STENOSIS AND INSUFFICIENCY 



669 



compression of the pulmonary artery. The increases 

 in initial tension and systolic summits, and the over-all 

 change in ventricular contour were similar to changes 

 observed in the left ventricle in acute experimental 

 aortic stenosis. The aortic pressure started to decline 

 when about 50 per cent of the pulmonary arterial 

 lumen was still patent, and the pressure fall was 

 marked as the constriction was increased. 



Right-sided failure in dogs was produced by con- 

 trolled progressive stenosis of the pulmonary artery 

 (44, 45). Failure occurred only when the diameter 

 of the artery was diminished to less than one-third 

 of its original size. The cardiac output decreased, 

 with marked increases in right ventricular systolic 

 and atrial mean pressures and a marked increase in 

 heart rate. The mean femoral arterial pressure usually 

 decreased. It is impossible to decide to what extent 

 the changes registered were due to the pulmonary 

 stenosis and to what extent to failure of the heart. 



Barger and collaborators (11) also produced pul- 

 monary stenosis in dogs. When the pulmonary steno- 

 sis was less than 50 per cent of the diameter, a slight 

 rise of right atrial pressure occurred with a further 

 rise in pressure during strenuous exercise. The work 

 capacity of these dogs was normal, and right heart 

 failure did not develop. Superimposed pulmonary 

 insufficiency produced only minor changes. Similar 

 experiences have been reported by others (i 13). 



Clinical studies of pulmonary stenosis started with 

 the introduction of the cardiac catheter (41, 52, 92). 

 Since then it has been demonstrated that pulmonary 

 stenosis is one of the common congenital lesions, and 

 is often symptom free. 



Normally, there should be no systolic pressure 

 gradient between the right ventricle and the pulmon- 

 ary artery. Under the conditions of study, often with 

 augmented blood flow due either to anxiety or to a 

 concomitant congenital shunt, pressure gradients of 

 around 10 mm Hg have been registered in the ab- 

 sence of anatomic stenosis. This is explained by the 

 pressure loss to velocity and the sucking effect by 

 the blood stream on the end hole of the catheter used. 



Several groups have classified patients with systolic 

 pressure gradients of less than 50 mm Hg as having 

 mild stenosis; with a gradient of 50 to 100 mm Hg 

 as having moderate stenosis; and only when the 

 gradient is above 1 00 mm Hg as having severe stenosis 

 (172). Only in cases with severe stenosis is the blood 

 flow decreased. 



During ejection, the blood is forced through the 

 stenosed valve in a jet, which can be demonstrated 

 by the use of angiocardiography. This jet has a high 



velocity at the orifice, but it slows down as it spreads 

 in the pulmonary artery and starts forming turbulent 

 eddies in the relatively stationary blood mass there. 

 The kinetic energy of the jet is converted into potential 

 energy which is measured as increased lateral pres- 

 sure. The turbulent eddies, which can be demon- 

 strated both by angiocardiography and in model 

 experiments, are most evident a few centimeters from 

 the orifice. The jet is most rapid in and just beyond 

 the orifice and gives rise to negative pressure laterally. 

 This has been demonstrated in model experiments. 



In pulmonary valvular stenosis, emptying of the 

 right ventricle is modified by the increa,sed resistance 

 in the pulmonary orifice. The pressure rise during the 

 ventricular contraction occurs more or less contin- 

 uously towards a peak, which is succeeded by a pres- 

 sure fall with the same continuous course. The more 

 severe the stenosis, the closer toward the end of systole 

 is the peak found. 



The right atrial pressure curve may be modified 

 in severe pulmonary stenosis with right ventricular 

 hypertrophy (147): The curve is dominated by a 

 high peaked a wave which is transmitted to tiie jugu- 

 lar venous pulse as well as to the liver (93). As early 

 as 1 91 3 LanbergandPezzi pointed out the presence of 

 this abnormal wave in the venous pulse, and inter- 

 preted it as a result of increased filling resistance in 

 the ventricle. It is of importance that this increased a 

 wave cannot be taken as a sign of tricuspid stenosis, 

 which can be ascertained only through simultaneous 

 or successive pressure tracings from the atrium and 

 ventricle. 



In pulmonary stenosis the pulmonary blood flow 

 and content is reduced, whether the narrowing afl'ects 

 the subvalvular outflow tract (infundibular stenosis), 

 the pulmonary valve itself, or the pulmonary artery. 

 At rest, o.xygenation is usually sufficient; but if the 

 stenosis is severe, exertion may cause cyanosis due to 

 inadequate pulmonary flow. The reported occurrence 

 of chronic cyanosis in pure pulmonary stenosis has 

 been discussed by Selzer & Carnes (179). Thev did 

 not find any decrease in arterial oxygen saturation 

 and consider the occurrence of peripheral cyanosis 

 in pulmonary stenosis to be comparable to that found 

 in mitral stenosis or other advanced heart lesions, 

 where the slow peripheral circulation, perhaps in 

 combination with local capillary damage, is respon- 

 sible for the cyanotic skin changes. 



The pressures in the pulmonary veins and the pul- 

 monary artery are low, with normal pulmonary vas- 

 cular resistance. The right ventricular systolic pres- 

 sure is elevated; and when hypertrophy, dilatation 



