Week 2- Control of breathing Flashcards
1
Q
Describe neural mechanisms that control breathing:
What areas of the brain are involved?
What is this group collectively known as?
What does each of these areas contain?
A
- Control of breathing relies on a number of brain centres collectively known as the respiratory centre in the Pons and Medulla.
- The pons modulates respiratory output, the medulla generates the central pattern of breathing, sends signals via cranial and spinal nerves to motor neurons that innervate respiratory muscles.
- In the pons/ pontine respiratory group there are two centres that can modulate respiratory output 1) the apneustic centre which stimulates inspiration (stimulates DRG, depth of breathing) and 2) the pneumotaxic centre which inhibits prolonged inspiration (promotes coordinated respirations, inhibits DRG) and can increase/control overall respiratory rate.
- In the medulla there are two respiratory groups:
- The Dorsal Respiratory group (DRG)- primarily sensory- coordinates input from peripheral chemoreceptors/pulmonary stretch receptors. Contains inspiratory neurones that synapse with motor neurones to respiratoy muscles. Generates normal pattern and active in quiet breathing.
- The Ventral Respiratory group (VRG)- primarily Motor- contains both inspiratory and expiratory neurones. Has regions that drive expiration and synapse with motor neurones that innervate accesory muscles of expiration (forced expiration). Has regions that drive inspiration- signals to muscles of pharynx and larynx. Active during forced inspiration/expiration.
2
Q
Describe how normal breathing occurs during quiet respiration
What promotes inspiration?
What promotes expiration?
A
- During quiet respiration, the DRG in the medulla sends stimulatory signals via the phrenic nerve to the diaphragm and via intercostal nerves to the external intercostal muscles.
- Diaphragm contracts and flattens, external intercostals elevate ribs and sternum- increase in volume of thoracic cavity
- Via Boyle’s law (pressure of gas inversely proportional to volume): Decreased pressure of air in lungs, atmospheric pressure higher, air into lungs.
- DRG stimulation ceases, Diaphragm and external intercostals relax.
- Expiration is passive- due to elastic recoil of the lungs.
3
Q
What sensory afferents do the respiratory centres receive?
Describe each one.
A
- The respiratory centres in the brainstem and medulla receive sensory afferents from:
- Peripheral chemoreceptors in the carotid and aortic bodies that primarily detect changes in pO2. They also respond to pCO2 and pH which enhances sensitivity to hypoxia.
- Central chemoreceptors on the brain side of the BBB. Primarily detect pCO2 by changes in the pH of cerebrospinal fluid.
- Pulmonary stretch receptors in the lung- terminate inspiration, prevent overinflation.
- Higher brain centres- modulate breathing pattern to allow for speaking/swallowing/vomiting etc.
4
Q
Describe the feedback loop that controls breathing
A
- Sensory afferents primarily from peripheral and central chemoreceptors that detect changes in arterial blood gases and pH (pO2, pCO2, pH).
- Some sensory afferent from pulmonary stretch receptors but only in the event of overinflation (does not contribute to normal respiratory control).
- Afferent signals sent via glosspharyngeal (CNIX) and Vagus (CNX) to the respiratory centres in the medulla to modulate efferent output.
- Modulatation of efferent output from the medulla to the respiratory muscles and modulation of rate and depth of breathing.
- Correct arterial blood gas back to the norm.
5
Q
What is the name of the reflex that prevents overinflation of the lungs?
A
Hering-Breuer reflex
6
Q
Describe the Hering-Breuer reflex
How important is it for normal control of breathing?
A
- Hering- Breuer reflex is initiated by pulmonary stretch receptors in the lung that signal back to the DRG of the medulla via vagal afferents which in turn modulates output to the respiratory muscles.
- Pulmonary stretch receptors are mechanosensors within the tracheobronchial tree that detect stretch and therefore volume of the lungs.
- Signal to the DRG of medulla via vagal afferent.
- Inhibits output of the phrenic motor neurones
- Protects lungs from overinflation.
- Reflex may be important in eupnea (normal breathing pattern) in infants
- Only activated above normal tidal volume in adults.
7
Q
What is low pCO2 in arterial blood called?
What is high pCO2 in arterial blood called?
What is low pO2 in arterial blood called?
A
- Hypocapnia - low pCO2
- Hypercapnia- high pCO2
- Hypoxia- Low pO2
8
Q
Why is the response to high pCO2 stronger than the response to low pO2?
A
- The need to protect acid base balance means the response to high CO2 is more powerful thatn the response to low pO2.
9
Q
Describe the physiological effects of hyperventilation and hypoventilation
A
Hyperventilation:
- In the event of increased inspiration, and when O2 usage and CO2 production remain the same in the tissues:
- pO2 in the alveoli will rise - increased delivery
- pCO2 in alveoli will decrease - increased removal
Hypoventilation:
- In the event of decreased inspiration, and when O2 usage and CO2 production remain the same in the tissues:
- pO2 will fall - decreased delivery
- pCO2 will rise- less excretion from lungs
10
Q
Describe the location and function of peripheral chemoreceptors
What do they primarily respond to?
What other stimuli can they respond to?
Which is the more important set of chemoreceptor?
What do they signal via?
What do they signal to?
What is the response when these chemoreceptors are activated?
Is the response rapid or slow?
A
- Peripheral chemoreceptors are located in the aortic and carotid bodies. The aortic bodies are located under the arch of the aorta. The carotid bodies are located at the bifurcation of the common carotid.
- They respond primarily to changes in pO2 in arterial blood but can respond to high pCO2 and low pH which increase their sensitivity to hypoxia.
- They are small structures, formed of glomus cells which detect the arterial blood gas concentrations and receive a very high blood flow.
- The concentration of arterial blood gas at the carotid body is virtually the same as the systemic arteries.
- Most important in detecting change are the carotid bodies which signal via the glossopharyngeal nerve (CNIX) to the DRG of the medulla. Role of aortic bodies less clear and signals via Vagus nerve (CNX).
- Afferent signals from peripheral chemoreceptors synapse with neurons in the DRG to increase respiratory rate and depth of respiration to restore pO2 back to the normal.
- Rapid response within 1-3 seconds of hypoxia being detected.
11
Q
What is the response to hypoxia?
What is the issue if hypoxia is not accompanied by hypercapnia?
When could this situtation arise?
A
- detected by peripheral chemoreceptor in carotid body
- Signal sent via glossopharyngeal nerve to DRG in medulla
- Modulation of output via DRG to increase respiratory rate and depth to restore pO2.
- If hypoxia is not accompanied by hypercapnia the increase in respiratory rate induced by the carotid bodies will also lead to hypocapnia.
- Hypocapnia will upset acid-base balance.
- This situation can arise at high altitude and during ventilation perfusion mismatch.
12
Q
When does ventilation increase markedly during hypoxia?
A
- Ventilation rate will increase markedly once alevolar partial pressure of oxygen falls below 8kPa.
13
Q
What is the main/most important serum buffering system?
What equation does this relate to?
What is key about the ratio in this equation?
A
- Serum buffering relies mainly on the bicarbonate buffering system which relies on the concentration of [HCO3-] in the blood.
- Under normal circumstances bicarbonate is maintained at a high level which enables it to buffer moderate increases in pCO2.
- CO2 is a weak acid and reaches an equilibrium with its conjugate base - HCO3-.
- This relates to the Henderson- Hasselbach equation which states:
- pH= pK + log(10) [HCO3-]/ pCO2 x solubility factor (0.23).
- The key ratio in this equation is the 20:1 ratio of HCO3- to CO2.
14
Q
What is the normal range for pH?
What is an acidosis? what is an alkalosis?
What types of acidosis/ alkalosis are there?
What causes them?
A
- Normal pH range lies between 7.35- 7.45.
- Acidosis is blood pH under 7.35:
- Metabolic acidosis refers to low serum pH caused by low serum [HCO3-]
- Respiratory acidosis refers to low serum pH caused by high pCO2 (hypercapnia)
- Alkalosis is blood pH over 7.45:
- Metabolic alkalosis refers to high serum pH caused by high [HCO3-]
- Respiratory alkalosis refers to high serum pH caused by low pCO2 (hypocapnia)
15
Q
Describe the location and response of central chemoreceptors
1) where are they located
2) what do they primarily detect?
3) what is the response?
A
- Central chemoreceptors are located on the ventral side of the medulla on the brain side of the blood brain barrier, close to the DRG.
- Central chemoreceptors primarily detect changes in pCO2- hypercapnia- indirectly via changes in the pH of cerebrospinal fluid (CSF).
- Central chemoreceptors are major source of feedback for tonic drive of breathing.
- CSF is secreted by cells of the choroid plexus. The pH of CSF is determined by the secretion of HCO3 by choroid plexus cells and by [H+] from the diffusion of CO2 from arterial blood across the BBB into CSF.
- H+ and HCO3- are unable to cross the BBB but CO2 is freely diffusible, thus CSF pH determined by pCO2 in arterial blood.
- When CO2 is high, the pH of CSF becomes more acidic/ decreases which causes signalling from the central chemoreceptors to the DRG to increase ventilation rate to excrete more CO2.
- A rise in CSF pH (hypocapnia) induces reduction in ventilation rate to increase alveolar pCO2.
17
Q
Describe briefly/generally principles of pH control in the blood serum
i.e- acid production/ serum buffering/ excretion of acid/ synthesis of base
A
- pH normally controlled by serum bicarbonate buffer
- Acids produced by metabolism are buffered with HCO3- which is present in large amounts in the blood
- HCO3- used in this reaction regenerated by the kidneys which reabsorb all bicarbonate and synthesises it.
- CO2 produced by metabolising tissues is excreted as volatile acid via the lungs.
- Buffering is limited by reaction reaching equilibrium in the tissues.
18
Q
Describe how metabolic acidosis may occur and how it may be compensated.
Why doesn’t overcompensation occur?
A
- Metabolic acidosis (pH less than7.35) can occur with excess ingestion of acid/ production of acid (diabetic ketoacidosis)/insufficient reabsorption/synthesis of HCO3 via kidneys
- Detected by central chemoreceptors and to lesser extent peripheral chemoreceptors
- Induce increase in ventilation rate via DRG in medulla- HYPERVENTILATION
- Increased excretion of CO2, reduced partial pressure of CO2 in alveolus (PACO2) and arterial blood gas (PaCO2)- RESPIRATORY ALKALOSIS
- reduced CO2 in arterial blood, 20:1 of HCO3: CO2 ratio restored- pH restored to normal value
- However both HCO3 and pCO2 are lower than normal physiological values.
- Overcompensation does not occur as pH induced hyperventilation ceases when pH reaches normal value.
19
Q
Describe how metabolic alkalosis may occur and how it may be compensated?
A
- Metabolic alkalosis (pH above 7.45) can occur with excess loss of acid (eg prolonged vomiting).
- pH raises with loss of acid and shift in the equilbrium to the left.
- Detected by central chemoreceptor and peripheral chemoreceptors- signal to DRG, reduce ventilation rate
- Reduced minute volume, raises pCO2 in alveolus (PACO2) and in arterial blood (PaCO2)- RESPIRATORY ACIDOSIS
- Raised pCO2 in arterial blood helps restore 20:1 ratio of HCO3 to CO2.
- pH restored to normal physiological range- however both HCO3 and pCO2 are not within normal physiological concentrations- both are raised.
