Pulmonary Blood Flow
I. "Dual" Circulation of the lung:
A. Bronchial circulation - arterial supply of tracheobronchial tree (as far as the terminal bronchioles), and other thoracic structures. About 2% of cardiac output. Some connections with pulmonary circulation, but normally no effect on the pulmonary circulation. Part of venous drainage is via the pulmonary veins (Levitzky Fig. 4-2).
B. Pulmonary circulation - site of gas exchange between alveolar air and capillary blood. Mixed venous blood in pulmonary artery.
II. Functional anatomy of the pulmonary circulation:
A. Main pulmonary artery is much thinner-walled than the aorta. Much less smooth muscle in the walls of the vessels of the pulmonary arterial tree. No highly muscular "arterioles".
1. Consequences of anatomy of pulmonary arterial tree:
a. Low resistance to pulmonary blood flow. Pulmonary vascular resistance (PVR) is about 1/10 of systemic vascular resistance (SVR) (Levitzky Fig. 4-1).
b. Pulmonary vessels are more distensible than systemic vessels.
c. Distribution of pulmonary resistance: about 30% arteries, 40% capillaries; 30% veins. This can change with lung inflation or during hypoxia.
2. Consequences of differences in pressure between left and right circuits:
a. Greater hydrostatic forces must be overcome by left side in order to perfuse greater vertical distances.
b. Higher pressure head makes regulation of left circuit possible. Can alter distribution of cardiac output among different vascular beds.
c. Greater stroke volume and metabolic demand of left ventricle.
B. Pulmonary capillaries in the adult: 280 billion capillaries supply 300 million alveoli - 50-100 m2 surface area. Diffusion distance normally less than ½ micron.
III. Pulmonary vascular resistance:
A. Low intravascular pressures and high vascular distensibility lead to a much greater importance of extravascular effects ("passive factors") on the pulmonary circulation.
1. Must consider transmural pressure; consider two different kinds of pulmonary blood vessels (Levitzky Fig. 4-3).
a. Small "alveolar" vessels: exposed to alveolar pressure; stretched and compressed as lung expands.
b. Larger "extra-alveolar" vessels: exposed to intrapleural pressure traction of lung parenchyma.
c. Therefore as lung expands (Levitzky Fig. 4-3): Alveolar vessels increased R; Extra- alveolar vessels decreased R. As lung volume decreases, the opposite occurs. Therefore pulmonary vascular resistance is lowest near the functional residual capacity and increases if lung volume increases or decreases.
2. Although pulmonary vascular resistance is very low at rest, it can decrease further, as in exercise, during which blood flow increases (Levitzky Fig. 4-5).
a. Possible mechanisms (Levitzky Fig. 4-6)
i. Recruitment
ii. Distensibility
b. Both mechanisms probably occur
B. Active factors influencing pulmonary vascular resistance:
1. Neural
a. Sympathetic nerves to larger vessels - NE released. Effects somewhat controversial - most likely increases pulmonary vascular resistance and decreases distensibility of larger vessels.
b. Parasympathetic - Ach decreases PVR if tone elevated.
2. Humoral
a. Increase PVR: Norepinephrine, alpha adrenergic agonists, serotonin, prostaglandins F2 and E2, angiotensin, endothelin, alveolar hypoxia (hypoxic pulmonary vasoconstriction), alveolar hypercapnia, low pH of mixed venous blood. Histamine constricts pulmonary veins.
b. Decrease PVR: Acetylcholine, beta adrenergic agonists, bradykinin, prostaglandin E1 and I2 (prostacyclin), nitric oxide.
IV. Regional distribution of pulmonary blood flow:
A. 133Xe - insoluble in blood; when reaches pulmonary capillaries released into alveoli. Distribution of radioactivity reflects the distribution of blood flow.
B. In the normal upright lung blood flow increases from top of lung to bottom. This is due to hydrostatic pressure effects and greater recruitment and distention of dependent lung (Levitzky Fig. 4-8) vessels. Intravascular pressures are greater in lower lung regions, so there is more recruitment and distention and therefore less resistance to blood flow.
V. “Zones of the Lung” (Levitzky Fig. 4-9)
|
|
Driving Pressure for Blood Flow |
|
Zone 1: PA >Pa> Pv |
- |
|
Zone 2: Pa >PA> Pv |
Pa - PA |
|
Zone 3: Pa >Pv> PA |
Pa - Pv |
VI. Hypoxic Pulmonary Vasoconstriction (Levitzky Fig. 4-10):
A. Active local response to alveolar hypoxia (and probably atelectasis).
B. Appears to occur at precapillary site.
C. Mechanism - likely a direct effect on vessels. Hypoxia appears to decrease an outward potassium current, which causes the pulmonary vascular smooth muscle to contract.
D. Advantage of response. Lowers intrapulmonary "shunt" flow by diverting blood flow away from poorly ventilated alveoli. Improves matching of ventilation and perfusion.
VII. Pulmonary Edema-causes (Levitzky Fig. 4-11):
Increased capillary permeability
Increased capillary hydrostatic pressure
Decreased interstitial pressure
Decreased plasma colloid oncotic pressure
Increased interstitial colloid oncotic pressure
Lymphatic insufficiency
Copyright © 2000 M. G. LEVITZKY
Last updated Monday, July 15, 2013 4:10 PM
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