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MD3001 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

The diaphragm:

  • Change from periphery to central area?
  • Motor and sensory supply?
  • During inspiration what happens?
A
  • Is muscular at its periphery and tendinous centrally
  • Motor and sensory supply from the phrenic nerve (C2,4,5)
  • During inspiration the domes descend, causing negative intrathoracic pressure but raising intra-abdominal pressure
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2
Q

Attachments of the diaphragm?

A

Anterior: To xiphoid process opposite T8/9

Deep surface of ribs and costal cartilages 7-12

(The costodiaphragmatic recess is the narrow, potential space between the periphery of the diaphragm and the ribs)

Posteriorly 5 ligaments (2 crura, 3 arcuate):

  • Muscular crura (Left crus from bodies of L1 and 2, right crus from bodies of L1,2 and 3)
  • Median arcuate ligment at T12, between the crurua
  • Medial arcuate ligament between body and transverse process tip of L1
  • Lateral arcuate ligament between tip of L1 transverse process to 12th rib.
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3
Q

Structures passing through the diaphragm

A

T8: IVC, Right phrenic nerve
T10: Oesophagus, R+L vagus nerves, left gastric vessels
T12: Aorta, thoracic duct, azygos veins

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4
Q

How do the following structures pass through the diaphragm:

  • Splanchnic nerves?
  • Sympathetic trunk?
  • Subcostal vessels and nerves?
A
  • Splanchnic nerves: Through the crura
  • Sympathetic trunk: Behind medial arcuate ligament
  • Subcostal vessels and nerve: Behind lateral arcuate ligament
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5
Q

Where does the phrenic nerve receive sensory innervation from?

A

Central tendon, parietal pleura and pericardium

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6
Q

Arteries alongside the phrenic nerve?

A

Superior and inferior phrenic

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7
Q

What mechanisms are involved in inspiration and exhalation?

A

Inspiration:

  • Increases diameters of the thorax to create a negative pressure (which sucks are into the lungs)
  • Diaphragmatic contraction causes the descent of its dome to increase vertical diameter
  • Rib elevation pushes the sternum up and forward, and the ribs outward, to increase anterioposterior and lateral diameters

Exhalation (i.e. normal, quiet expiration):

  • Muscle relaxation
  • Elastic recoil (in lungs and bronchi elastic tissue)
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8
Q

How does contraction of diaphragm assist in quiet inspiration?

A
  1. Contraction of the diaphragm
    - Contraction flattens the domes of the diaphragm
    - Increases the vertical thoracic diameter
    - Increases the volume of the thorax
    - Decreases intrathoracic pressure
    - Air is drawn into the lungs
    - Most important inspiratory activity in adult
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9
Q

How does contract of intercostal muscles assist in quiet inspiration?

A
  1. Contraction of intercostal muscles
    - As the shaft of the rib passes obliquely downwards, contraction of the intercostal muscles to raise the shaft of the rib towards the one above also lifts the sternum and pushes it anteriorly
    - Increases the anteroposterior diameter and the thoracic volume
    - Decreases intrathoracic pressure
    - Air is drawn into the lungs

ALSO

  • Raises the ribs 5-10 towards the one above and lifts the CC and pushes the rib laterally
  • Lateral splay by ribs with oblique CC only
  • Increases the lateral diameter and the thoracic volume
  • Decreases intrathoracic pressure
  • Air is drawn into the lungs
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10
Q

Describe the “bucket-handle” mechanism that occurs in forced inspiration?

A
  • Occurs in ribs 8-10 that have flat costo-transverse joints that permit gliding
  • Once the central tendon of the diaphragm is “anchored” by its attachment to the pericardium, further muscle contraction pulls on the ribs and causes them to evert
  • Gives a small, additional increase in the lateral thoracic diameter and therefore the volume
  • Even more air is drawn into the lungs by this additional decrease in intrathoracic pressure
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11
Q

Role of accessory muscles of respiration in forced inspiration and expiration?

A

Add more power of contraction but CANNOT further increase the thoracic diameters

Muscles involved:

  • Pectoralis major and minor (inspiration)
  • Latissimus dorsi (possibly helps compress ribs in forced expiration, but more superior parts may help raise ribs in forced inspiration)
  • Abdominal wall muscles (raise intra-abdominal pressure to push diaphragm up in forced expiration)
  • Neck and back muscles (trapezius, sternocleidomastoid, scalene muscles) help to fix the ribs
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12
Q

What is the involvement of intercostal muscles in inspiration and expiration?

A

External intercostal is more active during inspiration

Internal intercostal is more active during expiration

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13
Q

What is mesothelium?

A

Simple squamous epithelium that secretes a miniscule amount of serous fluid to lubricate the surfaces of viscera

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14
Q

Parietal pleura is attached firmly to ??

A
  1. Thorax wall (costal pleura)
  2. The fascia at the thoracic inlet (cervical pleura)
  3. Fibrous pericardium (mediastinal pleura)
  4. Diaphragm (diaphragmatic pleura)
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15
Q 
Pleural cavities surface markings of reflections:
Rib, 2cms above clavicle?
2nd CC ?
4th LCC?
6th CC:
8th rib?
10th rib?
12th rib?
Midline?
A 
Rise to level of neck of 1st rib, 2cms above clavicle
2nd CC -Lie adjacent in the mid line
4th LCC- notch for heart
6th CC- Deviates laterally
8th rib-  Lies in midclavicular line
10th rib- lies in mid axillary line
12th rib- Lies in the mid scapular line
Midline - Level with T12 (just below 12th rib)
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16
Q

What are the two pleural recesses?

A

Costodiaphragmatic recess: Potential space inferiorly around the periphery of the diaphragm

Costomediastinal recess: Anteriorly where pleura wrap around the mediastinum. Larger on left

Recesses= Sites of fluid accumulation

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17
Q

What is the difference between the surface markings of the lungs and the pleura?

A

Pleura:
8th rib- Lies in midclavicular line
10th rib- lies in mid axillary line
12th rib- Lies in the mid scapular line

Lungs:
6th rib: Lies in midclavicular line
8th rib- lies in mid axillary line
10 th rib- Lies in the mid scapular line and mid line

[i.e. lungs are two spaces higher than pleura]

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18
Q

What are the surface markings of the oblique fissure (R+L lung)?

A

Spine of T4, down across the 5th rib, follows line of the 6th rib around the thorax

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19
Q

What are the surface markings of the horizontal fissure (R lung only)?

A

4th CC, horizontally back across 5th rib. Meets oblique fissure in the mid-axillary line

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20
Q

Function of the pleural membrane

A

Surface tension between the parietal and visceral pleura “pulls” the visceral layer (and lung) with the movements of the thorax wall
Elastic recoil of the lung tissue means that lungs are tending to deflate
The surface tension creates a slight negative pressure that maintains the lung in slight inflation even at the end of expiration

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21
Q

Result of pneumothorax

A

If air enters the pleural cavity the surface tension and negative tension are lost
–> Lung collapse

If severe, the affected side shows:

  • No thoracic movement
  • Elevated hemi diaphragm
  • Shift of mediastinum to affected side
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22
Q

What is the result of fracture of ribs or sternum during inspiration?

A

That whole segment would float freely, i.e. a flail segment or flail chest, and on inspiration the segment would be sucked inwards, instead of lifting upwards: paradoxical respiration

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23
Q

Describe the cephalo-caudal and lateral folding of the trilaminar disc?

A

Starts towards the end of 3rd week
Head and tail folds to meet 2 lateral folds at umbilicus
Creates endodermal tube of pharynx and oesophagus; septum transversum between thorax and abdomen

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24
Q

What is the significance of the intra-embryonic body cavity?

A

Formed between the somatic and splanchnic mesoderm
Will contribute to the pericardial, pleural and peritoneal cavities.
The cavities are continuous via the pericardio-peritoneal canals until the diaphragm forms.

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25
Q

The pharyngeal pouch and _____moving towards each other, forming a membrane where they ____, and forming _____ arches between each pouch plus cleft

A

the pharyngeal pouch and CLEFT moving towards each other, forming a membrane where they MEET, and forming MESODERMAL arches between each pouch plus cleft

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26
Q

The 6 pharyngeal arches are composed of which elements?

A
  • .Cartilaginous element (derived from neural crest cells)
  • An artery (an aortic arch)
  • A nerve (cranial nerve)
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27
Q

What important structures are formed from pharyngeal pouches?

A 
1st gives rise to tympanic cavity
2nd: Tonsils
3rd: Thymus
3rd + 4th: The parathyroid glands
 [The thyroid gland comes from the root of the tongue]
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28
Q

What is the respiratory diverticulum?

A

Ventral outgrowth fromt he foregut (endoderm) early in the 4th week
Develops as the laryngotracheal groove in the floor of the pharynx.
As the trachea separates it maintains communication with the pharynx through the laryngeal orifice (that is also derived from the laryngotracheal groove)

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29
Q

Epithelium of the respiratory tract is derived from the ______
Cartilage, vasculature and muscle are derived from ________ ___________

A

Epithelium of the respiratory tract is derived from the ENDODERM [Epi, Endo]
Cartilage, vasculature and muscle are derived from OVERLYING MESODERM

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30
Q

Septum transversum separates what?

A

Septum Transversum between heart in pericardial cavity and GI tract in peritoneal cavity

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31
Q

Describe the formation of the trachea-oesophageal septum from the respiratory diverticulum?

A

The respiratory diverticulum grows and two trachea-oesophageal ridges expand inwards from each side of the tube to fuse and form the TRACHEO-OESOPHAGEAL SEPTUM.
This separates the lung bud (trachea) ventrally from the gut tube (oesophagus) dorsally.
Leaving the only connection of the larynx to the pharynx

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32
Q

What can abnormalities in the trachea-oesophageal septum cause?

A

Oesophageal atresia
Tracheo-oesophageal fistulas (TEFs)
[Occurs in 1/3000 births]

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33
Q

Consequences of:

  • Oesophageal atresia?
  • TEFs?
A

Oesophageal atresia
1. During a normal pregnancy, the foetus swallows amniotic fluid which is resorbed from the gut and returned to the maternal circulation
If oesophageal atresia develops, this circulation of fluid is prevented and
polyhydramnios develops (excess amniotic fluid)
2. After birth, when the baby attempts to feed, milk enters the trachea, causing choking and possible development of pneumonitis and pneumonia

TEF: Often linked to other developmental defects
-Renal, cardiac, vertebral and ano-rectal

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34
Q

90% of trachea-oesophageal fistula and atresia involve ??

A

Upper oesophageal atresia and

Fistula between the lower part of the oesophagus and the trachea

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35
Q

Development of bronchi and lungs

A
  1. 2 Bronchial buds form from the respiratory diverticulum
  2. 5th Week – they form the right and left 1y bronchi
  3. Then left forms two secondary (lobar) bronchi; the right three
  4. Lungs expand and invaginate into the body cavity i.e. the pericardio-peritoneal canals that are continuous with the peritoneal and pericardial cavities
  5. The pericardio-peritoneal canals are the primitive pleural cavities

[The mesoderm will become the pleura, cartilage and vasculature]

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36
Q

The ______ that is associated with the developing pleurae is closely associated with the developing _______ and the septum ______ that forms the central tendon of the diaphragm; this accounts for the _____ nerve supply of these structures: phrenic nerve C _____

A

The MESODERM that is associated with the developing pleurae is closely associated with the developing PERICARDIUM and the septum TRANSVERSUM that forms the central tendon of the diaphragm; this accounts for the COMMON nerve supply of these structures: phrenic nerve C 3, 4, 5

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37
Q

What are the 4 stages of lung development?

A
  1. Pseudoglandular
  2. Canalicular
    ^(Not compatible with life)
  3. Terminal saccular
  4. Alveolar
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38
Q

Describe the events that take place in the “1. Pseudoglandular” stage of lung development?

A

6-16 weeks
Major elements have formed as far as terminal bronchioles (i.e. not those involved with gaseous exchange and therefore not compatible with life)

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39
Q

Describe the events that take place in the “2. Canalicular” stage of lung development?

A

16-26/28 weeks

  • Terminal bronchioles have 2/3 respiratory bronchioles, which branch to form 2-6 alveolar ducts
  • Become increasingly well vascularised

Still not compatible with life

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40
Q

Describe the events that take place in the “3. Terminal saccular” stage of lung development?

A

Period 24/26- 36 weeks/birth
1. Thin walled sacs (primordial alveoli) lined by squamous epithelial cells (type 1 pneumocytes) become well vascularised

  1. From 20 weeks type 2 pneumocytes begin to secrete surfactant (phospholipids that lower surface tension and facilitate expansion of alveoli), but there is wide individual variation
  2. At 28 weeks 1000gram babies can survive: sufficiently well developed
    - Large enough surface area for gaseous exchange
    - Sufficient surfactant secretion
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41
Q

Describe the events that take place in the “4.Alveolar period” stage of lung development?

A

28/36 weeks to Birth/Childhood (8yrs)

  • 5/6 alveoli develop postnatally
  • Increase in number of alveioli, not size
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42
Q

What are the 3 necessities for survival during respiratory development?

A
  1. The close association of thin walled alveolar ducts with a rich capillary bed
  2. The close association of alveoli with a rich capillary bed
  3. Surfactant reduces surface tension and facilitates expansion of the alveoli. Not sufficient until 28 weeks when survival is possible
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43
Q

What is surfactant?

A

A complex mixture of phospholipids that reduces the surface tension and facilitates expansion of the alveoli. Type 2 pneumocytes begin to secrete surfactant at 20 weeks but it may not be sufficient until 28 weeks when a normal foetus reaches 1000gm and survival is possible.

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44
Q

Are breathing movements seen before birth?

A

Breathing movements occur before birth and may be seen in ultrasound scans.
The movements force amniotic fluid into the lungs
The pattern of movements changes just before birth and may be used to predict the onset of labour
At birth, the lungs are half full of fluid which is quickly resorbed into the pulmonary vessels

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45
Q

What is Respiratory Distress Syndrome (RDS)?

A

Caused by: Insufficient surfactant results in the collapse of the alveolar
wall during expiration

Treatment to reduce RDS associated mortality: Recent development of artificial surfactant and treatment with
glucocorticoids to stimulate surfactant secretion

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46
Q

Examples of abnormal lung development?

A
  1. Pulmonary agenesis

2. Lung hypoplasia

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47
Q

4 sources of origin of the diaphragm?

A
  1. Septum transversum - central tendon of diaphragm
    - Between the pericardial and peritoneal cavities and two pericardioperitoneal canals, lies a thick plug of mesoderm (the SEPTUM TRANSVERSUM). This forms the central part of the diaphragm

2.Two pleuroperitoneal membranes project towards and fuse with the septum transversum and close the pericardio-peritoneal canals

3,Mesentery of the oesophagus from which the crura develop

  1. Ingrowth from the body wall
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48
Q

Other name for RDS?

A

Hyaline membrane disease

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49
Q

Why does the Phrenic nerve provide whole motor supply of the diaphragm?

A

The septum transversum contains myoblasts from the somites in C3, 4, 5 and they migrate into 2, 3, and 4 (listed above) to form the muscle of the diaphragm

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50
Q

How does congential diaphragmatic hernia occur?

A

Normal development and fusion do not always occur in the diaphragm
So the absence of a pleuro-peritoneal membrane has left a hole in the diaphragm, allowing the gastro-intestinal contents of the abdomen to herniate into the thorax and suppress lung development

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51
Q

What are the 3 different types of hernia to occur int he diaphragm?

A
  1. Postero-lateral (Bochdalek)
  2. Anterior (Morgagni)
  3. Central
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52
Q

Change in volume –> change in ____ –> movement of air

A

Δ volume → Δ pressure → movement of air

Air flows from a high pressure area to a low pressure area. To lower the pressure inside the lungs we expand the size of the chest and lungs.

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53
Q

What is the Intrapulmonary pressure?

A

Pressure within the alveoli which rises and falls over on respiratory cycle

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54
Q

What is the intrapleural pressure? Compare to alveolar?

A

Always more negative than alveolar. The elastic nature of the lung tissue versis ribcage and thorax trying to pull apart visceral from parietal pleura
-4mmHg

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55
Q

Mechanics of inspiration:

  • Role of diaphragm and intercostals?
  • Changes in volume
  • Changes in pressures?
A

Role of diaphragm: Main muscle of respiration. Contraction flattens domes. Abdominal wall relaxes t allow abdominal contents to move downwards.
Role of intercostals: External (with first rib fixed). Two movements; forward movement to lower end of sternum, upwards + outwards movement of ribs.

Increase thorax volume by 500ml (normal tidal volume)

Intrapleural pressure drops to -6mmHg
Decreases intrapulmonary pressure by 1mmHg

Accessory muscles used in forced inspiration (ie in respiratory distress) is the trapezius

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56
Q

Quiet expiration, mechanics (Muscles involved, changes in volume and pressure??)

A

Passive- no direct muscle action normally
Cessation of muscle contraction
Elastic recoil = drives air out of the lungs
Thoracic volume decreases by 500ml
Intrapulmonary pressure increases
Air moves down pressure gradient

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57
Q

Forced expiration, mechanics?

A

Contraction of abdominal walls, forces abdominal contents up gradient against diaphragm
Internal intercostals pull ribs downwards

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58
Q

What is the transpulmonary pressure?

A

Difference between intrapulmonary and intrapleural pressure

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59
Q

At the end of each respiratory cycle the intrapulmonary pressure is back to…

A

Atmospheric pressure

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60
Q

During breather, energy is required to… (5)

A
  1. Contract the muscles of inspiration
  2. Stretch elastic elements
  3. Overcome airway resistance
  4. Overcome frictional forces arising from the viscosity of the lung an chest wall
  5. Overcome inertia of air and tissues
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61
Q

Airway resistance:

  • Significance?
  • Equation?
  • Contributing factors?
  • Where is it highest?
A

Significance: Most significant non-elastic source of resistance

Equation: F = ΔP/R

Contributing factors:
-Turbulence likely to uccir in high velocity, large diameter airways

Greatest resistance to airflow is found in the segmental bronchi

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62
Q

Changes in airway resistance

A
  1. In inspiration, airway resistance decreases (and vice versa)
  2. Insignificant in health
  3. Becomes an issue in disease states where airway resistance is increased
  4. In asthma inflammatory mediators changing smooth muscle tone – narrowing airways – increases resistance
  5. Patients with COPD tend to have over-inflated chests (barrel-chested)
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63
Q 
Compliance:
Definition?
Change in volume of the chest that results from a given change in \_\_\_\_\_\_\_\_\_\_ pressure
Major determinants?
Normal compliance?
A

Definition: Describes the distensibility (or ease of stretch of lung tissue) when external forced applied
I.e. the ease with which the lungs expand under pressure

Change in volume of the chest that results from a given change in INTRAPLEURAL pressure.

Major determinants: Elastic components, alveolar surface tension

Normal compliance: 1L per kPa/7.5mmHg

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64
Q

Compliance can be reduced by… (4 factors)

A
  1. Replacing elastic tissue with non-elastic tissue (e.g. in pulmonary fibrosis the lungs become stiffer)
  2. Blocking smaller respiratory passages
  3. Increasing alveolar surface tension
  4. Decreasing the flexibility of the thoracic cage or its ability to expand
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65
Q

Compliance can be increased by…

A

Pulmonary emphysema.
Due to alveoli rupture, creating larger air space and thus reducing surface area of lung. Impaired elastic recoil leads to poor deflation, trapping more air.

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66
Q

Why is there a different in ventilation between the apex and base of the lung?

A

Lung compliance varies with lung volume. (Small vol = high compliance)

Lung volume at base is less because it is compressed compared to apex. For the same change in intrapleural pressure at inspiration the base of the lung expands more than apex.

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67
Q

What is alveolar surface tension?
It’s importance?
Produced by?
Function?

A

Due to the polar nature of water. Prevents alveolar collapse.
If the lungs were lined with pure water, they would collapse. Presence of surfactant reduces this.
Produced by type II alveolar cells.
Increases lung compliance by reducing surface tension, allows greater expansion for a given change in pressure

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68
Q

Respiratory volumes and pulmonary function tests?

A

Spirometry
Vitalograph
Peak flow meters
Alveolar ventilation and minute ventilation

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69
Q

What are the 4 volumes of air in the lungs?

A

Tidal Volume TV
Inspiratory Reserve Volume IRV
Expiratory Reserve Volume ERV
Residual Volume RV

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70
Q

What is tidal volume?

A

Volume of air breathed in and our in a single breath

71
Q

What is inspiratory reserve volume?

A

Volume breathed in by max inspiratory at end of normal inspiration

72
Q

What is expiratory reserve volume?

A

Volume expelled by max effort at the end of normal expiration

73
Q

What is residual volume?

A

Volume of air in lungs at the end of maximum expiration

74
Q

What is inspiratory capacity (IC)

A

TV + IRV

Volume of air breathed in by max inspiration at the end of a normal expiration

75
Q

What is functional residual capacity (FRC)?

A

ERV + RV
Volume of air left in lungs at end of normal expiration. Buffer against extreme changes in alveolar gas levels in each breath

76
Q

What is vital capacity (VC)?

A

IRV +TV + ERV

Volume of air that can be breathed by max inspiration following a max expiration

77
Q

What is total lung capacity (TLC)?

A

VC + RV

Only a fraction of TLC used in normal breathing

78
Q

What lung volume cannot be measured with a spirometer?

A

Residual volume

79
Q

What is dead space:
Anatomically?
Alveolar?
Physiologically?

A

Anatomical: Areas of airways not involved in gaseous exchange (nose –> Bronchioles) 150ml on average

Alveolar: Gas exchange suboptimal in some parts of lung (ventilation less than 5ml)

Physiological (anatomical plus alveolar): In normal person about the same as anatomical due to low alveolar dead space. In lung disease ventilation, perfusion ration alters and alveolar dead space can increase.

80
Q

Where does the rhythmic activity of ventilation originate?

A

The respiratory muscles themselves do not have an intrinsic rhythmicity (unlike the heart).
The brainstem contains all the components to generate a rhythmic pattern of respiration.

Respiratory rhythm is generated in the MEDULLA

81
Q

Respiration is regulated by two mechanisms, nervous and chemical.
Explain each.

A

Nervous:

  • Breathing originates in the brainstem, in the medulla and the pons
  • Involves respiratory ‘centres’, afferent and effect nerves
82
Q

Respiration is regulated by two mechanisms, nervous and chemical.
Explain each.

A

Nervous:

  • Breathing originates in the brainstem, in the medulla and the pons
  • Involves respiratory ‘centres’, afferent and effect nerves
83
Q

Respiratory centres:

  • Location?
  • Function?
  • Names?
A

-Centres located in the medulla oblongata and pons

  • Collect sensory information about the levels of O2 and CO2 in blood, and determines signal sent to respiratory muscles
  • Stimulation produces alveolar ventilation
  • Pattern of breathing is aimed to minimise the amount of work done

Pontine centres: Pneumotaxic, apneustic
Medullary centres: Inspiratory, expiratory

84
Q

For the following MEDULLARY CENTRES name the location, aka and function:

  1. Inspiratory centre
  2. Expiratory centre
A
  1. Inspiratory centre
    Location: Upper part of medulla oblongata
    Aka: Dorsal Respiratory Group (DRG)
    Function: Concerned with inspiration, exclusively inspiratory neurons
  2. Expiratory centre
    Location: In medulla oblongata, anterior and lateral to the inspiratory centre
    Aka: Ventral Respiratory Group (VRG) Mixture of inspiratory and expiratory neurons
    Function: Centre is inactive during quiet breathing and when inspiratory centre is active. During forced breathing or when inspiratory centre is inhibited it becomes active.
85
Q

For the following PONTINE CENTRES name the location and function:

  1. Pneumotaxic centre
  2. Apnuestic centre
A
  1. Pneumotaxic centre
    Location: Situated in upper pons
    Function: Controls medullary respiratory centres, especially the inspiratory centre through the apneustic centre. It influences inspiratory centre so that duration of inspiration is under control
  2. Apnuestic centre
    - Situated in lower pons
    - Function: Increases depth of inspiration by acting on inspiratory
86
Q

What are the nervous connections for breathing?

A

Afferent pathways:

  • Deliver impulses via vagus and glossopharyngeal nerves
  • Respiratory centre gets impulses according to movement of thoracic region and lungs
  • Also from chemoreceptors

Efferent pathways:

  • Deliver signals that drive inspiration and expiration
  • Nerves from respiratory centre leave brain in anterior part of lateral column in spinal cord
  • Terminate in motor neurons in cervical and thoracic segments of spinal cord
  • Supply phrenic nerve that control diaphragm
  • Supply fibres for intercostal muscles
87
Q

Factors affecting respiratory centres?

A
  1. Impulses from higher centres (i.e. cerebral cortex, limbic system, hypothalamus)
  2. Hering-breur reflex (slowly adapting stretch pulmonary receptors). Smooth muscle of upper airways has slowly adapting stretch receptors.
  3. “J” Receptors or pulmonary C-fibres
88
Q

What is Hering-breur reflex?

A

Stretch receptors of lung= Slowly adapting pulmonary receptors
Smooth muscle of upper airways = Slowly adapting stretch receptors

When lung is inflated these neurones send impulses to DRG via the vagus nerve. This input in inhibitory, limiting inspiration, prevents overinflation of lungs.
Active more in
-First year of life
-During strenuous exercise when TV > 1L

89
Q

How do “J” receptors ( or pulmonary C-fibres) affect respiratory centres?

A

Juxtacapillary receptors present in wall of alveoli, in
close contact with pulmonary capillaries
• Stimulated during conditions like pulmonary oedema/ congestion/ pneumonia. Also from endogenous chemicals such as histamine
• Stimulation of J receptors induced apnea (temporary suspension of breathing) followed by rapid shallow breathing

90
Q

What are irritant receptors?
Where are they found?
How do irritant receptors of the lungs affect the respiratory centres?

A

What are they? Rapidly adapting receptors which are powerfully stimulated by inhalation of irritants (e.g. ammonia, cigarette smoke)
Location: Walls of bronchi and bronchioles

Function:

  • Induces rapid shallow breathing, mainly from shortening of expiration.
  • Also induces long deep augmented breaths taken to reverse slow collapse of lungs that occurs during quiet breathing
91
Q

Where are proprioreceptors found?

What is their function in respiration?

A

Found in:

  • Joints: To measure velocity of rib movement
  • Tendons: Detects strength of muscle contraction in muscles of respiration e.g. Diaphragm and intercostals
  • Muscle spindles: Monitors length of fibres (both statically and dynamically) and velocity

Function: Reflexes from muscles and joints to stabilise ventilation during changing mechanical conditions

92
Q

Affect of thermoreceptors on respiratory centre?

A

Cutaneous supply of signals to cerebral cortex.

Stimulates respiratory centre and hyperventilation

93
Q

Affect of pain receptors on respiratory centre?

A

Supply signals to cerebral cortex

Stimulates respiratory centre and induces hyperventilation

94
Q

What is the cough reflex?

Affect of cough reflex on respiratory centre?

A

Cough reflex= Protective reflex caused by irritation of parts of respiratory tract beyond nose e.g. Larynx, trachea and bronchi

Affect: Stimulates vagus nerve and cough induced.

  1. Deep inspiration followed by forceful expiration with closed glottis.
  2. Glottis opens and explosive outflow of air at high velocity
95
Q

Cause of sneezing reflex?

Affect on respiration?

A

Sneezing reflex caused by irritation of nasal mucous membranes

Affect: Deep inspiration followed by forceful expiration with opened glottis

96
Q

What is the deglutition reflex?

Affect on respiration?

A

Deglutition reflex: Respiration arrested during swallowing of food
Affect on respiration: Swallowing/deglutition apnea

97
Q

Chemoreceptors:

  • Responds to??
  • Classification?
A

Chemoreceptors: Respond to change sin chemical constituents of blood or CSF (e.g. Hypoxia, Hypercapnea, Increased H+ conc)

Classification:

  1. Central chemoreceptors
  2. Peripheral chemoreceptors
98
Q

What is hypercapnea?

A

Elevated CO2 in blood

99
Q

Central chemoreceptors:

  • Location?
  • Aka?
  • Action?
A

Location: Medulla oblongata close to DRG
AKA: Chemosensitive area
Action:
-Sensitive to increase in H+ concentration
-H+ concentration rise across the BBB or CSF barrier due to CO2 crossing barrier and dissociating to H+ and bicarbonate.
-Increase in PaCO2 in CSF has greater effect on pH vs in blood

CENTRAL CHEMORECEPTORS SENSISITIVE TO ARTERIAL PaCO2 NOT ARTERIAL H+ (or PaO2)

100
Q

Peripheral chemoreceptors:

  • Location?
  • Effect?
  • Sensitivities?
A

Location: Around carotid sinus and aortic arch
Effect: Carotid bodies have the greater effect on respiration
Sensitivities:
-PaO2
-PaCO2 (less sensitive than central receptors)
-pH,
-Blood
-Temperature

101
Q 
Effect of neuromuscular disorders on respiratory function:
CNS
Strokes
Poliomyelitis
Dipheria
Bolulism
DMD
A

CNS: Trauma to brain and spinal cord = partial/total loss of respiratory function. Uncontrolled activity of airways innervation can lead to: Vasoconstriction, hypertension, mucus secretion, oedema

Strokes: Hemispheric strokes interfere with voluntary pathways of breathing. Brainstem strokes that affect dorsal medullary centres cause fatal apnoea

Poliomyelitis: Mechanical ventilation required during acute phase. Reinnervation of fibres can recover respiratory muscle strength

Diptheria: Demyelinating neuropathy can lead to respiratory failure

Bolutism: Innervation of respiratory muscles seems particularly vulnerable, ventilation for extended period

DMD: Age 10 onwards vital capacity declines. Nocturnal hypoxaemia develops first. Causes of death 1. Pulmonary infection 2. Respiratory failure

102
Q

What is Dalton’s Law of Partial Pressures?

A

Each individual gas exerts a proportion of atmospheric pressure, according to its partial pressure

103
Q

How to calculate a gas’ partial pressure?

A

Nitrogen:
0.7808 x 760 mmHg = 593mmHg

Oxygen:
0.2095 x 760 mmHg = 150 mmHg

CO2:
0.00039 x 760mmHg = 0.26mmHg

104
Q

What is atmospheric pressure?

A

760mmHg
or
101.325 kPa

105
Q

What is Henry’s law?

A

When a mixture of gases is in contact with a liquid, each gas will dissolve in the liquid in proportion with its partial pressure.
[E.g. 10x more gas will dissolve into solution if its partial pressure is 10kPa than if it were 1kPa.
If the partial pressure in the liquid > in the air, gas will move out of the liquid ]

BUT the absolute level of gas dissolved in a liquid depends on the solubility of the gas

106
Q

If the gas enters into a chemical reaction (e.g.
producing bicarbonate) the _____ amount of the gas in
the liquid is the amount dissolved plus that _____ bound in solution.

A

If the gas enters into a chemical reaction (e.g.
producing bicarbonate) the TOTAL amount of the gas in
the liquid is the amount dissolved plus that CHEMICALLY bound in solution.

107
Q

For all gases, the amount dissolved is ______ to the partial pressure
The absolute amount dissolved also depends on its _______
Examples?

A

For all gases, the amount dissolved is PROPORTIONAL to the partial pressure
The absolute amount dissolved also depends on its SOLUBILITY

Examples:
CO2 = Most soluble
O2= 1/20 solubility of CO2
N2= Barely soluble

108
Q

What is composition of alveolar gas?

A

Alveolar gas is not atmospheric air due to humidifying actions of conducting passageways of respiratory system.
Warmed/moistened air water vapour pressure = 47mmHg
Hence 760-47 = 713mmHg….. 713 x 0.2093 = 149 mmHg

109
Q

Why are the partial pressures of gases in the lungs different to the alveolar PPs?

A

O2 is lower
CO2 is higher
Water vapous is higher

Because alveolar air is made up of “fresh air! plus the air that remained in the lungs after the last breath. Rest of different is due to constant flux, O2 is moving out of alveolar and CO2 in

110
Q

What are the different factors that alter the rate of diffusion of gases in respiration?

A

Proportional to:

  • Surface area
  • Solubility
  • Concentration gradient (different in partial pressure)

Inversely proportional to:

  • Tissue thicken
  • molecular mass root
111
Q

How do the following pathologies alter ventilation/diffusion:

  1. Oedema
  2. Emphysema
  3. Mucus, inflammation of airway, tumours
A
  1. Oedema
    - Wall thickness increases
    - Full transit time may not be sufficient to complete full gas exchange
    - O2 more affected than CO2 as CO2 has greater solubility
  2. Emphysema
    - If SA decreases, gas exchange is reduced
  3. Mucus, inflammation of airway, tumours
    - Gas exchange is inhibited
    - Gas exchange is reduced
112
Q

What are the results of the following on the physiology of ventilation/diffusion:

  1. Altitude
  2. Diving
A
  1. Altitude
    - Atmospheric pressure is reduced
    - Inspired + alveolar PO2 reduced, PCO2 reduced
    - Haemoglobin sat is reduced
    - Increase release of erythropoietin occurs
  2. Diving
    - Increased risk of air embolism and decompression sickness
    - Increase in atmospheric pressure by 760mmHg
    - Air enters lung at increased pressure
    - N2 can be forced into the bloodstream. Hence rapid ascent can cause gas bubbles of N2 to form
113
Q

Problems associated with N2 bubbles?

A
  • Can form lethal emboli
  • Bubble in the pulmonary circulation
  • Joint = extremely painful
  • Brain = stroke
  • Decompression sickness
  • Hyperbaris chambers used to slowly decompress divers we come up too quickly
114
Q

Risk of rapid ascension without exhaling?

A
  • Shallower water = decrease in atmospheric pressures
  • Volume of air in lungs increases (P1 x V1 = P2 x V2)
  • Causes rupture of alveoli and gas bubbles enter circulation
  • Usually lodge in cerebral circulation

–> Seizures, fits, unconsciousness

115
Q

What are the two modes of oxygen transport?

A
  1. Dissolved in plasma
    - Proportional to partial pressure
    - O2 is poorly soluble hence this is not an efficient mode of delivery as tissue requirements are too high
  2. Attached to haemoglobin
    - O2 forms an easily reversible combination (HbO2)
    - 4 binding sites
    - “Positive co-operative binding” ie Once first O2 is bound, the next 3 bind easily.
    - Produces sigmoidal oxygen-haemoglobin dissociation curve
116
Q

Increases in which substances influence haemoglobin saturation?
Bohr effect

A

Increased in temp, H+, CO2 and 2,3-bisphosphoglycerate (all shift curve to the right)

  • Modifies structure of Hb, decreasing its affinity for oxygen
  • Bohr effect: Increased CO2 leads to an increase in H+ which weakens the Hb-O2 interaction

At the lungs the curve shifts to the left and haemoglobins affinity for oxygen is increased (as there is decreased CO2)

117
Q

How to calculate amount of O2 carried in the blood?

A

Total = ([Hb] x max o2 capacity x %saturation) + amount dissolved

118
Q

For 100 ml of normal arterial blood:

  • [Hb] is 15 g Hb/100 ml blood
  • Capacity is 1.35 ml O2/g Hb (lies between 1.35 and 1.39 normally)
  • PO2 is 100 mmHg
  • % saturation is 98%
  • The amount dissolved is 0.3 ml O2/100ml

Calculate total amount of O2 carried in the blood

A

Total = ([Hb] x max o2 capacity x %saturation) + amount dissolved

Total = (15 * 1.35 * 98%) + 0.3
= 20 ml O2/100 ml blood, or 200 ml O2/litre

119
Q

How is CO2 transported in the blood by the following mechanisms:

  1. Bound to haemoglobin
  2. As bicarbonate
A
  1. Dissolved in plasma
    - 7-10% of total transported CO2
    - Greater solubility than O2
  2. Bound to haemoglobin
    - 10-20% of total transported CO2
    - Forms carbaminohaemoglobin
    - Binds to the amino acids, not the haemo, so doesn’t compete with o2
    - Loading and unloading is directly related to PCO2 and degree of oxygenation of Hb
    - Haldane effect
  3. As bicarbonate
    -70-80% of total transported CO2
    -When CO2 dissolves in water it produces carbonic acid, which breaks down to H+ and HCO3 (bicarbonate)
    CO2 + H20 H2CO3 H+ + HCO3-
    -Formed bicarbonate diffuses into plasma from RBC. H+ binds to Hb
    -Chloride shift (Chloride ions move into RBC to maintain electrical balance)
    -In lungs, the process is reversed so that CO2 is produced and released into alveoli
120
Q

What is the Haldane effect?

A

Deoxygenation of Hb increases its ability to bind CO2 (e.g. in the tissues) and vice versa in the lungs, oxygenation of Hb releases CO2 into plasma for transport into alveoli

Increase O2 binding -> CO2 release

121
Q

What enzyme is present in RBC and not in plasma that alters the reaction of CO2 dissolving?

A

Carbonic anhydrase in RBC speeds up the first stage of the reaction:
CO2 + H2O ↔ H2CO3

122
Q

The influence of CO2 on blood pH?

A

Alteration of alveolar ventilation (i.e. altering CO2 elimination) can change acid-base status of blood

Either changing the bicarbonate levels OR the CO2 levels

123
Q

How is pH of blood calculated?

A

HENDERSON-HASSELBACK equation used to calculate pH of blood
pH = pK + log [bicarbonate]/[CO2]

pK= 6.1
[bicarbonate] is measured
[CO2] is calculation accordin to the solubility of the gas and the PCO2

124
Q

How are respiratory acidosis and alkalosis caused?

A

Respiratory acidosis: -Decrease in ventilation

  • > CO2 increases
  • > pH falls
  • > HCO3 increased

Respiratory alkalosis:

  • Hyperventilation
  • > Blowing of more CO2
  • > pH rises
  • > HCO3 levels falls
125
Q

What are the variations in ventilation across the lungs and why?

A

In the upright human, inspired air is not evenly distributed throughout the lung. More gas goes to the base of the lung than the apex. The base of the lungs changes volume more than the apex.

Why?

  • Not entirely due to gravity. Weight of lungs pulls down on pleura so the alveoli are more extended already
  • Lower ribs are more curved and mobile than upper
  • Action of diaphragm
  • Upper lobes attached to main bronchi and upper airways so less easily stretched
  • Lower lobes have greater compliance
126
Q

What is ventilation?

A

Ventilation is the change in volume of the alveolus through the respiratory cycle

127
Q

Variations in perfusion across the lung

A

Two circuits supply the lung tissue: Pulmonary (98%) and bronchial circulation

Pulmonary:

  • Forms respiratory portion of circuit
  • Almost entire output of right ventricle
  • Mixed-venous blood
  • Pulmonary artery branches to supply lobes alongside bronchial tree (until bronchioles where a dense capillary network is formed)
  • Oxygenated blood returns through pulmonary venules and veins to the left atrium

Bronchial:

  • Branches of descending aorta
  • Forms conducting portion, re-joins circulation in pulmonary vein, thus diluting slightly the oxygenated blood with deoxygenated.
  • Supplies O2 to lung parenchyma (Airway smooth muscle, pulmonary arteries and veins) and pleura
  • Involved in conditioning of inspired air
128
Q

The pulmonary circulation is a low ________, ___ resistance system

A

The pulmonary circulation is a low PRESSURE, LOW resistance system

129
Q

What is transmural pressure?

A

The balance between alveolar pressure and blood pressure

130
Q

What is the distribution of blood flow in the lungs in upright position?

A

At apex = low perfusion
At base = high perfusion
Due to hydrostatic pressure difference between base and apex of lung (23mmHg) or pressure in capillaries is lower at apex

Blood will only flow if blood pressure is greater than alveolar pressure

131
Q

What are the consequences of changing the hydrostatic pressure of blood in the different zones?

A

In the apex (zone 1), if the alveolar pressure> blood hydrostatic pressure the capillary will be closed.

  • May occur with low bp or raised alveolar pressure
  • If capillaries are closed then they are ventilated but not perfused. Hence are called alveolar dead space

In zone 2, alveolar pressure

132
Q

Why (under normal conditions) is there no zone 1?

A

Because normally there is sufficient pressure to perfuse the apices

133
Q

How does the ventilation (V) and perfusion (Q) ratio (V/Q) alter throughout the lung?

A

Whole lung ratio = 0.85 (ideally 1)

Base ratio= 0.6 (due to more perfusion)
2/3 up from base ratio = 1
Apex ratio= 3 (Due to more ventilation)

134
Q

What are the 3 scenarios of ventilation and perfusion matching?

A
  1. Perfect matching. Well ventilated alveoli with a good perfusion of blood. Blood will equilibrate with alveolar air and be rich in oxygen and low CO2
  2. Poorly ventilated alveoli with rich blood supply.
    Alveolar air will equilibrate with the blood and the blood will tend towards the same composition as venous. Low P02, high PCO2
  3. Well ventilated alveoli which are poorly perfused with blood. Blood leaving the alveoli with be low in CO2 but as haemoglobin is full saturated there will be a slight increase in PO2
135
Q

Why is lowered PO2 of blood leaving poorly ventilated
parts of the lung is not compensated for by blood
leaving well ventilated areas?

A

As poorly ventilated areas have low 02 content

Whilst well ventilated areas have normal O2 content. PO2 is no higher than normal.

136
Q

What is hypoxic vasoconstriction and its importance?

A

Active control of blood flow away from poorly ventilated areas.
Intrinsic effect
Importance: At birth, before 1st breath the lungs are vasconstricted and resistance is high. At first breath, vasoconstriction and resistance drop.

137
Q

What afferent inputs can influence the basic pattern of ventilation generated in the medulla?

A
  1. Other areas of the brain
  2. Proprioceptors
  3. Stretch receptors
  4. Irritant receptors
  5. Chemoreceptors
138
Q

The control of ventilation: Voluntary control?

A

Effect of the cortex and other influences
Both cortical and other areas can by-pass the medulla and affect the lower motor neurones directly.

During voluntary control:

  1. There are signals from the cerebral cortex to the medulla (influencing basic pattern generation by the DRG).
  2. Direct pathway from cortex to the lower motor neurones to influence diaphragm and intercostals
139
Q

Involuntary control of ventilation:
Driven by?
Monitored by?

A

Driven by levels of O2, CO2 and H+ in the blood
Monitored by:
-Peripheral chemoreceptors (such as carotid body and aortic body)
-Central chemoreceptor (in ventro-lateral medulla)

140
Q

Peripheral chemoreceptors:

  • Location?
  • What are they?
  • Signal journey?
  • Carotid/aortic dominance?
  • Stimulation?
A

Location: Near to baroreceptors (carotid artery and aorta)

What are they: Specialised receptor cells (glomus type I)

Signal journey: These cells synapse with afferent nerves which run to brainstem. (Sensory portion of CN X from aortic bodies and CN IX from carotid bodies)

Carotid/aortic dominance: Carotid more important in respiration

Stimulation: Decrease in PO2 and increase in H+, that occurs as a result of increased CO2

141
Q

Central chemoreceptors:

  • Location?
  • Provides what information?
  • Stimulation?
A

Location: In medulla

Information: Provides excitatory input to the DRG

Stimulation: By an increase in H+ in CSF. (Although H+ cannot cross the BBB so detects increase in PCO2)

142
Q

Influence of PCO2 increase and decrease on of ventilation?

Normal value of PCO2?

A

Normal PCO2 = 40mmHg or 5.3 kPa

Increase PCO2:

  1. CO2 crosses BBB so as it rises can cause hypercapnia in blood leading to the pH of CSF decreasing.
  2. Excitory input sent to DRG in medulla
  3. Increased ventilation to “blow off” CO2
  4. PCO2 returns to normal, pH returns too normal and stimulus for respiration is reduced

Decreased PCO2:

e. g. during hyperventilation
1. Firing rating from chemoreceptors falls
2. Decrease in excitation to DRG
3. Respiration inhibited

143
Q

Central chemoreceptors are stimulates by acidification of the _________

A

CSF and ECF

As BBB prevents passage of H+ and HCO3- the CO2 passes through BBB then breaks down

144
Q

Peripheral chemoreceptors are sensitive to ___

A

PO2

145
Q

What occurs when PO2 level is 60mmHg or 8kPa?

A

The PO2 is must drop below 60mmHg before PO2 becomes a major stimulus for ventilation

146
Q

In COPD how is control of ventilation altered?

Associated dangers?

A
  1. PCO2 is chronically elevated due to poor ventilation
  2. The central and peripheral chemoreceptors become insensitive to PCO2
  3. Patient relies on decline in PO2 to stimulate breathing (hypoxic drives)

Risk: If placed on a 100% O2 mask, they will cease breathing as firing rate of peripheral chemoreceptors will fall and depress ventilator drive

147
Q

Decrease in pH causes increase/decrease in ventilation?

A

Increase

(Decrease in pH, increase in H+, need to drive of CO2 from lungs, increase ventilation)

If PCO2 is normal, the peripheral chemoreceptors control the change in ventilation

148
Q

What bone forms both the lateral wall and floor of the nasal cavity as the hard palate? The maxilla

A

The maxilla

149
Q

What bone forms the posterior nasal choanae and gives of attachment to the wall of the nasopharynx? The medial pterygoid of the sphenoid

A

The medial pterygoid of the sphenoid

150
Q

Bones that form the conchae?

A

Ethmoid forms superior and middle

Inferior is a separate bone

151
Q

Which bones are excavated into air sinuses?

A

Frontal
Maxilla
Ethmoid
Sphenoid

152
Q

What separates the nasal cavity from the cranial cavity and the brain?

A

The cribriform plate

153
Q

What is above and below the superior concha?

A

The spheno-ethmoidal recess above

The superior meatus below

154
Q

What is the nervous and arterial supply for the antero-superior lateral nasal wall?

A

Nervous: Branches of the ophthalmic (V1) division of the trigeminal nerve
Arterial: Ophthalmic artery branches

As the nerves and vessels have passed through the ethmoid bone they are named anterior ethmoidal

155
Q

What is the nervous and arterial supply for the postero-inferior lateral nasal wall?

A

Nervous: Branches of the maxillary (V2) division of the trigeminal nerve
Arterial: Maxillary artery

Mainly via the greater and lesser palatine nerves and arteries

156
Q

What happens to the auditory (pharyngotympanic) tube in the nasopharynx during swallowing?

A

The tube is opened by palatine muscles that partially arise from the tube.

157
Q

Other name for nasopharyngeal tonsil?

Position?

A

Adenoid

Roof and posterior wall of the nasopharynx

158
Q

Common site of epitaxis (nose bleed)?

A

Little’s or Kiesselbach’s area as it is the site of arterial anastomosis

159
Q

What is the nervous and arterial supply for the antero-superior septal wall?

A

Nervous: Anterior ethmoidal nerve which is a branch of the ophthalmic division of the trigeminal nerve (V1)
Arterial: Anterior ethmoidal artery (branch of ophthalmic artery)

160
Q

What is the nervous and arterial supply for the postero-inferior septal wall?

A

Nervous: Nasopalatine nerve (branch of the maxillary division V2 of trigeminal nerve)
Arterial: Sphenopalatine artery (branch of the maxillary artery)

161
Q

Where does the sphenoidal air sinus open into the nasal cavity?

A

The spheno-ethmoidal recess above the superior concha

162
Q

Which meatus does the the nasolacrimal duct opens to drain tears from the conjunctival sac?

A

The inferior

163
Q

What is the site for emergency access to the airway?

A

The cricothyroid membrane

164
Q

What do the superior laryngeal nerve and artery supply?

A

Pass through the thyrohyoid membrane to supply the laryngeal mucous membrane above vocal folds

165
Q

Where is the aryepiglottic fold found?

A

The free upper edge of the quadrangular membrane passing from the arytenoid (Post) to epiglottis (ant)

166
Q

Where is the piriform fossa of the pharynx found?

A

Outside quadrangular membrane, between it and thyrohyoid membrane

167
Q

Where is the vestibular fold found?

A

The free, lower edge of the quadrangular membrane

168
Q

Where is the vocal fold found?

A

The free upper edge of the cricovocal membrane. Passes from the vocal process of the arytenoid (Post) to the thyroid cartilage (ant)

169
Q

Ventricle of larynx found between which two folds?

A

Vestibular and vocal

170
Q

Action of cricothyroid?
Action of thyro-arytenoid?

Actions of cricothyroid + thyro-arytenoids + vocalis ?

A

Action of cricothyroid: Rocking of thyroid cartilage anteriorly to LENGTHEN the vocal folds
Action of thyro-arytenoid: Rocking the thyroid backwards to SHORTEN the chorda
Actions of cricothyroid + thyro-arytenoids + vocalis = Alter the length/thickness of the vocal folds to determine PITCH of voice

171
Q

The left and right recurrent laryngeal nerves supply all the muscles of the larynx except _______

A

Cricothyroid

Cricothyroid is supplied by the external branch of the superior laryngeal nerve

172
Q

Which muscles of the larynx contribute to the following actions:

  1. Opening of rima glottis (i.e. abducts the vocal folds)
  2. Closes glottis
  3. Acts as a “purse string” to contribute to laryngeal inlet closure
A
  1. Posterior crico-arytenoid
  2. Lateral crico-aryteniod and transverse (or inter) arytenoid
  3. Oblique arytenoid
173
Q

How do you calculate residual volume?

A

RV = ((C1/C2)-1) * volume of the spirometer

[Where C1 is the concentration of He at the start of the experiment, C2 is the concentration of He at the end of the experiment]

MD3001 (12 decks)

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