Physiology, Pulmonary Circulatory System


Pulmonary circulation includes a vast network of arteries, veins, and lymphatics that function to exchange blood and other tissue fluids between the heart, the lungs, and back. They are designed to perform certain specific functions that are unique to the pulmonary circulation, such as ventilation and gas exchange. The pulmonary circulation receives the entirety of the cardiac output from the right heart and is a low pressure, low resistance system due to its parallel capillary circulation. The system can be divided into the following components:

  • The arterial circuit arises from the main pulmonary artery arising from the right ventricle and runs a course of only 5 cm before dividing into right and left main branches and many subsequent branches to form an extensive network of small arteries, arterioles, and capillaries. The pulmonary arteries are thinner (one-third the thickness of their counterpart systemic vessels) and have a larger diameter. The combined effect makes them much more distensible and compliant (approximately 7mL/mmHg).
  • The venous circuit begins with the venules that drain the capillaries. They join to form smaller veins and eventually merge to form the main pulmonary veins draining into the left atrium. Like the arteries, the pulmonary veins are thinner and more distensible than the counterpart systemic veins and accommodate more blood because of their larger compliance.
  • Lymphatics play a crucial role in maintaining a dry alveolar membrane and preventing accumulation of tissue fluid around the pulmonary circulation. They can be found close to the terminal bronchioles and drain the mediastinal lymphatics before emptying into the right lymphatic duct.

It is appropriate to mention that a similar system of lymphatics and vessels exists between the parietal and visceral pleurae, draining the pleural fluid which plays an important role in providing a viscous medium for expansion of lungs during their respiratory excursion. The large negative pleural pressure (approximately -4 to -7 mmHg) exists because of an efficient efferent venous and lymphatic system that keeps the alveoli closely tethered to the visceral pleura and prevents them from collapsing inwards.

In addition to the pulmonary circulation, the lung parenchyma receives oxygenated blood via the bronchial circulation (accounting for about ~1% of the cardiac output) which arises from the aorta, and thus left ventricle. The bronchial circulation has superifical and deep systems. The superficial system drains into the hemiazygos and azygos veins, which ultimately drain into the right heart with the systemic venous return. However, the deep circulation drains into the pulmonary vein and thus left ventricle. As a result, the deep bronchial system effectively functions as an arteriovenous shunt. However, its venous return to the left heart is minimal (0-0.5% of cardiac output) and does not affect cardiac output to any significant degree as volumes between right and left ventricles are nearly identicle. [1]

Issues of Concern

Pulmonary circulation is essential for the body to ensure a continuous supply of oxygenated blood. Any compromise can have grave consequences and lead to tissue dysfunction secondary to hypoxia.

Some of the common pathologies of the pulmonary circuit include but are not limited to the following:

Pulmonary edema: Any disturbance in the starling forces (see below, pathophysiology) operating in the pulmonary circulation can lead to an accumulation of fluid in the alveoli, impairing gas exchange, and causing respiratory distress. Pulmonary edema can either be cardiogenic or non-cardiogenic. Causes include elevated hydrostatic pressure (i.e heart failure), decreased serum oncotic pressure (i.e. low albumin), decreased lymphatic clearance (i.e. lymphedema), increased vessel permeability (i.e. inflammation), and decreased surfactant (i.e. prematurity).[2]

Pulmonary embolism: A dislodged clot from a distant source (most commonly a deep venous thrombus) can embolize to the pulmonary circuit and lead to ischemia and, if prolonged, infarction of the lung parenchyma as well as severely impaired gaseous exchange. It is important to note that the peripheral parenchyma is more prone to infarcation as it is purely reliant on the pulmonary circulation for oxygenation (see below, function).[3]

Pulmonary hypertension: An increase in the mean pulmonary artery pressure beyond 25 mmHg is known as pulmonary arterial hypertension. It leads to impaired gas exchange and commonly manifests as exertional dyspnea. If prolonged, it can lead to right ventricular stain and right heart failure, a phenomenon known as cor-pulmonale.[4]

Pleural effusion: A disturbance in the starling forces (see below, pathophysiology) of the pleural circulation can lead to accumulation of fluid in the pleural space, a phenomenon known as pleural effusion. This manifests as pleuritic chest pain and respiratory distress.[5]


The fetal circulation begins to form as early as 15 days after conception in the form of immature placental vessels and slowly grows to form a fully functional four-chambered heart, beating independently from the maternal circulation by the fourth week of gestation.[6]

The growing fetus receives its nutrients and excretes metabolic waste products via the placental vessels that connect the umbilical veins, which in turn drain into the inferior vena cava and then into the right atrium. The fetal circulation is designed to shunt blood across the liver and lungs during fetal life via the ductus venosus, foramen ovale, and the ductus arteriosus. The blood from the right atrium makes its way to the systemic circulation without actually reaching the lungs. The pulmonary vessels remain closed under high pressure, and it is only after birth as the newborn takes its first breaths that the pulmonary artery pressures fall, shunts existing in the fetal life close, and blood begins to enter the lungs for exchange of gases for the fetus is no longer dependent on the placental circulation. A failure in this process sometimes leads to persistent pulmonary hypertension, causing respiratory distress in the newborn. The condition requires multi-disciplinary management using supplemental breathing, artificial surfactant, and vasodilators to lower the pulmonary artery pressure.[7][8]


The pulmonary circulation has many essential functions. Its primary function involves the exchange of gases across the alveolar membrane which ultimately supplies oxygenated blood to the rest of the body and eliminates carbon dioxide from the circulation. The bronchial circulation provides oxygenated blood to the lung parenchyma. There is an overlap between the bronchial and pulmonary circulations in terms of oxygenating the lungs, especially near central regions. The peripheral aspects of the lungs becoming increasingly dependent on the pulmonary circulation and is more prone to infarction as a result. The low-pressure venous system and an intricate system of lymphatics ensure that there is no build-up of edema fluid in healthy lungs.


An understanding of the pressure gradients across the pulmonary circuit is important in realizing that minor derangements in these pressures can lead to adverse outcomes such as pulmonary edema and respiratory shunts.

The pressure gradients can be summarized as follows:

Chamber/Vessel/Pressure Gradient (systolic/diastolic) (in mmHg)

  • Right ventricle - 25/0
  • Pulmonary artery - 25/8
  • Pulmonary capillaries - 7/0
  • Left atrium/wedge pressure - 5/0

It is important to note that low pressures in the pulmonary capillaries allow for easy exchange of gases in the lung alveoli. The pressure in the left atrium is difficult to measure directly, and a surrogate pressure, known as the pulmonary capillary wedge pressure (PWP), is often used. PWP can differentiate between primary and secondary pulmonary hypertension. A high PWP suggests a cardiac origin, whereas a low PWP suggests a pulmonary origin.

At the time of exercise, there is a markedly increased blood flow which is accommodated by the pulmonary circulation in the following ways:

  • Recruiting and opening new capillary beds
  • Dilating existing vessels to up to twice their original diameter (recall that the pulmonary vessels are highly compliant) as well as increasing blood flow rate
  • Finally, increasing the pulmonary arterial pressure. The first two mechanisms compensate well enough such that in practice, the pulmonary artery pressure remains unchanged at times of increased blood flow.[9]

Zones of Pulmonary Blood Flow

A hydrostatic pressure gradient exists, by virtue of gravity, from the apex of the lung to the base: 23 mmHg (distributed as -15 mmHg from the level of the heart to the apex of the lung and +8 mmHg from the level of the heart to the base of the lung). This results in a 5-fold greater blood flow at the base of the lung as compared to the apex of the lung. Three zones of pulmonary blood flow can be delineated based on the pulmonary capillary pressure (Pcp)and the pulmonary alveolar air pressure (Ppac).

Zone 1: The Pcp is always less than the Ppac here, and there is no blood flow in the pulmonary capillary bed during any phase of the cardiac cycle. Zone 1 circuits are not seen in the normal lung and are only seen in certain conditions, such as after massive blood loss or if a person is breathing against a positive airway pressure (PEEP). PEEP, in basic terms, overventilates the lung and increases alveolar pressures in order to improve alveolar ventilation in an unhealthy lung.

Zone 2: Here the Pcp rises above the Ppac only during systolic blood flow, and so gas exchange occurs only during systole and not in diastole. Zone 2 blood flow is seen at the apices of the normal lung.

Zone 3: Here the Pcp remains greater than the Ppac in all phases of the cardiac cycle, allowing for an efficient exchange of gases. At the time of exercise, the pulmonary blood flow increases and all Zone 3 lung converts to Zone 2.[10]

Related Testing

N-Terminal Pro-BNP

This is a peptide released by the left ventricular myocardium in response to elevated filling pressures and blood volumes. It is a very sensitive and specific marker of cardiogenic edema. High levels of Pro-BNP strongly suggest a cardiogenic cause while low levels can effectively rule out a cardiogenic cause; however intermediate values have little significance and require further investigation.[11][12][13]

Swanz-Ganz Catheter

This is an invasive tool used to evaluate the pulmonary capillary wedge pressure (PWP). It entails the insertion a catheter from a peripheral access site to the pulmonary artery. A value greater than 18 mmHg is highly suggestive of a cardiogenic cause of pulmonary edema as it corresponds to an elevated left atrial pressure.[14]


Pulmonary edema is the accumulation of free fluid in the alveoli resulting in a decrease in the capacitance of the parenchyma and impairing gas exchange across the alveolar membrane. Acute onset pulmonary edema can lead to severe respiratory distress and death in 20 to 30 minutes.

To understand the pathophysiology of pulmonary edema, it is essential to understand the starling forces operating to maintain a homeostatic flow across the pulmonary capillary bed.

Outward Driving Force

7 mmHg (capillary hydrostatic pressure) + 8 mmHg (negative interstitial fluid pressure) + 14 mmHg (interstitial colloid osmotic pressure) = 29 mmHg

Inward Driving Force

28 mmHg (plasma colloid osmotic pressure)

Therefore, the net pressure of +1 mm Hg drives fluid out of the pulmonary capillaries and is taken away by an efficient network of pulmonary venules and lymphatics.

An imbalance in these forces in the form of raised pulmonary hydrostatic pressure (for diastolic: left ventricular failure), decreased plasma osmotic pressure (e.g., protein-losing enteropathy) or increased capillary membrane permeability (e.g., infections like pneumonia, inhalation of toxic gases like carbon monoxide) leads to pulmonary edema.[2]

Pulmonary Edema Protection Factor

In accordance with the starling forces, excess edema fluid will accumulate when the interstitial tissue fluid overwhelms the capillary osmotic pressure (>28 mmHg).

Since the baseline left atrial pressure (and hence the pulmonary capillary wedge pressure) is 7 mmHg, this gives a protective factor of 21 mmHg, i.e., the left atrial pressure can rise by an additional 21 mmHg before pulmonary edema develops. However, beyond this value, the rate of accumulation of fluid is rapid, and pressures beyond 30 mmHg can lead to death due to pulmonary edema in 20 to 30 minutes (i.e. acute cardiogenic shock). However, in long-standing cases (i.e. chronic mitral stenosis), the pulmonary capillary wedge pressure may be as high as 40 mmHg before edema develops as both the heart and lungs have had time to compensate.[15]

Starling Forces Equation

Starling forces can be used to determine the direction of net water movement, thus evaluating filtration out of or absorption into the capillary. The starling equation for fluid flux (volume per time) can be found below.

Jv = Kf [(Pc-Pi)-σ(Πc - Πi)]

Jv: net fluid direction, Kf: filtration coefficient (vascular permeability to water, e.g. inflammation, burns); P: hydrostatic pressure, Π:oncotic pressure; c: capillary, i: interstitium, σ: reflection coefficient (movement of protein across the membrane)

In the lungs there are additional forces to be considered, alveolar air pressure and surface tension, with air pressure driving fluid into the vasculature, and surface tension pulling water into the lungs.

Another factor to consider is the net filtration pressure (NFP). This NFP reflects the driving force: Net Filtration Pressure = [(Pc-Pi)-(Πc - Πi)]

Clinical Significance

Acute pulmonary edema can have a cardiogenic or non-cardiogenic origin. The differentiation can be made clinically. Cardiogenic edema is commonly preceded by an acute coronary event and is usually associated with elevated left ventricular filling pressures. Non-cardiogenic causes are commonly included in the umbrella term of acute respiratory distress syndrome (ARDS) which is associated with wide-spread systemic inflammation and release of cytokines causing increased permeability of the pulmonary alveolar capillaries and causing an exudative edema as compared to a transudative edema as seen in acute heart failure. ARDS is commonly seen in settings of systemic sepsis, burns, or massive blood transfusions.

Patients commonly present with tachypnea and chest pain. An arterial blood gas analysis shows respiratory alkalosis and hypoxemia. Chest X-ray changes suggestive of bilateral infiltrates are an early and hallmark finding in ARDS and are evident in the first 24-hours of presentation. Findings in cardiogenic pulmonary edema evolve over 2 to 3 days and show considerable overlap with that of ARDS. N-pro BNP levels may be used to differentiate between the two etiologies if there is uncertainty. Further management of ARDS relies on early diagnosis and management of underlying cause of systemic inflammation such as antibiotics for infections or conservative fluid resuscitation in case of burns and acute pancreatitis. Management of cardiogenic edema relies on the early mobilization of fluid and reduction of left ventricular fluid overload using diuretics and vasodilators in addition to treating the cause of decompensated heart failure.[16][17]

Management of pulmonary edema depends a lot on the etiology. Ventilatory support, and oftentimes diuretic therapy, forms an essential cornerstone of all cases. Use of low tidal volume and positive end-expiratory pressure ventilation has been shown to significantly improve mortality.[18]

Article Details

Article Author

Vardhmaan Jain

Article Author

Stephen Bordes

Article Editor:

Abhishek Bhardwaj


5/24/2020 7:53:33 PM



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