Control Of Breathing

Question 1

What is the primary respiratory control center?

Answer 1

Medullary respiratory center

Question 2

Mention function of DRG

Answer 2

• When the DRG neurons fire, the inspiratory muscles contract and inspiration starts.
• When the DRG cease firing, inspiratory muscles relax and expiration begins.

Question 3

VRG is brought into action when …..

Answer 3

The demands for ventilation are increased

Question 4

Describe the function of VRG

Answer 4

During active expiration, DRG stimulates VRG expiratory neurons and send impulses to expiratory muscles (abdominal & internal intercostals).
During deep inspiration DRG stimulated VRG inspiratory neurons.
Thus VRG is called by DRG, as an overdrive mechansim.

Question 5

The basic respiratory rhythm is set by

Answer 5

Neurons in pre-Botzinger complex

Question 6

What happens in lesions of DRG or VRG?

Answer 6

Respiratory activity is not abolished but it is deregulated

Question 7

Site & function of pneumotaxic center

Answer 7

Upper pons

DRG inhibit inspiratory neurons, shortens duration of inspiration, increases breathing rate.

Question 8

Site & function of apneustic center

Answer 8

In lower pons

Driving effect on DRG inspiratory neurons exciting and stimulating them.

Question 9

Apneustuc center recieves inhibitory impulses from …&…

Answer 9

Pneumotaxic center & vagus

Question 10

Mention the dominating pontine center and why

Answer 10

Pneumotaxic center to stop breathing at proper time thus allowing normal expiration

Question 11

What happens in case of damage to pneumotaxic center OR bilateral vagotomy

Answer 11

Their inhibitory effect is lost and partially compensated by the other so breathing becomes slower and deeper.

Question 12

What happens in case of damage to pneumotaxic center AND vagi

Answer 12

Apneusis resulting in prolonged inspiratory gasps interrupted by very short expiration.

Question 13

Mention the mechanism & importance of Hering-Breuer reflex

Answer 13

Stretching of lungs above normal tidal volume results in stretch of bronchi & lung parenchyma stimulating stretch receptors producing an impulse which travels through vagus to medullary respiratory center.
Protective mechanism preventing overinflation of the lung

Question 14

Mention substances affecting ventilation

Answer 14

CO2, O2 & H+

Question 15

Role of central chemoreceptors in ventilation regulation

Answer 15

Rise in arterial blood CO2 which crosses the BBB, then causes increase in H+ by carbonic anhydrase reaction which stimulates the central chemo.
However, changes in arterial H+ don’t affect them as it doesn’t cross BBB

Question 16

Role of peripheral chemoreceptors in ventilation regulation

Answer 16

They respond to decreased PO2, increased CO2 & H+ in arterial blood.
They are the aortic bodies & carotid body.

Question 17

Impulses from carotid body are carried by …., while those from aortic body are carried by ….

Answer 17

Glosso-pharyngeal nerve (IX)

Vagus (X)

Question 18

GR: Aortic & carotid bodies do not sense anemic hypoxia or CO poisoning

Answer 18

Beacuse they has very large blood supply thus their oxygen needs are only met by physically dissolved form, thus they respond to changes in PO2 and not O2 content.

Question 19

Describe the ventillatory response to dec arterial O2

Answer 19

Peripheral chemoreceptors are stimulated when PO2 drops below 60 mmHg, they send impulses to stimulated medullary inspiratory neurons, such reflex is considered emergency life-saving mechanism.

Question 20

What happens if: peripheral chemoreceptors are absent?

Answer 20

Drop in arterial PO2 will cause direct depression of brain including respiratory centers with more reduction of PO2 till death occurs.

Question 21

Mention sites which respond to increased arterial PCO2

Answer 21

Mainly central chemoreceptors (70%) and peripheral to lesser extent (30%)

Question 22

What happens in case of increased arterial PCO2 more than 70-80 mmHg

Answer 22

Direct depression of entire brain including central chemoreceptors and respiratory center & marked hypoventilation.

Question 23

What happens when arterial PCO2 decreases below normal

Answer 23

Decrease the rspiratory drive by central chemoreceptors and accumulation of CO2 produced by cellular metabolism.

Question 24

Compare CO2 drive & hypoxic drive

Answer 24

CO2 drive is primary factor stimulating respiration in normal individuals where an increase in PCO2 more than 40 mmHg causes stimulation of respiration
Hypoxic drive occurs in patients with severe chronic lung diseasem where the kidneys respond to chronic acidosis by reabsorption of more bicarbonate ions which neutralize H+ in brain ECF so central chemoreceptors become insensitive to CO2 increase & and the decreased arterial PO2 becomes the primary respiratory stimulus.

Question 25

GR: O2 therapy should be given with caution to patients with severe chronic lung disease.

Answer 25

As removal of hypoxic drive can cause more depression of respiration.

Question 26

Describe ventilatory responses to pH changes

Answer 26

They are sensed solely by peripheral chemoreceptors, they stimulate respiration when pH decraeses and supress it when pH increases.

Question 27

In normal conditions, which is more powerful in stimulating respiration, dec O2, inc CO2 or inc H+?

Answer 27

Inc CO2 is most powerful, as dec PCO2 by 5% increases ventilation 3-4 times Dec O2 by 40% from 100 to 60 mmHg does not effect ventilation Inc H+ only stimulates peripheral receptors while CO2 stimulates both types of receptors

Question 28

Hypoxia is the respiratory drive in which situations?

Answer 28

- Chronic lung disease with decreased sensitivity to PCO2 - In cases of very high level of PCO2 (narcosis) - At high altitude where PCO2 is normal PO2 is low

Question 29

Why does breaking point occur?

Answer 29

Due to accumulation of CO2 in blood followed by increased H+ in ECF of brain, stimulating central chemoreceptors, override the voluntary inhibition, and breathing returns.

Question 30

How to prolong duration of voluntary apnea?

Answer 30

1. Hyperventilation before breath holding | 2. Breathing 100% CO2 before test

Question 31

Compare cough reflex & sneezing reflex

Answer 31

C: forced expiration against a closed glottis S: violent expiration while the glottis is continuously closed

Question 32

What happens when J-receptors are activated?

Answer 32

Apnea followed by rapid breathing, hypotension & bradycardia. Also activated by capsaicin

Question 33

Mention sites of mechanoreceptors

Answer 33

Chest muscles, tendons & ligaments | Skeletal muscles, joints, tendons & ligaments

Question 34

Role of arterial baroreceptors

Answer 34

Causes reflex inhibition of respiration when arterial blood pressure increases, which is the underlying mechanism of adrenaline apnea

Question 35

Gut reflexes effect on respiration

Answer 35

Inhibition & closing of glottis during swallowing & vomiting

Question 36

Mention role of hypothalamus in ventilation regulation

Answer 36

Modulates respiration in depth & rate in response of strong emotions & pain Also stimulates resp center in hot weather

Question 37

In moderate exercise ventilation increases in ….., while in heavy ex it increses in ….

Answer 37

Depth | Depth & rate

Question 38

During exercise arterial PCO2 & PO2 …….

Answer 38

Remain contsant due to hyperventilation

Question 39

GR: O2 extraction is greatly increased during exercise.

Answer 39

Increase alveolar-capillary PO2 gradient due to fall in PO2 in venous blood. Shift of Hb-O2 dissociation curve to the right by inc in CO2, H+ & 2,3-DPG

Question 40

What happens to arterial pH during exercise

Answer 40

In moderate: no change | In heavy: decreased due to lactic acid production

Question 41

The respiratory rate after exercise reaches basal levels only after ….

Answer 41

The O2 debt is repaid

Question 42

Explain: the abrupt increase in ventilation at onset of exercise.

Answer 42

Psychic stimuli via cerebral cortex Afferent impulses from proprioceptors in muscles This occurs in a feed-forward regulatory mechanism

Question 43

The main respiratory stimulant in heavy exercise & why?

Answer 43

Lactic acidosis since arterial PO2 inc & PCO2 decrease by hyperventilation

Question 44

GR: Ventilation increases gradually during moderate exercise although gases remain relatively constant

Answer 44

Increased temp, K+ stimulated peripheral chemoreceptors, increased fluctuations of arterial PCO2 & PO2, increased sensitivity of respiratory center to PCO2, sympathetic stimulation.

Question 45

GR: Extra O2 consumption during the recovery of muscle

Answer 45

Resaturate myoglobin, resynthesize ATP, remove lactic acid (80% is converted to glycogen, 20% metabolized to CO2 & H2O).

Question 46

Describe the effect of high altitude on ventilation

Answer 46

At 10,000 feet, PO2 is about 60 mmHg so pulmonary hyperventilation begins Above 10,000 feet, PO2 drops to the steep portion of Hb-O2 dissociation curve O2 lack stimulated respiration, leading to hyperventialtion & alkalosis

Question 47

GR: Occurence of Acute mountain sickness

Answer 47

Persons who ascend rapidly to altitudes of 10,000 feet or more

Question 48

Mention the compensatory mechanisms that develop in ascend to high altitude

Answer 48

Increased diffusion capacity, O2 carrying capacity, O2 liberation by inc 2,3-DPG, inc oxidative enzymes and myoglobin, inc number of capillaries, increased urinary excretion of HCO3- (alkaline urine)

Question 49

Mention disadvatages of compensatory measures to high altitude

Answer 49

Increased no of RBCs , inc resistance to blood flow, inc viscosity & inc cardiac work to pump blood.