A 70 kg old athlete was posted for surgery, Patient was administered succinylcholine due to unavailability of vecuronium. It was administered in intermittent dosing (total 640 mg). During recovery patient was not able to respire spontaneously & move limbs. What is the explanation
Xenon [Ref: Morgan's Anaesthesia 4/e p 781, 166, 167; Miller's Anaesthesia p 626, 6491 Xenon seems to be the best answer because all other inhalational anaesthetics mentioned in the question produce some cardiovascular effects that may harm the patient with mitral stenosis. Mitral stenosis is a disorder where cardiac output remains relatively fixed. Decrease in cardiac output should he avoided at any cost. - Any drug that increases the hea rate will reduce the cardiac output in patient with M.S. All the inhalational agents mentioned in the question decrease systemic vascular resistance and also increase the hea rate. Decrease in systemic vascular resistance leads to fall in blood pressure. Moreover, they may also decrease B.P. by their cardiodepressant action on myocardium. Therefore these drugs should not be used in patients with M.S. "Xenon has no effects on cardiac output or cardiac rhythum and is not thought to have significant effect on systemic vascular resistance It also does not affect pulmonary function and is not known to have any renal or hepatic toxicity". The main drawback of Xenon is its high cost and insufficient availability. -Xenon is an ine gas which is quite difficult to obtain and hence extremely expensive. - Xenon has received considerable interest in the last few years because it has many characteristics approaching those of an "ideal" inhaled anaesthetics. Mitral stenosis Due to mitral stenosis less blood .flows through the mitral valve to left ventricle. Left ventricle functions normally but is small and poorly.filled. Initially the left ventricle dilates keeping the pulmonary aery pressure low. As disease progresses pulmonary aery pressure increases and medial hyperophy develops resulting in chronic reactive pulmonary hypeension. The right hea hyperophies to pump against a pressure overload, then.fails. The pressure gradient across the narrow mitral orifice increase with the square of cardial output. Rapid hea rates, especially with atrial fibrillation decreases diastolic .filling time and markedly decreases cardiac output. Li / .filling is optimized by slow hea rate. Hemodynamic goals Low normal hea rate 50-70/min, treat tachycardia aggressively with /8 blockers. Maintain sinus rhythmus if possible. Maintain adequate preload Maintain high normal systemic vascular resistance Avoid hypercarbia, acidosis and hypoxia which may exacerbate pulmonary hypeension. The cardiac output is relatively fixed, maintain adequate afterload, slow the hea rate and avoid hypovolemia. Measure CVP and PAOP and maintain high preload. Avoid rapid decrease in afterload.
Pseudocholinesterase deficiency increasing action of syccinylcholine
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Undiagnosed muscular dystrophy and muscular weakness
Muscular weakness due to fasciculation produced by succinylcholine