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Flashcards in COPD Deck (27)
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1

Define COPD in lay terms (NHS website) 

Name for a group of lung conditions that cause breathing difficulties 

2

Define Ventilation (V)

The amount of air travelling INTO THE alveoli 

3

Define Perfusion (Q)

The amount of blood flowing to the alveoli 

4

Levels of perfusion and ventilation and vary at different areas of the lungs. 

State the average V/Q ratio and describe how the ratio changes at different levels of the lung. 

On average, the V/Q ratio is 0.8.  The ideal V/Q ratio would be 1, however, the ratio varies depending on the part of the lung. For example, the ratio is roughly 3.3 in the apex of the lung, and only 0.63 in the base. As such the overall value in the average human is closer to 0.8.

 

The ventilation to perfusion ratio is HIGHER at the APEX of the lung

The ventilation to perfusion ratio is LOWER at the base of the lung 

Levels of perfusion and ventilation INCREASE as you go down the lung, but Perfusion increases to a greater degree than ventilation 

 

 

Gravity plays a significant role on the V/Q ratio:

  • Pleural pressure is increased at the base of the lungs, resulting in more compliant alveoli and increased ventilation
  • Hydrostatic pressure is decreased at the apex of the lung, resulting in decreased flow and decreased perfusion

5

Why is it important that the V/Q ratio is near 1?

To allow for as effecient gas exchange 

6

Explain the difference between a shunt and dead space making reference to the VQ ratio 

  • Shunt - Perfusion with no ventilation - VQ of 0
  • Dead space - Ventilation with NO perfusion - VQ of infinity 

7

What is meant by V/Q mismatch? 

V/Q mismatch means that in some areas of the lungs, the alveoli and capillaries don't line up or there is anatomical dead space. This can mean that in some areas of the lung, there are more capillaries than alveoli, so they are better perfused by blood than ventilated. In other areas, there may be more alveoli with fresh oxygen than capillaries to pick up that oxygen, so they are better ventilated than perfused.

Some degree of mismatch occurs normally, but when it increases beyond a certain point, it causes problems.

8

State what is meant by the VQ ratio 

9

Describe how a V/Q ratio decrease is occuring 

  • Ventilation is not keeping pace with perfusion.
  • The alveolar oxygen levels will decrease, which will lead to a decrease in arterial oxygen levels (PaO2)
  • The alveolar CO2 levels will increase (we're not getting rid of it as fast), also leading to an increase in arterial CO2.

10

State how VQ mismatch affects gas exchange?

  • basically higher of lower, gas exchange is less 

11

What are the two types of VQ mismatch? Define them 

Dead space: ventilation of poorly perfused alveoli

Shunt: Perfusion of poorly ventilated alveoli 

12

Describe how an increase in VQ ratio is occuring

  • decrease in capillary blood flow 
  • increase ventilation 

13

Define COPD 

  • Chronic obstructive pulmonary disease
  • Umbrella term that covers diseases that have airflow limitation that is not fully reversible and destruction of the lung parenchyma 

14

What is the cause of COPD?

The airflow limitation is progressive and is caused by abnormal inflammatory response of the lungs to noxious particles/gases

15

Describe the process of elastic recoil, and briefly discuss how this is affected in emphysema 

  • The elastic fibres in the alveoil allow the alveoli to stretch (when taking in a fresh breath) and contract (thus compressing the air inside and expelling it)
  • They provide general structural support for the aiirways 
  • The elasticity in emphysema is reduced due to degradation of the elastic fibres by neutrophil elastase, meaning the lungs are less able to both stretch to accomodate air and recoil to expell air 
  • Furthemore, the reduced support as a result of the reduced elastin makes the airway prone to collapse, which can result in trapped air 

16

What are the main risk factors of COPD? 

  • Smoking - accounts for 90% of cases 
    • Development of COPD is proportional to the number of cigarettes smoked per day
  • Climate and high air pollutionn are lesser causses of COPD 

17

There are 3 primary routes of pathogenesis for COPD

 

Describe how cigarette smoking contributes to the pathogenesis of smoking 

  • noxious particles from smoke 
  • exposure to cigarette smoke leads to activtion of several patern recognition receptors on alveolar macrophages  via DAMPS released by epithelial cells 
  • This leads to release of proinflammatory cytokins and ATTRACTS neutrophils, monocytes and lymphocytes into the lung 
  • Neutrophils in particular can release elastases (just a class of proteases) and other proteases such as NEUTROPHIL ELASTASE, MMPs 
  • Conversley, there is a reduction in anti-proteases such as Alpha-1-antitrypsin which normally inhibits protease activity 
    • ​ALPHA-1-ANTITRYPSIN IS INHIBITED BY CIGARETTE SMOKE 
  • Cigarette smoke is also thought to cause irritation to airways, resulting in mucous gland hypertrophy 

18

There are 3 main routes for the pathogenesis of COPD

Describe how alpha1 antitrypsin deficiency can lead to COPD

  • Alpha 1 antitrypsin is produced in the liver 
  • it is a protease inhibitor
  • It diffuses in lungs, where it inhibits enzymes proteolytic enzymes such neutrophil elastase ( is a protease) - this is bad since neutrophil elastase can degrade alveolar wall connective tissue 
    • 3 main phenotypes of this deficiency:
      • MM(normal), MZ(heterozygous deficeincy), ZZ (homozygous deficiency) 

19

What is 3 path of development of COPD?

Infection 

20

Study the pathogenesis causes of COPD 

 

Note the imbalance of oxidants and antioxidants 

21

Describe the chronic bronchitis part of the pathophysiology of COPD

  • Increase in number of goblet cells AND increased mucus secretion- especially in larger bronchi, can lead to hypersecretion of mucus - which can block airways 
  • Infiltration of bronchial walls - main lymphocyte infiltrate is CD8 T cells (as opposed to Th2 in asthma) 
  • Ulceration of the columnar epithelium, which in time is replaced by squamous cells - this further down the line can cause mucocilliary disfunction - since the cillia are normal on columnar cells 
  • Inflammaton is followed by scarring and thickening of walls - this narrows the airway
  •  Small airways are particularly affected, initially without symptoms. This inflammation of the small airways is reversible in early stages, but in later stages it is not 
  • Progressive squamous cell metaplasia continues to occur, and scarring of the connective tissue of bronchial walls can occur - further narrowing the airways 
  • ALL OF THIS LEADS TO REDUCED AIRFLOW, as a result of narowed airways 
  • The lack of oxygen getting through to the alveoli, and the lack of CO2 going out causes a V/Q mismatch leading to hypoxemia and hypercapnia - resulting in ACIDOSIS - lower oxygen and higher  CO2
    • ​To compensate for this, the body will try to compensate to make more red blood cells (POLYCYTHEMIA - volume of red blood cells in the blood is elevated)
    • The acidosis and polycythemia contributes to cyanosis - hence BLUE BLOATERS  
  • Another thing that happens in alveolar hypoxia is the pulmonary vessels constrict, shunting blood away from the alveoli which are low in oxygen and diverting it to alveoli that have more oxygen 
    • However by doing this (pulmonar vasoconstriction), you can get an increas in pulmonary vascular pressure - PULMONARY HYPERTENSION
    • Pulmonary hypertension can cause backflow to right side of heart and can cause in RIGHT HEART FAILURE 
    • Another possible (although mainly in more severe cases) effect of the pulmonary hypertension is that it blood being supplied to the left side of the heart is also reduced, and therefore decreased circulatory volume
    • This is bad, because the Renin-angiotensin-aldoesterone system is activated, and you get more fluid retention

22

Define emphysema and describe it's role in the pathophysiology of COPD 

("Pink Puffers')

  • Abnormal, permenant enlargement of airspaces DISTAL to the terminal bronchioles accomapnied by the destruction of their walls (such as resp bronchioles and alveoli)
  • There is also damage to surrounding pulmonary capillary beds (also from neutrophil proteases)
  • Emphysema causes loss of elastic recoil of the lung - this makes it harder for the alveoli to fill and empty
  • This can result in air getting trapped in the airways and result in the small airways in expieration to COLLAPSE and restrict expiration flow, making breathing out really hard - both of these reasons lead to BARRELL CHEST 
  • Due to alveolar damage (reduced elasticity and wall damage)and pulmonary capillary damage  the gas exchange is also poor 
    • ​The result is a decrease in both VENTILATION and PERFUSION - this is called a MATCHED VQ defecit 
  • In blood, you will see hypoxia and hypercania 

23

State the symptoms for COPD

  • Dsypnea 
  • Chronic Cough 
  • Sputum Production 
  • Frequent chest infections
  • Wheezing 

 

 

24

Describe the difference between centri-lobular emphysema and panlobular emphysema 

Centrilobuar 

25

What does a V/Q of 0 indicate?

Airway obstruction

26

What does V/Q of inifite indicate?

Blood flow obstruction 

27