Control of Breathing

DR NOOR KAMIL
ILOs
■ Locate the pre-Bötzinger complex and describe its role in producing spontaneous respiration.
■ Identify the location and probable functions of the dorsal and ventral groups of respiratory neurons,
the pneumotaxic center, and the apneustic center in the brain stem.
■ List the specific respiratory functions of the vagus nerves and the respiratory receptors in the carotid
body, the aortic body, and the ventral surface of the medulla oblongata.
■ Describe and explain the ventilatory responses to increased CO2 concentrations in the inspired air.
■ Describe and explain the ventilatory responses to decreased O2 concentrations in the inspired air.
■ Describe the effects of each of the main nonchemical factors that influence respiration.
■ Describe the effects of exercise on ventilation and O 2 exchange in the tissues.
■ Define periodic breathing and explain its occurrence in various disease states.
Regulation of the Respiratory Center
Activity of the respiratory center can be modified in
response to inputs from other brain regions, receptors in
the peripheral nervous system, and other factors in order to
maintain the homeostasis of breathing.
Respiratory Center
(Central)
 The size of the thorax is altered by the action of the breathing muscles,
which contract as a result of nerve impulses transmitted from centers in
the brain and relax in the absence of nerve impulses.
 Voluntary (Cerebrum)
 Involuntary
 These nerve impulses are sent from clusters of neurons located bilaterally in
the brain stem.
 This widely dispersed group of neurons, collectively called the respiratory
center, can be divided into two principal areas on the basis of location and
function:
 (1) the medullary respiratory center in the medulla oblongata and
 (2) the pontine respiratory group in the pons
 Locations of areas of
the respiratory center

The respiratory center is composed of

neurons in the medullary respiratory center
in the medulla plus the pontine respiratory
group in the pons.
Medullary Respiratory Center (Involuntary)
 The medullary respiratory center is made up of two collections of
neurons called the dorsal respiratory group (DRG), formerly called
the inspiratory area, and the ventral respiratory group (VRG),
formerly called the expiratory area (suppressed by Drugs).
 Located in the VRG is a cluster of neurons called the pre-Bötzinger
complex (BOT-zin-ger) that is believed to be important in the
generation of the rhythm of breathing
 The VRG becomes activated when forceful breathing is required,
such as during exercise, when playing a wind instrument, or at high
altitudes
Roles of the medullary respiratory center in controlling (a) normal quiet breathing and (b) forceful breathing.
Pontine Respiratory Group
 The pontine respiratory group (PRG) (PON-teˉn), formerly
called the pneumotaxic area, is a collection of neurons in the
pons (Switch off point of inspiration)
 The neurons in the PRG are active during inhalation and
exhalation.
 The PRG transmits nerve impulses to the DRG in the medulla.
 The PRG may play a role in both inhalation and exhalation by
modifying the basic rhythm of breathing generated by the
VRG, as when exercising, speaking, or sleeping.
Cortical Influences on Breathing (Voluntary)
 Because the cerebral cortex has connections with the respiratory center, we
can voluntarily alter our pattern of breathing.
 We can even refuse to breathe at all for a short time. Voluntary control is
protective because it enables us to prevent water or irritating gases from
entering the lungs.
 The ability to not breathe, however, is limited by the buildup of CO2 and H+ in
the body.
 When PCO2 and H+ concentrations increase to a certain level, the DRG neurons
of the medullary respiratory center are strongly stimulated, nerve impulses are
sent along the phrenic and intercostal nerves to inspiratory muscles, and
breathing resumes, whether the person wants it to or not.
 It is impossible for small children to kill themselves by voluntarily
holding their breath.
 If breath is held long enough to cause fainting, breathing resumes
when consciousness is lost.
 Nerve impulses from the hypothalamus and limbic system also
stimulate the respiratory center, allowing emotional stimuli to alter
breathing as, for example, in laughing and crying.
CHEMICAL CONTROL OF RESPIRATION
(Peripheral)
 The ultimate goal of respiration is to maintain proper
concentrations of O2, CO2, and hydrogen ions in the
tissues.
 Excess CO2 or excess hydrogen ions in the blood mainly act
directly on the respiratory center, causing greatly increased
strength of both the inspiratory and the expiratory motor
signals to the respiratory muscles.
Chemoreceptor Regulation of Breathing
 Certain chemical stimuli modulate how quickly and how deeply we breathe.
 The respiratory system functions to maintain proper levels of CO2 and O2 and is
very responsive to changes in the levels of these gases in body fluids.
 Chemoreceptors in two locations of the respiratory system monitor levels of CO2,
H+, and O2 and provide input to the respiratory center
 Central chemoreceptors are located in or near the medulla oblongata in the central
nervous system. They respond to changes in H+ concentration or PCO2, or both, in
cerebrospinal fluid.
 Peripheral chemoreceptors are located in the aortic bodies.
 These chemoreceptors are part of the peripheral nervous system and are sensitive
to changes in PO2, H+, and PCO2 in the blood.
Locations of peripheral
chemoreceptors.
 Because CO2 is lipid-soluble, it easily diffuses into cells where, in the
presence of carbonic anhydrase, it combines with water (H2O) to
form carbonic acid (H2CO3).
 Carbonic acid quickly breaks down into H + and HCO3. Thus, an
increase in CO2 in the blood causes an increase in H+ inside cells, and
a decrease in CO2 causes a decrease in H+.
 Normally, the PCO2 in arterial blood is 40 mmHg. If even a slight
increase in PCO2 occurs—a condition called hypercapnia (hıˉ-per-
KAP-neˉ-a) or hypercarbia—the central chemoreceptors are
stimulated and respond vigorously to the resulting increase in H+
level.
 The peripheral chemoreceptors also are stimulated by both the high
PCO2 and the rise in H+.
 In addition, the peripheral chemoreceptors (but not the central
chemoreceptors) respond to a deficiency of O2. When PO2 in
arterial blood falls from a normal level of 100 mmHg but is still
above 50 mmHg, the peripheral chemoreceptors are stimulated.
 Severe deficiency of O2 depresses activity of the central
chemoreceptors and DRG, which then do not respond well to any
inputs and send fewer impulses to the muscles of inhalation.
 The chemoreceptors participate in a negative feedback system that
regulates the levels of CO2, O2, and H+ in the blood
 As a result of increased PCO2, decreased pH (increased H+), or
decreased PO2, input from the central and peripheral hemoreceptors
causes the DRG to become highly active, and the rate and depth of
breathing increase. Rapid and deep breathing, called hyperventilation,
allows the inhalation of more O2 and exhalation of more CO2 until PCO2
and H+ are lowered to normal.
 If arterial PCO2 is lower than 40 mmHg—a condition called hypocapnia
or hypocarbia—the central and peripheral chemoreceptors are not
stimulated, and stimulatory impulses are not sent to the DRG.
 People who hyperventilate voluntarily and cause hypocapnia can hold
their breath for an unusually long period. Swimmers were once
encouraged to hyperventilate just before diving in to compete.
Proprioceptor Stimulation of Breathing
 When start exercising, rate and depth of breathing increase, even
before changes in PO2, PCO2, or H+ level occur.
 The main stimulus for these quick changes in respiratory effort is
input from proprioceptors, which monitor movement of joints and
muscles.
 Nerve impulses from the proprioceptors stimulate the DRG of the
medulla.
 At the same time, axon collaterals (branches) of upper motor
neurons that originate in the primary motor cortex (precentral
gyrus) also feed excitatory impulses into the DRG.
Regulation of breathing in response to
changes in blood PCO2, PO2, and pH (H+)
via negative feedback control.
The Inflation Reflex
 Similar to those in the blood vessels, stretch-sensitive receptors called baroreceptors or stretch
receptors are located in the walls of bronchi and bronchioles. When these receptors become
stretched during overinflation of the lungs, nerve impulses are sent along the vagus (X) nerves to
the dorsal respiratory group (DRG) in the medullary respiratory center.
 In response, the DRG is inhibited and the diaphragm and external intercostals relax. As a result,
further inhalation is stopped and exhalation begins. As air leaves the lungs during exhalation, the
lungs deflate and the stretch receptors are no longer stimulated.
 Thus, the DRG is no longer inhibited, and a new inhalation begins. This reflex is referred to as the
inflation reflex or Hering–Breuer reflex (HER-ing BROY-er). In infants, the reflex appears to function
in normal breathing. In adults, however, the reflex is not activated until tidal volume (normally 500
mL) reaches more than 1500 mL.
 Therefore, the reflex in adults is a protective mechanism that prevents excessive inflation of the
lungs, for example, during severe exercise, rather than a key component in the normal control of
breathing.
Other Influences on Breathing
Other factors that contribute to regulation of breathing include the following:
• Limbic system stimulation. Anticipation of activity or emotional anxiety may
stimulate the limbic system, which then sends excitatory input to the DRG,
increasing the rate and depth of breathing.
• Temperature. An increase in body temperature, as occurs during a fever or
vigorous muscular exercise, increases the rate of breathing.
A decrease in body temperature decreases breathing rate.
A sudden cold stimulus (such as plunging into cold water) causes temporary
apnea (AP-neˉ-a; a- without; -pnea breath), an absence of breathing.
• Pain. A sudden, severe pain brings about brief apnea, but a prolonged somatic pain increases
breathing rate. Visceral pain may slow the rate of breathing.
• Stretching the anal sphincter muscle. This action increases the breathing rate and is
sometimes used to stimulate respiration in a newborn baby or a person who has stopped
breathing.
• Irritation of airways. Physical or chemical irritation of the pharynx or larynx brings about an
immediate cessation of breathing followed by coughing or sneezing.
• Blood pressure. The carotid and aortic baroreceptors that detect changes in blood pressure
have a small effect on breathing. A sudden rise in blood pressure decreases the rate of
breathing, and a drop in blood pressure increases the breathing rate.
Exercise and the Respiratory System
 The respiratory and cardiovascular systems make adjustments in response to both the intensity
and duration of exercise.
 As cardiac output rises, the blood flow to the lungs, termed pulmonary perfusion, increases as
well.
 In addition, the O2 diffusing capacity, may increase threefold during maximal exercise because
more pulmonary capillaries become maximally perfused.
 When muscles contract during exercise, they consume large amounts of O2 and produce large
amounts of CO2. During vigorous exercise, O2 consumption and breathing both increase
dramatically.
 At the onset of exercise, an abrupt increase in breathing is followed by a more gradual
increase.
 With moderate exercise, the increase is due mostly to an increase in the depth of breathing
rather than to increased breathing rate.
 When exercise is more strenuous, the frequency of breathing also increases.
 The abrupt increase in breathing at the start of exercise is due to neural changes that send
excitatory impulses to the dorsal respiratory group (DRG) of the medullary respiratory center in
the medulla.
 These changes include (1) anticipation of the activity, which stimulates the limbic system; (2)
sensory impulses from proprioceptors in muscles, tendons, and joints; and (3) motor impulses
from the primary motor cortex (precentral gyrus).
 The more gradual increase in breathing during moderate exercise is due to chemical and
physical changes in the bloodstream, including (1) slightly decreased PO2, due to increased O2
consumption; (2) slightly increased PCO2, due to increased CO2 production by contracting
muscle fibers; and (3) increased temperature, due to liberation of more heat as more O2 is
utilized.
 During strenuous exercise, HCO3 buffers H+ released by lactic acid in a reaction that liberates
CO2, which further increases PCO2.
 At the end of an exercise session, an abrupt decrease in breathing is followed by a more
gradual decline to the resting level.
 The initial decrease is due mainly to changes in neural factors when movement stops or slows;
the more gradual phase reflects the slower return of blood chemistry levels and temperature
to the resting state.
Terminologies
Abdominal thrust maneuver (Heimlich) First-aid procedure designed to clear the airways of
obstructing objects. It is performed by applying a quick upward thrust between the navel and costal
margin that causes sudden elevation of the diaphragm and forceful, rapid expulsion of air in the
lungs; this action forces air out the trachea to eject the obstructing object. The abdominal thrust
maneuver is also used to expel water from the lungs of near-drowning victims before resuscitation is
begun.
Asphyxia (as-FIK-se¯-a; sphyxia pulse) Oxygen starvation due to low atmospheric oxygen or
interference with ventilation, external respiration, or internal respiration.
Aspiration (as-pi-RA¯-shun) Inhalation of a foreign substance such as water, food, or a foreign body
into the bronchial tree; also, the drawing of a substance in or out by suction.
Black lung disease A condition in which the lungs appear black instead of pink due to inhalation of
coal dust over a period of many years. Most often it affects people who work in the coal industry.
Bronchiectasis (brong-ke¯-EK-ta-sis; -ektasis stretching) A chronic dilation of the bronchi or
bronchioles resulting from damage to the bronchial wall, for example, from respiratory infections.
Bronchoscopy (brong-KOS-ko-pe¯) Visual examination of the bronchi through a bronchoscope, an
illuminated, flexible tubular instrument that is passed through the mouth (or nose), larynx, and
trachea into the bronchi. The examiner can view the interior of the trachea and bronchi to biopsy a
tumor, clear an obstructing object or secretions from an airway, take cultures or smears for
microscopic examination, stop bleeding, or deliver drugs.
Cheyne–Stokes respiration (CHA¯N STO¯ KS res-pi-RA¯-shun) A repeated cycle of irregular breathing
that begins with shallow breaths that increase in depth and rapidity and then decrease and cease
altogether for 15 to 20 seconds. Cheyne–Stokes is normal in infants; it is also often seen just before
death from pulmonary, cerebral, cardiac, and kidney disease.
Dyspnea (DISP-ne¯-a; dys- painful, difficult) Painful or labored breathing.
Epistaxis (ep-i-STAK-sis) Loss of blood from the nose due to trauma, infection, allergy, malignant
growths, or bleeding disorders. It can be arrested by cautery with silver nitrate, electrocautery, or firm
packing. Also called nosebleed.
Hypoventilation (hypo- below) Slow and shallow breathing.
Mechanical ventilation The use of an automatically cycling device (ventilator or respirator) to assist
breathing. A plastic tube is inserted into the nose or mouth and the tube is attached to a device that
forces air into the lungs. Exhalation occurs passively due to the elastic recoil of the lungs.
Rales (RA¯LS) Sounds sometimes heard in the lungs that resemble bubbling or rattling. Rales are to
the lungs what murmurs are to the heart. Different types are due to the presence of an abnormal
type or amount of fluid or mucus within the bronchi or alveoli, or to bronchoconstriction that causes
turbulent airflow.
Respirator (RES-pi-ra¯-tor) An apparatus fitted to a mask over the nose and mouth, or hooked directly
to an endotracheal or tracheotomy tube, that is used to assist or support ventilation or to provide
nebulized medication to the air passages.
Respiratory failure A condition in which the respiratory system either cannot supply sufficient O2 to
maintain metabolism or cannot eliminate enough CO2 to prevent respiratory acidosis (a lowerthan-
normal pH in interstitial fluid).
Rhinitis (rı¯-NI¯-tis; rhin- nose) Chronic or acute inflammation of the mucous membrane of the nose
due to viruses, bacteria, or irritants. Excessive mucus production produces a runny nose, nasal
congestion, and postnasal drip.
Sleep apnea (AP-ne¯-a; a- without; -pnea breath) A disorder in which a person repeatedly stops
breathing for 10 or more seconds while sleeping. Most often, it occurs because loss of muscle tone in
pharyngeal muscles allows the airway to collapse.
Sputum (SPU¯-tum to spit) Mucus and other fluids from the air passages that is expectorated
(expelled by coughing).
Strep throat Inflammation of the pharynx caused by the bacterium Streptococcus pyogenes. It may
also involve the tonsils and middle ear.
Tachypnea (tak-ip-NE¯ -a; tachy- rapid; -pnea breath) Rapid breathing rate.
Wheeze (HWE¯Z) A whistling, squeaking, or musical high-pitched sound during breathing resulting
from a partially obstructed airway.