Accelerated idioventricular rhythm is defined as a ventricular rhythm of 60-100 beats per minute or a ventricular tachycardia that does nor exceed 120 beats per minutes. Although, it rarely converts to a fatal arrhythmia like ventricular fibrillation, it needs to be differentiated from AIVR, which is from another origin. AIVR may occur due to ischemic heart disease (ST elevated myocardial infarction), cardiomyopathy, rheumatic fever and digitalis intoxication. We report here on a case of AIVR that was related to desflurane administration.
Accelerated Idioventricular Rhythm ; Anesthesia ; Arrhythmias, Cardiac ; Cardiomyopathies ; Digitalis ; Isoflurane ; Methyl Ethers ; Myocardial Ischemia ; Rheumatic Fever ; Tachycardia, Ventricular ; Ventricular Fibrillation

Cisatracurium was initially characterized to have no evident histamine-releasing potential with excellent cardiovascular stability. However, severe anaphylactic reactions to cisatracurium that resulted in bronchospasms and cardiovascular collapse have been reported worldwide. Two cases of severe anaphylactic reactions after the administration of cisatracurium are presented. The anesthetics used in both cases were lidocaine, midazolam, propofol (microemulsion propofol in the second case), remifentanil and cisatracurium. After the administration of these drugs, bronchospasm and hypotension manifested, leading to the diagnosis of anaphylaxis and appropriate treatment. Skin intradermal testing confirmed that both cases were due to immune-mediated anaphylaxis to cisatracurium, despite the fact that neither of the patients had been exposed to the allergen previously. The anaphylaxis may be due to cross-reactivity between neuromuscular blocking agents and substances with quaternary ammonium ions. Anesthesiologists should be aware that cisatracurium has the potential to trigger severe anaphylactic reactions via an immune-mediated mechanism.
Anaphylaxis ; Anesthesia, General ; Anesthetics ; Atracurium ; Bronchial Spasm ; Humans ; Hypotension ; Intradermal Tests ; Ions ; Lidocaine ; Midazolam ; Neuromuscular Blocking Agents ; Piperidines ; Propofol ; Quaternary Ammonium Compounds ; Skin

BACKGROUND: Melatonin has been shown to attenuate the reflex sympathetic increases that arise in response to orthostatic challenges. We tested the hypothesis that the attenuated sympathetic increase induced by melatonin premedication may weaken the arterial blood pressure (ABP) preserving the capability during acute hypotension, thereby altering dynamic cerebral autoregulation and causing a further decrease in cerebral blood flow (CBF). METHODS: Acute hypotension was induced in 12 healthy subjects by releasing bilateral thigh cuffs before and after an oral dose of melatonin (0.2 mg/kg). Heart rate (HR), arterial blood pressure (ABP), Modelflow estimate of cardiac output (CO), total peripheral resistance (TPR) and cerebral blood flow velocity (CBFV) by transcranial Doppler were measured. RESULTS: Steady state HR, the mean arterial pressure and CBFV were not altered 60 minutes after melatonin ingestion. Reduced systolic arterial pressure (DeltaSAP), changes in HR (DeltaHR), CO (DeltaCO), and TPR (DeltaTPR), DeltaHR/DeltaSAP and percentage restoration of SAP were not affected after a temporal decrease in ABP induced by thigh cuff release. In the cerebral circulation, melatonin did not affect changes in CBFV, cerebrovascular resistance index, the rate of regulation and percentage restoration of CBFV following a sudden decrease in ABP. CONCLUSIONS: Contrary to our hypothesis, melatonin did not affect the rapid vasodilatory and recovery responses of cardiovascular and dynamic cerebral autoregulation. These results suggest that melatonin premedication may not impair ABP and CBF preserving capability induced by sudden postural changes or hemorrhage.
Arterial Pressure ; Blood Flow Velocity ; Blood Pressure ; Cardiac Output ; Cerebrovascular Circulation ; Eating ; Heart Rate ; Hemorrhage ; Homeostasis ; Humans ; Hypotension ; Male ; Melatonin ; Premedication ; Reflex ; Thigh ; Vascular Resistance

The addition of thoracic epidural anesthesia to general anesthesia during cardiac surgery may have a beneficial effect on clinical outcome. However, epidural catheter insertion in a patient anticoagulated with heparin may increase the risk of epidural hematoma. We report a case of epidural hematoma in a 55-year-old male patient who had a thoracic epidural placed under general anesthesia preceding uneventful mitral valve replacement and tricuspid valve annular plasty. During the immediate postoperative period and first postoperative day, prothrombin time (PT) and activate partial thromboplastin time (aPTT) were mildly prolonged. On the first postoperative day, he complained of motor weakness of the lower limbs and back pain. An immediate MRI of the spine was performed and it revealed an epidural hematoma at the T5-6 level. Rapid surgical decompression resulted in a recovery of his neurological abnormalities to near normal levels. Management and preventing strategies of epidural hematoma are discussed.
Analgesia ; Anesthesia, Epidural ; Anesthesia, General ; Back Pain ; Catheters ; Decompression, Surgical ; Hematoma ; Hematoma, Epidural, Spinal ; Heparin ; Humans ; Lower Extremity ; Male ; Middle Aged ; Mitral Valve ; Partial Thromboplastin Time ; Postoperative Complications ; Postoperative Period ; Prothrombin Time ; Spine ; Thoracic Surgery ; Tricuspid Valve