Control Of Breathing Flashcards
What is the primary respiratory control center?
Medullary respiratory center
Mention function of DRG
- When the DRG neurons fire, the inspiratory muscles contract and inspiration starts.
- When the DRG cease firing, inspiratory muscles relax and expiration begins.
VRG is brought into action when …..
The demands for ventilation are increased
Describe the function of VRG
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.
The basic respiratory rhythm is set by
Neurons in pre-Botzinger complex
What happens in lesions of DRG or VRG?
Respiratory activity is not abolished but it is deregulated
Site & function of pneumotaxic center
Upper pons
DRG inhibit inspiratory neurons, shortens duration of inspiration, increases breathing rate.
Site & function of apneustic center
In lower pons
Driving effect on DRG inspiratory neurons exciting and stimulating them.
Apneustuc center recieves inhibitory impulses from …&…
Pneumotaxic center & vagus
Mention the dominating pontine center and why
Pneumotaxic center to stop breathing at proper time thus allowing normal expiration
What happens in case of damage to pneumotaxic center OR bilateral vagotomy
Their inhibitory effect is lost and partially compensated by the other so breathing becomes slower and deeper.
What happens in case of damage to pneumotaxic center AND vagi
Apneusis resulting in prolonged inspiratory gasps interrupted by very short expiration.
Mention the mechanism & importance of Hering-Breuer reflex
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
Mention substances affecting ventilation
CO2, O2 & H+
Role of central chemoreceptors in ventilation regulation
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
Role of peripheral chemoreceptors in ventilation regulation
They respond to decreased PO2, increased CO2 & H+ in arterial blood.
They are the aortic bodies & carotid body.
Impulses from carotid body are carried by …., while those from aortic body are carried by ….
Glosso-pharyngeal nerve (IX)
Vagus (X)
GR: Aortic & carotid bodies do not sense anemic hypoxia or CO poisoning
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.
Describe the ventillatory response to dec arterial O2
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.
What happens if: peripheral chemoreceptors are absent?
Drop in arterial PO2 will cause direct depression of brain including respiratory centers with more reduction of PO2 till death occurs.
Mention sites which respond to increased arterial PCO2
Mainly central chemoreceptors (70%) and peripheral to lesser extent (30%)
What happens in case of increased arterial PCO2 more than 70-80 mmHg
Direct depression of entire brain including central chemoreceptors and respiratory center & marked hypoventilation.
What happens when arterial PCO2 decreases below normal
Decrease the rspiratory drive by central chemoreceptors and accumulation of CO2 produced by cellular metabolism.
Compare CO2 drive & hypoxic drive
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.
GR: O2 therapy should be given with caution to patients with severe chronic lung disease.
As removal of hypoxic drive can cause more depression of respiration.
Describe ventilatory responses to pH changes
They are sensed solely by peripheral chemoreceptors, they stimulate respiration when pH decraeses and supress it when pH increases.
In normal conditions, which is more powerful in stimulating respiration, dec O2, inc CO2 or inc H+?
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
Hypoxia is the respiratory drive in which situations?
- 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
Why does breaking point occur?
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.
How to prolong duration of voluntary apnea?
- Hyperventilation before breath holding
2. Breathing 100% CO2 before test
Compare cough reflex & sneezing reflex
C: forced expiration against a closed glottis
S: violent expiration while the glottis is continuously closed
What happens when J-receptors are activated?
Apnea followed by rapid breathing, hypotension & bradycardia.
Also activated by capsaicin
Mention sites of mechanoreceptors
Chest muscles, tendons & ligaments
Skeletal muscles, joints, tendons & ligaments
Role of arterial baroreceptors
Causes reflex inhibition of respiration when arterial blood pressure increases, which is the underlying mechanism of adrenaline apnea
Gut reflexes effect on respiration
Inhibition & closing of glottis during swallowing & vomiting
Mention role of hypothalamus in ventilation regulation
Modulates respiration in depth & rate in response of strong emotions & pain
Also stimulates resp center in hot weather
In moderate exercise ventilation increases in ….., while in heavy ex it increses in ….
Depth
Depth & rate
During exercise arterial PCO2 & PO2 …….
Remain contsant due to hyperventilation
GR: O2 extraction is greatly increased during exercise.
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
What happens to arterial pH during exercise
In moderate: no change
In heavy: decreased due to lactic acid production
The respiratory rate after exercise reaches basal levels only after ….
The O2 debt is repaid
Explain: the abrupt increase in ventilation at onset of exercise.
Psychic stimuli via cerebral cortex
Afferent impulses from proprioceptors in muscles
This occurs in a feed-forward regulatory mechanism
The main respiratory stimulant in heavy exercise & why?
Lactic acidosis since arterial PO2 inc & PCO2 decrease by hyperventilation
GR: Ventilation increases gradually during moderate exercise although gases remain relatively constant
Increased temp, K+ stimulated peripheral chemoreceptors, increased fluctuations of arterial PCO2 & PO2, increased sensitivity of respiratory center to PCO2, sympathetic stimulation.
GR: Extra O2 consumption during the recovery of muscle
Resaturate myoglobin, resynthesize ATP, remove lactic acid (80% is converted to glycogen, 20% metabolized to CO2 & H2O).
Describe the effect of high altitude on ventilation
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
GR: Occurence of Acute mountain sickness
Persons who ascend rapidly to altitudes of 10,000 feet or more
Mention the compensatory mechanisms that develop in ascend to high altitude
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)
Mention disadvatages of compensatory measures to high altitude
Increased no of RBCs , inc resistance to blood flow, inc viscosity & inc cardiac work to pump blood.
