636 .\NNOTATIONS Am. Heart J.

.April, 1960

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Warren, J. V., Walter, C. W., Romano, J., and Stead, E. .A.: Blood Flow in the Hand and Forearm After Pamvertebral Block of the Sympathetic Ganglia. Evidence AAgainst Sympathetic Vasodilator iYer\-es in Extremities of Man, J. Clin. Invest. 21:665, 1942.

SarnoT92jJ., and Simeone, F. A.: \:asodilator Fibers in Human Skin. J. Clin. Invest. 26:453,

,Arnott, \V. hl., and MacFie. J, bl.: Effect of Ulnar Nerve Block on Blood Flow in the Re- flexly Vasodilated Digit, J. Physiol. 107:233, 1948.

Gaskell, P.: Are There Sympathetic Vasodilator bierves to the Vessels of the Hands? J. Physiol. 131:647, 1956.

Roddie! 1. C., Shepherd, J. T., and \Vhelan, I<. F.: A Comparison of the Heat Elimina- tlon From the Normal and Nerve-Blocked Finger During Body Heating, J. Physiol. 138:445, 1957.

Roddie, I. C., Shepherd, J. ‘I‘.! and \Vhelan, Ii. F.: The Contribution of Constrictor and Dilator Nerves to the Skm Vasodilatation l)uring Body Heating, J. Physiol. 136:489, 1957.

Hurleqr,.H. J.. and Mescon, J.: Cholinergic Innervation of the Digital ;\rteriovenous Anasto- moses of Human Skin. 12 Histochemic,ll Localization of Cholinesterase, J, Appl. Physiol. 9:82, 1956.

Armin, J,, Grant, Ii. T., Thompson, 1:. H. S., and Tickner, ;\.: An Explanation for the Heightened Vascular Reactivity of the 1)cnervated Rabbit’s Ear, J. Physiol. 121:603,

Barcroft, H., Brad. J., Haves, J. P. L. A., and Iiirai5r\-i, Ii.: ‘The Effect of Mental :\rithmetic on the Blood Flow & the Hand, J. Physiol. 145:51’, 1959.

Doupe, J,, Cullen, C. >I., and Macaulay! L. J.: Studies in Denervation; Circulation in the Skin of the Proximal Parts of the Lnnbs, J. Xeurol. & Psychiat. 6:129, 1943.

Edholm, 0. G., Fox, Ii. H., and MacPherson, 12. Ii.: Vasomotor Control of the Cutaneous Blood Vessels in the Human Forearm, J. I’hysiol. 139:455, 1957.

Koddie, I. C., Shepherd, J. T., and \\%elan, R. F.: The Vasomotor Nerve Supply to the Skin and nluscle of the Human Forearm, Clin. SC. 16:67, 19.57.

Hertzman, I\. B.: Some Relations Between Skin ‘l‘cmperature and Blood Flow, Am. J. Phys. Med. 32:233! 1953.

Fox, K. II.. and HIlton, S. M.: Bradykinin Formation ill Human Skin as a Factor in Heat Vasodilatation, J. Physiol. 142:2 19, 1958.

Hilton, S. M., and Lewis, G. I’.: The Relationship Betwren Glandular Xctivit>., Bradykinin Formation, and Functional Vasodilatation in the Submandibular Salivary Gland, J. Physiol. 134:471, 1956.

Acute Rheumatic Fever in Adults

Friedberg’ has recently pointed out the rarity of acute rheumatic fever in adults over 2.5 years old who have not previously had the disease. The diagnosis is frequently made on the basis of arthritis alone. The finding of subcutaneous nodules, erythema marginatum, and chorea is very rare. A diagnosis of rheumatic carditis is also difficult to establish in adults, since other forms of heart disease are common. Friedberg believes that rheumatic carditis can be diagnosed only when a diastolic murmur appears under observation. He also challenges the concept that .%schoff bodies are evidence of clinically active rheumatic fever, since there is poor correlation between clinical status and the pathologic findings in auricular biopsies taken at operation.

All of these difficulties in making a diagnosis of acute rheumatic fever in adults are considered in a paper by Pader and Elster.2 Using the rather strict criteria of Friedberg, a good many of the 30 patients reported would not qualify for a diagnosis of acute rheumatic fever, and the authors suggest that the Jones criteria for the diagnosis of rheumatic fever in children be liberalized when applied to adults.

The main stumbling block is the diagnosis of rheumatic carditis. A prolongation of the P-Ii interval, changing murmurs, a pericardial friction rub, an enlarged heart, or heart failure are 11ot specific signs of acute rheumatic carditis and can be interpreted only tentatively.

One further concept of Friedberg is of great interest. He states that he has never seen a patient who developed his first attack of rheumatic fever after the age of 25 who has gone on to develop rheumatic valvular damage. Unfortunately, there are reports in the literature of patients developing their first attack as an adult, with progressive involvement of the heart valves and death from heart failure. What we do not know is how often this occurs. If it is as infrequent as

Vulume 59 Number 4 ANNOTATIONS

Friedberg suggests, this is added evidence that there are significant differences between acute rheumatic fever in children and that in adults.

Douglas Carroll, M II. Baltimore, Md.

1. Friedberg, C. K.: Kheumatic Fever in the Adult: Criteria and Implications (Editorial), Circulation 19:161, 1959.

2. Pader, E., and Elster, S. K.: Studies of Acute Rheumatic Fever in the Adult. I. Clinical and Laboratory Manifestations in Thirty Patients, Am. J. Med. 26:424, 19.59.

Classification of Systolic Murmurs

The advantages of careful clinical auscultation of the heart are frequently forgotten, due in part, perhaps, to the feasibility of precise physiologic studies. In the current literature, systolic murmurs are frequently described in the classic descriptive terms of intensity, location, radiation, and quality, but without mention of duration. Leatham I.2 first proposed a classification of systolic murmurs into two types: ejection and pansystolic.

Ejection systolic murmurs are found in conditions associated with increased turbulence of blood flow through the semilunar valves. Blood flow through the semilunar valves does not occur throughout the whole of systole, but is limited to the period of systolic ejection. Thus, the ejec- tion murmur starts slightly after the first sound, the delay corresponding to the period of iso- metric contraction. The murmur is loudest during the period of maximal ejection in mid-systole, and diminishes as intraventricular pressure falls and flow through the valves declines. It ceases before the second sound.

.Aortic ejection murmurs are found classically when there is aortic stenosis, but also in aortic valvular deformity without stenosis, subvalvular stenosis, dilatation of the aorta, and increased aortic flow.

The ejection systolic murmur of pulmonary stenosis is a little more difficult to recognize,3 because it is frequently longer and its relation to the second sound is complicated by the fact that the second (pulmonary) component of the second heart sound is usually absent, allowing the pulmonary ejection murmur to persist until the onset of the first (aortic) component of the second heart sound. This illusion of the murmur persisting to the end of systole will not deceive the ausrultator who pays to the second heart sound in the pulmonary area the strict attention that it deserves.4 The features of onset slightly after the first heart sound and mid-systolic accentuation are further aids in the recognition of the pulmonary ejection murmur. A pulmonary ejection murmur is found in atria1 septal defect because of the greatly increased flow through the pulmonary- artery and the dilatation of that vessel.

An ejection systolic murmur at both pulmonary and aortic areas may be heard in complete heart block (increased stroke volume), as well as in such conditions as fever, anemia, and thy- rotoxicosis. Phonorardiography records a slight ejection murmur in most normal individuals, and the exaggeration of this phenomenon accounts for many innocent murmurs. Other varieties of the innocent systolic murmur6 are the apical Late systolic murmur and the short, low-pitched murmurs frequently audible at the lower left sternal edge.

In contrast to the ejection murmurs which by their very nature are limited to the period of systolic ejection, other murmurs are due to abnormal flow that occurs throughout the whole of systole, and they are, therefore, pansystolic. In mitral and tricuspid incompetence there is a pres- sure gradient between ventricle and atrium, with regurgitant flow and murmur all through systole. The pansystolic or regurgitant murmur of atrioventricular valve incompetence, therefore, begins with the first heart sound and ends with the second sound. This situation is in marked contrast to that which obtains at the semilunar valves, where gradient, flow, and murmur are confined to the period of systolic ejection. Similarly, in uncomplicated ventricular septal defect the pressure gradient between the left and right ventricles is present throughout systole and, in consequence, the flow and the murmur are pansystolic. ‘This pansystolic murmur can be differentiated clinical11