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HOM > Respiration > Flashcards

Respiration Flashcards

1
Q

How does the airway change as it goes deeper into the lung (3)

A

Becomes
Narrower
Shorter
More numerous

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2
Q

How is the airway divided anatomically

A

24 regions

Numbered 0-23

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3
Q

How are the 24 generations divided

A

The first 17 generations are the conducting zone (anatomical dead space)

Generations 17-23 are the respiratory zine

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4
Q

What is the role of the conducting zone (3)

A

To warm and humidify the air inspired

To distribute air into the depths of the lung

To serve as a bodily defence against dust and bacteria

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5
Q

Describe the structure of the conducting zone

How does this lead into the respiratory zone

A

Trachea —> main bronchus —> lobar and segmental bronchi —> terminal bronchioles

—> respiratory bronchioles —> alveolar ducts —> alveoli

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6
Q

What is the smallest airway that does not allow gas exchange

A

Terminal bronchioles

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7
Q

Which parts of the airway are subject to thoracic pressure

How do they not collapse from the increased intrathoracic pressure during forced expiration

A

First 4 regions

They have cartilage arranged in U shaped rings

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8
Q

How does the arrangement of cartilage change through the airway

A

Initially in U Shaped rings on first 4 regions
Then becomes plates of cartilage in the lobar and segmental bronchi

It disappears in the bronchioles

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9
Q

How are bronchiolar airways maintained

A

By elastic connections to the parenchyma

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10
Q

What is the conducting zone supplied by

A

The bronchial circulation

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11
Q

What is the volume of the respiratory zone

A

~2.5 to 3 litres

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12
Q

How fast do RBC flow through pulmonary circulation

A

Less than a second

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13
Q

How does inspired air enter the lungs

A

Inspired air flows down by bulk flow, but the increased area of the conducting zone reduces the forward velocity of airflow

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14
Q

Give an advantage of the reduced airflow velocity to the alveoli

A

Dust and pollutants usually settle out before the alveoli

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15
Q

What is the driving force of oxygen/ CO2 exchange

A

Pressure gradient across the alveoli/ blood interface

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16
Q

Give the equation for Net Flux

A

(C1-C2) x (area/thickness) x D

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17
Q

How many alveoli in an adult human

A

300-500 million

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18
Q

How close can blood come to the air in the alveoli

A

0.5μm

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19
Q

How does the body manipulate Fick’s law to maximise diffusion

A

Large alveolar surface area and close association to the capillaries

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20
Q

Give 2 equations for flow for respiratory physiology

A

Flow = Δpressure x K

Or

Flow = Δpressure/ resistance

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21
Q

Why is the equations for flow important for respiration

A

A pressure gradient must be produced when breathing

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22
Q

Describe the thoracic pleura

A

Visceral pleura encases the lungs and is separated from the parietal pleura by a ~10μm thick layer of fluid

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23
Q

What determines the volume of the thoracic cavity

What is normal intrapleural pressure

A

The balance of the inward elastic recoil of the lungs and the outward elastic recoil of the chest wall

-5cmH2O

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24
Q

How is a pressure gradient created in the lungs

A

Increase thoracic volume and decrease intrapleural pressure
This is done by contraction of the diaphragm and the movement of the intercostal muscles, widening the thorax and raising the sternum

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25
Q

What happens if the lung is punctured

A

Pressure within would equilibrate with the atmosphere and the lungs would collapse due to their inward elastic recoil. This is pneumothorax

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26
Q

What stops both lungs collapsing in a right pneumothorax

A

The mediastinal membrane divides the thoracic cavity into 2 airtight compartments

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27
Q

What is eupnea

A

Quiet respiration

A passive process whereby Respiratory muscles relax, allowing the elastic potential of the lungs to recoil.

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28
Q

Does eupnea always occur

A

No

During exercise other muscles are recruited, such a abdominal muscles helping to raise the diaphragm

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29
Q

What are trans mural pressures

A

Pressures across a wall

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30
Q

How many trans mural pressures are there In The basic thoracic cavity

How are they all worked out

A

Transpulmonary
Trans chest wall
Trans total system

The pressure differential of the inside minus the outside

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31
Q

What is trans pulmonary pressure in normal humans

The greater the trans pulmonary pressure the ____ the lungs expand

A

always Positive

More

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32
Q

How do diaphragmatic contractions and thoracic cage expansion affect pleural pressure and trans pulmonary pressure

A

Decrease from -5 to -8cmH2O

Trans pulmonary increases

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33
Q

What is distending pressure

A

The pressure that keeps the lungs inflated

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34
Q

Why does airflow at the end of inspiration stop

A

Alveolar pressure equals atmospheric pressure

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35
Q

Why does air flow into the alveoli basically

A

Alveolar pressure is greater than atmospheric pressure and air flows from the lungs to the mouth until alveolar pressure= atmospheric pressure

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36
Q

When is capacity used for the spirometer

A

When a lung volume can be broken down into two or more smaller volumes

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37
Q

Are gases collected by the spirometer at body temperature

A

Nope

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38
Q

How is water vapour an imperfect gas

A

It changes its state from vapour to liquid with temperature changes within the physiological range

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39
Q

Give the ideal gas equation for respiration And the units

A

PV=nRT

P=mmHg
V= litres
T=K

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40
Q

What is R in the respiratory ideal gas equation

Give the units

A

62.36mmHg x L x mol-1 x K-1

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41
Q

How many litres does one mole of gas occupy at STPD

A

22.4

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42
Q

What is the relationship between a constant amount of gas at 2 different sets of temperature and pressure defined by

A

P1 x V1. P2 x V2
———— = ———-
T1. T2

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43
Q

How to calculate the new volume of saturated gas using the PV=nRT equation

A

Use P1V2/T equation
Use Table to find PH2O at new temperature and subtract that from the original partial pressure.
Input this new value into P1V1/T1=P2V2/T2

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44
Q

What is BTPS

A

Body temperature and Pressure standard

The physiological conditions within the body

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45
Q

What is the partial pressure of O2 in alveolies

A

13.2%

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46
Q

What is the partial pressure of CO2 in alveolies

A

5.3%

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47
Q

What is the partial pressure of N2 in alveoli

A

75.4%

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48
Q

What is the partial pressure of Water in alveolies

A

6.2%

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49
Q

Why do PCO2 and PO2 vary around the mean

A

Breathing is intermittent

A small amount of air is taken into the lungs with each breath relative to the volume of gas that is not exchanged (FRC)

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50
Q

What is indicator dilution technique used for

A

To determine residual volume and functional residual capacity

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51
Q

What is physiologic dead space

A

Alveolar dead space + anatomic dead space

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52
Q

Give typical breathing frequency and tidal value at rest

A

12 breaths/ min

500ml

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53
Q

What is the total normal inspired ventilation rate (Vi)

How much tidal volume actually gets to the alveoli for exchange

A

6 L/min

350ml

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54
Q

Is dead space constricted to the conducting zone

A

No

Doen alveoli have no blood flow or may have reduced blood flow

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55
Q

How much dead space is there in a seated individual weighing 170lb

A

170ml

Dead space ~ person’s weight in pounds

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56
Q

What is VE

A

Expired minute volume

VE= Vt x breathing frequency

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57
Q

What assumption is VE based on

A

Volume inspired=volume expired

Not quite true as our western diet means less CO2 is produced than O2 consumed

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58
Q

What is the volume of fresh air reaching the alveoli known as

Give the equation

A

Alveolar ventilation

Va=(Vt-Vd) x f

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59
Q

What is Vd

A

Volume of dead space

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60
Q

How can alveolar ventilation be estimated

A

From the volume of CO2 expired ina given time and the fractional concentration of CO2 in alveolar gas. All the expired gas must have come from the alveoli

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61
Q

Give the equation for volume of CO2 expired per minute

A

Va x FACO2

(Where FA CO2 is the fractional concentration of CO2 in alveolar gas

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62
Q

Va=?

A

Volume CO2 expired/ min
————————-
Fractional concentration of CO2

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63
Q

How is FA CO2 obtained

A

Sampling end tidal volume

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64
Q

What does VA=
To convert to correct units

Give units of each

A

Va(L/min)=(VE CO2 / PA CO2) x K

VE CO2: (ml/min)
PA CO2 (mmHg)
K: (mmHgx L/min

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65
Q

Va is at _____ and VE CO2 is at ____

A

BTPS

STPD

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66
Q

What is the conversion constant usually for Va

A

0.865 mmHg xL/ml

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67
Q

How are Va and PACO2/ FA CO2 relates

A

Inversely proportional

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68
Q

How does PA CO2 relate to CO2 in arterial blood

A

In equilibrium

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69
Q

How does hyperventilating affect P CO2 in arteries

A

Halves arterial P CO2

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70
Q

How does hypoventilation affect arterial PO2

A

Doubles arterial P CO2

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71
Q

How is Pa CO2 monitored by an anaesthetist

A

Using an infrared CO2 analyser on end tidal expiration

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72
Q

If a patient under anaesthetic had a PA CO2 of 80mmHg what would the anaesthetist do

Why

A

Double ventilation

Ratio of VE CO2/ Va is twice normal ratio

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73
Q

How does exercise affect VE CO2 and therefore Va

A

If VE CO2 Increase 5x, alveolar ventilation must be increased to maintain arterial P CO2 at 40 mmHg

Respiratory regulation is designed to keep arterial P CO2 at 40 mmHg despite changes to CO2 production

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74
Q

What happens when arterial P CO2 increases

A

Alveolar PO2 must decrease as total pressure cannot exceed atmospheric pressure

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75
Q

Does doubling alveolar Ventilation lead to a doubling of arterial PO2?

A

No

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76
Q

Why is the quantitative relationship between alveolar ventilation and arterial PO2 complex

A

PO2 does not equal 0

Respiratory exchange ratio (R) is not usually 1

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77
Q

What does it mean to say that R does not equal 0

A

More oxygen is removed than CO2 added

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78
Q

When would R be 1

A

If we only ate carbs

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79
Q

What is the alveolar gas equation

A

PA O2= PIO2 - PACO2 [FIO2+(1-FIO2)/ R]

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80
Q

What is PIO2 and FIO2

A

Partial pressure of inspired oxygen

Fractional concentration of O2 in the inspired air

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81
Q

What is the R value in a normal resting individual

A

0.82

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82
Q

What are normal alveolar values of PO2 and PCO2 at sea level

A

~100 and 40mmHg respectively

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83
Q

Why is alveolar PN2 increased

A

R<1

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84
Q

How does total venous pressure compare to atmospheric pressure

A

Venous is lower as PO2 decreases more than PCO2 increased

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85
Q

Which 2 physical characteristics of the respiratory components affect effectiveness of alveolar ventilation

A

Elastic properties of the lung and chest wall

Resistance of the respiratory tree

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86
Q

How does lung volume at any point in deflation compare to volume in inflation

A

Lung volume at any given pressure during deflation is larger than during inflation

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87
Q

When does lung volume fall to 0 if there is no trans pulmonary pressure

A

NEVER

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88
Q

What is static compliance

A

The volume change per unit increase in trans pulmonary pressure when there is no air flow

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89
Q

What is the normal range of trans pulmonary pressure

A

-2 to -10 cmH2O

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90
Q

How compliant is the lung? Give a value

A

0.2L/cmH2O

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91
Q

At larger lung volumes the lung is _____ compliant

What kind of curve does this give

A

Less

Flatter slope of pressure volume curve

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92
Q

Specific compliance=?

A

Compliance
——————
FRC

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93
Q

What is FRC?

A

Functional residual capacity

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94
Q

How does the specific compliance compare from mice to elephants ?

A

It is a similar value for all mammals (0.08/cmH2O)

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95
Q

Is compliance uniform throughout the lung?

A

No the top is less compliant than the base (regional compliance)

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96
Q

How does regional compliance occur

A

The downward pull of gravity results in lower pleural pressure (more negative) at the apex than the base

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97
Q

What does regional compliance result in

A

Higher trans pulmonary pressure at the apex results in alveoli being expanded more than alveoli at the base.

This volume difference places the alveoli in the apex in a less compliant portion of the pressure volume curve relative to the base

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98
Q

The base of the lung undergoes a _____ change in volume for a given pressure change relative to the apex

A

Greater

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99
Q

Why can the lower lung undergo a great increase in volume

A

It is at a lower volume

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100
Q

As one takes a breath in from FRC a greater proportion of the tidal volume goes to which lung region

A

Base

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101
Q

Where does greater alveolar ventilation occur

Prove it

A

The base of the lung

Use Xe 133 and a radiation camera at different levels of lung
This shows lower zone has higher ventilation/ unit volume than middle and low zone

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102
Q

Why do lower lung zones ventilate more

A

As the lung approaches residual volume, intrapleural pressure> atmospheric pressure
This compresses the base of the lung

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103
Q

When can ventilation of the lower lung occur

A

Only once intrapleural pressure falls below atmospheric pressure

The apex ventilates well whenver

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104
Q

What is the compliance like in a distensible lung

A

Abnormally high

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105
Q

Give the consequences of reduced lung compliance

A

Stuff lung -> more working for same level of ventilation -> cost of breathing increases

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106
Q

Name some causes on reduces lung compliance

A

Fibrosis

Scarring of alveoli such as when respiratory system is overloaded with pollutants

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107
Q

Name 4 pollutants, what they cause and whose lungs are most frequently affected

A

Carbon particles: “black lung” in miners
Silica particles: “silicosis” in glass workers
Asbestos particles: “asbestosis” in boiler workers
Cellulose particles: “brown lung” in textile workers

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108
Q

What happens in emphysema?

A

Increased lung compliance due to alveolar damage leading to a flabby lung

There is no problem inflating the lung but they have great trouble exhaling.

This is caused by a loss of elastic recoil

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109
Q

When are the opposing chest wall and lung pressure equal

A

At FRC

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110
Q

How to work out trans mural pressure of the lung and chest wall together

A

Add their individual values

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111
Q

How does reduced compliance affect FRC?

A

FRC is reduced

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112
Q

What dictates chest walls compliance

A

Rigidity and shape

Also depends on diaphragm and abdominal structures

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113
Q

How does obesity affect chest wall compliance

A

Compliance can be decreased if chest wall is deformed

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114
Q

Other than obesity what else may decrease chest walk compliance

A

Elevation of diaphragm (eg tumour)

Spasticity or rigidity of musculature

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115
Q

How does surface tension occur

A

Arises at air-liquid interfaces
Attractive forces between water molecules are stronger than those between molecules and the air
The surface therefore because as small as possible

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116
Q

Give LaPlace’s Law

A

Pressure=4x surface tension/ r

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117
Q

What is LaPlace’s Law applied to alveoli?

Why is it different?

A

P= 2x surface tension/ radius

The alveolus has only 1 air-liquid interface

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118
Q

Who first appreciated the importance of lung surface tension

A

Von Neergaard in the late 1920s

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119
Q

Describe Von Neergaard’s experiments

What were the conclusions (2)?

A

Cat lung was inflated and deflated using air then deflated with saline

1) Saline inflation gives a steeper pressure volume relationship. (Without the air-water interface, the lungs are more compliant)
2) There is greater hysteresis between air filling and emptying curves than for saline filled lungs

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120
Q

How much does surface tension account for in lung elastic recoil

A

2/3 to 3/4

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121
Q

What did scientists testing noxious fumes find

What discovery resulted

A

Edema foam coming from the lungs had very stable air bubbles due to reduced surface tension

Pulmonary surfactant

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122
Q

What is pulmonary surfactant

A

Secreted by cells lining the alveoli (particularly alveolar type 2 cells) that lowers surface tension
It is a rich phospolipid

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123
Q

How does pulmonary surfactant reduce surface tension

How is it made

A

DPPC

Dependant upon availability of precursors (ie glucose, palmitate and choline) supplied by pulmonary circulation

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124
Q

How is the effect of surfactant on surface tension studied

A

With a surface balance/ Langmuir trough
A v stable tray containing saline
The area of the surface is expanded and compressed simulating inflation and deflation
Saline, detergent and lung washings are added separately and results of relative area(y) vs surface tension(x) are compared

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125
Q

What are the effects of adding saline, detergent and lung washings to a Langmuir trough

A

Pure saline: surface tension of 70dynes/cm, irrespective of surface area

Detergent: reduces surface tension, independent of surface area

Lung washings: reduces surface tension but dependent on area with a marked hysteresis. At very low area surface tension falls to vvv low values

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126
Q

What is the role of surfactant

A

To reduce surface tension in alveoli to increase compliance

Allows alveoli of different sizes to coexist

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127
Q

What would happen to differently sized alveoli without surfactant

A

LaPlace’s Rule means there would be greater pressure in the smaller alveoli, forcing air into the larger. Therefore at low lung volumes small alveoli would collapse (this process is called atelectasis)
Surfactant stabilises the small alveoli by reducing surface tension in smaller alveoli

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128
Q

How does surfactant decrease surface tension

A

Molecules of DPPC are hydrophobic at one end and hydrophilic at the other

When aligned on the inner alveoli surface the IMF oppose the attractive forces between surface water molecules

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129
Q

What is the reduction of surface tension dependant on

When is it greatest

A

The amount of surfactant per unit area

When the film is compressed

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130
Q

When is the reduction in surface tension greatest and why is this?

A

When the film of surfactant is compressed because at small surface areas the DPPC Molecules are crowded close together resulting in greater repulsion and thus the opposition of surface tension is increased

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131
Q

What happens to DPPC at low lung volumes

What happens when the lungs expand

A

DPPC molecules are compressed and some molecules are pushed out of alignment, off the surface layer

Alveoli inflate so amount of DPPC per unit area will be less, resulting in a decreased ability to resist surface tension. New surfactant is required to form a new film.
This redistribution of the film may account for hysteresis

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132
Q

Why might patients who have undergone thoracic or abdominal surgery find it hard to breathe deeply

A

Alveoli expand more than usual in a deep breath so more surfactant is required
These patients may have poor surfactant spreading, which leads to atelectasis due to increased surface tension

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133
Q

When is the foetal lung triggered to fully mature

A

85-90% of the gestation period

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134
Q

Why is the lung functionally immature before 85% of gestation period

A

It does not have adequate surfactant production

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135
Q

Which respiratory disease is a common cause of death in premature babies?
Describe

A

Infant Respiratory Distress Syndrome (IRDS)
JFK lost a child to IRDS

Laboured breathing due to increased surface tension and the decreased compliance
Children would “magically” get better after ~18 days. This is because Type 2 lung cells are late to develop even after birth

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136
Q

How is Hylem Membrane Disease/ IRDS treated

A

Ventilatory delivery is kept at a positive pressure head so that the pressure is always above atmospheric, keeping the alveoli open, until development of Type 2 cells
This change increased survival rate from 20% to 80%

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137
Q

What do some physiologists believe is the most important role of surfactant

A

Keeping the alveoli dry

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138
Q

How does surfactant keep alveoli dry

A

The inward contracting force that collapses alveoli also lowers interstitial pressure ( making it more negative)
This pulls fluid in from the capillaries
Surfactant reduces this by lowering the surface tension

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139
Q

Where does turbulent air flow occur

A

In large airways such as the trachea and large bronchi at high flow rates (eg during exercise)

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140
Q

Where does laminar flow in the respiratory tree occur

A

Small airways where flow is slow

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141
Q

What kind of airflow is most prominent in the bronchial tree

A

Transitional

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142
Q

Give the equation that defines laminar flow

A

Flow= ΔP/ resistance

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143
Q

What did Poiseuille say resistance =?

A

8nl/πr^4

n= viscosity 
L= tube length 
r= tube radius
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144
Q

What is more important for resistance of a fluid: viscosity or density

A

Viscosity

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145
Q

Why would you assume that the small airways would provide the most resistance

Where in fact is the site of real resistance

A

Small radius: if you decrease the radius by a half, the resistance increases 16 fold

Medium sized bronchi

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146
Q

Why do the v small airways not account for the largest reduction in resistance

A

There are many small airways in parallel. Individual resistance is high but the large number increases cross sectional surface area

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147
Q

What is the equation for resistance in parallel

A

1/R total = 1/R1 +1/R2 +…+1/Rn

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148
Q

What is the problem with small airways only accounting for a small % of total resistance

A

Diseases often start in the small airways but go undetected for a long time before the increased airway resistance is detected

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149
Q

What suspends small airways

A

Parenchyma which acts as guy wires

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150
Q

Discuss autonomic control of bronchial smooth muscle

A

Parasympathetic stimulates of cholinergic fibres causes bronchial constriction and stimulation of mucus secretion

Sympathetic stimulation of adrenergic fibres results in dilation and inhibition of glandular secretions

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151
Q

What drugs can cause bronchial dilation

When are they often used

A

Isoproterenol and adrenaline cause dilation by stimulation of the β2 adrenergic receptors in the airways

To treat asthma attacks and marked bronchial constrictions induces by environmental insults eg smoke and dust particulates

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152
Q

How do PCO2 levels affect airway constriction

A

Increased PCO2 in conducting airways induces dilation while decreased PCO2 induces airway constriction

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153
Q

Why is helium used in underwater breathing simulations

A

Helium reduces the resistance of breathing

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154
Q

What does the fact that both density and viscosity affect airflow suggest about airflow

A

Airflow is not simply laminar

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155
Q

Describe a flow vs volume graph for forced expiration

What is on the X axis

A

Flow increases to a peak but most of the flow is an effort independent decrease

Volume (from TLC to RV)

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156
Q

What is EPP (respiratory)

A

Equal pressure point

The point in the airway during forced expiration where trans airway pressure is 0

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157
Q

Why can’t peak flow rate be increased

A

Increased effort increases intrapleural pressure as well as alveolar pressure so trans airway pressure remains constant

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158
Q

What are maximum flow rates primarily determined by and why?

A

The lungs’ elastic recoil

This is what generates alveolar pressure and therefore the alveolar-intrapleural pressure

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159
Q

How does maximum flow rate change as lung volume decreases

What is the main reason for this

A

Decreases

Due to the decrease in elastic recoil

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160
Q

How do healthy lungs “push” the EPP up the lung

What happens in emphysema

A

Because of elastic recoil, the normal lung has added pressure that overcomes intrapleural pressure so EPP is pushed up airway to where the airways won’t collapse due to cartilaginous rings

Less elastic recoil therefore less added alveolar pressure and EPP is moved lower and airways can collapse

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161
Q

What causes wheezing in patients with emphysema

A

Smaller airways collapse due to lowered EPP so there is no airflow here
Airway pressure in collapsed segments rises to equal alveolar pressure and airway reopens

EPP is set by lung compliance

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162
Q

What is FVC and how is it measured

A

Forced vital capacity

Measured by forced maximal exhalation

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163
Q

What is FEV1 and how is it normalised

A

Forced expiratory volume of air in one second

Normalised for lung size by expressing it as a fraction of FVC (FEV1/FVC)

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164
Q

What is FEV1/FVC in normal conditions

A

0.8

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165
Q

What is FEF25-75%

A

Forced expiratory flow rate over the middle 50% of the FVC

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166
Q

What is net diffusion dependant on

A

Surface area
Diffusion pathway
Diffusion gradient for both O2 and CO2
Diffusion coefficient

167
Q

Give Henry’s Law

Why is this useful

A

Concentration = partial pressure x solubility

It is more useful to talk about partial pressure of respiratory gases than concentration

168
Q

Give Fick’s equation using partial pressure and solubility

A

Net flux=

ΔP x s x area/thickness x D

169
Q

What is D

A

Diffusion coefficient of gas

170
Q

What is d

A

The diffusion constant for a specific constant In a specific medium

d is proportional to solubility/ square root of Mr

171
Q

Is a smaller molecule faster or slower to diffuse

A

Faster

172
Q

Give solubility constant for CO2 and O2

Give the units

A

O2: 0.03
CO2: 0.7

(C)O2/ litre plasma/ mmHg

173
Q

How much more soluble is CO2 than O2 in plasma?

A

23x

174
Q

How much faster does CO2 diffuse

A

20x faster than O2

175
Q

What is the transit time from the beginning to the end of the pulmonary capillary

A

<1s

176
Q

What is a diffusion reserve

A

When gas equilibration is accomplished with room to spare

177
Q

What is adequate equilibration of respiratory gases at the alveoli dependant on

A

Appropriate matching of alveolar ventilation with alveolar blood perfusion

178
Q

How much O2 is dissolved in arterial blood at 100mmHg

Give cardiac output in heavy exercise

Therefore what is O2 delivery to the periphery

A

3ml/O2 litre

30L/min

3x30=90ml/min

179
Q

2 ways that O2 is transported around the body

A

Dissolved

Bound to Haemoglobin

180
Q

How many polypeptide chains in a molecule of Hb

A

4

2 α and 2 β

181
Q

What happens to Hb type F after birth

A

This is foetal Hb so is replaced by Hb type A (for adult)

182
Q

What is Hb Type S

Discuss its structure and how this affects its functioning

A

Sickle cell haemoglobin

It has a small amino acid substitution in β chain, reducing oxygen affinity and alters the Hb solubility in deoxy form. This results in crystallisation and fragile, sickle shaped RB cells

183
Q

Briefly describe the oxygen binding structure of a Hb molecule

A

Each chain has a hydrophobic pocket containing a Fe2+ porphyrin moiety

The 4 subunits bind sequentially to O2 and each reaction improves the affinity of the remaining subunits

184
Q

Name 4 things that also affect Hb’s affinity for O2

A

H+,
CO2,
Diphosphoglycerate
Temperature

185
Q

What is the [dissolved oxygen] proportional to?

A

The solubility coefficient and the PO2

186
Q

You have 2 sealed containers separated by a semi Permeable membrane containing 2 solutions with different PO2 levels. What will happen?

What happens if haemoglobin is added to one side (and cannot pass through membrane)?

A

They will equilibrate with equal PO2 on both sides

The PO2 of the Hb side will drop as dissolved O2 binds to the Hb. Only dissolved O2 counts towards PO2 so the O2 from the other side will diffuse across to equilibrate PO2. The PO2 will be equal but the side with Hb will have more O2 total

187
Q

How much O2 can 1g of Hb carry

A

1.39ml

188
Q

How much Hb does blood have per 100ml

A

5g of Hb/100

189
Q

What is the oxygen capacity of blood given 1g of Hb can carry 1.39 ml of O2 and normal blood has 15g of Hb per 100ml

A

20.8 ml of O2 per 100ml of blood

190
Q

What is the O2 saturation of Hb at arterial PO2 of 100mmHg

What about mixed venous blood with a PO2 of 40mmHg

A

97.5%

75%

191
Q

Discuss the loading plateau of Hb

A

Hb is largely saturated at all PO2>60mmHg
Therefore quantity of O2 carried by the blood is not much affected by PO2 until it drops below 60mmHg
The quantity of O2 in arterial blood remains the same over large variations in ventilation rate

192
Q

What does the loading plateau mean for barometric pressure

A

Fluctuations in barometric pressure have little effect on the quantity of O2 carried in the blood

193
Q

What shifts the pO2 vs Hb Saturation curve to the right

A

Increased temperature
Decreased pH
Increased PCO2
Increased DPG

194
Q

ventilation rarely affects total O2 in the blood, what does this mean

A

Ventilation can be changed to regulate arterial PO2 without affects oxygen supply to tissues

195
Q

What happens if PO2 drops below 60

A

Hb saturation falls rapidly

The steepness of the curve means any right shift will result in Hb giving up O2

196
Q

Describe the RBC environment in exercising muscle

Therefore…

A

Acidic
Hypercarbic
Warm

An increase in these factors cause O2 to be offloaded more easily

197
Q

What is the Bohr Effect

A

The effect of CO2 and H+ (decrease pH) on affinity of Hb for O2

198
Q

What is 2,3 DPG and how does it affect the dissociation curve

A

2,3 diphosphoglycerate

Shifts it right

199
Q

Where are 2,3 DPG levels highest

A

In RBCs

200
Q

How do RBCs make 2,3 DPG

Why would it want to do this

A

Shunt 1,3DPG to 2,3DPG by DPG
Dismutase

2,3DPG has a high affinity for adult Hb so displaces O2 to the tissue

201
Q

How does foetal and adult Hb compare in relation to 2,3DPG

A

F type Hb is less sensitive to 2,3 DPG so the dissociation curve is shifted left. This increases the affinity for O2 at low PO2

202
Q

Why do F type Hb have high affinity for O2

A

Foetal PO2= 30mmHg which would give a 55% saturation in adults but it is 75% in foetuses

203
Q

What happens if the blood bank is depleted of 2,3 DPG

A

Offloading of O2 is impaired

Especially a problem if lots of blood is transfused

204
Q

What are the 2 important factors to remember regarding the relationship between PO2, O2-Hb, and oxygen content

A

Arterial pO2 is related to the amount of O2 dissolved in the plasma

Oxygen content/ Hb saturation is what keeps us alive

205
Q

Give equation for [blood O2]

A

1.39x[Hb]x %saturation) + (0.003 x PO2)

206
Q

What are the 4 categories of hypoxia

A

Hypoxic
Anaemic
Circulatory
Histotoxic

207
Q

Which hypoxia refers to a reduced O2 carrying capacity of blood

A

Anaemic hypoxia

208
Q

What is hypoxic hypoxia

A

Low arterial PO2 accompanied by inadequate Hb saturation

209
Q

What is circulatory hypoxia

A

When too little oxygenated blood is delivered to tissues

210
Q

What is histotoxic hypoxia

A

Characterised by normal o2 delivery to tissue but the cells are unable to use the oxygen available

211
Q

What does cyanide poisoning result in

A

Histotoxic hypoxia

212
Q

What is hyperoxia

A

When an above normal arterial PO2 occurs

213
Q

What is it called when you have excess CO2 in the blood

A

Hypercapnia

214
Q

What is hypocapnia and how does it occur

A

Below normal arterial PCO2 levels

Hyperventilation

215
Q

Why is carbon monoxide deadly

A

CO has an affinity for Hb 240x greater than that of O2 so binds to Hb instead of O2 forming COHb

216
Q

If there is 0.1% CO in the air, how much of our Hb will bind to CO

How will PO2 be affected

A

60%

PO2 will not be changed but total O2 will be dramatically reduced

217
Q

Why is CO dangerous (5)

A

1) High Hb affinity
2) left shift in o2 dissociation curve making it difficult to unload the little O2 that may still be bound
3) arterial PO2 is normal, impairing any feedback mechanisms
4) no physical signs of hypoxia because blood stays bright red when CO binds to Hb
5) odourless, colourless, non- irritating

218
Q

What is the first sensor of CO poisoning

A

The brain (when the individual loses consciousness)

219
Q

How can CO poisoning be treated

A

Pure O2 therapy to compete off CO from Hb

220
Q

3 forms of transporting CO2 in the blood

A

Dissolved
Bicarbonate
Carbamino compounds

221
Q

What does concentration =

A

Partial pressure x solubility

222
Q

How much of the carries CO2 is dissolved in the blood

A

5-10%

223
Q

Which form of CO2 is the largest fraction in blood

A

As HCO3-

90%

224
Q

How is HCO3- formed

A

Hydration of CO2 (by the action of carbonic anhydrase) and the dissociation of carbonic acid

225
Q

What is the dissociation constant for carbonic acid

What does this mean at physiological level

How fast is the hydration of CO2

A

6.1

pH =7.4 so many H+ generated

VERY slow

226
Q

Give the equation of CO2 to HCO3-

A

CO2+H2O ↔️H2CO3↔️ H+ + HCO3-

227
Q

How does CO2 form carbamino acids

How is plasma and Hb well suited for this

A

Proteins can reversibly bind CO2 to their amine groups

Plasma is 7% proteins so provides a large source
The RBC is 30% Hb

228
Q

What do most carbamino compounds exist as

Why

What is the issue

A

RNHCOO-

The dissociation constant of RNHCOOH <6

Induces a large pH change unless adequate buffering occurs

229
Q

Describe the Haldane Effect

A

The opposite of the Bohr effect

Deoxy-Hb is a weaker acid so at physiological pH it will bind more H+ so CO2↔️HCO3- equation shifts to the right
HCO3- increases and more is carried by the blood

Deoxy Hb also forms more carbamino compounds
Decreased PO2 increases amount of CO2 carried

230
Q

How do CO2 and O2 move from blood to tissue

A

Down their respective partial pressure gradient

231
Q

What are the H+ generated by formation of HCO3- buffered by

A

Imidazole groups on His amino acid residues of α and β chains of Hb

These residues have a pK of ~7 making them good buffers in the physiological range

232
Q

How does HCO3- leave the RBC

What must hAppen

A

Down it’s concentration gradient

Charge movement is balanced by an influx of Cl- and RBCs accumulate Cl- in exchange for HCO3-

233
Q

What is Hamburger’s phenomenon

Where does it occur

A

The influx of Cl- to compensate for the charge movement of HCO3- out of the RBC and the subsequent accumulation of Cl- in exchange for HCO3-

Capillary beds

234
Q

Why is the Cl- shift so fast

A

High anion permeability of RBC membrane

235
Q

What do the extra intracellular HCO3- and Cl- do

A

Increase intracellular osmolarity and osmotic pressure resulting in water influx and cell swelling

236
Q

What maintains the gradient for CO2 diffusion into the RBC

A

Continued efflux of HCO3-
Production of carbamino compounds
H+ buffering by Hb

237
Q

What does an increase in [H+] and PCO2 facilitate in RBCs

And what does this in turn facilitate

A

The release of O2 via the Bohr effect

Greater proton binding as a result of the Haldane effect

238
Q

How is the pH resulting from the solution of CO2 in the blood worked out

A

Henderson Hasselbach Equation

pH= pKa + log(HCO3-)/(CO2)

239
Q

What is the pH of blood

A

7.4

240
Q

Why is the Henderson Hasselbach equation important for blood pH

A

pH= 6.1 + log(HCO3-)/(0.03PCO2)

Therefore it is the ratio of HCO3- : dissolved pH that determines blood pH
Thus if the ratio remains the same (20), pH will be 7.4

241
Q

Why is blood a poor buffer system based on physical chemistry

A

The pK (6.1) is very far from the pH

242
Q

Despite physical chemistry, why is the blood a good buffer?

A

The lungs can alter [CO2] by changing alveolar ventilation

It is an open buffer system

243
Q

How much carbonic acid do the lungs excrete per day

A

10,000 mEq

244
Q

What organ primarily controls HCO3- levels

A

Kidney

245
Q

How well does full compensation occur

A

Never in real life

246
Q

What are the 3 things measured when checking the CO2:HCO3- ratio

What are the 3 categories for classification

A

PCO2, HCO3-, pH

Acidosis/ alkalosis;
Respiratory/ metabolic;
Acute/ compensated.

247
Q

How will you know if a blood shift is respiratory or metabolic

A

change in CO2 = respiratory

Change in HCO3- = metabolic

248
Q

How can you tell if a change is acute or compensated

A

If both CO2 and HCO3- levels have changed

249
Q

What are normal levels for:

a) pH
b) PCO2
c) HCO3-

A

a) 7.4
b) 40mmHg
c) 26mmol

250
Q

Classify someone who has pH 7.6,
PCO2: 43mmHg
HCO3-: 34mmol

What has likely happened

A

Acute metabolic alkalosis

Vomiting

251
Q

What are the 2 distinct circulations in the lungs

A

The bronchial and The pulmonary

252
Q

Give the purpose of the bronchial circulation

A

Supplies conduction zone and supporting structures

Source of warmth and humidity

253
Q

How is the pulmonary circulation associated with the respiratory zone

A

Intimately

Each time the airways branch, the airways also branch

254
Q

Give the 3 non respiratory functions of the pulmonary circulation

A

Blood reservoir

Filtration

Metabolism of vasoactive hormones

255
Q

Discuss the pulmonary circulation’s role as a blood reservoir

A

Blood volume in pulmonary capillary bed is approximately equal to stroke volume of the right heart
Contains approximately 500ml or 10% of total blood
Equal distribution between arterial and venous

256
Q

Discuss the filtration function of the circulation

A

Protects the critical organs from circulating obstruction such as emboli (fat globules, air, blood clots)
Small pulmonary arterial vessels and capillaries trap these emboli and prevent them from entering systemic circulation and blocking coronary, cerebral, or renal blood flow
Endothelial cells release fibrinolytic agents that dissolve blood clots
Pulmonary capillaries can absorb air emboli

257
Q

What can be a disadvantage of the lung’s filtration function

A

Emboli Can cause death if they are very numerous and/ or block a large pulmonary vessel thus impairing gas exchange

258
Q

Discuss the metabolic function of the pulmonary circulation

A

Involved in selective metabolism of vasoactive agents
Eg Angiotensin I, which is converted to angiotensin II by angiotensin converging enzyme
Angiotensin II is a potent vasoconstrictor

Noradrenaline, bradykinin, serotonin etc are inactivated
Adrenaline, histamine, and vasopressin are unaffected by passage through the pulmonary circulation

259
Q

Where is angiotensin converting enzyme found and how effective is jt

A

On the cell surface of pulmonary endothelial cells

Activation is v fast with 80% of angiotensin I is converted to II during a single passage through pulmonary vasculature

260
Q

What is the pressure that the whole cardiac output travels through the pulmonary circulation

How is this

A

10mmHg (compared to 80-90mmHg in systemic circulation)

Flow=ΔP/ R
Many vessels to accommodate flow (like a dense capillary bed)
Vessels are dilated so low resistance

261
Q

What primarily controls the resistance in pulmonary circulation

A

Local passive control (not really autonomic)

262
Q

What happens to resistance when pulmonary venous pressure is increased

A

Resistance decreases

263
Q

Why does resistance decrease in pulmonary circulation when pressure increases (2)

A

Capillary recruitment

Capillary distension

264
Q

Discuss capillary recruitment in pulmonary circulation

A

When blood flow increase pressure rises and collapsed vessels are opened, lowering overall pressure

265
Q

Discuss capillary distension in pulmonary circulation

A

Vessels have high compliance

Therefore the small increase in pressure increases the vessel diameter decreasing resistance

266
Q

Discuss pulmonary vascular resistance in regional hypoxia

A

Localised vasoconstriction to divert blood away from hypoxic region so there is only a small change in pulmonary arterial pressure

267
Q

Discuss pulmonary vascular resistance in general hypoxia

A

General vasoconstriction
Generalised increase in pulmonary vascular resistance
Increased arterial pressure leads to pulmonary hypertension and oedema

Low PO2 is thought to directly act on smooth muscle cells of the pulmonary vasculature

268
Q

What is net fluid exchange across the capillary determined by

A

The hydrostatic and colloid osmotic pressure across the wall

269
Q

Are their equal amounts of protein in the interstitial fluid all around the body

A

No
There is more in the lung as pulmonary capillaries are more permeant to proteins than capillaries in the systemic circulation

270
Q

What drains the interstitial fluid

Why is this important

A

Lymph

Stops fluid entering alveoli

271
Q

What ensures interstitial fluid doesn’t enter the capillaries (2)

A

Interstitial pressure is negative thus pulling water away from the alveoli

Surfactant serves to act as a barrier to fluid movement that attempts to enter the alveoli via capillary action

272
Q

What happens in the pulmonary circulation if filtration exceeds removal by lymph

What can cause this (5)

A

Oedema

An increase in capillary pressure due to left heart failure or general hypoxia

Increased capillary permeability due to oxidative damage (eg by ozone toxicity) or endotoxins

Decrease in capillary colloid osmotic pressure

Increased surface tension which increases negative interstitial pressure

Lymph blockage

273
Q

What can cause a

a) decrease capillary colloid osmotic pressure
b) increase in surface tension

A

a) Loss of plasma protein in starvation

b) loss/ lack of surfactant as occurs in acute respiratory distress syndrome

274
Q

What happens during drowning in fresh water

A

Fresh water inspired
Rapid diffusion of pure water across alveolar membrane into capillaries due to high colloid osmotic pressure in capillary
This leads to RBC lysis due to hypotonicity
The dilution of extracellular Na and the release of K+ from RBCs leads to cardiac fibrillation and death

275
Q

What leads to death in sea water drowning

A

Aspiration of salt water with an osmolarity > plasma results in net flow of water out of capillaries into interstitial space
Increases space of capillary from alveoli
RBCs do not lyse but patient dies of asphyxiation

276
Q

How much of the lung’s weight is blood

A

~50%

277
Q

1mmHg = ?cmH2O

A

1.36

278
Q

What is the pulmonary arterial pressure in the top of the lungs compared to the middle

A

11mmHg less

279
Q

What are the 3 zones that the lungs is divided into to represent the distinct interactions between pulmonary arterial pressure, alveolar pressure, and pulmonary venous pressure

A 
Zone 1 (upper lung)
Zone 2 (middle lung)
Zone 3 (lower lung)
280
Q

How do pulmonary arterial pressure, alveolar pressure, and pulmonary venous pressure vary in Zone 1 of the lungs

What does this mean for blood flow in zone 1

A

Alveolar > arterial > venous

Pulmonary capillaries are collapsed and there is no flow

281
Q

How do pulmonary arterial pressure, alveolar pressure, and pulmonary venous pressure vary in Zone 2 of the lungs

How does this come about

What does this mean for blood flow

A

Arterial> alveolar > venous

There is increased hydrostatic influence due to Zone 2’s increased proximity to the heart

The blood flow in this region of the heart is determined by the difference between arterial and alveolar pressure

282
Q

How do pulmonary arterial pressure, alveolar pressure, and pulmonary venous pressure vary in Zone 3 of the lungs

How is blood flow determined here?

A

Arterial>venous> alveolar

Using normal arterial-venous pressure difference

283
Q

When does venous pressure have influenced over blood flow in the lungs

A

When it exceeds alveolar pressure

284
Q

Are the conditions in zone 1 of the lungs normal?

A

No these do not usually occur in healthy people since arterial pressure in the upright lung is normally sufficient to overcome the small alveolar pressures

285
Q

When may the conditions in zone 1 occur, pathologically or otherwise?

A

If pulmonary arterial pressure falls (eg in severe haemorrhage) or if alveolar pressure is increased (eg forced ventilation)

286
Q

What are regional ventilation-perfusion ratios

A

Comparisons of the alveolar air flow to the flow of blood in different lung regions

287
Q

What is normal alveolar ventilation

What is normal total pulmonary blood flow

A

4 litres per minute

5 litres per minute

288
Q

What is the normal average VA/Q ratio

What’s the units

A

Normal ventilation perfusion ratio = 0.8

No units as it is a ratio

289
Q

Where is ventilation best

Why

Where is perfusion best? Why?

A

At the base of the lung

The effects of gravity on intrapleural pressure and thus the compliance of the lung

At the base of the lung also due to the effect of gravity in pulmonary arterial pressure

290
Q

How do airflow and blood flow change across the lung

Why

A

Increase down the lung

Ventilation and perfusion are gravity dependent

291
Q

Where is blood flow proportional greatest

What about ventilation

A

Base of lung

Apex of lung

292
Q

What is the difference between blood flow between the top and bottom of the lungs

A

5 fold difference

293
Q

What is the difference between airflow between the top and bottom of the lungs

A

2 fold difference

294
Q

How does VA/Q ratios change from the base to the apex of the lung

A

0.7 at the base and 3 at the top

However the VA/Q ratio does not change much over the lower 2/3 of the lung

295
Q

How does the VA/Q ratio change in the bottom 2/3 of the lung?

What about in the top

A

the VA/Q ratio does not change much over the lower 2/3 of the lung

Over The upper 1/3 of the lung the ratio increases dramatically as a result of the fall in blood flow

296
Q

Why are VA/Q ratios useful

A

Mismatches between ventilation and perfusion have marked effects upon alveolar gas exchange

297
Q

Where does tuberculosis occur typically

Why here?

A

The apex of the lung

The high VA/Q ratio which is a result of over ventilation relative to blood flow provides a high PO2 environment which is favourable for the mycobacterium tuberculosis

298
Q

How does the body compensate for a low VA/Q ratio

A

Increase overall ventilation - this is an acute response as this will result in over ventilation in normal lung units, leading to a deficiency in PCO2 in the alveoli and venous blood

Regional vasoconstriction induces by localised hypoxia will shunt blood away from poorly ventilated alveoli

299
Q

How does the body compensate for high VA/Q ratios

A

Local arterial PCO2 will fall, increasing pH. Increased pH

Causes localised increases in airway resistance, shunting ventilation to alveoli with normal VA/Q ratios

300
Q

How do venous admixtures affect systemic arterial PO2

A

Lower PO2 to approximately 95mmHg

301
Q

What is “wasted blood” in the lungs

A

Any fraction of blood that does not get fully oxygenated

302
Q

What is a venous admixture

A

The mixing of oxygenated blood with non oxygenated blood

303
Q

What are the 2 main causes of venous admixtures

A

Shunting

Low VA/Q

304
Q

What are the 2 kinds of shunt that cause venous admixtures

A

Right to left anatomic shunt

Alveolar shunt

305
Q

What is a right to left anatomic shunt

A

Blood passes through an anatomic channel that does not pass the alveoli
There might be a septal defect or the fact that a portion of the venous drainage of the bronchial circulation is dumped into the pulmonary vein, which enters the left heart to be pumped round the body

306
Q

Are right to left shunts normal?

A

All individuals have some degree of right to left anatomic shunt

307
Q

How much of cardiac output is venous admixture in a normal person

A

1-2% due to bronchial circulation drainage into the pulmonary vein

308
Q

What is alveolar shunting

A

When a portion of cardiac output goes past alveoli without coming into contact with alveolar air

309
Q

Why might an alveolar shunt occur

A

Pneumonia
Pulmonary oedema
Atelectasis

310
Q

Other than shunting, how may a venous admixture occur

A

Low VA/Q ratio - the normal regional distribution of VA/Q ratios contributes to venous admixture

311
Q

In the normal lung how much of the venous admixture is due to shunting and how much is low VA/Q ratios

A

20% = shunting

80% is a result of low VA/Q ratios at the base of the lung

312
Q

What is the name for quiet automatic breathing

What is the most important respiratory muscle here?

A

Eupnea

The diaphragm

313
Q

What is the excitatory activity like in the diaphragm when we inhale

What is this activity responsible for

A

Dramatic and linear

Responsible for the increases Negative intrapleural pressure leading to the reduction in alveolar pressure, causing lung expansion

314
Q

Describe the electrical activity of the diaphragm during breathing

A

Linear increase during inspiration
Inspiration is marked by an abrupt cessation of electrical activity which is followed by passive expiration due to the elastic recoil of the lungs

315
Q

Which instrument was surprisingly vital to our understanding of the role of the brainstem structures in the generation of cyclic breathing

Who did more delicate brainstem transections than this? When?

A

The guillotine (invented 1789)

Lumsden (1920s)

316
Q

How is breathing affected after sectioning above the pons

A

Breathing is unaffected when the vagus (carrying afferent information from the lungs) is intact

317
Q

How is breathing affected if you cut the vagi after sectioning above the pons

A

Reduced breathing frequency and increased tidal volume

318
Q

How is breathing affected if you cut below the medulla

A

Complete cessation of breathing

319
Q

How is breathing affected after sectioning above the central medulla

How would a vagotomy affect this

A

Rhythmic but irregular breathing

Slows the irregular pattern

320
Q

How is breathing affected if you cut at the level of the upper pons (below pneumotaxic and above apneustic centres)

What happens if both vagi are then cut

A

Slowed respiration and increases tidal volume

Either cessation of breathing at fuckk inspiration (apneusis) or inspiratory spasms interrupted by intermittent expirations (apneustic breathing)

321
Q

What were the findings of Lumsden’s experiments in the 1920’s

A

The central pattern generator for breathing is located in the medullary centre

The apneustic centre prolongs inspiration

The pneumotaxic centre inhibits the inspiratory phase

The Vagal afferent input is important in terminating inspiration

322
Q

What are the 2 key areas of the medullary respiratory centre

A

Dorsal respiratory group (DRG)

Ventral respiratory group (VRG)

323
Q

What is the DRG of the medulla associated with

A

Inspiration

These neurons project to the upper level motor neurone pool inner sting inspiratory muscles

324
Q

What is the VRG of the medulla associated

A

Both inspiratory and expiratory neurons and neuronal projections

325
Q

What is one theory of the control of Central Pattern Generation

What is the evidence

A

Inspiratory area cells have the property of intrinsic periodic firing, underlying the basic periodicity of breathing

When all afferent stimuli are abolished, the inspiratory cells generate repetitive bursts of APs to the diaphragm and other inspiratory muscles

326
Q

What is the inspiratory ramp

How is it turned off

A

The linear increase in electrical activity signalling from the inspiratory brainstem cells to inspiratory muscles

Turned off prematurely by inhibitory impulses from the pneumotaxic centre

327
Q

What allows modulation of breathing frequency

A

The pneumotaxic centre inhibiting the inspiratory ramp, shortening inspiration

328
Q

True or false:

The VRG and DRG are bilaterally paired and synchronised by cross communication

A

True

This results in the symmetry of respiratory movement

329
Q

What part of the pneumotaxic centre inhibits inspiration

A

The pontine respiratory group (PRG)

330
Q

What does the PRG in the pneumotaxic centre do

What is the experimental evidence for this

A

Switches off inspiration, regulating tidal volume and breathing frequency

Direct electrical stimulation of the pneumotaxic centre attenuates the inspiratory ramp

331
Q

What may play a role in fine tuning the period of the respiratory rhythm

A

The PRG

332
Q

Can a normal rhythm exist without the PRG

A

Yes

333
Q

What does the apneustic centre do

Evidence?

A

Prolongs the inspiratory ramp

An intact apneustic centre results in a regular inspiratory phase of the breathing cycle

334
Q

How does the apneustic centre prolong the inspiratory ramp

A

Impulses from the centre have an excitatory effect on the inspiratory area of the medulla, prolonging ramp action potentials

335
Q

How much voluntary control do we have over breathing?

A

We have override the automatic control of breathing by holding our breath etc but automatic control will eventually reassert control

There is a careful coordination between voluntary and involuntary for activities such as singing and speaking

336
Q

The feedback system for breathing is a negative feedback system. True or false?

A

True

337
Q

What is the variable under closest control in respiration under normal conditions

A

Arterial PCO2

338
Q

Name 6 things (not arterial PCO2) that are measured in the regulation of breathing

A

Chemical composition of peripheral blood and CSF (1 and 2)

state of lung expansion

Distortion of the king’s connective structure

Presence of irritants

Proprioceptive status of the chest wall

339
Q

Input from Which sensors are overwhelming modulators of respiration

A

Sensors interrelated with arterial PCO2 eg [H+]

340
Q

How is breathing activity related to arterial blood PO2

What about to PCO2 and [H+]

A

Inversely

Directly related

341
Q

What is a subject’s respiratory drive

A

The gradient of the graph of alveolar PCO2 (x) vs pulmonary ventilation (y)

342
Q

What is an effective stimulus to decrease ventilation rate

A

A reduction in arterial PCO2

343
Q

How might we suppress the drive to breathe for a short time

A

By hyperventilating and thus reducing arterial PCO2

344
Q

Why might an anaesthetised patient stop breathing briefly

A

If over ventilated by the anaesthetist

345
Q

Where is the response to PCO2 Levels dominate

A

In the CNS

346
Q

Who showed that there were CNS sites sensitive to PCO2 changes

When

Where

A

Mitchell

1960s

The ventral surface of the medulla (bilaterally located at the level of cranial nerve roots 8-11; additionally chemosensors have been found caudally in the area of the XII nerve root)

347
Q

How deep are the sites sensitive to PCO2 in the medulla

A

Very superficial - 200μm below the surface

348
Q

What is the area between the cranial and caudal PCO2 chemosensitive for?

A

It is an intermediate zone - an integrator of the 2 areas

349
Q

Are the PCO2 areas in the brainstem distinct from the DRG-VRG complex

A

Yes

They have been physiologically identifier but their exact anatomical identification has not been achieved

350
Q

How do we know the PCO2 sensitive areas are sensitive to PCO2 and affect breathing

How do we know it is neural

A

Direct local application of saline that is acidic or in equilibrium with high PCO2 values results in breathing

Application of cold solutions or anaesthetic depress ventilation

351
Q

What are the chemoreceptors controlling breathing surrounded by

A

Brain ECF (composed of ECF, CSF, and local metabolites)

352
Q

Which component of the brain ECF is most important for the CO2 chemoreceptors for respiration

Why

A

CSF

The area is close to the medulla and therefore close the the CSF

353
Q

How is CSF separated from the brain

A

By a layer of permanent ependymal cells

354
Q

What do the blood brain barrier mechanisms allow

A

Precise regulation of the chemical composition of CSF and brain ECF, preventing noxious agents from easily coming in contact with neural tissue

355
Q

Where is CSF found in the brain

A

Fills the 4 ventricles of the brain and outer surfaces of the brain

356
Q

How is CSF formed

A

Formed within the ventricles by highly vascularised tissues / the choroid plexuses

357
Q

what stops CSF being simply plasma filtrate

A

It is separated from the cerebral circulation by the blood brain barrier so it is a selective secretion

358
Q

What are the distinct characteristics of CSF

A

Low in: protein, HCO3-, K+, Ca2+

High in: Na+ and Cl-

359
Q

What is the only form of proton buffering in the CSF

A

HCO3-

360
Q

How permeable to H+, CO2, and HCO3- is the blood brain barrier

A

It relatively impermeable to H+ and HCO3-

The cerebral capillary endothelium are permeable to CO2

361
Q

What are interstitial changes in pH in the brain governed by

A

The diffusion of CO2 across the barrier and the [HCO3-] in the CSF

362
Q

What is the usual pH of CSF

A

7.3

363
Q

How can we determine whether CO2 chemoreceptors in the brain respond to CO2 directly or the change in pH?

A

Superfusing the CSF with a high PCO2, which results in a drop in pH, stimulates ventilation

Suffusing the area with a solution of high PCO2 but at a constant pH (by increasing HCO3- equally) has no effect on ventilation

Therefore we can conclude the chemoreceptors are responding to [H+] which rises when CO2 diffuses into the CSF when blood PCO2 is high

364
Q

How does increased ventilation stimulated by decreased PCO2 stop

A

Increased ventilation reduced PCO2 in the arterial blood and in the CSF and brain interstitial space

365
Q

What accompanies increased arterial PCO2 to facilitate CO2 exchange between the arterial blood and the CSF

A

Cerebral vasodilation

366
Q

Why is a greater change in pH detected in the CSF than peripheral interstitium

What happens if CSF pH is displaced over a long period of time? Why might this be dangerous?

A

The protein concentration is much lower in the CSF so it has a weaker ability to buffer

A compensatory increase in CSF HCO3- levels
A person with chronic lung disease (resulting in prolonged elevated PCO2) would have a normal CSF pH, leaving them with low ventilation than is required for their abnormally high arterial PCO2

367
Q

Other than chronic lung disease, what might cause someone to have a normal CSF pH but high PCO2 resulting in inappropriate ventilation rate

A

If the individual has been breathing 3% CO2 for a period of days

368
Q

Are the PCO2 chemoreceptors in the brain sensitive to O2?

A

No therefore changes in PO2 must be detected at a different site

369
Q

Where are the carotid bodies

Where are the aortic bodies

A

At the bifurcation of the common carotid arteries

Above and below the arch of the aorta

370
Q

What are the chemosensitive cells in the carotid bodies

What do they detect

A

Type 1 or glomus cells

These may also be in the aortic bodies

Changes in PO2, PCO2, and pH

371
Q

What happens if the glomus cells are stimulated by an fall in PO2

What other changes would provoke a similar response

A

Inhibition of K+ channel activity, cell depolarisation, and Ca2+ entry leading to NT release. This results in afferent signalling to the medulla and increased ventilation

Increased PCO2, reduced pH

372
Q

What is hypercapnia

A

Increased PCO2

373
Q

How much of the ventilatory response to hypercapnia can be attributed to the peripheral chemoreceptors

What about the response to hypoxia

A

20-40%

Peripheral chemoreceptors are solely responsible for this response

374
Q

What are the most important chemoreceptors in the body for ventilatory response to hypoxia

A

Carotid bodies

375
Q

How can we unmask the effect of hypoxia upon ventilation without letting CO2 affect results

A

By controlling alveolar, and subsequently arterial, PCO2 and then testing the effects of hypoxia - CO2 is added to inspired air to keep it constant in the face of changes in ventilation

376
Q

What happens to ventilation as PO2 drops below 60mmHg

A

Ventilation increases

377
Q

When is the marked increase in ventilation as PO2 drops

Why is this value important

A

When PO2 drops below 60mmHg

It is ideally mated with the O2 dissociation curve - at 60mmHg, Hb is ~90% saturated with O2 under normal conditions so above 60mmHg increased ventilation would have little effect. However, below 60mmHg, Hb saturation drops rapidly, so increases ventilation is required.

378
Q

What mediates the response to increased ventilation when PO2 drops below 60mmHg

How do we know

A

Carotid bodies

Without them, severe hypoxia depresses ventilation as a result of suppression of neural activity in the CNS. The loss of hypoxic ventilatory drive has been shown in patients with bilateral carotid body resection

379
Q

At what level does increased PCO2 result in increased ventilation

A

Any level

380
Q

If PCO2 is increased, at what level of PO2 does ventilation increase

A

100mmHg

381
Q

What are the 6 peripheral receptors that have been proposed to contribute to the control of ventilation via neural feedback on respiratory centres

A 
Pulmonary stretch receptors
Irritant receptors
C Fibre Endings
Proprioreceptors
Baroreceptors
Pain and temperature
382
Q

What is inspired PO2 on the summit of Everest

What is the issue with this

How do we overcome this

A

43mmHg BTPS

At a normal ventilation rate, our PA O2 is -3.8mmHg

Increasing ventilation 5 fold (hyperventilating), reducing PCO2 to 8mmHg and increasing the alveolar PO2 to 33mmHg

383
Q

What is the problem with the hyperventilation response to low PO2

A

The trigger to hyperventilate (LoS arterial PO2) is opposed by the braking effect of the fall in PCO2 when hyperventilating, detected by the central chemoreceptors

384
Q

How do we stop the brake reducing hyperventilating

A

Hyperventilating makes the blood alkaline which reduces central chemoreceptor stimulus to increase hyperventilation. Only when HCO3- Levels are reduced can this braking signal be inhibited - then the sustained arterial hypoxic stimulation will be dominant and ventilation rate will increase further

385
Q

Other than Central chemoreceptor compensation how does continued increase of alveolar ventilation occur

A

New experimental evidence suggests Input from peripheral chemoreceptors further increase ventilation in response to sustained exposure to hypoxia

386
Q

When can oxygen diffusion be rate limiting in respiration

A

At altitude under conditions of high cardiac output

387
Q

How can oxygen output be increased at altitude

A

Polycythemia (increased RBC concentration)

388
Q

Why is polycythemia useful at altitude

Give an example

A

Increased Hb means although CO2 and O2 saturation is diminished, O2 content is normal

Locals in Peruvian Andes (4600m): arterial blood PO2 is 45mmHg and Hb saturation is 81% but high RBC count means [Hb]= 19.8g/100ml and arterial [O2] =22.4ml/100ml blood

389
Q

Compare arterial pO2 in locals of the Peruvian Andes and the normal sea level value

A

Andes: 22.4ml/100ml of blood
Normal: 20ml/100ml

390
Q

Why might compensatory mechanisms to maintain arterial O2 content in hypoxia be deleterious

A

Alveolar Generalised hypoxia can lead to pulmonary vasoconstriction but all alveoli are hypoxic so all vessels construct, leading to pulmonary hypertension and eventually pulmonary oedema

391
Q

How is 2,3DPG involved in the response to hypoxia

How is this response different to effect of pH, increased PCO2 and increased temperature

A

Increased production of 2,3DPG shifts oxygen dissociation curve to the right, allowing oxygen to be unloaded more easily at the tissues

However, this is a permanent right shift leading to impairment of oxygen loading at the lungs

2,3DPG permanently shifts oxygen dissociation curve to the right, the other effects are reserved in the lungs

392
Q

How do scuba divers overcome the pressure of the water on their thorax

A

The air tank’s regulator’s second stage senses the surrounding pressure and provides air to the diver at a pressure approaching that of the surrounding environment

393
Q

What happens to gases in the body under hyperbaric conditions

A

Increased pressure forces the poorly soluble gas into solution in body tissues. This occurs particularly in fat where N2 is high

394
Q

What happens to N2 under hyperbaric conditions

A

N2 is high in fat but adipose tissue has poor blood supply and blood can carry v litter N2 anyway

Therefore equilibration of N2 between tissues and the environment is slow, taking hours

395
Q

What happens to N2 as divers ascend from hyperbaric depths

What if ascension is too fast

A

N2 is removed from tissues

Decompression is rapid and bubbles of N2 form in the blood

396
Q

Are bubbles of N2 in the blood dangerous

A

If they are small they can be removed from the circulation

If they are large, they can be painful, even lethal. The nitrogen emboli accumulate in the joints

397
Q

What is the ‘Bends’

A

When nitrogen bubbles accumulate in the joints causing severe pain
It is named after patients bending over in pain

398
Q

What happens in severe cases of the bends

A

Large numbers of bubbles can result in neurological disorders and death if they make their way to the brain or heart and occlude cerebral or coronary vessels

399
Q

How might you treat the bends

How can the risk be reduced

A

Immediate compression then slow decompression

Use specific diving tables to know the best rate of ascent for a given time at certain depths

Use a helium-oxygen mixture

400
Q

Why does a He-O2 mixture reduce your chance of getting the bends

A

He is half as soluble as N2 so less is dissolved in tissues under pressure and it is 1/7 the Mr of N2 so diffuses more rapidly through tissue

401
Q

Other than to reduce the risk of the bends, why would you use He-O2 mixture when diving

A

At depths of 160ft, N2 behaves as a narcotic, producing feelings of euphoria which is obviously dangerous

He, among other gases, is used to overcome this side effect

This mixture also reduces resistance to flow that occurs as a result of increased density at depth

402
Q

Which of the following is the rate limiting step in exercise:
Supplying sufficient oxygen
Removing CO2

A

Neither

Limitation of performance appears to lie at the level of the muscle and its ability to metabolically produce energy and external work

403
Q

During grades exercise which muscle units are recruited first

What is ventilation rate like accompanying this

A

Slow, oxidative muscle units

A near linear increase

404
Q

What happens after we run out of slow oxidative motor units during graded exercise

Give a positive and negative of this

A

We are forced to recruit fast glycolytic motor units

These have high energy output but use anaerobic respiration, producing large amounts of lactic acid

405
Q

How does lactic acid from exercise produce CO2

A

Acid enters the blood, increasing [H+] so blood HCO3- buffers this, forming CO2 which is then expired

406
Q

What causes ventilation to increase when anaerobic metabolism begins during exercise

A

Lactic acid is produced and exceeds the buffering capacity of the blood so H+ accumulates, activating peripheral chemoreceptors, which signal to increase ventilation

407
Q

What is the point of inflection in the ventilation workload graph

A

The increase in ventilation when the peripheral chemoreceptors are activated by excess lactic acid

It is the anaerobic threshold (AT)

408
Q

What is the importance of the anaerobic threshold

A

Important in endurance activity as it is associated with recruitment of glycolytic motor units and production of metabolic acids

Many training regiments aim to delay the onset of the AT

409
Q

Formula for trans thoracic pressure

A

Transmural + trans pulmonary

410
Q

Why can’t residual volume be measured by spirometry

A

Spirometry measures volumes you breathe out and You can’t breather that amount out

411
Q

How would you tell if a pathology is restricting lung inflation?

Give assessments of possible results

A

FEV1/FVC

Should be 80%
If >90% pathology is restrictive (eg emphysema)
If <70% it’s obstructive (eg fibrosis)

412
Q

A reduce in just a wall compliance will result in what

A

A decreased functional residual capacity

413
Q

Give the features of obstructive lung disease

Eg?

A

Decreased FEV
Decreased FVC
Increased RV
FEV/FVC=~42%

Asthma, tumour, bronchitis, emphysema

414
Q

Give the features of restrictive lung disease

Eg?

A

Decreased FEV
Decreased FVC
Decreased RV
FEV/FVC=0.9

Fibrosis

HOM (11 decks)

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