Introduction
The lung receives the entire cardiac output, accommodating a large amount of blood. It is low pressure and low-resistance system. The pulmonary artery has its origin in the right ventricle. The pulmonary artery of pulmonary circulation has deoxygenated blood, and its function is gas exchange. Bronchial arteries arise from the aorta of systemic circulation having oxygenated blood, and its function is to supply nutrition to the respiratory tree up to the terminal bronchiole.
Pulmonary Arteries:
The main pulmonary artery measures approximately five centimeters and is entirely enveloped within the pericardium. The artery at the level of the fifth thoracic vertebra divides into the longer right and the shorter left branches that supply blood to the lungs. The left pulmonary artery goes above the left main bronchus to enter the hilum and divide into two branches - ascending and descending. The ascending branch further bifurcates immediately into an apicoposterior branch and an anterior segmental branch which supply the left upper lobe. A branch that arises from the descending branch goes to the lingula, and further, the descending branch divides into two segmental arteries - a superior and an inferior lingular segmental artery. The superior segmental artery is the next branch arising from the descending branch, which supplies the superior segment of the left lower lobe. And the consecutive branches supply the remaining areas of the left lower lobe.
The right pulmonary artery goes under the arch of the aorta, and before entering the hilum, it bifurcates into the ascending, truncus anterior, and descending, interlobar branches. The ascending branch gives rise to apical, anterior, and posterior segmental branches. The interlobar artery gives off the middle lobe artery, which further separates into two branches - the lateral and medial branches, and the right lower lobe artery, which supplies the superior part of the right lower lobe. As on the left side, consequent branches supply the remaining four segments of the right lower lobe.
Bronchial Arteries:
The bronchial arteries vary in number and place of origin. In approximately 70 percent of cases, the bronchial arteries originate from the descending thoracic aorta, between the fifth and sixth thoracic vertebra levels. In addition, two to four bronchial arteries may arise independently or from a common trunk.
The right bronchial artery usually arises from a common stem, with the first aortic intercostal arising from the posteromedial aspect of the descending part of the aorta. A superior and inferior branch exists, originating from the descending thoracic aorta. These arteries travel down to the hilum, dividing parallel and close to the bronchus to reach the peripheral airways. The diameter of these arteries is small, approximately 1 to 1.5 mm at its origin within the mediastinum. Anomalous bronchial arteries, known as bronchial arteries that originate outside the levels of the fifth and sixth thoracic vertebra, are found in approximately twenty-one percent of patients with hemoptysis. In most cases, these anomalous arteries arise from the aortic arch.
Pulmonary circulation is influenced by intrathoracic pressure. It acts as a filter as it prevents emboli from reaching systemic circulation due to the presence of a fibrinolytic system. They have rapidly tapered ends which act as sieves to trap the emboli and blood cells, fat cells, cancer cells, and gas bubbles.
What Is the Significance of Hypoxic Pulmonary Vasoconstriction?
Hypoxic pulmonary vasoconstriction (HPV) plays an important role in patients presenting with heterogeneous respiratory diseases such as atelectasis, chronic obstructive pulmonary disease (COPD), pneumonia, and acute respiratory distress syndrome (ARDS). In the case of severe hypoxemia, it is reduced by maintaining the ventilation-to-perfusion (V/Q) ratio in different parts of the lungs. Whereas, when there is severe hypoxia, such as high altitude, sleep apnea, and pulmonary fibrosis, HPV can be detrimental, resulting in pulmonary hypertension and acute cor pulmonale owing to a gradual increase in right ventricular afterload. HPV also plays a crucial role during one-lung ventilation (OLV) and pneumatological procedures to decrease the intrapulmonary shunt and maintain blood oxygenation levels.
What Are the Factors that Can Increase Hypoxic Pulmonary Ventilation?
HPV is enhanced by
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Acidosis.
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Beta-adrenergic blockade.
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Epidural blockade.
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Low-dose Serotonin.
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Inhibition of cyclo-oxygenases such as Aspirin and Indomethacin or Nitric oxide (NO) synthase such as L-arginine analogs.
These two effects indicate that HPV is attenuated acutely by endogenous NO and prostacyclin.
What Are the Factors that Decrease Hypoxic Pulmonary Ventilation?
HPV is decreased by a variety of mediators of the blood or secreted from lung parenchyma, like
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Substance P, a neuropeptide.
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Calcitonin gene-related peptide.
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Atrial natriuretic peptides.
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Vasodilators like prostacyclin and NO are derived from the endothelium.
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Alpha-adrenergic blockade.
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Beta-adrenergic stimulation.
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Increased left atrial pressure.
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Increased alveolar pressure.
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Peripheral chemoreceptor stimulation.
Conclusion
It is a protective physiological mechanism that redirects the blood flow away from the regions of hypoxia to the regions with better ventilation and oxygenation. Factors influencing HPV are pH, partial pressure of carbon dioxide, age, temperature, and iron status. It is a physiological process to match the regional ventilation-perfusion and plays a pivotal role in maintaining oxygenation. It causes vasoconstriction of small pulmonary vessels and dilation of large systemic vessels. It plays a significant role in chronic respiratory diseases such as pneumonia or chronic obstructive pulmonary disease. Maintaining normal gaseous exchange depends on the ventilation-perfusion ratio, which is influenced by hypoxic pulmonary vasoconstriction. The heterogeneity of the lungs in these diseases refers to a local, regional response, such as with HPV, which helps in adequate long-term oxygenation. Inadequate delivery of supplemental oxygen in such cases, along with some drugs, can attenuate HPV, aggravate the V/Q mismatch, and, thereby, lead to deterioration in oxygenation. Chronic exposure to areas of high resistance also contributes to right ventricular hypertrophy, pulmonary hypertension, and cor-pulmonale. It also plays a crucial role in acute respiratory diseases such as asthma, pneumonia, pulmonary edema, and pulmonary emboli. It is likely to offer a beneficial effect in these clinical settings by redirecting pulmonary blood flow to areas of the better-ventilated lung, thereby improving the V/Q matching.
