Control of Ventilation Flashcards

1
Q

Definition of apneusis

A

Prolonged inspiration, holding breath

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2
Q

Definition of apnoea

A

No breathing, no change in phasic respiration

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3
Q

Definition of eupnoae

A

Normal pattern of breathing

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4
Q

Definition of pulmonary congestions

A

Occurs in heart failure, decreased CO => back up of fluid in venous circulation
P here increases => fluid goes into alveoli

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5
Q

Describe the 2 methods of neural control in the pons and their functions

  • pneumotaxic center
  • apneustic center
A

Pneumotaxic center

  • inhibit inspiration
  • without it => apneusis

Apneustic center

  • prolongs inspiration
  • without it => gasping
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6
Q

Describe the 2 methods of neural control in the medulla and their functions
-what nuclei make up each group?

  • dorsal resp group
  • afferents and efferents
  • ventral resp group
  • efferents
A

Dorsal resp group
-NST => phrenic, intercostals

  • inspiratory neurones only, fire before, during respiration => controls depth, rate, basal rhythm
  • inhibits expiratory neurones in ventral/pons group

Ventral resp group
-NA, NRA, BC, PBC (key to resp rhythmogenesis) => phrenic, intercostals

  • inspiratory and expiratory neurones
  • active only in forced inspiration and expiration
  • expiratory neurones inhibit inspiratory neurones
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7
Q

Name the 7 afferents that affect ventilation rate

A
  • stretch receptors
  • juxtapulmonary receptors
  • irritant receptors
  • proprioceptive afferents
  • pain receptors
  • V
  • arterial baroceptors
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8
Q

Describe the site, function, reflexes of the stretch receptors (medulla)

A

Bronchial SM

Makes inspiration shorter

Hering Breuer, inflation, inhibits inspiration
Deflation reflex, argument inspiration

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9
Q

Describe the site, function of the juxtapulmonary receptors (medulla)
What stimulates these receptors

A

Alveolar/bronchial walls near capillaries

Apnoea/rapid shallow breaths => decreased HR, BP
Laryngeal constriction
Skeletal muscle relaxation

React to dyspnoea
Increased alveolar wall fluid
Oedema
Pulmonary congestion
Microembolisms
Inflammatory mediators
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10
Q

Describe the site, function of the irritant receptors (medulla)
What stimulates these receptors

A

Airway

Trachea => cough
Lower airway => hyperapnoea

Irritant gases, smoke, dust
Inflammation
Lung collapse under weight

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11
Q

Describe the site, function of the proprioceptive afferents to the medulla
Why are they important?

A

Resp muscles

Shortenings load of non resp muscles => increase BR

Increased load => increased tension => increased BR => increased TV

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12
Q

How do pain receptors affect the breathing rate

A

Result in brief apnoea => increased breathing

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13
Q

How does the trigeminal region affect breathing rate

A

Results in apnoea/spasm => decrease in HR, sneeze

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14
Q

How does the arterial baroreceptor affect the breathing rate

A

Stimulation decreases ventilation

Increased BP => decreased BR

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15
Q

What is the main principle of chemical control

How is CO2 prod, O2 consumption, H+ prod estimated

A

Ventilation must match metabolism

CO2 production estimated from PaCO2
O2 consumption estimated from PaO2
H+ production estimated from pH

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16
Q

Describe how the rate of ventilation changes with PaCO2

A

In the normal physiological range, as PaCO2 increases, ventilation rate increases

If PaCO2 exceeds normal physiological range => CO2 narcosis

If PaCO2 is below normal physiological range, there is always a basal level of ventilation

17
Q

Describe how the rate of ventilation changes with changing pH and PaCO2

A

In the normal physiological range, as PaCO2 increases, ventilation rate increases

pH too low => hypoventilation/metabolic acidosis
PACO2 increases => vent increases

pH too high => hyperventilation/metabolic alkalosis
PACO2 increases => vent increases

18
Q

Describe how the rate of ventilation changes with changing PaO2

  • what happens if PaO2 is too low (<8kPa)
  • what happens if PaO2 is too high

What is the relationship between hypoxia and hypercapnia

A

As PaO2 falls below 8kPa, rate of ventilation rapidly increases.
If too low => respiratory depression

If too high => respiratory depression

Synergistic relationship between hypoxia and hypercapnia => increase ventilation

19
Q

Describe the central chemoreceptor

  • location
  • structure
  • how does it function
  • what is it affected by
A

Location
-IX, X exit in medulla

Structure

  • HCO, H crosses CSF brain barrier
  • CO2, O2 crosses BBB
  • chemoreceptor surrounded by glial cell

Functions

  • HCO buffer
  • PCO2 => [H+] increases due to buffer, pH change detected by chemoreceptor

Properties

  • only affected by PCO2
  • 20s to respond
20
Q

How do central chemoreceptors respond to altitude

A

Initially driven by hypoxic drive => alkali CSF

Vent drive decreases => restore pH => hypoxic drive continues

Cycles between the 2

21
Q

How do central chemoreceptors respond to prolonged hypercapnia

  • why is this bad
  • what should we do to help
A

Hypercapnia => low pH => increase vent

Over time, chemoreceptor threshold decreases so vent drive falls

But still hypercapnia, hypoxic, must provide low flow O2 to continue the hypoxic drive

22
Q

Describe the peripheral chemoreceptors

  • location
  • structure
  • function
  • properties
A

Location

  • IX, carotid body => pons
  • X, aortic bodies => pons

Structure

  • T1 glomus cell surrounded by T2 sheath cell
  • nerve fibres go to pons

Function

  • Detect large changes in PO2
  • increase vent rate in hypoxia

Properties

  • only affected by PO2
  • instant response
23
Q

Describe the 2 types of sleep apnea
-how do they arise

  • obstructive
  • central
A

Obstructive
-thoracic movement present but airway closed => decreasing SaO2 => disturbed sleep

Central
-no thoracic movement due to neuromuscular/brainstem problems
=> won’t breathe

24
Q

What is Cheyne Stokes breathing

  • what changes
  • what can cause this
A

Rapid cycling of SaO2

  • Opioids
  • HF
  • Stroke