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EXCELLENT studies * have resulted in one of the most important recent diagnostic developments in electrocardiography, that is, identification of the electrocardiographic pattern of disturbances in electrolyte equilibrium and metabolism. It has been known for many years that ill health of many types can change the T waves, but interest in disturbances in electrolytes has been limited primarily to calcium. The duration of the Q-T interval is known to vary inversely with the ionic concentration of calcium in the plasma, whereas the configuration of the T wave remains unchanged except for duration.9 Changes in duration of the S-T segment and T wave are primarily responsible for changes in duration of the Q-T interval.10 Until recently, the U wave was considered to possess no clinical significance and was purely of physiologic interest. However, studies in animals and in man by Winkler and his associates 1; Nadler, Bellet, and co-workers,2

It HAS been suggested that the tone of the veins is increased in chronic congestive heart failure,* but, because the evidence has been indirect and unconvincing, the concept has not been fully accepted.† Some of the data reported ‡ may be interpreted to support an increase in venous tone. Because the neck veins are distended in patients suffering with congestive heart failure, the blood volume is considered by many to be increased and venous tone to be decreased. That this is not necessarily true has been indicated by previous studies,§ as well as by the observation that blood volume may be only slightly to moderately increased, if at all, in congestive heart failure.∥ Thus, it is desirable to study venous tone in congestive heart failure further.A venous occlusive pneumoplethysmographic method has recently been developed in this laboratory that permits simultaneous measurements of the continuous curves of the time courses

This study describes aspects of the specific changes which occur in the myocardial cells of Coxsackie B4virus infected suckling mice. These changes consisted of cellular shedding, membrane-vesicle complex formation, disappearance of Golgi body, nuclear shrinkage and densification of chromatin and an increase in ribosomal population. These changes are in addition to the nonspecific changes which probably result as a nonspecific cellular response to injury.

Responses of the small pulmonary veins to systemic intravenous infusion of angiotensin II were measured directly in 15 intact anesthetized dogs. Systemic and pulmonary venous pressures were essentially unchanged. Change in pulmonary arterial pressure was not marked and probably due to action of angiotensin on the pulmonary arterial system. Systemic arterial pressure increased markedly while cardiac output decreased. Thus, angiotensin II in the doses used constricts precapillary systemic vessels but at the same time has little effect on the pulmonary and systemic veins and on the pulmonary arterial system.

Intravenous infusion of histamine phosphate in intact lightly anesthetized dogs produced a consistent increase in pressure in small pulmonary veins, slight reduction in stroke volume and decrease or lack of change in left atrial pressure. The rise in pulmonary venous pressure was due to an active increase in tone of these veins without change in their caliber, since the pulmonary blood volume did not change significantly.

Coxsackie virus B4has been shown to produce significant lesions in the large and small blood vessels of 2-day-old and 12-day-old mice. The Coxsackie virus B4-infected mice developed focal endothelial cell degeneration and necrosis with subsequent desquamation and denudation of intima of the aorta, coronary arteries, large veins, and other blood vessels.Viral infections in man are common, but infection of the great blood vessels remains little studied. Viral lesions are suggested as an initiating factor in the production of vascular diseases in man, possibly including atherosclerosis.

The effects of intravascular injection of glucagon (50 μg/kg) on systemic and pulmonary circulations were studied in urethane- and pentobarbital-anesthetized intact dogs. Maximal effects of glucagon were noted at 10 to 15 min after injection in both groups of dogs. Glucagon produced little change or a decrease in cardiac output and a decrease in stroke volume in urethane-anesthetized dogs, whereas it produced a consistent increase in cardiac output in pentobarbital-anesthetized dogs and slight decrease in stroke volume. Heart rate increased and femoral artery pressure decreased significantly in both anesthetic groups. Systemic resistance decreased in pentobarbital-anesthetized dogs and tended to decrease also in urethane-anesthetized dogs. These findings suggest a vasodilator effect of gulcagon. An initial transient rise in pulmonary artery pressure occurred in both groups due to glucagon. This pressure rise was blocked by pretreatment with phenoxybenzamine. Thus, it was at least alpha-adrenergically mediated. Respiratory rate was increased in both groups following glucagon administration.These studies show that some hemodynamic phenomena are influenced by certain general anesthetics used for animal preparation and that the hemodynamic effects of glucagon should be interpreted with this in mind.

ALTHOUGH the vectorcardiogram has been studied extensively during the past 15 years, its clinical value is still unsettled. This is due in part to the fact that fundamental problems regarding the physical properties of the heart's electric field remain unsolved. The lack of precise knowledge concerning the electric field of the heart raises difficulties in deciding upon proper electrode placement and recording techniques. Arguments based on physical concepts which condemn a particular lead system as unsound may also be applied to any of the electrocardiographic leads. Nevertheless, no one could reasonably deny the clinical value of the electrocardiogram. This is true even though electrocardiography has been regarded by many as an empiric science. Through the correlation of many thousands of records with clinical and autopsy data, the diagnostic and prognostic reliability of the electrocardiogram has become established. The vectorcardiogram must also be put to this test to determine its

IT HAS BEEN SHOWN that a hot and humid environment increases the cardiac output, work, and power of the right and left ventricles,1 the average increase in cardiac output being 57% for 10 subjects exposed to the hot and humid summer weather of New Orleans (92° F., 71% R.H. [relative humidity]) over that for the same subjects in an air-conditioned, comfortable ward (73° F., 59% R.H.). When subjects were exposed to even higher temperatures and relative humidities (111° F., 86% R.H.) in our experimental climatic rooms, the stress on the heart was greater. Under these circumstances patients with congestive heart failure were able to increase their cardiac output, work, and power only slightly.2 The increase in cardiac output and work in a man subjected to a hot and humid environment is a normal physiologic response to maintain thermal equilibrium. Patients in congestive heart failure are unable to perform the extra

IT HAS been noted that a hot and humid environment precipitated acute congestive heart failure in patients who are compensated sufficiently to be comfortable when at rest in bed in a comfortable environment.1 Failure was precipitated more readily if the patients were removed from a comfortable room atmosphere to a given hot and humid environment in the laboratory during the winter season than during the summer. This difference may be an expression of physiologic adjustments of acclimatization. That acclimatization is responsible for this apparent seasonal difference is supported by the well-known high fatality rates during sudden severe heat waves which occur in the cooler areas of this country and the relatively low rates in the warmer areas.2The fact that a hot and humid environment precipitates acute congestive heart failure is not surprising when it is realized that such environmental conditions produce an extra load or stress upon

Since the original description of sickle cell anemia, by Herrick1 in 1910, much has been written about this disease with little attention given to the problem of the sedimentation of the erythrocytes. A review of the literature since 1935 revealed 65 publications on sickle cell anemia. These articles contained 248 reports of cases, 149 being fairly detailed. In only 37 of these reports was the sedimentation rate mentioned. In 9 of the 37 the method used was not indicated, and in 24 there was no mention of the degree of anemia. Although these data are difficult to interpret, it would appear that in 7 instances the sedimentation rate was slow. Diggs2 recorded the sedimentation rate in 27 of a series of 37 cases and found it to be slow in manyinstances. He noted a decided variation even in the same subject. No attempt was made to explain these

Hill1and Kuno and Ikeuchi2inhibited sweating in human subjects by cooling isolated portions of the body. They made no attempt to correlate the temperature of the bath cooling the part, the temperature and humidity of the environment, and the size of the area cooled, with the quantity of sweat and the comfort of the subjects. Nor were attempts made to evaluate the efficiency of local cooling on the adaptation of a man to a very uncomfortable, hot, and humid environment. The present studies were undertaken to throw light upon these problems.Methods and Materials.The studies were conducted in an air-conditioned room with the temperature and relative humidity controlled at 75° ± 1°F and 50% ± 2%, respectively. The temperature and relative humidity of the room could be raised within 15 minutes to the desired levels as indicated below. The room in which the subjects rested contained very little of the recording apparatus in order to reduce the psychic disturbance to a minimum. Twenty-six (25 white and one negro) young adults, trained subjects who had had considerable experience around research laboratories, were used. They varied from 22 to 37 years of age. Three of the subjects were females.The rate of water loss was measured from the skin of the right index fingertip, right forearm, and midepigastrium by a method described by Neumann, Cohn and Burch,3The oral and rectal temperatures were measured and recorded photographically by means of copper-constantan thermocouples. The variations in the volume of pulsations of the right index fingertip and right second toetip were measured by means of a modification of the sensitive pneumoplethysmographic method of Turner.4

Cardiac causalgia is a pain syndrome frequently occurring in patients with ischemic heart disease or in patients who have suffered cardiac trauma. The term "cardiac causalgia" was chosen because the syndrome resembles causalgia of the extremities.Cardiac causalgia minor is characterized by pain over the precordial region, often burning in nature, and of varying intensity. Tender areas of the chest are present. Cardiac causalgia major includes symptoms of cardiac causalgia minor and, in addition, swelling of the arms and hands, trophic changes of chest and arm skin, pulmonary edema, pneumonitis, pericarditis, arthritis, and other systemic features (eg, postcardiotomy, postcommissurotomy syndrome). Five patients presented with the clinical spectrum of the syndrome and its unifying features.

It has been noted previously1-4 that a warm and humid environment increases the output of the heart. Cardiac output was measured by the direct Fick method in five volunteer subjects resting in bed in wards of the Charity Hospital during the New Orleans tropical weather of July and August, 1957.3 The cardiac output in all patients was found to be higher (mean about 50%) when they were in a warm and humid ward open to the outside weather than when in an air-conditioned and comfortable one. Because of the importance of these findings it was considered advisable to repeat these studies in five more volunteer patients during the New Orleans tropical weather of August, 1958. This report is concerned with the data obtained during the summers of 1957 and 1958. MATERIALS AND METHODS Five additional adult Negro subjects (Subjects 6 through 10), four of whom had no

The new diuretic agent, chlorothiazide (6-chloro-7-sulfamyl-1,2,4-benzot benzothiadiazine-1,1-dioxide),* is useful in the treatment of many clinical disorders, including congestive heart failure, cirrhosis, nephrosis, essential hypertension, premenstrual edema, and toxemia of pregnancy.1-9 Among its various clinical advantages are (1) remarkable effectiveness when administered orally; (2) prompt diuretic action, consisting of water diuresis, natruresis, and chloruresis but only minimal kaluresis; (3) persistent activity and lack of tolerance until edema subsides; (4) antihypertensive action, and (5) minimal side-effects or toxic reactions.Basic pharmacologic studies have demonstrated that chlorothiazide inhibits carbonic anhydrase in vitro but not significantly in vivo,2 and clinical trials in man indicate that its diuretic action is qualitatively similar to that of the mercurial diuretics. In short-term animal experiments,1 maximal diuresis was observed at 40 minutes after intravenous administration, with a total duration of effect of about 4 hours. The peak response after oral administration occurred at 4 hours,

Great scientific accomplishments require methodical, orderly, logical, and deliberate organization of thought and work. The planning of a good experiment is an experience limited to few men. A clear definition of objective, properly oriented within existing knowledge and previous publications, necessitates considerable effort, including self-conferences through scientific thought, with critical evaluation of any decision. Satisfactory and lucid planning requires leisurely but concentrated thought, even to the exclusion of one's entire environment or contact with reality.Discipline in scientific thought is developed, self-taught, but nurtured by a good scientific environment, especially by minds of great scientists. Unfortunately, greatness is too often unrecognized by associates, for great people are simple, humble, modest people. To be considered great by some does not necessarily confer greatness. Too often, a man's prejudiced followers join to establish greatness in their "hero." Similarly, lack of contemporary recognition does not disqualify a great thinker. Time tells! It is

Because venous tone is such an important, unsolved problem concerned with hemodynamic phenomena in congestive heart failure, it was considered desirable to present thoughts and experimental investigations on this subject. The early, important studies of McMichael and Sharpey-Schafer 1 and Starr and Rawson 2 on venous tone in congestive heart failure, as well as the opposing investigations of others,* should be studied by all. DEFINITIONS Congestive heart failure is a clinical syndrome associated with failure of the heart as a pump.The clinical pattern of ascites, hepatomegaly, generalized systemic venous hypertension, anasarca, bilateral pulmonary basal rales, dyspnea, and other symptoms and signs may have several etiologic associations, but the congestive type of failure of the heart should be considered the cause only when this syndrome is produced by or associated with failure of the heart to pump adequate quantities of blood to the tissues. According to this definition, therefore,

There has been considerable interest in the hemodynamic phenomena associated with aortic insufficiency,* but most studies heretofore have been concerned with the heart and large central vessels. The works of Wiggers † and others, as well as the interesting theoretic discussions of Gladstone,18 include considerations of relationships between intraventricular and aortic pressure and volume during left ventricular systole and diastole. The rates of volume and pressure ejection in aortic insufficiency were found to be increased over the average normal circulatory states during systole and to decline rapidly long before diastole began.‡ Wiggers considered the hemodynamic changes to be due in part to regurgitation of blood but also to the sudden rise and fall of intraventricular pressure and volume ejection during systole. Changes in peripheral circulation have been considered to contribute to the production of the water hammer capillary pulsations and other hemodynamic manifestations of aortic valvular insufficiency, but these concepts