Citations

The artificial pacemaker has been compared to a physiologic ventricular parasystolic focus. In hearts being driven by a pacemaker, in the absence of atrioventricular (AV) block, capture (interference) phenomena are constantly seen. While variations in QRS complexes have been observed when the external pacemaker stimulus occurs early in the T-wave period of a sinus conducted beat, no sequence of aberrant beats has been observed. One patient showed occasional sinus beats interpolated between ventricular beats arising from the artificial pacemaker, and these occurred at a very narrow time band suggesting that AV conduction was permitted by phenomenon of a supernormal phase. At a later date this patient showed also retrograde conduction believed related to a supernormal phase during recovery of junctional tissue penetrated by an impulse entering from above, though the impulse itself was blocked. Records of two patients are used to illustrate grossly aberrant QRS complexes produced by the stimulus of the electric pacemaker when this fell in the semirefractory period. Noteworthy was the presence of a latent period before potentials of the propagated impulse were recorded, there being evident stimulus-to-QRS delays. The situation wherein the rhythm is most chaotic is that where AV block is absent, the sinus rate is fast, and the electric pacemaker rate is relatively slow. In two patients, retrograde activation of the atria occurred as a stable mechanism. In one patient, nodal rhythm of the RP type occurred, and sequences of the records suggested that the AV node might have become synchronized with the extrinsic pacemaker cycle. In this last instance three independent centers of effective impulse formation coexisted, the sinus node, AV node, and stimulating electrodes of the electronic pacemaker. A marked increase in the refractory period of the ventricle, as measured by its response to the set stimulus of the electric pacemaker delivered at varying instants with respect to the sinus mechanism, occurred in one case within a few days. The possibility that reserpine therapy contributed to this change is possible but has not been established, for the effective refractory period, as measured, later remained constant over a period of many weeks.

Nineteen patients with ventricular septal defect and severe aortic valvular incompetence have been operated on at the Mayo Clinic. There were two early deaths and two late deaths. The ventricular septal defect was located high and anteriorly in the septum and was often small. Aortic valvular incompetence was due, in most cases, to a deformed, prolapsing right coronary cusp. Mild to moderate degrees of infundibular pulmonary stenosis coexisted in nine patients. Repair of the ventricular septal defect was readily accomplished in most cases by direct suture, and relief of obstruction to right ventricular outflow was effected, when required, by resection of the crista supraventricularis. Repair of the aortic incompetence was attempted by a variety of means, but the incidence of persistent significant regurgitation was high, except when prosthetic cusp replacement was used. It is currently our policy to defer operation in children unless there are significant symptoms. When the patient is past the age of about 12 to 14 years, operation is advised under proper circumstances, and it consists generally of suturing of the ventricular septal defect and replacement of the right coronary cusp of the aortic valve.

Sixteen patients were studied immediately and for 3 days following surgical closure of ventricular septal defect. In eight patients with absent or mild pulmonary vascular disease, convalescence was uneventful and only small deviations from normal in cardiac output, blood gas levels, and acid-base profile were observed. The remaining eight patients had pre-existing moderate or severe pulmonary vascular disease. Values for cardiac output were abnormally low at some time in the postoperative period in all but two of these eight patients. Failure to survive was clearly related to a low cardiac output in four of the five nonsurvivors. Reduction in cardiac output observed in this group of patients is believed to be based in major part on the pre-existing increased resistance to blood flow through the pulmonary vascular bed and also to impaired right ventricular function following operation. No evidence was obtained to suggest that major changes in pulmonary vascular resistance occurred in the immediate postoperative period in patients with moderate or severe pulmonary vascular disease following closure of ventricular septal defect. Right ventricular function following atriotomy or transverse ventriculotomy was less impaired than after vertical ventriculotomy.

A method is described for detecting and quantitating small left-to-right shunts by recording continuously and simultaneously the changes in blood oxygen saturation at a systemic artery and at selected sites in the right heart chambers or great vessels produced by a few breaths of an inert gas such as helium or nitrogen. The advantages of this technic for detecting and quantitating left-to-right shunts are (1) the same instrument, namely, the cuvette oximeter, used to determine blood oxygen saturation and indicator-dilution curves in conjunction with routine diagnostic catheterization procedures, also is used to record the inert gas curves, (2) only one right heart catheter is needed, (3) the method is relatively simple, (4) the shunt can be quantitated, and (5) shunts of less than 10 per cent of pulmonary flow can be detected. It is concluded that the technic is of considerable practical value as a means of excluding the presence of or demonstrating and determining the magnitude of small left-to-right shunts.

Sodium ortho-iodohippurate (Hippuran) I 131 renography has been performed by a standardized technic in patients with renal artery stenosis, pyelonephritis, primary aldosteronism, pheochromocytoma, and renal tubular acidosis with nephrocalcinosis, as well as in patients in whom the hypertension was apparently not secondary. Fifty of 94 patients studied were found to have abnormal renograms. In patients with renal artery stenosis, all of 37 patients studied had values on the renogram that were outside the range for normal subjects. Although the renographic findings were not considered diagnostic of renal artery stenosis, certain abnormalities of the renogram were commonly observed in the presence of such lesions. When a unilateral delay in the appearance of maximal radioactivity was associated with delayed disappearance ot the medium, renal artery stenosis was frequently observed. Less pronounced differences in the function of the two kidneys were observed in patients with bilateral renal artery stenosis. A state of antidiuresis was often found helpful in the detection of less severe differences in renal function. In patients with predominantly unilateral pyelonephritis, the renographic abnormalities were qualitatively consistent with the degree of impairment of renal function. Bilateral abnormalities were observed in two patients who had bilateral parenchymal disease. The abnormalities on the renogram did not permit distinction between renovascular and renal parenchynal disease. Pyelonephritis associated with obstructive uropathy revealed findings highly suggestive of renal artery stenosis. Distinction from renovascular lesions could be determined with the aid of urographic studies. Only three of 44 patients with essential hypertension had abnormal renograms. The renograms, normal and abnormal, revealed essentially equal function of the two kidneys. The patients with abnormal renograms were not found by other technics to have evidence of secondary hypertension. The patients who were found to have pheochromocytoma and primary aldosteronism had normal isotope renograms. The patient with renal tubular acidosis and nephrocalcinosis had a bilaterally abnormal renogram and severe impairment of total renal function. The presence of a normal isotope renogram, as performed in our laboratory, is considered strong evidence against the existence of a renal or renovascular cause for secondary hypertension.