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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



FIG. 22. Pressures obtained through 

 cardiac catheter as tip was withdrawn 

 from right ventricle to right atrium in 

 a case of tricuspid stenosis and mild re- 

 gurgitation. Note that even in longest 

 cardiac cycles, atrial fibrillation being 

 present, right ventricular diastolic pres- 

 sure does not reach level of right atrial 

 pressure. Pressure waves in right atrium 

 with each ventricular systole (V-waves) 

 are presumably caused by tricuspid re- 

 gurgitation. 



more common lesions involving this valve are ac- 

 quired. With tricuspid stenosis there is an increased 

 diastolic volume of blood in the right atrium as a 

 result of incomplete emptying through the narrowed 

 valvular orifice. The increased stretch of the right 

 atrium results in a more forceful atrial contraction 

 with at least a temporary restoration of normal 

 cardiac output. During this process of compensation 

 the right atrium becomes dilated and hypertrophied. 

 Because of the limited compensatory capacity of the 

 right atrial wall, systemic venous distention occurs 

 early. This then seems to diminish the outflow from 

 the right side of the heart. The effect of tricuspid 

 stenosis is somewhat similar to that of constrictive 

 pericarditis in that it obstructs the inflow of blood 

 into the right ventricle. 



In tricuspid stenosis the striking feature of the 

 atrial pressure tracing is the presence of giant A 

 waves. The right atrial pressure is elevated, u-sually to 

 a mean pressure between lo and 25 mm of mercury 

 instead of the normal of 6 mm. There also is an 

 abnormal pressure gradient between right atrium and 

 right ventricle during diastole (fig. 22). Killip & 

 Lukas (152) observed that a mean diastolic gradient 

 of more than i .9 mm of mercury while at rest and of 

 more than 2.6 mm during exercise occurred in 

 patients with tricuspid stenosis. The two major 

 hemodynamic alterations in tricuspid stenosis were a 

 decrease in cardiac output and an increase of right 

 atrial pressure. Their data suggest that a tricuspid 

 orifice smaller than i .0 cm- per m- of body surface is 

 associated with a decrease in cardiac output. 



TRICUSPID REGURGiT.-^TioN. In tricuspid regurgitation 

 as in stenosis of the tricuspid valve, there is an in- 

 creased volume of blood in tlic right atrium. This is 

 due to regurgitation of blood into the right atrium 

 durin<j; right \cntricular contraction. The right 

 atrium dilates and eventually liecomes hyper- 



trophied. Right atrial emptying is less complete than 

 usual, and pressure is elevated. 



The right atrial pressure may show many of the 

 typical features of the left atrial pulse in mitral 

 regurgitation. The contour of the right atrial pulse 

 shows a diminution in the negative X wave or replace- 

 ment by the ascending limb of the \' wave. The \' 

 wave is elevated and descends rapidly with the onset 

 of ventricular diastole (33, 102). However, this 

 positive venous pulse may be absent in tricuspid 

 regurgitation if the right atrium is greatly dilated so 

 that the regurgitant stream has little effect on its large 

 content. 



McMichael & Shillingford (176) observed that 

 during exercise tricuspid regurgitation increased with 

 a corresponding fall in forward cardiac output, which 

 is in contrast with what is seen in mitral regurgitation. 



Communications Between Right and Left Ventricles 

 and Between Pulmonarv and Systemic Arteries 



It is convenient to combine the discussion of these 

 two types of defects, for although they are different 

 anatomicallv their major hemod\namic effects are 

 similar. Therefore, although most of the discussion 

 here will be concerned with \entricular septal defects, 

 it will, in large part, apply as well to patent ductus 

 arteriosus and other aortic-pulmonary communica- 

 tions. 



GENERAL CONSIDERATIONS. Sincc commimications be- 

 tween the ventricles and between the pulmonary and 

 systemic arteries are between high and low-pressure 

 chambers and vessels, it is to be expected that the 

 blood will flow from the left to the right side of the 

 heart if the rest of the circulatory system is normal. 

 This is indeed the case when the defects are small. 

 Willi lar'je defects, however, balanced shunts or even 



