Physiology, Airway Resistance


Article Author:
Joshua Hurley
Jeremy Hensley


Article Editor:
Jeremy Hensley


Editors In Chief:
David Wood
Andrew Wilt
Hajira Basit


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
8/4/2019 11:32:38 AM

Introduction

The lungs are an intricately designed organ that acts as the bodies center for gas exchange, inhaling and exhaling approximately 7 to 8 mL of air per minute while exchanging oxygen for carbon dioxide. Airway resistance is an essential parameter of lung function and results from the frictional forces of the airways, which oppose airflow. At physiologic levels, airway resistance in the trachea is responsible for turbulent airflow, while airway resistance in the bronchi and bronchioles allows for more laminar airflow, in which air smoothly flows to the distal segments of the lungs. When airway resistance is elevated, as seen with certain pulmonary diseases, air can become trapped in the lungs, limiting gas exchange and possibly causing respiratory failure in severe cases.[1]

Development

Lung development traditionally subdivides into three main periods: embryonic, fetal, and postnatal. The major airways form during the embryonic period at 4 to 7 weeks. The rest of the airways form during the fetal period with the bronchial tree developing between 5 and 17 weeks, and the most distal airways form between 16 and 26 weeks.[2]

At the start of bronchial tree formation, the lung looks like a tubular gland. At 4 to 7 weeks, outgrowth and branching of the terminal bud occur, creating bronchial buds, which will later become bronchi. The bronchial buds then bifurcate, ultimately resulting in the formation of bronchioles. This branching continues, and by approximately 26 weeks, the first 20 generations of airways are evident.[3]

Fetal breathing movements begin around week 10 in humans. These breathing movements allow for amniotic fluid to move in and out of the lungs, resulting in stretching of the lung tissue, which ultimately increases the caliber of the airways.[4]

Mechanism

The standard airway resistance that is present with the laminar flow of normal breathing is largely a function of the Hagen-Poiseuille equation[1]:

R = 8hl /πr

Where h = viscosity, l = length, and r = radius 

Given this equation, it is clear that radius is the most important factor in airway resistance and that small changes in radius can lead to significant changes in the airway resistance. For example, if the radius of the tube doubles, the resistance decreases by a factor of 16.

The medium-sized bronchi collectively have the smallest radius. If we use the principle outlined above, it makes sense that since the medium-sized bronchi collectively have the smallest radius, then they would also be the site of greatest airway resistance. Using this same principle, we can also conclude that the terminal bronchioles have the lowest resistance since collectively they have the largest radius.[5]

Airway radius is not static and can be significantly altered by airway smooth muscle, which lines all of our conducting airways, except for the trachea where airway smooth muscle gets confined to the anterior wall.[1] The sympathetic nervous system causes the relaxation of airway smooth muscle. Stimulation of beta-2 receptors on airway smooth muscle induces bronchodilation and decreases airway resistance. The parasympathetic nervous system innervates airway smooth muscle triggering contraction when stimulated. This contraction of airway smooth muscle decreases the airway lumen, increasing airway resistance.[6]

Airway resistance also changes between inspiration and expiration. The majority of airways within the lung parenchyma are tethered by alveolar attachments that transmit an outward force on these airways, which increases as the lungs expand. This increasing outward force increases airway radius, thus decreasing airway resistance. On expiration, this outward tethering force diminishes, and inward elastic recoil forces increase causing a decrease in airway radius, which leads to increased airway resistance.[1]

Related Testing

Whole-body plethysmography is the most common method for measuring airway resistance. A plethysmograph is an air-tight chamber that the participant sits inside, which contains a tube that the patient puts in their mouth. There are two transducers within the plethysmograph: one located in the chamber that measures chamber pressure, and one inside of the tube that measures mouth pressure. There is also a flowmeter in the tube that measures the flow rate. During the test, the patient is asked to breathe normally while the tube is left open. When the participant breaths into the open tube, mouth pressure, and flow rate are recorded. A shutter then occludes the tube, and the participant is asked to try to breathe normally. With the participant attempting to breathe against the closed tube, there is no airflow and mouth pressure approximates alveolar pressure.[7] After obtaining the values for mouth pressure (kPa), alveoli pressure (kPa), and flow rate (L/s), airway resistance (kPa s L) can be calculated using the equation below.

R = (Pm – Pa) / Vo

Where Pm = pressure in the mouth, Pa = pressure in the alveoli, and Vo = flow rate.[8]

Pathophysiology

One of the diseases that highlights the importance of normal airway resistance is asthma. Asthma develops due to chronic inflammation of the conducting airways, particularly the bronchi and bronchioles. This chronic inflammation results in contraction and hypertrophy of the airway smooth muscle, increased mucus production, and thickening of the lamina reticularis (a layer of connective tissue that surrounds the airways). Asthma is characterized as an “obstructive” lung disease because these maladaptive changes to the airways result in narrowing or even complete occlusion of the airway lumen, which leads to an increase in airway resistance that “obstructs” air from exiting the lungs.[9]

The increased airway resistance associated with asthma is responsible for many of the signs and symptoms a patient will experience during an asthma exacerbation, including wheezing, dyspnea, chest tightness, and air trapping. Air trapping within the distal segments of the lungs is due to an inability to produce enough expiratory pressure to overcome the airway resistance of the more proximal bronchi and bronchioles. Since this airway resistance cannot be overcome, the air gets trapped in the distal segments of the lungs.[9][10]

Clinical Significance

Multiple medications can reduce airway resistance through various mechanisms. Many of these drugs are used to treat obstructive lung diseases like Asthma and COPD.

Albuterol is an inhaled short-acting beta-2 agonist that stimulates beta-2 receptors on the surface of airway smooth muscle. The increased sympathetic tone causes the relaxation of airway smooth muscle, which causes dilation of the bronchi and bronchioles, reducing airway resistance.

Heliox is often an adjunctive therapy alongside albuterol for reducing airway resistance. With severe airway narrowing, gas velocity increases, and airflow becomes turbulent. This turbulent airflow increases airway resistance. Helium is seven-times less dense than air, and when mixed with oxygen to form heliox, the lower density causes the turbulent airflow to revert to a state of laminar flow, decreasing airway resistance. This return to laminar flow and reduced resistance helps albuterol get to the distal airways where it can act on distant beta-2 receptors and also helps to maintain ventilation to the distal airways, preventing progression to respiratory failure.

Ipratropium is another inhaled agent that works in the opposite way of albuterol. Ipratropium is an anticholinergic agent that works by blocking parasympathetic cholinergic receptors, which results in decreased parasympathetic tone on the airway smooth muscle, which prevents stimulation and contraction of airway smooth muscle, dilating bronchi and bronchioles and resulting in decreased airway resistance. 

Inhaled corticosteroids are a common therapy option in the treatment of persistent asthma. They act to decrease airway inflammation and mucus production. This reduction in inflammation and mucus increases the caliber of airways, reducing airway resistance. Since these are inhaled corticosteroids, they have few if any systemic side effects.[11]


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Physiology, Airway Resistance - Questions

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A 32-year-old male on a hiking trip just finished climbing the tallest mountain in West Virginia. Due to the intense exertion, he begins to feel short of breath and starts to experience chest tightness with wheezing. Which of the following factors will help the most to prevent air trapping in his lungs?



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A 12-year-old male presents to the emergency department with dyspnea. He states that he first developed symptoms one hour ago while dusting his room. On physical exam, bilateral inspiratory wheezes are heard on auscultation of the lungs, and intercostal retractions are seen, indicating an increased work of breathing. Vitals show a heart rate of 89 bpm, respiratory rate 28 bpm, and blood pressure of 118/78 mmHg. O2 saturation is 95% on room air. A chest x-ray is obtained and demonstrates air trapping in both lungs. Which of the following is the most likely mechanism causing this patient's dyspnea?



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A 9-year-old female presents to the office with dyspnea and chest tightness. She states that he first developed symptoms one hour ago while riding her bike outside with friends on a hot summer day. On physical exam, bilateral inspiratory wheezes are heard on auscultation of the lungs, and intercostal retractions are seen. Vital signs demonstrate a heart rate of 75 bpm, respiratory rate of 26 bpm, and blood pressure of 122/82 mmHg. O2 saturation is 96% on room air. A chest x-ray is obtained which demonstrates air trapping in both lungs. Which of the following is the most likely mechanism of action of the first-line medication used to treat her condition acutely?



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A 4-year-old male with a history of Down syndrome is being taken to the operating room for an appendectomy. Preoperatively, his mother says that after having his tonsils removed at age 2, the anesthesiologist told her that his son was difficult to intubate and had a “small airway.” In the operating room, the child is difficult to ventilate after mask induction with sevoflurane and oxygen. Lung sounds are decreased bilaterally without wheezing, and stridor is noted. Which of the following would be the best treatment?



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A 65-year-old male is undergoing surgery for urethral stent placement to relieve urinary tract obstruction. Anesthesia is induced with lidocaine, propofol, fentanyl, and succinylcholine. An endotracheal tube is placed, and breath sounds are noted in bilateral lung fields. Anesthesia is then maintained with 1 minimum alveolar concentration (MAC) of sevoflurane. As the succinylcholine begins to wear off, and the patient begins to breathe spontaneously, it is noted that the patient now has an increased work of breathing compared to what their respiratory effort was before induction of anesthesia, and the patient requires pressure support from the ventilator to maintain adequate gas exchange. Which of the following is the most likely cause of this patient's increased work of breathing?



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Physiology, Airway Resistance - References

References

Bates JH, Systems physiology of the airways in health and obstructive pulmonary disease. Wiley interdisciplinary reviews. Systems biology and medicine. 2016 Sep;     [PubMed]
Schittny JC, Development of the lung. Cell and tissue research. 2017 Mar;     [PubMed]
Kitaoka H,Burri PH,Weibel ER, Development of the human fetal airway tree: analysis of the numerical density of airway endtips. The Anatomical record. 1996 Feb;     [PubMed]
Koos BJ,Rajaee A, Fetal breathing movements and changes at birth. Advances in experimental medicine and biology. 2014;     [PubMed]
Kaminsky DA, What does airway resistance tell us about lung function? Respiratory care. 2012 Jan;     [PubMed]
van der Velden VH,Hulsmann AR, Autonomic innervation of human airways: structure, function, and pathophysiology in asthma. Neuroimmunomodulation. 1999 May-Jun;     [PubMed]
DUBOIS AB,BOTELHO SY,COMROE JH Jr, A new method for measuring airway resistance in man using a body plethysmograph: values in normal subjects and in patients with respiratory disease. The Journal of clinical investigation. 1956 Mar;     [PubMed]
Criée CP,Sorichter S,Smith HJ,Kardos P,Merget R,Heise D,Berdel D,Köhler D,Magnussen H,Marek W,Mitfessel H,Rasche K,Rolke M,Worth H,Jörres RA, Body plethysmography--its principles and clinical use. Respiratory medicine. 2011 Jul;     [PubMed]
Mims JW, Asthma: definitions and pathophysiology. International forum of allergy     [PubMed]
Gono H,Fujimoto K,Kawakami S,Kubo K, Evaluation of airway wall thickness and air trapping by HRCT in asymptomatic asthma. The European respiratory journal. 2003 Dec;     [PubMed]
Pardue Jones B,Fleming GM,Otillio JK,Asokan I,Arnold DH, Pediatric acute asthma exacerbations: Evaluation and management from emergency department to intensive care unit. The Journal of asthma : official journal of the Association for the Care of Asthma. 2016 Aug;     [PubMed]

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