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Life Support Systems (LSS) > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

Define alveolar ventilation.

A

The volume of air reaching the respiratory zone per minute.

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2
Q

Define anatomical dead space.

A

The capacity of the airways unable to undertake gas exchange (e.g. trachea, main bronchi).

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3
Q

What is alveolar dead space?

A

The capacity of the airways which should be able to undertake gas exchange but can’t, e.g. hypo-perfused airways.

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4
Q

What is the equation for physiological dead space?

A

Sum of alveolar and anatomical dead space.

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5
Q

Define hyperpnoea, hypopnoea, apnoea, dyspnoea, bradypnoea, tachypnoea and orthopnoea.

A 
Increased / decreased depth of breathing
Cessation of breathing
Difficulty 
Abnormally slow/fast
Positional difficulty (e.g. when lying down)
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6
Q

What is the inspiratory capacity?

A

Sum of the tidal volume and inspiratory reserve volume.

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7
Q

What is vital capacity?

A

Sum of tidal volume and inspiratory and expiratory reserve volumes.

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8
Q

What is functional residual capacity?

A

Expiratory reserve volume and residual volume.

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9
Q

What is the pleural cavity?

A

The gap between the visceral and parietal pleura: it is a FIXED VOLUME.
Contains protein-rich pleural fluid.

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10
Q

What happens to air as it passes down the respiratory tree?

A

It is warmed, humidified, slowed and mixed. PCO2 and PH20 increase.

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11
Q

What is Dalton’s law?

A

The pressure of a gas mixture is equal to the sum of partial pressures.

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12
Q

What is Charles’ Law?

A

VOLUME is directly proportional to TEMPERATURE (at a constant pressure)

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13
Q

What is the difference between HbA, HbA2 and HbF?

A

HbA: 2x Hb alpha and 2x Hb beta
HbA2: 2x Hb alpha and 2x Hb delta
HbF: 2x Hb alpha and 2x Hb gamma

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14
Q

What does 2,3-DPG (2,3-diphosphoglycerate) do?

A

It binds to deoxyhaemoglobin and shifts the oxygen dissociation curve to the right. This means O2 is released more readily at P(O2) found in tissues.

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15
Q

What causes left and right shifts of oxygen dissociation curves?

A

Left Shift: decrease in temperature, decrease in 2,3-DPG, alkalosis and hypocapnia.
(LEFT = DECREASE in temp, 2,3-DPG, H+ and CO2)
Right Shift: increase in temperature, increase in 2,3-DPG, acidosis and hypercapnia.
(RIGHT = INCREASE in temp, 2,3-DPG, H+ and CO2)

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16
Q

What causes an upward and downwards shifts of oxygen dissociation curves?

A

Upwards: POLYCYTHAEMIA (abnormally high conc of Hb) - represents increased oxygen-carrying capacity
Downwards: anaemia

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17
Q

What shift in the oxygen dissociation curve does HbCO (carboxyhaemoglobin) cause?

A

Downwards (due to decreased capacity) and left (due to increased affinity).

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18
Q

How is CO2 carried in the blood?

A

Dissolved in blood
Bound to amine end of Hb: carbaminohaemoglobin (HbCO2)
Converted into carbonic acid by carbonic anhydrase. Dissociates and undergoes chloride shift with hydrogencarbonate ion (bicarbonate).

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19
Q

Why are ventilation and perfusion greater at the base of the lung than the apex?

A

VENTILATION: Alveoli smaller and more compliant
PERFUSION: higher intravascular pressure, more recruitment, less resistance and a higher flow rate.

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20
Q

Highlight the roles of goblet cells and ciliated epithelium cells in COPD.

A

Goblet cell hyperplasia with more mucus secretions. Modified gel phase traps cigarette smoke but also traps and harbour microorganisms.
Ciliated cell depletes and beat asynchronously (as opposed to metasynchronously).

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21
Q

What are club cells?

A

Secretory cells which detoxify, repair and act as progenitor cells and comprise roughly 20% of epithelial cells.

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22
Q

Describe type I and type II alveolar epithelial cells.

A

Type I: thin, flat for facilitating gas and solute exchange.
Type II: secretory and progenitor functions (can transdifferentiate).
Type I: II = 1:2
However Type I cover 95% of alveolar surface

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23
Q

Describe surfactant storage and release in alveoli

A

Type II cells store surfactant in lamellar bodies.
Released onto the air-liquid interface.
Prevents alveolar collapse on expiration.

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24
Q

Describe alveolar fibrosis.

A

Increased type II cells without differentiation into type I. Increases fibroblasts and collagen deposition (type II cells can differentiate into fibroblasts).

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25
Q

What do goblet, club and type II (the secretory cells) have in common?

A

They all carry out xenobiotic metabolism, for example processing and detoxifying foreign compounds such as carcinogens in cigarette smoke.

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26
Q

Describe the xenobiotic metabolism pathway.

A

Club and type II cells and macrophages contain phase I enzymes which convert the procarcinogen into the active compound. Normally, a phase II enzyme makes the carcinogen water soluble and it is excreted.

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27
Q

How are mucins stored in goblet cells?

A

They are stored in a highly condensed from in mucin granules.

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28
Q

Define asthma.

A

A clinical syndrome characterised by increased airway responsiveness to a variety of stimuli.
Symptoms include dyspnoea, wheezing and coughing.

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29
Q

Define alkalaemia and acidaemia.

A

Alkalaemia is higher than normal pH of blood.

Acidaemia refers to lower than normal pH of the blood.

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30
Q

What is alkalosis?

A

Describes circumstances which decrease the concentration of protons and increases pH.

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31
Q

Give the Sorensen equation for pH.

A

-log(H+)

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32
Q

Which source, respiratory or metabolic acid, contributes the most?

A

Respiratory acid 100:1.

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33
Q

How can changes in ventilation and kidney function maintain blood pH?

A

Ventilation changes stimulate a rapid compensatory response to changes in CO2.
Changes in kidney retention/secretion of HCO3-/H+ stimulate a SLOW compensatory response to increase/decreased pH.

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34
Q

What is the base excess (BE)?

A

The amount of HCO3- measured compared to expected at the CO2 of the patient.
-2 to +2 mmol/L is considered normal.

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35
Q

In partially compensated respiratory acidosis, what comprises the acute and chronic phase reactions?

A

Acute phase: CO2 enters RBC and is converted into HCO3-

Chronic phase: kidneys increase HCO3- retention.

36
Q

What are the acute and chronic phases for compensating respiratory alkalosis?

A

There is NO acute phase compensation.

The chronic phase compensation involves decreasing HCO3- retention.

37
Q

Describe the possible causes of lung hypersensitivity.

A

Immunological: IgE mediated.

Non-immunological: intolerance; enzyme deficiency; pharmacological.

38
Q

Define allergy

A

An exaggerated immune response to a foreign substance (allergen) which is either inhaled, swallowed, injected or comes into contact with the skin or eye.
Allergy is a MECHANISM: not a disease.

39
Q

What is atopy and when is it characterised as an allergic reaction.

A

Atopy is the hereditary predisposition to produce IgE antibodies against common environmental allergens.
Atopic diseases: allergic rhinitis, asthma and atopic eczema.
Allergic tissue reactions are characterised by infiltration of Th2 cells and eosinophils.

40
Q

What is the O2 cascade?

A

Decreasing oxygen tension from inspired air to respiring cells.

41
Q

What is hypoxia induced diuresis?

A

Water loss form humidifying inspired air at high altitude.

42
Q

Define acclimation

A

Acclimatisation induced by an artificial environment, like a hypobaric chamber or by breathing hypoxic gas.

43
Q

What is acetazolamide?

A

A carbonic anhydrase inhibitor which accelerates the slow renal compensation (causes kidneys to excrete bicarbonate ions) acidifying the blood and resulting in hyperventilation, increasing PO2.

44
Q

Give some innate adaptations to high-altitude living (hypoxia).

A

Barrel chest (+O2 in), increased haematocrit (+O2 blood), larger heart (+pulmonary perfusion), increased mitochondrial density (+O2 used).

45
Q

What causes chronic mountain sickness?

A

Secondary polycythaemia: high blood viscosity, which sludges through systemic capillary beds, impeding O2 delivery.

46
Q

What is the difference between type I and II respiratory failure?

A

Type I: hypoxaemia with hypo- or normocapnia. Result of impaired gas exchange.
Type II: hypoxaemia with hypercapnia. Result of impaired ventilation.

47
Q

What is Boyle’s law?

A

VOLUME of a gas is INVERSELY proportional to the PRESSURE.

48
Q

What are the purposes of a cough?

A

A defence mechanism protecting the lower respiratory tract from inhaled foreign material and excessive mucous secretion.

49
Q

Describe the pseudoglandular phase of lung development (5-17 weeks).

A

Pre-acinar airways all present by 17 weeks.
Development of cartilage, gland and smooth muscle tissue.
Lung buds: epithelial cells at tips are highly proliferative and multipotent.
Branching morphogenesis matched by vasculogenesis.

50
Q

Describe the canalicular phase of lung development (16-27 weeks).

A

Airspaces at the periphery enlarge.
Thinning of the epithelium underlying capillaries allows gas exchange.
Epithelial differentiation into type I and II cells.
Surfactant first detectable at 24-25 weeks (24 weeks –> babies become viable).

51
Q

Describe the saccular/alveolar phase of lung development (28-40 weeks).

A

Alveoli appear from 29 weeks and multiply up to 9-12yo.

1/3 - 1/2 adult number by term.

52
Q

Describe what happens to the lung at birth.

A

Volume of the lung is small and related to body weight.
All airways are present and differentiated.
There is a decrease in pulmonary vascular resistance.
10 fold rise in pulmonary blood flow.
Arterial lumen increases in size and walls thin.

53
Q

What is hypoplasia?

A

Bronchus and rudimentary lung present but all elements are reduced in size and number.

54
Q

Compare the volumes and pressures of systemic circulation and pulmonary circulation.

A

CO: 5L/min in both. Volume of systemic system is 4.5L, 0.5L for pulmonary system.
MAP = 93mmHg systemic. MAP = 13mmHg pulmonary.
Resistance 18.1 vs 1.8
Velocity of blood faster in systemic system than pulmonary system.

55
Q

What are the 3 functions of pulmonary circulation?

A

Gas exchange, metabolism of vasoactive substances (by ACE) and filtration of blood (small emboli are removed in pulmonary circulation).

56
Q

Why is the venous return to the left atrium greater than to the right atrium?

A

Bronchial circulation drains into the pulmonary vein which drains into the left atrium.

57
Q

How does the pulmonary circulation respond to an increased cardiac output?

A

Increased pulmonary artery distension and more perfusion of HYPOPERFUSED beds means there is negligible MAP change, minimal fluid leakage.
No onset of pulmonary oedema and no detriment in pulmonary function.

58
Q

What is the difference between systemic and pulmonary responses to hypoxaemia?

A

Systemic vascular response is vasodilation.

Pulmonary vascular response is vasoconstriction.

59
Q

What is the mechanism of pulmonary vascular constriction in response to hypoxaemia?

A

Hypoxaemia causes closure of O2 sensitive K+ channels, meaning there is reduced K+ efflux. This means the membrane depolarises as the membrane potential increases. Depolarisation means the Ca2+ channels open, causing VSMC constriction.

60
Q

Describe the differences between minute ventilation and oxygen saturation when awake and asleep.

A

Minute ventilation: drops by 10%

Oxygen saturation: drops by 1%

61
Q

What happens to PCO2 during sleep and what is the significance of this?

A

PCO2 increases which allows breathing to continue. Hypercapnia is mandatory for breathing during sleep. If PCO2 doesn’t rise above the apnoeic threshold during sleep, breathing will stop: central sleep apnoea.

62
Q

What is the difference between obstructive sleep apnoea and central sleep apnoea.

A

In obstructive sleep apnoea, there is effort to breathe. In central sleep apnoea, there is no effort to breathe.

63
Q

What can cause obstructive sleep apnoea?

A

Reduced upper airway muscle activity (no cartilage), extra luminal pressure, negative intra-luminal pressure all lead to the occlusion of the phalangeal airway.

64
Q

How is heart failure related to central sleep apnoea?

A

50% of HF patients hyperventilate so have a low PaCO2 (below apnoeic threshold). These people experience central sleep apnoea.

65
Q

Give the cycle of obstructive sleep apnoea.

A

Patent airway (open, unobstructed). Ventilation increases. Sleep. Less upper airway muscle function. Apnoea: hypoxia and hypercapnia. Arousal - termination of apnoea.

66
Q

What is the respiratory exchange ratio?

A

Co2 production / O2 consumption (=1)

67
Q

What does RER > 1 indicate?

A

Anaerobic respiration.

68
Q

Give the RER values for metabolisms of different energy sources.

A

Saccharides: 1
Proteins: 0.82
Lipids: 0.7

69
Q

What is the difference between small cell lung cancer and non-small cell lung cancer?

A

Small cell lung cancer grows much faster and metastasises much earlier.

70
Q

What are the 3 components of COPD?

A

Bronchitis, emphysema and small airways disease.

71
Q

What is the difference between an obstructive and a restrictive lung disease?

A

An obstructive lung disease reduces the lung’s ability to EXHALE air completely from the lungs (e.g. COPD, asthma, bronchitis).
A restrictive lung disease reduces the lung’s ability to INHALE air completely into the lungs, e.g. pulmonary fibrosis.

72
Q

How would you differentiate between an obstructive and restrictive lung disease using spirometry?

A

Obstructive disease has a REDUCED FEV1/FVC ratio.

Restrictive has a NORMAL FEV1/FVC ratio.

73
Q

How does hypoxia cause vasoconstriction of pulmonary vasculature?

A

Oxygen dependent K+ channels close, K+ efflux decreases, depolarisation leading to Ca2+ influx, contraction.

74
Q

How does inspiration happen?

A

Intercostal muscles and diaphragm contract, pulls parietal pleura away from visceral pleura.
Wider pleural space leads to a decrease in intrapleural pressure.
The pressure gradient between the pleural space and alveoli widens, causing inflation of the alveoli.
Inflation of the alveoli causes the pressure in the alveoli to decrease.
Air flows down its concentration gradient into the alveoli.

75
Q

Describe changes in structure as you descend the pulmonary tree.

A

Epithelial change from pseudostratified ciliated columnar epithelium in trachea and bronchi to simple columnar in tertiary bronchi and bronchioles.
Mucous cells/ submucosal glands decrease in number.
Cartilage in plates rather than rings and bronchioles have no cartilage at all.
Muscularis mucosa between lamina propria and submucosa introduced at bronchi and becomes more prominent as you descend.

76
Q

Give 3 causes of pulmonary oedema.

A

Increased pulmonary hydrostatic pressure (e.g. obstruction of mitral valve)
Decreased plasma oncotic pressure (e.g. low albumin from liver failure).
Impaired lymphatic drainage (e.g. metastatic infiltration).

77
Q

How do restrictive and obstructive lung diseases affect compliance, elastance and airway resistance?

A

An obstructive disease increases compliance, decreases elastance and INCREASES resistance.

A restrictive disease doesn’t affect resistance, but decreases compliance and increases elastance.

78
Q

Why do central chemoreceptors detect changes in PCO2 only?

A

Since CO2 can easily and rapidly cross the BBB to influence the CSF bathing the central chemoreceptors.
(H+ crosses at a much slower rate).

79
Q

What does sympathetic innervation do to pulmonary vasculature and why?

A

Causes constriction of the vessels, which occupy less space and “thin” the mucosa allowing the airways to dilate.

80
Q

What are conchae?

A

Protrusions in the nasal cavity, involved in humidifying and warming air.

81
Q

Why does breathing not stop when you are awake when the PaCO2 is below the apnoeic threshold?

A

Since the central regulator receives input from other areas of the brain - principally the primary somatosensory cortex but also the limbic system.

82
Q

How does respiratory distress syndrome lead to decreased gas exchange?

A

A layer of hyaline cartilage forms over the alveolar surface, decreasing the SA.

83
Q

Why is there loss of touch perception on the same side as the cut, but a loss of pain sensation of the opposite side?

A

Nociceptive afferents decussate in the spinal cord whereas proprioceptive afferents decussate in the medulla. Hence, nociceptive afferents have already crossed over at the point where the cut was made, so you lose pain sensation on the opposite side.

84
Q

What does parasympathetic innervation to the respiratory system do?

A

Bronchoconstriction.
Vasodilation (increase mucosal thickness).
Mucous secretion.
Uses ACh (muscarinic receptors).

85
Q

Why is Streptococcus Pneumoniae a particularly virulent cause of pneumonia?

A

It has a negatively charged capsule, making it difficult to bind to the epithelium - instead invades bloodstream to cause bacteraemia.

86
Q

What is bronchiectasis?

A

Abnormal widening of the bronchi or their branches, causing increased risk of infection.

87
Q

In chronic inflammation, what is the main cause of damage to lung tissue?

A

The increased number of neutrophils secrete so much protease that the anti-proteases in the lung are overwhelmed and so the surrounding structures are broken down.
(Most common = alpha-1 antitrypsin).
Elastin may be broken down, which gives structure to bronchioles.

Life Support Systems (LSS) (6 decks)

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