Physiology Note - Respiratory Mechanics during Spontaneous Breathing

 

 RESPIRATORY MECHANICS DURING SPONTANEOUS BREATHING


Contributed by Emy Ambooken, Thrissur

INTRODUCTION:

Respiratory mechanics refers to the expression of lung function through measures of pressure and flow. Pressure difference between the atmosphere and inside the lungs acts as a driving force to accomplish spontaneous breathing.

WHAT HAPPENS DURING SPONTANEOUS BREATHING?

During inspiration: The Diaphragm descends, increasing longitudinal length of the thoracic cavity and external intercostal muscles raise the ribs, thereby increasing the circumference of the thorax. Contraction of the diaphragm and external intercostal muscles provides the energy necessary to drive airflow and overcome the impedance offered by the lungs and chest wall. Accessory muscles of inspiration are also used during maximal inspiration.

During expiration: Inspiratory muscles relax, diaphragm moves upward, and the ribs return to their resting position. This reduces volume of the thoracic cavity and air is forced out of the alveoli. During maximal expiration, the accessory muscles of expiration are also used to compress the thorax

 

Fig 1: On inspiration, the dome-shaped diaphragm contracts, the abdominal contents are forced down and forward, and the rib cage is widened. Both increase the volume of the thorax. On forced expiration, the abdominal muscles contract and push the diaphragm up.

 

 

 

 GAS FLOW AND PRESSURE GRADIENTS DURING BREATHING:

Airway opening pressure (Pawo) or airway pressure (Paw) : It is the airway opening pressure.

 Intrapleural pressure (Ppl): It is the pressure in the potential space between the parietal and visceral pleurae.Ppl is normally about −5 cm H2O at the end of expiration during spontaneous breathing. It is about −10 cm H2O at the end of inspiration. Esophageal pressure (Pes) is used to estimate pressure changes in the pleural space.

Alveolar pressure (Palv) or intrapulmonary pressure:It is the pressure of the air within the alveoli, which changes during the different phases of breathing. It normally changes as the intrapleural pressure changes. During spontaneous inspiration, Palv is about −1 cm H2O, and during exhalation it is about +1 cm H2O.

 Transairway Pressure (PTA): Is the pressure difference between the airway opening and the alveolus. PTA =Pawo -Palv.PTA is therefore the pressure gradient required to produce airflow in the conductive airways.

 Transthoracic Pressure (PTT): It is the pressure difference between the alveolar space or lung and the body’s surface. It represents the pressure required to expand or contract the lungs and chest wall at the same time.  PTT= Palv − Pbs

Transpulmonary Pressure or transalveolar pressure (PL or PTP):It is the pressure difference between the alveolar space and the pleural space. It is the pressure required to maintain alveolar inflation.PL =Palv – Ppl.

 Transrespiratory pressure (PTR): It is the pressure difference between the airway opening and the body surface: PTR =Pawo -Pbs

 Fig 2: Various pressures and pressure gradients of the respiratory system.

THE MECHANICS OF SPONTANEOUS VENTILATION AND THE RESULTING PRESSURE WAVES

During inspiration, as the volume of the thoracic space increases, the intrapleural pressure becomes more negative in relation to atmospheric pressures and drops from about -5 cm H2O at end expiration to about -10 cm H2O at end inspiration. The negative intrapleural pressure is transmitted to the alveolar space, and the alveolar (Palv), pressure becomes more negative relative to atmospheric pressure. The transpulmonary pressure (PL), or the pressure gradient across the lung, widens and alveoli has a negative pressure during inspiration.

 The pressure at the airway opening is still atmospheric, creating a pressure gradient between the mouth and the alveolus of about -3 to -5 cm H2O. The trans airway pressure gradient (PTA) is approximately (0- [ -5]), or 5 cm H2O. Due to this gradient, air flows from the mouth or nose into the lungs, causing the alveoli to expand. As air continues to fill the alveoli, the pressure within alveoli rises until it equalizes with atmospheric pressure, and airflow ceases. This marks the end of inspiration.

 During expiration, the muscles relax, and the elastic recoil of the lung tissue results in a decrease in lung volume. The thoracic volume decreases to resting, and the intrapleural pressure returns to about- 5 cm H2O. The pressure inside the alveolus during exhalation increases and becomes slightly positive (+5 cm H2O). Hence the pressure is now lower at the mouth than inside the alveoli, and the trans airway pressure gradient causes air to move out of the lungs. Exhalation ends when the pressure in the alveoli and mouth are equal.

 

Fig 3: The mechanics of spontaneous ventilation and the resulting pressure waves (During inspiration, intrapleural pressure (Ppl) decreases to -10 cm H2O. During exhalation, Ppl increases from -10 to -5 cm H2O.

 

Changes in transpulmonary pressure during spontaneous ventilation

 Pressure

End Expiration

 End Inspiration

Intra alveolar (intrapulmonary)

0 cm H2O

 0 cm H2O

 Intrapleural

-5 cm H2O

-10 cmH2O

 Transpulmonary

 PL =0 -( -5) =+5cmH2O

  PL = 0- ( -10) =10 cmH2O

 

LUNG CHARACTERISTICS DURING BREATHING:

Two types of forces oppose inflation of the lungs: elastic and frictional forces. Elastic forces are due to elastic properties of the lungs and chest wall. Frictional forces are due to the resistance of the tissues and organs as they are displaced during breathing and the resistance to gas flow through the airways.

Compliance:

Lung compliance is the relative ease with which the lung distends, and elastance is the tendency to return to its original form after being stretched.

       C = ∆V/∆P, where C is compliance, ∆V is change in volume, and ∆P is change in pressure.

       The inverse of compliance is elastance (E ~ 1/C).

Compliance of the respiratory system is the sum of the compliances of both the lung parenchyma and the surrounding thoracic structures. During spontaneous breathing, the total respiratory system compliance is about 0.1 L/cm H2O (100 mL/cm H2O); varies with posture, position, and whether actively inhaling or exhaling during the measurement. It can range from 0.05 to 0.17 L/cm H2O (50 to 170 mL/cm H2O).

1/CRS = 1/CCW +1/CL

CRS =Compliance of respiratory system. CCW=Compliance of chest wall. CL=Compliance of lung

Measurement of compliance in spontaneous breathing:

       By measuring spontaneous breathing efforts with spirometry

           Body Plethysmography: gold standard for non-invasive lung function testing.

       Esophageal manometry: enables estimation of pleural pressure, offering a precise   assessment of transpulmonary pressure and lung compliance

 Conditions causing reduced compliance: ARDS, kyphoscoliosis, pulmonary fibrosis, alveolar oedema, atelectasis

 Conditions causing increased compliance: Emphysema, normal aging lung.

 Resistance:

 Resistance is a measurement of the frictional forces that must be overcome during breathing. Resistance is due to the anatomical structure of the airways and the tissue viscous resistance offered by the lungs, adjacent tissues and organs.

 Raw =PTA/flow, where Raw is airway resistance and PTA is the pressure difference between the mouth and the alveolus, or the trans airway pressure.

Flow (Q) is the gas flow measured during inspiration and it depends on the pressure gradient (ΔP) and is inversely related to the resistance to flow (R). Q = ΔP/R. In the lungs, two types of flow are present – laminar flow and turbulent flow. Turbulent flow is present in large airways and major bifurcations, whereas laminar flow is present in the more distant airways. The type of flow present in an airway is influenced by the rate of flow (V), the airway radius (r), the density of gas (p), and the viscosity of gas (η). Reynold's number is a calculation of the above variables and it determines whether flow will be turbulent or laminar. Reynold's number = 2Vrp/η, and values greater than 2300 indicate that flow will have a turbulent component. Flow with a Reynold's number greater than 4000 is completely turbulent.

Factors determining airway resistance:

1)Lung Volume: As lung volume decreases, airway resistance rises rapidly

2)Bronchial airway smooth muscle contraction: As bronchial smooth muscle narrows, airway resistance increases. Parasympathetic stimulation causes broncho constriction and β2 receptor stimulation relaxes bronchial smooth muscles

3)Fall of PCO2 in alveolar gas increases airway resistance by direct action on bronchiolar smooth muscles

4)Density and viscosity of inspired gas: Higher the density and viscosity, the more the airway resistance

 

In a normal individual, maximal inspiratory flow is limited only by muscle strength and total lung and chest wall compliance. Maximal expiratory flow is initially limited only by expiratory muscle strength (when the airway radius is large and resistance is minimal). However, as the airway lumen decreases, resistance to flow will increase and flow is limited by resistance. The accurate measurement of airway resistance during spontaneous breathing requires an oesophageal balloon to estimate pleural pressure and determination of the transpulmonary pressure at any given lung volume

 

The flow–volume loop demonstrates airflow at different points in the respiratory cycle. A normal flow–volume loop is shown in Fig. 4.

Text Box: Fig 4: A flow–volume loop with exhalation above the horizontal axis and inspiration below.

 

Time constants:

Lung units are heterogeneous, with compliance and resistance values of a terminal respiratory unit (acinus) varying from those of another unit. Time constant approximates the amount of time required to fill or empty a lung unit.It is the length of time (in seconds) required for the lungs to inflate or deflate to a certain amount (percentage) of their volume

Time constant is the product of compliance (C) and resistance (Raw)

 Time constant =C x Raw

 One-time constant equals the amount of time it takes for 63% of the volume to be inhaled (or exhaled), two-time constants represent the amount of time for about 86% of the volume to be inhaled (or exhaled), three-time constants equal the time for about 95% to be inhaled (or exhaled), and four-time constants are the time required for 98% of the volume to be inhaled (or exhaled)

Fig 5: Time constant (compliance x resistance) is a measure of how long the respiratory system takes to passively exhale or inhale.

Work of breathing:

WOB describes the energy required as flow begins to perform the task of ventilation. Work is defined as the product of pressure and volume (W = P × V). WOB can be determined through analysis of a PV plot, where work is the area under the curve. 

Work Done on the Lung

Text Box: Fig 6: Pressure volume curve of lung showing the inspiratory work done overcoming elastic forces (area 0AECD0) and viscous forces (hatched area ABCEA)

 During inspiration, the intrapleural pressure allows the curve ABC, and the work done on the lung is given by the area 0ABCD0. Of this, the trapezoid 0AECD0 represents the work required to overcome the elastic forces, and the hatched area ABCEA represents the work overcoming viscous (airway and tissue) resistance (Fig 6). On expiration, the area AECFA is work required to overcome airway (+ tissue) resistance. The difference between the areas AECFA and 0AECD0 represents the work dissipated as heat

Total work of breathing: Total work done moving the lung and chest wall is difficult to measure although estimates are obtained by artificially ventilating paralyzed patients in an iron-lung type of ventilator.

Surface Tension:

Surface tension is another factor in the pressure-volume behaviour of lung lining the alveoli.  This tension tends to collapse the alveoli, which reduces lung compliance. Type II pneumocytes produce surfactant, dipalmitoyl phosphatidylcholine (DPPC). It lowers surface tension and stabilizes the alveoli, preventing their collapse and facilitating homogeneous ventilation. In the absence of surfactant, smaller alveoli will collapse, resulting in reduced lung compliance, alveolar atelectasis, and a tendency for pulmonary edema.

CLINICAL IMPLICATIONS:

Dynamic Compression of Airways

Limits air flow in normal subjects during a forced expiration. It may occur in diseased lungs at relatively low expiratory flow rates, thus reducing exercise ability. During dynamic compression, flow is determined by alveolar pressure minus pleural pressure and is there effort independent. It is exaggerated in some lung diseases by reduced lung elastic recoil and loss of radial traction on airways. Expiratory flow limitation (EFL) is the maximal expiratory flow achieved during tidal breathing, and it is characteristic of intrathoracic airflow obstruction. EFL during tidal breathing promotes dynamic pulmonary hyperinflation (DH) and intrinsic positive end-expiratory pressure (PEEPi), with concomitant increase of work of breathing, functional impairment of inspiratory muscle function, dyspnoea, and adverse effects on haemodynamics.

Measures to reduce airway resistance:

β2 adrenergic agonist used in asthma and COPD to decrease airway resistance. Parasympathetic activity increases airway resistance, as with acetylcholine. Also, the density and viscosity of the inspired gas affect airway resistance. Heliox gas mixture helps to decrease density and thereby airway resistance.

Work of breathing in acute respiratory failure:

Work of breathing is usually associated with inspiratory effort, as expiration is a passive process. However, in patients with air trapping or acute respiratory failure, expiration can be an active process and requires significant work. As the WOB increases, increased demand is imposed on the respiratory muscles. The respiratory muscles of patients in acute respiratory distress will use an increasing percentage of the cardiac output. As the demand increases, the respiratory muscles will eventually fatigue. As the diaphragm fatigues, the accessory muscles of respiration are recruited, and the respiratory rate is increased. When fatigue leads to inadequate ventilation, carbon dioxide levels in the blood increase and arises the need for mechanical ventilation.

 

REFERENCES:

(1)West’s respiratory physiology: the essentials / John B. West, Andrew M. Luks. Tenth edition;2016

(2)Philbeams mechanical ventilation, physiological and clinical applications/ J.M. Cairo. Eighth edition;2020

(3) Clinical Application of Mechanical Ventilation, Fourth EditionDavid, W. Chang,2013

(4) Grinnan, D.C., Truwit, J.D. Clinical review: Respiratory mechanics in spontaneous and assisted ventilation. Crit Care 9, 472 (2005). https://doi.org/10.1186/cc3516

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