The mechanics of breathing

Histology

The overall histologic architecture of the bronchial tree is relatively consistent from the trachea to the bronchioles, with a sharp transition at the respiratory portion.

• Trachea

  • Fibroelastic connective tissue lined by two cell types

    • Ciliated columnar epithelial cells

    • Mucus producing goblet cells

  • C-shaped rings of hyaline cartilage provide support along anterior and lateral surfaces ( Fig. 13.2 ).

    

  • Semirigid support with high elastin content resists collapse but also accommodates changes in size:

    • Expansion during inspiration

    • Recoil during expiration

      Clinical Correlation Box 13.1

      The mucociliary elevator represents a joint effort of the ciliated epithelial cells and mucus-secreting goblet cells to move mucus and trapped debris to the pharynx. Toxins from cigarette smoking damage the ciliated epithelial cells. This results in accumulation of secretions and debris from the lungs.

• Distal conducting airways

  • Cartilage rings less frequent, disappearing completely in bronchioles.

  • Cilia shorten with fewer goblet cells. See Clinical Correlation Box 13.1

  • Smooth muscle layer increases (more control of diameter).

• Alveoli

  • Type I pneumocytes.

    • Thin, flat cells that form gas-diffusion barrier.

  • Type II pneumocytes.

    • Rounded, infrequent.

    • Produce surfactant which lowers surface tension in alveoli, which prevents alveolar collapse (see Fast Fact Box 13.1 ).

Gross anatomy

The lung may be divided into lobes, which are not symmetrical because of the need to accommodate the heart on the left side ( Fig. 13.3 A).

• Right

  • Upper

  • Middle

  • Lower

• Left

  • Upper

    • Lingula, a small portion of this lobe, corresponds to the “middle” lobe.

  • Lower

The lobes are further subdivided into bronchopulmonary segments, which are shaped like pyramids with apices pointing toward the hilum of the lung ( Fig. 13.3 B). Each is supplied by:

• Segmental bronchus. See Clinical Correlation Box 13.2

  Clinical Correlation Box 13.2

  A state known as atelectasis results when one or more bronchopulmonary segments collapse. This might happen when a mucus plug obstructs a segmental bronchus, blocking the movement of air into that segment. Atelectasis can occur after surgery or another cause of limited mobility. Such patients often spontaneously sigh in an unconscious manner to expand the collapsed alveoli. Collapse of entire lung, however, cannot be corrected by this strategy, however, and requires an invasive procedure such as placement of a chest tube.

• Segmental artery (branch of pulmonary artery).

• Segmental vein (branch of pulmonary vein).

There are no attachments between the lungs and the chest wall except at the hilum, where the lungs are suspended by the mediastinum, primary bronchi, pulmonary arteries, and pulmonary veins.

The pleura, which has two layers, surrounds the lungs ( Fig. 13.4 ).

• The visceral pleura adheres to the lung.

• The parietal pleura adheres to the chest wall and diaphragm, the principal muscle of breathing.

• The potential space between them is called the pleural space.

  • This contains only a small amount of pleural fluid, secreted by the superficial mesothelium of the pleura, which lubricates the movement of the lungs inside the chest wall.

  • Lymph ducts continually drain the fluid from the pleural space into the hilar lymph nodes and from there conveys it to the thoracic duct.

  • This drainage keeps the pleural space a potential space; a near vacuum. See Clinical Correlation Box 13.3

    Clinical Correlation Box 13.3

    Note that if the pleural space is punctured and air is introduced into the pleural space (pneumothorax) this space will no longer have a negative pressure, but will be equal to atmospheric pressure. Thus the lung collapses on that side. If the pneumothorax is a tension pneumothorax (i.e., air can enter but not escape from the puncture wound), air progressively accumulates in the pleural space and pushes the mediastinum to the opposite hemithorax. This can block venous return to the heart with devastating effects. Please see the pathophysiology section at the end of this chapter for a more complete discussion.

As a result, during inhalation, when the diaphragm pulls down on the parietal pleura, the parietal pleura cannot be pulled away from the visceral pleura. The diaphragm contracts and pulls the parietal pleura, which is vacuum-suctioned to the visceral pleura, and the lung is pulled open (see Clinical Correlation Box 13.4 ).

The chest wall is the semirigid musculoskeletal apparatus (ribs, sternum, spine, respiratory musculature) that serves to:

• Protect and support the heart and lungs

• Modify the volume of the thoracic cavity during breathing.

The most important muscle in this system is the dome-shaped diaphragm, which forms the floor of the thoracic cavity.

• The diaphragm contracts in a downward direction during inspiration, generating negative intrathoracic pressure to expand the lungs.

• The diaphragm relaxes during expiration, moving upwards and thus increasing intrathoracic pressure to empty the lungs.

• The diaphragm is innervated by the phrenic nerves, which originate at cervical roots C3, C4, and C5 (see Fast Fact Box 13.2 ).

Accessory breathing muscles may assist the diaphragm during exercise or in disease states that compromise breathing function.

• Intercostal muscles

  • Divisions

    • External intercostal muscles

    • Internal intercostal muscles

    • Innermost intercostal muscles

    • Transversus thoracis muscles

  • Function

    • Manipulate the ribs to increase or decrease the dimensions of the thoracic cavity.

    • Recruited during forced or active inspiration.

• Scalenes

• Sternocleidomastoids

  • Elevates the sternum and is only activated at increased respiratory volumes.

• Anterior serrati

• Alae nasi

  • Flare the nostrils.

Under respiratory stress, such as in the case of an asthma attack, these accessory muscles of inspiration can become overworked.

Pulmonary pressures and compliance

Transmural pressure and elastic recoil pressure

A transmural pressure is defined as the difference between the pressure inside and outside of the container.

P _transmural = P _in – P _out

A positive transmural pressure (P _in >P _out ) works to expand a container. A negative transmural pressure (P _in <P _out ) works to collapse a container.

There are three transmural pressures that determine the dynamics of ventilation:

• Pressure across the lungs and airways, or transpulmonary pressure (P _L )

• Pressure across the chest wall (P _CW )

• Pressure across the respiratory system (P _RS )

The transpulmonary pressure (also known as P _lung or P _L ) is the transmural pressure across the lungs ( Fig. 13.5 ). It determines the degree of inflation of the lungs.

P _{transpulmonary} = P _alveoli – P _{pleural space} = P _alv – P _pl = P _L

• P _pl is generally negative.

• In static conditions (i.e., before a breath is inhaled or exhaled), P _alv = P _mouth .

• If P _alv <0, the lung tends to contract and leads to expiration. If P _alv >0, the lung tends to expand and leads to inspiration (see Genetics Box 13.1 , Development Box 13.1 and Pharmacology Box 13.1 ).

GENETICS BOX 13.1

Some of patients with early onset emphysema have α1 antitrypsin deficiency because of a mutation in SERPINA1. This gene encodes the protein that antagonizes the enzyme neutrophil elastase. There are multiple alleles of this gene, the normal version being designated M, whereas others like the Z and S alleles have point mutations that impair the protein’s function. Patients with the MM genotype (homozygous for the normal gene) have no disease, whereas those with an ZZ, SS, or SZ have the disease.

DEVELOPMENT BOX 13.1

Although chronic obstructive pulmonary disease affects middle age to older adults who often have a history of smoking more than 10 to 15 years, patients with alpha 1 antitrypsin deficiency tend to be younger (age 20–50 years) and often are nonsmokers. They progressively lose elastic recoil of lung tissue because of the unopposed action of neutrophil elastase. This disrupts the balance of forces that help keep the airways open, resulting in air trapping in their overly compliant lungs. Symptoms include dyspnea, cough, wheezing, and sputum.

PHARMACOLOGY BOX 13.1

Like other patients with chronic obstructive pulmonary disease, patients with symptomatic α1 antitrypsin deficiency respond to inhaled bronchodilators, such as albuterol and ipratropium with decreased airflow obstruction. But the intravenous administration of α1 antitrypsin pooled from human donors, a form of replacement therapy called “intravenous augmentation” directly addresses the pathobiology of the disease and helps preserve the elastic recoil of lung tissue and potentially slowing disease progression.

In static conditions, P _L is equivalent to the elastic recoil pressure (P _el ) of the lung.

• The lung has an innate tendency to collapse that is counterbalanced by the tendency of the elastic chest wall to “spring out.”

• This pressure difference creates a “vacuum” in the pleural space (see Clinical Correlation Box 13.6 ).

  Clinical Correlation Box 13.6

  Coughing, or exhalation at high velocity, is initiated by irritant receptors in the large airways and mediated by the medulla.

  • Initiates tremendous inspiration

  • Seals the epiglottis and vocal cords

  • Abdominal muscles contract to generate high intrathoracic pressure

  • Seal is abruptly released, driving air out at high velocity

  The trachea can add resistance through contraction of the smooth muscle connecting its cartilage rings, resulting in a smaller diameter.

  • Recall that A ₁ V ₁ = A ₂ V ₂ (A = cross sectional area, V = fluid velocity)

  • Thus smaller diameter → higher velocity

  • High intrathoracic pressures generated by abdominal musculature overcome the tendency of increased resistance to limit flow (Q=P/R)

  Thus this high speed mobilizes debris and helps to clear phlegm and mucus.

• The force with which the lungs tend to collapse is the elastic recoil pressure, which is defined as the difference between the pressure outside of the lung (P _pl ) and inside the lung wall (P _alv ):

  P _el = P _alv – P _pl

The pressure of expansion or contraction (P expansion or contraction, or P _E/C ) for the lungs is defined as the net result of recoil pressure and transmural pressure across the lungs.

P _E/C = P _L + P _el

• When the lungs are neither expanding nor contracting, P _L and P _el are equal and opposite and P _E/C =0.

• In general, the positive transpulmonary pressure opposes the lungs’ recoil pressure because of connective tissues in the lung parenchyma, such as elastin and collagen. However, it is the recoil pressure of the lung that drives contraction and exhalation.

The tendency for the chest wall to “spring out,” increasing the intrathoracic volume, is the P _CW may be represented as:

P _CW = Ppleural space – Pbody surface = P _pl – P _bs

Thus the transmural pressure across the entire respiratory system is represented as a balance between elastic recoil and chest wall expansion:

P _RS = P _alv – P _atm = (P _alv – P _pl ) + (P _pl – P _bs ) = P _alv – P _bs

Compliance

The shape of transmural pressure-volume (PV) curves for elastic containers like the lung is determined by the elastic recoil properties of the container walls.

• When recoil pressure is constant overall volume, the transmural PV has a linear relationship.

  • ↑ Transmural pressure against a constant recoil pressure → ↑ container volume in a direct proportion to change in transmural pressure.

  • Higher recoil force = decreased slope (more pressure required to achieve same change in volume).

  • Lower recoil force = increased slope (less pressure required to achieve same change in volume) ( Fig. 13.6 ).

    

Compliance (C) is defined as the slope of this curve, or the change in volume in the lung (∆V) that occurs for a given change in transmural pressure (∆P) ( Fig. 13.7 ). Compliance is thus inversely proportional to elastic recoil.

C = ∆V/∆P

Recall that the linear relation between transmural pressure and volume implies a recoil force that is uniform over all volumes. However, the transmural PV curves are not linear in the lung and chest wall ( Fig. 13.8 ).

• Like a rubber band being stretched, greater ΔV leads to greater recoil force (and thus greater difficulty in expanding the lungs).

• This tends to progressively flatten the transmural PV curve.

The lung/chest wall counterbalance and the breathing cycle

The transmural PV curves for the lungs and chest wall in isolation differ due their differences in recoil properties.

• Lungs ( Fig. 13.9 )

  • If transmural P is ≤ 0, the recoil force of the lung acts unopposed and the lung collapses (atelectasis).

  • At larger lung volumes, ↓ C because of ↑ recoil force.

  • Eventually, volume expansion cannot occur and further ↑ in pressure leads to alveolar rupture (barotrauma).

  

• Chest wall ( Fig. 13.10 ).

  • As transmural P becomes increasingly negative, C approaches zero/

  • If transmural P = 0, the chest wall tends to maintain 60% of thoracic capacity volume because of inherent recoil outwards.

  • As transmural P becomes more positive, the chest cavity will continue to expand.

  • However, at a certain point, the chest wall’s recoil forces direct inward (similar to the lung) and resist further expansion.

  

However, in a living person, the lung and chest wall work in unison as a single container (the chest wall/lung system) with its own elastic recoil properties.