Abnormal Respirations

Lacey Whited; Derrel D. Graham.

Author Information

Last Update: July 30, 2019.

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Introduction
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.[1][2]

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Function
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.

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Issues of Concern
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, its 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.[3][4]

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Clinical Significance
The types of clinically relevant normal and abnormal respiration patterns include the following:

 Eupnea is normal breathing.

 Sighing is an involuntary inspiration that is 1.5 to 2 times greater than normal tidal
volume. Sighing breathing is observed in subjects suffering from anxiety with no
observed organic pathology.
 Dyspnea is the subjective sensation of difficulty breathing.
 Paroxysmal nocturnal dyspnea is described as attacks of severe shortness of breath that
wake the patient from sleep.  They have to sit up to catch their breath. Most commonly,
this is a symptom of heart failure.
 Orthopnea also is seen in heart failure.  Patients are unable to breathe comfortably lying
flat. They must be in a sitting or propped up to breathe without difficulty. 
 Cheyne-Stokes is a pattern of crescendo-decrescendo respirations followed by a period of
apnea. This pattern of breathing was first described by John Cheyne, a British Physician
and William Stokes, an Irish Physician. It is well described in patients with heart failure.
Usually observed while asleep and is the result of disordered central control of breathing.
Its presence has implications for outcome in that cardiac resynchronization therapy
improves outcomes in patients with Cheyne-Stokes Respirations.
 Bradypnea is a respiratory rate that is lower than normal for age.
 Tachypnea is a respiratory rate that is greater than the normal for age.
 Hyperpnea in increased volume with or without an increased rate of breathing.  Blood
gasses are normal.
 Agonal breathing is characterized by slow, very shallow irregular respirations that result
from anoxic brain injury. This will often progress to apnea depending on the underlying
cause.
 Apnea is the absence of breathing. This signals a life-threatening situation in which the
patient will quickly succumb unless rescue breathing is instituted immediately. 
 Hyperventilation is over-ventilation above that needed for the body’s CO2 elimination.
This results in a decrease in PaCO2 and respiratory alkalosis. Hyperventilation can be
driven by chemoreceptor stimulation due to metabolic acidosis.
 Hypoventilation is under-ventilation below that needed for the body’s CO2 elimination. It
is inadequate to maintain a normal PaCO2.
 Kussmaul respirations were originally observed and described by Dr. Adolf Kussmaul in
1874. He made his observation in diabetic patients who were comatose and in the late
stages of diabetic ketoacidosis. As classically described, Kussmaul respirations are a
deep, sighing respiratory pattern. Dr. Kussmaul actually described it as “air hunger.” This
is probably the most important of the abnormal respiratory patterns.
 Kussmaul respiratory pattern occurs due to increased tidal volume with or without an
increased respiratory rate. It is a form of hyperventilation. It results from stimulation of
the respiratory center in the brain stem by low serum pH. The effect is the lowering of the
partial pressure of carbon dioxide in the alveoli, thereby compensating for metabolic
acidosis.  Initially, in acidosis, the respiratory pattern is rapid and shallow, but as the
acidosis progresses, the inspirations become deeper. It is only in the later stages that true
Kussmaul respirations are seen. Kussmaul respirations can be seen with any disorder that
causes significant acidosis. Toxic ingestions, particularly alcohols, are another common
cause of Kussmaul respirations. Salicylate toxicity is also a cause. Kussmaul was also
classically described in patients with uremia. It can also be seen in any disorder that
results in lactic or ketoacidosis. 
 Acidosis results from the abnormal accumulation of ketones, lactate, urate or exogenous
acid in the blood. A fall in pH significant enough to induce Kussmaul’s respirations is a
sign of decompensation. As described by Dr. Kussmaul, this respiratory pattern is a
perimortem event. Failure to recognize this respiratory pattern can result in delayed
recognition and treatment of the underlying cause. Such delays can result in increased
morbidity and even mortality for the patient. 
 The Biot respiratory pattern was first described by Camille Biot, a French physician, in
1876. He made his observations while studying the pattern of breathing described by
John Cheyne and William Stokes. Biot respiratory pattern is characterized by regular
deep respirations interspersed with periods of apnea. It is caused by damage to the pons
due to stroke, trauma, or uncal herniation. As the insult to the pons progresses, the pattern
becomes irregular. At this point, the pattern deteriorates to ataxic breathing. Biot
respiratory pattern can also be induced by opiate intoxication.
  Apneustic breathing is another abnormal breathing pattern. It results from injury to the
upper pons by a stroke or trauma. It is characterized by regular deep inspirations with an
inspiratory pause followed by inadequate expiration. This respiratory pattern is often
associated with severe brain injury and carries a poor prognosis. Apneustic breathing can
be temporarily induced by ketamine.
 Central neurogenic hyperventilation is persistent hyperventilation typically caused by
head trauma, severe brain hypoxia, or lack of cerebral perfusion. It is usually due
to midbrain and upper pons damage. Central neurogenic hypoventilation occurs when the
medulla respiratory centers are not responding to
appropriate stimuli.Central neurogenic hypoventilation may occur with head trauma,
cerebral hypoxia, and narcotic suppression.

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.[5][6][7]

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Enhancing Healthcare Team Outcomes

All healthcare workers should have some idea what is abnormal respiration. There are several
types of abnormal respiration and each has many causes. The key is to ensure that
the appropriate specialist is notified promptly. Failure to recognize abnormal respiration can
prove fatal and lead to litigation.

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Questions
To access free multiple choice questions on this topic, click here.

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References
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3.
Stewart J, Howard RS, Rudd AG, Woolf C, Russell RW. Apneustic breathing provoked
by limbic influences. Postgrad Med J. 1996 Sep;72(851):559-61. [PMC free article]
[PubMed]
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Hopper K. Respiratory Acid-Base Disorders in the Critical Care Unit. Vet. Clin. North
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Haddad S, Aldawood AS, Alferayan A, Russell NA, Tamim HM, Arabi YM.
Relationship between intracranial pressure monitoring and outcomes in severe traumatic
brain injury patients. Anaesth Intensive Care. 2011 Nov;39(6):1043-50. [PubMed]
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Zhou W, Liu W. Hypercapnia and hypocapnia in neonates. World J Pediatr. 2008
Aug;4(3):192-6. [PubMed]
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