CARDIAC INDEX = (.9 L /mm /m' 



FIG. 20. Simultaneously recorded left atrial, left ventricular, 

 and aortic pressure pulses (redrawn to identical pressure scale) 

 from a 24-year-old man with "pure" mitral regurgitation 

 (operative diagnosis). Note characteristic differences in con- 

 tours of left atrial pulses recorded in "pure" regurgitation from 

 those recorded in "pure" stenosis (fig. 19). For discussion see 

 text. 



is present; 2) there is no apparent C wave, since the 

 trough or X wave between the C and V waves is 

 absent; j) if the C wave could be distinguished at the 

 beginning of ventricular systole, its amplitude would 

 be far exceeded by the V wave; and 4) there is a 

 rapid descent of the V wave at the termination of 

 ventricular systole. 



Since the pulmonary capillary (or wedge) pressure 

 is dependent for its level on left atrial pressure, it 

 follows that this contour of the wedge pressure pulse 

 would also reflect the changes in left atrial pressures 

 (66); thus hemodynamic studies using pulmonary- 

 artery wedge pressures have been carried out (173). 

 Gorlin and associates (119) have studied the hemo- 

 dynamic status of patients with mitral regurgitation. 

 They showed that in such patients a normal aortic 

 output was usually maintained, but at the expense of 

 a large increase in total left ventricular output. 



McMichael & Shillingford (176) noted that any 

 factor tending to lower the peripheral resistance and 

 thus lessen the obstruction to aortic outflow would at 

 the same time reduce the backfiow through the mitral 

 valve relative to the forward flow tiirough the aortic 

 valve. This can occur during exercise. They found 

 that administration of amyl nitrate caused the aortic 

 output to increase whereas the regurgitant flow 

 decreased. 



PULMONARY STENOSIS. Stenosis of the pulmonary 

 valve, without other significant intracardiac mal- 



formations, accounts for more than 2 per cent of 

 congenital cardiac anomalies. The essential disturb- 

 ance in isolated pulmonary stenosis is an increased 

 pressure in the right ventricle with a normal or 

 diminished pressure in the pulmonary artery. Nor- 

 mally, the pressure gradient across the pulmonary- 

 valve varies from o to 5 mm of mercury, but with 

 severe pulmonary stenosis this gradient may be 100 

 mm or more. The right ventricular pressure may 

 actually exceed the left ventricular systolic pressure. 

 The right ventricular hypertension leads to hyper- 

 trophy of the right ventricle. Normal cardiac output is 

 usually maintained despite the obstruction. Even- 

 tually, however, the right side of the heart may fail 

 and, as a result, cardiac output falls and the right 

 ventricular diastolic, right atrial, and .systemic venous 

 pressures rise. 



Numerous studies have been carried out in experi- 

 mental animals on the acute effects of constriction of 

 the pulmonary artery. The critical level of occlusion 

 at which circulatory failure is produced has been 

 demonstrated to be approximately 60 per cent of the 

 cross-sectional area of the pulmonary artery (103, 

 246). Taquini and associates (246) found that in 

 open-chest dogs the right ventricle was capable of 

 attaining a pressure of approximately 60 mm of 

 mercury without alteration of cardiac output. Up to 

 this level the increased systolic force of the right 

 ventricle occurred without apparent changes in the 

 diastolic pressure or volume of the right ventricle. In 

 general, an increase in resistance beyond this level 

 was followed by a fall in cardiac output, a fall in 

 left ventricular pressure and later a fall in right 

 ventricular pressure, and by progressive failure. 



Amorim and colleagues (g) studied the hemo- 

 dynamic effects of acute obstruction of the pulmonary 

 artery in normal closed-chest dogs produced by 

 means of a balloon catheter and confirmed the 

 findings of Taquini et al. (246). There appeared to 

 be no hemodynamic change other than the increase 

 in right ventricular pressure up to 60 mm of mercury. 

 When the right ventricular pressure was raised beyond 

 this level, however, a marked elevation of mean right 

 atrial pressure and a striking decrease in cardiac 

 output and systemic arterial pressure occurred. 

 Pressure recordings from the right atrium and 

 indicator-dilution techniques demonstrated the de- 

 velopment of significant degrees of tricuspid regurgita- 

 tion under these circumstances. The deterioration of 

 right ventricular function in dogs with intact cardiac 

 septa appears to be related a) to overdistention of the 

 right \entricle, and h) possibly to a disproportionate 



