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CVR > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is Atmospheric Pressure?

A

760mmHg

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2
Q

What is Intrapulmonary Pressure?

A

760mmHg

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3
Q

What is Intrapleural Pressure?

A

756mmHg

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4
Q

What is the Collapsing Force of The Lungs?

A

4mmHg

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5
Q

What happens in Inspiration? (7 Steps)

A
  1. Inspiratory Muscles contract
  2. Thoracic Cage Expands
  3. Intrapleural Pressure becomes more negative
  4. Transmural Pressure increases and causes Alveoli to swell and open
  5. Intra-alveolar pressure falls relative to atmospheric pressure
  6. Air flows down pressure gradient from atmosphere into alveoli
  7. At the end of Inspiration–> No airflow, Intra-alveolar Pressure = Atmospheric Pressure
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6
Q

What happens in Passive Expiration?

A

Relaxation of the Expiratory Muscles

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7
Q

What happens in Active Expiration?

A
  1. Contraction of abdominal muscles

2. Contraction of internal intercostals

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8
Q

What are the 3 types of Muscles of Respiration?

A
  1. Primary
  2. Accessory
  3. Airway
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9
Q

What are the Primary Muscles of Respiration?

A
  1. Diaphragm

2. External Intercostals

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10
Q

What is the function of the Diaphragm?

A

Responsible for 75% of breathing, flattens upon contraction

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11
Q

What is the function of the External Intercostals (in relation in breathing)?

A

They lift the ribs upwards and outwards

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12
Q

What are the Accessory Muscles of Respiration?

A
  1. Scalene

2. Sternomastoid

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13
Q

What is the function of the Scalene Muscles (in relation to breathing)?

A

Raise the first 2 ribs

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14
Q

What is the function of the Sternomastoid (in relation to breathing)?

A

Raise the Sternum

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15
Q

What are the Airway Muscles of Respiration?

A
  1. Laryngeal
  2. Pharyngeal
  3. Genioglossus
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16
Q

What is the function of the Airway Muscles of Respiration

A

Enlarge and Stabilise the airway

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17
Q

What is Tidal Volume (TV)?

A

Volume of air breathed in and out each breath

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18
Q

What is the Inspiratory Reserve Volume (IRV)?

A

Inspiratory Capacity minus Tidal Volume

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19
Q

What is the Inspiratory Capacity (IC)?

A

Volume of air breathed in during maximal inspiration

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20
Q

What is the Expiratory Reserve Volume (ERV)?

A

Vital Capacity minus Inspiratory Capacity

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21
Q

What is the Residual Volume (RV)?

A

Volume of air in the lungs after maximal exhalation

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22
Q

What is the Functional Residual Capacity (FRC)?

A

Expiratory Reserve Volume + Residual Volume

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23
Q

What is the Vital Capacity (VC)?

A

Maximum volume of air able to be exhaled after a maximal inspiration

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24
Q

What is the Total Lung Capacity (TLC)?

A

Vital Capacity + Residual Volume

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25
Q

What is the Forced Vital Capacity (FVC)?

A

Maximal Inhalation followed by fast exhalation

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26
Q

What is the Forced Expiratory Volume in 1 Second (FEV1)?

A

Determined in Pulmonary Function Test

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27
Q

How is the Total Lung Capacity affected in Obstructive Respiratory Disease?

A

Not affected

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28
Q

How is the Total Lung Capacity affected in Restrictive Respiratory Disease?

A

Decreased

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29
Q

How is the Residual Volume affected in Obstructive Respiratory Disease?

A

Increased

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30
Q

How is the Residual Volume affected in Restrictive Respiratory Disease?

A

Not affected

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31
Q

How is the Forced Vital Capacity (FVC) affected in Obstructive Respiratory Disease?

A

Not affected or slightly decreased

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32
Q

How is the Forced Vital Capacity (FVC) affected in Restrictive Respiratory Disease?

A

Decreased

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33
Q

How is the FEV1 affected in Obstructive Respiratory disease?

A

Decreased

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34
Q

How is the FEV1 affected in Restrictive Respiratory Disease?

A

Decreased

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35
Q

How is the FEV1/FVC affected in Obstructive Respiratory Disease?

A

Decreased

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36
Q

How is the FEV1/FVC affected in Restrictive Respiratory Disease?

A

Not affected

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37
Q

What are the methods for Lung Volume Measurement?

A
  1. Peak Expiratory Flow Meter
  2. Helium Dilution Technique
  3. Body Plethysmography
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38
Q

What does Peak Expiratory Flow Meter measure?

A

Maximum speed of expiration–> measure of airway resistance

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39
Q

What does the Helium Dilution Technique measure?

A

Functional Residual Capacity (FRC)

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40
Q

What is the equation for FRC in the Helium Dilution Technique?

A

FRC = (C1 x V1) / (C2 - V1)

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41
Q

What does Body Plethysmography measure?

A

Functional Residual Capacity (FRC)

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42
Q

How does Body Plethysmography measure a patient’s Functional Residual Capacity (FRC)?

A

The Patient sits in an airtight chamber and tries to breathe through a closed mouthpiece. The patient’s chest and lungs expand, and the pressure in the lungs decrease. Meanwhile, the air volume in the chamber decreases and the pressure in the air chamber increases.

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43
Q

What is the equation for FRC in Body Plethysmography?

A

Change in Volume (Initial Pressure minus Change in Pressure) ÷ Change in Pressure

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44
Q

What is Boyle’s Law?

A

P1V1 = P2V2

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45
Q

What is Dead Space?

A

Volume occupied in lung by gas not involved in gas exchage

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46
Q

What are the different types of Dead Space in the lung?

A
  1. Anatomical Dead Space
  2. Alveolar Dead Space
  3. Physiological Dead Space
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47
Q

What is Anatomical Dead Space?

A

Anatomical Dead Space Volume = Tidal Volume - Alveolar Volume

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48
Q

How is Anatomical Dead Space measured?

A

Measured by Fowler’s Method (Nitrogen Washout)

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49
Q

Describe Fowler’s Method (Nitrogen Washout)

A
  1. Pure oxygen is breathed in, causing Nitrogen Concentration = 0
  2. During expiration, the nitrogen concentration is measured. Vd is when the Nitrogen concentration starts increasing from 0
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50
Q

What is Alveolar Dead Space?

A

Air in the alveoli in areas without blood flow

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51
Q

What is Physiological Dead Space?

A

Total Dead Space–> Alveolar Dead Space + Anatomical Dead Space

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52
Q

How is Physiological Dead Space measured?

A

Bohr’s Method

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53
Q

Describe Bohr’s Method

A

Vd is calculated using partial pressures of Carbon Dioxide in alveoli and expired air–> VD = VT [(PaCO2 - PeCO2)] / PaCO2

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54
Q

What is the effect of Dead Space on Ventilation?

A

Alveolar Ventilation = (VT - VD) x Breaths/min

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55
Q

What are 2 types of work of breathing?

A
  1. Compliance (Elastic) Work

2. Frictional/ Resistive Work

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56
Q

What is Compliance (Elastic) Work of the Lungs?

A

Compliance = The Stretching of the Lungs and Chest Wall = Change in Volume of the Lungs ÷ Change in Transmural Pressure

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57
Q

What is Transmural Pressure?

A

The pressure difference between the intra-alveolar pressure and the intrapleural pressure

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58
Q

What are the 3 types of Compliance?

A
  1. Static Compliance
  2. Dynamic Compliance
  3. Specific Compliance
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59
Q

When is Static Compliance measured?

A

When there is no airflow

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60
Q

When is Dynamic Compliance measured?

A

During Airflow

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61
Q

How is Dynamic Compliance measured?

A

Using a Hysteresis Loop

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62
Q

What is a Hysteresis Loop?

A

Graphical Representation of relationship between volume change and pressure change during quiet breathing

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63
Q

What is the work of breathing in a Hysteresis loop?

A

The area in the loop

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64
Q

What does Specific Compliance measure?

A

Measures the elastic properties of the lungs

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65
Q

What are the 2 things that contribute to Specific Compliance?

A
  1. Tissue Elasticity

2. Surface Tension

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66
Q

Describe Tissue Elasticity (Lung Compliance)

A

During Inhalation, Energy is required to stretch the lungs open–> In exhalation, the lungs makes use of the elastic recoil (due to elastin fibres in the connective tissue)

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67
Q

Describe Surface Tension (Lung Compliance)

A

Surface Tension = Phenomenon where the surface of liquid acts like a thin elastic sheet–> Will cause lung or alveolar collapse. High Surface Tension = Low Compliance

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68
Q

What counteracts Surface Tension in the lungs?

A

Pulmonary Surfactant

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69
Q

What is the function of surfactant?

A

Reduce surface tension by interfering with water molecule interactions –> increase compliance of the lung and stabilises alveoli of different sizes

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70
Q

What is the composition of surfactant?

A
  1. 40% Dipalmitoyl-Phosphotidylcholine (DPCC)
  2. 40% Other phospholipds including phosphotidylglycerol (7%)
  3. 5% Surfactant-Associated Proteins
  4. Cholesterol
  5. Traces of other substances
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71
Q

How is surfactant synthesised?

A
  1. Formation of Phosphatidylcholine (Lechtin) from: CDP-diacylglycererol + Alcohol or diacylglycerol + CDP-Choline/Ethanolamine
  2. Phosphatidylcholine –> Dipalmitoyl-Phosphotidylcholine (DPCC)
  3. DPCC joins to Apolipoproteins to form unique lipoprotein–> surfactant
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72
Q

What are the Surfactant Apolipoproteins?

A

SP-A,B,C and D

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73
Q

Which surfactant apolipoproteins are hydrophillic?

A

A and D

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74
Q

Which surfactant apolipoproteins are hydrophobic?

A

B and C

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75
Q

What is the function of hydrophillic surfactant apolipoproteins?

A

Crucial role in pulmonary immunity

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76
Q

What is the function of hydrophobic surfactant apolipoproteins?

A
  1. Reduce Alveolar Surface Tension
  2. Phospholipid Packaging
  3. Organisation of Surfactant Structure
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77
Q

What are the different types of cells in the lung?

A
  1. Smooth muscle cells
  2. Lung macrophages
  3. Mast Cells
  4. Gobet Cells
  5. Endothelial Cells
  6. Type 1 Alveolar Cells
  7. Type 2 Alveolar Cells
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78
Q

Where are the smooth muscle cells of the lungs located?

A

Bronchi

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79
Q

Where are the Lung Macrophages located?

A

They are Interspersed, found along the length of the respiratory tract

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80
Q

Where are the mast cells of the lungs located?

A

They are found along the length of the respiratory tract

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81
Q

Where are the Goblet cells of the lungs located?

A

They are present from Bronchioles upwards–> in the epithelium

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82
Q

Where are the Pulmonary Endothelial cells located?

A

Alveolar Wall

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83
Q

Where are the Type 1 Alveolar Cells located?

A

Alveoli–> Makes up 95% of the respiratory zone–> fuses with the Pulmonary Endothelium

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84
Q

Where are the Type 2 Alveolar Cells located?

A

Alveoli

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85
Q

What is the function of Smooth Muscle Cells in the lungs?

A
  1. Control the diameter and tension of the bronchi
  2. Involved in Asthma
  3. Produces Cytokines IL-5, IL-13
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86
Q

What is the function of Lung Macrophages?

A

Important for immune defence–> Phagocytosis, produce antimicrobial (Proteases) and antiviral (interferons) agents

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87
Q

What is the function of the mast cells in the lungs?

A
  1. Speed Immune Response

2. Important in Asthma

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88
Q

What is the function of the Goblet Cells in the lungs?

A

Secrete Mucus

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89
Q

What is the function of the Endothelial Cells?

A
  1. Environment for alveolar capillaries
  2. Produces Vasoactive Peptides–> tPA and ACE
  3. Control blood flow, fluidity, pressure and viscosity
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90
Q

What is the function of Type 1 Alveolar Cells?

A

Gas exchange

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91
Q

What is the function of Type 2 Alveolar Cells

A
  1. Synthesis, Storage and Secretion of Surfactant

2. Can replace themselves or other pulmonary cell types after injury

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92
Q

What is Frictional/Resistive Work of the Lungs?

A

Airway Resistance

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93
Q

What affects Airway Resistance in the Lungs?

A
  1. Diameter of Airway
  2. Distance Air needs to travel
  3. Flow type/Pattern
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94
Q

What affects the Diameter of Airway and the Distance air needs to travel in the lungs?

A
  1. Cross-sectional area of the Bronchial tree
  2. Lung volume (increased lung volume = decreased resistance)
  3. Bronchial Smooth Muscle Tone
  4. Mucus/Secretions
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95
Q

What is Hagen-Poiseuille Law?

A

Resistance = (8 x viscosity x length) ÷ (π x radius^4)

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96
Q

Where is the greatest resistance in the airways?

A

In Large Airways

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97
Q

What are the types of air flow?

A
  1. Laminar–> streamline & well-ordered

2. Turbulent –> Chaotic, Increases resistance

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98
Q

When does Turbulent Flow of air occur?

A

Occurs if Reynold’s number is greater than 2000

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99
Q

What is the Partial Pressure of Oxygen in Inspired air?

A

150mmHg

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100
Q

What is the Partial Pressure of Oxygen in Expired Air?

A

120mmHg

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101
Q

What is the Partial Pressure of Oxygen in Alveolar Air?

A

100mmHg

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102
Q

What is the Partial Pressure of Carbon Dioxide in Inspired Air?

A

0mmHg

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103
Q

What is the Partial Pressure of Carbon Dioxide in Expired Air?

A

30mmHg

104
Q

What is the Partial Pressure of Carbon Dioxide in Alveolar Air?

A

40mmHg

105
Q

What is the thickness of the Alveolar-Capillary Membrane?

A

0.5 microns

106
Q

What is the Solubility Index of Oxygen?

A

1

107
Q

What is the Solubility Index of Carbon Dioxide?

A

20

108
Q

What is the Partial Pressure difference of Oxygen between the alveoli and the pulmonary artery?

A

60mmHg

109
Q

What is the Partial Pressure difference of Carbon Dioxide between the alveoli and the Pulmonary Artery?

A

6mmHg

110
Q

What is Diffusing Capacity?

A

The volume of gas that diffuse through the respiratory membrane per minute for each mmHg of Gas Partial Pressure Difference

111
Q

How do you measure Diffusing Capacity?

A

Measured using Carbon Monoxide–> because the partial pressure difference is equivalent to the alveolar partial pressure of carbon monoxide

112
Q

How is Diffusing Capacity calculated?

A

Diffusing Capacity = Rate of Transfer of Gas from Lung to Blood ÷ Partial Pressure Diffference

113
Q

Why is there an Alveolar-Arterial PO2 gradient?

A

Due to Anatomical Shunts where deoxygenated blood joins up with oxygenated blood–> overall still oxygenated

114
Q

Describe the Ventilation/Perfusion Ratio

A

More air goes to the base than the apex of the lung due to intrapleural pressure and gravity–> therefore the base is relatively underventilated and overperfused while the apex is overventilated and underperfused

115
Q

What causes a low Ventilation/Perfusion ratio?

A

Shunting, causing arterial hypoxaemia–> Obstruction in airway–> Emphysema

116
Q

What causes a high Ventilation/Perfusion ratio?

A

Blockage of blood vessel–> Pulmonary Embolism

117
Q

What happens if Blood Flow > Ventilation?

A

Decreased Alveolar PO2, Increase Alveolar PCO2–> Vasoconstriction and Bronchodilation–> Decrease Blood Flow and Increase Ventilation

118
Q

What happens if Blood Flow < Ventilation?

A

Increased Alveolar PO2, Decreased Alveolar PCO2–> Vasodilation and Bronchoconstriction–> Decrease Ventilation and Increase Blood Flow

119
Q

How is oxygen carried in the blood?

A
  1. Combine with Haemoglobin

2. Physically dissolved in Plasma

120
Q

What is %Saturation of Oxygen?

A

Oxygen Content ÷ Oxygen Capacity

121
Q

What is Oxygen Capacity?

A

The volume of oxygen carried when Haemoglobin is 100% saturated = 20mL%

122
Q

What is the crucial PO2?

A

8kPa (60mmHg)–> Once PO2 falls below crucial PO2, the % saturation of Oxygen will significantly decrease and the tissues will not receive adequate oxygen

123
Q

What is the Bohr Effect?

A

An increase in CO2 and H+ causes Haemoglobin to release more O2

124
Q

What causes a similar effect to the Bohr Effect?

A
  1. Increased Temperature

2. Increased 2,3-DPG

125
Q

When is 2,3-DPG increased?

A
  1. Exercise
  2. Altitude
  3. Anaemia
  4. Respiratory Disease
126
Q

When is 2,3-DPG reduced?

A

In stored blood

127
Q

Why does Fetal Haemoglobin bind O2 better than Adult Haemoglobin?

A

There are no ß-chains for 2,3-DPG to bind to in Fetal haemoglobin

128
Q

What is P50?

A

PO2 when Haemoglobin is 50% saturated

129
Q

What does P50 measure?

A

The affinity of Oxygen for Haemoglobin–> Low P50 = High Affinity

130
Q

What is the effect of Anaemia on Oxygen Transport?

A

Arterial PO2 is normal but the O2 content is reduced

131
Q

What is Methaemoglobinaemia?

A

The Fe2+ of haemoglobin is oxidised to Fe3+

132
Q

What is Carboxyhaemoglobinaemia?

A

When Haemoglobin binds to Carbon Monoxide

133
Q

What is Sickle-Cell Anaemia?

A

When an abnormal Haemoglobin causes deformation of the Red Blood Cell

134
Q

What is Cyanosis?

A

Blue colouration of skin and mucus membranes when arterial blood is 85% saturated or when capillary blood is 70% saturated

135
Q

What are the 2 types of Cyanosis?

A
  1. Central

2. Peripheral

136
Q

What is Central Cyanosis?

A

Cyanosis due to arterial blood desaturation

137
Q

What is Peripheral Cyanosis?

A

Cyanosis due to reduced tissue blood flow

138
Q

How is Carbon Dioxide transported in the blood?

A
  1. Physically Dissolved
  2. Carbamino Compounds
  3. Bicarbonate
139
Q

What is the Haldane effect?

A

Deoxygenation allows Haemoglobin to bind more CO2 and H+

140
Q

What is the pH of arterial blood?

A

7.4

141
Q

What is the pH of Venous blood?

A

7.35

142
Q

What is Hyperventilation?

A

When the PaCO2 is less than 40mmHg

143
Q

What is Hypoventilation?

A

When the PaCO2 is greater than 40mmHg

144
Q

What causes Respiratory Alkalosis?

A

Hyperventilation

145
Q

What causes Respiratory Acidosis?

A

Hypoventilation

146
Q

What is Eupnoea?

A

Normal Quiet Breathing

147
Q

What is Hyperpnoea?

A

Increased Ventilation

148
Q

What is Tachypnoea?

A

Increased Respiratory Rate

149
Q

What is Hypocapnia?

A

PCO2 less than normal

150
Q

What is Hypercapnia?

A

PCO2 greater than normal

151
Q

What is Hypoxia?

A

PO2 less than normal

152
Q

What is Hyperoxia?

A

PO2 greater than normal

153
Q

What is Hypoxaemia?

A

PO2 less than normal in blood

154
Q

What is Asphyxia?

A

Hypoxia and Hypercapnia

155
Q

What is Dyspnoea?

A

Stressful Breathing

156
Q

What is Apnoea?

A

Absence of Breathing

157
Q

What are the components of the Respiratory Control Centre

A
  1. Higher Centres
  2. Inspiratory Centre
  3. Expiratory Centre
158
Q

Where does the Inspiratory Centre receive signal from?

A
  1. Blood PO2, PCO2, pH
  2. Lung expansion
  3. Airway irritants
  4. Pain
  5. Body Temperature
  6. Limb Movements
  7. Muscle Contractions
159
Q

What are the Pons Respiratory Centres?

A
  1. Pneumotaxic Centre

2. Apneustic Centre

160
Q

What does the Pneumotaxic Centre do?

A

Drives Inspiration

161
Q

What does the Apneustic Centre do?

A

Turns off Inspiratory Centres

162
Q

What are the Medullary Inspiratory Centres?

A
  1. Pre-Bötzinger Complex
  2. Dorsal Respiratory Group
  3. Ventral Respiratory Group
163
Q

What makes the Pre-Bötzinger Complex special?

A

It has pacemaker activity

164
Q

What will a disruption to the Respiratory Control Centre cause?

A

Hypoventilation and Hypoxaemia

165
Q

How can the Respiratory Control Centre get disrupted?

A
  1. Depressant drugs
  2. Spinal cord injury in the cervical region
  3. Damage to motor nerves
  4. Muscle diseases
  5. Dysfunction of Respiratory Apparatus
166
Q

What are the Airway/Lung Receptors?

A
  1. Stretch Receptors
  2. irritant Receptors
  3. Juxtacapillary ‘J’ Receptors
167
Q

Where are the Stretch Receptors located?

A

Airway smooth muscle

168
Q

What are the Stretch Receptors stimulated by?

A

Stretch during inspiration

169
Q

What is the function of Stretch Receptors?

A
  1. Inhibit the Inspiratory Centre–> Hering-Breuer Inflation Reflex
170
Q

Where are the Irritant Receptors located?

A

Near the airway epithelial cells

171
Q

What are the irritant Receptors stimulated by?

A

Dust
Cold air
Cigarette smoke
Noxious gases

172
Q

What are the functions of the Irritant Receptors?

A

Cause reflex Bronchoconstriction or coughing–> involved in asthma

173
Q

Where are the J Receptors located?

A

Near the Capillaries in the alveoli

174
Q

What are the J Receptors stimulated by?

A

Factors that affect the interstitial spaces in the lung e.g. pulmonary congestion and oedema

175
Q

What are the functions of J receptors?

A

Cause reflex apnoea or rapid shallow breathing

176
Q

What are the Chemoreceptors in the Respiratory System?

A
  1. Peripheral

2. Central

177
Q

Where are the Peripheral Chemoreceptors?

A
  1. Carotid bodies–> signal via the Hering Nerve and Glossopharyngeal Nerve
  2. Aortic Bodies–> signal via the Vagus Nerve
178
Q

What percentage of the Chemoreceptors are peripheral?

A

20%

179
Q

What percentage of the Chemoreceptors are central?

A

80%

180
Q

What do the Peripheral Chemoreceptors respond to?

A
  1. Decreased Arterial PO2
  2. Increased Arterial PCO2
  3. Decreased pH
181
Q

Where are the Central Chemoreceptors located?

A

In the medulla separate from the respiratory control centres

182
Q

What do the Central Chemoreceptors respond to?

A

Increased Arterial PCO2 and Increased Brain ECF H+–> Arterial H+ cannot cross the Blood Brain Barrier

183
Q

What does Hypocapnia cause?

A

Increased neuromuscular excitability and tetany

184
Q

What does Hypercapnia cause?

A

Depression of the nervous system and coma

185
Q

What are the different types of Hypoxia?

A
  1. Hypoxic
  2. Anaemic
  3. Stagnant
  4. Histotoxic
186
Q

What is Hypoxic Hypoxia?

A

PaO2 is less than normal

187
Q

What is Anaemic Hypoxia?

A

PaO2 is normal but O2 content is less than normal

188
Q

What is Stagnant Hypoxia?

A

PaO2 and O2 content are all normal but O2 delivery to tissues is reduced due to decreased blood flow

189
Q

What is Histotoxic Hypoxia?

A

PaO2, O2 Content and O2 delivery are all normal but tissue cannot use the O2 due to metabolic poisoning

190
Q

What causes Respiratory Diseases?

A
  1. Decreased ventilation
  2. Decreased Alveolocapillary Diffusion
  3. Decreased O2 and CO2 transport
191
Q

What are the effects of high altitude on a person’s respiratory system?

A

Similar to Hypoxia and Hypoxaemia

192
Q

What are the Acute Effects of high altitude on the Respiratory System?

A
  1. Ventilation increases by 65%, improving Alveolar PO2

2. Alveolar and Arterial PCO2 decrease

193
Q

What are the Acute Effects of high altitude on the Cardiovascular system?

A
  1. Pulmonary Hypertension due to arteriole vasoconstriction in lungs
  2. Increased Heart Rate and Cardiac Output
194
Q

What are the Acid-Base Acute Effects of high altitude?

A

Respiratory Alkalosis

195
Q

What are the Acute Effects of high altitude on the CNS?

A
  1. Drowsiness
  2. Decreased manual dexterity
  3. Judgement and Memory
  4. Euphoria
196
Q

What are the chronic effects of high altitude on the Respiratory System?

A
  1. Ventilation increases by 300-500%

2. PaCOs levels decrease a lot

197
Q

What are the chronic effects of high altitude on the Cardiovascular system?

A
  1. Cardiac Output and Heart Rate return towards normal but not pulmonary arterial pressure
  2. Increased Tissue vascularity
  3. Increased Erythropoietin, HCT, Haemoglobin, Blood Volume, 2,3-DPG, P50 and Diffusing Capacity
198
Q

What are the Acid-Base chronic effects of high altitude?

A

Renal compensation–> retention of H+, Excretion of HCO3-

199
Q

What are the Symptoms of Acute Mountain Sickness?

A
  1. Dyspnoea, palpitations fatigue, muscular weakness
  2. Drowsiness, Sleepiness, Dizziness, Headache, Nausea
  3. Anorexia, decreased visual acuity, Cerebral Oedema
  4. Pulmonary Hypertenion, Pulmonary Oedema
200
Q

What are the treatments for acute mountain sickness?

A
  1. Descent
  2. Acetazolamide
  3. Gamow Bag
201
Q

What is the mechanism of action of Acetazolamide?

A

It is a Carbonic Anhydrase Inhibitor–> reduce H+ secretion in renal cells so that more HCO3- will be excreted in urine

202
Q

What causes Asthma?

A
  1. Bronchospasm
  2. Pulmonary Inflammation
  3. Increased Mucus Secretion
  4. Cholinergic Nerve Over-Activity
203
Q

What happens in the Initial Phase of Asthma?

A

Mast Cell IgE releases Histamine to cause Bronchoconstriction

204
Q

What happens in the Intermediate Phase of Asthma?

A

Release of chemokines stimulate Leukocytes, causing inflammation and mucosal oedema

205
Q

What happens in the Late Phase of Asthma?

A

Release of Lymphocytes, Neutrophils and Eosinophils, causing Lung Epithelial Damage

206
Q

What are the symptoms of Chronic Obstructive Pulmonary Disease (COPD)?

A
  1. Dyspnoea, Cough, Sputum production
  2. Frequent chest infections
  3. increased risk of developing cardiovascular disease
207
Q

What are the causes of COPD?

A
  1. Long term exposure to gases
  2. Persistent airflow limitation, progressive and largely irreversible
  3. Damaged Respiratory Cilia
  4. Chronic Colonization of lower airways by bacteria due to excessive mucus
208
Q

What are 2 examples of COPD?

A
  1. Chronic Bronchitis

2. Emphysema

209
Q

What causes chronic bronchitis?

A
  1. Decreased bronchial luminal diameter
  2. Wall thickening due to inflammation
  3. Increased mucus and mucus plugs
210
Q

What causes Emphysema?

A
  1. Enlargement of alveoli and bronchioles
  2. Destruction of Alveolar walls
  3. Loss of lung elastic recoil–> chest hyperextension
211
Q

What is used in the Quick Relied of Bronchospasm in COPD?

A
  1. 2-4 puffs of rapid-acting ß2-agonist

2. Antibiotics for acute exacerbations with purulent sputum

212
Q

What is used in an Accident/Emergency situation in the acute management of COPD?

A
  1. 24-48% oxygen via face mask
  2. Antibiotics for acute exacerbations with purulent sputum
  3. Nebulised ß2 agonist and Ipratropium
  4. Oral or IV Steroids
213
Q

What is used in a Life-Threatening situation in the acute management of COPD?

A
  1. IV Aminiphylline or Salbutamol

2. If persistently hypoxic/acidotic, Consider NIPPV or Invasive Ventilation

214
Q

What is NIPPV?

A

Nasal Intermittent Positive Pressure Ventilation

215
Q

What is used in the chronic management of COPD?

A
  1. Smoking cessation
  2. Avoid occupational inhaled pollutants
  3. Vaccinations
  4. Bronchodilators: ß2 agonists, M3 antagonists, Xanthines
  5. Anti-Inflammatory Drugs: Inhaled Glucocorticoids
  6. Long-term oxygen therapy
  7. Pulmonary rehabilitation/nutrition/air travel
  8. Surgery
216
Q

What is alpha1-Antitrypsin Deficiency

A

Autosomal Co-dominant disorder where there are mutations on the SERAPINA1 gene on chromosome 14

217
Q

What are the mutations on the SERAPINA1 gene in alpa1-Antitrypsin Deficiency?

A

Z(Glu342Lys) and S(Glu264Val) mutation

218
Q

What are the symptoms of Alpha 1- Antitrypsin Deficiency?

A
  1. Shortness of Breath
  2. Wheezing
  3. Emphysema
219
Q

What is the cause of Alpha 1- Antitrypsin Deficiency?

A

Alpha 1-Antitrypsin is not around to inhibit neutrophil elastins. which cause damage to and reduced elasticity of the alveoli–> can also build up in liver to cause hepatitis

220
Q

What are the treatments for Alpha 1- Antitrypsin Deficiency?

A
  1. Standard COPD Treatments
  2. Augmentation Therapy
  3. In future: gene therapy etc.
221
Q

What is Augmentation Therapy in the treatment of Alpha 1- Antitrypsin Deficiency?

A

Infusions of purified pooled human Alpha 1- Antitrypsin to restore normal levels

222
Q

What is Respiratory Failure?

A

When the Arterial PO2 is low (below 8kPa at atmospheric sea level)

223
Q

What is Type 1 Respiratory Failure?

A

When PO2 is low but PCO2 is normal/low

224
Q

What causes Type 1 Respiratory Failure?

A
  1. Ventilation/Perfusion Mismatch–> If low = asthma, if high = Pulmonary Embolism
225
Q

How is Type 1 Respiratory Failure managed?

A
  1. Giving inhaled O2

2. Mechanical Ventilation if arterial O2 cannot be maintained

226
Q

What is Type 2 Respiratory Failure?

A

When PO2 is low but PCO2 is high

227
Q

What causes Type 2 Respiratory Failure?

A

Hypoventilation throughout lungs e.g. COPD, Sedative& Opoid overdose

228
Q

How is Type 2 Respiratory Failure Managed?

A
  1. Low-dose inhaled O2 (24%)
  2. Respiratory Stimulants
  3. NIPPV but only Mechanical Ventilation for acute cases
  4. Treatment of underlying cause
229
Q

What is cough?

A

Protective reflex which helps clear respiratory passages from fluids, irritants, foreign particles and microbes

230
Q

What is the mechanism of cough?

A
  1. Stimulation of mechanoreceptors or chemoreceptors
  2. Afferent impulses to cough centre in the medulla
  3. Efferent impulses via parasympathetic and motor nerves to diaphragm, intercostal muscles and lung
  4. Increased contraction of diaphragm, abdominal and intercostal muscles
231
Q

What causes cough?

A
  1. Acute Respiratory Infection (URTI, Pneumonia)
  2. Chronic Respiratory Infections (Cystic fibrosis, Bronchiectas)
  3. Airways disease (Asthma, COPD)
  4. Interstitial Lung Disease (Pulmonary Fibrosis)
  5. Irritant (smoke, dust etc.)
  6. Drug-Induced (ACE Inhibitors, Inhaled drugs)
232
Q

What are the 3 types of medications used in the management of cough?

A
  1. Expectorants
  2. Antitussives
  3. Mucolytics
233
Q

What is the mechanism of action of Expectorants?

A
  1. Increase fluidity of secretions

2. Help cough out the mucus

234
Q

What are examples of Expectorants?

A
  1. Guaifenisine

2. Iodine

235
Q

What are the 2 types of Antitussives?

A
  1. Centrally-acting

2. Peripherally-Acting

236
Q

What is the mechanism of action of centrally-acting Antitussives?

A

opoids–> at doses below those needed for pain relief, increase the threshold for the stimulation of neurons in the medullary cough centre

237
Q

What are examples of Centrally-acting Antitussives?

A
  1. Codeine

2. Dextrometorphan

238
Q

Why is Dextrometorphan preferred to Codeine in the management of cough?

A
  1. Not addictive

2. Does not cause constipation

239
Q

What is the mechanism of action of peripherally-acting Antitussives?

A

Reduce the sensitivity of cough receptors

240
Q

What are examples of peripherally-acting Antitussives?

A
  1. Local Anaesthetics
  2. Menthol Vapour
  3. Eucalyptus Oil/Menthol Lozenges
241
Q

What is the mechanism of action of Mucolytics?

A

Break down disulphide bonds in mucus–> reduces the viscosity of mucus

242
Q

What are examples of Mucolytics?

A
  1. Carbocysteine

2. Dornase Alfa

243
Q

What is significant about Dornase Alfa?

A

It is the only mucolytic agent with proven clinical benefit

244
Q

What are the ventilatory adjustments to exercise?

A
  • Increased extraction of O2–> Arteriovenous difference for O2 changes from 5mL% (normal) to 15mL% (exercise)
245
Q

What is Maximal Oxygen Consumption (VO2Max)?

A

Measured by measuring the VO2 plateau which occurs as exercise intensity is raised

246
Q

What is the VO2Max in Sedentary People (normal people with little exercise)?

A

40mL/min/Kg

247
Q

What is the VO2Max in Trained Athletes?

A

60mL/min/Kg

248
Q

What is the VO2Max in Elite Endurance Athletes?

A

> 80mL/min/Kg

249
Q

What is Oxygen Debt?

A

The VO2 in excess of resting VO2 after the end of exercise

250
Q

What is the Anaerobic Threshold?

A

When the metabolic demand for O2 exceeds O2 delivery so that muscles begin to use glycolysis in addition to aerobic metabolism–> leads to lactic acidosis

251
Q

What are the effects of training in the Respiratory System?

A
  1. Increased VO2Max
  2. Increased O2 Debt
  3. Increased Anaerobic Threshold
252
Q

What is unaffected by training in the Respiratory System?

A
  1. VO2 at rest
  2. Diffusing Capacity
  3. Haemoglobin Concentration
  4. Maximum Heart Rate
  5. Cardiac Output at rest
253
Q

What is Neonatal Respiratory Distress Syndrome (NRDS)?

A

Insufficient surfactant in the lungs of a foetus–> rapid laboured breathing in newborn and sternal retraction due to partial lung collapse

254
Q

How do you test the Foetal Lung Maturity?

A
  1. Sample amount of surfactant in the amniotic fluid
  2. Test the Lechtin-Sphingomyelin Ratio–> 2:1 = Deficiency
  3. Test for the presence of Phosphotidylglycerol
  4. Test the surfactant/albumin ratio
255
Q

How do you treat Neonatal Respiratory Distress Syndrome (NRDS)?

A
  1. Treat mother with corticosteroids to increase surfactant lipid synthesis
  2. Treat neonate with exogenous surfactant immediately after birth
  3. Positive Pressure Mechanical Breathing

CVR (5 decks)

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