Summary: An understanding of the role of magnesium in cardiac conduction is complicated by the multiplicity of intracellular events coordinated by the magnesium ion. Several reports have cited magnesium deficiency as the cause of a variety of ventricular and supraventricular arrhythmias. On further inspection, the circumstances of each report strongly suggest the coexistence of significant potassium depletion; isolated hypomagnesemia as a cause of arrhythmia is not reported. This discussion brings together new data from basic science with that of clinical research to refute the suggestion that isolated hypomagnesemia is arrhythmogenic. However, there is sufficient evidence to indicate that hypomagnesemia will significantly exacerbate the proarrhythmic effect of hypokalemia, particularly if occumng in the presence of digoxin toxicity. Potassium and magnesium depletion are commonly concomitant, and simultaneous repletion of both ions in the presence of hypokalemia-induced arrhythrma would be both logical and effective. The beneficial effects of intravenous magnesium in the acute control of ventricular tachyarrhythmia are concluded to occur as a result of a separate antiarrhythmic action, quite independent of underlying magnesium balance.
SUMMARY In order to determine the significance of abnormalities of diastolic function in patients with left ventricular hypertrophy, exercise echocardiography to heart rates of 140 to 150 beats/min was performed in 18 normal subjects and 14 patients after aortic valve replacement. Simultaneous echo-, phono-, and electrocardiograms were recorded. Left ventricular cavity size was determined at end-diastole and end-systole. The timing of mitral valve opening and closure was measured, and hence left ventricular filling time derived, expressed either as ms/beat, or s/min when multiplied by heart rate. Isovolumic relaxation was taken as the interval between A2 and mitral valve opening. Systolic function, assessed from cavity dimensions, peak VCF, and QA2 interval was normal in all but two patients at rest and on exercise. Isovolumic relaxation was prolonged at rest in the patients to 85±8 ms (normal 69+9 ms), but left ventricular filling times were normal. With exercise, in normal subjects, isovolumic relaxation remained constant, but filling times dropped strikingly from 380±66 ms/beat, or 27±2 s/min at rest to 115± 10 ms/beat or 16+2 s/min. In patients with left ventricular hypertrophy, isovolumic relaxation dropped on exercise to 41+15 ms. Filling periods were normal at rest, 367+67 ms/beat or 27+3 s/min, but failed to show the normal drop with exercise, being 240±44 ms/beat or 28±4 s/min. At heart rates above 120/min, separation between the two groups was complete.Thus, striking abnormalities of left ventricular filling can be demonstrated on exercise in patients with left ventricular hypertrophy. They appear to represent loss of mechanisms whereby rapid diastolic filling is achieved in the normal subject.Numerous studies of left ventricular diastolic function have been performed in man at rest, both in normal subjects and in patients with disease. Several techniques, including haemodynamic,I ultrasound,2 and radionuclide3 have all confirmed a characteristic pattern of volume change consisting of an early period of rapid filling, a mid-diastolic period of diastasis, and a further volume increase during atrial systole. In patients with left ventricular hypertrophy, this pattern is significantly modified. Isovolumic relaxation is prolonged,4 peak rate of dimension increase during filling is reduced,5 and, in late diastole, passive stress strain relations may be abnormal.6 It was the purpose of the present study to examine early diastolic events in a group of such patients during exercise, and to compare the findings with normal. We have therefore determined a series of diastolic time intervals using echo-and phonocardiography in order to investigate Accepted for publication 8 February 1983 the manner in which the abnormal resting filling pattern is modified during exercise in those with left ventricular hypertrophy. Patients and methodsObservations were made on 14 patients studied five to 26 months after aortic valve replacement. Operation was for dominant aortic stenosis in 12, and aortic regurgitation in two. T...
151distended rectum was emptied manually. The limbs and jaw were hypotonic with absent jerks and normal sensation. The CSF protein was normal, and the serum potassium 1 8 mmol/l. Although 100 mmol intravenous and intragastric potassium was administered daily, it took 48 hours to raise the serum potassium to 2-5 mmol 1. He could breathe unaided after 36 hours. Recovery was uneventful.
Objective-To assess the electrophysiological and antiarrhythmic effects of pharmacological load manipulation by an angiotensin converting enzyme (ACE) inhibitor (captopril) and a direct vasodilator (hydralazine plus isosorbide mononitrate) in patients with inducible ventricular tachycardia and impaired left ventricular function.Design-Randomised open label crossover comparison of three regimens.Setting-Tertiary arrhythmia referral centre.
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