Part of the TeachMe Series

Pulmonary Circulation

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Original Author(s): Chloe Hill
Last updated: 13th February 2021
Revisions: 26

Original Author(s): Chloe Hill
Last updated: 13th February 2021
Revisions: 26

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The lungs have both a bronchial and pulmonary circulation. The bronchial circulation supplies O2 and nutrients to meet the metabolic requirements of the lungs.

The pulmonary circulation carries deoxygenated blood away from the heart to the lungs’ alveoli to undergo gas exchange and returns oxygenated blood back to the heart.

This article will consider the functions of both the bronchial and the pulmonary circulation and their special adaptations.

Overview of the Pulmonary Circulation

Deoxygenated blood leaves the right ventricle of the heart through the pulmonary valve and enters the pulmonary trunk. This divides into the right and left pulmonary arteries.

In the lungs the arteries divide further into smaller capillaries at the alveoli, allowing gas exchange to take place. Oxygen diffuses from the alveoli into the pulmonary capillaries while carbon dioxide diffuses from the capillaries into the alveoli.

This newly oxygenated blood leaves the lungs through the pulmonary veins to the heart’s left atrium, completing the pulmonary cycle. The blood is then distributed around the body via the systemic circulation.

Fig 1 Pulmonary circulation and alveolar capillaries

Since the right heart cannot work independently of the left heart, both the right and left ventricle must have the same cardiac output to prevent blood from building up in either the systemic or pulmonary circulation. This means the pulmonary circulation must be able to accept the entire cardiac output (5L).

 Adaptations

To facilitate high volumes of blood flowing through it, the pulmonary circulation has several adaptations.

  • Low pressure – The pulmonary circulation is a lower pressure system (mean arterial pressure of 5-15mmHg) compared to the systemic circulation (mean arterial pressure of 93mmHg). This is because the pulmonary arteries have thin vascular walls and high compliance, allowing them to carry more blood.
  • Low resistance – The pulmonary vessels are shorter and wider compared to vessels in the systemic circulation. Additionally, pulmonary capillaries run in parallel, rather than in series like the systemic circulation. There is also relatively little smooth muscle in the arterioles, which helps to reduce arterial tone. These properties allow the pulmonary circulatory system to operate at a lower resistance.

To promote efficient gas exchange with the alveoli and produce the maximum O2 and CO2 transport capacity, the pulmonary capillaries have:

  • A large surface area available for gas exchange due to the branching structure of the pulmonary tree.
  • A short diffusion distance – The combined thickness of the alveolar endothelium and the capillary endothelium is approximately 0.3µm. Moreover, the very high density of capillaries also means that the alveolar wall is always close to a capillary.
  • Hypoxic pulmonary vasoconstriction – This is an important mechanism which responds to low alveolar oxygen levels to increase the efficiency of gas exchange. See the Ventilation Perfusion Matching sub-section.

Ventilation Perfusion Matching

For efficient oxygenation of the blood, it is important that the ventilation of the alveoli is matched by their perfusion, with an optimal V/Q ratio of 0.8-1.0.

To maintain this V/Q ratio, blood must be diverted away from poorly ventilated alveoli and directed towards better-ventilated alveoli. This is ensured by hypoxic pulmonary vasoconstriction, whereby small pulmonary arteries constrict to redirect blood flow from poorly ventilated areas of the lung to better-ventilated lung areas.

Formation of Tissue Fluid

Starling forces determine fluid formation in tissues. The increased hydrostatic pressure of the blood in the capillaries pushes fluid out of the vessels at the arterial end. In contrast, oncotic pressure (exerted by large molecules such as plasma proteins) draws fluid back into the capillary at the venous end.

The low capillary pressure of the pulmonary vessels minimises fluid formation in the lungs. This means that only a small amount of fluid leaves the capillaries, and nearly all of this is reabsorbed. This a protective mechanism against fluid formation in the lungs.

Overview of the Bronchial Circulation

The bronchial circulation is not involved in gas exchange; its role is to supply fully oxygenated arterial blood to the lung tissues themselves.

The bronchial arteries receive blood from the thoracic aorta and the upper intercostal arteries. They enter the lung at the hilum and branch at the main bronchus.

One portion of these arteries supply the lower trachea, extrapulmonary airways, and supporting structures and drain into the superficial bronchial veins. These veins join the azygous (from the right lung), the accessory hemizygous or intercostal vein (from the left lung), before reaching the inferior vena cava to enter the right heart.

The bronchial arteries also supply the intrapulmonary airways up to the level of the terminal bronchioles, where they form extensive anastomoses with the pulmonary vasculature. This portion drains via deep bronchial veins within the lung and joins the pulmonary veins to travel to the left heart.

Clinical Relevance – Right Heart Failure

In chronic hypoxia, there is widespread vasoconstriction of the pulmonary vessels due to (the normally protective) hypoxic pulmonary vasoconstriction. This chronic hypoxic vasoconstriction causes a chronic increase in vascular resistance, leading to pulmonary hypertension.

This increases the afterload on the right ventricle, causing right ventricular hypertrophy and right-sided heart failure. Chronic hypoxia may also occur at high altitudes, or as a consequence of lung disease such as emphysema.

Fig 2 Right ventricular hypertrophy caused by pulmonary hypertension

Clinical relevance – Pulmonary Oedema

If the pressure inside the pulmonary capillaries rises, then more fluid will leave the capillaries. This can occur if the left atrial pressure rises (such as in mitral valve stenosis or left ventricular failure). Not all of this extra tissue fluid will be reabsorbed, and therefore builds up in the lung tissue. This is known as pulmonary oedema.

Pulmonary oedema impairs gas exchange by increasing the length of the diffusion pathway. It can be treated using diuretics and by treating the underlying cause.