Shallow breathing that repeatedly occurs during sleep is known as hypopnea, defined as abnormally slow or shallow breathing. An episode of hypopnea is typically defined as a reduction in airflow of at least 30%, lasting ten seconds or longer, and accompanied by a drop in blood oxygen levels or an arousal from sleep. This recurring reduction in oxygen supply and fragmentation of sleep can lead to long-term health complications, including an increased risk of heart problems, stroke, and excessive daytime sleepiness. Understanding the mechanisms behind this shallow breathing is the first step toward appropriate medical treatment.
The Physiology of Respiration During Sleep
The body’s control over breathing changes when a person transitions from wakefulness to sleep. While awake, breathing is driven by both voluntary control from the cerebral cortex and involuntary control from the brainstem. Upon falling asleep, the voluntary drive is lost, and breathing shifts entirely to automatic, involuntary control centers.
This transition makes the respiratory system more dependent on chemical signals, specifically the body’s sensitivity to carbon dioxide (\(\text{CO}_2\)) and oxygen. During non-rapid eye movement (NREM) sleep, the ventilatory response to rising \(\text{CO}_2\) levels becomes dulled, meaning a higher concentration of \(\text{CO}_2\) is needed to trigger a breath. This reduced sensitivity, combined with decreased metabolic demand, causes minute ventilation—the total volume of air breathed per minute—to naturally decrease, resulting in a slight increase in the body’s baseline \(\text{CO}_2\) level.
Another physiological change involves muscle tone, which decreases in the upper airway during sleep. This relaxation is most pronounced during rapid eye movement (REM) sleep, affecting all muscles except the diaphragm. The reduced tone in muscles like the genioglossus, which normally keeps the throat open, increases the vulnerability of the airway to collapse.
Shallow Breathing Caused by Airway Blockage
The primary cause of shallow breathing during sleep is a physical narrowing or partial collapse of the upper airway, known as obstructive hypopnea. This is a core feature of Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS), where the physical structure of the throat cannot maintain patency against the negative pressure created during inhalation.
During sleep, the muscles that hold the throat open, such as the genioglossus muscle in the tongue, relax. This relaxation allows the soft tissues in the throat—like the soft palate, uvula, and tongue—to fall backward and partially obstruct the airflow. This partial blockage causes air movement to be reduced, leading to the characteristic shallow breathing of a hypopnea event.
Several anatomical and non-anatomical factors increase the risk of this collapse. Obesity, for instance, leads to fat deposits in the neck and around the pharynx, which physically narrows the airway and increases its collapsibility. Other factors include a recessed jaw, an enlarged tongue, or hypertrophied tonsils and adenoids, all of which reduce the space available for air to pass. The distinction between a hypopnea and a full apnea is the degree of closure: hypopnea is a partial restriction, while apnea is a complete cessation of airflow for ten seconds or more.
Shallow Breathing Caused by Neural Control Issues
Shallow breathing can stem from a failure in the central nervous system to generate the proper breathing signal. This is termed central hypopnea and is a manifestation of Central Sleep Apnea (CSA), where the airway remains open but the brain fails to prompt the respiratory muscles to contract.
The brainstem’s respiratory control center, which regulates the rhythm and depth of breathing, becomes unstable or malfunctions. This results in a lack of respiratory effort from the diaphragm and chest wall muscles, causing a pause or a decrease in breathing depth and rate. A specific pattern often seen in CSA is Cheyne-Stokes breathing, where the person cycles between periods of rapid, deep breaths and long periods of shallow breathing or no breathing at all.
Central hypopnea is frequently a secondary condition caused by an underlying medical issue that affects the brain’s ability to regulate \(\text{CO}_2\). Conditions such as congestive heart failure, stroke, and certain neurological diseases can disrupt the respiratory control loop. Additionally, external factors like the use of opioid pain medications or sedatives can depress the central respiratory drive, significantly increasing the likelihood of central hypopnea events.
Shallow Breathing Caused by Lung Conditions
Chronic lung diseases can contribute to shallow breathing, particularly as the body attempts to compensate for reduced respiratory capacity while sleeping. Conditions like Chronic Obstructive Pulmonary Disease (COPD), severe asthma, and pulmonary fibrosis physically impair the ability of the lungs to fully inflate or efficiently exchange gas.
In COPD, the airways are chronically obstructed, and the lung tissue may be damaged, leading to a permanent reduction in the functional capacity of the respiratory system. When a person with a lung condition lies flat, changes in body position and the natural decrease in muscle tone during REM sleep further restrict the ability to breathe deeply. This physiological stress results in hypoventilation, where breathing becomes chronically shallow and ineffective, leading to elevated \(\text{CO}_2\) and reduced oxygen levels.
This exacerbation during sleep can worsen the underlying lung disease and is seen in cases where both COPD and obstructive sleep apnea are present, a combination known as “overlap syndrome.” The reduced efficiency of the lungs combined with the central or obstructive factors creates a cycle where the body struggles to maintain adequate gas exchange, forcing breathing to remain shallow and rapid.