# Breathing or Pulmonary Ventilation

Air enters the nose and the nasal cavity, where much of the dust and other foreign particles are filtered out by hairs and mucous.  The inhaled air is also warmed and humidified as it passes over the respiratory mucosa. (When the nasal passages are blocked by congestion, mouth breathing is an option. However air is not filtered or humidified during mouth breathing.) Then, the air proceeds into the pharynx (the throat). From there, the air travels into the larynx, commonly called the voice box. The opening between the pharynx and the larynx is the glottis; the movable flap that covers it during swallowing of food or liquids is the epiglottis. Air then flows into the trachea (the windpipe). The trachea branches into two bronchi, which enter the lungs. The bronchi divide into secondary, then tertiary bronchi, which branch into smaller tubes called bronchioles

The bronchioles lead into the clusters of sacs called alveoli. All the alveoli combined have an enormous surface area for gas exchange (about 3 x 108 alveoli whose total surface area is more than 40 times the area of the our entire body's surface). Alveoli are composed of a single cell layer of squamous epithelium which borders the endothelium of the blood capillaries which surround the alveoli. This close juxtaposition of the alveoli and the capillaries allows for efficient and fast gas exchange. Each alveolus is coated with a surfactant (a phospholipid) covering its inner surfaces to prevent water vapor from increasing the surface tension to the point where the alveolus could not expand. Figure 22.9 "Alveoli and the respiratory membrane" (Figure 22.9 text alternative) illustrates the alveoli and the respiratory membrane formed by the alveolar and capillary walls.  Be sure to examine the anatomy of the respiratory system shown in your text (Figures 22.1, 22.7, 22.8).

Figure 22.9 Alveoli and the respiratory membrane"

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The lungs are not muscular, but they do contain stretch receptors that send impulses through the sensory neurons to the medulla. The smooth muscles in the bronchioles receive motor neuron impulses from the autonomic nervous system; the parasympathetic impulses cause bronchiole constriction, and the sympathetic impulses induce dilation to enhance air exchange during fight or flight.

The act of breathing is possible due to the pressure differences created in the thoracic cavity, which is airtight except for the opening out of the trachea. Several muscles are involved in inspiration and in expiration. The muscles of inspiration include the diaphragm and the external intercostals. Contraction of the diaphragm and the external intercostals acts to expand the chest and increase lung volume so that a slight vacuum is created that helps draw air into the lungs. Normally, expiration is a passive process occurring as the inspiratory muscles relax and decrease the volume of the chest cavity. Forced expiration can be achieved when the abdominal muscles and the internal intercostals contract forcing air out of the lungs, as happens during strenous physical activity.

Pressure changes in the lungs are illustrated in Figure 22.13 "Pressure Changes in the Lungs" (Figure 22.13 text alternative)  (It is customary to let 760 mm Hg, normal atmospheric pressure, equal 0 mm Hg when discussing lung pressures.)

Figure 22.13 Pressure Changes in the Lungs

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You can see that the actual pressure in the lungs changes very little, but that it is decreased to pull air into the lungs in inspiration and increased to expel the air during expiration. These changes in pressure are caused by the action of the diaphragm and other respiratory muscles. The pleurae, double-layered serous membranes surrounding the lungs, play an important role in the inspiration and expiration processes. Since the somewhat elastic lungs tend to pull away from the wall of the chest, there is always a negative pressure in the pleural cavity, the narrow space between the two layers of pleura. This greatly facilitates inspiration. The serous fluid present between the two layers of the pleurae is slippery and reduces friction as the lungs expand and contract.

A number of terms are applied to the volumes of air in the lungs in various states of action or rest. These include tidal volume, inspiratory reserve volume, expiratory reserve volume, vital capacity, residual volume, and total lung capacity. These are defined in Figure 22.16 "Respiratory Volumes and Capacities" (Figure 22.16 text alternative). Note that, due to the residual volume, complete air exchange does not occur with each breath.

Figure 22.16 Respiratory Volumes and Capacities

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Breathing is regulated by the respiratory centers in the medulla and the pons. The regulation of breathing is not well understood, but it appears that the inspiratory neurons and the expiratory neurons are so linked that, as one set of neurons sends signals to the necessary muscles, the other set is inactive. This helps to create the rhythm of breathing. This rhythm is also maintained by the stretch receptors in the lungs. The stretch receptors create inflation reflexes, the Hering-Breuer reflexes, which signal the brain when the lungs are expanded or deflated to prevent over-expansion or over-deflation.

While the medulla controls the breathing rhythm, the pons regulates the rate and depth of respiration. Factors influencing these respiratory modifications include primarily the CO2 levels in the blood, and the H+ concentration in the blood, and, to a lesser extent, the O2 levels in the blood. This homeostatic regulation controlled by the medullary respiratory centers involves a negative feedback mechanism which can be seen in Figure 22.25 "Changes in PCO2 and blood pH regulate ventilation by a negative feedback mechanism." Make sure to click open and review the figure, before proceeding to the rest of the content.  Ventilation is also affected by exercise, sensory stimulation, arterial pressure, and speech

Figure 22.25 Changes in PCO2 and blood pH regulate ventilation by a negative feedback mechanism

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Of those regulatory mechanisms listed in the paragraph above, CO2 level is the primary regulator. We refer to the partial pressure of a gas when discussing gases in the respiratory system. (Consult your text for a discussion of partial pressures, if necessary.) Here's how the PCO2 regulates breathing. CO2 from the blood diffuses into the cerebrospinal fluid (CSF). There, it combines with water to form carbonic acid, H2CO3, which disassociates into a hydrogen ion and a bicarbonate ion:

$\begin{array}{l}C{O}_{2}+{H}_{2}O⇌{H}_{2}C{O}_{3}\\ {H}_{2}C{O}_{3}⇌{H}^{+}+HC{O}_{3}-\end{array}$

Then, H+ is detected by the central chemoreceptors in the medulla. (It is the decrease in pH that is actually detected, since an increased H+ concentration represents a lowered pH.)

When there is a decrease in pH in the cerebrospinal fluid, the central chemoreceptors are triggered to increase the rate and depth of breathing. This causes excess CO2 to be exhaled, returning the pH in the CSF to normal. (Question: Why does breathing into a paper bag prevent a person who is hyperventilating from passing out?)  In terms of body homeostasis, this regulatory mechanism acts as a physiological buffering system and combined with the kidneys (see p 1006 in the textbook) maintains blood pH within normal limits.