Thirty-three different electrocardiographic criteria for left ventricular hypertrophy have been evaluated in 360 autopsied hearts utilizing a chamber dissection technic. One hundred and sixty hearts had left ventricular hypertrophy, and 200 hearts did not (146 of these were normal, and 54 had right ventricular hypertrophy).The following five electrocardiographic criteria had a sensitivity of 56% but 10.5% to 14.5% false positives: Svi or Sv2 +RV5 '-35 mm, SV +±Rv5 or RV6 > 30 mm, Sv, or SV2 + Rv5 or RV6 > 35 mm, SV2 + RV4 or Rv5 > 35 mm, R + S > 40 mm. A point-score system employing a combination of criteria had a sensitivity of 54%, but lowered the false positives to 3%. The best limb-lead criterion was R aVL > 7.5 which had a sensitivity of 22.5% with only 3.5% false positives. The following criteria had no false positives, but the highest sensitivity was 19%: Svl, 24 mm, R aVL> 11 mm, RI + SI,, > 25 mm, RI > 13 mm, R aVL > 12 mm, RI > 15 mm, R aVL > 13 mm, and S aVR > 14 mm. Overall the precordial lead criteria were considerably more sensitive but less specific than the limb lead criteria. Since only six of the 200 hearts without left ventricular hypertrophy were in persons less than 30 years of age, this is not the major explanation for the high incidence of false positives in the more sensitive voltage criteria. The problems of using voltage criteria alone and the need for new criteria and approaches to the electrocardiographic diagnosis of left ventricular hypertrophy are discussed.

Although it has been recognized for some time that anoxia may result in an elevation of the pressure in the pulmonary artery, the mechanism of this response has not been satisfactorily explained.Von Euler and Liljestrand (1) in 1946 demonstrated in anesthetized cats that breathing 10%o to 11 %7o oxygen in nitrogen caused a rise in pulmonary artery pressure which was not affected by vagotomy or excision of the stellate ganglia, and which they therefore attributed to a direct effect of anoxia on the pulmonary vessels. Although left atrial pressure was sometimes recorded directly (2), no measurements of cardiac output were made, so that the pressor effects of changes in vascular resistance could not be separated conclusively from those due to variations in blood flow.Motley and his associates (3) in 1947 demonstrated the pulmonary hypertensive effect of anoxia in five unanesthetized human subjects, using the technique of cardiac catheterization. A slight fall in cardiac output occurred simultaneously with the rise in pulmonary arterial pressure and an inverse relationship between the two was suggested. Nevertheless, the two possible mechanisms of (a) stasis in the smaller pulmonary vessels associated with a decreased output of the left ventricle, or (b) pulmonary arteriolar constriction, could not be segregated except by inference.Recent reviews (4-6) of the pulmonary circulation in general, have accepted the role of anoxia in the pathogenesis of pulmonary hypertension, and have implied that the mechanism involved is pulmonary vasoconstriction. However, vasoconstric- tion with an increase in the pressure gradient and resistance to blood flow across the human pulmonary vascular bed has heretofore not been conclusively demonstrated to result from anoxia.The study of pressure in any closed fluid system requires not only a quantitative knowledge of the flow through the system, but an understanding of the resistance to that flow. In analyzing the resistance to the flow of blood from the pulmonary artery through the lungs to the left ventricle, the factor of left atrial or pulmonary venous pressure must be segregated from pulmonary vascular resistance. Without knowledge of the pulmonary venous or "capillary" pressure, it cannot be determined whether changes in pulmonary arterial pressure, themselves, are due primarily to changes in cardiac output or to variations in pulmonary arteriolar resistance.In 1948 Hellems and co-workers (7) described a method for determining pulmonary "capillary" pressure in man and have since given adequate proof that this pressure varies with the pulmonary venous pressure (8). When the pulmonary artery pressure, the pulmonary "capillary" pressure, and the cardiac output are determined simultaneously, the pulmonary arteriolar resistance may be calculated (9).It should be emphasized, as is mentioned by Dexter and his co-workers (10), that the term "arteriolar" resistance is used in the physiological sense, since no vessels having the anatomical characteristics of systemic arterioles are found in ...

Nor-epinephrine is a sympathomimetic drug similar in structure to epinephrine, but lacking a methyl group on the nitrogen atom contained in the latter compound (1). Its levo-isomer is twice as active as the optically inactive preparation. Some investigators believe that 1-nor-epinephrine is identical with sympathin E (1); others feel that it is more likely that nor-epinephrine is the precursor of epinephrine at adrenergic nerve endings (2, 3). Goldenberg and associates (1) found that in man l-nor-epinephrine increases total peripheral resistance, and in further contrast to epinephrine, does not increase the cardiac output. Goldenberg also (1) found a consistent elevation in pulmonary artery pressure during the infusion of l-nor-epinephrine in man. However, since he did not measure pulmonary venous pressure, one cannot determine from his study the primary site of action of l-nor-epinephrine in producing transient pulmonary hypertension. For these reasons it seemed desirable to investigate further the action of l-nor-epinephrine upon the pulmonary circulation.The purpose of the study reported here is to determine how l-nor-epinephrine produces pulmonary arterial hypertension in man. In man the pulmonary venous pressure may not ordinarily be measured directly. However, Hellems and coworkers (4) have described a method of obtaining pulmonary "capillary" pressure, and have shown that in animals the pulmonary "capillary" pressure varies with the pulmonary venous pressure. If pulmonary artery pressure, pulmonary "capillary" pressure and cardiac output are determined simultaneously, the pulmonary arteriolar resistance may be calculated (5 terial constriction, then a rise in pulmonary arteriolar resistance is to be expected during the pulmonary hypertension resulting from its exhibition. MATERIALThirteen subjects were studied. Eleven had normal hearts as shown by physical examination, X-ray, and the electrocardiogram. One (E. B.) was convalescing from beriberi heart disease, with only residual tachycardia. One (C. F.) had a systolic murmur at the cardiac apex and a pulmonary "capillary" pressure tracing suggestive of incompetency of the mitral valve (6). C. F. had also moderate elevation of the mean pulmonary arterial pressure while in the resting state. As controls, six subjects with various types of cardio-pulmonary disease were studied. METHODAll subjects except E. B. were studied in the fasting condition, sedated by 0.1 or 0.2 gm. of seconal given two to two and a half hours prior to study. Cardiac catheterization was performed as described previously (7). A double lumen catheter was used, so that pulmonary "capillary" pressure and pulmonary arterial pressure could be measured simultaneously. Pulmonary "capillary" pressure was obtained by the method of Hellems and co-workers (4). The criteria of satisfactory pulmonary "capillary" pressures were (1) the nature of the pressure curve, showing "a" and "c" waves; (2) the peripheral location of the catheter tip in the lung; and (3) the securing of a specimen of blood satur...

Three hundred fifty-four adult human hearts were dissected utilizing a technique similar to those previously described by Müller 1 and Lewis. 2 A classification was synthesized on the basis of anatomic characteristics of 100 normal hearts. Presumptive evidence of either left or right ventricular overload, provided by clinical and autopsy observation, served as essential corollary data in establishing normal limits. The existence of hypertrophy was readily recognized in hearts in which one or both ventricles increased in mass sufficiently to surpass the defined upper limit. Isolated ventricular hypertrophy of mild degree was recognized as a consequence of an abnormal LV+S/RV ratio in 58 hearts in which ventricular weights were within the normal range. Factors which would be expected to result in left or right ventricular overload were demonstrable in 42 of these cases. Atrial hypertrophy correlated well with hypertrophy of the corresponding ventricle and served as an invaluable aid in recognition of mild degrees of combined ventricular hypertrophy. This classification constitutes the basis for a subsequent correlative electrocardiographic study.