Respiration (30-32) Flashcards

1
Q

What is external respiration?

A

Exchange of oxygen and carbon dioxide between an organisms and external environment

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2
Q

What is the difference between breathing and ventilation?

A

Breathing → the physical act of muscle contraction/relaxation that move bones that change the volume of the lungs to move air in and out of the lung

Ventilation → movement of air from outside to inside the body for exchange of gas between air in the lungs and blood in capillaries within the alveoli - ventilating a patient: pushing air not breathing for them

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3
Q

What are the 3 aspects to the central control of breathing?

A

Reflex/automatic → generates respiratory rhythm coordinated in the ventral respiratory column
Voluntary/behavioural → control of breathing patterns
Emotional → can override respiratory patterning

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4
Q

What generates respiratory rhythm?

A

Reflexive/automatic control

Inspiratory rhythm → preBotzinger complex
Expiratory rhythm → parafacial respiratory group (pFRG)

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5
Q

Where does voluntary control of breathing originate?

A

Motor cortex
→ motor cortex neurones that modulate breathing synapse in the pons (part of your brainstem)

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6
Q

When can voluntary control of breathing not be maintained?

A

When stimuli, such as Pco2 or H+ become too intense → the breaking point

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7
Q

Can emotional control of breathing still occur in locked in syndrome?

A

Yes
→ volitional control does not occur

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8
Q

How does emotional control of breathing arise?

A

Through corticospinal projections

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9
Q

What feedback mechanisms pattern breathing?

A

Central/peripheral chemoreceptors (monitoring of blood gases)
Protective reflexes
Pulmonary stretch receptors

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10
Q

How does arterial Pco2 control breathing?

A

Arterial CO2 is the major chemical factor regulating minute breathing
→ excess CO2 (hypercapnia) leads to acidification
→ ability of Pco2 to control breathing associated with change in [H+]
→ central and peripheral chemoreceptors respond to high Pco2

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11
Q

How does hypoxia/hypercapnia modulate breathing?

A

Small increases in inhaled CO2 will stimulate breathing → 10% rise in CO2 - 100% rise in breathing, 20% rise more than trebles breathing
Hypoxia to a lesser degree → 35% drop in O2 - 20% increase in breathing, 55% drop in O2 - doubles breathing

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12
Q

What do peripheral chemoreceptors detect?

A

Alterations in blood gases - predominately oxygen (80% O2 detection, 20% CO2 detection)
→ carotid bodies, aortic bodies
→ respond to arterial blood changes (hypoxia, hypercapnia, acidosis)

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13
Q

What do central chemoreceptors detect?

A

Alterations in blood gases - predominantly CO2 (70% of CO2 detection, 30% of O2 detection)
→ mainly located in the medulla oblongata
→ respond to changes in cerebrospinal fluid (increased Pco2, changes in [H+]/pH)

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14
Q

What do slowly adapting pulmonary stretch receptors monitor?

A

Lung inflation
→ in smooth muscle on bronchi and trachea
→ signal lung volume to brain
→ inhibit inspiration and lengthen expiration (Hering-Breuer inflation reflex)
→ regulating respiratory rhythm e.g. exercise and sleep in neonates

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15
Q

What do rapidly adapting pulmonary stretch receptors monitor?

A

Irritants
→ in epithelial cells in larynx, trachea and airways
→ respond to mechanical stress: large inflation/deflation
→ respond to chemical environment of lung: noxious gases, dust, cold, histamine
→ constrict airway and promote rapid shallow breathing - responsible for ‘gasping inspirations of the newborn’
→ promote cough in trachea and larynx
→ promote signing due to gradual collapse of lungs (atelectasis) ~5 minutes

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16
Q

What are the two major determinants of lung compliance?

A

Lung compliance required so they can inflate and deflate - ability to expand lungs at any given change in trans pulmonary pressure
→ 1. stretchability of tissues
→ 2. surface tension within alveoli

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17
Q

How is surface tension within alveoli lowered?

A

By pulmonary surfactant
→ surface of alveoli is moist
→ surface tension at air-water interface resists stretching
→ pulmonary surfactant (lipids) lowers tension and increases compliance

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18
Q

What is pulmonary surfactant?

A

Lines the alveoli to lower surface tension
→ released from type II alveolar cells during sighing - prevents lungs collapsing
→ mixture of phospholipids and protein
→ makes lungs easier to expand

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19
Q

What are pulmonary protective reflexes?

A

Responses that protect the respiratory system from irritants
→ cough reflex: due to receptors in epithelial cells of upper airways
→ sneeze reflex: due to receptors in epithelial cells of nose of pharynx

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20
Q

What are the 3 phases of rhythmic breathing?

A

Breathing depends on the cyclical excitation of respiratory muscles
1. inspiration → active: initiated by activation of the nerves to the inspiratory muscles
2. post-inspiration → active: recruitment of post-inspiratory muscles
3. expiration → passive: inspiratory muscles relax and lungs recoil, active: activation of exploratory muscles

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21
Q

What happens when inspiratory muscles contract?

A

Contraction of inspiratory muscles draws air into the lungs
scalene → lift chest plate up
intercostals → open up rib cage

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22
Q

What is the function of the diaphragm?

A

Most important respiratory muscle (70% of tidal volume)
→ asymmetrically innervated
→ cruel diaphragm slows recoil
→ upon inhalation, the diaphragm contracts and flattens and the chest cavity enlarges
→ this contraction creates a vacuum, which pulls air into the lungs

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23
Q

What does contraction of the tongue support?

A

The airway and reduces resistance during inspiration
→ helps to move air efficiently

24
Q

What is the thorax?

A

A closed compartment separated from the abdomen by the diaphragm
→ contained by spinal column, sternum, ribs and intercostal muscles
→ lungs and wall of the thorax are covered by thin membranes - pleurae

25
Q

What are the different pleurae?

A

Visceral pleura → thin layer of epithelium covering each lung
Parietal pleura → lines inner surface of the walls of the thorax
Pleural cavity → maintains a partial vacuum which helps keep the lungs expanded

→ intra pleural fluid allows pleura to slide over one another - stops separation

26
Q

How is pressure generated inside the plura?

A

Differential set points of muscles and lungs
→ lungs want to be further apart - fluid prevents it

27
Q

What is transpulmonary pressure?

A

Ptp = Palv - Pip = 760 - 756 = 4mm Hg
(needs constant pressure so lungs don’t collapse)

Ptp → transpulmonary pressure: difference in pressure between the inside and outside of the lungs within the thorax
Pip → intra pleural pressure: the pressure outside the lungs in the thorax
Palv → alveoli pressure: the pressure inside the lungs

Palv > Pip - keeps the lungs inflated

28
Q

What causes pneumothorax (collapsed lung)?

A

Air in the plural cavity
→ occurs when perforation of the lung or chest wall allows air to enter intrapleual space
→ trans pulmonary pressure decreases
→ elastic recoil collapses the lung

29
Q

How does air move into the lung?

A

Air moves by bulk flow, from region of high pressure to one of low pressure

Ohms law: Q = (P1-P2)/R
Flow = (Patm-Palv)/R
Patm fixed to Palv must be altered to achieve air flow

30
Q

How does alveolar pressure change?

A

By changes in volume of the lungs

Boyle’s law → P1V1 = P2V2
for a given volume there’s a certain amount of collisions
→ if volume inside lungs is changed, pressure inside lungs will also change

31
Q

What happens to alveolar pressure during inspiration?

A

During inspiration
→ muscles of chest wall and diaphragm contract
→ ribs pulled upwards and diaphragm flattens
→ thorax enlarges Pip lowers, trans pulmonary pressure increases
→ chest volume increases to alveolar pressure decreases
Palv < Patm so air moves in

32
Q

How do O2 and CO2 move between alveoli and blood?

A

By diffusion
→ occurs from a region where partial pressure is high to a region where it is low

33
Q

What is the pressure of atmospheric air?

A

(total pressure is the sum of all the partial pressure of all the gases)
In atmospheric air: Patm = PN2 + PO2 + PCO2 = ~760mm Hg

34
Q

How is partial pressure of gases in tissue determined?

A

By combustion of glucose - breaking something down with CO2
→ consumes 70-100% of oxygen, tissue PO2 = 30mm Hg
→ produces 45-70 mm Hg PCO2, tissue PCO2 = 45mm Hg

35
Q

What are the two pulmonary dead spaces?

A

Anatomical dead space → volume of gas within the conducting airways, increases PCO2 in the alveoli
Physiological dead space → volume of gas not involved in gas exchange
→ two are almost equal in healthy lungs
→ dead space elevates CO2 levels within the body

36
Q

How does gas exchange occur in alveoli?

A

O2 diffuses from alveoli into the lung capillaries → alveolar Po2 > pulmonary Po2

CO2 diffuses from the lung capillaries into the lung → alveolar Pco2 < pulmonary Pco2

37
Q

How does gas exchange occur in tissues?

A

O2 diffuses from the tissue capillaries into the tissue → blood Po2 > tissue Po2

CO2 diffuses from the tissue into the tissue capillaries → blood Pco2 < tissue Pco2

38
Q

What is the respiratory quotient (RQ)?

A

The ratio of CO2 production to O2 consumption
→ varies between 0.7-1.0, average 0.8

alveolar PO2 = inspires PO2 - (blood PO2/RQ)

39
Q

How is oxygen primarily transported?

A

On haemoglobin
→ >98% of O2 reversibly combines with haemoglobin molecules in erythrocytes

→ <2% of O2 dissolved in the plasma and red blood cell water

40
Q

What is the purpose of haemoglobin’s saturation curve?

A

Haemoglobin holds oxygen in a reversible combination so it can be released to tissues
→ when Po2 is high (in alveoli) haemoglobin binds O2
→ when Po2 is low (in tissues) haemoglobin releases its stored O2 reserves

41
Q

What is the Bohr effect?

A

CO2 causes O2 to dissociate from haemoglobin, CO2 shifts the saturation curve to the right
→ CO2 causes haemoglobin to release more O2
→ CO2 diffuses from venous blood into alveolar space allowing more O2 to load onto haemoglobin
→ temperature and acidity promote O2 unloading
→ CO2 has a higher affinity for haemoglobin

42
Q

How is CO2 transported in the blood?

A
  1. dissolved in plasma (5%)
  2. in red blood cells (bound to Hb or dissolved in cytoplasm)
    → most CO2 is converted into carbonic acid by enzyme carbonic anhydrase
    → carbonic acid immediately dissociates into H+ and HCO3-
    → HCO3- ions are transported out of red blood cells in exchange for Cl- ions (70%) - chloride shift - Cl- allows for greater unbinding of CO2
43
Q

Why does carbon monoxide poisoning occur?

A

Because CO has a higher binding affinity for Hb
→ CO displaces O2 from Hb to form carboxyhaemoglobin, thus decreasing the amount of O2 that combines with haemoglobin in pulmonary capillaries
→ Hb saturation curve shifted to the left, thus decreasing the unloading of O2 from haemoglobin in the tissues

44
Q

How is the respiratory system organised?

A

Air is delivered to the lungs via the trachea → from the mouth and nose
There are two lungs, each divided into lobes → 3 lobes in right lung, 2 lobes in left lung
Bronchi and bronchioles distribute air throughout the lungs → respiratory bronchioles give rise to alveoli (site of gas exchange)
Respiratory tree → comprises the branching structures from the trachea to the alveoli

45
Q

What are the divisions of the respiratory system?

A

The upper/lower airways → anatomical divisions
The conducting zone
The respiratory zone

46
Q

What is the upper airways?

A

aka upper respiratory tract
→ mouth, nose, pharynx, larynx
→ infection symptoms: sneezing, nasal discharge, runny nose, nasal congestion, fever, sore throat - non
→ obstruction of the upper airways causes snoring during sleep

47
Q

What is the lower airways?

A

aka the lower respiratory
→ extends from the top of the trachea to the alveoli
→ infection symptoms: bronchitis, oedema, shortness of breath, weakness, fever, coughing, fatigue - affect gas exchange

48
Q

What is the conducting zone?

A

Extends from mouth and nose to terminal bronchioles
→ conducts air but does not exchange gas
→ provides low-resistance pathway for airflow
→ warms (or cools) and moistens the air
→ defends against microbes, toxic chemicals and other foreign matter
→ airway resistance decreases from bronchi to terminal bronchiole

49
Q

What defence mechanisms does the airway have?

A

Contraction of bronchioles via smooth muscle
Cilia → hair-like projecting from epithelial cells that line airways, constantly beat upward toward the larynx, immobilised by many noxious agents, smokers damage cilia - lots of mucus
Mucus → secreted by glands and epithelial cells lining the airways, particulate matter and bacteria in sipped air sticks to mucus, continuously moved by cilia, swallowed every 30s
Macrophages → phagocytic cells that are present in airways and alveoli, engulf and destroy inhaled particles and bacteria, injured by noxious agents (air pollutants, cig smoke)

50
Q

What is asthma?

A

Disorder of the conducting zone
→ chronic inflammation - causes airway smooth muscle to be hyper-sensitive to triggers
→ intermittent episodes of smooth muscle contraction increases airway resistance
→ reduced airway diameter increases work of breathing
→ reversible: short-acting beta2 adrenergic receptor agonist e.g. salbutamol (ventolin)

51
Q

What is bronchitis?

A

Disorder of the conducting zone
→ persistent inflammation of the bronchial walls, airways are inflamed and thickened
→ increase in mucus-secreting cells and loss of ciliated cells
→ obstruction of the airways, hindering both breathing and oxygenation of the blood

52
Q

What is the respiratory zone?

A

Extends from respiratory bronchioles to alveolar sacs
→ provides O2, eliminated CO2
→ regulates blood pH in coordination with the kidneys
→ influences arterial concentrations of chemical messengers
→ traps and dissolves blood clots arising from systemic veins

53
Q

What is the pulmonary circulation?

A

Includes blood pumped from the right ventricle through the lungs to the left atrium
→ large network of capillaries in the alveolar walls
→ low pressure (15mm Hg), 70ml blood
→ high-flow (5L blood/min) system, blood cells spend 0.75s in lung

54
Q

How is blood supplied to the respiratory zone?

A

Each alveoli associated with many pulmonary capillaries
→ inhaled air is brought close proximity to pulmonary blood
→ allows efficient gas exchange between air and blood, alveolar walls very thin

55
Q

How is gas exchange in alveoli optimised?

A

Thinness of barrier between blood within the alveolar wall capillary and the air within the alveolus
→ the vast surface area of alveoli in contact with capillaries
→ the moist surface of the alveolar cells

56
Q

What is emphysema?

A

Disorder of the respiratory zone
→ lungs undergo self-destruction by proteolytic enzymes secreted by leukocytes
→ adjacent alveoli fuse to form fewer but larger alveoli - reduces SA available for gas exchange
→ destruction of alveolar walls and collapse of lower airways
→ increased airway resistance due to inflammation - greatly increases the work of breathing

57
Q

What is chronic pulmonary disease?

A

Chronic bronchitis and emphysema
COPD 2011 4th leading worldwide cause od death
→ ~65mil suffered worldwide, ~ 3mil deaths per annum