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Year 1 LSS > Respiratory system: Mechanism > Flashcards

Respiratory system: Mechanism Flashcards

1
Q

Lung volumes and capacities:

A
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2
Q

Restrictive lung disease

A

difficulties with filling lung with air

“hugging bear disease”

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3
Q

Obstructive lung disease

A

Difficulties with exhaling air

(like hand in front of mouth)

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4
Q

Dead space (different types + volumes)

A

Physiological dead space: air that does not participate in gas exchange

Split into

  • anatomical dead space = air conducting system, normally 150ml
  • alveolar dead space= alveoli wihout blood supply –> normally 0ml
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5
Q

Boyles Law

A

Gas can be compressed (volume is determined by pressure)

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6
Q

Chest wall- Lung relationship

A

Are attached to each other via Pleura

Normally: chest would be bigger, lung would be smaller but form equilibrium in middle

–> this allows minimal changes around neutral pressure to have bigger effects on lung volume

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7
Q

The three compartment model

A

Three compartments with different pressures:

  • Atmospheric (Patm)
  • Interpleural pressure (P Ip/Pi) )
  • Inraalvelolar pressure (Palv)

Three Pressure Gradients can be calculated:

  • Transpulmonary pressure (PTp= PPi - PAlv)
  • Transthoracic pressure (PTT= Ppl- Patm)
  • Transrespiratory system pressure (PRS=PAtm - PAlv)

—> most importatn: drives inspiration+ expiration

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8
Q

Pulmonary function test: Protocol for Volume time curve

A

Protocol

  1. Patient wears noseclip
  2. Patient inhales to TLC
  3. Patient wraps lips around mouthpiece
  4. Patient exhales as hard and fast as possible
  5. Exhalation continues until RV is reached or six seconds have passed
  6. Visually inspect performance and volume time curve and repeat if necessary. Look out for:
  • a)Slow starts
  • b)Early stops
  • c)Intramanouevervariabiltiy
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9
Q

Explain volume-time curves, important measurements and effect of obstructive /restrictive lung disease on it

A

FVC= forced vital capacity

FEV1 = Forced expiration volume after one minute

–> Measures airway resistance and FVC

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10
Q

Peak flow

A

Measures peak flow (l/min)

Measures Airway resistance (how fast can be exhaled?)

The peak flow meter can measure it.

–> Normal ranges for sex, age, and height

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11
Q

Compare alveolar vs pulmonary ventilation

A

Pulmonary ventilation:

gas that is taken into the lungs in one breath

Alveolar ventilation:

air that reaches the alveoli (Tidal volume - dead space)

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12
Q

Classification of Lung disease

A
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13
Q

Control of airway function (Neurological pathway, hormonal way)

A

Parasympathetic innervation: contraction via Vagus nerve

Vasodilation (more blood supply to tissue)

Sympathetic: Dilation (via doral route ganglion and adrenaline)

BUT also NO synthesis (only species, causing relaxation)

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14
Q

Changes in Cells in Ashmah

A
  • overresponsiveness to stimuli causes airway obstruction
  • Airway inflammation –> remodeling
  • More mucus production (Hypertrophy/Hyperplasia of mucous glands)
  • Airway constriction (SM hypertrophy/Hyperplasia)
  • New vessels formation

–> positive feedback: inföammatory agents feedbak on rest

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15
Q

Daltons Law

A

the pressure of gas mixture = sum of the pressure of all partial pressures of the gases in it

P(gas mixture) = ∑P(gas 1) + P(Gas 2) ………P(<strong>Gasn</strong><strong>)</strong>

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16
Q

Ficks law

A

diffusion of a gas across a membrane is determined by

  • a concentration gradient (p1-P2)
  • and surface area(A)
  • the thickness of the surface(T)
  • and diffusion capacity of gas (D)

“V Gas”= 𝑨/𝑻∙𝑫∙[𝑷_𝟏−𝑷_𝟐]

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17
Q

Hernry’s law

A

solubility

is determined by Pressure (P) of gas and individual solubility

𝑪_( 𝑫 𝑮𝒂𝒔)=𝒂_( 𝑮𝒂𝒔) ∙ 𝑷_( 𝑮𝒂𝒔)

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18
Q

Boyle’s law

A

At constant temperature, the volume of a gas is inversely proportional to the pressure of a gas

P_(Gas)∝ 1/V_(Gas)

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19
Q

Charle’s law

A

At constant pressure, the volume of a gas is proportional to the temperature of a gas

𝑽_( 𝑮𝒂𝒔)∝ 𝑻_( 𝑮𝒂𝒔)

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20
Q

Differentiate between different form of Haemoglobin

A

1.“Normal” Haemoglobin (HbA) : Two alpha, two beta chains

When 4 O2 bind–> 5th binding site for 2,3-DPG appears (Allosteric –> effect on another binding site than ligand, regulatory function) –> when binding this “pushes” oxygen out

2. HbA2: two alpha, two delta chains

found in thalassemia

2. Fetal Haemoglbin (HBF): Two alpha, two gamma chains

– steals o2 from maternal haemoglobin –< higher affinity

3. Meta Haemoglobin (MetHb):

does not bind oxygen (F3+ already in middle) –< can convert into HbA (constant changing between two forms) by MetHb reductase

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21
Q

Cooperative binding

A

First O2 in haemoglobin in difficult to bind, following get easier

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22
Q

Myoglobin

A

haemoglobin in muscle –> stores 02 and extracts it from blood –> higher affinity for O2

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23
Q

When does a Sidewards shifts in the Oxygen dissociation curve occur?

A

Right shift (increased pressure required to get same saturation)

  • increase in temperature
  • acidosis
  • hypercapnia
  • increase 2,3, DPG

Left shift (less pressure required for same saturation

  • decreased temperature
  • alkalosis
  • hypocapnia
  • decreased 2,3, DPG
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24
Q

Up and downwards shifts in oxygen dissociation curves

A

Down: Anaemia: 100% saturated but not enough Hb available

UP: Too much Haemoglobin (e.g. doping, altitude), greater capacity of Hb to bind O2

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25
Q

Oxygen dissociation cuve

A

–> shows oxygen saturation of Hb (at normal Hb levels proportional to Oxygen in the blood)

Big range in Systemic circulation: (low partial pressure of O2) Oxygen can match tissue demand

Only small range in Pulmonary (high partial pressure of O2) circulation –> allows 02 to get saturated

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26
Q

Transport of Co2 in Blood

A

1. Solution with blood

–> non-enzymatic, low rate (H20+Co2= H2Co3)

2. In Erythrocyte

  • In solution with water –> enzymatic via carbonic anhydrase (increases rate by 5000 times)
  • –> Dissociation into H2Co3= HCo3- –> HCo3- get exchanged via AE1 transporters with Cl- and leaves Erythrocyte

3. In Erythrocyte: bound to haemoglobin

  • binds to amin Ends of globin chains –> Carbamino haemoglobin
  • H+ binds to h+ acceptors like Histidine on globin chain
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27
Q

CO2 dissociation curve

A

Co2 dissociation curve

Linear for used ranges –> Changes in partial pressure of CO2 and concentration are less significant for Co2

Also different for different saturations fo Hb –> when 100% O2 bound no Co2 bound

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28
Q

Alkaalemia and Acidaemia

A

Alkalaemia to proton concentration –> higher or lower than normal

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29
Q

Acidosis and alkalosis

A

conditions that influence pH –> they cause alkalaemia or acidaemia

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30
Q

Basic ranges for PO2

A

>10 kPa normal

8-10 = mild hypoxaemia

6-8= moderare hypoxaemia

<6 kPa= severe hypoxameia

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31
Q

How is an alkalosis compensated?

Compare respiratory compensation for pH to renal

A

Alkalosis needs acidosis to compensate (and another way around)

Respiratory: fast compensation

renal: slow (reuptake of H+/HCO3-)

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32
Q

Base exess (explenation and normal ranges)

A

Is calculated:

Difference between measured HCO3- and expected HCO3- based on PCO2

Normal ranges: -2 - 2 mmol/l

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33
Q

Normal ranges for PH, Po2, PCO2, HCO3-

A

pH= 7.35 to 7.45

pCO2 = 4.7 to 6.4 kPa (35 - 48 mm Hg)

PO2= >10 kPa (>80 mmHg)

HCO3-= 22-26 mEq/L

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34
Q

How to access/describe blood gases

A
  1. pH
  2. PCo2
  3. BE
  4. PO2
  5. Acid-base status
  6. Oxygenation

Example: Uncompensated respiratory alkalosis with severe hypoxaemia

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35
Q

Pressure-volume loops

(Name A-E)

A

A: Normal tidal breathing

B: Inhalation to Total Lung Capacity

C: Exhalation as hard as possible

D: Exhalation slows down

E: Immediate inhalation to TLC

–> produces a respiratory flow envelope (all values will lie within this values, anatomical restriction)

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36
Q

How does PVL changes in Obstructive Lung disease?

A
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37
Q

How do Pressure-Volume loops change in restrictive disease?

A
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38
Q

Differentiate between Hypoxia, Hypoxaemia and Ischaemia

A

Hypoxia= low PO2 in that environment

Hypoxaemia = low PO2 in blood

Ischaemia= lack of O2 in tissues

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39
Q

Summarise the oxygen cascade

A

decreasing oxygen tension from air to tissues /respiration cells

Two great points of loss of PO2:

  1. Mixing a fiar in lungs /upper airway
  2. In respiration tissues

How much arrives in tissues/vessels is dependant on Ficks law

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40
Q

What are the Challenges of high altitude?

A

Hypoxia (low Patm)

Thermal stress (cold)

Increased solar radiation

Hydration (dry air)

Dangerous(wind, hypoxia-induced confusion etc.)

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41
Q

Accomodation and Acclimatisation in high altitude

A
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42
Q

Prophylaxis in altitude sickness

A
  1. Cllimation = artificial exposure to an environemnt
  2. Acetoazolamide

–> carbonic acid inhibitor: accelerates renal compensation

43
Q

Chronic mountain sickness (cause, pathophysiology, symptoms, consequences, treatment)

A

Causes: unknown

Pathophysiology:

  • polycythaemia (high RBC) –> increases viscosity in blood
  • blood can only sludge through capillaries –> inadequate O2 delivery

Symptoms

  • Cyanosis, fatigue

Consequences:

  • ischaemic tissue damage
  • heart failure
  • death

Treatment

  • only known treatment: descending
44
Q

Acute mountain sickness (cause, patophysiology, symptoms, consequences, treatment)

A

Cause:

  • Maladaptation to high altitude

Patophysiology:

  • cerebral oedema

Symptoms:

  • nausea, vomiting, impaired decision making, fatigue, insomnia, –>“hangover”

Consequences

  • development of high altitude cerebral oedema, high altitude pulmonary oedema

Treatment:

  • stop ascent, analgesia, fluid, monitor symptoms, azetazolamide or hyperbaric O2, –> symptoms after 48h lower (renal adaptation)
45
Q

High altitude pulmonary oedema (pathophysiology and treatment)

A

Pulmonary arteries constrict due to hypoxia –> increased pulmonary pressure (and thereby increased leakage)

Treatment

descent, hyperbaric O2therapy, nifedipine (calcium antagonist), salmeterol(Sympathomimetics), sildenafil (vasodilation)

46
Q

High altitude cerebral oedema (pathophysiology and treatment)

A

vasodilation of vessels in response to hypoxaemia (to increase blood flow) more blood going into the capillaries increases fluid leakage

Treatment: immediate descent, O2therapy, hyperbaric O2therapy, dexamethasone (anti-inflammatory glucocorticoid)

47
Q

Type 1 Respiratory failure

A

Hypoxic respiratory failure

  • Low PO2 (<8)
  • Low or normal PCO2
  • –> Diffusion issue (oxygen can’t get into the body but normally Co2 can get out)

Reasons:

  • Pneumonia
  • Pulmonary oedema
  • High altitude
48
Q

Type 2 Respiratory failure

A

Type 2: Hypercapnic respiratory failure

“getting gas there problem”

  • High CO2 –> more production of CO2 and too little elimination of it
  • Most of the time: O2 aswell problematic low but not main problem

Causes:

  • Ventilation / Perfusion mismatch
  • Pulmonary fibrosis (increase in dead space)
  • obesity
  • neuromuscular disease, decreased CNS drive
49
Q

How do PVL change with an Extrathoracic obstruction?

A

Blunted inspiration

50
Q

How do PVL change with intrathoracic obstruction?

A

Blunted expiration

51
Q

How do PVC change with fixed airway obstruction?

A

Both: blunted inspration and expiration

52
Q

How does mechanical realtionship between pleura (pressure) and chest wall changes in lung diesease?

A
53
Q

Compliance

A

the tendency to distort under pressure

Compliance = ►V / ►P

–> A condom is more compliant than a balloon

54
Q

Elastance

A

The inverse of compliance

The tendency to go back to the original volume

Elastance = ►P / ►V

Balloon is more elastant than a condom

55
Q

Surfactant: Role of surfactant in alveoli

A

Normally: Surface tension of water would lead to collapsing of alveoli

But: Surfactant: phospholipid (bipolar) produced by type 2 pneumocytes

  • reduces surface tension –> prevents collapsing
  • increases compliance
  • Reduces work of breathing
56
Q

Factors which influence resistance in airway

A
  1. Generation

Resistance decreases with airway generation (counter-intuitive as radius decreases BUT so many airways –> sum increases)

  1. Lung volume

Airways dilate with breathing –> further reduce resistance

57
Q

Explain the Flow of air in collapsible tubes

A

Pressures determine if the flow is even possible:

If the pressure in pleura (outside) is bigger than on the inside (airway) e.g. in hard expiration

—> Airways might collapse

–> This is why airway is supported by Cartilage

58
Q

Changes to ventilation and Blood gases in Sleep

A
  1. Ventilation (tidal volume) drops
  2. very little changes to So2 (because of the plateau phase of ODC)
  3. BUT. Increased PCO2
59
Q

Which gas increases in sleep?

Why, how much and which effects can this cause?

A

CO2

  • The mechanism that keeps you breathing
  • in healthy people: by 0.5 kPa
  • because: sensitivity to Co2 decreases during sleep

–> induces apnoeic threshold

60
Q

Apnoeic threshold

A

stage/level of CO2 where you would not breathe during sleep because CO2 levels are too low

When CO2 levels are below this threshold: It can lead to Central sleep apnoea

61
Q

Central sleep apnoea

A

Nor effort to breath –> central drive is lost due to low CO2 (below apnoeic threshold)

62
Q

What can happen to airway during sleep? What does that cause?

A
  • Reduced muscular tone during sleep lead to
  • a decrease in intraluminal pressure (during inspiration)
  • Can be amplified by extra-luminal pressure (adipose tissue)

–> Airway blocked during sleep but still want to breath

There is still effort to breath (because of hypoxia)

This is called obstructive sleep apnoea

63
Q

Effects of sleep on COPD patients

A
  • Different oxygen dissociation curve
  • saturation of oxygen changes significantly with only little changes in PO2 changes
  • ventilation during sleep might be needed
64
Q

Effects of heart failure during sleep

A
  1. Leads to oedema
  2. Hyperventilation
  3. decreased in PCO2 below the apnoeic threshold
  4. Central sleep apnoea
65
Q

How is breathing (awake) being controlled?

A
66
Q

Which nerves control reflexes in breathing? What do they cause?

A

V

IX

X

–> all: irritant leading to a defensive mechanism (cough, sneeze)

X (Vagus) also stretch

67
Q

What controlles breathing?

A

PCO2

68
Q

How does the sensitivity of carotic receptors changes with the environment?

A

Increasing Sensitivity:

  • hypoxia ( Low PO2)
  • acidosis

Decreased sensitivity:

  • Alkalosis

Overall: Saturation of O2 (SO2 is stronger defended than PO”)

69
Q

Minute ventilation (definition, formula)

A

Ventilation in one minute

VE = Vt (tidal volume) x f(frequency)

70
Q

Three types of breathlessness

A
  1. Tightness –> restriction due to airway narrowing (inspiration)
  2. Increased work and effort –> High minute ventilation, high lung volume, against resistance (inspiratory or expiratory)
  3. Air hunger –> powerful urge to breath –> Mismatch between VE demand and VE achieved
71
Q

What scale can be used to measure breathlessness?

A

BORG scale

Subjective but still quite reliable and reproducible

72
Q

What are the main control centers for Breathing?

A

1. Medulla

  • central, involuntary breathing, controlled breathing via PCO2
  • Gets influence by limbic system and peripheral ( carotid chemoreceptors)

2. Behavioral center

  • cerebral cortex

1 always dominates 2

73
Q

Name the main difference between pulmonary and systemic circulation

A

Pulmonary circulation = low pressure (25/8 mmHg), high capacity circulation (10% of overall blood)

–> Thin walled arteries

74
Q

What is special about endothelial cells in pulmonary circulation?

A

Specialiced –> has ACE on suface

–> Angiotensin 1 to Ang2 converstion

+

break down of Bradykinin

75
Q

Bradykinin effects

A

Vasodilation

Increases leakiness of endothelial

76
Q

Explain the filter capacity of the pulmonary circulation

A

Is a very good filter: has a huge surface area

Can filter: small emboli as well (disseminates in pulmonary microcirculation)

77
Q

What are the three tasks of the pulmonary circulation?

A
  1. Gas transport
  2. Metabolic actions (ACE)
  3. Filtration of blood
78
Q

Shunting: explain the concept of shunting and provide and explain anatomical examples

A

Ways to bypass respiratory exchange surface (and therefore gas exchange)

  1. Anatomical
    * Bronchial circulation –> leaves via thoracic aorta and returns via pulmonary veins
  2. Fetal circulation
  • Ductus arterosus
  • Foramen ovale
  1. Congenital defect
  • atrial septal defect (patent foramen ovale)
  • ventricular septal defect

Congenital defects are generally okay it left ventricle is still stronger than right ventricle but because right ventricle has to operate under high pressure –> right ventricle gets stronger over time

This can lead to mixed venous blood bypassing pulmonary circulation —> Hypoxaemia

79
Q

Effects of increased Cardiac output on pulmonary circulation

A
  • increased diameter in arteries (compliant)
  • increased perfusion in hypoperfused beds (Apex of lungs)
  • This leads to minimal changes in MAP
  • Minimal changes in fluid leakage
80
Q

Effects of increased ventilation on pulmonary circulation

A

Vascular resistance changes with ventilation

At max expiration: extra-alveolar vessels compressed (too much pressure in the thorax)

At max inspiration: Alveolar so big that they compress capillaries

81
Q

Pulmonary hypoxic vasoconstriction: explain the importance, advantages and disadvantages of pulmonary hypoxic vasoconstriction in humans in health and disease and how this differs from the systemic response

A

In Hypoxia:

  • Vessels constrict to achieve good ventilation-perfusion matching

–> in areas that are poorly ventilated perfusion would be wast

  • Can be pathophysiologic in a hypoxic environment
  • In systemic response: vasodilation to ensure more blood flow –> better oxygen supply
82
Q

When is pulmonary hypoxic vasoconstriction beneficial?

A

During foetal development

  • •Blood follows the path of least resistance
  • •High-resistance pulmonary circuit means increased flow through shunts
  • •First breath increases alveolar PO2and dilates pulmonary vessels
83
Q

When is pulmonary hypoxic vasoconstriction very bad?

A

Chronic obstructive lung disease

  • •Reduced alveolar ventilation and air trapping
  • •Increased resistance in pulmonary circuit
  • •Pulmonary hypertension(Cor pulmonale)
  • •Right ventricular hypertrophy
  • •Congestive heart failure
84
Q

Pulmonary fluid balance: What factors influence pulmonary fluid balance? What might be the problem with changes?

A
  1. Hydrostatic pressure –> pushing force
  2. Oncotic pressure –> pulling force

(rest neglectable)

If lymphatic drainage fails or too high hydrostatic pressure –> pulmonary edema

85
Q

How can pulmonary hypertension cause heart problems?

A

Pulmonary hypertension e.g. in COPD –> vasoconstriction due to hypoxia

–> Increased resistance

leads to cor pulmonale –> hypertrophy of right ventricle

–> Might lead to Congestive heart failure

86
Q

What is an allosteric protein?

Why is haemoglobin an allosteric protein?

A

A protein that changes its affinity when other molecules bind to it

–> 2,3 DPG can bind to haemoglobin that helps to kick off O2 when 4 O2 already bound

87
Q

What is the definition of hypoxia?

A

It is a low PO2 environment

88
Q

Define hyoxaemia

A

Low PaO2 in the blood

89
Q

Define Ischaemia

A

Inadequate tissue perfusion of oxygen

90
Q

What happens to PaO2 with age?

A

It will decline because of poorer lung function

91
Q

What is Acclimation?

A

Like acclimatisation but stimulated by an artificial environment (e.g. hypobaric chamber or breathing hypoxic gas)

92
Q

What medical prevention could you prescribe when someone is planning to spend some time in high altitude?

A

Acetazolamide

  • Carbonic anhydrase inhibitor
  • accelerates renal acclimatisation to high altitude (hypoxia induced hyperventilation) (inhibts HCO3- reabsorbtion)
93
Q

What makes the pulmonary circulation a good filter?

What can it filter?

A

It is a good filter because it has a huge surface area!

It can e.g. filter small emboli (dissolved at end of vessels)

94
Q

What are the 3 functions of the pulmonary circulation?

A
  1. Gas exchange
  2. Metabolism of vasoactive substances (ACE)
  3. Filtration of blood (emboli)
95
Q

Which ion movements are involved in the hypoxia-induced vasoconstriction in pulmonary circulation?

A
96
Q

Where is perfustion of the lung greatest?

Where is ventilation in the lung greatest?

A

Apex: Alveoli large, less compliant + gravity less

–> Both less perfustion and ventilation

Base: ventilation (small alveoli, more compliant) + perfustion (gravity) bigger

97
Q

When is pulmonary vascular resistance highest?

A

It is highest at its extreme volume (Residual volume and Total lung capacity) because of pressure changes

98
Q

What is the most common cause of Hypoxaemia in lung disease?

A

Ventilation/Perfusion mismatch

If pulmonary blood flow isn’t reaching the ventilated alveoli, gas exchange can’t occur. Many lung diseases are associated with global V/Q mismatch

99
Q

Which weeks of gestation involve the embryonic phase of lung development?

What happens in this phase?

A

Embryonic phase: 0-7 Weeks

  • lung buds and main bronchi develop
  • (inkl. vascular supply)
100
Q

In which weeks of gestation does the Pseudoglandular phase of lung development occur?

What happens during this phase?

A

Pseudoglandular phase: 5-17 Weeks (2nd)

  • Around seven weeks: tertiary (segmental) bronchi form
  • By the end of 17th week: most structures have formed
  • Vessels: surround lung but gas-blood barrier not yet formed –> not viable yet
101
Q

During which weeks of gestation do the Canalicular period occur in lung development?

What happens during this phase?

A

It is the third phase (16-25w)

  • Tissue differentiation occurs (muscle, cartilage etc, alveoli)
  • Respiratory bronchioles form (after week 24)
  • 24-26 weeks: surfactant is secreted
  • Blood-Gas barrier starts to form
102
Q

During which weeks of gestation does the Saccular (terminal sac) period in lung development occur?

A

Saccular period: 24 Weeks - Parturation

  • number of terminal sacs develop
  • Immature alveoli form from week 32
103
Q

When does the alveolar phase in lung development occur?

What happens during this phase?

A

Late Fetal time to childhood

  • Further development of alveoli
  • Increase in lung size over first 3 years (increased number of alveoli and respiratory bronchioles)
  • –> More than 90% of alveoli are formed after birth!
104
Q

Which mechanisms lead to change from umbilical circulation to pulmonary circulation at birth

A
  1. First breath: expansion of lung
  2. Triggers production of vasodilatory agent + inhibition of vasoconstrictive agents
  3. O2 relaxed muscle
  4. Leading to reduced resistance –> increased blood flow to lungs

Year 1 LSS (12 decks)

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