18.1 Respiratory System

Upper Airway

The upper airway includes the trachea as its lowest part and structures above including the sinuses, nose, pharynx, epiglottis, glottis, and larynx. Behind the nose is a space that includes the nasal turbinates or conchae, which are composed of folded mucosal tissues. The nasal turbinates protect the airway from inhaled particles and increase the surface area in the nasal cavity, helping to warm and humidify inhaled air. The sinuses are bilateral cavities named based on the bones where they are located, including frontal (above each eye, maxillary), posterior to the maxillae bilaterally, sphenoid (near the pituitary gland and optic nerves and the sphenoid bone of the eye sockets), and the ethmoid (several small air-filled cells comprising front, middle, and rear groups, each with independent openings to the nasal cavity). The mucus lining the sinuses helps to humidify the air we breathe, and cilia lining the sinuses (hairlike fibers) help to trap and remove excess secretions and foreign objects from the upper airway.

Three regions comprise the pharynx:

• the nasopharynx—behind the turbinates at the posterior of the nasal cavity
• the oropharynx—located at the posterior of the oral cavity
• the laryngopharynx—below the oropharynx, extending to the larynx, familiarly referred to as the voice box

The epiglottis is a cartilaginous structure, which rests its loose end on the glottis, thereby protecting the trachea. When a person swallows, the epiglottis closes the opening from the esophagus (part of the gastrointestinal tract, which sits posterior to the trachea), thereby preventing food or fluid from flowing into the trachea. Located within the glottis are false and true vocal cords. The false vocal cords are also known as vestibular folds and are composed of mucus membrane tissue. True vocal cords have muscular attachments to the thyroid and to laryngeal cartilage; the movement of the inner aspects of the vocal cords provides the mechanism for sound production.

The trachea, commonly referred to as the windpipe, provides the pathway from the upper to lower airways. The esophagus carries fluids and chewed foods from the oral cavity to the stomach. A combination of cartilage and connective tissue gives the trachea its shape and maintains it open for the passage of air. Cilia line the trachea, continuing the process of trapping foreign objects and allowing for their removal, in the same fashion as in the higher structures of the upper airway. Where the trachea bifurcates into the left and right mainstem bronchi is the location of the carina. The carina is the border of the upper and lower airways.

Lower Airway

The lower airway consists of structures below the carina. The bronchi are the major structures of the lower airway and begin with the bifurcation of the right and left mainstem bronchi, which enter into the right and left lung, respectively. Subsequently, the mainstem bronchi continue paths through the lungs as the primary, secondary, and tertiary bronchi, becoming smaller, and branching further throughout the lungs. Bronchi continue to be lined with cilia and goblet cells for mucus production and have cartilaginous rings like the trachea, to provide support and prevent airway collapse.

From the tertiary bronchi, the branching of the airway becomes even smaller, as they are identified as bronchioles. These continue to their smallest form as terminal bronchioles; at this point, the airway is no longer supported by cartilage, and the muscles comprising the walls can dilate and constrict to control the flow of air. The tiny terminal (or respiratory) bronchioles reach alveolar ducts, which are also a combination of smooth muscle and connective tissues, where alveoli (the minuscule, round sacs of air involved in gas exchange) cluster together. These clusters of alveoli are where the most common type I alveolar cells and the smallest capillaries of the bloodstream exchange gases (primarily O₂ and CO₂) through a very thin alveolar-capillary membrane (Ball et al., 2023). Another alveolar cell type (type II) is responsible for the production of surfactant. A phospholipid substance that prevents the collapse of alveoli by reducing surface tension is called surfactant. The third type of alveolar cells, alveolar macrophages, remove foreign substances and waste products from this delicate and essential region.

Lungs

The lungs are responsible for respiration and house the smaller structures involved in the process of ventilation. The right and left lungs are slightly different in structure: the left lung is shaped to include the cardiac notch, which provides space for the heart. The left lung has two lobes: upper and lower; the right lung contains three lobes: upper, middle, and lower. Normal, healthy lungs are supple and yield in size and shape to the demands of respiration, including compliance, the ability to accommodate deep and shallow breaths, and elastic recoil, or the ability to bounce back to normal size and shape after the expansion of inhaling, during exhalation. Lungs are designed to be air-filled. When taxed by disease, fluid accumulation, or exposure to toxic or noxious gases, the lungs can lose effectiveness, and the respiratory processes may become compromised.

Within the lungs are the structures of the lower airway, including the right and left bronchi, primary, secondary, and tertiary, bronchioles, alveoli, and the alveolar-capillary bed, where the cardiopulmonary system interacts, and gases are exchanged. Deoxygenated blood undergoes removal of CO₂, and O₂ is brought into the system. These processes are studied in more detail in the next section, through exploration of the physiology of the respiratory system.

Gas Exchange in Alveoli

Alveoli are found in groups clustered around alveolar ducts, and when inflated, they resemble a cluster of grapes. There are three types of alveolar cells: type I, type II, and alveolar macrophages (Naeem et al., 2022). Type I cells cover approximately 90 percent, or 70 square meters, of surface area within the lungs. These cells are responsible for gas exchange (Figure 18.5). After inspiration, O₂ travels across the capillary-alveolar bed and attaches to hemoglobin, where it is transported throughout the bloodstream and to the body tissues. At the tissues, O₂ is released from the hemoglobin and taken up by the tissues as needed. It is also here that the waste product, CO₂, returns from the body by diffusion (a transport process that involves molecular movement driven by a concentration gradient) into the bloodstream and subsequently the lungs, where it is ultimately removed from the body by exhalation. The respiratory membrane is extremely thin, only about half of a micrometer, which enables gases to easily move to and from the bloodstream and air space within the lungs.

Figure 18.5 In the structures at the alveolar-capillary bed are where gas exchange occurs. (credit: modification of work from Biology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

For alveoli to easily reinflate, or to maximize inflation, surfactant is synthesized and released from type II alveolar cells. These cells are located among the type I cells and are made up of proteins and phospholipids. By coating the exterior of the alveoli, the cells reduce the surface tension, which prevents collapse (Naeem et al., 2022). Surfactant is produced by deep breaths, such as sighs, yawns, sobs, and gasps. Deep breaths often inspire coughing, and coughing causes deep breaths, which fosters continued production and release of surfactant and prevention of atelectasis (alveolar collapse). For this reason, patients are encouraged to cough and deep breathe when inspiration is limited. Nurses and respiratory therapists (RTs) instruct patients on the use of the incentive spirometer, which involves slow, deep breaths, often subsequent coughing, and tends to improve pulmonary function.

The third type of alveolar cell, the macrophages, like phagocytic cells elsewhere in the body, provide the immune system function of phagocytosis (Naeem et al., 2022). Alveolar macrophages are able to travel within the alveolar areas and isolate, consume, and remove foreign particles that have invaded the alveolar region. These cells are not involved directly in the gas exchange process.

Life-Stage Context

Incentive Spirometer Patient Education

With advanced age, some people experience hearing deficit or even total hearing loss (deafness). Older adults may also suffer from one of the cognitive impairments related to dementia. These sensory or cognitive deficits can influence a patient’s comprehension of a nurse’s teaching because the patient is unable to hear or understand the instructions.

Use of the incentive spirometer can be confusing to patients and requires education by the nurse and/or respiratory therapist to properly describe its use. In addition to telling the patient how to use the device, it is recommended the nurse evaluate the patient’s use of the incentive spirometer by demonstration. Often, patients assume that since the mouthpiece is attached to a strawlike hose, they should blow into it instead of the correct action of inhaling deeply through the mouthpiece. The device includes numbers representing volumes, and there is an indicator (piston) that moves with the patient’s inhalation (Figure 18.6). Nurses often write a line with a marker to indicate a goal volume for a particular patient.

Patients with hearing impairment or cognitive deficit may require a more active explanation of the use of the incentive spirometer, including a demonstration by the nurse (using an incentive spirometer dedicated to such patient education), which may also include gestures and dramatic movements to illustrate deep intake of breath through the mouthpiece instead of a blowing action. Again, the patient should provide a return demonstration so the nurse is able to assess proper understanding and use of the incentive spirometer. These patients may also respond well to having a goal indicated by a line on the device, and written reminders as to how often and how many inhalations should be done may be helpful, depending on the type and extent of impairment.

Figure 18.6 Explaining the incentive spirometer’s components and demonstrating its correct use can help patients understand the device’s importance. (credit: modification of work “Kendall Respiflo VS 5000, Atemtrainer, Incentive Spirometer” by Stefan Bellini/Wikimedia Commons, Public Domain)

Respiration

The term respiration is a rather general term, often synonymous with the word breathing. It also may be used interchangeably with the term ventilation, as it involves inhalation and exhalation. Respiration is associated with the process of gas exchange, the primary purpose of the respiratory system.

Respiration is a basic function, generated by the neurological system, with control centers within the medulla oblongata and pons. Regulation by these systems, including actions stimulating the length and depth of each breath, is controlled by opposing actions of the apneustic and pneumotaxic centers, in efforts to maintain homeostasis, or stability, throughout the body.

Respiration is a critical function and is included as one of the vital signs, which most commonly include respiratory rate, heart rate, temperature, and blood pressure. In addition to the respiratory rate, nursing assessment of the respiratory system also includes auscultation of breath sounds and observation of depth and regularity of breathing, symmetry, whether the patient relies on the use of accessory muscles to breathe, their desired position, and how they breathe (e.g., pursed lips, gasping, apneic pauses), as well as apparent anxiety. A noninvasive device called a pulse oximeter measures saturation of hemoglobin with O₂ and can be a valuable respiratory assessment tool. Arterial blood gas (ABG) testing offers important data in some circumstances of respiratory compromise and potential failure, but ABGs are invasive and typically considered painful. Additional diagnostics may include chest radiographs (x-rays), computed tomography or magnetic resonance imaging, ventilation-perfusion (V/Q) scan, and a variety of pulmonary function tests, depending on the diagnosis being explored.

Perfusion

Perfusion, as previously defined, is associated with the circulatory system and is evidenced by the cardiovascular system’s delivery of O₂ and nutrients to body tissues. Adequate perfusion indicates there is enough pumping action of the heart, which is referred to as contractility, and enough volume in the body’s vascular system, as shown by a normal blood pressure. Under conditions of adequate perfusion, patient assessment includes vital signs within normal ranges, normal or baseline mentation, pulses typified as 2+ (normal), no dependent edema noted, breath sounds that are clear without adventitious sounds, and skin that is warm, dry, and of normal color for race.

Inadequate perfusion tends to involve a variety of signs and symptoms. Examples of poor perfusion include deterioration of vital signs, which may include tachycardia (heart rate over 100 beats per minute), hypotension (low blood pressure, e.g., under 90 systolic), abnormal body temperature, tachypnea (respiratory rate over 20 breaths per minute), mental status or level of consciousness changes that may range from slight confusion to lethargy to unconsciousness, peripheral edema, potentially adventitious breath sounds like crackles, and skin that feels cool, clammy, and is notably changed in appearance from normal to demonstrating pallor.

Respiratory changes due to lack of perfusion are particularly important, as the respiratory system is often the first to display signs and symptoms indicative of this negative status change. The signs emanating from the respiratory system may be obvious, such as tachypnea or crackles, or may be reflected in a neurological change, such as a change in mental status.

Dyspnea

The medical term for the subjective feeling of shortness of breath or difficulty breathing is dyspnea. Patients can be asked to rate their dyspnea on a scale of zero to ten, similar to using a pain rating scale. The feeling of dyspnea can be very disabling for patients. Nurses can objectively assess the response to the experience by noting a climbing respiratory rate, shallow breaths, the use of accessory muscles, and whether the patient is able to speak only one word between breaths. Certain pathological changes to normal physiology, like asthma, heart failure (HF), chronic obstructive pulmonary disease (COPD), hypercapnia (elevated CO₂), and anxiety, may contribute to dyspneic episodes. Interestingly, anxiety can both cause and result from dyspnea, as struggling to breathe is one of the most helpless, frightening experiences most people can have.

Episodes of dyspnea may or may not require intervention from the healthcare team. Sometimes, the symptoms are mild and transitory, resolving as quickly as they began. However, if the patient’s respiratory status is compromised, prompt action may be necessary. Observations and assessments of respiratory deterioration may include a falling O₂ saturation as seen on pulse oximeter, exhaustion from sustained tachypnea and use of accessory muscles, intolerance of lying flat, and decreased breath sounds.

Hypoxia

A reduced level of tissue oxygenation is the definition of hypoxia. Hypoxia has many causes, ranging from respiratory and cardiac conditions to anemia. A specific type of hypoxia is hypoxemia, defined as decreased partial pressure of oxygen in the blood (PaO₂) indicated in an ABG result.

Early signs of hypoxia are anxiety, confusion, and restlessness. As hypoxia worsens, the patient’s level of consciousness and vital signs will worsen with an increased respiratory rate and heart rate and decreased pulse oximetry readings. Late signs of hypoxia include bluish discoloration of the skin and mucous membranes called cyanosis.

Hyperventilation

Rapid, deep breathing is referred to as hyperventilation. A faster respiratory rate and depth cause low levels of CO₂ in the blood. Hyperventilation can occur due to anxiety, panic attacks, pain, fear, head injuries, or mechanical ventilation. Acute asthma exacerbations, pulmonary embolisms, or other respiratory disorders can initially cause respiratory alkalosis as the lungs breathe faster in an attempt to increase oxygenation, which decreases the PaCO₂. After a while, however, these hypoxic disorders cause respiratory acidosis as respiratory muscles tire, breathing slows, and CO₂ builds up in the blood (Table 18.1).