Ludwig W. Eichna

Comparison of intracardiac and intravascular temperatures with rectal temperatures in man.

A study of intracardiac and intravascular temperatures was undertaken with the thought that such measurements might provide further information concerning the mechanisms which normally maintain body temperature within its narrow limits and also that they might help to explain the deviations from normal temperature in certain disease states. Whereas the temperature of the peripheral tissues may vary widely, homeothermic man maintains the temperature of the deep tissues, or of a critical deep tissue, fairly constant under widely varying conditions of heat loss and heat gain (2). The identity of the critical deep tissue is not completely understood but a considerable body of evidence places it in the diencephalon and in normal man small variations in its temperature are thought to initiate compensating mechanisms which return the temperature of the body to the homeothermic norm. Generally, rectal temperature has been considered to indicate deep tissue, and critical tissue, temperatures but often rectal temperature appears to be a lagging and unsatisfactory index; witness the onset, when the body is heated, of such compensating mechanisms as peripheral vasodilatation and sweating before a rise in rectal temperature has occurred; and conversely, in subjects who are cooled, the presence of vasoconstriction and pilomotor activity before a fall in rectal temperature has taken place. It seemed desirable, therefore, to look for some other index of critical deep tissue temperature. Considerations of the mixing of blood in the left ventricle, probably in proportion to the volume flow and temperature of the blood from all organs,

Low potassium syndrome due to defective renal tubular mechanisms for handling potassium

Abstract Prolonged observations were made on the characteristics and the mechanism of production of the low potassium syndrome in a forty-two year old Chinese male with nephritis of unknown etiology. The syndrome consisted of intermittent bouts of muscular weakness, atony of the bladder, constipation and electrocardiographic changes of a broad flattened T wave, prolonged Q-T interval, prolonged P-R interval and dropped beats, all associated with low serum potassium levels. The plasma potassium level varied between 1.5 and 2.3 mEq./L. when the patient was on a regular diet (104 mEq. potassium daily), fell as low as 1 mEq./L. on a low potassium intake (30 mEq. potassium daily) and rarely exceeded 4 mEq./L. even when the potassium intake was six times greater than normal (625 mEq. potassium daily). The potassium balance was negative on an average potassium intake and became positive only when the daily potassium intake was increased to 425 mEq. or more. In general the serum sodium levels were low and sodium balance tended to be negative except when sodium intake was high. A reciprocal relationship between the potassium and sodium balances was apparent when the potassium intake was varied. Variations in sodium intake and balance, however, were not attended by reciprocal changes in the potassium balance. The plasma chloride level was usually low and chloride balance appeared to be related to the sum of the sodium and potassium balance in that chloride was retained when base was retained and vice versa. Potassium depletion appeared to affect adversely muscle strength and the vegetative nervous system. The severity of signs and symptoms referable to these systems varied in the presence of a constant plasma potassium level; nor was development of symptoms inevitable at any particular plasma potassium level. The height of the T wave of the electrocardiogram could be correlated with the plasma potassium level in acute experiments after potassium administration. Although electrocardiographic abnormalities occurred only during periods of potassium depletion, the day-to-day correlation between the height of the T wave and plasma potassium levels was poor. Glomerular filtration rate, renal plasma flow and maximum capacities of the renal tubules to excrete p-aminohippurate and to reabsorb glucose were approximately one-third of normal. The rate of glomerular filtration, but not the other functions, varied directly although not precisely with the level of daily potassium intake. During periods of low potassium intake and in spite of very low plasma potassium levels the kidneys continued to excrete urine containing appreciable amounts of potassium. Loss of potassium in the urine was not due to inability of the kidneys to defend by the usual mechanisms against either alkalosis or acidosis. Under conditions of low potassium intake as much as 50 per cent of the potassium filtered at the glomeruli appeared in the urine (normal = less than 20 per cent). Tubular excretion of potassium was easily demonstrable whenever the patient was on a high potassium intake. Potassium given during a period of potassium depletion and at a time when an abnormal amount was being lost in the urine demonstrated that the tubules were capable of reabsorbing additional potassium. A similar experiment performed during a period of high potassium intake resulted in a greater increase in the amount of potassium in the urine than in the glomerular filtrate. It is probable that both decreased absorption and increased excretion of potassium were a part of the renal tubular defect responsible for the excessive loss of potassium in the urine.

ELECTROLYTE AND WATER EXCRETIONS AND RENAL HEMO-DYNAMICS DURING INDUCED CONGESTION OF THE SUPERIOR AND INFERIOR VENA CAVA OF MAN

It is apparent that the kidney is the organ ultimately responsible for the salt and water retention, hence the edema formation, in congestive heart failure, but why the kidney fails to excrete these substances normally in this disease state remains to be determined. Venous congestion, and renal venous congestion in particular, has been postulated as one of the factors playing a role in the decreased electrolyte and water excretions. Recent observations in animals and man lend support to this concept.

Cardiac asystole in a normal young man following physical effort

Abstract 1. 1. While standing erect following an episode of hard physical work, a normal young soldier suffered a syncopal attack during which a cardiac arrest for nineteen seconds occurred. 2. 2. Such an asystole raises again the question whether sudden death during and after physical exertion may be the result of a fatal vasovagal syncope.

Capillary blood pressure in man. Direct measurements in the digits of patients with Raynaud's disease and scleroderma before and after sympathectomy

Abstract 1.1. During vasospastic circulatory arrest, induced in the fingers by cold, (a) digital capillary blood pressure varied between 7.0 and 12.5 mm. Hg (average, 9.7 mm. Hg); (b) digital capillary blood pressure rose slowly in response to induced increases in venous pressure, but fell promptly when the increased venous pressure was suddenly lowered; (c) cessation of blood flow through the capillaries was caused by closure of vessels proximal to them. The capillaries, venules, and veins remained patent. 2.2. Erythrocytes in clumps or loose aggregations may be isolated outside the central capillary blood stream when the digital circulation returns after a period of vasospastic circulatory arrest. Localized constriction of the capillary, or stickiness of the capillary endothelium, or both, may account for this. 3.3. In fingers with intact innervation the average digital capillary blood pressure was as follows: arteriolar limb, 18.5 mm. Hg; summit, 22.4 mm. Hg; and venous limb, 19 mm. Hg. The gradient of fall of pressure through the capillary was small, usually less than 3 mm. Hg. 4.4. In fingers deprived of sympathetic innervation the average digital capillary blood pressure was as follows: arteriolar limb, 27.8 mm. Hg; summit, 25.2 mm. Hg; and venous limb, 21.6 mm. Hg. The somewhat greater capillary pressure in the arteriolar limb suggests release of arteriolar tone. The gradient of pressure in the capillary is still small (6 to 7 mm. Hg).