Regulation of respiration

Controls of Ventilation

A). Brain
1.Respiratory Center
i). Dorsal Respiratory Group
ii). Ventral Respiratory Group
iii) Pneumotaxic Area of the Pons
2). Hypothalamus:
3). Higher Cortical Functions

B). Chemical Signals

1). PCO2
2) H a Rate of breathing increases
3). PO2
Respiratory center (RC) is located in the medulla oblongata which is the
lowermost part of the brain stem. RC receives controlling signals of neural,
chemical and hormonal natures and controls the rate and depth of respiratory
movements of the diaphragm and other respiratory muscles. Injury to this center
may lead to central respiratory failure which necessitates mechanical ventilation
but usually the prognosis is grave

The groups of nerve cells in the brain which regulates the respiration rhythmically
are collectively known as respiratory centres. respiratory centre is composed of
several widely dispersed groups of neurons.

Groups: Respiratory centre is divided four major groups.

Respiratory Location Name of Function

centres nucleus

1. Inspiratory Dorsal portion of Nucleus of It causes inspiration

centre ( Dorsal medulla Tractus solitarius while stimulated.
respiratory oblongate
group)

2. Expiratory Antero- lateral Nucleus 1. It causes either

centre ( Ventral part of medulla, ambiguous and expiration or inspiration
respiratory about 5 mm nucleus retro depending upon which
Group) anterior and ambiguous. neuron in the group are
lateral to dorsal stimulated. But
respiratory group generally causes
expiration

2. It sends inhibitory
impulse to the
apneustic centre.

3. Pneumotaxic Upper part of Nucleus 1.It controls both rate

centre pons parabrachialis and pattern of
breathing

2. It sends impulses to
limit inspiration.
Apneustic centre In the lower part 1. It discharges
of the pons. stimulatory impulse to
the inspiratory centre
causing inspiration.

2. It receives inhibitory
impulse from
pneumotaxic centre and
from stretch receptor of
lung.

3. It discharges
inhibitory impulse to
expiratory centre.

(Ref. Guyton & Hall—11th P. 515)

Apneustic respiration
Apneustic respiration (apneusis) is an abnormal pattern of breathing
characterized by deep, gasping inspiration with a pause at full inspiration
followed by a brief, insufficient release.

Causes

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.

Nervous regulation of respiration/Rhythmic breathing

Inhaling & expiring of air at a regular interval of time is rhythmic breathing.
Process

• Spontaneous inspiratory ramp signal produced b inspiratory center. \

• Passing through phrenic & int costal nerves
after 2 sec. ramp signal switch-off by pneumotaxic center
• expiration fakes place by passive way.

Chemical regulation of respiration

The rhythmic discharge is regulated by alteration in arterial PO2, PCO2, & [H+] this
chemical control is supported by non-chemical influences.

A number of chemical factors such as

1) Elevated blood Pco2 for concentration of C02.
2) Elevated blood H+ (i.e. PH) and
3) Decreased blood P02 (or concentration of 02) are involved in chemical control
of respiration.

Effects of C02 on alveolar ventilation:

-- C02 itself has little direct effect in stimulating the respiratory centre.
-- Reflex action:
The C02 diffuses through the blood- brain barrier into CSF and combines with
water to form carbonic acid, which dissociates into H+ and HCO3- ions. The H+
then stimulates the central chemoreceptor area.

As a result the rate and depth of respiration is increased.

A maximal increase in CO2 can increase alveolar ventilation about 10- fold.

Effect of H+ (i.e. pH) on alveolar ventilation:

Increased blood H concentration (i.e. decreased pH increased alveolar ventilation.
The effects of blob H+ concentration on ventilation are thought to be mediated by
way of peripheral chemoreceptors in addition to direct effects on the respiratory
centre.
Central chemoreceptors are stimulated only slightly by increased, H+
concentration in the blood because the blood- brain barrier is relatively
impermeable to H+ A maximal increase in H+ concentration can increase alveolar
ventilation about 4-fold.

Effect of decreased O2 on alveolar ventilation:

Peripheral chemoreceptors in the carotid and aortic bodies are stimulated by
decreased 02 in the arterial blood. But, the arterial P02 must decrease to below
60 mm Hg for stimulation to occur.
 Signals from the stimulated peripheral chemoreceptor are transmitted to
the respiratory centre where they cause an increase in alveolar ventilation.
A maximal O2 (under acute conditions) can increase alveolar ventilation only
about one and two-thirds.

Control the rate & depth of respiration by Hering Breuer reflex:

Reflex control of rate & depth of respiration resulting from stimulation of lung
stretch receptors by inflation or deflation of lung is called Hering Breuer reflex.

Hering Breuer reflex is initiated by inflation of the lungs and functions to terminate
inspiration. Inflation of the lungs stimulates lung stretch receptors that are located
in the small airways. These receptors send impulses to the respiratory centres
via the vagus nerves that inhibit the pontine and medullry respiratory centres.
Conversely, in sustain deflation of the lungs with an occulded airway promotes
strong and frequent inspiratory efforts.

Inspiratory ramp Signal

- Called a ramp signal because it starts as a weak signal and gradually increases
in strength for 2 seconds and then abruptly stops for approximately 3 seconds
- This abrupt halt relaxes the diaphragm allowing for the elastic recoil of the lungs
and exhalation
- Advantage: a steady gradual increase in lung volume. Otherwise, we will breath
by gasping
 Exercise on respiration
Effect of exercise on respiration

Para meter Effect

1. O2 Consumption Increase

2. O2 Production and elimination Increase

3. Ventilation Increase

4. Arterial PO2 + PCO2 No overall change

5. Arterial pH No change in moderate exercise

Decreases in strenuous exercise

6. Venous PCO2 Increases

7. Pulmonary blood flow Increases ( which always equals the

cardiac out put)

8. Ventilation perfusion ratio More evenly distributed in lung

Regulation of respiration during exercise

During exercise, the rate of respiration increases. This increases in respiration is

controlled by both neural and chemical mechanisms.

1. Nervous factor or direct stimulation of respiratory centre from motor

cortex:

a. During exercise the brain transmitting impulses to, the contracting muscles
also transmit collateral impulses to the respiratory centre.

b. This stimulation of respiratory centre increases the rate of respiration.\

2. Chemical factors or stimulation caused by chemical substances:

a. During exercise, the Pco2 increases and O2 decreases due to excess

metabolism in the cells.
 b. This then stimulates chemosensitive area of brain through
chemoreceptors which then increase the rate of respiration.

3. . Indirect stimulation from proprioceptors

a. During exercise, the movements of the limbs and body excites the
proprioceptors

b. This then transmits impulse to the respiratory centres

c. This increase rate of respiration

4. Hypoxia: During exercise, hypoxia develops in the muscles that elicits

afferent nerve signal to the respiratory to excite respiration

How is extra amount of 02 supplied to the tissues during exercise?

Ans. Extra amount of O2 is supplied to the tissues during exercise by:

1. Breathing: Increase in pulmonary ventilation introduces large amounts of
fresh air into the lung.
2. O2 uptake in the lung: Large amount of oxygen are taken up from the
lungs by the blood. \
3. Supply of oxygen to the tissues: A great blood supply to the muscle due to
increased cardiac out put and redistribution of blood to the systemic
circulation.
4. Removal of oxygen by the tissues: This is effected as follows-
a. Dilatation and increase in the number of patent capillaries in the
muscles slows the rate of the blood how.
b. Low oxygen tension allows oxygen to diffuse more rapidly and to a
greater extent. \
c. High CO2 tension and raised temperature increases the extent and
rate of dissociation of oxyhaemoglobin,

Respiratory insufficiency

It means abnormalities in normal rate & depth of respiration.

Cause:
1. inadequate ventilation.
2. Reduce gaseous diffusion through respiratory membrane.
3. Abnormal ventilation—perfusion ratio.
•Eupnea: Means normal breathing.
 •Tachypnea: Means rapid breathing than normal.
• Bradypnea: Means slow breathing than normal.
•Hypoxia: Means decreased O2 in tissue.
•Anoxia: Means total lack of O2
•Hypoxaemia: Means reduced O2 in blood.
•Hypercapnia: Means excess CO2 in blood.
•Hypocapnia: Means depressed CO2 in blood.
•Dyspnoea: Means difficulty in breathing.
•Apnoea: Means temporary cessation of breathing.

HYPOXIA

Hypoxia is oxygen (O2) deficiency at the tissue level.

Types with causes:

1. Hypoxic hypoxia (anoxic anoxia): PO2 of the arterial blood is reduced.
When a person exposed to high altitude (e.g. - in the plane flying above
16,000 meters), Hypoxic hypox develops. It is due to a sudden drop in the
inspired Po2 (<20 mmHg). This may cause loss of consciousness in 10-20
minute & death in 4-5 minutes.
2. Anaemic hypoxia: the arterial PO2 in normal but the amount of
haemoglobin available to carry O2 It reduced.
3. Stangnant or ischemic hypoxia: the blood flow to a tissue is so low that
adequate O2 is not delivered to it despite a normal PO2 and Hb
concentration.
4. Histotoxic hypoxia:
In which the amount of O2 delivered to tissue is adequate but the tissue
cannot utilize the O2 due to presence of toxic substances.

Effect of hypoxia:
Severe hypoxia can cause death of the cells. But less sever hypoxia can cause
• Mental aberration:
• Impaired judgment
• drowsiness
• Dulled pain sensibility.
• Excitement.
• Disorientation.: loss of time sense.

causes of hypoxia.
:
1. Hypoxic hypoxia (anoxic anoxia): Disoders causing hypoxic hypoxia are:
i. Lung failure (gas exchange failure)
a. Pulmonary fibrosis
 b. Ventilation-perfusion imbalance.
ii. Shunt Venous to arterial shunt (right to left cardiac shunt).

iii. Pump failure (ventilatory failure)

a. Fatigue

b. Mechenical defects

c. Depression of respiratory controller in the brain.

2. Anaemic hypoxia: It occurs due to-

a. Lack of hemoglobin

b. CO poisoning
c. Abnormal Hb due to poisoning with nitrates, nitric oxide and other
metals.

3. Stagnant or ischaemic hypoxia: It occurs due to-

a. Decreased cardiac output due to heart failure.
b. Decreased blood flow to the organ.
c. Impaired venous return. haemorrhage and shock.

4. Histotoxic hypoxia: It occurs due to-

a. Poisoning with potassium cyanide which interferes tissue oxidation by
paralysis the enzyme cytocrom oxidase.
b. Narcotics also depressed tissue oxidation by interfere with dehydrogenous
system.

Acclimatization:
Acclimatization’ means the adjustment of the human body to suit in a new
climate. (E.g.-High altitude)

The five principal means by which acclimatization occur are:

1. ↑Pulmonary ventilation.
2. ↑Red blood cell & Hb (about 20 gm/dl)
3. ↑Diffusion capacity of the lungs.
4. ↑Vascularity of the tissues.
5. ↑Ability of the cells to utilize 02 despite low P02.

CYANOSIS
Bluish discoloration or skin of mucous membrane due to presence of large
amount of reduced Hb in subcutaneous vessels.
 •Amount of reduced fib showed the at least 5-7 gm/dl.
• Occurs in arterial hypoxia of stagnant hypoxia.
Causes:
o Formation of altered Hb
o Polycythemia
o Rt of left shunt of heart

Type:
Central Cyanosis- Caused by cardiac failure or pulmonary disorder. eg- Tip of
the tongue.
Peripheral cyanosis- Local vascular stains, shock, cold, temperature eg- Tip of
the fingers.

Hypercapnea

Hypercapnea means excess CO2 in the body fluid

Cause

1. Hypoventilation

2. Obstruction in respiratory

3. Respiratory diseases such as asthma

Clinical features:

1. Depression of CNS : confusion

2. Respiratory depression

3. Come & death.

Effects of hypercapnoea:
1. PCO2 more than 60 -75 mm Hg causes severe dyspnoea.
2. PCO2 more than 80-100 mm Hg causes a person lathergic some times even
semicomatoes.
3. PCO2 more than 100-150 mm Hg causes anaesthesia & death.
Cheyne stokes breathing

It is characterized by slow waxing & waning respiration occurring over again

every 40 — 60 sec.
Mechanism:
•When the respiration becomes much more rapid & deeper than usual,
the PCO2 in pulmonary blood decreases.
•This decreased PCO2 inhibit respiration by depressing respiratory center.
As a result, the pulmonary blood PCO2 increases.
•Then this blood enters into the respiratory center & stimulate respiration
again, thus making the person over breath once again & initiating a new cycle of
depressed respiration.
•The cycle thus continue on & on, causing Cheyne-stokes breathing.

Cheyne-Stokes breathing and its effect on arterial O2 saturation. Cheyne-

Stokes breathing occurs frequently during sleep, especially in subjects at high
altitude, as in this example. In the presence of preexisting hypoxemia secondary
to high altitude or other causes, the periods of
apnea may result in further falls of O2 saturation to dangerous levels.
Falling PO2 and rising PCO2 during the apnea intervals ultimately
induce a response and breathing returns, reducing the
stimuli and leading to a new period of apnea.
Ventilation-perfusion ratio
Ans.
Definition: The ratio of alveolar ventilation and alveolar blood flow is called
ventilation - perfusion ratio. It is about 0.8.
VA .... Alveolar ventilation (V)
This is expressed as Q ..... Cardiac output (Q)
4.2 L/min
5 L/min
= 0.84
• Explanation:
1. When VA & Q is normal for a given alveolus, The VA/Q will be normal.
2. When VA is zero but Q of the alveolus is normal, then VA/Q will he zero.
3. When VA is normal but Q is zero, then VA/Q will be infinity.
At a ratio of either zero or infinity, there is no exchange of gases through the
respiratory membrane of the affected alveoli.

Physiologic shunt
The total quantitative amount of shunted blood per minute is called physiologic
shunt. The greater the amount of physiologic shunt the greater the amount of
blood fails to be oxygenated as it passes through the lungs.
Respiratory exchange ratio

The ratio of’ carbondioxide outside to oxygen uptake is called the respiratory
e.\change ratio (R). That is.
Rate of carbon dioxide output
R = Rate of oxygen uptake

The value for R changes under different metabolic conditions. When a person is
using exclusively carbohydrates for body metabolism. R rises to 1.00.
Conversely, when the person is using exclusively fats for metabolic energy, the R
level falls to as low as 0.7.