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Respiratory Physiology > Control Of Breathing > Flashcards

Control Of Breathing Flashcards

1
Q

What is the primary respiratory control center?

A

Medullary respiratory center

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2
Q

Mention function of DRG

A
  • When the DRG neurons fire, the inspiratory muscles contract and inspiration starts.
  • When the DRG cease firing, inspiratory muscles relax and expiration begins.
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3
Q

VRG is brought into action when …..

A

The demands for ventilation are increased

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4
Q

Describe the function of VRG

A

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.

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5
Q

The basic respiratory rhythm is set by

A

Neurons in pre-Botzinger complex

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6
Q

What happens in lesions of DRG or VRG?

A

Respiratory activity is not abolished but it is deregulated

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7
Q

Site & function of pneumotaxic center

A

Upper pons

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

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8
Q

Site & function of apneustic center

A

In lower pons

Driving effect on DRG inspiratory neurons exciting and stimulating them.

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9
Q

Apneustuc center recieves inhibitory impulses from …&…

A

Pneumotaxic center & vagus

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10
Q

Mention the dominating pontine center and why

A

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

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11
Q

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

A

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

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12
Q

What happens in case of damage to pneumotaxic center AND vagi

A

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

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13
Q

Mention the mechanism & importance of Hering-Breuer reflex

A

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

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14
Q

Mention substances affecting ventilation

A

CO2, O2 & H+

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15
Q

Role of central chemoreceptors in ventilation regulation

A

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

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16
Q

Role of peripheral chemoreceptors in ventilation regulation

A

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

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17
Q

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

A

Glosso-pharyngeal nerve (IX)

Vagus (X)

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18
Q

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

A

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.

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19
Q

Describe the ventillatory response to dec arterial O2

A

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.

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20
Q

What happens if: peripheral chemoreceptors are absent?

A

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

21
Q

Mention sites which respond to increased arterial PCO2

A

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

22
Q

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

A

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

23
Q

What happens when arterial PCO2 decreases below normal

A

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

24
Q

Compare CO2 drive & hypoxic drive

A

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.

25
Q

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

A

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

26
Q

Describe ventilatory responses to pH changes

A

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

27
Q

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

A

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

28
Q

Hypoxia is the respiratory drive in which situations?

A
  • 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
29
Q

Why does breaking point occur?

A

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.

30
Q

How to prolong duration of voluntary apnea?

A
  1. Hyperventilation before breath holding

2. Breathing 100% CO2 before test

31
Q

Compare cough reflex & sneezing reflex

A

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

32
Q

What happens when J-receptors are activated?

A

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

33
Q

Mention sites of mechanoreceptors

A

Chest muscles, tendons & ligaments

Skeletal muscles, joints, tendons & ligaments

34
Q

Role of arterial baroreceptors

A

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

35
Q

Gut reflexes effect on respiration

A

Inhibition & closing of glottis during swallowing & vomiting

36
Q

Mention role of hypothalamus in ventilation regulation

A

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

37
Q

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

A

Depth

Depth & rate

38
Q

During exercise arterial PCO2 & PO2 …….

A

Remain contsant due to hyperventilation

39
Q

GR: O2 extraction is greatly increased during exercise.

A

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

40
Q

What happens to arterial pH during exercise

A

In moderate: no change

In heavy: decreased due to lactic acid production

41
Q

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

A

The O2 debt is repaid

42
Q

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

A

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

43
Q

The main respiratory stimulant in heavy exercise & why?

A

Lactic acidosis since arterial PO2 inc & PCO2 decrease by hyperventilation

44
Q

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

A

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

45
Q

GR: Extra O2 consumption during the recovery of muscle

A

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

46
Q

Describe the effect of high altitude on ventilation

A

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

47
Q

GR: Occurence of Acute mountain sickness

A

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

48
Q

Mention the compensatory mechanisms that develop in ascend to high altitude

A

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)

49
Q

Mention disadvatages of compensatory measures to high altitude

A

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

Respiratory Physiology (5 decks)

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