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It is easy to take for granted the seemingly effortless way cardiovascular surgeons are able to bypass atherosclerotic coronary arteries. The process used today was developed over many years of rigorous study, experimentation, success, and failure. Early cardiac surgery was performed blindly, through small incisions, on a beating heart. Advances in medicine allowed surgery to be performed on hearts stilled by cardioplegic arrest, while the circulation was continued through the use of a cardiopulmonary bypass (CPB) machine. The development of the CPB machine allowed surgeons to perform the delicate work of coronary artery bypass grafting (CABG), first attempted on dogs, and then humans. This article briefly outlines the historical evolution of cardiac surgery that led to the development of the technology necessary to perform off-pump coronary artery bypass grafting (OPCAB). A case report of a 72-year-old female who underwent OPCAB is outlined. Included is a discussion of some of the benefits and potential complications of CABG and OPCAB. Anesthetic considerations for OPCAB procedures also are presented.

Acute respiratory distress syndrome (ARDS) is the most severe lung injury caused by many pathologic states. We treated a patient who suffered from ARDS caused by splenic infarction. A 75-year-old patient had a gastric cancer with multiple lung and liver metastasis. During anti-cancer therapy, she developed a high fever (above 39 degrees C) and a chest and an abdominal CT scan revealed splenic infarction. Hypoxia progressed gradually and she was transferred to ICU with tracheal intubation. Mechanical ventilation was performed according to open lung strategy, but she did not recover. On ICU day 3, the bilateral infiltration shadow on her chest X-ray was pointed out, and she had a low central venous pressure. We diagnosed her ARDS. The administration of methylprednisolone was started according to Meduri\'s report. Hypoxia was improved gradually and on ICU day 7, she was weaned from mechanical ventilation, and extubated. On ICU day 8, she was returned to her ward without ventilatory support.

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We reported a case of motor neuropathy with pyramidal sign following prolonged administration of a high dose of muscle relaxant, pancuronium bromide (Myoblock). A 40-year-old male was admitted to our hospital with acute episode of pancreatitis. He was treated with artificial ventilation and Myoblock to manage delirious state, disseminated intravascular coagulation and multiple organ failure. Total dose of 823 mg (24 mg/day) of Myoblock was given intravenously over 36 days. After Myoblock was discontinued, he regained his consciousness and marked muscle weakness with atrophy was noted in both limbs, more severe in distal lower limbs, without any noticeable sensory and sphincter disturbances. Motor nerve conduction studies showed normal nerve conduction velocities with markedly decreased amplitude of compound muscle action potentials. Repetitive nerve stimulation studies revealed decrement response after tetanic stimulation, which disappeared later. Needle EMG showed active denervation potentials and marked polyphasic motor unit potentials. Muscle biopsy revealed neurogenic muscle atrophy with fragmented acetylcholine esterase-positive postsynaptic sites. Sural nerve biopsy showed slight to moderate degree of axonal degeneration of myelinated fibers. Clinical, electrophysiological, and pathological studies above indicated that the main affected sites were neuromuscular junctions including the terminal twigs of motor neurones and postsynaptic membrane, and pyramidal tracts, predominant in lower limbs. About one month after the recognition of the muscle weakness, his muscle strength improved gradually, however, spasticity with hyperreflexia and pathologic reflexes of both legs were found, and became more prominent thereafter. Intensive physiotherapy and rehabilitation led improvement to the point that he became able to ambulate with walking-aids about 7 months later, but marked spasticity persisted.(ABSTRACT TRUNCATED AT 250 WORDS)

There are different opinions about the efficiency of preventing the succinylcholine-induced increase of serum potassium by precurarization. The following case report demonstrates that this method is not practicable in risk patients. A case of severe cerebral trauma is reported, in whom after precurarization with 2,0 mg diallyl-nortoxiferine and with 1.5 mg pancuronium, too, there was an increase of a normal serum potassium level up to 9.35 respectively 9.20 mEq/l about 1-2 minutes after injection of succinylcholine. 20 minutes after the injection serum potassium decreased to a normal level again. Only a short lasting bradycardia was noticed during the hyperkaliaemic period. Similar results reported in the anaesthesiologic literature are discussed.

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