Disorders of Ventilation and Gas Exchange Flashcards

1
Q

Explain the concept of ventilation perfusion matching, why is this concept important

A

You match ventilation or air reaching the alveoli with blood flow to the alveoli. If you have a decrease in blood flow to an alveoli you’ll get bronchoconstriction and that alveoli will not be ventilated, the opposite is also true. If you have bronchoconstriction, blood flow to the alveoli will decrease. So you match ventilation with perfusion, it doesn’t matter which is first or second, you just match it. Function of ventilation perfusion matching is to optimize gas exchange between alveoli and blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pleural effusion

A

fluid in the pleural cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hydrothorax

A

accumulation of serous fluid - yellowish fluid
- seen in heart failure, renal failure, liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

empyema

A

infection in pleural cavity –> pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

chylothorax

A
  • lymph –> milky white
  • trauma, inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hemothorax

A
  • blood in the pleural cavity
  • chest injury
  • chest surgery
    requires drainage (thoracentesis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is pleural effusion dangerous

A

Too much fluid in the pleural cavity → separation of pleural membranes → collapsed lung → atelectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pneumothorax

A
  • air enters the pleural cavity
  • air takes up space, restricting lung expansion
  • partial or complete collapse of the affected lung
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

spontaneous or closed pneumothorax

A
  • rupture of air filled bleb or blister on the lung surface
  • air moves into pleural space and then the ruptured bleb is sealed off. no effect on unaffected lungs during inspiration/expiration
  • secondary spontaneous occurs n patients with lung disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

open pneumothorax

A
  • Air moves in and out of the opening in the chest wall. Heart shifts towards the unaffected lung during inhalation and back towards the affect lung during expiration → mediastinal flutter impairs venous return
  • Decreases the amount of air that enter the unaffected lung during inspiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

tension pneumothorax

A
  • Air moves in during inspiration, can’t move out during expiration so more and more air accumulated in the pleural cavity
  • Compression of the unaffected lung → shift of mediastinum to the opposite side
  • Compression of the vena cava and significantly reduce venous return and CO → life threatening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which pneumothorax is the most dangerous and why

A

tension pneumothorax because it significantly impairs venous return because it results in a bending or kinking of the inferior vena cava, so cardiac output goes way down)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

s/s of pneumothorax

A
  • Increased respiration rate
  • Ipsilateral lung pain
  • Asymmetry of the chest during inspiration
  • Decreased breathing sound on affected side
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

treatment of pneumothorax

A
  • Small spontaneous → air is reabsorbed on its own
  • Needle aspiration or closed drain system → one way valve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

extrinsic asthma

A

(atopic): trigger type I hypersensitivity reaction IgE mediated asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

intrinsic asthma

A

(nonatopic): trigger respiratory infection, cold, exercise, drugs → immune system not involved

17
Q

s/s of asthma

A
  • Cough, marked dyspnea, tight feeling in chest and agitation
  • Wheezing
  • Thick mucus is coughed up
  • Rapid breathing with use of accessory muscles
  • Tachycardia
18
Q

how is asthma treated

A
  • Avoid trigger factors
  • Inhalers → bronchiodilators (beta-2 adrenergic agonist, such as albuterol)
  • Glucocorticoid: reduce inflammation
  • Leukotriene antagonist: reduce inflammation
  • Cromolyn sodium: prophylactic medication which inhibits release of substances from sensitized mast cells in the respiratory tract and decrease the number of eosinophils → reduces the hypersensitivity of the tissue (no value during acute attacks)
19
Q

early phase of asthma

A

10 to 20 min

20
Q

late phase of asthma

A

4 to 8 hours

21
Q

Explain the pathophysiology of an asthma attack

A

Bronchi and bronchioles are excessively responsive to stimuli leading to bronchoconstriction, inflammation with edema, and increased secretion of thick mucus → interfere with air flow

22
Q

What is Cor Pulmonale and how does it develop

A

COPD may result in cor pulmonale – right sided congestive heart failure due to lung disease

23
Q

What are the different types of COPD

A
  • emphysema
  • chronic bronchitis
24
Q

Emphysema

A
  • increase compliance to air flow because of chronic or recurring expiratory obstruction
  • Breakdown of alveoli wall → decreases surface area
  • Loss of pulmonary capillaries → decreased gas exchange
  • Loss of elastic fibers → easy to get air in but not out
25
Q

cause of emphysema

A
  • smoking
  • genetics
  • exposure to air pollutants
26
Q

s/s of emphysema

A
  • Dyspnea
  • Hyperventilation with prolonged expiratory phase
  • Anorexia
  • Clubbed fingers with secondary polycythemia
27
Q

chronic bronchitis

A
  • Obstruction of small airways
  • Changes in bronchi – constant irritation from smoking or exposure to industrial pollution
  • Effects are irreversible and progressive
28
Q

cause of chronic bronchitis

A
  • Inflammation and obstruction
  • Repeated infection
  • Chronic coughing
  • Increased number of mucous cells
29
Q

s/s of chronic bronchitis

A
  • Constant productive cough
  • Shortness of breath
  • Mucous secretions are thick and purulent
  • Cough more severe in morning
  • Airway obstruction