There are multiple types of normal and abnormal respiration. They include apnea, eupnea, orthopnea, dyspnea, hyperpnea, hyperventilation, hypoventilation, tachypnea, Kussmaul respiration, Cheyne-Stokes respiration, sighing respiration, Biot respiration, apneustic breathing, central neurogenic hyperventilation, and central neurogenic hypoventilation. Each pattern is clinically important and useful in evaluating patients.
Evaluating respiratory patterns assists the clinician in understanding the patient's current physiologic status. Abnormal breathing patterns suggest the possibility of underlying injury or metabolic derangements. Early recognition of abnormal respiratory patterns can aid the clinician in early intervention to prevent further deterioration of the patient's condition.
Breathing is controlled centrally in the brainstem. It receives input from central and peripheral chemoreceptors as well as voluntary control from the cerebrum. The brainstem also receives input from the chemoreceptors and adjusts the rate and tidal volume based on pH and PaCO2.
The regular cycle of breathing originates in the medulla. The medullary respiratory center has several widely dispersed groups of neurons that are referred to the dorsal and ventral respiratory groups. There does not appear to be separate inspiratory and expiratory centers.
Bilateral dorsal respiratory groups (DRG) control the rhythm of breathing by producing inspiratory impulses. Neurons from this center send impulses to the motor neurons of the diaphragm and the external intercostal muscles. These nerves also extend to the ventral respiratory groups (VRG). Input from the airways, lungs, joint proprioceptors and peripheral chemoreceptors via the vagus and glossopharyngeal nerves modify the breathing pattern.
The ventral respiratory groups (VRG) are also bilateral collections of inspiratory and expiratory neurons in the medulla and are active in exercise and stress. These neurons send impulses to the diaphragm and external intercostals. They also stimulate the abdominal muscles and internal intercostals via neurons in the caudal area.
The interaction between the DRG and VRG produces an impulse, the inspiratory ramp signal. It starts low and gradual, then increases to produce a smooth inspiratory effort.
The pons contains two respiratory areas referred to as the pneumotaxic and apneustic centers. The pneumotaxic center has an inhibitory effect on the medulla. In effect, it’s stimulation causes the end of the inspiratory effort and therefore controls inspiratory time. Weak signals from the pneumotaxic center increase inspiratory time causing an increase in tidal volume. The apneustic center stimulates the inspiratory neurons in the medulla and inhibits the expiratory neurons. Overstimulation of this area produces long, gasping inspirations that are interrupted inadequately by occasional expirations. This pattern is called apneustic breathing.
The types of clinically relevant normal and abnormal respiration patterns include the following:
Breathing patterns associated with brain injury may not be observed due to mechanical ventilation and sedation. There is a complex interplay in cases that result in brainstem injury. Autoregulation of cerebral blood flow is affected by CO2 levels in the blood. As CO2 increased, cerebral vessels will dilate, and as they decrease, the cerebral vessels will constrict. In traumatic brain injury (TBI), the brain swells and cannot expand due to the fixed volume of the intact skull. Raised intracranial pressure can overcome perfusion pressure causing further anoxia and injury leading to brain death and/or herniation. Although hyperventilation can lower PaCO2, causing vasoconstriction and reduce swelling/ICP, it should be avoided. The effect is short-lived. In TBI, both hyperventilation and hypoventilation must be avoided. ICP is treated pharmacologically, surgically, and with medically induced coma.