I 7IO 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION' II 



fig. 38. Blood pressures re- 

 corded from the pulmonary 

 artery (PA) and right atrium 

 (RA) during quiet breathing in 

 a patient with chronic bronchitis 

 and emphysema. 



30 [— 

 mm Hg 



20 



5 

 



PA 



I — 



MMjuW 



M 



M 



RA 



process, venous return to the thorax may become ob- 

 structed as positive intrathoracic pressures are im- 

 posed on central venous pressures. However, until the 

 systemic venous valves (in the external jugular, sub- 

 clavian, axillary, and femoral veins) become incompe- 

 tent from central venous congestion, the rise in central 

 venous pressure is not transmitted to the peripheral 

 systemic veins. Therefore, during a forced expiration, 

 peripheral venous pressure rises only gradually, rep- 

 resenting the gradual filling of a distensible system 

 which is obstructed at its thoracic venous outlet. 



of the pulmonary vascular bed (397);/) the balance 

 of alveolar, pleural, left atrial, and pulmonary ar- 

 terial pressures which is required to make calculated 

 changes in resistance meaningful (354); and g) the 

 probable insignificance of alveolar surface tension in 

 determining pulmonary vascular resistance during 

 either positive (intrapulmonary) or negative (pleural) 

 pressure inflation of the lungs (398). This list also 

 serves to emphasize the fallibility of extrapolating 

 from artificial inflation of the lung to spontaneous 

 breathing. 



Inflation of the Lungs 



In 1 87 1, Quincke and Pfeiffer reported that positive 

 (intrapulmonary) inflation of the lungs decreases the 

 pulmonary blood volume and increases the resistance 

 to flow (324). Since then, physiologists have debated — 

 on the basis of a wide variety of experiments, models, 

 animal preparations, and intact animals — whether 

 resistance to perfusion increases as the lungs are in- 

 flated and if positive pressure inflation exerts the same 

 effects as negative (pleural) pressure inflation (39, 

 431). It now seems that the discordant results were to 

 be expected because of the nature of the experiments 

 and of the models (62). The principal bases for dis- 

 agreement seem to have been: a) the uncertain mean- 

 ing of the model under study (354); b) the failure to 

 distinguish between transmural pressure and luminal 

 pressure in determining vascular calibers (61); c) the 

 mechanical increase in resistance at exceedingly low 

 lung volumes, possibly due to kinking or collapse of 

 small vessels (61); d) the mechanical increase in re- 

 sistance at high degrees of pulmonary distension as 

 resistance vessels are stretched (354); e) the influence 

 of the pressure-volume behavior of the lung, and of 

 its enclosed pulmonary vasculature, on the resistance 



Positive Pressure Breathing 



In the isolated lung, or in the open-chest animal, 

 inflation of the lung from the collapsed position is 

 associated with an initial decrease in resistance as the 

 lung is moderately inflated, followed by an increase 

 in resistance as the lung is distended further (62). 

 Such U-shaped curves have been taken to represent: 

 a.) a decrease in resistance to blood flow as vessels in 

 the collapsed lungs are unkinked and opened (62), 

 followed by h) an increase in resistance due to both a 

 decrease in transmural distending pressure as alveolar 

 pressures increase (191, 215) and mechanical distor- 

 tion of the resistance vessels at the high lung volumes 



( 2I 5> 397)- 



In the closed-chest animal, positive pressure breath- 

 ing affects the pulmonary circulation by increasing 

 alveolar pressure and impeding systemic venous 

 return to the lungs: the systemic venous-right atrial 

 pressure gradient is decreased, thereby decreasing the 

 filling of the right ventricle and right ventricular out- 

 put (87, 253); the volume of the heart and pulmonary 

 vessels decreases. As a result of the combination of a 

 decreased right ventricular output and a sustained 

 left ventricular output, the pulmonary blood volume 



