Central Contol Of Ventilation Flashcards Preview

Cardio-respiratory Physiology And Pharmacology > Central Contol Of Ventilation > Flashcards

Flashcards in Central Contol Of Ventilation Deck (21)

What does minute alveolar ventilation depend on ?

Both rate and depth of breathing


How can expiration be a passive process during quiet breathing ?

Because the recoil of the lungs and chest wall is sufficient to cause expiration


What nerves innervate the diaphragm and the inter coastal muscles ?

Phrenic nerve innervate the diaphragm
Intercostal nerves innervate the intercostal muscles


Where are the respiratory control regions ?

In medulla and pons of BRAINSTEM
- contain inspiratory and expiratory neurons


Where are the 2 respiratory control centres of the medulla and what's contained in them ?

VRG - 2 groups of primarily expiratory neurons and 1 region of inspiratory neurons
DRG- contains primarily inspiratory neurons
Thought that inspiratory neurons control the motor neurones that control inspiratory neurones


What is the pattern of activity like in inspiratory neurones of the VRG and DRG ?

At expiration and rest here is little or no activity
Inspiration causes a low frequency to begin and then it ramps up as inspiration proceeds reaching crescendo at the peak
Then it terminates as expiration begins


What is the pontine respiratory group ?

Formerly refereed to as apneustic and pneumotaxic centres
Thought to affect the neurons in the medulla - primarily the inspiratory ones
- some have an excitatory effect
- others switch off or inhibit inspiration


What are the hypothesise for the central pattern generator being present in the medulla ?

1- certain cells have pacemaker activity but none have actually been identified yet
2- inputs from sensory receptors and other brain areas modifies the output from it


What are pulmonary stretch receptors ?

Located in airway smooth muscle
Activated by distension of the lungs
Main reflex effect to stimulating these receptors is a slowing of respiratory frequency due to an increase in expiratory time


What is the function of the PRG neurones ?

Regulate respiratory rate and depth and to fine tune the respiratory rhythm


What is the central pattern general pathway ?

Sensory inputs, pons and cortex all feed into the medulla which is proposed to have a network of neurons responsible for generating regular repeating pattern
Theses then project to the inspiratory neurons of the DRG and VRG and these then produce the breathing rhythm


What are the hering-Breuer reflexes and where are hey important ?

Thought to play an important role in determining rate and depth of breathing by modulating the activity of PRG neurons
These a relatively inactive in adult humans except at high lung volumes and they are important in other animal species


What happens when the arterial partial pressure of oxygen drops to below 60mmHg?

Ventilation is stimulated
Increasing the alveolar partial pressure of oxygen because alveolar air is replaced with fresh air more rapidly so the alveolar oxygen concentration is closer it the inspired oxygen concentration


What are the consequences of increased ventilation at altitude ?

Because increasing the ventilation increases the loss of carbon dioxide and the production of carbon dioxide is not altered significantly at altitude so it causes respiratory alkalosis
- decreasing PaCO2 and proton concentration
Theses effects are detected by central and peripheral chemoreceptors causing inhibition of ventilation


What effect does the decreased arterial partial pressure of carbon dioxide and increased pH at altitude do to the oxygen dissociation curve ?

Shifts it to the left
Increasing the affinity for haemoglobin to oxygen
Good at lungs but bad at tissues because it's not released


How is respiratory alkalosis compensated for ?

By decreasing the reabsorption of bicarbonate ions to decrease the concentration in the plasma


What are the immediate adjustments to acclimatisation to altitude ?

1- hyperventilation caused by hypoxic respiratory drive
2- increased CO at rest and during sub maximal exercise submaximal CO and HR can be increased by up to 50% above sea level values helping to increase system I and pull lady blood flow and compensate for the reduced arterial oxygen content


What are the short term adjustments to altitude acclimatisation ?

Increased ventilation causes respiratory alkalosis which is compensated for by increased excretion fo bicarbonate ions but this has important consequences:
1- it accompanies osmotic diuretics causing further fluid losses causing a reduction in plasma volume and therefore an increase in haematocrit
2- reduction in blood buffering capacity of non carbonic acids so it reduces the critical level of exercise that can be tolerated without causing blood lactate accumulation


What are the longer term adjustments for altitude acclimatisation ?

Initially the ventilatiation only increases by 2 fold but over 2-3 weeks it increases up to 5-7 fold
Main influence on this rise is due to increases in tidal volume which is a more efficient way of increasing alveolar ventilation


What is responsible for the secondary rise in ventilation?

Not known but through........
1- increas in sensitivity of peripheral chemoreceptors to low oxygen arterial pressure occurs over first few days at altitude
2- gradual restoration of near normal CSF pH may occur and this reduces the indirect effect of low atrial carbon dioxide pressure on the central chemoreceptors


What haemotological changes occur at altitude ?

1- increases in haemotocrit levels, initially due to reductions in plasma volume but it increases oxygen carrying capacity of each litre of blood
2- hypoxia stimulates the kidney to release EPO within 15 hours of ascent to altitude this results in an increase in red blood cell synthesis causing increased numbers of circulating rbcs
3- then the plasma volume returns to normal resulting in an increase in both blood volume and haemotocrit - haematocrit crit can increas by 60% in fully acclimatised individuals