Physiology, Pulmonary Circulatory System


Article Author:
Vardhmaan Jain


Article Editor:
Abhishek Bhardwaj


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
10/27/2018 12:31:49 PM

Introduction

Pulmonary circulation includes the 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, like exchanging gases in the lungs and acting as a reservoir for the storage of blood amongst others. The pulmonary circulation is divided into the following components:

  • Arterial circuit - It begins with the main pulmonary artery arising from the right ventricle and runs a course of only 5 centimeters before branching off into the right and left main branches and many subsequent branches to form an extensive network of small arteries and arterioles which culminate in the pulmonary capillaries. The pulmonary arteries are much 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 ), allowing them to accommodate a larger volume of blood in a limited amount of space
  • Venous circuit: It begins with the venules which 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:  The lymphatics play a crucial role in maintaining a “dry alveolar membrane” and preventing accumulation of tissue fluid around the pulmonary circulation. They begin close to the terminal bronchioles and drain the mediastinal lymphatics to culminate near the right lymphatic duct eventually.

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, the lung parenchyma receives oxygenated blood via the bronchial vessels (accounting for about 1% to 2 % of the cardiac output) arising from the left ventricle which ultimately drains into the left atrium after forming the bronchial veins. Hence, it is important to note that the cardiac output of the left ventricle is approximately 1% to 2 % greater than that of the right ventricle.[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 operating in the pulmonary circulation can lead to an accumulation of fluid in the alveoli, impairing gas exchange and causing respiratory distress.[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.[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 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]

Development

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 separately from the maternal circulation by the fourth week of gestation.[6]

The growing fetus gets its nutrients and excretes its 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 thus eventually 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 pressure falls, the 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 vaso-dilators to lower the pulmonary artery pressure.[7][8]

Function

Pulmonary circulation is involved in many essential functions. The primary function is the exchange of gases across the alveolar membrane which ultimately supplies oxygenated blood to the rest of the body and is also the chief mechanism by which the body eliminates carbon dioxide. Bronchial circulation provides oxygenated blood to be consumed by the lung parenchyma to carry out its own metabolic functions. The low-pressure venous system and an intricate system of lymphatics ensure that there is no build-up of edema fluid in the lungs.

Mechanism

The understanding of the pressure gradients across the pulmonary circuit is important to realize the fact that minor derangements in these pressures can lead to adverse outcomes like 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 the low pressure in the pulmonary capillaries allows for easy exchange of gases in the lung alveoli. Also, the pressure in the left atrium is difficult to measure directly, and a surrogate pressure, known as the pulmonary capillary wedge pressure, is often used.

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. This is about 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.

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 parts of the lung receive zone 3 blood flow.[10]

Related Testing

N-Terminal Pro-BNP

This is a peptide released by the left ventricular myocardium in response to elevated filling pressures and raised blood volumes and is a very sensitive and specific marker of the cardiogenic cause of pulmonary edema. High levels have been shown to strongly suggest a cardiogenic cause while low levels have been used to successfully 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 method of inserting a catheter from a peripheral access site to reach the pulmonary artery and ultimately evaluate the pulmonary capillary wedge pressure. A value greater than 18 mmHg has been shown to be highly suggestive of a cardiogenic cause of pulmonary edema (corresponding to raised left atrial pressures).[14]

Pathophysiology

Pulmonary edema is an 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 to 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. However, in long-standing cases like chronic mitral stenosis, the pulmonary capillary wedge pressure may be elevated to values up to 40 mmHg before edema starts to develop.[15]

Clinical Significance

Acute pulmonary edema can have a cardiogenic or non-cardiogenic origin. The differentiation can be done clinically based on the clinical settings in which it arises. 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.

Management of pulmonary edema depends a lot on the etiology. Ventilation support forms an essential cornerstone of all cases and a target saturation of 88% to 92%, and a Po2 level of 60 to 80 mm Hg is a modest approach for management of hypoxia. Use of low tidal volume and judicious use of positive end-expiratory pressure ventilation has been shown to significantly improve mortality in ARDS.[16]

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.[17][18]


Interested in Participating?

We are looking for contributors to author, edit, and peer review our vast library of review articles and multiple choice questions. In as little as 2-3 hours you can make a significant contribution to your specialty. In return for a small amount of your time, you will receive free access to all content and you will be published as an author or editor in eBooks, apps, online CME/CE activities, and an online Learning Management System for students, teachers, and program directors that allows access to review materials in over 500 specialties.

Improve Content - Become an Author or Editor

This is an academic project designed to provide inexpensive peer-reviewed Apps, eBooks, and very soon an online CME/CE system to help students identify weaknesses and improve knowledge. We would like you to consider being an author or editor. Please click here to learn more. Thank you for you for your interest, the StatPearls Publishing Editorial Team.

Physiology, Pulmonary Circulatory System - Questions

Take a quiz of the questions on this article.

Take Quiz
Which of the following properties of the pulmonary circulation allows is to carry a higher volume of blood in a smaller network of vessels as compared to the systemic circulation?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following parameters can be used to differentiate cardiogenic from non-cardiogenic causes of pulmonary edema?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 32-year-old man presents to the emergency department after a high-velocity road traffic accident where he was the restrained driver. On arrival, he is unconscious and is actively losing blood from open fractures of the upper and lower extremities. Pulse rate is 110/min, blood pressure 70/40 mmHg in the right brachial artery, and the respiratory rate 31/minute. Which of the following best describes the blood flow circuit in the apices of his lungs?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following components of the circulation carries the largest volume of blood?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 42-year-old man with a long-standing history of alcohol use syndrome presents to the emergency department with a two-hour history of severe epigastric pain radiating to the back. His wife reports that he has been binge drinking for the past 3 days and has not had anything to eat. He is alert, awake but in visible pain and respiratory distress. On the way to the hospital, he has had two episodes of non-blood tinged vomitus. He has not had any bowel movements in the past two days. Vitals are significant for a pulse rate of 104/min and regular, blood pressure of 90/60 mmHg in the right brachial artery, respiratory rate of 32/min. He is in marked respiratory distress. Chest x-ray shows bilateral ground glass opacities. Which of the following describes the of the patient’s current condition?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up

Physiology, Pulmonary Circulatory System - References

References

Boyette LC,Bhimji SS, Physiology, Pulmonary, Circulation null. 2018 Jan     [PubMed]
Mathew B,Lakshminrusimha S, Persistent Pulmonary Hypertension in the Newborn. Children (Basel, Switzerland). 2017 Jul 28     [PubMed]
Lakshminrusimha S,Mathew B,Leach CL, Pharmacologic strategies in neonatal pulmonary hypertension other than nitric oxide. Seminars in perinatology. 2016 Apr     [PubMed]
Chamarthy MR,Kandathil A,Kalva SP, Pulmonary vascular pathophysiology. Cardiovascular diagnosis and therapy. 2018 Jun     [PubMed]
Naeije R,Chesler N, Pulmonary circulation at exercise. Comprehensive Physiology. 2012 Jan     [PubMed]
Soohoo SL,Goldberg HS,Graham R,Jasper AC, Zone 2 and zone 3 pulmonary blood flow. Journal of applied physiology (Bethesda, Md. : 1985). 1987 May     [PubMed]
Tuder RM,Marecki JC,Richter A,Fijalkowska I,Flores S, Pathology of pulmonary hypertension. Clinics in chest medicine. 2007 Mar     [PubMed]
Karkhanis VS,Joshi JM, Pleural effusion: diagnosis, treatment, and management. Open access emergency medicine : OAEM. 2012     [PubMed]
Tarbox AK,Swaroop M, Pulmonary embolism. International journal of critical illness and injury science. 2013 Jan     [PubMed]
Murray JF, Pulmonary edema: pathophysiology and diagnosis. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. 2011 Feb     [PubMed]
Ware LB,Matthay MA, Clinical practice. Acute pulmonary edema. The New England journal of medicine. 2005 Dec 29     [PubMed]
Morrison LK,Harrison A,Krishnaswamy P,Kazanegra R,Clopton P,Maisel A, Utility of a rapid B-natriuretic peptide assay in differentiating congestive heart failure from lung disease in patients presenting with dyspnea. Journal of the American College of Cardiology. 2002 Jan 16     [PubMed]
Levitt JE,Vinayak AG,Gehlbach BK,Pohlman A,Van Cleve W,Hall JB,Kress JP, Diagnostic utility of B-type natriuretic peptide in critically ill patients with pulmonary edema: a prospective cohort study. Critical care (London, England). 2008     [PubMed]
Determann RM,Royakkers AA,Schaefers J,de Boer AM,Binnekade JM,van Straalen JP,Schultz MJ, Serum levels of N-terminal proB-type natriuretic peptide in mechanically ventilated critically ill patients--relation to tidal volume size and development of acute respiratory distress syndrome. BMC pulmonary medicine. 2013 Jul 9     [PubMed]
Neya K, [Swan-Ganz catheter (pulmonary artery catheter)]. Kyobu geka. The Japanese journal of thoracic surgery. 2009 Jul     [PubMed]
Wiesen J,Ornstein M,Tonelli AR,Menon V,Ashton RW, State of the evidence: mechanical ventilation with PEEP in patients with cardiogenic shock. Heart (British Cardiac Society). 2013 Dec     [PubMed]
Humphrey H,Hall J,Sznajder I,Silverstein M,Wood L, Improved survival in ARDS patients associated with a reduction in pulmonary capillary wedge pressure. Chest. 1990 May     [PubMed]
Mitchell JP,Schuller D,Calandrino FS,Schuster DP, Improved outcome based on fluid management in critically ill patients requiring pulmonary artery catheterization. The American review of respiratory disease. 1992 May     [PubMed]

Disclaimer

The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of Nurse-Physiology. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for Nurse-Physiology, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in Nurse-Physiology, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of Nurse-Physiology. When it is time for the Nurse-Physiology board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study Nurse-Physiology.