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MD3001 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

What is the diaphragm attached to anteriorly?

A

Xiphoid process opposite T8/9

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2
Q

What is the diaphragm attached to laterally?

A

Deep surface of ribs and costal cartilages 7-12

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3
Q

What is the diaphragm attached to posteriorly?

A
  • Median arcuate ligament T12 (between crura)
  • Median Arcuate ligament (body of L1 tip of transverse process of L1)
  • Lateral Arcuate ligament (tip of L1 transverse process to 12th rib)
  • 2 Muscular crura
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4
Q

Where is the left crus of diaphragm from?

A

Bodies of L1 & L2

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5
Q

Where is the right crus of diaphragm from?

A

Bodies of L1, 2 & 3

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6
Q

What passes through diaphragm at T8?

A
  • IVC

- Right Phrenic nerve

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7
Q

What passes through diaphragm at T10?

A
  • Oesophagus
  • Both Vagus nerves
  • Left gastric vessels
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8
Q

What passes through diaphragm at T12?

A
  • Aorta
  • Thoracic duct
  • Azygos veins
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9
Q

What happens during Quiet Inspiration: Contraction of diaphragm (1)?

A
  • Flattens domes of diaphragm
  • Increases vertical thoracic diameter
  • Increases volume
  • Decreases intrathoracic pressure
  • Air is drawn into lungs
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10
Q

What happens to the ribs and CC during Quiet Inspiration: Contraction of intercostal muscles?

A

Costal cartilages of ribs 5-10 pass obliquely upwards to the sternum, contraction of the intercostal muscles raise rib towards one above also lifts CC and pushes rib laterally

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11
Q

What happens to rib 1 during Quiet Inspiration: Contraction of intercostal muscles?

A

No lateral movement of 1st rib

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12
Q

What happens during Forced Inspiration?

A
  • Bucket-handle
  • Ribs 8-10
  • Central tendon of the diaphragm is “anchored” by attachment to pericardium, further muscle contraction pulls the ribs and causes them to evert like lifting the handle of bucket
  • Gives small increase in the lateral thoracic diameter & therefore the volume
  • Air is drawn into the lungs by this additional decrease in intrathoracic pressure
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13
Q

What 4 examples of Accessory Muscles can assist in both movements of inspiration and expiration when required?

A
  1. Pectoralis Major/Minor - inspiration
  2. Latissimus dorsi (compress ribs in forced expiration, raise ribs in forced inspiration)
  3. Abdominal wall muscles (raise intra-abdominal pressure to push
    diaphragm up in forced expiration)
  4. Neck and back muscles (trapezius, sternocleidomastoid, scalene
    muscles) help to fix the ribs
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14
Q

What type of respiration is external intercostal more active during?

A

Inspiration

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15
Q

What type of respiration is internal intercostal more active during?

A

Expiration

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16
Q

What is Mesothelium?

A
  • Simple squamous epithelium

- Secretes small amount of serous fluid to lubricate the surfaces of viscera

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17
Q

What are the surface marking of the Pleural cavity reflections?

A
  • Rise to neck of 1st rib, 2cms above clavicle
  • 2nd CC lie adjacent in midline
  • 4th Left CC notch for the heart
  • 6th CC deviate laterally
  • 8th rib lie in midclavicular line
  • 10th rib lie in midaxillary line
  • 12th rib lie in mid scapular line
  • Midline level with T12
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18
Q

What are the Pleural Recesses?

A
  1. Costodiaphragmatic Recess- around periphery of diaphragm

2. Costomediastinal Recess- anteriorly, larger on the left

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19
Q

What are Recesses?

A

Potential spaces and sites of accumulation of fluids

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20
Q

Where is the Oblique Lung Fissure on both lungs?

A
  • Spine of T4/body of T5
  • Down across 5th rib
  • Follow line of 6th rib around thorax
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21
Q

What is the clinical possibility of the apical segment of the inferior lobe?

A

Pneumonia

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22
Q

Where is the Horizontal Lung Fissure on right lung only?

A
  • 4th CC
  • Horizontally back across 5th rib
  • Mett oblique issue in midaxillary line
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23
Q

What does Surface tension of the Pleural membrane cause?

A
  • Between Parietal & Visceral pleural “pulls” visceral layer with movements of thoracic wall
  • Slight negative pressure that maintains lung in slight infiltration even at end of expiration
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24
Q

What happens to Surface tension of Pleural Membrane when Air enters the Pleural cavity?

A

Surface tension & negative pressure are lost and lung collapses

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25
Q

What are the severe side effects of air entering the pleural cavity?

A
  • No thoracic movement
  • Elevated hemi diaphragm
  • Shift of mediastinum to affected side
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26
Q

What is an example of Paradoxical Respiration?

A
  • Fracture of ribs and sternum causing the whole segment to float freely ie. flail segment
  • Inspiration the segment would be sucked inwards, instead of lifting upwards.
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27
Q

What does the ectoderm overlying the pharynx externally send during development?

A
  • Pharyngeal grooves/clefts inwards towards the endodermal pharynx
  • Most disappear but the first groove gives rise to the external auditory meatus
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28
Q

What is pharyngeal pouches?

A

Series of outgrowths which extend from the internal, endodermal aspect of the pharynx towards the grooves

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29
Q

Where does the pharyngeal membrane form?

A

Where the pharyngeal groove & pouch meet

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30
Q

What respiratory development occurs as a result of the cephalocaudal folding?

A

Endodermal tube of pharynx and oesophagus, septum transversum between thorax and abdomen

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31
Q

What/Where are the 6 pharyngeal arches?

A
  • Each with core of mesoderm

- Formed between each pharyngeal groove & pouch

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32
Q

What are the 6 pharyngeal arches have in them?

A
  • Cartilaginous element (from neural crest cells)
  • Artery (aortic arch)
  • Nerve (cranial nerve)
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33
Q

What do the 6 Pharyngeal arches give rise to?

A
  • Facial structures
  • Mandible
  • Tongue
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34
Q

What do the Pharyngeal pouches give rise to?

A
  • 1st to the tympanic cavity
  • 2nd to tonsils
  • 3rd to thymus
  • 3rd & 4th to parathyroid glands
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35
Q

What is the epithelium of the respiratory tract derived from?

A

Endoderm

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36
Q

What is cartilage, vasculature and muscle derived from?

A

Overlying Mesoderm

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37
Q

What is the respiratory diverticulum and when is it formed?

A
  • Ventral outgrowth from foregut (endoderm) early in the 4th week
  • Develops as the laryngotracheal groove in the floor of pharynx
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38
Q

What does the septum transversum seperate?

A

Heart in pericardial cavity and GI in peritoneal cavity

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39
Q

Where is the laryngeal orifice derived from?

A

Laryngotracheal groove

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40
Q

What does the tracheo-oesophageal septum do?

A

Separates the lung bud (trachea) ventrally from the gut tube (oesophagus) dorsally, leaving only the connection of larynx to pharynx

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41
Q

Give examples of the abnormalities that can occur in trachea-oesophageal septum?

A
  • Oesophgeal atresia

- Tracheo-oesophageal fistulas (TEFs)

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42
Q

What is 90% of Trachea-Oesophageal Fistula (TEF) cases?

A

Upper oesophageal atresia and fistula between lower oesophagus and the trachea

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43
Q

What amniotic fluid complication can occur as a result of oesophageal atresia?

A

Polyhydramnios (excess amniotic fluid)

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44
Q

What other defects are linked with TEF’s?

A
  • Renal
  • Cardiac
  • Vertebral
  • Ano-rectal
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45
Q

What structures are first to develop from the respiratory diverticulum for the lungs?

A

2 bronchial buds (week 5)

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46
Q

What will the pericardio-peritoneal cavities become?

A

Pleural cavities

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47
Q

How many secondary bronchi are on the left and right?

A
  • Left: 2

- Right: 3

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48
Q

What do the 2 bronchial buds do?

A
  • Subdivide into lung buds and push towards the pericardio-peritoneal canals
  • Also “picking up” mesoderm to become cartilage, muscle, vasculature and pleura
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49
Q

How many tertiary bronchi are on the left and right?

A

10 on both

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50
Q

When does the tertiary bronchi become the segmental bronchi?

A

End of 24 weeks

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51
Q

Which structures are associated with the same mesoderm, resulting in them all having C3,4,5 supply?

A

Pleura, developing pericardium and septum transversum

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52
Q

What are the 4 Stages of lung development?

A
  1. Pseudoglandular
  2. Canalicular
  3. Terminal Saccular
  4. Alveolar
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53
Q

When does Pseudoglandular stage of lung development occur?

What does it consist of?

A
  • 6-16 weeks
  • Major elements formed upto terminal bronchioles (not those involved with gaseous exchange and therefore not compatible for life)
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54
Q

When does Canalicular stage of lung development occur?

What does it consist of?

A
  • 16-26/28 weeks
  • Terminal bronchioles have 2/3 respiratory bronchioles, which branch to form 3-6 alveolar ducts
  • Become increasingly well vascularised
  • Not compatible for life
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55
Q

When does Terminal Saccular stage of lung development occur?

What does it consist of?

A
  • 24/26-36 weeks/birth
  • Thin walled sacs (primordial alveoli) lined by squamous epithelial type 1 pneumocytes become well vascularised and across which gaseous exchange can occur
  • From 20 weeks type 2 pneumocytes begin to secrete surfactant but there is wide individual variation
  • At 28 weeks 1000gram babies can survive
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56
Q

When does Alveolar stage of lung development occur?

What does it consist of?

A
  • 28-36 weeks, birth and into childhood (8 yrs)
  • 50 million alveoli at birth
  • However 5/6 of alveoli develop postnatally
  • No increase in size, increase in numbers of alveoli
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57
Q

What is Surfactant?

A

Complex mixture of phospholipids that reduces the surface tension and facilitates expansion of the alveoli

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58
Q

What are the 3 Necessities in lung development for foetal survival?

A
  1. Close association of thin walled alveolar ducts and alveoli with…
  2. Rich capillary bed
  3. Surfactant
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59
Q

What is Respiratory Distress Syndrome (RDS)?

A
  • Deficiency of surfactant resulting in collapse of alveolar wall during expiration
  • Also known as hyaline membrane disease
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60
Q

How has the mortality associated with Respiratory Distress Syndrome (RDS) been decreased?

A

Artificial surfactant & glucocorticoids to stimulate surfactant secretion

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61
Q

What is the Septum Transversum?

A
  • Lies between pericardial/thorax & peritoneal/abdomen cavities
  • Is a thick plug of mesoderm
  • Contains myoblasts from somites in C3/4/5
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62
Q

What are the Diaphragms 4 sources of origin?

A
  1. Septum Transversum- central tendon of diaphragm
  2. 2 pleuroperitoneal membranes project towards and fuse with the septum transverse and close the pericardia-peritoneal canals
  3. Mesentery of the oesophagus from which the crura develop
  4. Ingrowth from the body wall
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63
Q

What can occur if the components of the diaphragm don’t fuse properly?

A

Congenital Diaphragmatic Hernia

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64
Q

What is the name of the posterolateral hernia of the diaphragm?

A

Bochdalek Hernia

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65
Q

What is the name for an anterior hernia of the diaphragm?

A

Morgagni Hernia

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66
Q

What is intrapulmonary pressure?

A

Pressure within Alveoli

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67
Q

What is Intrapleural pressure?

A
  • Always more negative than alveolar

- Elastic nature of lung tissue versus ribcage and thorax trying to pull apart visceral from parietal pleura

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68
Q

What is the usual value for intrapleural pressure?

A

-4mmHg

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69
Q

What is the usual value of intrapulmonary pressure?

A

760 mmHg

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70
Q

What is the normal tidal volume?

A

500ml per inspiration

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71
Q

How much does intrapleural pressure drop in inspiration?

A

approx -6mmHg

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72
Q

How much does intrapulmonary pressure drop by in inspiration?

A

approx 1mmHg

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73
Q

What is the role of the diaphragm in respiration?

A
  • Main muscle
  • Contraction flattens domes
  • Abdominal wall relaxes to allow abdominal contents to move downwards
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74
Q

What is the role of intercostal muscles in respiration?

A
  • Forward movement of lower end of sternum

- Upward and outward movement of ribs

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75
Q

What is the accessory muscle in forced inspiration?

A

Trapezius

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76
Q

Describe what happens during Quiet Expiration?

A
  • Passive
  • Cessation of muscle contraction
  • Elastic recoil (air out of lungs)
  • Thoracic volume decreases by 500ml
  • Intrapulmonary pressure increases
  • Air moves down pressure gradient
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77
Q

Describe what happens during forced expiration?

A
  • Contraction of abdominal walls, forces abdominal contents up against diaphragm
  • Internal intercostals pull ribs downwards
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78
Q

What is energy used to do regarding breathing?

A
  • Contract muscles of inspiration
  • Stretch elastic elements
  • Overcome airways resistance
  • Overcome frictional forces arising from viscosity of lung and chest wall
  • Overcome inertia of the air and tissues
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79
Q

Where does 75% of energy expenditure in breathing go?

A

In quiet breathing, contraction of diaphragm

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80
Q

What is the most significant non-elastic source of resistance?

A

Airway resistance

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81
Q

How is the amount of air that flows (F) calculated?

A

ΔP/R

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82
Q

What 2 factors predisposes turbulent flow?

A
  1. High velocity

2. Large diameter airways

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83
Q

Where is the greatest resistance to airflow?

Why?

A
  • Segmental bronchi

- Cross sectional area is relatively low and airflow is high and turbulent

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84
Q

Which stage of respiritory cycle is airway resistance decreased?

A

Inhalation

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85
Q

What is the airway resistance in asthma patients?

Why?

A

Inflammatory mediators change smooth muscle tone and narrow airways leading to increased resistance

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86
Q

What is the definition of Compliance?

A
  • Describes the distensibility/ ease of stretch of lung tissue when external forces applied
  • Or ease with which the lungs expand under pressure
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87
Q

What are the major determinants of compliance?

A
  • Elastic components

- Alveolar surface tension

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88
Q

What is the compliance of a healthy individual?

A

approx 1L per kPa

1L per 7.5mmHg

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89
Q

How can compliance be reduced?

A
  • Replacing elastic tissue with non-elastic (pulmonary fibrosis)
  • Blocking smaller respiratory passages
  • Increasing alveolar surface tension
  • Decreasing the flexibility of the thoracic cage/its ability to expand
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90
Q

How can compliance be increased?

A
  • Alveoli rupture, creating larger air spaces & reducing surface area of the lung (pulmonary emphysema)
  • Impaired elastic recoil leads to poor deflation, trapping more air
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91
Q

Which lung volume is compliance the highest?

A

Low volume

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92
Q

Which part of lung has the greatest compliance and why?

A
  • Base of lung

- Compressed by surrounding tissues, so volume is less, so can expand more than the apex

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93
Q

What makes up the Alveolar surface tension?

A
  • Due to polar nature of water (pure water=collapse)

- Presence of surfactant prevents alveolar collapse pressure

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94
Q

Name Respiratory Volumes & Pulmonary Function Tests?

A
  • Spirometry (can’t measure residual volume)
  • Vitalograph
  • Peak flow meter
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95
Q

What is Tidal Volume (TV)?

A

Volume of air breathed in and out in a single breath (0.5L)

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96
Q

What is Inspiratory Reserve Volume (IRV)?

A

Volume breathed in by max inspiration at end of normal inspiration (3.3L)

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97
Q

What is Expiratory Reserve Volume (ERV)?

A

Volume of air expelled by max effort at the end

of normal expiration (1 L)

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98
Q

What is Residual Volume (RV)?

A

Volume of air in lungs at the end of maximum expiration ( 1.2 L)

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99
Q

What is Inspiratory capacity (IC)?

A
  • TV + IRV

- Volume of air breathed in by max inspiration at the end of a normal expiration (3.8 L)

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100
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 (2.2-2.4 L)
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101
Q

What is Vital capacity (VC)?

A
  • IRV+TV+ERV

- Volume of air that can be breathed by max inspiration following a max expiration (4.8 L)

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102
Q

What is the anatomical definition of Dead Space?

A

Areas of airway not involved in gaseous exchange
- Nose, mouth, pharynx, larynx, trachea, bronchi, bronchioles (little bit of alveolar aswell in physiological definition!)

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103
Q

How much ventilation occurs at dead spaces?

A

approx 150ml

104
Q

How much ventilation occurs in alveoli?

A

approx 5ml

105
Q

What does high compliance mean?

A

There is a large change in volume for a given change in pressure

106
Q

What is FEV1 and what measures it?

A
  • Forced exhalation volume per second

- Vitalograph measures it

107
Q

What is the characteristics of Respiration?

A
  • Automatic
  • Rhythmic
  • Adapts to meet changing requirements
108
Q

What happens to the activity of inspiration neurons during Inspiration?

A
  • Activity increases steadily

- Through positive feedback mechanism

109
Q

What happens to the activity of inspiration neurons at the end of Inspiration?

A

Activity shuts off abruptly and expiration takes place through recoil of elastic lung tissue

110
Q

Do respiratory muscles have/have not got intrinsic rhythmicity?

A
  • HAVE NOT

- Unlike heart

111
Q

What contains all the components to generate a rhythmic pattern of respiration?

A

The brainstem

112
Q

Where is the respiratory rhythm generated?

A

In the Medulla

113
Q

What 2 mechanisms regulate respiration?

A
  1. Nervous/Neural

2. Chemical

114
Q

What are respiratory “centres”?

A

They are diffuse networks, possibly at higher density which are active together to bring about the respiratory effect

115
Q

Where and what do the respiratory centres do?

A
  • Located in medulla oblongata and pons
  • Collect sensory information about levels of oxygen and carbon dioxide in blood that determines the signal sent to respiratory muscles
  • Stimulation of these muscles provides respiratory movements which produce alveolar ventilation
116
Q

What are the 2 Medullary Respiratory Centres called?

A
  1. Inspiratory centre

2. Expiratory centre

117
Q

Where and what does the Inspiratory centre do?

A
  • Located in upper part of medulla oblongata
  • Also called Dorsal Respiratory Group (DRG)
  • Function is exclusively with inspiration
118
Q

Where and what does the Expiratory centre do?

A
  • Located in medulla oblongata, anterior and lateral to the inspiratory centre
  • Also called Ventral Respiratory Group (VRG)
  • Inactive during quiet breathing and when inspiratory centre is active, but during forced breathing or when inspiratory centre is inhibited it becomes active
119
Q

What are the 2 Poutine Centres called?

A
  1. Pneumotaxic Centre

2. Apnestic Centre

120
Q

Where and what does the Pneumotaxic centre do?

A
  • Located in upper Pons
  • Controls medullary respiratory centres, especially the inspiratory centre through the apneustic centre
  • Influences inspiratory centre so that duration of inspiratory is under control
121
Q

Where and what does the Apneustic centre do?

A
  • Located in lower Pons

- Increases depth of inspiration by acting on inspiratory centre

122
Q

How do respiratory Afferent pathways deliver impulses?

A

Via vagus & glossopharyngeal nerves

123
Q

How does respiratory afferent signals occur?

A
  • Respiratory centre gets impulses according movement of thoracic region and lungs
  • Also from chemoreceptors
124
Q

How does respiratory efferent signals occur?

A
  • 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 controls diaphragm
  • Supply fibres for intercostal muscles
125
Q

What are the 10 Factors which affect respiratory centres?

A
  1. Impulses from higher centres
  2. Stretch receptors of lung slowly adapting pulmonary receptors
  3. “J” receptors/pulmonary C-fibres
  4. Irritant receptors of lungs
  5. Proprioreceptors
  6. Thermoreceptors
  7. Pain Receptors
  8. Cough Reflex
  9. Sneezing Reflex
  10. Deglutition reflex
126
Q

What are impulses from higher centres and how does it affect respiratory centres?

A
  • Limbic system, cerebral cortex, hypothalamus

- Can stimulate/inhibit respiratory centres directly

127
Q

What are “J” Receptors/Pulmonary C-fibres and how does it affect respiratory centres?

A
  • Juxtacapillary receptors present in wall of alveoli
  • Stimulated during conditions like pulmonary oedema, congestion, pneumonia. Also from endogenous chemicals such as histamine
  • Stimulation induces apnea
128
Q

What is Apnea?

A

Temporary suspension of breathing, followed by rapid shallow breathing

129
Q

What are Irritant receptors of lungs and how does it affect respiratory centres?

A
  • Rapidly adapting receptors
  • Situated on walls of bronchi & Bronchioles
  • Stimulated by chemicals like ammonia, cigarette
  • Induces rapid shallow breathing, mainly from shortening of expiration
  • But also, long deep augmented breaths, which are taken by mammals every 5-20mins on average to reverse slow collapse of lungs that occur during quiet breathing
130
Q

What are Proprioreceptors and how does it affect respiratory centres?

A
  • On chest wall
  • Reflexes from muscles and joints to stabilise ventilation in the face of changing mechanical conditions
  • Situated in joints
  • Tendons detect stretch of muscle contraction
  • Muscle spindles monitors length of fibres both statically and dynamically (length & velocity)
131
Q

What are Thermoreceptors and how does it affect respiratory centres?

A
  • Cutaneous
  • Supply signals to cerebral cortex
  • Stimulates respiratory centre
  • Hyperventilation
132
Q

What are Pain Receptors and how does it affect respiratory centres?

A
  • Supply signals to cerebral cortex
  • Stimulates respiratory centres
  • Hyperventilation
133
Q

What is Cough Reflex and how does it affect respiratory centres?

A
  • Protect reflex caused by irritation of parts of respiratory tract beyond nose (larynx, trachea & bronchi)
  • Stimulates vagus nerve
  • Deep inspiration followed by forceful expiration with closed glottis
  • Glottis opens and explosive outflow of air at high velocity
134
Q

What is Sneezing reflex and how does it affect respiratory centres?

A
  • Irritation of nasal mucous membranes

- Deep inspiration followed by forced expiration with opened glottis

135
Q

What is Deglutition reflex and how does it affect respiratory centres?

A
  • Respiration arrested during swallowing of food

- Swallowing apnea or deglutition apnea

136
Q

What doe Chemoreceptors Respond to?

A
  • Changes in chemical constituents of blood or CSF
  • Hypoxia
  • Hypercapnea: elevated CO2 in blood
  • Increased H+ connection (decreased pH)
137
Q

What are the 2 groups of chemoreceptors?

A
  1. Central chemoreceptors

2. Peripheral chemoreceptors

138
Q

Where and what do the Central Chemoreceptors do?

A
  • Located in medulla oblongata close to DRG
  • Sensitive to increase in H+ concentration
  • H+ cannot cross BBB or CSF barrier
  • CO2 can cross into CSF, form carbonic acid, which is unstable and rapidly dissociates to H+ and bicarbonate
  • Sensitive to arterial PaCO2, not arterial H+
  • NOT sensitive to PaO2
139
Q

Why are central chemoreceptors sensitive to arterial PaCO2 and not arterial H+?

A

Because there is less protein in CSF than plasma a rise in PaCO2 can cause a larger effect on pH in CSF than in blood

140
Q

Where and what do Peripheral Chemoreceptors do?

A
  • Situated around carotid sinus and aortic arch
  • Carotid bodies have the greater effect on respiratory
  • Sensitive to PaO2, PaCO2 (but about 10x less sensitive than central receptors), pH, blood flow, temp.
141
Q

What is CNS neuromuscular disorder?

A

Trauma to brain and spinal cord can cause partial or total loss of respiratory function
- Vasoconstriction, hypertension, mucus secretion, oedema can result from uncontrolled activity of airways innervation

142
Q

What do Hemispheric strokes interfere with?

A
  • Voluntary pathways of breathing

- Brainstem strokes that affect dorsal medullary centres cause fatal apnoea

143
Q

What is Poliomyelitis?

A
  • Viral Disease can cause temporary or permanent paralysis

- 25% require mechanical ventilation during acute phase

144
Q

What is Diptheria?

A

Demyelinating neuropathy that can lead to respiratory failure

145
Q

What is Botulism?

A
  • Food poisoning

- Innervation of respiratory muscles seems particularly vulnerable, ventilation may be required for extended period

146
Q

What happens if the brainstem is cut above the level of the pons?

A

Basic rhythm continues

147
Q

What is normal atmospheric pressure in mmHg and pascals?

A
  • 760mmHg

- 101kPa

148
Q

What is the partial pressure of nitrogen?

A

593mmHg

149
Q

What is the partial pressure of oxygen?

A

159mmHg

150
Q

What is the partial pressure of carbon dioxide?

A

0.29mmHg

151
Q

What happens to partial pressure when atmospheric pressure changes?

A

Partial pressure changes

152
Q

What is Trimix?

A

Nitrogen, Oxygen & Helium

153
Q

What is Heliox?

A

Oxygen & Helium

154
Q

What is Henry’s Law?

A
  • When mixture of gases is in contact with liquid, each gas will dissolve in liquid in proportion with its partial pressure
  • Absolute level of gas dissolved in a liquid also depends on solubility of the gas
155
Q

What happens to the gas when the partial pressure in liquid becomes greater than air?

A

Gas will move out of liquid

156
Q

Out of the atmospheric gases, which is the most soluble?

A

CO2

157
Q

What is the total amount of gas in liquid when a chemical reaction occurs?

A

Total amount of gas in liquid is the amount dissolved plus that chemically bound in solution

158
Q

Is alveolar gas same as atmospheric air?

A

NO

159
Q

What is the pressure of the water vapour in the alveoli?

A

47mmHg

160
Q

What is the alveolar partial pressure of O2?

A

104mmHg

161
Q

What is the alveolar partial pressure of CO2?

A

40mmHg

162
Q

What things is the rate of diffusion proportional to?

A

Surface area, solubility, concentration gradient, inversely proportional to tissue thickness and square root of molecular mass

163
Q

What is the concentration gradient?

A

Difference in partial pressure

164
Q

What is the partial pressure of oxygen in venous blood?

A

40mmHg

165
Q

How much more soluble is CO2 than O2?

A

20x

166
Q

How long does it take for a RBC to pass through pulmonary capillary at rest? Exercise? & Equilibrium?

A

REST- 1s
EXERCISE- 0.3s
EQUILIBRIUM- 0.25s

167
Q

What is the partial pressure of PCO2 in venous blood?

A

45mmHg

168
Q

What could be a cause of increase in thickness of respiratory membranes?

A

Oedema

169
Q

What may cause decrease in surface area for gas exchange?

A

Emphysema

170
Q

What may cause gas entry inhibition?

A

Gas exchange reduced by mucus, inflammation of airway, tumour

171
Q

Explain how altitude increases RBC count?

A
  • Lower atmospheric pressure, therefore lower partial pressure pO2
  • Haemoglobin saturation reduced
  • Increased erythropoietin release, compensation by increased Hb
172
Q

What are problems associated with N2 bubbles?

A
  • Lethal emboli
  • Bubbles in pulmonary circulation
  • Painful joints
  • Stroke
173
Q

How is decompression sickness treated in divers?

A

Hyperbaric chambers used to slowly decompress divers who surfaced too quickly

174
Q

What are the problems associated with rapid ascension without exhaling?

A
  • Volume of air in lungs increases (P1V1=P2V2)
  • Causes rupture of alveoli and gas bubbles enter circulation
  • Usually lodge in cerebral circulation
  • Can cause Seizures, unconsciousness
175
Q

What are the gas movements in the tissues?

A
  • CO2 moves into blood from tissues

- O2 moves out of blood into tissues

176
Q

What are the 2 ways oxygen is carried in the blood?

A
  1. Dissolved in plasma

2. Attached to haemoglobin

177
Q

What are the O2 tissue requirements at rest?

A

250ml O2/min

178
Q

How is O2 dissolved in plasma?

A
  • Proportional to partial pressure

- O2 poorly soluble

179
Q

What does PO2 mean?

A
  • Partial pressure of oxygen

- Reflects amount of oxygen gas dissolved in the blood

180
Q

How is O2 carried by haemoglobin (Hb)?

A
  • Easily reversible combination: HbO2
  • 4 binding sites
  • Affinity of Hb for O2 increases with amount of O2 previously bound (Positive co-operative binding)
  • Oxygen-haemoglobin dissociation curve with is sigmoidal
181
Q

What is the percentage saturation of haemoglobin at tissues and what is the partial pressure of O2?

A
  • Hb 75% saturated so you only lose 25%

- 40mmHg

182
Q

What is the significance of the flat upper plateau in Oxygen-haemoglobin dissociation curve?

A

If PO2 in lungs falls (low O2 environments), Hb saturation not greatly altered in lungs

183
Q

What is the significance of the steep lower part of the Oxygen-haemoglobin dissociation curve?

A

In low O2 tissues, only small change in n PpO2 req. for a large unloading of O2 from haemoglobin

184
Q

What is the significance of 25% of unloading in normal tissues?

A

Large reserve of O2 without even needing to increase Cardiac Output or respiratory rate

185
Q

What factors shift the Oxygen-haemoglobin dissociation curve to the right?

A

Increased temperature, H+, CO2, 2,3-bisphosphoglycerate

186
Q

How is the oxygen-haemoglobin dissociation curve moved to the right and what does this mean?

A
  • Factors modify the structure of haemoglobin

- Decrease Hb affinity for O2

187
Q

What is the Bohr Effect?

A

Increased CO2 leads to an increase in H+ which weakens the Hb-O2 interaction

188
Q

How is amount of O2 carried in blood worked out?

A

Amount of O2 carried by haemoglobin + amount dissolved

189
Q

How is amount carried by Hb worked out?

A

Hb concentration in blood X max O2 carrying capacity of Hb X % saturation of Hb

190
Q

What is the normal amount of Hb in blood?

A

15g/100ml

191
Q

What is the normal capacity of Hb for carrying O2?

A

1.35 ml (O2)/g (Hb)

192
Q

What is the % of saturation of Hb in 100ml of normal arterial blood?

A

98%

193
Q

How is carbon dioxide transported in the blood?

A
  1. Dissolved in plasma
  2. Bound to haemoglobin
  3. As bicarbonate
194
Q

How much CO2 is dissolved into the plasma?

A

7-10%

195
Q

How much CO2 is bound to haemoglobin?

A

10-20%

196
Q

How does CO2 bind to haemoglobin?

A
  • Carbaminohaemoglobin
  • Binds to amino acids, not the haevx m so does not compete with oxygen
  • Loading and unloading is directly related to PCO2 and degree of oxygenation of Hb
197
Q

What is the Haldane Effect?

A
  • Deoxygentation of Hb increases its ability to bind CO2

- Oxygenation of Hb releases CO2 into plasma for transport into alveoli

198
Q

How much CO2 is transported in blood as a bicarbonate?

A

70-80%

199
Q

What is the chemical reaction of CO2 dissolving in water?

A

CO2 + H2O –> H2CO3 –> H+ + HCO3-

200
Q

How is the conversion of CO2 to carbonic acid speed up?

A

Carbonic anhydrase in RBC

201
Q

What happens as a result of increased H+ ?

A

Chloride shift: chloride ions move into RBC to restore electrochemical gradient

202
Q

What happens in the lungs regarding CO2 travelling as bicarbonate?

A
  • Reversed
  • HCO3- moves back into RBC, reacts with H+ to form carbonic acid which is rapidly reacted by carbonic anhydrase to form CO2 & water
  • CO2 diffuses into alveoli space
203
Q

What equation can calculate the pH of blood?

A

Henderson-Hasselbach equation

204
Q

What is the Henderson-Hasselbach equation?

A

pH=pK+ Log(bicarbonate)/CO2

205
Q

What is the pK of bicarbonate?

A

6.1

206
Q

Changing the levels of what will change the pH of blood?

A

CO2 or Bicarbonate

207
Q

What is respiratory Acidosis?

A

If Ventilation decreases, CO2 increases, pH falls and HCO3- increases

208
Q

What is respiratory Alkalosis?

A

If patient hyperventilates, blowing off more CO2, pH rises and the levels of HCO3- falls

209
Q

What factors need to be closely matched in order to have effective gas exchange?

A

Ventilation & Perfusion

210
Q

What is ventilation?

A

Change in volume through the respiratory cycle

211
Q

Where does more gas go to in the lung during inspiration?

A

More goes to the base of the lung than the apex

212
Q

Why does the base of the lung receive more gas than the apex?

A
  • Lower ribs more curved & mobile
  • Diaphragm expands lower lobes more
  • Upper lobes are attached to main bronchi & upper airways so less easily stretched
  • Lower lobes have greater compliance
  • Weight causes apex to have more negative intracellular pressure, with so alveoli are more extended already
213
Q

Which 2 circuits nourish lung tissue?

A
  1. Pulmonary (approx 98% of blood to lungs)

2. Bronchial (approx 2% of blood to lungs)

214
Q

Describe the Pulmonary blood flow?

A
  • Respiratory Portion
  • Pulmonary artery flow considered equal to cardiac output
  • approx 5L enters each min
  • Stroke volume is ~70ml
  • ## Volume of pulmonary capillary network at rest ~100ml
215
Q

Describe the Bronchial blood flow?

A
  • Conducting portion, thus diluting oxygenated with deoxygenated blood slightly
  • Bronchial arteries are branches of descending aorta
  • Function to supply oxygen to lung parenchyma, airway smooth muscle pulmonary arteries, veins and pleura
  • Also conditioning (warming) of inspired air
216
Q

What is the pressure and resistance in pulmonary circulation?

A

Both LOW

217
Q

What is the clinical relevance of how pulmonary capillaries are surrounded in air?

A

Can collapse or be extended according to balance of blood pressure and alveolar pressure (transmural pressure)

218
Q

What is the mean arterial pressure in the lung?

A

~15mmHg

219
Q

What is the distribution of blood flow in an upright position and why?

A
  • Blood flow at apex is low
  • Blood flow at base is large
  • Due to hydrostatic pressure difference between base & apex ~23mmHg
  • Pressure in capillaries is lower at apex than at base of lung
220
Q

What are the consequences of the change in hydrostatic pressure at different levels of the lung?

A

In apex if alveolar pressure > blood hydrostatic pressure capillary will be closed

221
Q

What are the 3 Zones of the lungs?

A

Zone 1- Apex (PA = Pa)
Zone 2- Middle (Pa > PA)
Zone 3- Base (Pa&raquo_space; PA)

222
Q

What happens when the capillaries are closed in zone 1 of the lungs?

A

Apex of lungs are ventilated but not perfused so are considered alveolar dead space

223
Q

Why under normal conditions is there no Zone 1 in lungs?

A

Because there is sufficient pressure to perfuse the apices

224
Q

How is the flow determined in Zone 2 of the lungs?

A
  • Alveolar pressure (PA) is lower than systolic arterial pressure (Pa) but may be higher than diastolic arterial pressure and venous pressure
  • Flow is determined by arterial alveolar pressure difference
225
Q

How is the flow determined in Zone 3 of the lungs?

A
  • Alveolar pressure (PA) is lower than both arterial pressure (Pa) and venous pressure
  • Capillaries are distended as a consequence of the transmural pressure and there is continuous flow
226
Q

What is the V/Q?

A

Ventilation (V) and Perfusion (Q) ratio

227
Q

What is the V/Q ratio over the entire lung?

A

0.85

228
Q

What is the V/Q ratio at base?

A

0.6

more prefusion than ventilation

229
Q

Where is V/Q ratio 1?

A

2/3 up the base

230
Q

What is the V/Q ratio at apex of lung?

A

3

231
Q

What are the 3 Main Scenarios of Ventilation and Perfusion matching?

A
  1. Perfect matching- well ventilated alveoli, good perfusion of blood. Rich in O2, low in CO2
  2. Poorly ventilated alveoli with rich blood supply- low PO2, high PCO2
  3. Well ventilated alveoli, poorly perfused with blood- blood leaving alveoli will be low in CO2 but as Hb is fully saturated, no significant increase in O2 levels
232
Q

What happens to lowered P02 of blood leaving poorly ventilated parts of the lung?

A
  • NOT compensated for by blood leaving well ventilated areas
  • Poorly ventilated areas have low O2 content
  • Well ventilated areas have normal O2 content
233
Q

Describe effect on CO2 conc. at low VQ ratio?

A

As ventilation low, CO2 not removed rapidly, CO2 accumuates in the alveoli and higher steady state PCO2 occurs

234
Q

Describe effects on O2 conc. at low VQ ratio?

A

As ventilation low, O2 taken up by blood is not fully replenished by new air entering lungs, so O2 is depleted in alveolar air and a new steady state low PO2 occurs

235
Q

Describe effects on CO2 conc. at high VQ ratios?

A

CO2 diffusing from blood nearly all blown away. CO2 nearly depleted from alveoli until a new lower steady state level occurs

236
Q

Describe effect on O2 conc. at high VQ ratios?

A

O2 is not removed by blood as quickly so accumulates in alveoli.
Higher PO2 occurs

237
Q

What does Hypoxic Vasoconstriction do?

A
  • Intrinsic effect

- Diverts blood away from poorly ventilated areas

238
Q

Via which tract can lower motor neurone activity be affected by other upper motor neurones?

A

Corticospinal tract

239
Q

During voluntary control of ventilation, where are signals coming from and going to?

A

Come from cerebral cortex, travel to medulla (influence DRG) or go directly to lower motor neurones (influence intercostals/diaphragm)

240
Q

What is involuntary control of ventilation driven by?

A

Levels of O2, CO2, H+ in blood

241
Q

What is a glomus type 1 cell?

A

Peripheral chemoreceptor cell located in carotid bodies and aortic bodies

242
Q

What are glomus cells stimulated by?

A

Primarily Decrease in PO2, increase in H+ (caused by increase in CO2)

243
Q

What do glomus cells synapse with?

A

Afferent nerves which run to brainstem, sensory portion cranial nerve X (vagus) from aortic bodies and cranial nerve IX (glossopharyngeal) from carotid bodies

244
Q

Which of the 2 peripheral chemoreceptors is more important in respiration?

A

Carotid Body

245
Q

Where are the central chemorecpetors located?

A

Ventro-lateral medulla

246
Q

What are peripheral chemoreceptors sensitised by?

A

CO2 and pH

247
Q

Describe what keeps the glomulus cell quiescent/inactive?

A

When PO2 is high, K+ channel is open and glomus cell is inactive (REFRACTORY)

248
Q

Describe what happens when glomulus cell is activated

A
  1. PO2 falls and K+ channel closes, cell membrane depolarises
  2. Ca2+ channels open
  3. Ca2+ influx triggers neurotransmitter release
  4. Action potential travels along sensory afferents synpasing with glomulus cell
249
Q

Where does the central chemoreceptor input go?

A

DRG (dorsal respiratory group)

250
Q

What does CO2 do when it crosses BBB?

A
  • Causes hypercapnea in blood
  • pH of CSF decreases
  • Excitatory input to DRG in medulla and resulting increased ventilation “blows off” CO2, reducing arterial PCO2
251
Q

If CO2 is decreased (during hyperventilation) how is ventilation depressed?

A
  • Normal PCO2 there is resting discharge action potential from chemoreceptors
  • PCO2 falls the firing rate also falls so decrease in excitatory input to DRG, with result of respiration being inhibited
252
Q

What chemoreceptors are sensitive to PO2?

A
  • Peripheral chemoreceptors ARE

- Central chemoreceptors are NOT

253
Q

What must PO2 drop below to result in peripheral chemoreceptors becoming major stimuli for ventilation? What is the oxygen saturation of hB at this level?

A
  • 60mmHg (13.3kPa)

- 85%

254
Q

What happens to peripheral chemoreceptors in COPD & why does this become a problem?

A
  • Steady state PCO2 high due to poor ventilation
  • Central & peripheral chemoreceptors become insensitive to PCO2
  • Patient relies on peripheral stimulation from the low PO2 to stimulate breathing
  • If you give these patients O2 (100%) breathing stops
255
Q

What type of chemoreceptor controls change of pH if PCO2 is normal?

A

Stimulation of Peripheral chemoreceptors from PO2

256
Q

What happens to ventilation if pH decreases?

A

Ventilation increases

MD3001 (15 decks)

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