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. Alveolar pressure decreases, dilating the alveolar vessels, and decreasing alveolar blood vessel resistance.Meanwhile pleural pressure becomes less negative, compresses the extra-alveolar blood vessels, increasing extra-alveolar blood vessel resistance.

So, since total pulmonary resistance is the sum of alveolar vessel and extra-alveolar resistance, total pulmonary resistance is highest at either lung volume extreme: at maximum inspiration, when alveolar resistance is high; and at maximum expiration when extra-alveolar resistance is high.

Total pulmonary resistance is the lowest when vessel resistances are at their lowest which is at passive expiration, that’s the point just before either forced expiration or inspiration occurs.

Now another way to control pulmonary vasculature resistance is by vasoconstriction of the pulmonary arterioles which increases resistance; and vasodilation of the pulmonary arterioles, which decreases resistance.

Vasoconstriction and vasodilation are controlled by the smooth muscle that wraps around the arterioles. A trigger for smooth muscle contraction is a decrease in the partial pressure of O2 within the alveoli - this is called hypoxic vasoconstriction.

Typically, the partial pressure of O2 is 100 millimeters of mercury (mmHg). But, let’s say some area in the lung is diseased or damaged, like a pneumonia in the left lower lobe.

The partial pressure of O2 in those alveoli may be only 70mmHg, and that would decrease O2 delivery to the blood flowing to that region of the lung.

So what happens is that in response to the low levels of oxygen in the alveoli, the smooth muscle that’s wrapped around the arterioles just upstream of the alveoli, start to vasoconstrict.

This shuttles blood away from those damaged areas of the lung, and towards healthy lung tissue where the partial pressure of O2 is higher and the blood can be oxygenated more efficiently.

But hypoxic vasoconstriction can also happen globally throughout the entire lung, like at high altitudes; or during widespread lung disease, like emphysema; or in fetal circulation when the baby isn’t breathing.

These can all cause a decrease in partial pressure of oxygen throughout the lungs and that can lead to widespread vasoconstriction of pulmonary arterioles.

That leads to an increase in pulmonary vascular resistance, and increased resistance makes it harder for the right ventricle to pump out blood – a bit like pushing water through a narrow pipe as opposed to a wider one, so blood flow decreases.

To make the same amount of blood flow through the pulmonary arterioles, the right side of the heart has to generate increased pressure.

In chronic situations, that results in pulmonary hypertension. In fetal circulation, only about 15% of the blood from the right ventricle actually flows to the lungs and this lower level of blood flow is maintained by diverting the remainder of the blood to the left side of the heart so that it bypasses the lungs.In addition to hypoxia, another smooth muscle regulators is arachidonic acid, a 20-carbon fatty acid found in cellular membranes of many cells throughout the body.

In response to cellular injury and inflammation, arachidonic acid can be metabolized by some cells using the cyclooxygenase pathway.

The cyclooxygenase pathway results in thromboxane A2 and prostaglandin I2 - which are vasoactive metabolites that bind to and affect the smooth muscle cells.

Thromboxane A2 is produced by leukocytes in lung tissues and causes vasoconstriction, while prostaglandin I2 is produced by lung endothelial cells and causes vasodilation.

In addition, endothelial cells of the pulmonary vasculature produce nitric oxide. The nitric oxide then enters nearby smooth muscle cells and causes them to vasodilate.

##SummaryOK, so to recap: Pulmonary blood flow is the cardiac output of the right ventricle. It can be calculated using the formula Q= the difference in pressure between the pulmonary artery and the left atrium (delta P)/the resistance of the pulmonary vasculature (R).

The resistance of the vasculature can be changed by lung volume and vasoactive substances which can constrict or dilate the vasculature to ultimately regulate the pulmonary blood flow.

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