STENOSIS AND INSUFFICIENCY 



663 



exceeded the left atrial pressure by a wide margin 

 during most of systole. During diastole, however, this 

 margin was usually small, except at the time of the 

 height of the i^ wave. This indicates that the pul- 

 monary vascular resistance in these dogs also was 

 fairly low. 



It is of importance to consider that, in the experi- 

 mental animal, compensatory mechanisms, come into 

 play soon after the heart lesion develops, tending to 

 restore the condition to normal. Most notable among 

 these compensatory mechanisms are the increase in 

 I he pressure head of the left atrial activity, a pro- 

 longation of the time for diastolic filling, and an 

 augmentation of the sucking action of the left ven- 

 tricle, as evidenced by the steeper rise of the diastolic 

 portion of its pressure curve. The extent of the created 

 stenosis and the modifying effect of such compensatory 

 mechanisms may explain the different results in the 

 animal studies. 



The infrequent occurrence in dogs of terminal right 

 heart failure after the creation of mitral stenosis may 

 be due to the small increase in the load on the right 

 ventricle that is the consequence of most experi- 

 mentally produced mitral lesions. This is in contrast 

 lo the long standing and marked elevation of pul- 

 monary arterial pressure and right ventricular load 

 liiat accompanies the human disea.se. 



The extensive experience gained from right heart 

 catheterization studies in several laboratories around 

 the world has gi\en a rather complete picture of the 

 altered circulation in patients with mitral stenosis or 

 incompetence of varying degrees (9, 13, 23, 24, 40, 

 48, 50. 53. 58, 59. 70, 85-87, 90, 91, 136, 138, 140, 

 142, 177, 180, 192, 199, 208, 214, 215). Left heart 

 catheterization has added comparatively little to the 

 knowledge of the circulation in mitral stenosis (16, 

 17, 20, 26, 42, 152). Some of this information has, 

 however, been of extreme importance, as, for example, 

 the height of the left ventricular diastolic pressure. 



The constant and central finding in patients with 

 mitral stenosis in any degree is the increase of the 

 blood pressure in the left atrium and consequently 

 also in the pulmonary veins, the pulmonary artery, 

 and in the right ventricle during systole. In patients 

 with early or slight mitral lesions the pressures may be 

 normal at rest, only to increase on exercise with 

 loads that do not raise the pulmonary pressure in 

 normal individuals. With the gradual narrowing of 

 the mitral orifice, the left atrial pressure and pul- 

 monary arterial wedge pressure increase, up to a 

 limit of about 40 mm Hg. The pulmonary arterial 

 pressure increases in a similar fashion. The gradient 

 from pulmonary artery to pulmonary vein, which is 



low in normal individuals, is also low in patients with 

 mitral stenosis as long as the pressure in the pulmonarv 

 veins is relatively low — below 15 to 20 mm Hg. With 

 the gradual narrowing of the mitral orifice and the 

 increasing of the left atrial pressure, the pulmonary 

 gradient increases, leading to marked pulmonary 

 arterial hypertension and pulmonary arterial pressures 

 that may exceed those in the systemic arteries. 



A rise in pressure in the left atrium is an obvious 

 condition for maintaining normal diastolic filling of 

 the left ventricle through a narrowed mitral ostium. 

 This causes a corresponding rise in pressure in the 

 venous and capillary parts of the pulmonary circuit, 

 with a risk of development of pulmonary edema when 

 the pulmonary venous blood pressure approaches the 

 oncotic pressure of the blood. This critical value is 

 reached when the mitral orifice has decreased to less 

 than one-fourth of its normal width. The exact height 

 of the pressure is, however, a function not only of 

 mitral valve opening, but also of the cardiac output — 

 more specifically the diastolic flow — and thus also of 

 the heart rate. 



Contrary to what has been found in dogs or in 

 isolated lung segments, the pulmonary vascular 

 resistance, and consequently the pulmonary arterial 

 pressure in mitral stenosis in man, is elevated when 

 the disease is advanced and of long duration. Since 

 changes of comparable magnitude were not observed 

 in dogs over the periods of study by Hannon et al. 

 (95), it may be concluded that the rise of pulmonary 

 va,scular resistance in man is not a passive hydro- 

 dynamic phenomenon but rather results from slow, 

 chronic changes in the blood vessels that alter their 

 elastic and /or mu.scular properties. Some active 

 contraction of the hypertrophied small pulmonary 

 arterial branches may also add to this raised resistance 

 (103). 



The cardiac output has been found to \'ary con- 

 siderably at rest, depending on the degree of mitral 

 stenosis. In patients with stenosis of minimal or 

 moderate degree, it usually is within normal limits; 

 in those with more acK'anced stenosis, the output has 

 been reduced at rest. In patients with frank congestive 

 failure this reduction has been still more pronounced, 

 although the diflcrence usually is small. During 

 exercise, it has been found that the ability to increase 

 the output is relatively unimpaired in most patients 

 with minimal lesions. With increasing stenosis the 

 ability to increase the cardiac output ijecomes less and 

 less. In some patients, usually those in right heart 

 failure and with added tricuspid regiu-gitation, the 

 cardiac output is fixed and may actually fall during 

 exercise (188). 



