Respiratory System Flashcards

1
Q

What is Respiratory Physiology

A

Respiratory physiology is the study of how oxygen is brought into the lungs and delivered to peripheral tissues and how carbon dioxide is removed.

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2
Q

What are the functions of the respiratory system

A

Provides oxygen and eliminates carbon dioxide for homeostatic regulation of blood gases. Protects against microbial infection in an filtering action. Regulates blood in coordination with kidneys. Contributes to phonation, contributes to olfaction and reservoir for blood.

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3
Q

How is the respiratory system organized

A
Upper Airways
Trachea
Lungs
Muscles of Respiration
Rib Cage and Pleura
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4
Q

What makes up the upper airway of the respiratory system

A

They are the gateway to the lungs. It is made up of the nasal cavities, oral cavities, pharynx, and larynx.

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5
Q

What makes up parts of the lungs

A

Bronchi, bronchioles, alveoli, smooth muscles, connective tissue, and pulmonary circulation

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6
Q

What are upper airways

A

The upper airways will warm the air. The air travels from either the nasal cavity or oral cavity into the pharynx and then the larynx. The air then moves to the trachea.

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7
Q

What makes up the trachea and the bronchi

A

Trachea and primary bronchi are made up the c-shape cartilage and smooth muscle. Bronchi is made up plates of cartilage and smooth muscle. Bronchioles and terminal bronchioles there is only smooth muscle.

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8
Q

What is the process of continuous branching

A

We go from 1 branch being the trachea to upwards of 60,000 in the bronchioles.

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9
Q

What is the conducting zone

A

The conducting zone leads gas to exchanging region of the lungs, getting through the “anatomical dead space.” NO alveoli and NO gas exchange.

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10
Q

What is the respiratory zone

A

The respiratory zone is where the gas exchange happens and it contains alveoli.

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11
Q

Where is the higher surface area in the lungs

A

Even though the airways are smaller the more we progress into the lungs there is a higher surface area due to the sheer quantity of alveolar sacs and alveoli.

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12
Q

What are the alveoli in the lungs.

A

A tiny, thin-walled capillary-rich sac in the lungs where the exchange of oxygen and carbon dioxide takes place. There are about 500 million alveoli in the human lung and there are about 280 billion of capillaries in the lung.

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13
Q

What are type 1 alveoli

A

Most of the surface of alveolar walls are lined by a continuous monolayer of flat epithelial cells, they do not divide and they are susceptible to inhaled or aspirated toxins

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14
Q

What are type 2 alveoli

A

Type 2 alveolar cells (7% of alveolar surface) and produce SURFACTANT, a detergent-like substance made of lipoproteins that reduces the surface tension of alveolar fluid. They act as progenitor cells and when there is injury to type 1 cells they can be replaced by type 2 cells that can multiply and differentiate

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15
Q

What are the alveolar walls like

A

The alveolar walls also contain a dense network of capillaries and a small interstitial space (connective tissue and interstitial fluids)

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16
Q

How small are the capillaries in the alveolar walls

A

Capillaries are small (7 to 10 micrometers in diameter), just enough space for a red blood cell to pass.

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17
Q

How long do red blood cells spend in the capillaries of the respiratory system

A

Each red blood cell spends about 0.75 seconds in the capillary network and during this time probably traverses two or three alveoli.

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18
Q

How does Oxygen and Carbon Dioxide travel through respiratory membrane

A

The respiratory membrane is extremely thin and then can be easily damaged. Transfer of oxygen to carbon dioxide occurs by DIFFUSION through the RESPIRATORY MEMBRANE

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19
Q

What can damage the respiratory membrane

A

High blood pressure or too much pressure from intubation/respiration will distend the capillary and the rest of the respiratory circulation and may cause the epithelium to break; fluid/blood goes into the lungs and causes problems

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20
Q

What are the steps of Respiration

A
  1. Ventilation: Exchange of air between atmosphere and alveoli by bulk flow
  2. Exchange of Oxygen and Carbon Dioxide between alveolar air and blood in lung capillaries by diffusion
  3. Transport of Oxygen and Carbon Dioxide through pulmonary and systemic circulation by bulk flow
  4. Exchange of Oxygen and Carbon Dioxide between blood in tissue capillaries and cells in tissues by diffusion
  5. Cellular utilization of Oxygen and production of Carbon Dioxide
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21
Q

How is Respiratory Airflow (Ventilation) Produced?

A
  1. Central nervous system sends rhythmic excitatory (respiratory) drive to respiratory muscles
  2. Respiratory muscles contract rhythmically and in a very organized pattern
  3. Changes in volume and pressures at the level of the chest and lung occur
  4. Air flows in and out of the lungs
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22
Q

What are the respiratory muscles

A

Pump muscles
Airway muscles
Accessory muscles

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23
Q

What are the inspiration pump muscles

A

Diaphragm, external intercostals, parasternal intercostals

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24
Q

What are expiration pump muscles

A

Internal intercostals, and abdominal muscles

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25
Q

What are inspiration airway muscles

A

Tongue protruders, alae nasi, and muscles around the airways (pharynx and larynx)

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26
Q

What are expiration airway muscles

A

Constrictor muscles around the airways (pharynx and larynx)

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27
Q

What are inspiration accessory muscles

A

Sternocleidomastoid, scalene, and pectoralis.

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28
Q

How does the Diaphragm work

A

It is an inspiratory pump muscle and the most important muscle of inspiration. It is a dome shaped muscle which flattens during contraction (inspiration), abdominal contents are forced down and forward and rib is widened leading to an increase in volume of the thorax.

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29
Q

How does the external intercostal muscle work

A

It is an inspiratory pump muscle. It contracts and pulls the ribs upward increasing the lateral volume of the thorax and it moves in a bucket handle motion.

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30
Q

How does the parasternal intercostal muscle work

A

It is an inspiratory pump muscle. It contracts and pulls the sternum forward, increasing anterior and posterior dimensions of the rib cage. It works in a pump handle motion.

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31
Q

How do the abdominal muscles work

A

They are expiratory pump muscles. It is made up of external oblique, internal oblique, rectus abdominis, and transverse abdominis.

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32
Q

What do the abdominal muscles do at rest

A

They are relaxed at rest. They are involved in other physiological functions such as coughing, vomiting, defecation, and posture.

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33
Q

What do abdominal muscles do when you are active

A

Deeper, faster breathing requires active contraction of abdominal and internal intercostal muscles to return the lungs to its resting position. After exercise their goal is to return to the resting position

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34
Q

How do the internal intercostal muscles work

A

They are expiratory pump muscles. They are relaxed at rest. During exercise, internal intercostal muscles pull rib cage down, reducing thoracic volume

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35
Q

How do the accessory inspiratory work

A

Scalenes: Elevates upper ribs
Sternocleidomastoid: Raises the sternum
Pectoralis: Elevates ribs
These muscles contribute little to quiet breathing or at rest. They contract vigorously during exercise or forced respiration.

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36
Q

What muscles are involved during quiet inspiration

A

Quiet inspiration involves the external intercostal muscles and the diaphragm

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37
Q

What muscles are involved in forced inspiration

A

Forced inspiration involves the sternum, sternocleidomastoid, pectoralis, and diaphragm.

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38
Q

What muscles are involved in quiet expiration

A

During quiet expiration the diaphragm, and abdominal organs are involved

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39
Q

What muscles are involved in forced expiration

A

During forced expiration, the posterior internal intercostal muscles, diaphragm, abdominal muscles, and abdominal walls are involved. During forced (active) expiration abdominal muscles contract and push abdominal contents and diaphragm upward to reduce thoracic volume

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40
Q

How do upper airway muscles generate airflow

A

For inspiratory pump muscles to generate airflow, the upper airway must be open. Several muscles contribute to opening the upper airways and reduce airway resistance. These muscles include the tongue protruders, alae nasi, pharyngeal and laryngeal dilators for inspiration and pharyngeal and laryngeal constrictors for expiratory

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41
Q

What is obstructive sleep apnea

A

Reduction in upper airway patency during sleep such as snoring and sleep disturbances. This is caused by anatomical defects and a reduction in muscle tone. This is treated the CPAP machine called the continuous positive airway pressure

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42
Q

How does the conducting zone and “muco-ciliary escalator” work as filtering action

A

The conducting airways are lined by a superficial layer of epithelial cells which comprises mucus-producing (goblet) cells and ciliated cells. These cells function in a coordinated fashion to entrap inhaled biological and inert particulates and remove them from the airway.

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43
Q

How are deposited particles removed from the tracheobronchial tree

A

It is an effective clearance that requires both ciliary activity and respiratory fluids. The ciliated cells produce periciliary fluid (SOL LAYER) with low viscosity that is optimal for ciliary activity. Goblet cells produce mucus (GEL LAYER) distributed in patches that have high viscosity and high elastic properties and trap inhaled materials. The cilia movements downwards towards the nasopharynx and upwards towards the trachea.

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44
Q

What is the filtering action of the macrophages in the alveoli

A

It is the last defence against inhaled particles. They rapidly phagocytize foreign particles and substances as well as cellular debris. Silica dust and asbestos can cause pulmonary fibrosis and they kill the macrophages through disintegration.

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45
Q

What is spirometry

A

Pulmonary function test to determine the amount and the rate of inspired and expired air.

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46
Q

What are electronic spiromets

A

They act as airflow transducers. They digitally convert airflow rates and volumes into electronic signals, which can be digitally analyzed and displayed.

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47
Q

What is a spirometer

A

The spirometer is an apparatus used for measuring the volume of air inspired and expired by the lungs. It records the amount and rate of air that you breathe in and out over a period.

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48
Q

What is a spirogram

A

A test used to measure lung volume and capacities. The residual volume, functional residual capacity and total lung capacity cannot be measured by means of a spirometry test

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49
Q

What is residual volume

A

Residual volume is necessary and the amount of air that remains in the lungs after completely forced expiration - this is necessary, so our alveoli don’t collapse.

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50
Q

What is Tidal Volume

A

The volume of air moved IN OR OUT of the respiratory tract (breathed) during each ventilatory cycle.

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51
Q

What is Inspiratory Reserve Volume (IRV)

A

The additional volume of air that can be forcibly inhaled following a normal inspiration. It can be assessed by simply inspiring maximally to the maximum possible inspiration

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52
Q

What is Expiratory Reserve Volume (ERV)

A

The additional volume of air that can be forcibly exhaled following a normal expiration. It can be assessed by expiring maximally to the maximum voluntary expiration

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53
Q

How can you calculate residual volume

A

RV = FRC - ERV
RV: Residual Volume
FRC: Functional residual capacity
ERV: Expiratory Reserve Volume

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54
Q

What is Vital Capacity

A

The maximal volume of air that can be forcibly exhaled after a maximal inspiration

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55
Q

How can you calculate vital capacity

A
VC = TV + IRV + ERV
VC: Vital Capacity
TV: Tidal Volume
IRV: Inspiratory Reserve Volume
ERV: Expiratory Reserve Volume
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56
Q

What is Inspiratory Capacity

A

The maximal volume of air that can be forcibly inhaled

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57
Q

How do you calculate the inspiratory capacity

A

IC = TV + IRV
IC: Inspiratory Capacity
TV: Tidal Volume
IRV: Inspiratory Reserve Volume

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58
Q

What is functional residual capacity

A

The volume of air remaining in the lungs at the end of a normal expiration

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59
Q

How do you calculate functional residual capacity

A

FRC = RV + ERV
FRC: Functional Residual Capacity
RV: Residual Volume
ERV: Expiratory Reserve Volume

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60
Q

What is Total Lung Capacity (TLC)

A

The volume of air in the lungs at the end of a maximal inspiration

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61
Q

How do you calculate Total Lung Capacity

A
TLC = FRC + TV + IRV = VC + RV
TLC: Total Lung Capacity
FRC: Functional Residual Capacity
TV: Tidal Volume
IRV: Inspiratory Reserve Volume
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62
Q

What is minute (total) ventilation

A

Total amount of air moved into the respiratory system per minute

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63
Q

What is alveolar ventilation

A

Amount of air moved into the alveoli per minute. Alveolar ventilation is less than minute ventilation and it depends on anatomical dead space.

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64
Q

What are the effects that breathing pattern in alveolar ventilation

A

Increased DEPTH of breathing is more effective in increasing alveolar ventilation than an equivalent increase in breathing RATE

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65
Q

What is the forced expiratory volume in one second (FEV1)

A

A healthy person can normally blow out most of the air from the lungs in about 1 second

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66
Q

What is the ratio of FEV1:FVC (forced expiratory volume in one second:forced vital capacity)

A

The proportion of the amount of air that if blown out in 1 second.

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67
Q

What can a spirometry test show us

A

It can so us if the person is normal in regards to age, sex, weight, and height. We can also see if there is an obstructive pattern or a restrictive pattern.

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68
Q

What is an obstructive pattern

A

Patients affected by obstructive lung disease have shortness of breath due to difficulty in exhaling all the air from the lungs. Because of damage to the lungs or narrowing of the airways (bronchial constriction), exhaled air comes out more slowly than normal. At the end of a full exhalation, there an abnormally high amount of air that is still in the lungs

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69
Q

What can cause an obstructive pattern

A

Bronchial asthma, chronic obstructive disease and cystic fibrosis.

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70
Q

What does the spirometry test tell us about the obstructive pattern

A

FEV1 (forced expiration volume in 1 second) is significantly reduced
FVC (forced vital capacity) is normal/reduced
FEV1:FVC ratio is reduced.

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71
Q

What is a restrictive pattern

A

Patients affected by restrictive lung disease cannot fully fill their lungs with air. Their lungs are restricted from fully expanding. Restrictive lung disease most often results from a condition causing stiffness in the lungs themselves. In other cases, a stiffness of the chest tail, weak muscles, or damaged nerves may cause the restriction in lung expansion.

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72
Q

What causes restrictive patterns

A

Lung fibrosis, neuromuscular diseases (ALS, muscular dystrophy), or scarring of the lung tissues.

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73
Q

How does a spirometry show a restrictive pattern

A

Reduced vital capacity
FEV1 is reduced (forced expiratory volume in 1 second)
FVC is reduced (forced vital capacity)
FEV1:FVC is above average

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74
Q

What is the Helium Dilution Method

A

Helium is insoluble in blood and after several breaths, the helium will equilibrate. The concentration is measured at the end to see if there is an expiratory effort increase/decrease.

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75
Q

What are the static properties of the lung

A

Mechanical properties when no air is flowing (which are necessary to maintain lung and chest wall at a certain volume)

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76
Q

What are dynamic properties of the lung

A

Mechanical properties when the lungs are changing volume and air is flowing in and out (which is necessary to permit airflow)

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77
Q

What is ventilation

A

Exchange of air between the atmosphere and the alveoli (bulk flow - gas moves from high pressure to low pressure)

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78
Q

What is Boyle’s Law

A

For a fixed amount of an ideal gas kept at a fixed temperature, P [pressure], V [volume] are inversely proportional, so while one increases, the other decreases
P1V1 = P2V2 at a constant temperature

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79
Q

According to Boyle’s Law what happens when there is no net movement of air

A

Pressure between the two areas (atmosphere and alveoli) will have no net movement of the air

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80
Q

According to Boyle’s Law what happens the alveoli experiences an increase in volume

A

The alveoli increases in volume and decreases in pressure. The air moves from the atmosphere in the alveoli.

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81
Q

According to Boyle’s Law what happens where is an increase in pressure in the alveoli

A

When the alveoli decreases in volume and increases in pressure, the air moves from the alveoli to the atmosphere.

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82
Q

How do you get airflow

A

Once pressure difference is generated between inside and outside of lung, air moves via the flow from region of high pressure to the region of low pressure.

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83
Q

What happens to pressure and volume during inspiration

A

During inspiration we will increase the pulmonary volume the alveolar pressure (PALV) will decrease and increasing the atmospheric pressure (PATM)

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84
Q

What happens to pressure and volume during expiration

A

During expiration we will decrease the pulmonary volume, the alveolar pressure (PALV) increases to more than the atmospheric pressure (PATM) leading to an overall decreased pulmonary volume.

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85
Q

What is lung pressure

A

Lung pressure involved in lung volumes and in the movement of air and out of the lungs

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86
Q

What pressures are impacted during inspiration and expiration

A

During inspiration and expiration, the air moves in and out the lungs due to the variations in the intrapleural pressure (PIP), alveolar pressure (PALV), and transpulmonary pressure (PTP)

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87
Q

What is the pleurae

A

The pleurae form a thin double-layered envelope. The parietal pleura covers the thoracic wall and superior face of the diaphragm. The visceral pleura covers the external surface of the lung

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88
Q

What is the intrapleural fluid

A

There is ~10 mL and it reduces the friction of lungs against thoracic wall during breathing, it is extremely thin between 5-35 micrometers

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89
Q

What determines lung volume determined by

A

The interaction between the lungs and the thoracic cage determines the lung volume.

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90
Q

What is the elastic recoil of lung and chest wall

A

The lungs tend to collapse because of their elastic recoil. The chest wall tends to pull the thoracic cage outward because of their elastic recoil. At equilibrium, the inward elastic recoil of the lungs exactly balances outward elastic recoil of the chest wall.

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91
Q

How does the lungs and the chest wall interact

A

This interaction between lungs and chest wall does not occur by direct attachment but through the intrapleural space between the visceral and parietal pleura

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92
Q

What is intrapleural pressure (PIP)

A

Intrapleural pressure (PIP) is the pressure within the pleural cavity. It fluctuates with breathing, but it is always subatmospheric due to the opposing directions of the elastic recoil of lungs and thoracic cage. It acts as a relative vacuum.

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93
Q

What happens if the intrapleural pressure (PIP) and the alveolar pressure (PALV) are the same

A

If the Intrapleural pressure (PIP) equals alveolar pressure (PALV) the lungs would collapse

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94
Q

What is alveolar pressure (PALV)

A

Alveolar pessure is the air inside the alveolar. When the glottis is open and no air flows into and out of the lungs, the pressures in all parts of the respiratory tree, including the alveoli (PALV), are equal to atmospheric pressure. Alveolar pressure (PALV) is a dynamic event, directly involved in producing air flow

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95
Q

What is transpulmonary pressure (PTP)

A

It is the force responsible for keeping the alveoli open, expressed as the pressure gradient across the alveolar wall. Alveolar pressure (PALV) should always be more than Intrapleural Pressure (PIP), transpulmonary pressure more than 0 to maintain the lungs expanded in the thorax. Transpulmonary pressure (PTP) is a static parameter which does not cause airflow, but determines lung volume (VL).

96
Q

What are the impacts of pressures during inspiration

A
  1. Central nervous system causes the diaphgram and inspiratory intercostals to contract
  2. The thorax expands
  3. The intrapleural pressure becomes more subatmospheric
  4. The transpulmonary pressure increases
  5. The lungs expand
  6. Alveolar pressure becomes subatmospheric
  7. Air flows into the alveoli
97
Q

What are the impacts of pressure duing expiration

A
  1. The central nervous system causes the diaphragm and inspiratory intercostals to stop contracting
  2. The chest wall recoils inward
  3. The intrapleural pressure moves back toward the preinspiration value
  4. Transpulmonary pressure moves back towards preinspiration value
  5. The lungs recoil toward preinspiration size
  6. Air in alveoli becomes compressed
  7. Alveolar pressure becomes greater than the atmospheric pressure
  8. Air flows out of the lungs
98
Q

What are the resistive forces of airway

A

Inertia of the respiratory system which is neglible
Friction caused by lung tissue past itself during expansion, lung and chest wall tissue surfaces gliding past each other, and frictional resistant to flow of air through the airways represents 80% of total airways resistance

99
Q

What are the different kinds of airway patterns

A

Laminar
Transitional
Turbulent

100
Q

What is laminar airflow

A

The subject invests relatively little energy in airflow resistance; characteristic to the small airways that are distal to terminal bronchioles

101
Q

What is transitional airflow

A

It takes extra energy to produce vortices and the resistance increases; airflow is transitional throughout most of the bronchial tree

102
Q

What is turbulent airflow

A

The effective resistance to airflow is the highest; in the large airway (trachea, larynx, pharynx), where the airway radius is large and linear air velocities may be extremely high

103
Q

What is the resistance to airflow

A

For laminar flow Poiseullie’s law states that airway resistance is proportional to the viscosity of the gas and the length of the tube/airway, but is inversely proportional to the fourth power of the airway radius.

104
Q

What is airway resistance in the respiratory tract

A

It is inversely proportioanl with the 4th power of airway radius leads to each small airway has a high individual resistance. However, the approximately 65,000 terminal bronchioles aligned in parallel have a much lower aggregated resistance compared to the only few large airways

105
Q

How can the smaller airways detemine airflow resistance

A

In disease conditions the small airways play a large role because they are easily occluded by smooth muscle contraction in their walls, edma occurring in the walls of alveoli and bronchioles, and mucus collecting in the lumens of bronchioles

106
Q

What is lung compliance

A

Lung compliance is a measure of the elastic properties of the lungs and is a measure of how easily the lungs can expand.

107
Q

How is lung compliance measures

A

Lung compliance is the magnitude of the change in lung volume (V), produced by a given change in transpulmonary pressure (PTP). It is the slope measured in the Pressure-Volume Curve.

108
Q

What is lung compliance determined by

A

Elastic components of lungs and airway tissues - elastic and collagen
Surface Tension at the air-water interface within the alveoli. The surface tension at the air-water interface accounts for about two-thirds of the elastic recoil of the lungs and this leads to surface tesion decreasing lung compliance

109
Q

What is static compliacne of the lung

A

Static compliance represents lung compliance measured during periods of no gas flow, such as during an inspiratory/expiratory pause.

110
Q

How is static compliance of the lung determined

A

Static compliance of the lung is determied by P (pressure)/V (volume) slope when measured at functional residual capacity (FRC), that is at the end of an expiratory effort.

111
Q

What does the slope of static compliance look like with a patient with low compliance

A

Patients with low compliacen have an extremely low slope

112
Q

What does the slope of static compliance look like with a patient with high compliance

A

Patients with high compliacne typically have floppy lungs which result in increased volume, however, this is not beneficial because it is probably a loss of alveolar tissue.

113
Q

What is dynamic compliance of the lung

A

Dynamic compliance represents pulmonary compliance during periods of gas flow, such as during inspiration, this happens when the transpulmonary pressure (PTP) continuously changes.

114
Q

What does the dynamic compliance of the lung tell us

A

Since dynamic compliance is measured during airflow, it reflects not only the lung stiffness but also the airway resistance, against which distending forces must act.

115
Q

When does dynamic compliance of the lungs fall

A

Dynamic compliance falls when either lung stiffness or airway resistance increases. Dynamic compliance is always less than or equal to static lung compliance.

116
Q

What is the pressure-volume relationship during an hemothorax

A
  1. Stable Lung Volume (VL)
  2. Opening of airways
  3. Linear expansion of open airways
  4. Limit of airway inflation
117
Q

What is the importance of stable lung volume (VL) during a hemothorax

A

At low lung volumes it is difficult to pop open an almost completely collapsed airway; rising Transpulmonary pressure (PTP) has little effect on lung volume (VL)

118
Q

What is the importance of opening of airways during a hemothorax

A

The first increases in lung volume (VL) reflect the popping open of the proximal airways, followed by their expansion and recruitment of others.

119
Q

What is the importance of linear expansion of open airways during a hemothorax

A

When all the airways are open, making intrapleural pressure (PIP) more negative by chest wall expansion inflates the lungs and increases lung volume (VL) in a linear fashion

120
Q

What is the importance of limiting of airway inflation during a hemothorax

A

At high lung volume (VL) lungs compliance decreases

121
Q

What is hysteresis

A

Defines the difference between the inflation and deflation compliance paths. It exists because a greater pressure difference is required to open a previously closed (or narrowed) airway than to keep an open airway from closing

122
Q

What are the elastic components of the airways

A

Localized in alveolar walls, and around vessels and bronchi. Lung elastic behaviour has less to do with simple elongation of fibers that it does with their geometrical arrangements. Made of collagen which is like a strong twine, high tensile strength, and inextensible. Made of elastin which is like a weak spring, low tensile strength, and extensible.

123
Q

What is an emphysema

A

Floppy lungs because of elastin destruction and alveolar wall destruction. Increased compliance with much less elastic recoil - for little changes in the transpulmonary pressure (PTP) there are large changes in lung volume. Time to fill and empty the lungs is increased.

124
Q

What is pulmonary fibrosis

A

Collagen deposition in alveolar walls in response to lung injury, silica dust, or abestos. Reduction in lung compliance which leads to higher transpulmonary pressure (PTP) changes are necessary to generate changes in lung volume

125
Q

What is alveolar surface tension

A

Water molecules at the surface of a liquid-gas interface are attached strongly to the water molecules within the liquid mass. This cohesive force is called “surface tension.” Surface tension is a measure of the attracting forces to pull a liquid’s surface molecules together at an air-liquid interface.

126
Q

What are the factors affecting the pressure-volume relation

A

Surface tension is seen at all air-fluid boundaries that arises because of hydrogen bonding of water molecules. Importance of surface tension is clear in P(pressure)-V(volume) curve in which surface tension is eliminated with saline-filled lungs

127
Q

What is the effect of surface tension

A

The effect of surface tension is to “cause” the surface to maintain as small an area as possible. When lungs are inflated with liquid - no hysteresis and much lower inflation pressures occur.

128
Q

What is alveolar surfactant

A

Air entering the lungs is humidifed and saturated with water vapour at body temperature. The water molecules cover the alveolar surface. Surface water molecules create substantial surface tension. Alveolar surface tension creates inward recoil which leads to alveolar collapse.

129
Q

How does surface tension impact the alveoli

A

The surface tension acts like a belt tightening around one’s waist. It tends to decrease the volume of compressible gas inside the alveoli and increases its pressure. At equilibrium, the tendency pressure to example the alveolus balances the tendency of surface tension to collapse it.

130
Q

How does different size impact alveoli and the pressure and surface tension

A

Different alveolar size in normaly healthy lungs. If our lungs weren’t cared for by surface the small alveoli would collapse into the large ones but this is inhibited by the surfactant.

131
Q

How does surfactant impact surface tension

A

Surfactant makes the alveoli stable against collapse by lowering the surface tension of the lining fluid so we can breathe without too much effort. It reduces the surface tension of water but increases compliance which leads to an easier way to expand the lungs

132
Q

What is surfactant composed of

A

Due to its hydrophobic and hydrophilic properites, the surfactant gets into the air-water interface and decreases the density of water molecules. The most important components of the pulmonary surfactant are the phospholipids dipalmitoyl-phosphatidylcholines, phosphatidyl-choline, surfactant apoproteins and calcium ions.

133
Q

How is alveoli stablized by surfactant

A

Thickness of surfactant decreasses with increase of surface area. This tends to equalize pressures between alveoli of different sizes, which helps prevent collapse of the small alveoli into large alveoli. However, the dynamic properties of surfactant permit the alveolar surface tension to change with inflation and deflation, as the thickness of the surfactant layer viares inversely with surface area.

134
Q

What are the functions of surfactant

A
  1. Reduces the surface tension of alveolar fluid
  2. Improves lung compliance
  3. Stabilizes the alveoli
135
Q

Why do premature infants need help breathing

A

Premature infants lack of surfactant decreases lung compliance and increases the work of breathing which can lead to infant respiratory distress syndrome

136
Q

How can we measure regional differences in ventilation

A

Measurement of regional differences with radioactive xenon. When the gas is inhaled, its radiation can be detected by counters outside the chest. Note that the ventilation decreases from the lower to upper regions of the upright lung.

137
Q

How can the weight of the lungs impact pressure

A

The weight of the lungs increases pressure in regions near the bottom (makes intrapleural pressure PIP, less negative), therefore less pulling it open than regions at the top of the lung.

138
Q

What happens to the alveoli at the bottom of the lungs

A

Since alveoli at the bottom may be more deflated (if intrapleural pressure PIP, is less negative than the intrapulmonary pressure will be smaller), they are able to expand more. Thus, bottom regions of the lungs receive a larger portion of inspired air.

139
Q

What are the different forms of gas exchange

A

Exchange of oxygen and carbon dioxide between alveolar air and blood in lung capillaries by diffusion.
Exchange of oxygen and carbon dioxide between blood in tissue capillaries and cells in tissues by diffusion

140
Q

What controls the partial pressures of gases

A

Gas molecules are constantly in motion and this motion exerts a pressure. Pressure increases in response to anything that increases movement of gas molecules through temperature and the concentration of gas molecules

141
Q

What is Dalton’s Law

A

In a mixture of gas, each gas operates independently. Thus, total pressure is the sum of individual pressures

142
Q

What is Fick’s Law

A

The rate of a gas through a sheet of tissue/unit time (V; L/min) is proportional to the tissue area and the difference in a gas partial pressure between two sides, a diffusion constant, and inversely proportional to the tissue thickens.

143
Q

What is the diffusion constant

A

The amount of gas transferred between the alveoli and the blood/unit time (diffusion) is also proportional to the gas solubility in fluids or in tissues.

144
Q

Compare the solubility of carbon dioxide and oxygen

A

The solubility of carbon dioxide is much higher than oxygen

145
Q

What is Henry’s Law

A

The amount of gas dissolved in a liquid is directly proportional to the partial pressure of gas in which the liquids is in equilibrium

146
Q

What happens when we’re looking at partial pressures between gas and liquid or multiple gases.

A

While partial pressures are the same in gas and liquid, amount of gas in liquid is also determined by its solubility. Thus, if two gases are at the same partial pressure but differ in solubility, their content within solution will differ. Only the gas that is dissolved in solution contributes to the partial pressure.

147
Q

Why is the pressure of oxygen in air higher than the pressure in the alveoli?

A

Humidification of air in the respiratory tract which decreases pressure. Loss of oxygen to blood diffusion increases pressure. Mixing of inspired air with alveolar air (functional residual capacity) decreases pressure.

148
Q

What are the determinants of alveolar pressure of oxygen (PO2)

A

Pressure of oxygen (PO2) in the atmosphere
Alveolar ventilation (VA)
Metabolic rate
Perfusion

149
Q

What are the determinants of alveolar carbon dioxide pressure (PCO2)

A

Pressure of carbon dioxide (PCO2) in the atmosphere
Alveolar ventilation (VA)
Metabolic rate
Perfusion

150
Q

What happens to the alveolar gas pressure when they increase alveolar ventilation

A

Increasing alveolar ventilation (VA) will increase alveolar pressure of oxygen (PO2) and decrease alveolar pressure of carbon dioxide (PCO2)

151
Q

What happens to alveolar gas pressures when they increase metabolic rate

A

Increasing metabolic rate (oxygen consumption and carbon dioxide production), will decrease alveolar pressure of oxygen (PO2) and increase alveolar pressure of carbon dioxide (PCO2)

152
Q

What happens during hypoventilation

A

Carbon dioxide production is higher than carbon dioxide elimination

153
Q

What happens during hyperventilation

A

Carbon dioxide production is lower than carbon dioxide elimination

154
Q

What is the gas exchange between alveoli and blood

A

Blood gases equilibrate very quickly on their way through the lung. Partial pressure of gas in alveoli determines arterial levels.

155
Q

What is cardiac output

A

Is the volume of blood pumped by the heart per minute

156
Q

What is systemic circulation

A

High pressure system necessary to deliver blood in peripheral tissue (brain) and overcome high resistance system

157
Q

What is pulmonary circulation

A

Low pressure system, needs to deliver blood only to lungs and high pressures are risky (lung edema)

158
Q

Why is it necessary the pulmonary circulatory system be low pressure

A

It needs to pump blood only to the top of the lung. It is important for avoiding rupturing the respiratory membrane and edema formation

159
Q

Why is it necessary for the pulmonary circulatory system to be a low resistance system

A

Resistance is less than 1/10 of that in the systemic circulation due to the shorter and wider of vessels

160
Q

Why is it important for the pulmonary circulatory system to have high compliance vessels

A

Higher number of arterioles with a low resting tone. Due to thin walls and the paucity of smooth muscle can accept large amounts of blood. Can dilate in response to modest increase in arterial pressure.

161
Q

What are pulmonary capillaries

A

There are 280 billion highly anastomosing capillayr segments creating a gas exchange surface of 50-100 meters squared. Blood passes through the pulmonary capillaries about 0.75 seconds at rest and can be reduced to 0.3 seconds when the cardiac output increases.

162
Q

How can alveolar capillaries be collapsible

A

If the capillary pressure falls below alveolar pressure, the capillaries close off, diverting blood to other pulmonary capillary beds with higher pressures.

163
Q

What is the ventilation/perfusion ratio

A

The ventilation/perfusion (V/Q) ratio is the balance between lung ventilation. The ratio between the ventilation and the perfusion is one of the major factors affecting the alveolar and therefore arterial levels of oxygen pressure (PO2) and carbon dioxide pressure (PCO2)

164
Q

What happens when we increase ventilation through the ventilation/perfusion ratio

A

The greater the ventilation, the more closely alveolar pressure of oxygen (PO2) and pressure of carbon dioxide (PCO2) will approach their respective values of inspired air

165
Q

What happens when we increase perfusion in the ventilation/perfusion ratio

A

The greater the perfusion, the more closely the composition of the local alveolar air will approach that of mixed-venous blood.

166
Q

What is the Anatomical VD

A

Volume of conducting airways that do not participate in gas exchange

167
Q

What is alveolar VD

A

Regions of the lungs with a high ventilation perfusion (V/Q) ration. Regions that are relatively over ventilated (UNDERPERFUSED) so that a portion of the fresh air reaching these alveoli can not be taken up by the blood.

168
Q

What happens to alveoli that are not ventilated

A

Low ventilation perfusion (V/Q) ratio causes an airway obstruction will will lead to a necessary shunt. A portion of the venous blood doesn’t get oxygenated and goes back to arterial blood.

169
Q

What does perfusion depend on

A

Gravity and posture

170
Q

What is apical ventilation ratio

A

Increased in compared to the ideal ratio

171
Q

What is the basal ventilation perfusion ratio

A

Decreased compared to the ideal ratio

172
Q

What is the homeostatic mechanism that occurs for ventilation-perfusion matching

A

Homeostatic mechanism exists to limit the mismatch. Most important is th unique response of pulmonary capillaries to low oxygen

173
Q

What is pulmonary hypoxic vasoconstriction

A

Ventilation in alveoli is matched to perfusion through pulmonary capillaries. If ventilation decreases in group of alveoli the pressure of carbon dioxide increases and the pressure of oxygen decrease. Blood flowing past the alveoli doesn’t get oxygenated. The decreased tissue allows pressure of oxygen around underventilated alveoli and constricts arterioles, diverting blood to the overventilated alveoli.

174
Q

What is the matching ventilation and perfusion in alveoli

A
  1. Decreased airflow to region of lung and decreased flow to region of lung at the same time
  2. In the pulmonary blood there is a decrease in pressure of oxygen and in the alveoli decrease in pressure of carbon dioxide at the same time
  3. There is vasoconstriction of pulmonary vessels and bronchoconstriction at the same time
  4. There is decreased blood flow and decreased air flow at the same time
  5. There is local perfusion decreased to match a local decrase in ventilation and local ventilation decreased to match a local decrease in perfusion
  6. There is diversion of blood flow and airflow away from local area of disease to healthy areas of the lung
175
Q

How is oxygen carried in the blood

A

There is dissolved blood that is 2% and the rest is combined with hemoglobin (98%)

176
Q

What is dissolved oxygen subject to

A

Dissolved oxygen is subject to Henry’s law of solubility and it has a low solubility were we have roughly 3 mL of oxygen to 1 litre of blood

177
Q

How is oxygen transported in hemoglobin

A

Most oxygen is carried to hemoglobin in red blood cells

178
Q

What is hemoglobin

A

Protein composed of 4 amino acid subunits called globins (2 alpha and 2 beta) and 4 heme groups. Each heme group has a porphyrin ring structure that contains an iron atom in the ferrous (Fe2+) form, to which oxygen binds.

179
Q

How does oxygen bind to hemoglobin

A

Each hemoglobin (Hb) molecule can bind up to FOUR oxygen molecules per subunit and exists as deoxyhemoglobin (no oxygen bound), or oxyhemoglobin (oxygen molecules bound), this is a reversible process

180
Q

What is the oxygen dissociation curve

A

The percentage of hemoglobin binding sites that have oxygen.

181
Q

What is oxygen capacity

A

Maximum amount of oxygen that can be combined with hemoglobin

182
Q

What is hemoglobin saturation

A

Percentage of the available hemoglobin binding sites that have oxygen attached

183
Q

What is hemoglobin saturation in arterial blood

A

Hemoglobin saturation of arterial blood that is high (97.5%)

184
Q

What is hemoglobin saturation in mixed venous blood

A

It is relatively low (75%)

185
Q

What are the determinants of hemoglobin saturation

A

Arterial pressure of oxygen (PO2). Cooperative binding. The dissociation curve is also sensitive to pH, pressure of carbon dioxide, and temperature

186
Q

What is the cooperative binding of oxygen and heme group

A

When oxygen binds to a heme group, it deforms the shape of the heme group which changes the shape of its associated globin chan from tense to relaxed state. This cooperative binding action produces the characteristic sigmoidal oxygen binding curve of hemoglobin

187
Q

What happens when the globin chain changes shape

A

The change in the shape of one globin chain deforms the others, exposing the iron in their heme groups and facilitates binding of additional oxygen molecules.

188
Q

What are the important features of the sigmoidal dissociation curve

A

Plateau regions (60-100 mmHg) and steep regions and (10-40 and 40-60 mmHg)

189
Q

What is the plateau region of the sigmoidal dissociation curve

A

Many conditions result in reduced alveolar pressure of oxygen, and therefore arterial pressure of oxygen caused by pulmonary diseases and altitude. Due to the plateau, saturation says high over a wide range of alveolar pressure of oxygen. Plateau provides an excellent safety factor sot that even a significant limitation of lung function still allows almost normal oxygen saturation of hemoglobin.

190
Q

What is the 40-60mmHg steep region of the sigmoidal dissociation curve

A

Unload large amounts of oxygen with only small decrease of oxygen. At pressure of oxygen of 40 mmHg oxygen saturation is still at 75%. It is important that pressure of oxygen remains relatively high in the capillary of peripheral tissue since this pressure is necessary to drive diffusion of oxygen from red blood cells to blood to cells and mitochondria

191
Q

What is the 10-40mmHg steep region of the sigmoidal dissociation curve

A

Increases metabolic rate cause further decrease in tissue pressure of oxygen, which facilitates diffusion from plasma which leads to a drop in plasma pressure of oxygen, diffusion of oxygen from red blood cells, drop in pressure of oxygen in red blood cells, additional dissociation of oxygen from hemoglobin.

192
Q

How can anemia impact the oxygen dissociation curve

A

Reduction of hemoglobin amount in the blood so it is lower on the curve that a normal dissociation curve

193
Q

How can polycythemia show on the oxygen dissociation curve

A

An increase in hemoglobin amount in blood or reduction of blood volume will show as an increase on the dissociation curve.

194
Q

How can carbon monoxide show on the dissociation curve

A

Carbon monoxide has 200 times more affinity for hemoglobin compared to oxygen. So there is a shift downwards on the curve and there is an unloading of oxygen to tissues

195
Q

What is the oxygen movement in the lungs and tissues at the level of respiratory membrane

A

Before diffusion on the pressure of oxygen in the alveoli is higher than pressure of oxygen in the blood.
At equilibrium the pressure of oxygen in the alveoli is equal to the pressure of oxygen in the blood.
The Oxygen-Hemoglobin binding doesn’t contribute to the pressure of oxygen value.

196
Q

What is the oxygen movement in the lungs and tissues in the peripheral tissue

A

Before diffusion the pressure of oxygen in the blood is larger than the pressure of oxygen in the interstitial fluid, which is larger than the pressure of oxygen within the cell, which is large than the pressure within the mitochondria.
Net diffusion from the blood to cell and mitochondria. Reduction of pressure of oxygen in the blood reduces the affinity of oxygen for hemoglobin and more oxygen is released from the red blood cells.

197
Q

How can certain factors impact the oxygen dissociation curve

A

Metabolism, temperature, pressure of carbon dioxide, and an increase of hydrogen ions can lead to an oxygen affinity of hemoglobin being reduces which means a stronger unloading of oxygen than rest.

198
Q

How is carbon dioxide transported in the blood

A

Carbon dioxide is carried in the blood in 3 forms

  1. Dissolved (5%)
  2. Bicarbonate, HCO3- (60-65%)
  3. Carbamino compounds (25-30%)
199
Q

How does carbonic acid (H2CO3) and bicarbonate (HCO3-) work together in our blood

A

To maintain the electrical neutrality and allow for bicarbonate (HCO3-) to exit the cells through the anion exchange. Hydrogen ions (H+) is released from the carbonic acid and will increase in venous blood and therefore decrease pH

200
Q

How does carbon dioxide move in the lungs and tissues in the peripheral tissues

A

Pressures of carbon dioxide exit cells, is dissolved in interstitial fluid, and diffuses to blood. Here carbon dioxide remains in plasma as dissolved carbon dioxide and enters red blood cells and remains dissolved as carbon dioxide, is bound to deoxyhemoglobin or react with water to produce bicarbonate and hydrogen ions.

201
Q

How does carbon dioxide move in the lungs and tissues at the level of the respiratory membrane

A

Before diffusion the pressure of carbon dioxide in the alveoli is less than pressure of carbon dioxide in blood.
Dissolved carbon dioxide in blood diffuses into alveoli. Lower pressure of carbon dioxide in plasma recalls dissolved carbon dioxide from red blood cells and change equilibrium carbon dioxide/water reactions and carbon dioxide/hemoglobin reactions

202
Q

How are hydrogen ions transported between tissues and lungs

A

Deoxyhemoglobin has much higher affinity for hydrogen ions compared to oxyhemoglobin. A large proportion of hydrogen ions is bound to hemoglobin and not dissolved in blood cells or plasma. This way the pH of blood is preserved and the venous blood is slightly more acided than arterial pH.

203
Q

How can hemoglobin act as a buffer

A

Hemoglobin has a key role in buffering the production of hydrogen ions in the peripheral tissues and capillaries.

204
Q

How does hydrogen ions interact in the lungs

A

In the lungs, the equilibrium is reverted, and hydrogen ions interact with bicarbonate and hemoglobin is available for binding with oxygen

205
Q

What is the result of hypoventilation

A

When carbon dioxide production is higher than carbon dioxide eliminated. Not only pressure of carbon dioxide increases but also hydrogen ions which results in respiratory acidosis.

206
Q

What is the result in hyperventilation

A

When carbon dioxide production is less than carbon dioxide eliminated. Not only pressure of carbon dioxide decreases but also hydrogen ions decreases which is respiratory alkalosis

207
Q

What is metabolic acidosis

A

Increase in blood hydrogen ions concentration independent from changes in pressure of carbon dioxide

208
Q

What is metabolic alkalosis

A

Decrease in blood hydrogen ion s concentration independent of changes in pressure of carbon dioxide.

209
Q

What is the neural control of breathing

A

Rhythm of breathing is established in the central nervous system

210
Q

How is breathing controlled

A

Initiated in the medulla by specialized neurons. Modified by higher structures of the central nervous system and inputs form central peripheral chemoreceptors and mechanoreceptors in the lung and chest wall.

211
Q

How do neuronal networks work

A

Neuronal networks must establish the automatic rhythm for contraction of the respiratory muscles. Several groups of respiratory neurons are in the brainstem.

212
Q

What is the prebotzinger (PreBotC) group of neurons

A

In the ventral respiratory group are the group of neurons of the prebotzinger complex (PreBotC) is response for generating excitatory inspiratory rhythmic activity that excites inspiratory muscles (via polysynaptic pathway).

213
Q

What is the parafacial group of neurons

A

In the ventral respiratory group, another group of neurons (the parafacial respiratory group, pFRG) has been proposed to be important for generating active expiratory rhythmic activity that excited expiratory muscles (via polysynaptic pathway)

214
Q

How is the rhythm of breathing generated

A

Rhythm of breathing is generated in the ventral respiratory group in the medulla. Prebotzinger and parafacial neurons drive activity in premotor neurons, which excite motoneurons that activate rhythmically respiratory muscles. THe rhythmic activity is also influenced by sensory and neuromodulatory inputs originating from different regions within and outside the central nervous system.

215
Q

How is the neural networks adjusted

A

Based off of:
Metabolic demands - blood pressure of oxygen, blood pressure of carbon dioxide, and blood pH
Varying mechanical conditions - changing posture
Non-ventilatory behaviours - speaking, sniffing, and eating
Pulmonary and non-pulmonary disease.

216
Q

What is inspiration neuro-respiratory pathways to the intercostal muscles

A

Prebotzinger complex triggers the inspiratory premotor neurons which triggers the phrenic and thoracic inspiratory motoneurons and triggers the diaphragm and external intercostal muscles.

217
Q

What is inspiration neuro-respiratory pathways to the upper airways

A

Prebotzinger complex triggers the inspiratory premotor neurons trigger the cranial motoneurons and triggers the tongue and upper airway muscles.

218
Q

What is active expiration neuro-respiratory pathway

A

Parafacial neurons trigger the expiratory premotor neurons which triggers the thoracic and lumbar expiratory motoneurons which triggers the internal intercostal and abdominal muscles

219
Q

How does prebotzinger complex work with anesthetics and opioids

A

Activity of prebotzinger complex neurons is robust and they persist through life. The activity of prebotzinger complex neurons may be depressed by several drugs such as anesthetics and pain killers. Depression of prebotzinger complex neurons activity leads to respiratory depression and eventually respiratory arrest or death. Naloxone will treat the overdose.

220
Q

What is control of ventilation

A

Control of ventilation by pressure of oxygen, pressure of carbon dioxide, and hydrogen ion concentration.

221
Q

How can tidal volume and respiratory rate impact the control of ventilation

A

Tidal volume and respiratory rate are not fixed but they can increase or decrease over a range of values if activity of respiratory networks is appropriately stimualted or inhibited. Small variations in arterial pressure of carbon dioxide and pressure of oxygen occur with activities such as sleep, exercise, talking, and panting.

222
Q

What can impact chemical controls of ventilation

A

Hypoxia - low pressure of oxygen
Hypercapnia - High pressure of carbon dioxide
Acidosis - Low pH in the blood
All of these can cause an increase in ventilation, which tends to raise pressure of oxygen, to lower pressure of carbon dioxide, and to raise pH.

223
Q

What are chemoreceptors

A

Chemoreceptors are specialized structures that sense changes in pressure of oxygen, pressure of carbon dioxide, and pH.

224
Q

What are the kinds of peripheral chemoreceptors

A

Carotid and aortic bodies. They are different from carotid sinuses. They sense hypoxia but are also sensitive to pH.

225
Q

What are carotid bodies.

A

They are extremely small. They are chemosensitve. They are highly vascularized. They have high metabolic rate. They are broken down into glomus and sustentacular cells.

226
Q

What are glomus cells in carotid bodies

A

They are chemosensitive cells. They are type 1 glomus cells. They have a variety of voltage-gated ion channels. Depolarization triggers action potentials. Glomus cells have numerous intracellular vesicles containing a variety of neurotransmitters. Stimulation causes the release of neurotransmitters and control the firing of the sensory nerve endings.

227
Q

What are sustentacular cells

A

They act as support in the carotid bodies. They are type 2, sustentacular cells.

228
Q

What are glomus cells sensitive to

A

A decrease in arterial pressure of oxygen is the primary stimulus for the peripheral chemorecepotrs. Glomus cells display an increase in firing rate with lowering of pressure of oxygen. Glomus cells are also sensitive in pressure of carbon dioxide and pH.

229
Q

How do peripheral chemoreceptors impact the pressure of oxygen

A

Ventilation is stable over 60-120 mmHg range of arterial pressure of oxygen. Stimulation of peripheral chemoreceptors occurs at arterial pressure of oxygen value below 60 mmHg.

230
Q

What is the response to hypoxia mediated by peripheral chemoreceptors

A
  1. Decrease in inspired in pressure of oxygen
  2. Decrease in alveolar pressure of oxygen
  3. Decrease in arterial pressure of oxygen
  4. This leads of increasing firing of peripheral chemoreceptors.
  5. This causes a reflex via medullary respiratory neurons
  6. There is an increase in contractions of respiratory muscles
  7. There is an increase in ventilation
  8. Results in a return of alveolar and arterial pressure of oxygen toward normal.
231
Q

What are central chemoreceptors

A

Central chemoreceptors are specialized neurons located close to the ventral surface of the medulla - which are in close contact with blood vessels and cerebrospinal fluid. Other chemosensitive sites are in the medullary raphe and hypothalamus.

232
Q

What is the respiratory response to metabolic acidosis

A
  1. Increase in production of non-carbon dioxide acid
  2. Increase in arterial hydrogen ion concentration
  3. Increase in peripheral chemoreceptors firing
  4. There is a reflex via the medullary respiratory neurons
  5. There is an increase in contractions of respiratory muscles
  6. Increase in ventilation
  7. Decrease in alveolar pressure of carbon dioxide
  8. Decrease in arterial pressure of carbon dioxide
  9. Return to arterial hydrogen ion concentration toward normal.
233
Q

What is the chemical control of ventilation when there is a decrease in pressure of oxygen

A
  1. Decrease in arterial pressure of oxygen
  2. Increase in firing of peripheral chemoreceptors
  3. Firing of medullary inspiratory neurons
  4. Increase of firing of neurons to diaphragm and inspiratory intercostals
  5. Increase contractions of diaphragm and inspiratory intercostals
  6. Increased ventilation
234
Q

What is the chemical control of ventilation when there is an increase of the production of non-carbon dioxide acids

A
  1. Increase in production of non-carbon dioxide acids
  2. Increase in arterial hydrogen ions
  3. Increase firing of peripheral chemoreceptors
  4. Increase of firing of medullary inspiratory neurons
  5. Increase of firing of neurons to diaphragm and inspiratory intercostals
  6. Increase of contractions in the diaphragm and inspiratory intercostasl
  7. Increased ventilation
235
Q

What is the chemical control of ventilation when there is an increase of pressure of carbon dioxide

A
  1. Increase in arterial pressure of carbon
  2. Increase in brain extracellular fluid of pressure of carbon dioxide
  3. Simultaneous increase in brain extracellular fluid of hydrogen ion concentration and increase in arterial hydrogen ions
  4. Simultaneous increase of firing of peripheral chemoreceptors and central chemoreceptors
  5. Increase of firing of medullary inspiratory neurons
  6. Increase of firing of neurons to diaphragm and inspiratory intercostals
  7. Increase of contractions in the diaphragm and inspiratory intercostasl
  8. Increased ventilation