Describes physiology in respiratory nervous control

1. Group 27 presentation
• Discuss the control of respiratory rate and depth by the brainstem.
• How do the respiratory muscles coordinate during forced
breathing?
• Explain the process of ventilation-perfusion matching in the lungs.
• What happens during a bronchoconstriction and its effects on
airflow?
• Discuss the impact of altitude on respiratory physiology.
1. MUSIIMENTA GRACE VU-BPC-2301-0403-DAY
2. MUTONYI SHARON AMORA VU-BPC-2301-0071-DAY
3. MUTYABA MARTIN VU-BPC-2301-1562-DAY
4. MUYAMA GETRUDE VU-BPC-2301-1196-DAY

2. CONTROL OF RESPIRATORY RATE AND DEPTH BY THE
BRAINSTEM
The brainstem, particularly the medulla
oblongata and pons, plays a central role in
regulating these respiratory parameters.
The respiratory center receives input from a variety of sources, including:
The peripheral chemoreceptors, which are located in the carotid bodies and aortic
bodies. These receptors sense the levels of carbon dioxide (CO2) and oxygen (O2) in
the blood.
The central chemoreceptors, which are located in the medulla oblongata. These
receptors sense the pH of the cerebrospinal fluid.
The stretch receptors in the lungs. These receptors sense the amount of air in the
lungs.
The cerebral cortex. The cerebral cortex can voluntarily control breathing, but this is
usually overridden by the automatic control of the respiratory center.

3. Nervous control: respiratory neuronal center
 Composed of several groups of
neurons.
 Located in the entire length of the
medulla and pons.
 Can be divided into four major groups
of neurons:-
1-Dorsal respiratory group​.
2-Ventral respiratory group​.
3-The apneustic center​.
4-The pneumotaxic center.​
 Several mechanisms are involved which can be grouped into two main categories which
are closely integrated:-
1- Nervous control mechanism.​
2- Chemical control mechanism
CONTROL OF VENTILATION

4. Medullary Respiratory centers
1. Inspiratory area (Dorsal Respiratory Group)-DRG:
-Determines basic rhythm of breathing (rhythmicity center).
-Causes contraction of diaphragm and external intercostals.
-The rhythmicity center received impulses from:
1-Higher brain centers.
2-Centers in the brain stem (medulla and pons).
3-Special receptors (respiratory reflexes).
-The rhythmicity center sends excitatory impulses via
the intercostal and phrenic nerves to the external intercostal muscles
and diaphragm.
-The medullary respiratory center stimulates basic inspiration for
about 2 seconds and then basic expiration for about 3 seconds (5sec/
breath = 12breaths/min).

5. 2. Expiratory area (Ventral Respiratory Group)-VRG:
-Although it contains both inspiratory and expiratory neurons, It is inactive
during normal quiet breathing.
-Activated by inspiratory area during forceful breathing.
-Causes contraction of the internal intercostals and abdominal muscles (
mainly expiratory).
Pontine Respiratory centers
pons
1. Apneustic area:
Stimulates inspiratory area of medulla to prolong inhalation. Therefore, slow
respiration and prolonged respiratory cycles will result if it is stimulated. It receives
inhibitory impulses from the sensory vagal fibers and inhibitory impulses from
the pneumotaxic center.
2. Pneumotaxic area:
It transmits inhibitory impulses to the apneustic center and to the inspiratory area to
switch off inspiration.
Therefore, breathing is more rapid when pneumotaxic area is active.

6. Hering-Breuer inflation reflex
• When the lung becomes overstretched
(tidal volume is about 1.5 L), stretch
receptors located in the wall of
bronchi and bronchioles transmit
signals through vagus nerve to DRG
producing effect similar to
pneumotaxic center stimulation.
• Switches off inspiratory signals and
thus stops further inspiration .
• This reflex also increases the rate of
respiration as does the pneumotaxic
center.
• This reflex appears to be mainly a
protective mechanism for preventing
excess lung inflation

7. CHEMICAL CONTROL OF VENTILATION
The rhythmicity center is affected by chemical changes in the blood via two
types of chemoreceptors:-
1-Peripheral chemoreceptors​.
2-Central chemoreceptors​.

8. PERIPHERAL CHEMORECEPTORS:
• Located mainly in the carotid and aortic bodies, but may be found anywhere in
the circulatory system.​
• When stimulated, send excitatory impulses to the rhythmicity center
(via glossopharyngeal and vagus nerves)​.
• Highly sensitive to changes in arterial PO2 and to a lesser extent to PCO2 and
pH.​
• Fall of PO2, rise in PCO2 and fall of pH, stimulate the chemoreceptors to
increase ventilation​.
• Most probably located on the ventrolateral surface of medulla oblongata (which is
bathed with cerebrospinal fluid)​
• Highly sensitive to the hydrogen ion concentration of the CSF(cereprospinal fluid).
• evoked by arterial PCO2 (CO2 can freely cross the blood-brain barrier(BBB) into
CSF, while BBB is relatively impermeable to H+ and HCO-
3 ions)​

9. Effect of CO2 on central chemoreceptors
Although carbon dioxide has
little direct effect in stimulating
the neurons in the
chemosensitive area, it does
have a potent indirect effect. It
does this by reacting with the
water of the tissues to form
carbonic acid, which
dissociates into hydrogen and
bicarbonate ions; the hydrogen
ions then have a potent direct
stimulatory effect on
respiration.

10. Effect of CO2 and H Ion Concentration on
Chemoreceptor Activity.
 An increase in either carbon dioxide concentration or hydrogen
ion concentration also excites the peripheral chemoreceptors
and, in this way, indirectly increases respiratory activity.
 There is one difference between the peripheral and central
effects of carbon dioxide: the stimulation of the peripheral
chemoreceptors occurs as much as five times as rapidly as
central stimulation, so that the peripheral chemoreceptors might
be especially important in increasing the rapidity of response to
carbon dioxide at the onset of exercise.

11. Other Factors Influencing Respiration

12. FORCED BREATHING
Forced breathing, also known as active or deep breathing, occurs when
we need to increase the volume of air exchanged in our lungs. It is
typically required during physical exertion, such as exercise, or in
situations where we need to inhale more oxygen or exhale more carbon
dioxide than during normal, quiet breathing
During forced breathing, the respiratory muscles coordinate to expand the
chest cavity more than during normal breathing. This expansion allows for
a larger volume of air to be inhaled or exhaled.
The key respiratory muscles involved in forced breathing are the
diaphragm, intercostal muscles, and accessory muscles.
The coordination of these respiratory muscles is controlled by the
respiratory centers in the brainstem. These centers receive input from
various sensors in the body that monitor factors like oxygen and
carbondioxide levels in the blood. Based on this input, the respiratory
centers adjust the rate and depth of breathing, activating the appropriate
muscles for forced breathing when needed.

13. Active Inspiration
Active inspiration involves the contraction of the accessory
muscles of breathing (in addition to those of quiet inspiration, the
diaphragm and external intercostals). All of these muscles act to
increase the volume of the thoracic cavity:
• Diaphragm, a dome-shaped muscle located just below the
lungs, contracts and flattens during inhalation. This
contraction increases the vertical dimension of the thoracic
cavity, allowing the lungs to expand more fully. The diaphragm is
primarily responsible for the majority of the volume increase
during forced breathing
 Scalenes – elevates the upper ribs.
 Sternocleidomastoid – elevates the sternum.
 Pectoralis major and minor – pulls ribs outwards.
 Serratus anterior – elevates the ribs (when the scapulae are
fixed).
 Latissimus dorsi – elevates the lower ribs.

14. Active Expiration
• Active expiration utilises the contraction of several
thoracic and abdominal muscles. These muscles act to
decrease the volume of the thoracic cavity:
 Anterolateral abdominal wall – increases the intra-
abdominal pressure, pushing the diaphragm further
upwards into the thoracic cavity.
 Internal intercostal – depresses the ribs.
 Innermost intercostal – depresses the ribs.

16. Ventilation perfusion matching
• Ventilation is the amount of air used for gaseous exchange in the
alveolar while perfusion is the blood flow in the pulmonary capillaries
for gaseous exchange.
• Ventilation perfusion matching is a relationship between airflow in the
alveolar and blood flow in the pulmonary capillaries that maintains the
concentration gradient of the gases aiding diffusion of gases across the
respiratory membrane.
• Ventilation perfusion ratio is the ratio of airflow to blood flow. Written
as V/Q and has a range of 0.8-1.2. V/Q ratio is affected by; Gravity
affects perfusion and Lung conditions that obstruct the airway and
those that alter perfusion like pulmonary edema, asthma, COPD,
pulmonary embolism. These conditions lead to a disruption in the V/Q
ratio causing a mismatch.

17. Process
To match local blood flow and airflow at the respiratory
membrane, pulmonary capillaries can be adjusted by
vasoconstriction or vasodilation and the airways by
bronchoconstriction or bronchodilation.
If perfusion is greater than airflow, gases do not have enough
time to exchange properly. V/Q ratio is low, therefore:
• CO2 is high triggering bronchodilation to increase airflow
• O2 is low triggering vasoconstriction to decrease blood flow.
If blood flow is slower than airflow, excess gaseous takes place.
V/Q ratio is high, therefore:
• CO2 is low triggering bronchoconstriction to decrease airflow.
• O2 is high triggering vasodilation to increase blood flow.

18. V/Q Ratio
Normal ventilation is 4-6
L/min and pulmonary blood
flow has a similar range.
V/Q must be estimated on an
alveolar-capillary level, since
different units have different
ratios and not for the lungs
because it only gives an
approximate of the situation in
all alveolar-capillary units.
If V/Q ratio is not matched
then there is a mismatch or an
inequality (airflow and blood
flow ratio are not properly
corresponding).

21. Summary
• The magnitude of V and Q as well as their
distribution isimportant in determining pulmonary
gas exchange.
• Distribution of V and Q is predominately gravity
and intrinsic lung structure.
• V/Q ratiosare nonuniformin different regions of the
lungs.
• V/Q mismatch is the most important cause of
gaseous exchange abnormalities inlung diseases

22. Bronchoconstriction is defined as the abnormal contraction of the smooth muscles of
the bronchi and bronchioles resulting into narrowing of the airways in the lungs and
difficult breathing.
Air flow in air passages can get restricted in three ways: spasmodic state of the
smooth muscles in airway, inflammations of the bronchi and bronchioles and
excessive production of mucus.
Bronchoconstriction can cause symptoms such as wheezing, coughing, chest
tightness, and a feeling of breathlessness. These symptoms are common in conditions
like asthma and chronic obstructive pulmonary disease (COPD).
Bronchoconstriction

23. MECHANISM OF BRONCHIAL SPASM
1.Parasympathetic Nervous System Activation: When the parasympathetic nervous system is
activated, it leads to the release of acetylcholine.
2.Release of Acetylcholine: Postganglionic parasympathetic fibers release acetylcholine, which
acts as a neurotransmitter.
3.Muscarinic M3 Receptors: Smooth muscle cells surrounding the bronchi have muscarinic M3
receptors on their cell membranes. These receptors are activated by acetylcholine.
4.G Protein Activation: When acetylcholine binds to the M3 receptors, it activates an intracellular
G protein associated with these receptors.
5.Phospholipase C Pathway Activation: The activated G protein, in turn, activates the
phospholipase C pathway. Phospholipase C is an enzyme that cleaves a membrane phospholipid
to produce inositol trisphosphate (IP3) and diacylglycerol (DAG).
6.Intracellular Calcium Increase: IP3 acts on intracellular calcium stores (like the endoplasmic
reticulum), causing the release of calcium ions into the cytoplasm of the smooth muscle cell.
This results in an increase in intracellular calcium concentrations.
7.Smooth Muscle Contraction: Elevated intracellular calcium concentrations trigger the
contraction of the smooth muscle cells surrounding the bronchi.
8.Bronchial Constriction: As the smooth muscle contracts, it narrows the diameter of the
bronchus. This narrowing leads to increased resistance to airflow through the bronchus.

24. The effects of bronchoconstriction on airflow are:
• Increased resistance to airflow: The increased resistance to airflow
makes it more difficult for air to move in and out of the lungs. This
can cause shortness of breath and wheezing
• Decreased airflow rate: The decreased airflow rate means that less
air is able to reach the lungs with each breath. This can lead to
hypoxemia, which is a low level of oxygen in the blood
• Increased work of breathing: The increased work of breathing is the
effort that the respiratory muscles must make to breathe. This can
lead to fatigue and respiratory failure
• Decreased lung compliance: The decreased lung compliance means
that the lungs are less able to expand and contract. This can make it
difficult to breathe deeply.

25. IMPACT OF ALTITUDE ON RESPIRATORY PHYSIOLOGY
As altitude increases, atmospheric pressure decreases. At sealevel, atmosphericpressure is
approximately 760mmHg(compared to approximately 253mmHgatthe peakofMountEverest). These
atmosphericpressurescanbe usedto calculatethe partial pressureofoxygen(pO2) in air. This shows
that thepO2is approximately159mmHgat sea level and 43mmHgatthe summitofMountEverest.

26. Acclimatisation
• Acclimatisation describes the normal physiological changes through
which the body adapts to decreasing levels of oxygen. It explains why
in parts of the world such as Tibet, many generations of people have
lived at high altitude whereas climbers have to take considerable care
when moving to high altitudes.

28. Changes in blood
Increased red blood cell production
Increased hemoglobin concentration to about 20g/dL due to increased erythropoietin
secretion
Increased hematocrit
Increased plasma volume
Increased production of 2,3-diphosphoglycerate (DPG)
Changes in respiratory system
Increased pulmonary ventilation and blood flow
Increased diffusion capacity by the lungs due to stimulation of chemoreceptors
Changes in cardio vascular system
Increased heart rate, cardiac output and BP
Increased blood flow to the vital organs like, brain, heart and muscles
Changes in tissue
Increased quantities of oxidative enzymes involved in metabolism present in cells
Increased mitochondria in cells
Increased myoglobin content

29. Acute mountain sickness (AMS)
is a group of symptoms that can occur when the body is not able to adapt to the
decreased oxygen levels at high altitude. Symptoms of AMS can include
headache, nausea, vomiting, dizziness, and fatigue. In severe cases, AMS can be
fatal.
AMS is most common at altitudes above 8,000 feet (2,400 m). The risk of AMS
increases with the altitude and with the rate of ascent.
severe cases of acute mountain sickness this can lead to a number of serious
complications, including:
• High altitude pulmonary edema (HAPE)
• High altitude cerebral edema (HACE)
Treatment options include
• Rest: This allows the body to rest and to recover from the stresses of ascent.
• Acetazolamide: This medication helps to reduce the symptoms of AMS.
• Descent: If symptoms are severe, it is important to descend to a lower
altitude.

30. High-Altitude Pulmonary Edema
(HAPE)
• Life threatening form of non cardiogenic
edema due to leaky capillaries
• Starts at first 1-2 days at high altitude
Symptoms include shortness of breath,
cough, rapid breathing, and cyanosis
• Treatment: immediate descent, oxygen,
and medications.
• HAPE is a medical emergency; timely
action is critical.