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MD3001 > WEEK 8 > Flashcards

WEEK 8 Flashcards

1
Q

What are the attachments of the diaphragm?

A
  1. Anterior to xiphoid process opposite T8/9
  2. Deep surface of ribs & CC 7-12
  3. Posterior attachments, 2 crura & 3 arcuate ligaments
    - median arcuate ligament: T12
    - medial arcuate ligament: body of L1 to tip of transverse process fo L1
    - lateral arcuate ligament: tip of L1 transverse process to 12th rib
    - muscular crura: Left crus from bodies of L1 & 2; Right crus from bodies of L1, 2, 3
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2
Q

What structures pass through the diaphragm? Give the vertebral levels at which they do so.

A

T8: IVC with R. phrenic nerve (remember the L. passes through the central tendon)
T10: oesophagus through right crus, with vagi & left gastric vessels
T12: aorta behind median arcuate ligament with thoracic duct & azygous veins
Crura: splanchnic nerves
Medial arcuate lig: sympathetic trunk
Lat. arcuate lig: subcostal vessels and nerve

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3
Q

What is the Costodiaphragmatic Recess?

A

The narrow, potential space between the periphery of the diaphragm & the ribs

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4
Q

What is the central tendon fused to? What does further contraction of the diaphragmatic muscle do?

A

The pericardium

- pulls on ribs 7-10 from the anchored central tendon

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5
Q

What is the innervation of the diaphragm?

A

Phrenic nerve C3, 4, 5

Motor & sensory from central tendon parietal pleura & pericardium

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6
Q

What are the diaphragmatic movements that occur during respiration?

A

Diaphragmatic contraction
- causes descent of domes to increase vertical diameter
- this increases the volume of the thorax => decreasing intrathoracic pressure so air is drawn into the lungs
NOTE: this is the most important inspiratory activity in adults

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7
Q

What is the function of the intercostal muscles in quiet inspiration?

A

As shaft of rib passes obliquely downwards contraction of intercostals raises the shaft of rib towards the one above. It also lifts the sternum anteriorly
- this increases A-P diameter & thoracic volume which decreases intrathoracic pressure => air drawn in
The raising of the ribs results in the CC being lifted which pushes the ribs laterally
- this increases lateral diameter & thoracic volume
- this movement does not occur with rib 1 and ribs 2-4 may twist slightly to increase lateral diameter as their CCs are short and horizontal

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8
Q

How does forced expiration occur?

A

Bucket handle, only in ribs 8-10 as they have flat costo-transverse joints which allow gliding
- once central tendon is anchored by its pericardial attachment, further contraction pulls on the ribs and causes them to evert like lifting the handle of a bucket giving a small additional increase in lateral thoracic diameter

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9
Q

What are accessory muscles of respiration?

A

Big muscles that attach to the head & upper limbs, as well as the abdominal muscles
- used when more power is required

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10
Q

Give specific examples of accessory muscles of respiration and what they assist with?

A
  1. Pec. major and minor - inspiration
  2. Lat. dorsi - can help compress ribs in forced expiration, but more superior parts may help 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 ribs
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11
Q

When is (i) External intercostals (ii) Internal intercostals primarily used?

A

(i) inspiration

(ii) expiration

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12
Q

Expiration is normally a passive process due to?

A

Muscle relaxation & elastic recoil of airway & lung tissue

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13
Q

What are the abdomen & pelvis lined by? What is mesothelium?

A

peritoneum

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

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14
Q

What is parietal pleura attached firmly to?

A
  1. Thorax wall
  2. The fascia at the thoracic inlet, at 1st rib and T1
  3. Fibrous pericardium and other mediastinal structures
  4. Diaphragm
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15
Q

What structures would be at risk with lateral movement of rib 1?

A

Subclavian vessels

Lower trunk of brachial plexus

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16
Q

What are the landmarks for the extent of the pleural cavity? (HINT: 2, 4, 6, 8, 10, 12)

A 
Rises to level of neck of 1st rib (2cm above clavicle)
2nd CC - lie adjacent in midline
4th L. CC - notch for heart
6th CC - deviation laterally
8th rib - lie in midclavicular line
10th rib - lie in midaxillary line
12th rib - lie in midscapular line
Mid line - level with T12 (just below 12th rib)
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17
Q

Where/what is the costomediastinal recess?

A

Located anteriorly where pleurae wrap around the mediastinum.
Is larger on the left

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18
Q

What is the differences between the lung & pleural surface markings? (NOTE: this is when the lungs are in quiet inspiration)

A

For the lungs: those that lie in mid clavicular, mid axillary & mid scapular are all 2 ribs higher than that of the pleura

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19
Q

What is the landmarks of the oblique fissure?

A

On both the R and L lungs

  • spine of T4 when palpating
  • body of T5 on radiograph
  • down across 5th rib, to follow the line of the 6th rib around the thorax
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20
Q

What segment/lobe of the lung(s) is prone to pneumonia?

A

The apical segment of the inferior lobe

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21
Q

What is the landmarks of the horizontal fissure?

A

Located in RIGHT lung only

- 4th CC then horizontally back across the 5th rib to meet the oblique fissure in the mid-axillary line

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22
Q

Describe the effect of surface tension?

A

Surface tension between the parietal and visceral pleurae “pulls” the visceral layer (and the lung) with the movements of the thoracic wall
- elastic recoil of the lung tissue means the lungs are tending to deflate but 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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23
Q

What is a pneumothorax? If severe, what does the affected side show?

A

When air enters the pleural cavity the surface tension and negative pressure are lost and the lung collapses
If severe, no thoracic movement, elevated hemi diaphragm, shift of mediastinum to affected side

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24
Q

What would happen if severe trauma caused fracture of the ribs and sternum?

A

The whole segment would float freely i.e. a flail segment or flail chest
- on inspiration the segment would be sucked inwards, instead of lifting upwards
= PARADOXICAL RESPIRATION

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25
Q

What are the (i) upper (ii) lower components of the respiratory system?

A

(i) nasal cavity, nasopharynx, larynx and trachea

(ii) primary bronchi and lungs

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26
Q

When does cephalo-caudal and lateral folding of the trilaminar disc occur? What does it create?

A

Starts towards end of 3rd week

- creates endodermal tube of pharynx and oesophagus, septum transversum between thorax and abdomen

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27
Q

When/how does the respiratory diverticulum appear? What does it develop as?

A

As a ventral outgrowth from the foregut early in the 4th week
- it develops as the laryngotracheal groove in the floor of the pharynx

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28
Q

As the trachea separates, how does it maintain communication with the pharynx?

A

Through the laryngeal orifice - which is also derived from the laryngotracheal groove

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29
Q

How are the trachea and oesophagus formed?

A

The respiratory diverticulum grows and two tracheo- oesophageal ridges expand inwards from each side of the tube to fuse and form the tracheo-oesophageal septum that separates the lung bud (trachea) ventrally from the gut tube (oesophagus) dorsally

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30
Q

What abnormalities can arise in the partitioning of the oesophagus and trachea? Describe the complications of said abnormalities.

A

Oesophageal atresia and tracheo-oesophageal fistulas (TEFs)
- during normal pregnancy foetus swallows amniotic fluid which is resorbed from gut and returned to maternal circulation BUT in oesophageal atresia, the circulation of fluid is prevented and polyhydramnios develops => when baby attempts to feed milk will enter the trachea (choking and potential pneumonitis/ pneumonia

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31
Q

What other developmental defects can TEF’s be linked with?

A

Renal
Cardiac
Vertebral
Ano-rectal

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32
Q

2 Bronchial buds form from the respiratory diverticulum. What do they form in the 5th week? What does that then form?

A

Form the right and left 1y bronchi

- then forms secondary lobar bronchi (2 on left, 3 on right)

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33
Q

What do the 2 bronchial buds subdivide into?

A

Lung buds which push towards the pericardio-peritoneal canals
- but also “picking up” mesoderm to become cartilage, muscle, vasculature and pleura

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34
Q

What are the first 2 stages of lung development? Describe each stage.

A

(1) PSEUDOGLANDULAR 6-16 wks
- major elements has formed as far as terminal bronchioles (i.e. no gaseous exchange yet so not compatible with life)
(2) CANALICULAR 16-26/28 wks
- terminal bronchioles have 2/3 resp bronchioles which branch to 3-6 alveolar ducts (=> becoming more vascularised) NOT COMPATIBLE WITH LIFE

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35
Q

What are the second 2 stages of lung development? Describe them.

A

(3) TERMINAL SACCULAR 24/26 - 36wks/birth
- thin walled sacs lined by squamous epithelial cells (type 1 pneumocytes) become well vascularised => gaseous exchange can occur
- from wk20, type 2 pneumocytes begin to secrete surfactant - there’s wide individual variation
- wk 28 1000g babies can survive as have large enough s.a. for gaseous exchange and sufficient surfactant secretion
(4) ALEVOLAR PERIOD 28/36wks - birth(and up to 8yo)
- 50 mil alveoli at birth, 5/6 of alveoli develop post natally

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36
Q

What are the 3 necessities for survival?

A
  1. Thin walled alveolar ducts and alveoli
  2. Rich capillary bed essential for gaseous exchange. Before the terminal saccular period, the s.a. is too small and not sufficiently vascularised to support gaseous exchange
  3. Surfactant = complex mix of phospholipids that reduces the surface tension and facilitates expansion of alveoli
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37
Q

What is respiratory distress syndrome (RDS)? What is the mortality associated with RDS and what is done to reduce this?

A

Insufficient surfactant results in the collapse of the alveolar wall during expiration which results in RDS
RDS is responsible for 20% of deaths among newborns
- development of artificial surfactant and treatment with glucocorticoids (to stimulate surface secretion) have reduced mortality

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38
Q

What are the 2 types of abnormal lung development?

A

Pulmonary agenesis

Pulmonary hypoplasia

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39
Q

What are the 4 sources of origin of the diaphragm?

A
  1. Septum transversum = central tendon
  2. 2 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
  4. Ingrowth from the body wall
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40
Q

What is a congenital diaphragmatic hernia?

A

The absence of a pleuro-peritoneal membrane has left a hole in the diaphragm
- this allows the GI contents of the abdomen to herniate into the thorax and suppress lung development

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41
Q

Define (i) intrapleural pressure (ii) intrapulmonary pressure.

A

(i) always more negative than alveolar. Elastic nature of lung tissue versus ribcage and thorax trying pull apart visceral from parietal pleura. -4 mmHg
(ii) pressure within the alveoli – falls and rises over one respiratory cycle.

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42
Q

Describe the processes involved in inspiration .

A

Change in volume leads to a change in pressure
Contraction of diaphragm flattens domes, abdominal wall relaxes to allow abdominal contents to move down. This increases the volume of thorax by approx 500ml, the intrapleural pressure drops to 6mmHg and intrapulmonary is decreased by 1mmHg
Accessory muscles used in forced expiration - trapezius

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43
Q

Describe the processes involved in quiet and forced expiration.

A

QUIET - no direct muscle action. Elastic recoil drives air out of the lungs and the thoracic volume decreases by 500ml. The intrapulmonary pressure increases and air moves DOWN a pressure gradient
FORCED - contraction of abdominal walls forces contents up against diaphragm and internal intercostals pull ribs down

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44
Q

Define the term: work of breathing, and list what the work of breathing involves.

A

Energy is required to:

  • contract inspiration muscles (in quiet breathing diaphragm contraction = 75% energy expenditure)
  • stretch elastic elements
  • overcome airway resistance
  • overcome frictional forced arising from the viscosity of the lung and chest wall
  • overcome inertia of the air and tissues
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45
Q

What is airway resistance? What determines it?

A

It is the most significant non-elastic source of resistance
F = change in P/R
the amount of air that flows determined by change in pressure divided by resistance
greatest resistance to airflow is found in the segmental bronchi because the cross sectional area is relatively low and airflow is high and turbulent

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46
Q

What is compliance? What is the value of compliance in a healthy individual?

A

The distensibility/ease of stretch of lung tissue when external force is applied, or the ease with which the lungs expand under pressure
approx. 1L per pKa (1 L per 7.5mmHg)

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47
Q

What does high compliance mean? What are the 2 major determinants of compliance?

A

It means that there is a large change in volume for a given change in pressure
Determinants = elastic components and alveolar surface tension

48
Q

How can compliance be (i) reduced (ii) increased?

A

(i) replacing elastic tissue with non - elastic as lungs become stiffer (pulmonary fibrosis)
block smaller resp passages
increasing alveolar surface tension
decreasing the flexibility of the thoracic cage/ its ability to expand
(ii) Pulmonary emphysema. Due to alveoli rupture, creating larger air space and thus reducing s.a of lung. Impaired elastic recoil leads to poor deflation => trapping more air

49
Q

How is alveolar surface tension reduced in health? Describe conditions when it would be raised.

A

The presence of surfactant and type II alveolar cells as they prevent alveolar collapse

50
Q

What are the 3 types of diaphragmatic hernias? Be sure to mention where they are located.

A
  1. Postero-lateral: Bochdalek hernia
  2. Anterior: morgagni hernia
  3. Central hernia
51
Q

What causes changes in airway resistance?

A
  1. In inspiration, resistance decreases, this becomes an issue in disease stated where airway resistance is increased - i.e. asthma
  2. Pts with COPD tend to have over-inflated chests (barrel-chested)
52
Q

What are the 4 volumes that air in the lungs is divided into?

A
  1. Tidal Volume (TV): Volume of air breathed in and out in a single breath (0.5 l)
  2. Inspiratory Reserve Volume (IRV): volume breathed in by max inspiration at end
    of normal inspiration (3.3 l)
  3. Expiratory Reserve Volume (ERV): volume of air expelled by max effort at the end
    of normal expiration (1 l)
  4. Residual Volume (RV): volume of air in lungs at the end of maximum expiration ( 1.2 l)
53
Q

What are the 4 types of pulmonary capacities? Describe them with relation to the volumes.

A
  1. Inspiratory capacity (IC): TV + IRV
    - Volume or air breathed in by max inspiration at the end of a normal expiration (3.8 l)
  2. Functional Residual Capacity (FRC): ERV+RV
    - Vol 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)
  3. Vital capacity (VC) IRV+TV+ERV
    - Vol of air that can be breathed by max inspiration following a max expiration (4.8 l)
  4. Total lung capacity (TLC) VC+RV – key point – only a fraction of TLC used in normal breathing (6 l)
54
Q

What can you measure and can’t you measure with a spirometer?

A

CAN: TLC, VC, IC, FRC, ERV, TV, IRV

CAN’T: Residual Volume

55
Q

What is a spirometer?

A

A spirometer is used to measure and record volumes of inspired and expired air - producing a spirogram

56
Q

What is anatomical dead space?

A

areas of airway not involved gaseous exchange – nose and mouth, pharynx, larynx, trachea, bronchi, bronchioles – 150 ml on average.

57
Q

What is the location of the primary respiratory centre?

A

MEDULLARY
(1) Inspiratory (i.e. Dorsal respiratory group DRG)
- upper part of medulla oblongata
- function = exclusively inspiratory neurons
(2) Expiratory (i.e. Ventral resp. group VRG)
- anterior and lateral to inspiratory centre
- mix of inspiratory and expiratory neurons
- function = during forced breathing or when inspiratory centre is inhibited
PONTINE
(1) Pneumotaxic centre
- in upper pons
- function = controls medullary centres (esp. DRG through ). Influences respiratory centre so duration of inspiration is under control
(2) Apnuestic centre
- in lower pons
- function is to increase depth of inspiration by acting on inspiratory centre

58
Q

What is the function of the respiratory centres?

A

they collect sensory information about the levels of oxygen & CO2 in the blood which determines the signal sent to respiratory muscles

59
Q

What factors affect respiratory centres?

A
  1. Impulses from higher centres - cerebral cortex, hypothalamus, can stimulate or inhibit respiratory centres directly
  2. Stretch receptors of lung slowly adapting pulmonary receptors (= Hering-Breur Reflex)
  3. J receptors or pulmonary C-fibres
  4. Irritant receptors of lungs
  5. Proprioreceptors
  6. Thermoreceptors
  7. Pain receptors
  8. Cough reflex
  9. Sneezing reflex
  10. Deglutition reflex
60
Q

What is the equation used to calculate residual volume?

A

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

61
Q

What are chemoreceptors? What can they respond to?

A 
Respond to changes in chemical cons1tuents of blood or CSF.
They can respond to
- hypoxia
- hypercapnea (elevated CO2 in blood)
- increased H+ conc
62
Q

What are the 2 groups that chemoreceptors are classified as?

A

CENTRAL
- in medulla close to DRG, known as the chemosensitive area
- function: sensitive to an increase in H+ conc.
(H+ cannot cross BBB or CSF barrier but CO2 can and forms carbonic acid, which is unstable and rapidly dissociates to H+ and bicarbonate
PERIPHERAL
- around carotid sinus and aortic arch
- the carotid bodies have the greater effect on respiration
- sensitive to PaO2, PaCO2 (10x less than central though), pH, blood flow, temp.

63
Q

What determines how much gas dissolves in a liquid?

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 go into solution if its partial pressure is 10kPa than if it were 1kPa

64
Q

What happens is the partial pressure in the liquid becomes greater than that in the air?

A

Gas will move out of the liquid

65
Q

What 2 mechanisms regulate respiration?

A

NERVOUS

CHEMICAL

66
Q

What are J receptors? What is their function?

A

Present in the wall of alveoli, in close contact with pulmonary capillaries
Stimulated in conditions like pulmonary oedema, congestion, pneumonia and from endogenous chemicals (i.e. histamine)
Stimulation of said receptors induces apnea (= temp. suspension of breathing followed by rapid shallow breathing)

67
Q

What are irritant receptors of lungs?

A

rapidly adapting receptors that are powerfully stimulated by inhalation of irritants. They are found on the walls of bronchi and bronchioles. They induce rapid shallow breathing, mainly from shortening of expiration
They can also induce long deep augmented breaths - this is confusing as these are taken by mammals every 15-20mins to reverse slow collapse of lungs

68
Q

What do (i) tendons (ii) muscle spindles detect/monitor?

A

(i) found within diaphragm and intercostals. They detect the strength of muscle contraction
(ii) Monitors length of fibres both statically and dynamically (length and velocity)

69
Q

What are the various neuromuscular disorders?

A

CNS - trauma to brain and SC can cause partial or total loss of respiratory function
Poliomyelitis - about 25% require mechanical ventilation during acute phase
Diptheria - demyelinating neuropathy
Botulism - ventilation may be required for extended period
DMD - common cause of death is respiratory failure, secondary to pulmonary infection

70
Q

What is Dalton’s Law of Partial Pressures?

A

Each individual gas exerts a proportion of atmospheric pressure, according to its partial pressure
=> if atmospheric pressure changes then partial pressure also changes
AND if the proportion of gas changes, its partial pressure changes.

71
Q

What is the value of normal atmospheric pressure?

A

760mmHg

101.325 kPa

72
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
=> 10x more gas will go into solution if its partial pressure is 10kPa rather than 1kPa

73
Q

What happens if the partial pressure of the liquid becomes greater than in air? How does this relate to the respiratory system?

A

The gas will move out of the liquid
- gives the basis for oxygen moving into the blood in the lungs, whereas carbon dioxide moves out of the blood in the lungs

74
Q

What does the absolute level of gas dissolved in a liquid depends on?

A

The solubility of the gas

75
Q

Describe the composition of Alveolar Gas.

A

It is NOT atmospheric air
- the conducting passageways of the respiratory system humidify the air (warmed and moistened air water vapour pressure of 47mmHg)
=> 760-47 = 713 mmHg

76
Q

What is the pressure of (i) oxygen (ii) carbon dioxide in the lungs?

A

(i) 104 mmHg

(ii) 40 mmHg

77
Q

What is the s.a of the lungs?

A

LARGE

50-100 m2

78
Q

What is the concentration gradient of oxygen between the alveoli and the venous blood of the pulmonary capillaries? What direction - as a result of this - does oxygen move in?

A

alveolar air = 104 mmHg
venous blood = 40 mmHg
=> oxygen diffuses rapidly from alveoli to pulmonary capillary

79
Q

How many times faster does CO2 diffuse compared to oxygen?

A

20 times

80
Q

How long does it take blood to pass through the pulmonary capillaries (i) at rest (ii) in exercise?

A

(i) 1 second

(ii) 0.3s

81
Q

What is the concentration gradient of carbon dioxide between the alveoli and the venous blood of the pulmonary capillaries? What way does it move?

A

alveolar = 40 mmHg
venous = 45 mmHg
moves from capillary -> alveoli

82
Q

What are various changes to respiratory membranes?

A

OEDEMA - thickness increases and the full transit time may not be sufficient to complete full gas exchange. It has a more marked effect on oxygen than carbon dioxide (this is due to the greater solubility of carbon dioxide)
EMPHYSEMA - s.a decreases so gas exchange reduced
MUCUS/AIRWAY INFLAMMATION/TUMOUR - gas entry inhibited =. exchange reduced

83
Q

Describe the movements of gases (CO2 and oxygen) at the tissues?

A

The gradients are reversed
=> CO2 moves INTO blood from lungs
O2 moves OUT of blood into tissues

84
Q

How does altitude affect PO2?

A

Atmospheric pressure is reduced => PO2 is also reduced

HB saturation reduced, Increased release of erythropoeitin

85
Q

What are the pressure values for Denver Colorado (5300 ft above sea level)?

A

Atmospheric = 632 mmHg (was 760)
Inspired PO2 = 125 mmHg (was 149)
Alveolar PO2 = 84 mmHg (was 104)
Alveolar PCO2 = 34 mmHg (was 40)

86
Q

What are the effects of high pressures on blood gases?

A

Increased risk of air embolism and decompression sickness
N2 can be forced into the bloodstream and bubbles form
- bubbles can cause lethal emboli, they are extremely painful in joints and can cause a stroke in the brain

87
Q

What are the 2 main ways that oxygen is carried in the blood? Describe them both.

A
  1. DISSOLVED IN PLASMA
    - proportional to partial pressure BUT remember O2 is poorly soluble
    => arterial blood with a PO2 of 100mmHg contains 0.3 ml O2/100ml.
    - Tissue requirements at rest are about 250ml O2/min but this would only deliver 15ml O2/min => not efficient way to deliver O2 to tissues
  2. CARRIAGE BY HAEMOGLOBIN
    - O2 forms an easily reversible combo with Hb
    - post co-operative binding = once the first oxygen is bound its much easier for the next 3 to bind (i.e. Hb saturation increases)
    - this produces an oxygen - haemoglobin dissociation curve that’s sigmoidal
88
Q

What are the various factors that influence Haemoglobin saturation? Describe them.

A
  1. Increased temperature, H+, CO2 and 2,3-bisphosphoglycerate all shift the curve to the RIGHT
    - they do this by modifying the 3D structure of Hb, decreasing its affinity for oxygen => shift to right
    - increased CO2 leads to increase in H+ which weakens HbO2 interaction = BOHR EFFECT
    - at the lungs the curve shifts to the left and Hb’s affinity for O2 is increased
89
Q

How is the amount of oxygen carried in the blood calculated?

A

= amount carried by Hb + amount dissolved

TOTAL = ([Hb]capacity%saturation) + amount dissolved

90
Q

What are the 3 ways that carbon dioxide is transported in the blood?

A
  1. DISSOLVED IN PLASMA
    - is about 7-10% of transported CO2
    - plasma has a greater solubility than oxygen => this mechanism has a more significant effect in respiration overall
  2. BOUND TO HB
    - 10-20% of transported CO2
    - Binds to the amino acids, not the haem (no comp with O2) = carbaminohaemoglobin
    - the loading and unloading is directly related to PCO2 and the degree of oxygenation of Hb
  3. AS BICARBONATE
    - 70 to 80% transported CO2
    - CO2 dissolves in water to form carbonic acid. This is unstable and rapidly breaks down to H+ and HCO3- (bicarbonate)
    - the first stage of this reaction is slow in plasma but presence of carbonic anhydrase in RBC makes v.rapid. H+ binds to Hb
    - Chloride shift = Cl- move into RBC to maintain electrical balance
91
Q

What is the Haldane effect?

A

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

92
Q

What influence does CO2 have on blood pH? Explain how the pH can be calculated.

A

Alteration of alveolar ventilation (i.e. altering CO2 elimination) can change the acid base status of blood
The pH can be calculated from Henderson-Hasselbach eqn : pH = pK + log [bicarbonate] / [CO2]

93
Q

What pH levels suggest (i) acidosis (ii) alkalosis? How does each come about?

A

(i) < 7.35
(ii) > 7.45
If ventilation decreases, CO2 increases, pH falls and HCO3- increases = respiratory alkalosis
If pt hyperventilates, blowing out more CO2, pH rises and levels of HCO3- falls = respiratory alkalosis

94
Q

What is ventilation?

A

The change in volume through the respiratory cycle
=> an alveolus that’s already open and extended at the start of the cycle will have less ventilation than a small, non extended one.
i.e. the change in volume compared to the resting volume

95
Q

Why does the base of the lung change volume more than the apex?

A
  1. The lower ribs are more curved and mobile
  2. The action of the diaphragm expands the lower lobes more than upper - partly because upper lobes are attached to main bronchi and upper airways => less easily stretched tissue
  3. Lower lobes have greater compliance (larger compliance means a larger change in volume)
  4. Small role = gravity
    - weight of lung pulls down on pleura => apex has more -ve intrapleural pressure so alveoli more extended already
96
Q

Describe the bronchial circulation.

A

Part of the systemic circulation as the bronchial arteries are branches of the descending aorta
Bronchial conducting portion re-joins circulation in pulmonary vein => ‘diluting’ slightly the oxygenated blood with deoxygenated
FUNCTION = supply O2 to lung parenchyma, airway smooth muscle pulmonary arteries and veins, and pleura
Also the conditioning (warming) of inspired air

97
Q

With regards to the pulmonary blood flow; (i) How much blood enters its circulation each min? (ii) What is the vol of the pulmonary capillary network at rest? (iii) stroke volume?

A

(i) about 5L
(ii) about 100 ml
(iii) about 70ml

98
Q

What is transmural pressure?

A

The balance between alveolar pressure and BP

Blood flow through the capillaries depends on this

99
Q

When will blood flow?

A

When the blood pressure is GREATER than the alveolar pressure

100
Q

What is the value of the hydrostatic pressure difference between the base and apex of the lung?

A

about 23 mmHg

101
Q

What happens at the apex of the lung is alveolar pressure is greater than blood hydrostatic pressure?

A

The capillary will be closed

- this means that they are ventilated but not perfused and so are considered alveolar dead space

102
Q

What is flow determined by in zone 2 of the lungs?

A

By arterial-alveolar pressure difference

103
Q

What is the pressure like in (i) zone 2 (ii) zone 3 of the lungs?

A

(i) alveolar pressure is lower than systolic arterial but may be higher than diastolic arterial and venous pressure
(ii) alveolar pressure lower than both arterial and venous pressure

104
Q

In zone 3, what are the state of the capillaries? Explain.

A

They are distended as a consequence of transmural pressure

- there is continuous flow

105
Q

What is the V/Q ratio of (i) the lung (ii) the base (iii) 2/3 up from base (iv) apex?

A

(i) 0.85
(ii) 0.6 (more perfusion than ventilation)
(iii) 1
(iv) 3

106
Q

What are the 3 main scenarios for V/Q matching?

A
  1. Perfect matching: well ventilated alveoli with good perfusion of blood, blood equilibrates with alevolar air and is rich in O2 (=> low in CO2)
  2. Poorly ventilated alveoli with rich blood supply: alveolar air equilibrates with blood and blood will tend towards the same composition as venous because less fresh air is being brought in. Low PO2, high PCO2
  3. Well ventilated alveoli poorly perfused with blood: blood leaving alveoli low in CO2 but as Hb is fully saturated, there won’t be a significant increase in O2 levels
107
Q

At low V to Q ratios (e.g. base of lung) what is the effect on on (i) CO2 conc (ii) O2 conc?

A

(i) CO2 diffuses from blood -> alveoli but CO2 isn’t taken away as rapidly (as V is low)
=> CO2 accumulates in alveoli and higher steady state PO2 occurs (42 instead of 40 mmHg normally)
(ii) O2 diffuses from alveoli into blood but since V is low, O2 taken up by blood isn’t fully replenished by new air entering the lungs. O2 depleted in alveoli and new steady state low PO2 occurs. (90 instead of 100mmHg normally)

108
Q

At high V to Q ratios (e.g. apex of lung) what is the effect on on (i) CO2 conc (ii) O2 conc?

A

(i) CO2 diffusing from blood is nearly all blown away => CO2 in alveoli is depleted till a new lower steady state level occurs (28 instead of 40 mmHg normally)
(ii) O2 diffusing from alveoli isn’t taken away by blood as much as normal because relative blood flow is lower BUT O2 is replenished with each breath O2 accumulates, diffusion carries on and a new higher PO2 level occurs (130 instead of 100 mmHg normally)

109
Q

What is hypoxic vasoconstriction? Why is this important at birth?

A

An intrinsic effect which diverts blood away from poorly ventilated areas
When first born (before 1st breath) the lungs are vasoconstricted and the resistance is high, with the first breath both vasoconstriction and resistance decrease

110
Q

What are the locations of peripheral and central chemoreceptors?

A

PERIPHERAL - carotid and aortic bodies

CENTRAL - ventro-lateral medulla

111
Q

What do the PCR and CCR monitor and respond to?

A

PCR = specialised receptor cells (glomus type I) that are stimulated primarily by a decrease in PO2 and an increase in H+ (which occurs as a result of increased PCO2) Carotid are more important than aortic in respiration. Both stimulated primarily by a decrease in PO2. Sensitised by CO2 and pH
CCR - excitatory input to DRG. Stimulated by an increase in H+ and CSF but H+ doesn’t cross BBB => are really detecting PCO2

112
Q

What is the consequence of a (i) raised PCO2 (ii) lowered PCO2?

A

(i) CO2 crosses BBB, => raised in blood, the pH of CSF decreases. This has excitory input to DRG in medulla and resulting increased ventilation “blows off” CO2, reducing arterial PCO2.
(ii) Ventilation is depressed, the firing rate from the chemoreceptors AP falls => decrease in excitatory input to DRG so respiration is inhibited

113
Q

What value must the PO2 drop below to become a stimulus for ventilation?

A

must drop below 60 mHg before it becomes a major stimulus for ventilation.

114
Q

What is the consequence of a (i) raised arterial pH (ii) lowered arterial pH?

A

(i) causes an increase in ventilation - metabolic acidosis (trying to drive off CO2)
(ii) causes a decrease in ventilation

115
Q

How do other inputs influence the control of ventilation?

A
  1. Muscle, joint receptors
    - sense: chest wall position and muscle tension
    - effect: normal breathing
  2. Irritant receptors
    - sense: chemicals, dust, cold air
    - effect: coughing and bronchoconstriction
  3. Stretch receptors
    - sense: lung inflation
    - effect: inflation terminates
  4. J receptors
    - sense: chemicals, stretch, pulmonary oedema
    - effect: shallow breathing, bronchoconstriction, mucus secretion

MD3001 (14 decks)

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