Effects of glucagon on myocardial contractility and cardiac output.
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Biomedical subjects
Publications and source records attributed to J Hamer.
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The Frank system vectorcardiogram has been studied in 61 patients with severe mitral valve disease to determine the value of the vectorcardiogram in the recognition of the relative degree of left and right ventricular hypertrophy in this situation. The appearance of the usual evidence of right ventricular hypertrophy is delayed in mitral valve disease by the vertical electrical position of the heart which may be due to alterations in the intrathoracic electrical field produced by left atrial enlargement. Voltage criteria for the recognition of isolated left or right ventricular hypertrophy in the vectorcardiogram are not applicable to combined ventricular hypertrophy in mitral valve disease. The present analysis is based on the spatial pattern of the QRS loop. The vectorcardiograms show a continuous gradation from posterior to anterior direction, the extremes indicating dominant left and right ventricular hypertrophy, respectively. Five groups are recognized from the appearance in the horizontal plane. Long posterior loops (Fig. 1) are associated with severe left ventricular hypertrophy, open posterior loops (Fig. 2) with left ventricular dominance, and wide posterior loops (Fig. 3) with moderate hypertrophy of both ventricles. Wide crossed loops (Fig. 4) indicate right ventricular dominance, and anterior clockwise loops (Fig. 5) are found with severe right ventricular hypertrophy. The vectorcardiogram rarely showed large QRS voltages in left ventricular hypertrophy, though these changes were often evident in the conventional electrocardiogram. The vectorcardiogram appeared to be more successful than the electrocardiogram in the recognition of severe right ventricular hypertrophy. An unusual rightwards displacement of the QRS loop was found in patients with tricuspid valve disease. It is concluded that the vectorcardiogram gives useful additional information for the recognition of ventricular hypertrophy that is not evident in the conventional electrocardiogram in mitral valve disease.
Haemodynamic studies have been performed in 9 patients whose blood pressures had been satisfactorily controlled with oral propranolol for 7 to 29 months. A postural drop of blood pressure or a fall of blood pressure on exercise did not occur. Pulse rate and cardiac output were below normal at rest and on exercise; peripheral resistance was high. The results are similar to those obtained in a comparable group of hypertensives after acute administration of propranolol. These findings are discussed in relation to the mode of action of propranolol in hypertension.
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Exchangeable sodium and potassium, total body water, and sulphate space were measured in 42 patients with severe valvular heart disease who were free of oedema. Compared with normal subjects of the same height, no increase in exchangeable sodium was found but a mean potassium depletion of 27% was shown. This depletion was not related to diuretic therapy, and no relationship between the degree of depletion and postoperative arrhythmias was found. It is concluded that the major cause of the low exchangeable potassium is the reduction in cell mass that occurs in chronic heart disease, and that there is no significant fall in the intracellular potassium concentration.