Psl 301: Lec 23

Front 1

1) Describe the lung volume changes with respect to inspiration and expiration.

s4

Back 1

1) Brainstem sends signals to the phrenic nerve which activates diaphragm -> inspiratory muscles contract -> thoracic volume increases -> lung expands -> air goes in

At end of inspiration (reached max air volume), stretch receptors activate in the alveoli -> diaphragm contracts -> a bit further diaphragm relaxes, chest contracts -> air continues to go out until done

Front 2

1) Describe the steps of inspiration with respect to the muscles

s5

Back 2

1) -> Rib cage and thoracic cavity expand: Sternocleidomastoids andscalenes contract. The external intercostal muscle as well. The tongue muscle contracts slightly before diaphragm to allows air to go in. -> diaphragm muscle contracts and moves down

-> pressure in thoracic cavity decreases and lungs expand: Pressure inside lungs decreases, air moves in

Front 3

1) Describe the action of the intrapleural space

s6

Back 3

1) fluid filled with a few mL of fluid. Liquid is non expandable, so lungs follow volume changes of the thorax. The pleural membranes are adherent to the lungs and to the thoracic wall by connective tissue. Intrapleural space has -3 mmHg subatmospheric pressure, so it acts as suction cups.

Front 4

1) What is Pneumothorax condition?

s8

Back 4

1) Have air in pleural cavity breaks the fluid bond holding the lung to the chest wall. So have air instead of fluid. Now when the cage is expanding, the lungs don't follow. Lung collapses to unstretched size

-> Can apply wet dressing on the wound to act as a one way valve out and positive pressure at the mouth to inflate lungs

Front 5

1) Describe the Hydrothorax condition, the symptoms, causes and treatments.

s11

Back 5

1) -> Blood accumulating in the pleural cavity

-> Symptoms: Tachypnea (Faster breathing), dyspnea (feeling difficulty of breathing), cyanosis (Get blue, lack of o2), low breathing sounds

-> cause: traumatic, from blunt or penetrating injury to thorax

-> Removing source of bleeding and by draining the blood already in thoracic cavity

Front 6

1) What is ventilation and what is the formula?

2) How does air flow into the lung and what is the formula?

s12

Back 6

1) Ventilation moves air between environment and the alveoli.

V (with dot on top) = Rate x volume L/min

2) Because of pressure gradient

Flow = deltaP / R

less resistance, higher flow

Front 7

1) What is Boyle's law?

2) Describe the steps of breathing with respect to pressure changes.

s15

Back 7

1) P1 V1 = P2 V2

2) Inspiration: inspiratory muscles contract, alveolar pressure drops by 1 mmHg.

end of inspiration: volume of air at max, alveolar pressure equal to atmospheric

expiration: inspiratory muscles cease. Elastic recoil of the lungs returns the diaphragm and the rib cage to original position. Air pressure in lung increases 1 mmHg above atm pressure.

active expiration: Occurs when hyperventilation or CO2 increase. Internal intercostal and abdominal muscles.

intrapleural pressure in inspiration: -3 mmHg before inspiration, and P alv = P atm. At inspiration, intrapleural P goes to -6, P alv = P atm - 1

Front 8

1) Describe the different components of lung volume.

s17

Back 8

1) Quiet breathing: 0.5 L

Shallow breathing: 0.3 L

These 2 make the 0.35 L (70%) of air used for gas exchange.

Remaining 0.15 L comes from dead space volume (air remaining in trachea, bronchi, and/or poorly perfused alveoli)

Front 9

1) What is spirometry?

2) What is the residual lung volume?

3) What is vital capacity?

4) What is the tidal volume?

5) What is the functional residual capacity (FRC)?

s18

Back 9

1) Measure volume of air inspired and expired by the lungs. The chamber measures it and records the volumes.

2) The volume of air remaining in lungs after maximum voluntary expiration

3) Maximum amount of air that can be intaken.

4) The normal amount of air going in and out of air (like non voluntary)

5) Volume of air in lung at end of normal expiration

Front 10

1) What is emphysema?

2) What is pneumothorax?

3) What is pulmonary fibrosis?

s20

Back 10

1) Elevated FRC; Destruction of tissue around alveoli by smoking. alveoli are flappy and can't expand/contract a lot, not very elastic. So can't fully contract and there we will be higher air left.

2) Lowered FRC. If lots of air in pleural cavity, push against lung and compress. FRC will go down.

3) Fibrous tissues accumulating close to alveoli, due to pollutants e.g. environment, tobacco, abestos, coal. FRC Lowered, lower space for alveoli

Front 11

Lung volume disease; explain how they affect

1) Diaphragmatic hernia

2) COPD (obstruction of airways), Asthma (inflammation of airways)

3) Obstructive sleep apnea.

s21

Back 11

1) Organs go in pleural cavity, compress lungs. lower FRC

2) Expiratory reserve volume decreases

3) Tidal volume decrease, higher pressure. Apnea = cessation of breathing e.g. due to bad brain signals, etc.

Front 12

1) What is hyperpnea?

2) What is eupnea?

s22

Back 12

1) Increased rate and volume in response to changes in metabolism e.g. increase when excercising.

2) Normal quiet breathing

Front 13

1) Describe lung compliance property. What happens when you have low compliance

s23

Back 13

1) Degree the lungs comply by changing their volume when subjected to change in intrapleural pressure or the ability of lung to stretch.

-> Influenced by elastin fibre network and surface tension in alveoli

-> When have low compliance, hard to expand, get restrictive lung disease such as fibrotic lung disease

Front 14

1) Describe airway resistance property.

s23

Back 14

1) Force that opposes movement of air.

-> Influenced by type of flow or airway diameter. If you have inflammation of airway, have less space in airway and harder to move air.

-> High resistance: asthma, obstructive sleep apnea

Front 15

1) How is lung compliance calculated?

s24

Back 15

1) CL = delta long volume (L) / delta P (mmHg)

Low compliance = hard to expand alveoli and lungs

High compliance = too elastic, too easy to expand

Front 16

1) How does the elastin fiber network work.

2) What happens in pulmonary fibrosis? What are the symptoms and how is compliance and FRC affected?

s26

Back 16

1) Tiny cells between alveoli, contract and push against wall of alveoli. They are cross linked and can contract or stretch

2) Scaring of the lungs. Fibrious connective tissues around the lung that can destroy alveoli over time

-> Symptoms: shortness of breath, chronic dry, hacking coughing, fatigue and weakness, chest discomfort, loss of appetite and rapid weight loss.

-> Low compliance and low FRC

Front 17

1) What are the types of flows that can affect airway resistance?

s28

Back 17

1) -> Laminar flow: Smooth flow in normal airways, e.g. trachea and bronchi

-> Turbulent flow: e.g. when have mucus or secretion, would be harder for air to move e.g. in asthma. Can give heliox, mix of oxygen and helium, which is lighter than oxygen

Front 18

1) How is resistance measured?

2) What are the factors that can affect airway diameter.

s29

Back 18

1) R = L (length of tube) * n (gas viscosity) /r^4

2) -> Upper airway diameter: If closed, can't move air in and out. Diameter depends on the activity of the upper airway muscles. If not, then the airway too small and will collapse cause negative pressure.

In OSA (Obstructive sleep apnea), get relaxation of upper airway muscles.

-> bronchoconstriction: Can happen due to allergy or inflammation. Can give histamine.

Front 19

1) What is COPD? What happens in it, what are causes and symptoms.

s31

Back 19

1) Chronic obstructive pulmonary disease: common in smoking. Get inflammation and mucus secretion in airways (get bronchitis) and emphysema (destruction of lung tissues). Increases airways resistance, decrease compliance and reduce gas exchange.

-> Symptoms: Chronic cough, dyspnea, less intense breath sounds, airflow limitation

-> Cause: by noxious gas or particles, commonly from tobacco smoking, abnormla inflammatory response.

Front 20

1) What happens in OSA?

s32

Back 20

1) -> reduction of upper airway muscle activity

-> diaphragm activity but too low.

-> Rib cage and abdomen movements are opposite: rib cage expands and abdomen contracts

-> Arousal and breathing resumes

Airway collapses ^

Front 21

1) What is hypopnea? What are OSA symptoms?

s34

Back 21

1) Have apnea, no breathing for some time, but movement of abdomen.

-> Hypopnea: reduction of the apnea, still have little flow. But have lots of abdomen movement.

-> Apnea-Hypopnea index measures the intensity of episodes in an hour.

-> Symptoms: daytime sleepiness, depression, hyperactive behaviours, repeated desaturation during night.

Front 22

1) What are long term consequences of OSA?

Treatments?

Causes?

s35, 36

Back 22

1) -> casdiovascular diseases - hypertension, stroke

-> treatments: losing weight, continuous positive airway pressure (CPAP) in the night

-> Relaxation of upper airway muscles, accumulation of fat (narrowing the upper airway). Alcohol worsens muscle relaxation

-> Fluid shift from legs to neck in the night

-> Weight of muscle of tongue by gravity, weight of neck,