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Physiology > Lecture 22: Regulation of Respiration > Flashcards

Lecture 22: Regulation of Respiration Flashcards

1
Q

What is the importance of respiration?

A

Maintaining O2 levels

Eliminating CO2 waste

pH regulation (by extension of CO2)

Managing respiratory work and expenditure

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2
Q

How does respiration regulate pH?

A

CO2 + H2O H2CO3 HCO3- + H+

CO2 build up (hypercapnia) = respiratory acidosis

Excessive clearance of CO2 = respiratory aklalosis

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3
Q

Respiratory control organisation

A

See figure

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4
Q

What are the respiratory control centres?

A

Neurons in the brain stem

Medullary rhythmic centre

Pons respiratory centres

See figure

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5
Q

Functions of the neurons in the brain stem as respiratory control centres

A

Generate rhythm of breathing (exhalation and inspiration cycles)

Stimulate respiratory muscles

Integrate feedback signals

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6
Q

What are the components of the medullary rhythmic centre?

A

Pre-Botzinger complex

Dorsal respiratory group

Ventral respiratory group

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7
Q

What are the components of the pons respiratory centres?

A

Apneustic area

Pneumotaxic area

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8
Q

Pre-Botzinger complex (PBC) - what? Function?

A

Basal pacemaker and initiation

Generates some neural activity (even in the absence of all external signals, under significant pharmacological blockage and in severe brain damage)

Not a stable, rhythmic output (needs outside help)

Does not directly stimulate inspiration, but ensures activation of the dorsal respiratory group

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9
Q

Dorsal Respiratory Group (DRG) - Function

A

Exerts primary control over basal breathing (at rest)

Principal Inspiratory centre

Critical integrator/effector of respiratory control

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10
Q

What are oscillations and/or maintenance in DRG activity due to?

A

Multiple sensory inputs

Pre-Botzinger complex

Apneustic centre

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11
Q

Graph of DRG activity

A

DRG activity ramps up over 2 seconds to cause inspiration (slow and gradual crescendo)

Somewhat self-inhibitory

Halting of activity over 3 seconds causes passive expiration

See figure

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12
Q

DRG downstream innervation

A

Phrenic nerve -> diaphragm (contraction)

External intercostal nerves/muscles -> ribcage expansion (open chest)

See figure

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13
Q

Phrenic nerve and regulation of breathing

A

Bursts of phrenic nerve activity contract principal inspiratory muscles

More rapid firing, bigger and deeper breaths (active ventilation)

More frequent bursts, faster breathing rate

See figure

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14
Q

What type of breathing is driven by the ventral respiratory group (VRG)?

A

Inactive during normal, quiet breathing

Principally drives active expiration during exercise, dyspnea, some lung diseases (failure of passive expiration - COPD, asthma, emphysema)

Also provides supplementary inspiratory control (pectorals, scalene)

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15
Q

What efferent activity does the VRG control?

A

Internal intercostal nerves/muscles -> ribcage compression

Abdominal muscles -> push diaphragm up

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16
Q

How is the VRG engaged?

A

Activated by spillover from the DRG

The VRG is only activated AFTER the DRG (the two cannot be activated at once) = the expiration is delayed and out of phase

Bursts of internal intercostal nerve activity contract the expiratory muscles

See figure

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17
Q

When is activation of the VRG required?

A

Under periods of high respiration

When there is failed passive expiration

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18
Q

Function of the Apenustic centre (APC)

A

Activates DRG

APC actively prolongs inspiration: prevents DRG from switching off, maintained phrenic nerve activity, longer/deeper breaths, shortened expiration

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19
Q

Function of the pneumotaxic centre (PRG)

A

Inhibits APC

Turns off inspiration, allows expiration

Routinely activated by DRG: delayed and out pf phase, key part of flip-flop circuit

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20
Q

Characteristics of apneustic breathing

A

Gasping

Prolonged inspiration, shallow expiration

See figure

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21
Q

How can apneustic breathing come about?

A

Brainstem injury (severe stroke or trauma)

Loss of input from mechanoreceptors

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22
Q

Simple respiratory centre feedback

A

See figure

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23
Q

What is responsible for central chemoreception in regulation of breathing?

A

Neurons of retrotapezoid nucleus (RTN)

Seem to interface with pre-Botzinger complex

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24
Q

How do the central chemoreceptors modulate respiration?

A

Minute-by-minute ventilatory control (not fast, but slow, gradual changes)

Most sensitive to PaCO2

Somewhat sensitive to pHa (indirectly)

Insensitive to PaO2 (oxygen is not a primary regulator)

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25
Q

How does the central chemoreceptor sense changes in respiratory system?

A

Through pH of CSF (does not directly measure CO2)

CO2 diffuses across the BBB, into the cerebrospinal fluid.

H+, H2CO3 and HCO3- cannot cross the BBB

In the CSF, CO2 is converted into HCO3- and H+.

Change in pH is sensed by the RTN

See figure

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26
Q

What is the normal pH of the CSF?

A

7.32

Weakly buffered = High change in pH for small changes in CO2

Sensitive and linear

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27
Q

RTN chemoreceptor CO2 response graph

A
  1. Room CO2 (0.4 %)
  2. CO2 goes up to 10% (takes 5 minutes for RTN to kick in)
  3. CO2 decreased back to room air = allow decrease in firing

See figure

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28
Q

How can the RTN system get confused?

A

When there are long term changes of CO2 in the system, there can be an adaptation of CSF bicarbonate

Choroid plexus releases more HCO3- into the CSF to account for the high CO2, which is causing high H+. pH changes are no longer detectable.

Patients begin to tolerate the hypercapnia and start hypoventilating

H+ builds up in the blood and there is respiratory acidosis

See figure

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29
Q

What are the peripheral chemoreceptors? Role?

A

Carotid body

Aortic body

Sense arterial blood at high flow sites

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30
Q

How does the carotid body sense and transmit signals?

A

Sensor: type I glomus cell

Glossopharyngeal nerve (IX) transmits

Afferent interface to DRG

See figure

31
Q

What does the carotid body respond to

A

Principally: Low PaO2

NOT THE O2 CONTENT

Also responds to: PaCO2, pHa (CO2 independent)

Non adapting (should always be able to respond to O2)

32
Q

Carotid body response mechanism

A

Carotid body has low basal firing rate

When PaO2 goes below 60 mmHg = dramatic increase

Typical of emergency mechanism (oxygen falls, but there is no problem. Suddenly, threshold is reached and there is a massive stimulus from cells)

NOTE: integrated respiratory response is still heavily dependent on PaCO2

See figures

33
Q

Importance of aortic body in central chemoreception? Where is it important?

A

Less important than carotid body

Aortic body response is weak, but it can adapt/increase if the carotid body is damaged

Principal role is baroreception for blood pressure

34
Q

How does the aortic body sense and transmit signals?

A

Sensor: Type I gloms cells

Interfaces and activates DRG

Afferent through vagus nerve (X)

35
Q

Comparison of chemoreceptors - role in normal and emergency breathing, transmission, interface site, primary and secondary stimuli, no stimuli, response speed, response type, adaptation

A

See figure

36
Q

What do pulmonary receptors and nerves help regulate?

A

Inspiration

Expiration

Emergency or protective responses

37
Q

What do the pulmonary receptors and nerves operate through? What stimulates them? Outcomes?

A

Vagus nerve

Stimuli: Mechanical, chemical

Outcomes: inhibitory, excitatory

38
Q

Lung mechanoreceptors - respond to? Types?

A

Respond to stretch

Slowly adapting receptors (SARs): continual firing during normal, slow inspiration

Rapidly adapting receptors (RARs): fire during rapid inspiration

See figure

39
Q

What are the hiring-breuer reflexes?

A

Classic respiratory control discovered in 1868

Inflation reflexes and deflation reflexes

40
Q

Hering Breuer reflexes - inflation

A

Mechanoreceptors terminate at APC and DRG

Inhibitory neurons

Act to suppress inspiratory activity (stop stretching of lungs)

SARs help turn gentle inspiration to expiration

RARs prevent lung overinflation

See figure

41
Q

Hering Breuer Reflexes - deflation

A

Small group of mechanoreceptors

Excitatory neurons

Terminate at DRG

Compression acts to restart inflation at low lung volumes

See figure

42
Q

Where are irritant and cough receptors located? Nerve?

A

Airway epithelium

Afferent through vagus nerve

43
Q

Where are cough receptors located? What do they respond to?

A

Nerves in trachea and high bronchi

Respond to mechanical and chemical stimuli

44
Q

Where are irritant receptors located? What do they respond to?

A

Nerves in bronchioles

Respond to chemical stimuli only

45
Q

What does stimulation of irritant and cough receptors cause?

A

Stimulation causes spasm of multiple effector muscles

No clearly defined cough centre

46
Q

Comparison of mechano- and irritant- receptors- location, transmission, nerve ty[e, interface site, stimuli, reflex action

A

See figure

47
Q

What are the components of cortical control of breathing?

A

Conscious control of muscles: singing and talking, holding breath

Subconscious control of respiratory centres: emotion, pain, fear, temperature

48
Q

When can hypercapnia be tolerated?

A

If respiratory effort is high, possible situations:

High gas pressure/density

Heavy weight on chest

49
Q

What wins in a fight: autonomic or cortical control?

A

Autonomic

50
Q

Spinal cord damage and effects on breathing

A

See figure

51
Q

What happens if C1-C4 phrenic and intercostal nerves are severed?

A

Full ventilator dependency

52
Q

What happens if C4-C6 are damaged, but phrenic nerve is intact

A

Weak but functional breathing driven by diaphragm

53
Q

What happens is T6-T12 afferent nerves are severed?

A

Loss of cough reflex (efferent)

Mechano- and chemo- reception intact (vagus and glossopharyngeal nerves are outside spine)

54
Q

What happens during altitude sickness?

A

Low inspired pO2 = hypoxemia at carotid bodies

Acute hyperventilation may help to improve PaO2

Excessive CO2 loss = respiratory alkalosis and suppression of central chemoreceptors

Symptoms arise from hypoxemia and/or alkalosis: nausea, lightheadedness, headaches, fatigue and confusion, insomnia

55
Q

Altitude feedback loop

A

See figure

56
Q

Adaptation to altitude

A

Chronic adaptation (1-2 days) comes from kidneys

Therapeutic options

Increased O2 carrying capacity of blood

57
Q

How does chronic adaptation to altitude occur?

A

Comes from kidneys

Normally: HCO3- retention, H+ consumed/excreted, CO2 expired

Hypoxia: HCO3- secreted, H+ retention, pHa falls

58
Q

What is the therapeutic option for adaptation to altitude?

A

Acetazolamide

Carbonic anhydrase inhibitor = forces HCO3- secretion, pHa falls

May assist CO2 retention in the brain

59
Q

How does increased O2 carrying capacity of the blood occur during adaptation to altitude?

A

EPO secretion downstream of hypoxia inducible factors

PaO2 stays low, so hypoxemia-driven respiration remains high

Combined benefits are essentially altitude training

60
Q

Adapted altitude feedback loop

A

See figure

61
Q

What happens if there is failed adaptation to altitude?

A

High altitude pulmonary deem (HAPE)

High altitude cerebral deem (HACE)

62
Q

Characteristics of HAPE?

A

Chronic hypoxic vasoconstriction in lungs (V/Q matching)

Fluid build up in alveoli

Treatment as for pulmonary hypertension (nifedipine)

63
Q

Characteristics of HACE?

A

Chronic hypoxic vasodilation in brain (improve O2 delivery)

Cerebral endothelium becomes leaky

VEGF; NO and other molecules implicated

Dexamethasone treatment, steroidal, anti-inflammatory, vasoconstrictive

64
Q

What ventilation occurs during metabolic acidosis? Causes?

A

Hyperventilation

Longstanding diarrhea (HCO3- loss)

Diabetic type 1 - ketoacidosis

Some kidney dysfunctoins

65
Q

What ventilation occurs during metabolic alkalosis? Causes?

A

Hypoventilation

Excessive vomiting (H+ loss)

Chronic diuretic use (HCO3- retention)

Some kidney dysfunctions

66
Q

What occurs in the respiratory system of people with chronic lung disease (Emphysema, chronic bronchitis)

A

Persistent mild hypercapnia and hypoventilation

Central chemoreceptor adaptation

Supplemental O2 often necessary: suppresses emergency breathing, additional risk factors, sudden respiratory failure

67
Q

What happens during exercise?

A

Increased O2 consumption, increased CO2 production

Anticipatory breathing precedes exercise (learned/trained feed-forward response, subconscious and conscious)

Mechanoreceptors in exercising muscles (type III/IV afferent fibers, interface in medulla, possible DRG)

Circulating catecholamines (dopamine, adrenaline, noradrenaline)

Activation/spillover from aortic body baroreceptors (hypoxia-like response under normal O2 conditions)

Limit to exercise is mostly cardiac output

68
Q

What do opiates do to respiration?

A

Suppress multiple aspects of rhythm generation (especially DRG)

Suppress cortical control

Reversed by opioid antagonist: naloxone

See figure

69
Q

What are typical findings in sudden infant death syndrome

A

SIDS

Infant 1-12 months

Asleep on stomach

Soft bed and tight blankets or in bed with parents

No sign of struggle

70
Q

Triple risk model of SIDS

A

Critical period (1-12 months, rapid changes in homeostatic control)

Vulnerable infant (abnormalities in brain stem)

Outside stressors (smoke, infection, overheating, mechanical factors)

71
Q

What is the key pathology in SIDS?

A

Poor ventilation

CO2 rebreathing

Poor response to PaCO2

Emergency responses fail

72
Q

What are other stressors and vulnerabilities in SIDS?

A

Serotonin deficiency in SIDS group

RTN defects in 71% of cases (faulty interface between central chemoreceptors and PBC)

Peripheral chemoreceptors under-developed and possibly abnormal

73
Q

SIDS feedback loop

A

See figure

74
Q

What occurs in CO poisoning

A

CO prevents hemoglobin from releasing O2

Reduces oxygen carrying capacity, but not PaO2

O2 delivery to tissue drops without triggering carotid body

No change in PaCO2 or pHa

Slowly suffocate without a gasp/rescue response

Treatment: 100% O2 or hyperbaric O2 therapy

Physiology (19 decks)

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