Regulation of pulmonary blood flow

Okay - so pulmonary circulation starts with the right ventricle.

From there - blood is pumped into the large pulmonary trunk, which splits to form the two pulmonary arteries – one for each lung.

The pulmonary arteries divide into smaller arteries known as pulmonary arterioles and then eventually into pulmonary capillaries which surround the alveoli - which are the millions of tiny air sacs where gas exchange happens.

At that point, oxygen enters the blood and carbon dioxide enters the alveoli.

The pulmonary capillaries drain into small veins that join to form the two pulmonary veins exiting each lung, and these pulmonary veins complete the circuit by delivering oxygen-rich blood into the left atrium.

Pulmonary blood flow (Q) is the volume of blood usually in milliliters, that’s being pumped out of the right ventricle over time, usually in 1 minute.

Said differently, pulmonary blood flow is the cardiac output of the right ventricle.

And cardiac output is the stroke volume, the volume of blood pumped per beat from the right ventricle of heart, expressed as mL per heartbeat; multiplied by the heart rate in beats per minute.

Now pulmonary blood flow is directly proportional to the difference in pressure between the pulmonary artery and the left atrium, or the delta P; and inversely proportional to the resistance of the pulmonary vasculature (R).

The blood pressure and resistance in the pulmonary circulation is normally much lower than the systemic blood pressure.

The normal pulmonary artery pressure is about 25/10 mmHg with a mean arterial pressure of 15 mmHg.

If pulmonary blood flow needs to change in response to a situation or vasoactive substance, it’s done by changing the resistance of the vasculature, particularly the arterioles, which is related to the diameter of the blood vessels.

Specifically, a decrease in the diameter of the arterioles causes an increase in resistance, and that leads to a decrease in blood flow.

On the other hand, an increase in the diameter of the arterioles causes a decrease in resistance, and that leads to an increase in blood flow.

Now - in the lungs, tiny capillaries surrounding the alveoli are called alveolar vessels; whereas those that located further away, like arterioles, are called extra-alveolar vessels.

And the sum of the resistance in both the alveolar blood vessels and extra-alveolar blood vessels determines the total resistance of the pulmonary vasculature.

Alveolar blood vessel resistance depends on alveolar air pressure because the blood vessels share a basement membrane with alveoli and therefore feel the pressure directly.

As a result, if alveolar air pressure is high, that can crushed or close up an alveolar blood vessel, and if alveolar air pressure is low, that can allow the alveolar blood vessel to open up.

In contrast, extra-alveolar blood vessel resistance depends on pressure in the pleural space which lies between the parietal pleura, which is stuck to the chest wall, and the visceral pleura, which is stuck to the lungs.

Pressure within the pleural space is established by two main opposing forces. One is the muscle tension of the diaphragm and chest wall which contract and expand the thoracic cavity outwards, and the other is the elastic recoil of the lungs, which try to pull the lungs inward.

The two forces pull on each other creating a slight vacuum in the pleural space - which results in a pressure of -5 centimeters of water relative to the pressure of 0 centimeters of water in both the thoracic cavity and within the alveoli of the lungs.

Based on this, one way to control pulmonary vasculature resistance is through changes in lung volume.

When lung volume is high, like at the end of maximum inspiration, alveoli are extended and the alveolar pressure increases, pressing down on and applying increased pressure on the alveolar blood vessels. The result is the alveolar vessels constrict and resistance increases.

But also during maximum inspiration, pleural pressure is negative and that means that lung tissue expands outward, pulling open the extra-alveolar vessels and decreasing their resistance.

When lung volume is low, like at the end of maximum expiration, everything is reversed.