Patterns of Respiration
BY
AHMAD YOUNES
PROFESSOR OF THORACIC MEDICINE
Mansoura faculty of medicine
The central pattern generator is composed of
predominately three neuronal groups
1- Dorsal respiratory group
2- Ventral respiratory group
3- Pontine respiratory group.
– The dorsal respiratory group is in the ventrolateral
subnucleus of the nucleus tractus solitarius. This
neuronal group is primarily active during inspiration
receiving input from pulmonary vagal afferents.
Many of these neurons excite lower motor cranial
nerves that dilate the upper airway prior to excitation of
the contralateral phrenic and intercostal neurons in the
spinal cord. This coordinated output must occur in the
correct timed sequence to permit the movement of air
through a patent airway.
Ventral respiratory group
• The ventral respiratory group is located in the ventral lateral
medulla from the top of the cervical cord to the level of the
facial nerve.
• This group contains the Botzinger complex, the preBotzinger
neurons, the rostral portion of nucleus ambiguous, and
nucleus retroambigualis.
• The Botzinger complex contains neurons that are active
during expiration and inhibit inspiration.
• The preBotzinger complex contains propriobulbar neurons that
participate in generating the rhythm of respiration.
• The caudal portion of this group is primarily composed of
expiratory neurons that project to intercostal, abdominal, and
external sphincter motor neurons.
Ventilatory control
• The medullary centers respond to direct influences from
the upper airways, intra-arterial chemoreceptors, and
lung afferents by the 5th, 9th, and 10th cranial nerves,
respectively.
• The dorsal respiratory group seems to be active
primarily during inspiration .
• The ventral respiratory group, contains both inspiratory
and expiratory neurons. Ventral respiratory group
output increases in response to the need for forced
expiration occurring during exercise or with increased
airways resistance.
• Respiratory effector muscles are innervated from the
ventral respiratory group by phrenic, intercostal, and
abdominal motoneurons.
Pontine respiratory centers
• The pneumotaxic center in the rostral pons consists of the
nucleus parabrachialis and the Kolliker-Fuse nucleus.
• This area seems primarily to influence the duration of inspiration
and provide tonic input to respiratory pattern generators.
• The apneustic center, located in the lower pons, functions to
provide signals that terminate smoothly inspiratory efforts.
• The pontine input serves to fine tune respiratory patterns and
may additionally modulate responses to hypercapnia, hypoxia, and
lung inflation.
• The automatic central control of respiration may be influenced and
temporarily overridden by volitional control from the cerebral
cortex (motor area , area 4,6) for a variety of activities, such as
speech, singing, laughing, intentional and psychogenic
alterations of respiration, and breath holding.
Descending motoneurons include two
anatomically separate groups:
• The corticospinal and corticobulbar tracts for the volitional
control of respiration and
• The reticulospinal tracts for the automatic control of
respiration .
• volitional respiratory act is associated with a suppression
of the background spontaneous breathing (automatic
respiratory rhythm). Such an inhibition is obvious in
specific respiratory acts such as breath holding, during
speech, and when playing a wind instrument.
• These voluntary modifications of breathing pattern (both in
term of amplitude and frequency) can be made for long
periods of time without any superimposed automatic
rhythmic activity at least as long as PaCO2 does not rise.
Central chemoreceptors
• Central chemoreceptors, located primarily within the
ventrolateral surface of medulla, respond to changes in
brain extracellular fluid [H1] concentration.
• Other receptors have been recently identified in the
brainstem, hypothalamus, and the cerebellum.
• These receptors are effectively CO2 receptors because
central [H1] concentrations are directly dependent on
central PCO2 levels.
• Central [H1] may differ significantly from arterial [H1]
because the blood-brain barrier prevents polar solute
diffusion into the cerebrospinal fluid. This isolation results
in an indirect central response to most peripheral acidbase disturbances mediated through changes in PaCO2.
• Central responses to changes in PCO2 levels are also
slightly delayed for a few minutes by the location of
receptors in the brain only, rather than in peripheral
vascular tissues.
Peripheral chemoreceptors
• Peripheral chemoreceptors include the carotid bodies
and the aortic bodies.
• The carotid bodies, located bilaterally at the bifurcation
of the internal and external carotid arteries, are the
primary peripheral monitors.
• They are highly vascular structures that monitor the
status of blood about to be delivered to the brain and
provide afferent input to the medulla through the 9th
cranial nerve.
• The carotid bodies respond mainly to PaO2, but also to
changes in PaCO2 and pH.
• They do not respond to lowered oxygen content from
anemia or carbon monoxide toxicity.
Other afferent pathways
• Pulmonary stretch receptors are located in proximal
airway smooth muscles, and respond to inflation,
especially in the setting of hyperinflation. Pulmonary
stretch receptors mediate a shortened inspiratory
and prolonged expiratory duration.
• Additional input is also provided by rapidly adapting
receptors that sense flow and irritation. J receptors
are located in the juxtacapillary area and seem to
mediate dyspnea in the setting of pulmonary vascular
congestion.
• Bronchial c-fibers also affect bronchomotor tone and
respond to pulmonary inflammation.
Other afferent pathways
• Afferent activity from chest wall and respiratory
muscles additionally influences central controller
activity.
• Feedback information regarding muscle stretch,
loading, and fatigue may impact both regulatory
and somato-sensory responses.
• Upper airway receptors promote airway patency
by activation of local muscles including the
genioglossus.
During sleep
• During sleep, the metabolic rate falls (hence,
decreased CO2 production), but this is offset by
a proportionately greater fall in minute
ventilation with the result that the PaCO2
increases slightly.
• The fall in ventilation is due to increased upper
airway resistance and decreased
chemosensitivity as well as the loss of the
wakefulness stimulus to breathe.
• The result is that the PaCO2 rises and the PaO2
falls slightly
Because of the normal position on the flat portion of the O2Hb
dissociation curve, there is little change in the SaO2 as a result of the
fall in PO2 associated with sleep . If the baseline awake PaO2 is lower,
the fall in SaO2 will be greater for the same drop in PaO2.
• In patients with lung disease and a lower awake PO2,
even a normal sleep-related drop in PO2 will be
associated with a larger decrease in the SaO2.
• The change in ventilation with sleep is due to a fall in Vt
with minimal change in the RR.
• During the transition from wake to stage N1 and early
stage N2, the ventilation can be slightly irregular.
However, in stable stage N2 and stage N3, the Vt and RR
are nearly constant.
• During REM sleep, ventilation is irregular with periods of
decreased Vt associated with bursts of eye movements.
• The FRC decreases from wake to sleep.
• During sleep, the hypercapnic ventilatory response
and hypoxic ventilatory response are reduced during
NREM compared with wake and decreased in REM
sleep compared with NREM sleep .
• Both hypoxia and hypercapnea may trigger
arousals from sleep, resulting in a return to the
more tightly regulated ventilatory control
associated with wakefulness.
• Arousal thresholds for hypercapnia range
between 65 and 66 mmHg and do not vary
consistently among the different sleep stages.
• The threshold for arousal in response to hypoxia
is more variable and seems less reliable. Severe
oxygen desaturations in some individuals do not
uniformly result in arousals.
Alveolar hypoventilation
• Alveolar hypoventilation during wakefulness is defined as an
PaCO2 of 45 mm Hg or higher.
• If the sleeping PaCO2 is ≥10 mm Hg above the awake value,
Sleep hypoventilation is said to be present.
Hypoxemia is defined as a low arterial partial pressure of
oxygen (PaO2) relative to predicted values.
A PaO2 < 55 mm Hg while breathing room air is considered
severe and an indication for chronic 24-hour supplemental
oxygen therapy.
Milder degree of hypoxemia can be identified by comparing a
PaO2 with a predicted value for age.
• A simple estimate of a normal predicted PaO2
Pao2=105 – 1/2 age (yr).
Normal respiration
• Eupnea: Normal breathing at a rate of 12-20 bpm
e g. normal physiology
• Normal respiration at rest for healthy subjects:
- inhalation is 1.5-2 s
- exhalation is 1.5-2 s
- automatic pause of almost no breathing is 2 s
- tidal volume (the depth of inhalation) is 500-600 ml
- breathing frequency is 10-12 breaths/min.
Abnormal respiration
• Bradypnea: Slow respiratory rate <12 bpm.
e g. normal during sleep, brain tumors, diabetic coma, drugs
(alcohol, narcotics), increased intracranial pressure, metabolic
acidosis, uremia
• Tachypnea: Increased respiratory rate >20 bpm, regular rhythm
e g. anxiety ,asthmatic, atelectasis, brain lesions, drugs (aspirin),
exercise, fever, hypercapnia, hypoxemia, metabolic acidosis,
pain
• Hypopnea: decreased depth with normal rate and rhythm e g.
normal during sleep , circulatory failure, meningitis,
unconsciousness
• Hyperpnea: increased depth, normal rate and rhythm e g.
exertion, fever, pain.
Bradypnea
• Bradypnea (Greek from bradys, slow + pnoia, breath; British
English spelling bradypnoea) refers to an abnormally slow
breathing rate.
• The rate at which bradypnea is diagnosed depends upon
the age of the patient.
Age ranges and bradypnea
• Age 0–1 year < 30 breaths per minute
• Age 1–3 years < 25 breaths per minute
• Age 3–12 years < 20 breaths per minute
• Age 12–50 years < 12 breaths per minute
• Age 50 and up < 13 breaths per minute
Causes:
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Normal during sleep,
Brain tumors
Diabetic coma
Drugs (alcohol, narcotics
↑ICP, metabolic alkalosis
Hypothyroidism
Tachypnea
• Tachypnea (or "tachypnoea") (Greek: "rapid
breathing") is the condition of rapid breathing.
• In adult humans at rest, any rate between 12-20
breaths per minute is normal and tachypnea is
indicated by a respiratory rate >20 breaths per
minute.
Hyperventilation
• Hyperventilation or overbreathing is the state of
breathing faster or deeper than normal,
(hyperpnoea)[causing falling Paco2 below normal
(35–45 mmHg).
• Stress or anxiety commonly are causes of
hyperventilation; as a consequence of various lung
diseases, head injury, or stroke (central neurogenic
hyperventilation, apneustic respirations, ataxic
respiration, Cheyne–Stokes respiration or Biot's
respiration) and metabolic acidosis, In the setting of
diabetic ketoacidosis, this is known as Kussmaul
breathing – characterized by long, deep breaths.
Hypoventilation
• Hypoventilation (also known as respiratory
depression) occurs when ventilation is inadequate
to perform needed gas exchange.
• It causes an increased concentration of carbon
dioxide (hypercapnia) and respiratory acidosis.
• Hypoventilation during wakefulness is defined
as an PaCO2 equal to or greater than 45 mm Hg.
During sleep, Score hypoventilation during sleep if
there is a ≥10 mm Hg increase in PaCO2 during
sleep in comparison with an awake supine value.
Kussmaul breathing
• Kussmaul breathing is a deep and labored
breathing pattern often associated with severe
metabolic acidosis, particularly diabetic
ketoacidosis but also renal failure.
• In metabolic acidosis, breathing is first rapid and
shallow but as acidosis worsens, breathing
gradually becomes deep, labored and gasping. It
is this latter type of breathing pattern that is referred
to as Kussmaul breathing.
Kussmaul breathing
Apneustic Respiration
• The apneustic center of the lower pons appears to promote
inspiration by stimulation of the Inspiratory neurons in the medulla
oblongata providing a constant stimulus.
• The apneustic center of pons sends signals to the dorsal
respiratory center in the medulla to delay the 'switch off' signal of
the inspiratory ramp provided by the pneumotaxic center of pons. It
controls the intensity of breathing.
• The apneustic center is inhibited by pulmonary stretch receptors.
However, it gives positive impulses to the inspiratory neurons.
Apneustic Respiration
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Apneustic respiration is an abnormal pattern of breathing characterized by
deep, gasping inspiration with a pause at full inspiration followed by a
brief, insufficient release, with an increase in the ratio of inspiratory to
expiratory time.
• It is caused by damage to the pons or upper medulla caused by strokes or
trauma.
• Specifically, concurrent removal of input from the vagus nerve and the
pneumotaxic center causes this pattern of breathing.
• It can also be temporarily caused by some drugs, such as ketamine.
• It is an ominous sign, with a generally poor prognosis.
Apneustic respiration in patients with achondroplasia ( congenital small
foramen magnum which compress the distal medulla and upper cervical
cord )
Apneustic respiration during wakfullness..
•Apneustic respiration during NREM N1
and N2.
Ataxic Breathing
• This type of breathing is characterized by clusters of
cyclic irregular breathing followed by recurrent periods
of apnea.
• The apnea length is greater than the ventilatory phase.
• Ataxic breathing is often noted in medullary lesions.
Biot’s breathing is a special type of cluster breathing
(ataxic breathing) characterized by breaths of nearly
equal volume separated by long periods of apnea.
• This is really a variant of ataxic or cluster breathing and
may be found in patients with medullary lesions.
Ataxic Respiration
• As the breathing pattern deteriorates, it merges with agonal
respirations.
• It is caused by damage to the medulla oblongata due to
strokes or trauma. It generally indicates a poor prognosis,
and usually progresses to complete apnea.
• The term is sometimes used interchangeably with Biot's
Respirations, but technically, Biot's respirations refers to
groups of similar-sized breaths alternating with regular
periods of apnea.
Agonal Respiration
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Agonal respiration is an abnormal pattern of breathing characterized by
gasping, labored breathing, accompanied by strange vocalizations and
myoclonus.
Possible causes include cerebral ischemia, extreme hypoxia or even
anoxia.
Agonal breathing is an extremely serious medical sign requiring immediate
medical attention, as the condition generally progresses to complete apnea
and heralds death.
The term is sometimes (inaccurately) used to refer to labored, gasping
breathing patterns accompanying organ failure (e.g. liver failure and renal
failure), SIRS, septic shock, and metabolic acidosis (see Kussmaul
breathing, or in general any labored breathing, including Biot's respirations
and ataxic respirations.
Correct usage would restrict the term to the last breaths before death.
Myoclonus
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Myoclonus is a brief, involuntary twitching of a muscle or a group of
muscles.
It describes a medical sign and, generally, is not a diagnosis of a disease.
Brief twitches are perfectly normal.
Contractions are called positive myoclonus; relaxations are called negative
myoclonus.
The most common time for people to encounter them is while falling asleep
(hypnic jerk), but myoclonic jerks are also a sign of a number of
neurological disorders.
Hiccups are also a kind of myoclonic jerk specifically affecting the
diaphragm.
Most often, myoclonus is one of several signs in a wide variety of nervous
system disorders such as multiple sclerosis, Parkinson's disease, some
forms of epilepsy, and occasionally in intracranial hypotension.
Agonal Respirations
•Agonal respirations are also commonly seen in cases of
cardiogenic shock or cardiac arrest where agonal
respirations may persist for several minutes after
cessation of heartbeat.
• The presence of agonal respirations in these cases
indicates a more favorable prognosis than in cases of
cardiac arrest without agonal respirations.
• In an unresponsive, pulseless patient in cardiac arrest,
agonal gasps are not effective breaths.
•Agonal respiration is not the same as, and is unrelated to,
the phenomenon of death rattle.
Death Rattle
• A death rattle is a medical term that describes the sound
produced by someone who is near death when saliva
accumulates in the throat.
• Those who are dying may lose their ability to swallow,
resulting in such an accumulation.
• Related symptoms can include shortness of breath and
rapid chest movement.
• While death rattle is a strong indication that someone is
near death. it can also be produced by other problems
that cause interference with the swallowing reflex, such
as the case with brain injuries.
• It is sometimes misinterpreted as the sound of the person
choking to death.
• In palliative care, drugs such as atropine may be used for
their anticholinergic effects to reduce secretions and
minimize this effect.
Cheyne-Stokes and Cheyne-Stokes
Variant Patterns of Breathing
• Cheyne-Stokes breathing (CSB) is a special type of central apnea
manifested as cyclic changes in breathing with a crescendodecrescendo sequence separated by central apneas .
• The Cheyne-Stokes variant pattern of breathing is distinguished by the
substitution of hypopneas for apneas.
• AASM scoring CSB if there are at least 3 consecutive cycles of cyclical
crescendo-decrescendo change in breathing amplitude accompanied
by at least one of the following:
1- five or more central apneas and hypopneas per hour of sleep; and
2- a cyclic crescendodecrescendo change in breathing amplitude and
duration of at least 10 consecutive minutes.
• The cycle length is most commonly in the range of 60 seconds but must
be at least 45 seconds in duration.
• The arousals typically occur in the middle of the hyperventilation cycle.
• This breathing pattern is most prominently seen in NREM sleep,
particularly stages 1 and 2, and attenuates or disappears during REM
sleep.
Cheyne-Stokes and Cheyne-Stokes
Variant Patterns of Breathing
• In neurologic disorders, the Cheyne-Stokes type
of breathing is mostly noted in bilateral cerebral
hemispheric lesions and it worsens during
sleep, whereas Cheyne-Stokes variant patterns
of breathing may also be noted in brain stem
lesions, in addition to bilateral cerebral
hemispheric disease.
• This pattern of breathing is noted in patients
with severe congestive cardiac failure.
Dysrhythmic Breathing
• Dysrhythmic breathing is characterized by nonrhythmic respiration of irregular rate, rhythm, and
amplitude during wakefulness with or without O2
desaturation that becomes worse during sleep
• Dysrhythmic breathing may result from an
abnormality in the automatic respiratory pattern
generator in the brain stem.
Inspiratory Gasp
• Inspiratory gasp is characterized by a short inspiration
time and a relatively prolonged expiration (reduced
inspiratory-expiratory time ratio).
• Gasping or irregular breathing has been noted after
lesion in the medulla.
Apraxia
• Apraxia (from the Greek root word praxis, for an act, or
preceded by a privative a, meaning without) is
characterized by loss of the ability to execute or carry
out learned purposeful movements, despite having the
desire and the physical ability to perform the
movements.
• It is a disorder of motor planning, which may be
acquired or developmental, but is not caused by
incoordination, sensory loss, or failure to comprehend
simple commands (which can be tested by asking the
person to recognize the correct movement from a
series).
Apraxia
• It is caused by damage to specific areas of the
cerebrum.
• Apraxia should not be confused with ataxia, a lack
of coordination of movements; aphasia, an inability
to produce and/or comprehend language; abulia,
the lack of desire to carry out an action; or
allochiria, in which patients perceive stimuli to one
side of the body as occurring on the other.
Apraxia
• Apraxia is neurological condition characterized by loss
of the ability to perform activities that a person is
physically able and willing to do.
• Apraxia is caused by brain damage related to conditions
such as head injury, stroke, brain tumor, and
Alzheimer's disease.
• The damage affects the brain's ability to correctly signal
instructions to the body.
Forms of apraxia include the inability to say some words
or make gestures.
Causes and symptoms
• Apraxia is caused by conditions that affect parts of the
brain that control movements .
• Apraxia is a result of damage to the brain's cerebral
hemispheres. These are the two halves of the cerebrum
and are the location of brain activities such as voluntary
movements.
• Apraxia causes a lapse in carrying out movements that
a person knows how to do, is physically able to perform,
and wants to do .
• A person may be willing and able to do something like
bathe. However, the brain does not send the signals that
allow the person to perform the necessary sequence of
activities to do this correctly.
Types of apraxia
• Buccofacial or orofacial apraxia is the inability of a person to follow
through on commands involving face and lip motions. These
activities include coughing, licking the lips, whistling, and winking.
It is the most common form of apraxia.
• Limb-kinetic apraxia is the inability to make precise movements
with an arm or leg .
• Ideomotor apraxia is the inability to make the proper movement in
response to a command to pantomime an activity like waving .
• Constructional apraxia is the inability to copy, draw, or build simple
figures .
• Ideational apraxia is the inability to do an activity that involves
performing a series of movements in a sequence. A person with
this condition could have trouble dressing, eating, or bathing. It is
also known as conceptual apraxia .
• Oculomotor apraxia is characterized by difficulty moving the eyes .
• Verbal apraxia is a condition involving difficulty coordinating mouth
and speech movements. It is referred to as apraxia of speech
Respiratory apraxia
• Respiratory apraxia is defined as failure to
perform voluntary respiratory movement on
command with the lack of pyramidal defect.
SLEEP-RELATED RESPIRATORY DYSRHYTHMIA
Sleep Apnea
• Three types of sleep apnea have been noted: central,
upper airway obstructive, and mixed.
• Normal individuals may experience a few episodes of
sleep apnea, particularly central apnea, at the onset of
NREM sleep and during REM sleep.
• To be of pathologic significance, the sleep apnea should
last at least 10 seconds and the apnea index (number of
apneas per hour of sleep) should be at least 5.
• In addition to a duration of 10 seconds ,apnea is scored
when the peak amplitude drops by 90% or more of the
baseline, and this amplitude reduction must last for at
least 90% of the event’s duration.
Sleep Apnea
• Cessation of airflow with no respiratory effort
constitutes central apnea. During this period there is no
diaphragmatic and intercostal muscle activity or air
exchange through the nose or mouth.
• Upper airway obstructive sleep apnea (OSA) is
manifested by absence of air exchange through the
nose or mouth but persistence of diaphragmatic and
intercostal muscle activity.
• During mixed apnea, initially airflow ceases, as does
respiratory effort (central apnea); this is followed by a
period of upper airway OSA.
• On rare occasions this pattern may be reversed,
resulting in an initial period of OSA followed by central
apnea
Sleep-Related Hypopnea
• Reduction of nasal pressure signal excursion (or that of
the alternative airflow sensor) by 30% or more of the
baseline amplitude lasting for a period of at least 10
seconds and accompanied by a 4% or more
desaturation from the pre-event baseline.Furthermore,
at least 90% of the event’s duration must meet the
amplitude reduction criteria for hypopnea.
• An alternative is a reduction of the amplitude excursion
in the nasal pressure signal (or that of the alternative
airflow sensor) by 50% or more of the baseline lasting
for at least 10 seconds and accompanied by oxygen
desaturation of 3% or more from the pre-event baseline,
or the event is associated with an arousal. This
amplitude reduction must be present for at least 90% of
the event’s duration.
Sleep-Related Hypopnea
• Sleep-related apneas and hypopneas in neurologic diseases are
secondary sleep apnea syndromes, in contrast to primary OSA
syndrome, in which no cause except for minor deviations of the upper
airway anatomic configuration is found to account for the appearance of
apnea.
• The neurologic illness may be aggravated by the secondary sleep apnea
because of the adverse effects of sleep induced hypoxemia and
hypercapnia, and repeated arousals with sleep fragmentation.
Paradoxical Breathing
• The thorax and abdomen move in opposite directions during
paradoxical breathing, indicating increased upper airway
resistance.
• In upper airway resistance syndrome,this may be noted without any
change in oronasal airflow;
• In OSA, paradoxical breathing is accompanied by reduction or
absence of oronasal airflow.
Sleep-Related Hypoventilation
• sleep-related hypoventilation, a type of respiratory
dysrhythmia without any apnea or hypopnea, is
seen commonly in neuromuscular and intrinsic
pulmonary and thoracic restrictive disorders,
and sometimes in brain stem lesions.
• Sleep-related hypoventilation is characterized by an
increase in the partial pressure of PaCO2 of 10
mm Hg above the supine awake values during
sleep. This abnormal rise in PaCO2 is accompanied
by severe sleep-related hypoxemia that is not due
to apnea or hypopnea
Documentation of an increased partial pressure of carbon dioxide
(PCO2) during sleep. Note the alveolar plateaus (black circles).
PCO2 = exhaled PCO2 waveform tracing; PETCO2 = end-tidal reading;
SpO2 = pulse oximetry.
Catathrenia
• Catathrenia (respiratory dysrhythmia with bradypnea
and groaning), characterized by prolonged expiration
with the characteristic groaning noise.
• This may be mistaken for a central apnea but is really
not an apnea , and there is no oxygen desaturation
during the episode .
• It is considered a parasomnia, and the etiology and
mechanism are at present unknown.
Catathrenia: a rare parasomnia which may mimic central sleep apnea on
polysomnogram. Note prolonged expiration in the flow and effort
channels followed by arousals without oxygen desaturation in stage 2
NREM sleep .
Other Abnormal Breathing Patterns
• Nocturnal stridor causing severe inspiratory
breathing difficulty
• Prolonged periods of central apnea accompanied
by mild O2 desaturation in relaxed wakefulness,
as if the respiratory centers “forgot” to breathe.
• Transient occlusion of the upper airway or
transient uncoupling of intercostal and
diaphragmatic muscle activity,
• Transient sudden respiratory arrest