Airway Conductance

Summary / Explanation

The respiratory system comprises two sets of airways connected in series. The conducting airway begins at the nose and mouth and continues into the pharynx, larynx, epiglottis, vocal cords, trachea, bronchi, and bronchioles, respectively. This system transmits inhaled gases to the respiratory airways, which continue as respiratory bronchioles, alveolar ducts, and terminal alveolar sacs, which exchange gas.[1] Appropriate air conductance through these passageways is crucial for normal physiologic airway function. Here, we present an overview of the physical principles underlying this movement and the pathophysiology, diagnosis, and management of reduced airway conductance.

Physics of Conductance

An interaction between the density of the flowing gas, the length and diameter of the airway, and the pressure gradient across the system determines conductance through the airways. Classically, these interactions have been described by the Hagen-Poiseuille equation, written as:

Q = ΔPπR⁴/8ηL

Where 

• Q = Flow
• P = Pressure
• R = Airway radius
• η = Viscosity of the flowing gas
• L = Airway length

Alternatively, the inverse of this equation may be written to describe airway resistance.

According to this equation, conductance is directly proportional to pressure gradient and airway radius and inversely proportional to airway length and gas viscosity. Thus, airflow can be improved by increasing the driving pressure or airway radius, shortening the airway, or decreasing the viscosity of inhaled gases.

A related principle is the Reynolds number (Re), which is a dimensionless number describing the ratio of inertial to viscous forces in a flowing fluid.[2] It is calculated as:

Re = ρVL/μ 

Where 

• ρ = Density of the flowing gas
• V = Velocity of the flowing gas
• L = Airway length
• μ = Viscosity of the flowing gas

The significance of this relationship becomes apparent when the Reynolds number exceeds 2000. At these high values, airflow transitions from laminar to turbulent with the development of eddy currents, which increase resistance, decrease conductance, and may increase the work of breathing.[3]

Diseases of Reduced Airway Conductance

Multiple pathologic states are associated with reduced airway conductance. Mechanistically, these are related to changes in the variables described by the Hagen-Poiseuille equation, most commonly reductions in airway driving pressure or reductions in airway diameter.

Frequent causes of reduced driving pressure include diseases of neuromuscular weakness (eg, Guillain-Barré syndrome, myasthenia gravis, amyotrophic lateral sclerosis, high cervical spine injuries), residual postoperative neuromuscular blockade, opioid overdose, or insufficient ventilator support in intubated patients.[4]

Reduction of airway diameter is seen secondary to static narrowing (eg, laryngeal, pharyngeal, or mediastinal malignancies; subglottic stenosis, undersized endotracheal tube), reactive narrowing (eg, asthma, cholinesterase inhibitor toxicity), or dynamic narrowing (eg, tracheomalacia, bronchomalacia).[5]

Diagnosing Impaired Conductance

Clinical signs

Presentation of impaired airway conductance may be nonspecific, chronic, or acute and will typically depend upon the severity of impairment. Common symptoms include tachypnea, dyspnea, stridor, or wheezing.[6] Tachypnea is an indication of increased work of breathing and may be present early or late in the course of disease progression. Sudden resolution of tachypnea should be investigated immediately, as this may herald respiratory collapse as the respiratory muscles transition from a state of fatigue to failure. Dyspnea occurs secondary to a sensation of air hunger in the setting of hypoxemia. Dyspnea may be less severe in compensated patients with chronic hypoxemia. Stridor is a high-pitched musical sound associated with upper airway obstruction. Inspiratory stridor is an indication of extrathoracic lesions, expiratory stridor indicates intrathoracic lesions, while biphasic stridor indicates lesions at the glottis or just below the glottis.[7] Alternatively, wheezing is associated with lower airway obstructions. Wheezing may be localized or widespread, and sudden cessation of wheezing should be considered an ominous sign, as it may indicate a severe reduction of airway conductance and insufficient airflow to produce audible wheezing.[8]

Imaging

Upright chest X-rays should be obtained as part of the routine evaluation of patients with signs and symptoms of impaired conductance. Diaphragmatic flattening and hyperinflation of the lungs indicate air trapping in conditions such as asthma or chronic obstructive pulmonary disease (COPD). However, many other pathologies may not present on plain radiographs. Computerized tomography (CT) can help identify mass lesions and areas of airway narrowing.

Pulmonary Function Testing (PFTs)

Pulmonary function testing (PFTs) may help identify abnormal respiratory muscle function and differentiate upper versus lower and fixed versus dynamic airway obstruction. Flattening of the inspiratory loop indicates dynamic extrathoracic obstruction, while flattening of the expiratory loop indicates dynamic intrathoracic obstruction. Reductions in both expiratory and inspiratory loops indicate fixed upper airway obstruction.[9]

Ventilator Settings

Once intubated, a patient's ventilator settings can help diagnose reduced conductance. Increased peak pressures in the setting of normal plateau pressures indicate upper airway obstruction, such as from masses, undersized endotracheal tubes, mucus plugging, bronchoconstriction, or kinking of the endotracheal tube or ventilator circuit. This will often be seen as a sharp "peak" preceding the plateau of a pressure waveform. Increases in both peak and plateau pressures indicate reduced chest-wall system compliance, such as occurs in acute respiratory distress syndrome (ARDS), pneumothorax, or circumferential burn injuries.[10]

Treatment Principles

The treatment of reduced airway conductance is aimed at optimizing flow (Q) and minimizing the work of breathing. The first treatment step usually involves administering supplemental oxygen (eg, nasal cannula, simple face mask, non-rebreather face mask), as patients are often hypoxemic at presentation. This will help increase alveolar oxygen concentration independent of changes in airway flow patterns. Noninvasive positive pressure ventilation(eg, continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP)) may be used if patients continue to experience dyspnea or show signs of increased work of breathing. CPAP and BiPAP will improve and reduce the work of breathing by increasing airway driving pressure (ΔP) without increasing patient effort.[11]

For patients presenting with airway constriction due to reactive airway narrowing, bronchodilator or antisialogogue therapy may be warranted. Treatment with β-agonists (eg, albuterol, racemic epinephrine, terbutaline), muscarinic antagonists (eg, glycopyrrolate, ipratropium), or steroids (dexamethasone, hydrocortisone, methylprednisolone) improve by reducing airway swelling and clearing airway secretions, and thus increasing the diameter of narrowed airways (R).[12]

Patients with fixed airway obstructions may benefit from helium-oxygen mixtures, commonly called heliox. Helium is a low-density (ρ) gas compared to oxygen. Thus, by administering a helium-oxygen mixture, the Reynolds number is reduced, which promotes the transition from turbulent to laminar flow in the upper airways and reduces the work of breathing.[13] A limitation of this therapy is the patient's ability to tolerate a low inspired oxygen concentration (FiO₂).

Patients who fail these therapies may require urgent or emergent endotracheal intubation. This will help bypass restricted flow due to upper airway obstruction and provide a secure airway to administer invasive positive pressure ventilation. Additionally, anesthetic gases such as desflurane, sevoflurane, and isoflurane may be administered as bronchodilator therapy in intubated patients.[14] Some patients may develop reduced conductance following intubation due to an undersized endotracheal tube, mucus plug formation, or kinking of portions of the ventilator system. In this case, treatment involves ensuring an appropriately sized endotracheal tube, identifying any areas of reduced flow, and possibly replacing circuit components.

Patients who continue to experience reduced airway conductance despite maximal ventilator and medical therapy, such as in refractory status asthmaticus, may require extracorporeal membrane oxygenation (ECMO).[15] This will allow bypassing of the respiratory system entirely to provide oxygenation and ventilation support while other therapies are ongoing.

Ultimately, treatment aims to correct the underlying disease state through long-term bronchodilator therapy, treatment of airway edema, surgical correction of airway narrowing or airway masses, or resolution of neuromuscular failure. When surgical correction is not possible, or when a patient is unable to liberate from a ventilator, a tracheostomy may be required. This may help improve conductance by bypassing the narrowing in the upper airway and shortening the length of the airway (L), thus increasing and improving the work of breathing.[16]

Reductions in airway conduction may lead to significant clinical decline and life-threatening airway compromise. Establishing a multidisciplinary team and evidence-based practices is critical to ensuring optimal outcomes in this patient population. This begins with the ability for triaging providers to quickly mobilize specialties experienced in difficult airway management, including anesthesiology, surgery, and otolaryngology, and for those centers that provide ECMO, teams such as cardiothoracic surgery and critical care medicine. Respiratory therapists should be well-versed in the tools required by intubating physicians, such as video laryngoscopes, fiberoptic bronchoscopes, and heliox administration. Such collaboration will help improve outcomes at every stage of managing these challenging conditions.