What is irregular breathing pattern called?

DEFINITIONS

Patterns of breathing during sleep may be categorized into one of several types. Primary snoring (PS) consists of snoring without a change in sleep architecture, alveolar ventilation, or gas exchange abnormalities. The incidence of PS on a habitual basis ranges from 7% to 10% of children.3 Most children with PS do not progress to SDB.4

Upper airway resistance syndrome (UARS) describes the effect of negative intrathoracic pressure changes on inspiration during sleep. These changes are caused by airway obstruction that may lead to electroencephalographic arousals and major sleep fragmentation, but not to frank apnea. In addition to the repeated transient electroencephalographic arousals, an increase in snoring occurs just prior to the arousal. Changes in the respiratory pattern include an increase in the time of inspiration and a coinciding decrease in the time of expiration, but no change in gas exchange abnormalities.5 UARS is found most often during rapid eye movement (REM) sleep. It is difficult to document in children because it usually requires direct measurement of intrathoracic pressure in the esophagus, a procedure difficult to perform in most children. In assessing the quality of life in children with SDB, de Serres and associates have shown that UARS is more common than obstructive apnea.6

Obstructive apnea (OA) is the absence of any gas exchange that results from complete obstruction of the upper airway during a respiratory effort. During sleep, these obstructive episodes result in electroencephalographic arousals, sleep fragmentation, and gas exchange abnormalities.

During an episode of central apnea, there is an absence of gas exchange that results from an absence of a respiratory effort. Episodes of central apnea are abnormal if they are longer than 20 seconds in duration or associated with one of the following: oxygen desaturation below 90%, bradycardia, or nighttime arousals.7,8 Mixed apnea episodes contain both obstructive and central elements.

Hypopnea is a partial obstruction during sleep that may result in electroencephalographic arousal, sleep fragmentation, and changes in ventilation and gas exchange. In children, there has been a lack of consensus of what actually constitutes a hypopnea. Catterall and colleagues have described a hypopnea as breath with a 50% reduction in airflow.9 Gould and co-workers have described it as a 50% reduction in respiratory effort.10 Guilleminault and associates have reported both a reduction in airflow and associated oxygen desaturation.11 Block and colleagues have suggested a reduction in airflow and respiratory effort in association with a fall in oxygen saturation.12 Complete (obstructive apneas) and partial obstructions (hypopneas) intermingled with periods of normal sleep and ventilation are defined as the obstructive sleep apnea syndrome (OSAS).

A respiratory event–related arousal (RERA) is a gradual increase in the end-inspiratory negative intrathoracic pressure of at least 5 cm H2O during five or more breath cycles, followed by an arousal or awakening.13 This subtle measure of a significant respiratory disturbance may be more important in children than in adults.

Observation of Breathing Patterns

Breathing patterns vary among individuals and may be influenced by pain, emotion, body temperature, sleep, body position, activity level, and the presence of pulmonary, cardiac, metabolic, or nervous system disease (Table 4-4). The optimal time, clinically, to examine a patient's breathing pattern is when he or she is unaware of the inspection because knowledge of the physical examination can influence the patient's respiratory pattern.

Observation of breathing pattern should include an assessment of rate (12 to 20 breaths per minute is normal), depth, ratio of inspiration to expiration (one to two is normal), sequence of chest wall movement during inspiration and expiration, comfort, presence accessory muscle use, and symmetry.

 Clinical Tip

If possible, examine a patient's breathing pattern when he or she is unaware of the inspection because knowledge of the physical examination can influence the patient's respiratory pattern. Objective observations of ventilation rate may not always be consistent with a patient's subjective complaints of dyspnea. For example, a patient may complain of shortness of breath but have a ventilation rate within normal limits. Therefore the patient's subjective complaints, rather than the objective observations, may be a more accurate measure of treatment intensity.

7 How can the respiratory pattern and brainstem reflexes help in the assessment of the comatose patient?

Respiratory pattern and rate are often helpful in identifying the cause of coma. Hyperventilation, as an example, may be a response to hypoxemia, metabolic acidosis, toxins, or dysfunction within the pons. Cheyne-Stokes breathing may indicate diencephalic lesions or bilateral cerebral hemisphere dysfunction, for example, increased ICP or metabolic abnormalities. Cluster breathing is associated with high medulla or lower pontine lesions. Brainstem reflexes should be examined and focal motor abnormalities, as well as reflex asymmetry, recorded. Equal and reactive pupils may indicate toxic or metabolic causes, whereas a unilateral fixed and dilated pupil usually indicates oculomotor palsy possibly as a result of uncal herniation. Bilateral pinpoint pupils with minute reaction suggest a pontine lesion, and bilateral fixed and dilated pupils may indicate medullary injury, global anoxia, or hypothermia. Ocular bobbing (a repetitive rapid vertical deviation downward and slow return to neutral position) indicates a pontine lesion often seen in basilar artery occlusion, whereas ping-pong or windshield-wiper eye movements usually indicate bilateral cerebral dysfunction. Eye movements can safely be elicited in the comatose patient without cervical spine injury by performing the oculocephalic maneuver (often called “doll's eyes”), that is, by rapidly rotating the head from side to side. If the paramedian pontine reticular formation and the vestibular system are intact, the eyes should move smoothly in the direction opposite to that in which the head is rotated.

If cervical spine stability is in question, or no response to oculocephalic maneuvers occurs, the oculovestibular response (often called “cold calorics”) can be tested instead. One tympanic membrane is irrigated with 30 mL of ice-cold water and the response observed. When the underlying brainstem structures are intact, both eyes will deviate laterally toward the side where the cold water is instilled. If cortical structures and parts of the frontal lobe are intact, there will be nystagmus with the fast phase toward the nonirrigated ear. In metabolic or toxic coma the clinician usually sees intact gaze deviation toward the irrigated ear but absent or abnormal nystagmus indicating cortical dysfunction. In many comatose patients with structural brainstem injury, the oculovestibular system is impaired, and deviation of the eyes is absent or abnormal.

Physical Examination

Pattern of breathing (e.g., splinting, use of pursed lips or accessory muscles), body habitus (e.g., cachexia, obesity), posture (e.g., leaning forward on elbows to recruit pectoralis muscles as ventilatory muscles, as in COPD), skeletal deformity, and emotional state may be important clues to the underlying diagnosis. Cough on deep inspiration or expiration suggests asthma or interstitial lung disease. A generalized decrease in the intensity of breath sounds suggests emphysema or moderate to severe bronchoconstriction, whereas a localized decrease may result from pneumothorax, pleural effusion, localized airway obstruction, or elevated hemidiaphragm of any cause. Forced expiratory maneuvers may elicit focal or diffuse wheezing. Cardiac examination may suggest pulmonary hypertension (e.g., right ventricular heave or prominent P2) or right ventricular failure (e.g., jugular venous distention, right-sided S3 gallop). Clubbing of the digits is an easily overlooked sign of many processes, notably cancer or purulent lung disease (e.g., bronchiectasis). Cyanosis, a bluish coloration of the perioral region or nails, indicates there are at least 5 g of deoxygenated hemoglobin per 100 mL of blood (note: hypoxemia in the presence of significant anemia may not cause cyanosis because of insufficient hemoglobin). Edema of the lower extremities suggests congestive heart failure if symmetrical and thromboembolic disease if asymmetrical. Assessment of the patient's emotional status may be helpful.84

If a patient's history includes a report that he or she develops dyspnea walking a short distance (e.g., <200 yards), one should consider walking the patient in a corridor or up a flight of stairs near the examination room to provoke his or her symptoms. When the patient becomes dyspneic, observe the patient, repeat the vital signs, reexamine the chest and heart, and check the oxygen saturation with pulse oximetry. The development of an abrupt increase in heart rate and blood pressure (e.g., pulse pressure product) or onset of basilar crackles or acute wheezing suggests a rapid increase in pulmonary capillary pressure and interstitial edema. Rapid shallow breathing may be a sign of stiff lungs or chest wall. Occasionally the patient will walk farther than one would expect from the history; motivation and the inability of the patient to tolerate any respiratory discomfort may, in fact, be the cause of the patient's limitation. It is not uncommon for patients who lead extremely sedentary lives, especially if they have been told they have a condition that may cause shortness of breath, to interpret any increase in ventilation as pathologic.

A Anesthetic Depth and Respiratory Pattern

The respiratory pattern is altered by the induction and deepening of anesthesia. When the depth of anesthesia is inadequate (less than MAC), the respiratory pattern may vary from excessive hyperventilation and vocalization to breath-holding. As anesthetic depth approaches or equals MAC (light anesthesia), irregular respiration progresses to a more regular pattern that is associated with a larger than normal Vt. However, during light but deepening anesthesia, the approach to a more regular respiratory pattern may be interrupted by a pause at the end of inspiration (a “hitch” in inspiration), followed by a relatively prolonged and active expiration in which the patient seems to exhale forcefully rather than passively. As anesthesia deepens to moderate levels, respiration becomes faster and more regular but shallower. The respiratory pattern is a sine wave losing the inspiratory hitch and lengthened expiratory pause. There is little or no inspiratory or expiratory pause, and the inspiratory and expiratory periods are equivalent. Intercostal muscle activity is still present, and there is normal movement of the thoracic cage with lifting of the chest during inspiration.

The respiratory rate is generally slower and the Vt larger with nitrous oxide–narcotic anesthesia than with anesthesia involving halogenated drugs. During deep anesthesia with halogenated drugs, increasing respiratory depression is manifested by increasingly rapid and shallow breathing (panting). On the other hand, with deep nitrous oxide–narcotic anesthesia, respirations become slower but may remain deep. In the case of very deep anesthesia with all inhaled drugs, respirations often become jerky or gasping in character and irregular in pattern. This situation results from loss of the active intercostal muscle contribution to inspiration. As a result, a rocking boat movement occurs in which there is out-of-phase depression of the chest wall during inspiration, flaring of the lower chest margins, and billowing of the abdomen. The reason for this type of movement is that inspiration is dependent solely on diaphragmatic effort. Independent of anesthetic depth, similar chest movements may be simulated by upper or lower airway obstruction or by partial paralysis.

Abnormal Respiratory Patterns

Central causes uncommonly result in respiratory failure. Many supraspinal neurological disorders produce a “restrictive” pattern on pulmonary function tests, which is often clinically insignificant. Respiratory failure is not a major problem unless other medical complications occur. Rare exceptions to this caveat include central hypoventilation syndromes resulting from congenital or acquired disorders of medullary respiratory center or apneic seizures. By and large, central disorders produce certain characteristic respiratory patterns in the context of acute devastating neurological illnesses. Most of these patterns, such as Cheyne-Stokes respiration, central neurogenic hyperventilation, apneustic breathing, and ataxic breathing, affect primarily the rate and rhythm of breathing. A number of nonneurological conditions can also produce these respiratory patterns.