Respiratory control

Question 1

What initiates inspiration?

Answer 1

-Motor neurons to the intercostal muscles and diaphragm

Question 2

Where is primary control of neural inspiration initiation?

Answer 2

-Medulla oblongata contains the medullary respiratory centre it contains;
1. neurons of the dorsal respiratory group (DRG), these fire during inspiration and have input to the spinal motor neurons that activate resp muscles involved in inspiration (intercostal muscles and diaphragm )
primary - diaphragm (phrenic nerve, c3,4,5)

2. ventral respiratory group (VRG). This rhythm generator appears to be composed of pacemaker cells and complex neural network that together set the basal respiratory rate
   - contains expiratory neurons that are most important during strenuous exercise when large increases in ventilation are needed

Question 3

What neural processes occur during quiet breathing?

Answer 3

• The respiratory rhythm generator activates inspiratory neurons in the VRG, (ventral respiratory group) this depolarizes the inspiratory motor neurons causing the inspiratory muscles to contract
• When these neurons stop firing the muscles relax allowing passive expiration

Question 4

What area of the brain do medullary inspiration neurons receive input from?

Answer 4

• The medullary inspiration neurons receive a rich sympathetic input from neurons in various areas of the pons
• This input fine tunes the output of the medullary inspiratory neurons and may help terminate inspiration by inhibiting them
• a lower area of the pons, the apneustic centreis is the major source of this output. But an upper area, the pneumotaxic centre, modulates the activity of the apneustic center
• The pneumotaxic centre (or pontine respiratory group) helps to smooth the transition between inspiration and expiration
• The respiratory nerves in the medulla and pons also recieve synaptic inout from higher centres of the brain such that the pattern of respiration is controlled by voluntarily during speaking, diving and even emotion and pain
• stretch receptors

Question 5

What is the Hering-Breuer reflex?

Answer 5

1. Pulmonary stretch receptors which lie in the airway smooth muscle are activated by large lung inflation
2. Action potentials are sent to medulla and pneumotaxic center of the pons to inhibit inspiration so that overstretching during inspiration does not occur and so that expiration occurs
3. This reflex prevents over stretching of the lungs
   - this reflex is only active in conditions of large tidal volumes, eg strenuous exercise

Question 6

How do peripheral chemoreceptors affect respiratory centres?

Answer 6

Peripheral chemoreceptors -

• located high in the neck at the bifurcation of the common carotid arteries (carotid bodies-monitor oxygen supply of the brain) and in the thorax on the aortic arch (aortic bodies)
• stimulated by a decrease in arterial PO2 and increase in arterial H+ conc
• the cells communicate synaptically with neuron terminals from which afferent nerves fibres pass to the brainstem, there they provide excitatory synaptic input to the medullary inspiratory neurons
• The carotid body is dominant in control of respiration

Question 7

How do central chemoreceptors affect respiratory centres?

Answer 7

Central chemoreceptors

• located in the medulla
• provide excitatory synaptic input to the medullary inspiratory neurons
• stimulated by an increase in H+ in the brains ECF (mainly due to changes in blood P CO2)
• H+ penetrates BB slowly, Co2 penetrates very quickly

Question 8

What reflex is mediated by the peripheral chemoreceptors ?

Answer 8

• low arterial O2 (only large reduction affects this reflex due to the disociation curve of Hb and O2) increases the rate that the receptors discharge, resulting in an increased number of action potentials travelling up afferent nerve fibres and stimulating medullary inspiratory neurons
• increased ventilation = more oxygen
• decreases in arterial O2 could be due to lung disease or high altitude
• mild to moderate anemia does not activate the response or carbon monoxide as the amount of O2 dissolved in plasma does not change

Question 9

What is metabolic acidosis?

Answer 9

normal or pathological situations in which H+ is increased due to a cause other than a change in PCO2
eg, addition of lactic acid causes hyperventilation due to peripheral chemoreceptors, then is because brain H+ conc is increased very slowly and H+ penetrates the BB very slowly. CO2 penetrates very quickly changing the H+ conc.

Question 10

What is metabolic alkalosis?

Answer 10

normal or pathological situations in which H+ is decreased due to a cause other than a change in PCO2
eg, loss of HCL when vomiting, peripheral chemoreceptors detect and ventilation is reduced

Question 11

What chemoreceptors (central or peripheral) play the major role in altering ventilation in cases of metabolic acidosis or metabolic alkalosis?

Answer 11

Peripheral chemoreceptors

Question 12

What stimulates ventilation during exercise?

Answer 12

1. CO2? - very little change to arterial CO2
2. O2? - very little change to arterial O2
3. increased H+? - a little increase in strenuous exercise due to lactic acid release
4. reflex inout from mechanoreceptors in joints and muscles
5. increase in body temp
6. inputs to respiratory neurons via branches of axons descending from the brain to motor neurons suppling the muscles (central command)
7. increase in plasma epinephrine
8. increase in plasma K conc
9. conditioned (learned) response mediated by neural input to resp centres

4 and 6 are most likely!
abrupt increase and decrease at beginning and end of exercise - unlikely to be chemical or body temp!

Question 13

Protective reflexes

Answer 13

The reflexes protect the respiratory system from irritants
-Cough (sensory receptors in the larynx, trachea and bronchi)
when receptors initiating a cough are stimulated the medullary respiratory neurons cause deep inhalation and a violent expiration. This moves particles and secretions from smaller to larger airways and aspiration of materials into the lungs is also prevented.
-Sneeze (sensory receptors in the nose or pharynx)
-the immediate cessation of respiration when noxious agents are inhaled (chronic smoking may inhibit this reflex)

(alcohol inhibits the cough reflex, this may be way alcoholics are more susceptible to choking and pneumonia)

Question 14

Voluntary control of breathing

Answer 14

• descending pathways from cerebral cortex to the motor neurons of the respiratory muscles
• this voluntary control cannot be maintained duringintense involuntary stimuli eg elevated PCO2 or H+
• speaking, singing, swallowing

Question 15

J-receptor reflexes

Answer 15

• located in the lungs in capillary walls or in the interstitium
• normally dormant
• stimulated by an increase in interstitial pressure caused by the collection of fluid in the interstitium
• this increase occurs during the vascular congested caused by either occulsion of a pulmonary vessel (pulmonary embolism) or left ventricular heart failure
• also strenuous exercise in healthy people
• the reflex results in rapid breathing (tachypnea) and a dry cough
• the J receptors also give rise to sensations of pressure in the chest and dysnea (the feeling that breath is labored or difficult)

Question 16

What is hypoxia

1. Hypoxic hypoaxia/hypoxemia
2. Anemic hypoxia/carbon monoxide hypoxia
3. Ischemic hypoxia/hypoperfusion hypoxia
4. Histotoxic hypoxia

Answer 16

Hypoxia is a deficiency of oxygen at tissue level

1. Hypoxic hypoaxia/hypoxemia in which arterial PO2 is reduced - most common cause of hypoxia
2. Anemic hypoxia/carbon monoxide hypoxia in which arterial PO2 is normal but total oxygen content is low due to reduced Hb content, or due to competition with carbon monoxide
3. Ischemic hypoxia/hypoperfusion hypoxia in which blood flow to tissues is low
4. Histotoxic hypoxia in which the quantity of oxygen reaching the tissues is normal but the cell is unable to utilize the oxygen because a toxic agent cyanide for example has interfered with the cells machinery

Question 17

What can cause hypoxic hypoaxia

Answer 17

1. hyperventilation
   a, defect on resp control pathway
   b. severe thoracic cage abnormalities
   c. major obstruction of the upper airway
2. diffusion impairment - from thickening alveolar membranes or decrease in SA, this means blood O2 and alveolar O2 do not equilibrate (often only apparent during exercise) Co2 is either normal because it diffuses more readily than oxygen or reduced is ventilation is stimulated
3. A shunt
   a. anatomical abnormality of the cardio system that causes mixed venous blood to bypass ventilated alveoli in passing from R side of heart to L
   b. an intrapulmonary defect in which mixed vanous blood perfuses unventilated alveoli. hypooxemia stimulates hyperventilation reflex
4. Ventilation-perfusion inequalities
   this occurs in chronic obstructive lung disease and other lung diseases
   CO2 - normal or increased due to hyperventilation

Question 18

What is Emphysema?

Answer 18

Emphysema (chronic obstructive pulmonary disease)
-loss of elastic tissue and destruction of alveolar walls leading to an increase in compliance, and loss of pulmonary capillaries originally in the alveolar walls
-the merging of alveoli reduces the total surafce area avaible for diffusion, this impairs gas exchange
-also atrophy and collapse of upper airways (from terminal bronchioles down) can occur -lung elastic tissue is destroyed
-the lungs self-destruct due to proteolytic enzymes secreted by leukocytes in response to a variety of factors
-cigarette smoking stimulates release of proteolytic enzymes and destroys enzymes that normally protect the lung against them
-also ventilation-perfusion inequalities as the destructive changes are not uniform throughout the lungs
-large increase in airway resistance due to collapsed airways, this greatly increases the work of breathing and may cause hyperventilation (this is way it is classed as an obstructive disease)
=results in hypoxia

Question 19

High altitude

Answer 19

-decrease in atmospheric pressure as altitude increases

Question 20

What is mountain sickness?

Answer 20

Also known as altitude sickness this is when people ascend to altitudes of 10,000 ft too quickly
*breathlessness, headache, nausea, vomiting, insomnia, fatigue and impairment of mental processes

• PULMONARY EDEMA - this is leakage of fluid from pulmonary capillaries into alveolar walls and air spaces, this is due to the development of pulmonary hypertension (pulmonary arterioles reflexively constrict in the presence of low oxygen)
• BRAIN EDEMA -
• *supplemental oxygen and diuretic therapy are used to treat mountain sickness; diuretics help to reduce blood pressure by promoting loss in the urine
• Over several days the symptoms of mountain sickness usually dissappear - although maximal physical capacity remains reduced

Question 21

How does acclimatization to high altitude occur?

Answer 21

1. peripheral chemoreceptors stimulate ventilation due to low CO2
2. Erythroprotein (secreted by kidney) stimulates erythocyte synthesis - this results in increased erthocyte and hemoglobin conc in blood - and an increase in oxygen-carrying capacity of the blood
3. DPG increases and shifts O2-Hb dissociation curve to the right so that oxygen unloading occurs (however at very high altitudes this is maladaptive as it also impairs oxgyen loading in the lungs)
4. Increases in skeletal muscle capillary density (due to hypoxia-induced expression of genes that code for angiogenic factors), number of mitochondria, and muscle myoglobin occur, all of which increase oxygen transfer
5. Plasma volume can be decreased, this results in an increased conc of erythrocytes and hemoglobin in the blood

Question 22

What non-respiratory functions does the lung carry out?

Answer 22

• The lungs can partially or fully remove some substances (neurotransmitters and paracrine agents for example) from the blood and thereby prevent them from reaching the other locations in the body via the arteries. This is done by the endothelial cells that line the pulmonary capillaries.
• The lungs can also produce new substances, some play local roles within the lungs but if enough if secreted they may diffuse into the pulmonary capillaries and be carried to the rest of the body. eg, inflammation in the lung may release histamine that could alter systemic flow or angiotensin II
• The lungs also act as a sieve that traps small blood clots preventing them from reaching the systemic arterial blood where they could occlude other blood vessels in the body

Question 23

What are the functions of the respiratory system?

Answer 23

1. provides oxygen
2. eliminates carbon dioxide
3. regulates H+ conc with kidneys
4. Phonation - speech
5. defends against microbes
6. influences arterial conc of chemical messages, by removal or production
7. traps blood clots arising from systemic veins