Respirations

Chapter: Respirations
McMaster Section Editor(s): Nathan Hambly
Section Editor(s) in Interna Szczeklika: Ewa Niżankowska-Mogilnicka, Filip Mejza
McMaster Author(s): Anurag Bhalla, Nathan Hambly
Author(s) in Interna Szczeklika: Wojciech Szczeklik, Miłosz Jankowski
Additional Information

Definition and EtiologyTop

1. Respiratory cycle:

1) Respiratory rate (in adults normal respiratory rates at rest range from 12-20 breaths/min):

a) Tachypnea (increased respiratory rate): Caused by anxiety or panic disorder, pain, exertion, elevated body temperature, sepsis, pregnancy, acidosis, anemia, endocrine disease (hyperthyroidism, pheochromocytoma, hypocalcemia), pulmonary disease, cardiovascular disease, primary myopathy or neuromuscular disorders, and deconditioning (rates >30 breaths/min are often associated with the onset of respiratory failure in patients with pulmonary or cardiovascular disorders).

b) Bradypnea (decreased respiratory rate): Caused by central nervous system (CNS) disorders (eg, elevated intracranial pressure, disorders of the brain stem), opioid or benzodiazepine overdose, hypothyroidism, metabolic alkalosis.

2) Depth of breathing (depth of inspiration):

a) Hyperpnea (increased volume with or without an increased respiratory rate) may develop in patients with metabolic acidosis. Kussmaul breathing involves a deep, gasping, and labored respiratory pattern (increased frequency and tidal volume) that is often seen in severe metabolic acidosis (often associated with diabetic ketoacidosis but can also occur in toxic alcohol ingestion, lactic acidosis, renal failure, or salicylate toxicity).

b) Hypopnea (shallow breathing) may develop in patients with respiratory failure, particularly in the case of exhaustion of the respiratory muscles (this is followed by gasping and apnea). Chest wall disorders and neuromuscular weakness can also result in a shallow breathing pattern. Agonal breathing is slow and very shallow breathing that may develop in patients with anoxic brain injury of any cause and may lead to apneas.

c) Hyperventilation is overventilation (increase in the rate or tidal volume) that is necessary for elimination of carbon dioxide. It leads to hypocapnia. Causes: acidosis, stress, anxiety or panic disorder, high altitude, brain injury, stroke, anemia, pulmonary or cardiovascular disorders as described above.

d) Hypoventilation is underventilation that is required for adequate gas exchange. It leads to hypercapnia. Causes: obesity, stroke involving brainstem, medication overdose (benzodiazepines and narcotics), alkalosis.

3) Inspiration-to-expiration ratio: Under normal conditions expiration is slightly longer than inspiration. Prolonged expiration occurs in patients with exacerbation of obstructive lung diseases (asthma, chronic obstructive pulmonary disease [COPD]).

4) Other abnormalities:

a) Cheyne-Stokes respiration: An irregular breathing pattern described as a cyclical crescendo-decrescendo pattern with periods of central apnea. Respirations gradually increase in depth and rate and then become less frequent and shallow with periods of apnea. Causes: heart failure, stroke, metabolic or drug-induced encephalopathy, traumatic brain injury, brain tumor, carbon monoxide poisoning, altitude sickness, and sometimes at the end of life.

b) Biot respirations: A rapid, shallow, irregular breathing pattern with increasing episodes of apnea (10-30 seconds). Causes: elevated intracranial pressure, CNS lesion at the level of the medulla oblongata, drug-induced coma (opioids). This breathing pattern is sometimes lumped with ataxic breathing, which refers to irregular frequency and tidal volumes intermixed with unpredictable episodes of apneas.

c) Breathing interrupted by deep inspirations (sighing respirations): Isolated deep inspirations and expirations occurring between normal breathing cycles, often with audible sighing. Causes: anxiety and psycho-organic disorders.

d) Apnea and shallow breathing during sleep (see Obstructive Sleep Apnea).

2. Mechanism of breathing: The mechanism of breathing is complex and regulated by 2 anatomically distinct but functionally integrated elements involving central (brainstem, metabolic) and voluntary respiratory control centers. Rhythmic control is regulated by central and peripheral chemoreceptors sensing carbon dioxide, pH, and oxygen, as well as lung mechanoreceptors (eg, pulmonary stretch receptors). In the medulla, the dorsal respiratory group is responsible for generating inspiratory impulses while the ventral respiratory group triggers expiration. The pons contains 2 additional respiratory areas: the pneumotaxic center has an inhibitory effect on inspiration while the apneustic center has an excitatory function. Breathing effectors include diaphragm, intercostal muscles, and abdominal and accessory muscles. The diaphragm is the principle muscle of respiration.

1) Thoracic breathing uses external intercostal muscles and is more frequent in women. In patients with severe ascites, large abdominal tumors, and diaphragm paralysis, as well as in advanced pregnancy, it is the only breathing mechanism.

2) Abdominal (diaphragmatic) breathing uses the diaphragm and is more common in men than in women. It is most frequently seen in patients with ankylosing spondylitis, paralysis of the intercostal muscles, and severe pleural pain.

3. Mobility of the chest:

1) Unilateral impairment of chest mobility (with normal mobility on the contralateral side): Caused by unilateral disease process including airway obstruction, pulmonary edema or fibrosis, pleural disease (significant effusion or fibrosis [fibrothorax]), structural immobility or defect (thoracoplasty or rib fracture), and diaphragmatic paralysis.

2) Paradoxical chest movement: Recession of the thoracic wall on inspiration. Causes: trauma leading to fracture of >3 ribs in >2 places (so-called flail chest) or fracture of the sternum causing paradoxical mobility of a part of the thoracic wall. Flail chest associated with respiratory failure is the only indication for consideration of rib fracture fixation. Paradoxical chest movement may occasionally occur in patients with respiratory failure due to other causes.

3) Paradoxical diaphragmatic movement (diaphragmatic paradox or paradoxical breathing) occurs during respiration when the abdominal and chest wall move in opposite directions. Normally during inspiration the chest wall expands and the diaphragm moves downwards, causing outward expansion of the abdominal wall. Diaphragmatic weakness (paresis or exhaustion) results in its passive upward movement into the chest, especially in the setting of high negative intrathoracic pressure (respiratory effort), and consequently abnormal inward movement of the abdominal wall on inspiration.

4) Increased work of accessory muscles of respiration (sternocleidomastoid, trapezius, scalene muscles): This is found in patients in whom the external intercostal muscles and diaphragm are not sufficient to maintain normal gas exchange (causes as in dyspnea). On physical examination intercostal retractions are visible and the patient may assume a tripod position, which involves stabilizing the shoulder girdle by resting the upper limbs against a hard surface (eg, edge of the bed). In patients with chronic respiratory failure, hypertrophy of the accessory muscles of respiration may occur, as can be seen in patients with COPD and neuromuscular weakness.

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