Cases reported "Bradycardia"

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1/29. Fatal cardiac ischaemia associated with prolonged desflurane anaesthesia and administration of exogenous catecholamines.

    PURPOSE: Four cardiac ischaemic events are reported during and after prolonged anaesthesia with desflurane. CLINICAL FEATURES: We have evaluated desflurane in 21 consecutive patients undergoing advanced head and neck reconstructive surgery. Four deaths occurred which were associated with cardiac ischaemic syndromes either during or immediately after operation. All patients in the study received a similar anaesthetic. This comprised induction with propofol and maintenance with alfentanil and desflurane in oxygen-enriched air. Inotropic support (either dopamine or dobutamine in low dose, 5 micrograms.kg.min-1) was provided as part of the anaesthetic technique in all patients. Critical cardiovascular incidents were observed in each of the four patients during surgery. These were either sudden bradycardia or tachycardia associated with ST-segment electrocardiographic changes. The four patients who died had a documented past history of coronary heart disease and were classified American Society of Anesthesiologists (ASA) II or III. One patient (#2) did not survive anaesthesia and surgery and the three others died on the first, second and twelfth postoperative days. Enzyme increases (CK/CK-MB) were available in three patients and confirmed myocardial ischaemia. CONCLUSION: These cases represent an unexpected increase in the immediate postoperative mortality for these types of patients and this anaesthetic sequence.
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2/29. bradycardia and asystolic cardiac arrest during spinal anaesthesia: a report of five cases.

    Sudden, severe bradycardia/asystolic cardiac arrest are considered infrequent, but are certainly the most serious complications of spinal anaesthesia. We report four cases of primary asystole and one of severe bradycardia in young to middle-aged, healthy patients scheduled for minor surgery at the day surgery unit. bradycardia/asystole were not related to respiratory depression or hypoxaemia/hypercarbia; they occurred at different time intervals after the onset of spinal anaesthesia (10-70 min) and, apparently, were not dependent on the level of sensory block, which varied between T3 and T8. One patient was nauseated seconds before the asystole, otherwise there was no warning signs. All the patients were easily resuscitated with the prompt administration of atropine and ephedrine and, in the case of cardiac arrest, cardiac massage and ventilation with oxygen. One patient was treated with a small dose of adrenaline. Four patients had the surgery, as planned; one had the surgery postponed. All the patients were discharged from hospital in good health and did not suffer any sequelae.
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3/29. Can a dose of 2microg.kg(-1) caudal clonidine cause respiratory depression in neonates?

    A case of multiple life-threatening postoperative apnoeas in a term neonate undergoing inguinal herniorrhaphy and orchidopexy who received light inhalation anaesthesia combined with caudal block with 1 ml.kg-1 ropivacaine 0.2% plus 2 microg.kg-1 clonidine is reported. The patient showed no apparent risk factors for postanaesthetic apnoea. Oxycardiorespirography five days after surgery only showed minor abnormalities. clonidine though administered caudally in the usual dose of 2 microg.kg-1 appeared to be the most likely cause for postanaesthetic apnoea in this neonate.
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4/29. Profound bradycardia and hypotension following spinal anaesthesia in a patient receiving an ACE inhibitor: an important 'drug' interaction?

    An 86-year-old man on whom a transurethral resection of prostate was performed under spinal anaesthesia developed profound bradycardia and hypotension with disturbance of consciousness during transfer to the recovery room. Initial treatment with atropine produced rapid improvement in cardiovascular and cerebral function. A further hypotensive episode (without bradycardia) occurred approximately 1 h later but responded rapidly to methoxamine. The patient made a full recovery during an overnight stay on the High Dependency Unit. Possible mechanisms for this event are discussed, with the proposal that the concomitant administration of captopril and the relative unavailability of angiotensin ii may have significantly contributed to the problem.
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5/29. Asystole during electroconvulsive therapy: a case report.

    OBJECTIVE: The objective of the report is to describe a case of asystole lasting for 18 s, which developed after a subconvulsive stimulus during electroconvulsive therapy (ECT) in a patient without pre-existing cardiovascular abnormality. A brief review of the relevant literature is also provided. CLINICAL PICTURE: The patient was a 65-year-old Chinese man with a 2-year history of depression and good past medical health. Earlier he had responded well to a course of ECT without adverse effects. This time he presented with low mood, anhedonia, poor appetite and constipation. He did not respond to adequate trials with several antidepressant medications. When a subconvulsive stimulus was administered to determine the seizure threshold, no seizure activity was detected. However, immediately after the stimulus the patient developed an 18-s asystole, followed by bradycardia of 40 beats per minute for 10 s. The bradycardia resolved spontaneously before therapeutic intervention was effected. TREATMENT: Intravenous atropine was employed as premedication and suprathreshold stimulus was used in further ECT sessions. OUTCOME: Asystole did not recur in the subsequent six ECT sessions. CONCLUSION: When proper precautions are taken, asystole does not necessitate the suspension of further ECT sessions but intravenous atropine should be considered as premedication in such cases. Inducing anaesthesia with methohexital, avoiding excessive amounts of succinylcholine and employing suprathreshold stimulus and unilateral electrode placement may further lessen the likelihood of asystole in susceptible cases.
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6/29. Anaesthetic management of severe bradycardia during general anaesthesia using temporary cardiac pacing.

    There are few reports of management of severe bradycardia with temporary cardiac pacing. We describe a 65-yr-old female patient who developed bradycardia and hypotension on two occasions during general anaesthesia for laryngoscopy. The first episode was treated with atropine, ephedrine, and colloid infusion and the second with a temporary pacemaker and ephedrine.
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7/29. Wenckebach type heart block following spinal anaesthesia for caesarean section.

    A case is described of complete heart block during spinal anaesthesia for Caesarean section in a fit 23 yr-old-woman. This developed shortly after the institution of the block, with the height of the block below T5 and in the absence of hypotension. The patient was resuscitated successfully with vagolytic and alpha-agonist drugs. A Wenckebach block persisted for a short period postoperatively. The importance of instituting monitoring before the beginning of anaesthesia and the immediate availability of atropine and alpha-agonists before the initiation of spinal anaesthesia is stressed.
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8/29. Cardiac arrest due to a vagal reflex potentiated by thoracic epidural analgesia.

    reflex bradycardia and cardiac arrest may be the result of a vagal reflex, which can occur during a variety of surgical procedures. We report a patient who developed cardiac arrest as a result of a vagal reflex that was potentiated by thoracic epidural analgesia during general anaesthesia. A 53-year-old man was scheduled for subtotal gastrectomy because of an early gastric adenocarcinoma. After an epidural catheter had been inserted, general anaesthesia was induced. During surgery, an abdominal self-retaining retractor was set up but bradycardia and cardiac arrest developed. The patient returned to a normal sinus rhythm after successful resuscitation. We conclude that bradycardia as a result of a vagal reflex is mediated by potent abdominal wall traction and is potentiated by epidural analgesia. early diagnosis and proper treatment can allow a full recovery, even in high-risk patients.
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9/29. Is phenytoin administration safe in a hypothermic child?

    A male neonate with a Chiari malformation and a leaking myelomeningocoele underwent ventriculoperitoneal shunt insertion followed by repair of myelomeningocoele. During anaesthesia and surgery, he inadvertently became moderately hypothermic. Intravenous phenytoin was administered during the later part of the surgery for seizure prophylaxis. Following phenytoin administration, the patient developed acute severe bradycardia, refractory to atropine and adrenaline. The cardiac depressant actions of phenytoin and hypothermia can be additive. Administration of phenytoin in the presence of hypothermia may lead to an adverse cardiac event in children. As phenytoin is a commonly used drug, clinicians need to be aware of this interaction.
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10/29. Renal transplantation and diabetic autonomic neuropathy.

    This report describes six episodes of cardiovascular collapse in the perioperative period of a young diabetic woman undergoing general anaesthesia for renal transplantation and a similar episode after a second anaesthetic. She was subsequently found to have an autonomic neuropathy. Recommendations for the management of similar patients are made.
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