may cause severe hypotension. This change is triggered by reduced cardiac venous return as well as episodes of emotional stress, excitement or pain. Occasionally, these vasovagal responses may be unpredictable and may dramatically proceed to asystole with circulatory collapse, and may even result in death. In these circumstances, hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilatation. Regional anesthesia, decreased venous return, hemorrhage and abnormal fetal presentation cumulatively increase the risk of vasovagal syncope in cesarean section patients. When a vasovagal response occurs, ephedrine is the drug of first choice because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anesthesia.

Perioperative Vasovagal Syncope with Focus on Obstetric Anesthesia

Chen

Taiwanese Journal of Obstetrics and Gynecology

2006

British Journal of Anaesthesia

Perioperative bradycardia and asystole: relationship to vasovagal syncope and the Bezold–Jarisch reflex

Kinsella

Tuckey

2001

288

237

Reflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, the Bezold-Jarisch reflex and neurocardiogenic syncope. The circulatory response changes from the normal maintenance of arterial pressure, to parasympathetic activation and sympathetic inhibition, causing hypotension. This change is triggered by reduced cardiac venous return as well as through affective mechanisms such as pain or fear. It is probably mediated in part via afferent nerves from the heart, but also by various non-cardiac baroreceptors which may become paradoxically active. This response may occur during regional anaesthesia, haemorrhage or supine inferior vena cava compression in pregnancy; these factors are additive when combined. In these circumstances hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilation. Treatment includes the restoration of venous return and correction of absolute blood volume deficits. Ephedrine is the most logical choice of single drug to correct the changes because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anaesthesia.

Non‐drug related asystole associated with anaesthetic induction

Keane¹,

Hennis²,

Bink‐Boelkens³

1991

Anaesthesia

SummaryA patient is presented where routine venepuncture associated with anaesthetic induction resulted in bradycardia and asystole. The case highlights the need for special caution with, and ECG monitoring throughout induction for, patients with a history of syncope. It also demonstrates the need for caution when attributing cardiovascular events during induction to the effect of the induction agents used. Key words Anaesthesia; intravenous.Complications; asystole.Arrythmias associated with the effect of anaesthetics or other medication on the cardiac conducting tissues are often reported. It is unusual to find a patient where the mildly painful procedures associated with an intravenous induction result in a profound bradycardia and cardiac arrest. This report describes such a patient. Case HistoryA 20-year-old male patient was scheduled for a routine follow-up cardiac catheterisation. He had had a total correction of a Fallot's tetralogy in 1976, and the operation had achieved a good result, with slight residual pulmonary stenosis. His general health and exercise tolerance were good, and he had been receiving no medication since this operation. His pre-procedure ECG showed a high-normal P-R interval (0.2 second) with no other abnormality.The procedure was commenced in the usual manner. ECG monitoring was applied and lignocaine 1 % was infiltrated subcutaneously over the femoral area. The patient had a short syncopal episode when the introducing needle was inserted into this area, with a heart rate of 20/minute. This spontaneously recovered in 20 seconds and the procedure was continued. A similar sinus bradycardia with a heart rate of 20/minute occurred when the venous sheath was inserted, with recovery taking 40 seconds. It was decided to postpone the catheterisation and do it later under general anaesthesia. The patient had not complained of any painful sensation during this attempted procedure, and a postoperative ECG showed no change from that before the procedure.The patient was premedicated with oral diazepam 15 mg before the second catheterisation attempt and appeared adequately sedated. However, when a 22-gauge cannula was inserted into the dorsum of his hand he developed bradycardia. This rapidly progressed to asystole, which was associated with a tonic-clonic convulsion. Oxygen 100% was given and cardiac massage was performed. A bolus dose of intravenous atropine 1 mg resulted in a sinus rate of 80/minute. The procedure was again abandoned. A subsequent detailed family history revealed that two of the patient's immediate family, his mother and twin brother, had experienced similar syncopal attacks under stressful circumstances, but had not had a documented cardiac arrest, nor any history of hospital treatment. A repeat ECG was identical to the pre-arrest one. A 24-hour Holter recording showed occasional multifocal ventricular ectopics with a short period of nocturnal Wenckebach A-V heart block with a maximal pause of 2.9 seconds. Such changes alone would not explain these attacks and a neurogenic basi...