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Clinical Nursing Skills

18.1 Respiratory System

Clinical Nursing Skills18.1 Respiratory System

Learning Objectives

By the end of this section, you will be able to:

  • Identify the structures and functions of the respiratory system
  • Recognize the physiology of the respiratory system
  • Describe the regulation of the respiratory system

The primary purpose of the respiratory (or pulmonary) system is gas exchange, which is necessary to support human life. The gas exchange happens where the capillaries and alveoli meet, with a very thin membrane between them—the capillary-alveolar bed (or membrane). The process of breathing—inspiration (inhaling) and expiration (exhaling)— provides O2 and removes CO2 waste. The cardiovascular system provides the means of transport for O2 and other nutrients and the removal of waste products. The blood vessels provide the medium for the exchange of gases by the pulmonary circulation through interaction with respiratory alveoli. The joining of these systems as the cardiopulmonary system combines the actions of cardiac perfusion (vascular circulation powered by the pumping heart, which delivers O2 and other nutrients to the body) with respiratory ventilation to provide the essential processes of oxygenation and perfusion. Prior to considering the complexity of the combined cardiopulmonary system, each system is explored individually, and these concepts are investigated more deeply later in this section.

This chapter also considers dysfunctions of the cardiovascular and pulmonary systems, diagnostics for recognition and assistance in planning care, and management of patients, particularly nursing actions and skills. The following section explores the structure and function, physiology, and regulation of the respiratory system.

Structures and Functions of the Airway

What is considered the airway consists of structures from the head and face through the pulmonary cavity in the chest (Figure 18.2). The study of the structure (anatomy) of the airway tends to be considered as two components: upper and lower airways. The upper airway extends from the sinuses and nose through the trachea to the carina, where the airway bifurcates into left and right bronchi and continues into the lungs. This helps to focus on the different locations of the sections of the airway, as well as the normal function of each, and the variation of pathophysiology when things go awry. Disturbed function may arise from a variety of issues, including microbial invasions, exposure to noxious or toxic gases, and injuries. This section explores the structures of the upper and lower airways and their function, physiology of the respiratory system, and respiratory system regulation.

A diagram of the respiratory system.
Figure 18.2 Air enters the respiratory system through the nasal cavity and pharynx and then passes through the trachea and into the bronchi, which brings air into the lungs. (credit: modification of work from Biology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

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.

Real RN Stories

Endotracheal Suctioning

Nurse: Danisha, RN
Clinical setting: Intensive care unit (ICU)
Years in practice: Less than one year at the time
Facility location: Dallas, Texas

As a student, I took an elective course between junior and senior years of nursing school—it was a course modeled after senior capstone and included 400 clinical hours with a preceptor. My placement was night shift in the ICU. My first night’s patient was an older adult Asian female who was intubated and on mechanical ventilation; she was on pressors to maintain her blood pressure adequately. I remember coming in with lofty goals in mind, and when I saw this patient with all the tubes and wires and the monitor and ventilator, I was overwhelmed. One of the first tasks necessitated by the patient’s status was to suction her through an inline suction catheter that passed through the endotracheal tube. She was coughing, and my nurse preceptor showed me how to advance the suction catheter through the tube; she demonstrated the suction control, and while withdrawing the catheter, she suctioned the patient of moderate secretions.

As the patient recovered between passes, she asked how I would know if the catheter had advanced to touch the carina. At that point in my nursing education, I had no idea. “She’ll cough,” she told me, “The carina is sensitive, so when it’s touched, the patient will cough, and you’ve gone too far. Ideally, you want to pay attention to how far that is, so you don’t go that far again.” Through over ten years in the ICU, I never forgot that recommendation and tried not to stimulate the discomfort of hitting the carina when suctioning.

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.


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.

Physiology of the Respiratory System

The exchange of gases, primarily O2 and CO2, is the purpose of the respiratory system. The removal of CO2 during expiration also helps to regulate the body’s acid-base balance. Acid-base balance is measured by pH level. The body is sensitive to alterations in pH, and there is a narrow range of normal for pH: 7.35 to 7.45. In circumstances when the body’s pH has fallen out of range, the respiratory system is able to adjust quickly in an effort to normalize it (Daniels, 2020). By increasing the rate and depth of respirations, excess CO2 is released through exhalation, and an acidic pH (less than 7.35) may be improved. An alkalotic pH (over 7.45) may be corrected by shallow, slow breaths, allowing the accumulation of CO2 to bring pH closer to normal.

Cilia and mucus throughout the respiratory system provide mechanisms for isolating and removing foreign substances, such as inhaled gases and microbiota. Cilia move pathogens and other inhaled particles that become trapped in mucus out of the lungs and into the bronchi, where expectoration is assisted through coughing.

The lungs also play a role in the conversion of angiotensin I to angiotensin II, in conjunction with the renin-angiotensin-aldosterone system (RAAS) (Figure 18.3) (Fountain et al., 2023). Angiotensin II is recognized for its powerful vasoconstriction properties and therefore increases blood pressure. Angiotensin I is produced by a combination of the enzyme renin from the renal system and angiotensinogen. Angiotensin I is not a potent vasoconstrictor, but when combined with angiotensin-converting enzyme (ACE), it is transformed into angiotensin II and increases blood pressure by its properties of vasoconstriction. Capillaries within the lungs are a major location for ACE production.

A diagram of the renin-angiotensin-aldosterone system.
Figure 18.3 The renin-angiotensin-aldosterone system regulates fluid output and blood pressure. (credit: modification of work from Anatomy and Physiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Oxygenation involves interactions between the respiratory and cardiovascular systems, including air movement through the lungs, where O2 and CO2 are exchanged through the alveoli and capillaries as the respiratory and circulatory systems connect and interact at the alveolar-capillary bed. Physiological processes involved include ventilation (the movement of air in and out of the lungs) and perfusion. This combination of respiratory ventilation and cardiovascular perfusion provides O2 (and other nutrients) to the body’s tissues and removes waste products including CO2 from the tissues.

The part of the respiratory cycle whereby the diaphragm and intercostal muscles contract, which enlarges the space within the thorax, is called inspiration. This enlargement lowers the pressure within the alveoli, and air flows into the lungs. During expiration, the muscles that expanded the thoracic cavity now relax, and elastic recoil reduces the pressures in the lungs and surrounding thorax. The pressure within the intrapulmonary system is momentarily higher than atmospheric pressure, and air is passively exhaled from the lungs. Lungs that are compliant and retain the properties of elastic recoil are able to increase and decrease in size and shape with each respiratory cycle (Figure 18.4).

An image showing how the lungs move for inhalation (left side) and expiration (right side).
Figure 18.4 (a) Inhalation (breathing in) and (b) expiration (breathing out). The orange arrows indicate chest and diaphragm movement as air is inhaled and exhaled. (credit: modification of work from Biology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Potential problems of the respiratory system include any changes to the normal structure and/or function of any part of the system. This may include injuries, such as rib fracture(s) or burns to any part of the airway. Pathophysiological changes from diseases such as asthma or chronic obstructive pulmonary disease can alter the structure of the airways and the processes and effectiveness involved in gas exchange.

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.

A diagram showing the different parts of the alveolar-capillary bed.
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.

A photo of a spirometer.
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)


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.


Diffusion is a transport process that involves molecular movement driven by a concentration gradient. Molecules move from areas of high concentration to those with low concentration. In the case of respiratory gas exchange, diffusion is the primary process for the transport of gas molecules, moving the gas that is in high concentration to a low concentration area. Concentration gradients and the diffusion process are responsible for the exchange of gas between blood, with a high concentration of CO2 and low O2 concentration from the body, and the air in the lungs, which is high in O2 concentration and has low CO2 levels. The diffusion process is often very dynamic, as is the case in the respiratory system, as the molecules are not static. The concentration of gases changes with each breath and as tissues take up O2 and release wastes.


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.

Regulation of the Respiratory System

The respiratory system is controlled by the neurological system. As a basic function of life, respiration is an involuntary effort. Control of several involuntary respiratory and cardiovascular functions, and some movement of the muscular system, originates within the brainstem and cerebellum.

The medulla oblongata, the primary respiratory center in the brainstem, is responsible for signaling to respiratory muscles that allow the process of ventilation. The two sets of respiratory muscles are the ventral and the dorsal respiratory groups, and they cause muscle movement for expiration and inspiration, respectively. Some reflex responses like sneezing, vomiting, and coughing are also under the control of the medulla.

The respiratory rate is controlled by the pons. There are two centers within the pons that are involved in this process. First is the apneustic center, which is involved in signals for length and depth of breaths, or tidal volume. The intensity of respirations is limited by stretch receptors of the muscles involved in breathing and by further signaling from the pneumotaxic center. Inhibitory signals from the pneumotaxic center also provide fine-tuning of respiratory rate control by limiting the action of the phrenic nerve. The actions of the pneumotaxic center lead to diminished tidal volume.


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.

Clinical Judgment Measurement Model

Recognize Cues: Patient with Dyspnea

Mr. Wu is a 73-year-old Asian immigrant who moved to California when he was 27 years old. Mr. Wu has been smoking two packs of cigarettes a day since he was 15 years old and was diagnosed with emphysema ten years ago. He presents to the emergency department stating he cannot breathe. Mr. Wu is sitting upright on the gurney and leaning forward onto the bedside table.

The nurse asks about his health history, and Mr. Wu is only able to say one word before he has to pause to try to catch his breath. The nurse auscultates Mr. Wu’s breath sounds and can barely hear inspiratory and expiratory sounds from either front or back.

Mr. Wu’s vital signs are as follows:

  • HR 118 beats per minute
  • BP 162/94
  • RR 26 breaths per minute
  • T 99.3°F
  • SaO2 75 percent

The nurse considers this patient’s subjective and objective presentation and determines the following: Important information includes medical history and vital signs (HR, BP, RR, SaO2). Priority information includes SaO2 and severely diminished breath sounds. Ventilation and oxygenation are the nurse’s immediate concern.


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.


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).

Physiological Challenge Respiratory Pattern Subsequent Acid-Base Imbalance Resultant Compensatory Change Ideal Result
Anxiety, pain, fear, asthma exacerbation, pulmonary embolus Hyperventilation Respiratory alkalosis (pH >7.45; PaCO2 <35 mm Hg) Hypoventilation in response to alkalosis Normal pH (acid-base balance) with return to normal respiratory rate and depth
Decreased level of consciousness, obesity, weak respiratory muscles Hypoventilation Respiratory acidosis (pH < 7.35; PaCO2 >45 mm Hg) Hyperventilation in response to acidosis Normal pH with return to normal respiratory rate and depth
Table 18.1 Hyperventilation and Hypoventilation

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