Muscles of Respiration Accessory

While quiet, effortless breathing is powered by your diaphragm and external intercostals, your body has a powerful backup system for times of physiological stress. The accessory muscles of respiration are recruited during labored inhalation and forced exhalation, transforming your thorax into a more efficient pump when demands for oxygen increase or when airways are obstructed. Understanding these muscles is not just an anatomical exercise; it’s crucial for diagnosing respiratory distress, interpreting physical exam findings, and managing conditions from asthma to heart failure.

Foundational Anatomy: The Primary vs. Accessory Distinction

To appreciate the accessory muscles, you must first understand the baseline. Quiet inspiration is primarily driven by the diaphragm and the external intercostal muscles. The diaphragm contracts and flattens, increasing the vertical dimension of the thoracic cavity. The external intercostals elevate the ribs, contributing to the "bucket handle" and "pump handle" motions that increase the transverse and anteroposterior dimensions, respectively. This coordinated action creates negative intrapleural pressure, drawing air into the lungs. Quiet expiration is a passive process; it relies on the elastic recoil of the lungs and chest wall as these inspiratory muscles relax.

The accessory muscles of respiration are recruited when the work of breathing increases significantly. They are not typically active during rest but become essential during exercise, airway obstruction (e.g., asthma, COPD), or when lung compliance is decreased (e.g., pulmonary fibrosis). Their activation is a clear clinical sign of increased respiratory effort or distress.

Accessory Muscles of Inspiration

When a deeper, more forceful inhalation is required, your body calls upon additional muscles to further elevate the rib cage and sternum. The major players are the sternocleidomastoid, scalenes, and pectoralis minor.

The sternocleidomastoid (SCM) muscles are the most prominent accessory inspiratory muscles. When both sides contract, they elevate the sternum, directly increasing the anteroposterior diameter of the thorax. You can feel them contract by placing your fingers on the sides of your neck just above the clavicles while taking a deep, forceful breath. In severe respiratory distress, hypertrophy of these muscles can even become visually apparent.

The scalene muscles (anterior, middle, and posterior) are often considered primary inspiratory muscles as they may have slight activity during quiet breathing. However, their role becomes pronounced during labored breathing. They elevate and fix the first two ribs, providing a stable platform from which other muscles can act. Dysfunction here can contribute to certain thoracic outlet syndromes.

The pectoralis minor assists by elevating the third, fourth, and fifth ribs when the scapula is fixed. This action is particularly leveraged when a person leans forward and braces their arms on a table or their knees—a position known as the tripod position. This posture is a classic compensatory mechanism in patients with COPD, as it allows these accessory muscles to function more effectively.

Accessory Muscles of Forced Expiration

Normal expiration is passive, but situations like coughing, sneezing, singing, or blowing require active, forceful expulsion of air. This is achieved by muscles that compress the abdominal cavity, forcing the diaphragm upward, and by muscles that directly depress the rib cage.

The abdominal muscles are the principal force generators. This group includes the rectus abdominis, external obliques, internal obliques, and transversus abdominis. When they contract, they increase intra-abdominal pressure. This pressure pushes the relaxed diaphragm superiorly into the thoracic cavity, rapidly decreasing thoracic volume and increasing pleural pressure to expel air. A strong cough is entirely dependent on coordinated abdominal muscle contraction.

For forced exhalation that also involves depressing the ribs, the internal intercostal muscles are key. Unlike their external counterparts, the internal intercostals (except for the interchondral part) have fibers that run in a direction to pull the ribs downward and inward. This action decreases the transverse diameter of the thorax, further compressing the thoracic cavity to force air out. During a maximal forced exhalation, these muscles work in concert with the abdominals.

Clinical Integration and Pathophysiology

Recognizing the use of accessory muscles is a fundamental clinical skill. Their activation is a hallmark of increased work of breathing. In an asthma attack, for example, bronchoconstriction and inflammation dramatically increase airway resistance. To overcome this, patients vigorously recruit the SCM and scalenes, often sitting upright in a tripod position to engage the pectoralis minor. You may observe supraclavicular and intercostal retractions, where the skin is pulled inward between the ribs and above the clavicles during inspiration—a sign of high negative intrathoracic pressure.

In chronic obstructive pulmonary disease (COPD), patients often develop a "barrel chest" and rely permanently on accessory muscles due to hyperinflation. The flattened, inefficient diaphragm cannot generate adequate force, making the accessory muscles the primary drivers of inspiration. This is metabolically costly and contributes to the weight loss and muscle wasting sometimes seen in advanced disease. Conversely, injury to the spinal cord in the cervical region can paralyze these accessory muscles, leaving the diaphragm (innervated by C3-C5) as the only functioning inspiratory muscle, resulting in profoundly restricted ventilation.

Common Pitfalls

Misinterpreting Quiet Breathing: A common mistake is to list the sternocleidomastoid or abdominal muscles as primary muscles for normal tidal breathing. Remember, their activation is a red flag for physiological strain. On an exam, a question about "normal, quiet inspiration" is testing your knowledge of the diaphragm and external intercostals.

Overlooking the Scalenes: It's easy to focus on the prominent SCM and forget the scalenes. Recognize that the scalenes are critical for stabilizing the upper ribs. In questions about muscle actions, remember that elevating the first rib is a key function of the scalenes, not the SCM (which primarily lifts the sternum).

Confusing Internal vs. External Intercostals: Mixing up the actions of the intercostal layers is a frequent error. Use this mnemonic: External intercostals Elevate for Inspiration. Internal intercostals (except the interchondral part) are for forced expiration. Thinking about fiber direction can help: external fibers run "down and forward" like your hands in your pockets, pulling the ribs up and out.

Ignoring the Clinical Picture: In isolation, muscle origins and insertions are dry facts. The pitfall is failing to integrate this anatomy with pathophysiology. Always ask: Why is this muscle being used? What disease process would lead to hypertrophy of the abdominal musculature as it relates to breathing (e.g., chronic bronchitis with constant coughing)?

Summary

• The accessory muscles of respiration are recruited during labored breathing, exercise, or airway obstruction, and are not primary drivers of normal, quiet respiration.
• Major accessory inspiratory muscles include the sternocleidomastoid (elevates sternum), scalenes (elevate first two ribs), and pectoralis minor (elevates ribs 3-5), all acting to further increase thoracic volume.
• Forced expiration requires active contraction of the abdominal muscles (rectus abdominis, obliques) to increase intra-abdominal pressure and the internal intercostals to depress the rib cage, compressing the thoracic cavity.
• Clinically, the use of accessory muscles (visible SCM contraction, supraclavicular retractions) is a key sign of increased work of breathing and respiratory distress, seen in conditions like asthma, COPD, and pulmonary fibrosis.
• Understanding the transition from primary to accessory muscle use provides critical insight into a patient's respiratory status and the underlying pathophysiology of their disease.