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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



strated a lowering of pulmonary artery pressure and 

 pulmonary vascular resistance, both at rest and during 

 exercise (191). This did not cause any pulmonary 

 edema or breathing difficulties, although both the 

 heart rate and cardiac output usually increased. The 

 "protection" afforded by the high resistance thus did 

 not seem to be needed. The infusion of acetylcholine 

 also caused a decrease in arterial oxygen saturation, 

 indicating changes in the ventilation perfusion ratio of 

 the lungs. Thus the increased resistance may be second- 

 ary to anoxic changes in the ventilation to perfusion 

 ratio, rather than to the increased left atrial pressure 

 per se (67, 159, 202). The rapid decrease of the pul- 

 monary vascular resistance seen in some patients 

 after the mitral block has been removed by commis- 

 surotomy also speaks in favor of its functional nature. 



The anatomical lesions found in the lungs of pa- 

 tients with long-standing left heart disease may in 

 itself, cause both increased resistance and rapid 

 changes in resistance during different conditions of 

 flow. As suggested by Folkow, even minor thickening 

 of the inner layer of the vessel walls of the arteries of 

 the systemic circulation causes a marked narrowing 

 of the lumen and thereby increased resistance (75, 

 76). A similar mechanism operating in the pulmonary 

 vascular bed could well explain the observed figures 

 for pressures and flows in pulmonary hypertension 

 in mitral stenosis. Also the rapid increa.se in resistance 

 seen during exercise studies when heart rate and 

 cardiac output (and presumably the pulmonary 

 blood volume) increase, could be due to purely 

 anatomical alterations. 



Taking all facts into consideration, it may be con- 

 cluded that the increased pulmonary vascular resist- 

 ance seen in patients with left-sided heart disease 

 is due partly to functional vasoconstriction within 

 the lung, and partly to patho-anatomical changes 

 of the small arterial branches. The extent to which 

 one or the other mechanism is responsible for the 

 changes in any given case may vary considerably. 



Some studies of the pulmonary blood volume have 

 been made using several indicator dilution techniques 

 (24, iig, 127, 128). They have usually shown an 

 absence of increased pulmonary blood volume in 

 patients with mitral stenosis. The uncertain technique, 

 combined with difliculties in obtaining comparable 

 figures in normal individuals or patients with other 

 heart lesions, invalidates any conclusions from most 

 of the results published. It seems obvious furthermore 

 that a '"normal"' figure for the amount of blood in the 

 chest of a patient with marked perivascular puliiKMi- 

 ary fibrosis, interstitial edema, and enlarged heart 



in itself may signify engorgement of the pulmonary 

 vessels. 



No studies regarding the lymph flow in pulmonary 

 congestion have been reported. It is, however, a 

 frequent finding, during surgery for mitral stenosis, 

 that the pulmonary lymph vessels are markedly 

 dilated and may have a diameter of i cm or more. 

 This indicates the importance of good lymph drainage 

 to maintain the lungs edema-free in conditions with 

 elevated left atrial pressure. 



In the discussion of the importance of increased 

 pulmonary vascular resistance for the dexelopment 

 of the progressive clinical picture in mitral stenosis, 

 it is often stated that the cardiac output can no longer 

 be increased when the pulmonary arterial pressure 

 increases to systemic loads. There are, in reality, 

 only a few such cases reported in the literature where 

 the high arterial pressure existed in tlie absence of 

 other hemodynamic abnormalities. In almost all 

 cases signs of right ventricular failure were also pres- 

 ent, with or without tricuspid incompetence. A 

 similar inability to increase the cardiac output on 

 exercise has also been found in patients with secondary 

 myocardial changes, with much less pulmonary 

 hypertension, or even almost normal pulmonary 

 pressure. The primary importance of the high pul- 

 monary arterial pressure for the regulation of the 

 cardiac output in patients with mitral stenosis thus 

 seems to have been exaggerated. 



REGIONAL AND PERIPHERAL BLOOD FLOW 



Regional blood flow has been studied only to a 

 limited extent in various valvular heart disorders. 

 Most interest has been directed to the renal blood 

 flow in view of the possible connections between 

 changes in renal hemodynamics and the development 

 of the syndrome of congestive heart failure (10-12, 

 109, 199). When it was demonstrated, in 1946, that 

 markedly decreased renal blood flow and glomerular 

 filtration rate occurred in patients with chronic con- 

 gestive failure, this gave rise to a large series of studies 

 on the behavior of the kidney in patients with heart 

 disease. It was soon found that similar renal changes 

 could be demonstrated in some patients with valvular 

 heart disease long before any signs of congestive failure 

 had appeared. In a large series of patients with mitral 

 stenosis, where the renal dynamics were studied 

 simultaneously with the pulmonary circulation (199), 

 it was foiuici thai the resting values for renal ijlood 

 flow were close to normal in those patients who had 



