PERFUSION



The pulmonary vascular bed serves as a source of nutritive blood to the alveolar membrane, but its most important role is in pulmonary gas ex­change. It delivers the entire venous return to the pulmonary capillary bed, where exchange of 02 and C02 occurs. While it receives the same blood flow per minute as the systemic circulation, there are many differences between the vascular beds. First, since the pulmonary vascular resistance cal­culated as pulmonary artery pressure - left arterial pressure cardiac output is also only about one tenth of systemic vascular resistance, the pressure in the pulmonary vascular bed is consequently only one tenth of that in the systemic circulation. Second, all structures within the thorax, including the pulmonary vas­cular bed, the heart, and the great vessels, are ex­posed to the surrounding pressures, both pleural and alveolar, which vary during respiration.

Many factors affect the pressure-flow relation­ships in the pulmonary circulation. When blood flow increases in upright man, as during exercise, pulmonary vascular pressure increases, but pul­monary vascular resistance actually falls owing to the ability to recruit new vessels and distend the ones already open. This allows large increases in blood flow with lesser increases in pressure, thus preventing the transudation of fluid into the lungs due to a higher microvascular pressure. Pulmo­nary vascular resistance is also affected by lung volume and is lowest at FRC.

In addition to these passive influences, a num­ber of factors actively affect pulmonary vascular tone. The most important is alveolar hypoxia, which results in constriction of the perfusing ar­tery by asyet-unknown mechanisms. This may be a conservative mechanism when alveolar hypoxia is localized, since reduction in perfusion to poorly ventilated alveoli reduces the abnormality of gas exchange, which is otherwise inevitable. During generalized hypoxia, its beneficial nature is not always apparent, as in sojourners at high altitude, in whom it may be a major cause of pul­monary edema. Acidosis causes a vasoconstrictor response of lesser magnitude. Other vasoactive compounds produced in the body, such as pros­taglandins and adrenergic substances, may also alter pulmonary vascular tone.

Blood entering the lung at the hilum must either be pumped upward toward the lung apex or flow down with the help of gravity toward the base. Thus pulmonary arterial pressures display great variation from the apex to the lung base, whereas the alveolar pressure is the same throughout the lung. The blood flow through any alveolus and therefore the distribution of blood in the lung de­pend on the interaction of the vascular pressure across the capillary bed (arterial-venous differ­ence) and the surrounding alveolar pressure (Fig. 17-4). At the apex, pulmonary artery pressure is usually just able to overcome alveolar pressure. However, a fall in arterial pressure or any rise in alveolar pressure (positive pressure breathing) may cause alveolar pressure to exceed arterial pressure, with cessation of flow. This is known as Zone 1 conditions. Below this lies Zone 2, where the alveolar pressure is less than arterial pressure but greater than venous pressure. Thus, blood flow depends on the difference between arterial pressure and the surrounding alveolar pressure. Blood flow continues to increase with increasing arterial pressure and eventually reaches a point, Zone 3, where venous pressure exceeds alveolar pressure and flow becomes dependent on arterial-venous pressure difference.