DYNAMICS OF PULMONARY CIRCULATION 



I709 



cells is less than that of the plasma [cell transit time 

 plasma transit time = 0.91 ± .05 (310)]. In man, 

 the total (systemic plus pulmonary) circulation time 

 is of the order of 15 to 18 sec (184). Approximately, 

 one quarter to one third of the total time is spent in 

 traversing the pulmonary circulation; the circulation 

 time between the right ventricle and the pulmonary 

 capillaries is estimated to be 2 to 3 sec (87). Despite 

 the many measurements of the pulmonary circula- 

 tion time, both in normal subjects and in patients 

 with cardiopulmonary disorders, there is still an 

 inadequate fund of information concerning the pre- 

 cise pulmonary vascular pathways traversed by the 

 test substance between the sites of injection and 

 sampling (75). 



INFLUENCE OF RESPIRATION ON 

 PULMONARY CIRCULATION 



In the pulmonary circulation, blood pressures, 

 volume, and flow change during each breath. The 

 precise nature of these changes has been debated for 

 two centuries (50, 324). Nonetheless, many aspects 

 remain unsettled largely because of the technical 

 difficulties involved in simultaneously recording 

 transient respiratory and circulatory events in the 

 intact animal or man. 



The attempts to circumvent the technical diffi- 

 culties have created problems of their own: a) the 

 recourse to simplifying physical models (fig. 37) 

 and artificial preparations has led to dubious gener- 

 alizations about natural breathing (61, 354); b) 

 the experimental control of some respiratory in- 

 fluences at the expense of others, has tended to 

 exaggerate the physiological importance of some 

 parameters while denying others — such as the degree 

 and type of inflation — their full due (215, 380); and 

 c) complicated experimental designs have created 

 artificial situations in which the usual calculation of 

 pulmonary vascular resistance either does not apply 

 or is very difficult to translate into terms of pul- 

 monary vascular dimensions (315, 354). 



Spontaneous Breathing 



During inspiration, as pleural pressure becomes 

 more negative, luminal pressure (referred to atmos- 

 phere) decreases. On the other hand, transmural 

 pulmonary arterial pressures — systolic, diastolic, and 

 mean — increase. During expiration, these changes are 

 reversed. 



There is no unanimity concerning the mechanisms 

 responsible for the increase in pulmonary arterial 

 transmural pressure during inspiration. Most certain 

 is an increase in pulmonary blood flow, arising from 

 the decrease in intrathoracic pressure and from the 

 increase in systemic venous return which it promotes 

 (17, 49); much more equivocal is a reduction in the 

 outflow from the pulmonary vascular bed so that the 

 pulmonary blood volume is increased (225, 253). 

 Such a combination of increased inflow and reduced 

 outflow would imply pulmonary vascular distension 

 and, hence, a decrease in pulmonary vascular 

 resistance. 



However, there are experimental results which do 

 not fit this picture: a) under some circumstances, in- 

 spiration has been found to increase — rather than to 

 decrease — pulmonary vascular resistance (49, 1 1 5, 

 309); b) measurements of transmural atrial pressures 

 suggest that the pulmonary veins empty uninterrupt- 

 edly during inspiration (187); and e) experiments on 

 models and dogs indicate, that, under circumstances 

 which promote an unusual emptying of the extra- 

 thoracic veins, the veins may collapse during inspira- 

 tion as they enter the thorax, thereby preventing an 

 increase in venous return (308). 



At least part of the divergent opinions about the 

 effects of inspiration on the pulmonary circulation 

 seem to arise from failure to take full cognizance of the 

 experimental setting: during an ordinary quiet 

 breath, pulmonary blood flow and volume do appear 

 to increase; if resistance does change, the change is 

 small (354). Moreover, collapse of extrathoracic veins 

 is not apt to occur under ordinary physiological cir- 

 cumstances even though it may conceivably occur in 

 the resting subject who is breathing with enormous 

 tidal volumes (354). 



As long as fluctuations in intrathoracic pressure 

 are small and venous return to the right heart remains 

 ample throughout the respiratory cycle, the pulmo- 

 nary arterial pressure pulses are fairly uniform. How- 

 ever, in clinical conditions associated with low 

 systemic venous return, in chronic pulmonary disease 

 (fig. 38), during exercise and during voluntary deep 

 breathing, marked swings do occur in the pulmonary 

 arterial pressure pulses. These reflect not only the 

 swings in intrathoracic pressure but also changes in 

 blood flow, volume, and resistance (187, 253). 



During natural expiration, the filling of the right 

 heart is decreased as intrathoracic pressures approach, 

 or even exceed, caval pressures; the pattern described 

 for inspiration is reversed. In patients with pulmonary 

 disease, in whom expiration has become an active 



