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Block 2 > Week 2: CTB > Flashcards

Week 2: CTB Flashcards

1
Q

Define SIRS (Qualitative)

A
  • Systemic Inflammatory Response Syndrome

- Inflammatory response to infection / non-infectious insult (trauma, severe burns) that affects the whole body

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2
Q

Define Infection (Qualitative)

A
  • Invasion & Multiplication of pathogenic microbes in an area of the body where they are not normally present, which usually leads to disease.
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3
Q

Define Sepsis (Qualitative)

A
  • Life-threatening organ dysfunction due to a dysregulated host response to infection
  • Infection + SIRS = Sepsis (2001)
  • Sepsis = Infection + SOFA score >/= 2 or qSOFA >/= 2 (2016)
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4
Q

Define Severe Sepsis (Qualitative)

A
  • Sepsis + Organ Dysfunction (including septic shock due to cardiovascular system dysfunction)
  • Kidneys particularly vulnerable to AKI from Sepsis
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5
Q

Define Septic Shock (Qualitative)

A
  • A subset of sepsis where profound circulatory, cellular, & metabolic abnormalities substantially increase mortality
  • Sepsis + Cardiovascular system failure
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6
Q

What can cause Systemic Inflammatory Response Syndrome (SIRS)?

A
  • Infection
  • Pancreatitis
  • Burns
  • Trauma
  • Other
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7
Q

Relate the process of acute inflammation to the Pathogenesis and Presentation of Sepsis

A
  • Begins with stimulation of immune system (innate/adaptive) which leads to release of pro-inflammatory cytokines
  • Fever symptoms, vasodilation, Increased capillary permeability, Increased WBC numbers & Activity, Decreased Myocardial function
  • Leads to hypovolaemia (vasodilation + Increased capillary permeability), hypoxaemia (More oxygen used less oxygen from lungs), & Hypotension (vasodilation & reduced myocardial function)
  • Anaerobic respiration & Acidosis
  • End organ damage & Multi-organ failure
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8
Q

Define SIRS (Quantitate)

A
  • Systemic Inflammatory Response Syndrome: 2/+ of:
  • Temperature <36 >38 C
  • Heart rate >90/min
  • Respiratory rate >20/min or pCO2 <32mmHg
  • WCC <4x10^9/dl or >12x10^9/dl or >10% immature WBCs
  • Blood glucose >7.7mmol/l (unless DM present)
  • Confusion or Decreased Conscious Level (GCS)
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9
Q

Define Severe Sepsis (Quantitative)

A
  • Purpuric rash (purple) - Characteristic of meningococcal infection - causes meningitis + Sepsis
  • Heart rate >130/min
  • Systolic BP <90mmHg / mean arterial BP <65mmHg
  • Respiratory rate >25/min
  • Oxygen saturation <91%
  • Decreased conscious level (GCS)
  • Lactate >2mmol/l
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10
Q

What is meant by SOFA score?

A
  • Sepsis Clinical Criteria = confirmed/suspected Infection + Change in Sepsis-related Organ Failure Assessment (SOFA) >/= 2
  • Identifies pt’s with sepsis and thus poor outcomes early on. Comprehensive scoring system used in intensive care: 6 advanced physiological and laboratory measurements.
  • PaO2, Hypotension/vasopressors, Platelets, Glasgow coma scale, bilirubin (liver dysfunction), creatinine (kidney function)
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11
Q

What is qSOFA?

A
  • Sepsis Bedside Criteria - Quick Sepsis-related Organ Failure Assessment
  • Respiratory rate >/= 22/min
  • Altered cognition
  • Systolic blood pressure
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12
Q

Describe the Sepsis 6 to Initial treatment of Sepsis

A
  • Within 1 hour of suspecting severe sepsis:
    1. Give high-flow oxygen
    2. Take blood cultures
    3. Give Empirical IV antibiotics
    4. Measure FBC & Serum lactate
    5. Start IV fluid resuscitation
    6. Start accurate urine output measurements
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13
Q

Where to access care pathways/guidelines/policies (Local & National) relevant to sepsis

A
  • Surviving Sepsis Campaign - Very detailed sepsis protocols & bundles
  • British National Formulary - Chapter 5: Include generic antibiotic guidelines
  • But also check local sepsis antibiotic guidelines, based on local data (maybe particular patterns of infection so have a best choice antibiotics or protocol in the area)
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14
Q

What is the Sepsis Hysteria (2019) Cancern?

A
  • Paper Singer et al, The Lancet into heightened sepsis awareness and no evidence to support recommendation for antibiotics within 1 hour of presentation for all sepsis cases
  • Antibiotic use in ED doubled since 2015 –> Diagnostic problems (if giving antibiotics before taking cultures, don’t know if treated pt correctly or inappropriately afterwards) & Concerns regarding antibiotic resistance
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15
Q

Identify the key regions & Nerves involved in control of breathing

A
  • Cranial nerve X
  • Thoracic spinal cord
  • Phrenic nerve
  • Pons
  • Cervical spinal cord
  • Medulla
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16
Q

What is the principle region of the brain involved in creating the normal pattern of regular breathing?

A

Brainstem

  • Medulla region - Main respiratory centre controlling normal pattern of respiration + reflexes
  • Pons region - Fine tunes normal pattern, altering timing and depth of inspiration and expiration
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17
Q

What does Decerebrate mean?

A

Whole cerebrum/part of brainstem damaged

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18
Q

What does Decorticate mean?

A

Indicates cortical and deep cortical regions above brainstem mainly affected

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19
Q

What can the brainstem Medulla and Pons regions in breathing detect and respond to? How?

A
  • Lung volume - Increasing lung capacity activates mechanoreceptors
  • Blood gas composition - Blood pH, oxygen, CO2 levels detected by chemoreceptors
  • Can increase/decrease rate and depth of breathing to maintain blood homeostasis
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20
Q

What are the divisions of neutrons involved in control of respiration within the Medulla?

A
  • Ventral Respiratory group

- Dorsal Respiratory group

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21
Q

Describe the Ventral Respiratory Group

A
  • Brainstem respiratory centre within the Medulla
  • Controls inspiration (rostral regions) and forced expiration (caudal regions).
    Pacemaker cells in the rostral group which activate cells responsible for causing inspiration to give natural rhythm of breathing
  • Ventral surface also contains cells that detect chemical composition of CSF and informs the respiratory groups about this
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22
Q

Describe the Dorsal Respiratory group

A
  • Brainstem respiratory centre of the Medulla
  • Contains cells that integrate info from central chemoreceptors (on dorsal side of medulla - changes in CSF) and peripheral chemoreceptors + mechanoreceptors
  • Send info to main respiratory groups to control inhalation
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23
Q

What is meant by pneumotaxic centre of Breathing

A
  • Timing - Switch between inspiration and Expiration

- Pons - Pontine Respiratory Group thought to control this

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24
Q

What is meant by Apneustic Centre of Breathing

A
  • Depth of breathing

- Pons - Pontine Respiratory Group thought to control this

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25
Q

You’re walking along the corridor, minding your own business, when a colleague jumps out at you and shouts ‘boo!’ at you through a megaphone! What will be happening in your brainstem respiratory centres?

A
  • Body enters flight, fight or fright mode
  • Pontine centres controlling pattern of breathing and depth will increase the rate and length of inspiration to increase uptake of oxygen and blow off CO2 produced as result of this exertion
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26
Q

What are the 2 main locations for chemoreceptors involved in control of Breathing?

A
  • Central Chemoreceptors - Surface of medulla in brainstem

- Peripheral Chemoreceptors - Carotid artery and aortic arch

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27
Q

Where are Central Chemoreceptors located?

A
  • Ventral surface of medulla in close contact with ventral respiratory group
  • Fourth ventricle, contact cells in dorsal respiratory group
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28
Q

What do Central Chemoreceptors detect?

A
  • H+ (pH)
  • PaCO2
  • NOT oxygen
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29
Q

Where are peripheral chemoreceptors located?

A
  • Carotid bodies - At bifurcation of carotid artery

- Aortic bodies - Aortic arch

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29
Q

Where are peripheral chemoreceptors located?

A
  • Carotid bodies - At bifurcation of carotid artery

- Aortic bodies - Aortic arch

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29
Q

Where are peripheral chemoreceptors located?

A
  • Carotid bodies - At bifurcation of carotid artery

- Aortic bodies - Aortic arch

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29
Q

Where are peripheral chemoreceptors located?

A
  • Carotid bodies - At bifurcation of carotid artery

- Aortic bodies - Aortic arch

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30
Q

If PaO2 has decreased and PaCO2 has increased, what is the best way to restore normal blood gas composition?

A

By increasing ventilation rate alone the oxygen and carbon dioxide levels can both be reversed

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31
Q

What do Peripheral Chemoreceptors detect?

A
  • H+
  • PaCO2
  • PaO2
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32
Q

Which nerve will carry signals to the diaphragm to control ventilation rates?

A

Phrenic

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33
Q

Which nerves carry the Peripheral Chemoreceptor Information to the Brainstem?

A
  • Cranial Nerves IX (Glossopharyngeal) and X (Vagus)

- Carry to dorsal respiratory centre for integration with central information

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34
Q

At what value in mmHg is PaCO2 normally maintained at?

A

40mmHg by controlling pace and depth of breathing

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35
Q

If a patient’s normal ventilation is 6l/min PaCO2 (with a tidal volume of 500ml) and their PaCO2 is raised to 43 mmHg, what will their new respiratory rate be?

A
  • For each 1mmHg PaCo2 increase, 3l/min increase in ventilation rate
  • New ventilation rate 15 l.min x1000 / 500
  • 30 breaths per minute
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36
Q

At high altitude it is harder to breath. What changes to cause this?

A
  • As increase altitude the fall in atmospheric pressure decreases partial pressure of inspired oxygen and changes the rate of gas exchange in the lungs
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37
Q

Recall Boyle’s Law and its relation to altitude

A
  • If temperature remains constant, the relationship between the ventilation rate and atmospheric pressure is correlated
  • Can calculate how much harder the lung will have to work by comparing pressure at altitude to that at sea level
  • Respiratory rate = Respiratory rate at 1atm (sea-level)/Atmosphere at altitude (atm)
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38
Q

What type of breathing may aid ventilation at altitude?

A
  • Slow, deep breathing

- Allows for maximum transfer of oxygen and improved ventilation at altitude

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39
Q

How does increased 2,3-DPG alter the oxyhaemoglobin dissociation curve?

A

Shifts to right - Increasing 2,3-DPG reduces the affinity of Hb for O2, so that it is released into tissues

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40
Q

What physiological adaptations aid people living at high altitudes?

A
  • Increased red blood cell count
  • Increased levels of 2,3-DPG (to allow easy release of O2)
  • Decreased bicarbonate levels
  • Pulmonary hypertension.
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41
Q

Describe the diving reflex

A
  • On submersion:
  • Apnea - Breathing cessation
  • Bradycardia - Slowing of heart rate
  • Stops aspiration and protects from drowning
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42
Q

A medical student climbs Ben Nevis for Charity. Due to freak weather conditions, temperature remained constant for the climb. Air pressure at the top of the mountain is 0.86 atm. At sea level his normal respiratory rate is 12 breaths per minute.

What is his respiratory rate at the top of the mountain?

A
  • 14 breaths per minute

- Bpm at sea level x pressure at sea level 1atm/ pressure at altitude 0.86atm

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43
Q

If a patient has reduced oxygen levels but their carbon dioxide levels are constant, what will be the effect of increasing their oxygen intake?

A
  • Increasing ventilation rate will lead to restored oxygen levels, but HYPOCAPNIA - Reduced carbon dioxide levels (as more CO2 removed on exhalation
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44
Q

Explain the Oxygen Cascade

A
  • Outlines the steps by which PO2 decreases from air to mitochondria
  • Humidification - Alveolar gas equation - Diffusion - Physiological shunt
  • Final part of cascade from Artery - Mitochondria - Veins
  • Some blood bypasses capillaries via arteriovenous anastomoses
  • Rate of oxygen diffusions into mitochondria dependent on rate of metabolism
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45
Q

Outline Humidification of Oxygen in the Oxygen Cascade

A
  • Gas is humidified in the trachea during inspiration to 37C and 100% relative humidity
  • PiO2 = FiO2 x (PB - PSVP water)
  • Dilution of Oxygen
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46
Q

Explain the principles underlying the alveolar gas equation

A
  • How much O2 is supplied by alveolar ventilation + How much O2 diffused into bloodstream is removed by pulmonary capillaries
  • Equation allows prediction of how PAO2 changes with ventilation - If ventilation increases PAO2 will increase
  • Increase in Fraction of Inspired Oxygen (FiO2) will increase PAO2 more than hyperventilation, important when treating pt with low oxygen levels.
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47
Q

What is PIO2

A
  • Partial Pressure of Inspired oxygen

- FIO2 (PB - PSVPwater)

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48
Q

What is the Alveolar Gas Equation?

A
  • Allows to calculate PAO2 for a given PiO2 and respiratory exchange ratio (removal of O2 by pulmonary capillaries + O2 supply by alveolar ventilation)
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49
Q

What effect will breathing a gas mixture with 40% oxygen have on PAO2, assuming everything else stays the same?

A

It will Increase the PAO2

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50
Q

What effect will standing at the top of Mount Everest have on PAO2, assuming everything else stays the same?

A
  • Will decrease PAO2
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51
Q

Describe influences on oxygen and carbon dioxide transfer from atmosphere to blood (Diffusion - Oxygen Cascade)

A
  • Diffusion rate (Fick’s Law) = (A x D x Difference in P)/T

- In clinical practice, can only change Partial Pressure Difference e.g. FiO2

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52
Q

Describe and apply the pathophysiological concept of impaired diffusion

A
  • Disease which affect the diffusion barrier e.g. pulmonary fibrosis, get thickening of diffusion barrier, affect oxygen diffusion to a much greater degree than carbon dioxide diffusion.
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53
Q

Describe and apply the pathophysiological concept of impaired diffusion

A
  • Thickening of alveolar-capillary membrane e.g. pulmonary fibrosis, get thickening of diffusion barrier, affects oxygen diffusion to a much greater degree than carbon dioxide diffusion. Reduces rae of diffusion –> Lower PaO2 - Hypoxaemia
  • Strenuous exercise -> Effects of reduced transit time due to increased cardiac output exacerbated by disease effecting alveolar-capillary membrane
  • Altitude - Reduced Different in Pressure and rate of diffusion –> Effects exacerbated by disease or exercise
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54
Q

What is meant by Pulmonary Limited O2 Transfer

A
  • Under normal conditions diffusion of O2 is perfusion limited
  • Because O2 reaches diffusion equilibrium 1/3 way along capillary and no more net diffusion of O2
  • Can only be increased by increasing blood flow - Will determine net O2 transfer
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55
Q

What is Hypoxaemia

A
  • Low Partial pressure of Oxygen in blood leaving capillaries of lung
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56
Q

Give the Alveolar Gas Equation

A
  • PAO2 = FiO2(PB - PSVPwater) - (PaCO2/RQ)
  • FiO2 - Fraction of inspired O2
  • PB - Atmospheric pressure in kPa
  • PSVPwater - Saturates vapour pressure of water in kPa
  • RQ - Respiratory exchange ratio (CO2 production/O2 consumption)
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57
Q

A healthy person has a PaCO2 of 5.6kPa. Calculate their PAO2 (assume FIO2 of 0.21, atmospheric pressure of 101.3 kPa, the saturated vapour pressure of 6.3 kPa, and RQ of 0.8).

A
  • PAO2 = FiO2(PB - PSVPwater) - (PaCO2/RQ)
  • PAO2 = (0.21 x (101.3 - 6.3) - (5.6/0.8)
  • = 12.95 kPa
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58
Q

Why is oxygen diffusion perfusion limited in people with healthy lungs under normal conditions?

A
  • As Oxygen diffusion equilibrates 1/3 way across the capillary unless blood flow is changed. There will be no net oxygen diffusion past this point.
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59
Q

A patient with pulmonary fibrosis has a reduced PaO2. The oxygen transfer in their lungs is said to be diffusion-limited. What is the underlying pathology for their low PaO2?

A
  • They have a thickened diffusion barrier/membrane which decreases the rate of oxygen diffusion as per Fick’s law. This reduces the PaO2
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60
Q

Explain the physiological shunt in A-a Gradient

A
  • Blood that bypasses alveoli and does not participate in gas exchange
  • Anatomical shunt - Oxygenated blood entering from left side of the heart for anatomical reasons, e.g. bronchial blood flow + Venous drainage from myocardium via thebesian veins into left side of heart
  • Functional shunt - Blood that passes areas with low V/Q ratio (local V/Q mismatch) e.g. base of lungs
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61
Q

Describe Pathological causes of Increased A-a gradient

A
  • Severe diffusion impairment: Thickened alveolar membrane e.g. pulmonary fibrosis. Decreased alveolar surface area e.g. emphysema (damage to alveoli)
  • Right-to-left shunt e.g. ventricular septal defect (blood shunted from right side of heart to left side of heart without passing through pulmonary circulation)
  • V/Q Mismatch: Pulmonary shunt, Dead space
  • N.B - A-a will be normal in hypoventilation
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62
Q

Describe and apply the concept of V/Q matching in abnormal circumstances - In V/Q Mismatch - Dead Space

A
  • V/Q Mismatch: Dead space
  • Alveoli ventilated but not perfused
    V/Q = Infinite
  • Can be caused by: Pulmonary embolism - Blood flow impeded by embolus in pulmonary vessel.
  • Also caused by: Reduced right ventricular stroke volume e.g. due to hypovolaemia, right ventricular infarction, pericardial tamponade
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63
Q

Describe and apply the concept of V/Q matching in abnormal circumstances - In V/Q Mismatch - Pulmonary Shunt

A
  • Alveoli perfused but not ventilated
  • O/Perfusion –> V/Q = 0
  • Causes:
  • Pneumonia
  • Pulmonary oedema
  • Pneumothorax
  • Acute exacerbation of asthma
  • Atelectasis
  • Mucous plugging
  • Acute respiratory distress syndrome
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64
Q

Describe Hypoxaemia in Mild and Large V/Q Mismatch

A
  • Mild V/Q mismatch - Increasing FiO2 can increase PaO2 by increasing PAO2 in poorly ventilated alveoli, increases pressure gradient, so more O2 into blood
  • Large V/Q mismatch - Increasing FiO2 will not significantly increase PaO2 - As blood cannot take up anymore O2, e.g. in Right to left shunt.
  • PaCO2 tends to remain in normal range due to increased elimination in high V/Q areas and increased alveolar ventilation
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65
Q

What is Hypoxia

A
  • Inadequate level of tissue oxygenation for aerobic respiration:
  • Hypoxaemic hypoxia - Low PaO2
  • Anaemic hypoxia - O2 carrying capacity reduced
  • Stagnant (circulatory) hypoxia - O2 delivery reduced
  • Cytotoxic hypoxia - Mitochondria fail to utilise O2 effectively
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66
Q

What can cause Hypoxaemic Hypoxia?

A
  • Low PaO2 - Reduces saturation of Hb and CaO2
  • Caused by:
  • Low Partial pressure of inspired O2 (PiO2), e.g. altitude
  • Hypoventilation
  • V/Q mismatch
  • Right to left shunts
  • Diffusion abnormality
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67
Q

What can cause Anaemic Hypoxia?

A
  • O2 carrying capacity reduced
  • Anaemia
  • Carbon monoxide poisoning
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68
Q

What can cause Stagnant (circulatory) hypoxia?

A
  • O2 delivery reduced
  • Cardiogenic shock –> Reduced cardiac output
  • Ischaemia due to local lack of perfusion
69
Q

What can cause Cytotoxic Hypoxia

A
  • Mitochondria fail to utilise O2 effectively
  • Cyanide poisoning
  • Severe Sepsis
70
Q

What does the A-a gradient represent?

A
  • The difference between mean calculated Alveolar PO2 and measured systemic arterial PO2
71
Q

A patient has taken an overdose of opioids and has a respiratory rate of 6 breaths per minute. How will PAO2 be affected?

A
  • Decrease due to decreased ventilation
72
Q

A patient has taken an overdose of opioids and has a respiratory rate of 6 breaths per minute. How will PaO2 be affected?

A
  • Decrease
73
Q

A patient has taken an overdose of opioids and has a respiratory rate of 6 breaths per minute. How will A-a gradient be affected?

A
  • Remain the same. Mean PAO2 calculated using alveolar gas equation will be reduced/ If calculated PAO2 and PaO2 are both reduced. Difference will be unaffected
74
Q

A patient with hypoxia is diagnosed with a tension pneumothorax
Would you expect their V/Q ratio to be increased or decreased compared to normal?
What type of hypoxia is this most likely to be?

A
  • V/Q ratio would be decreased compared to normal
  • Because Tension Pneumothorax = Accumulation of air in pleural space under pressure, lung can collapse, impairing ventilation to affected part of lung
  • Hypoxaemic Hypoxia as pt PaO2 will be reduced due to reduced oxygenation
75
Q

Define respiratory failure using physiological outcome and gas tensions.

A
  • When respiratory system is no longer able to meet the metabolic demands of the body by failure of oxygenation, with or without failure of carbon dioxide removal
  • Characterised by severe hypoxaemia: PaO2 <8 kPa on FiO2 of 0.21
76
Q

Define Type 1 Respiratory Failure + Outline causes

A
  • Hypoxaemia
  • PaO2 <8 kPa on FiO2 of 0.21
  • PaCO2 is normal or low
  • Caused by V/Q mismatch e.g. Pneumonia, Pulmonary oedema, Acute exacerbation of asthma, Pulmonary embolism, etc
77
Q

Define Type 2 Respiratory Failure

A
  • Two gases wrong - Hypoxaemia and Hypercapnia
  • PaCO2 >6.5 kPa
  • Caused by: Failure to ventilate whole lungs
78
Q

Why is PaCO2 normal or low in Type 1 Respiratory Failure?

A
  • V/Q mismatch may result in an initial increase in PaCO2, but this stimulates chemoreceptors and induces a compensatory hyperventilation. Increased elimination of CO2 via the unaffected alveoli (an increase in ventilation decreases the partial pressure of CO2 in the unaffected alveoli, increasing the partial pressure gradient, and increasing diffusion of CO2 out of the blood).
  • However, as the disease progresses, hyperventilation may no longer be able to compensate and type 2 respiratory failure can develop
79
Q

Describe causes of Type 2 Respiratory Failure

A
  • Insufficient Respiratory Drive - Secondary to Opiates, Central Neurological damage
  • Impaired Lung Movements - E.g. Chest wall deformity, Obesity, Neurological Impairment
  • Work of breathing is excessive - COPD, Near Fatal Asthma attack
80
Q

Explain the clinical and physiological consequences of Type 1 Respiratory Failure.

A
  • Hypoxaemia stimulates hyperventilation - Increase in rate and depth of breathing
  • Hypoxia (Dyspneoa, Confusion, Drowsiness, Restlessness and agitation)
  • Cyanosis - Haemoglobin desaturation
81
Q

Explain the clinical and physiological consequences of Type 2 Respiratory Failure.

A
  • Hypoxaemia stimulates hyperventilation - Increase in rate and depth of breathing
  • Hypoxia (Dyspneoa, Confusion, Drowsiness, Restlessness and agitation)
  • Hypercapnia - Only Type 2 (Headaches, Tachycardia with bounding pulse, Peripheral vasodilation (flushing, warm extremities), CO2 retention flap (asterixis), Papilloedema, Respiratory acidosis
82
Q

Why does respiratory acidosis occur in Type 2 Respiratory Failure?

A

An increase in PaCO2will lead to an increase in carbonic acid, an increase in H+ionconcentration, andthe pH will decrease (acidaemia).

83
Q

Explain the compensatory mechanisms for respiratory failure - Hypoxia (Type 1 + 2)

A
  • Hyperventilation
  • Hypoxic pulmonary vasoconstriction - Redistributes perfusion of blood away from poorly ventilated areas of lung to better ventilated lung
  • Increase in cardiac output and regional blood flow, particularly to brain
  • Increase Hb Concentration - Splenic contraction (transient), Increased erythropoietin production (long term)
  • Oxyhaemoglobin dissociation curve - Displaced to right by increase in 2,3-DPG
84
Q

Explain the compensatory mechanisms for respiratory failure - Hypercapnia (Type 2 only)

A
  • Hyperventilation (unless unable)

- Renal compensation of respiratory acidosis - By retention of bicarbonate (HCO3-)

85
Q

Explain the Use of Arterial Blood Gas (ABG)

A
  • Small sample of blood taken from usually radial artery, run through gas analyser, used to assess pt respiratory status:
  • Assess adequacy of oxygenation and ventilation
  • Assess respiratory function and identify evidence of respiratory failure
  • Determine acid-base balance and identify acid-base abnormalities
  • Identify evidence of compensatory mechanisms
  • Measures of other parameters such as lactate, glucose, electrolytes etc.
86
Q

Outline the Process of ABG Interpretation

A
  • Patient Name and Details
  • Are they on oxygen? If so how much and by what route?
  • Look at PaO2: Normal range 11-15 kPa. If PaO2 <8 kPa on air is severe hypoxaemia and respiratory failure
  • Look at pH: Within normal range? Acidaemia/Alkalaemia
  • Look at PaCO2 - Respiratory component. Normal or abnormal?
  • Look at HCO3- - Metabolic Component. Normal or abnormal? Compensation?
  • Look at other components: Lactate (septic), Glucose, Electrolytes
87
Q

A patient with COPD has an arterial blood gas performed on room air which reveals a PaO2 of 7.6 kPa (normal range: 11-15 kPa), pH of 7.33 (normal range: 7.35-7.45) PaCO2 of 7.8 kPa (normal range 4.6 - 6.4 kPa), and HCO3- of 31 (normal range 22 - 30 mmol/L).
How would you describe the patient’ acid-base status?
Does this patient have respiratory failure and if so what type?

A

a) Partially compensated Respiratory Acidosis

b) Type 2 Respiratory failure: Hypoxia <8kPa and Hypercapnia

88
Q

A patient has an arterial blood gas performed on room air which reveals PaO2 of 7.2 kPa (normal range: 11-15 kPa), pH of 7.45 (normal range: 7.35-7.45) PaCO2 of 4.2 kPa (normal range 4.6 - 6.4 kPa), and HCO3- of 22 (normal range 22 - 30 mmol/L).
What type of respiratory failure does this patient have?

A

Type 1 Respiratory Failure: Hypoxia PaO2 <8 kPa with normal or low PaCO2

89
Q

In a patient experiencing an acute exacerbation of asthma, why does a PaCO2 in the normal range indicate life-threatening asthma?

A
  • Patient normally compensate initially by hyperventilating and increasing alveolar ventilation to unobstructed lung, leading to decrease in PaCO2. Result in Type 1 Respiratory Failure
  • However, as exacerbation progresses compensatory hyperventilation impaired by increasing functional residual capacity, progressive airway narrowing, and muscle fatigue. Leads to increasing PaCO2, urgent ITU intervention.
  • Normal PaCO2 - Life-threatening asthma
  • Raised PaCO2 - Near-fatal asthma
90
Q

If plasma pH was low (acidaemia) and the underlying cause was respiratory in origin, what would you expect PaCO2 to be?

A

Increased - Respiratory acidosis/acidaemia

91
Q

Causes of Respiratory Acidosis

A
  • Neurological disorders
  • COPD
  • Opiod overdose
  • Near-fatal exacerbation of asthma
  • Chest wall deformities
92
Q

Causes of Respiratory Alkalosis

A
  • Panic attack
  • Excessive mechanical ventilation
  • High altitude
  • Pulmonary embolism
93
Q

If the plasma pH was low (acidaemia) and the underlying cause was metabolic in origin, what would you expect the HCO3- concentration to be?

A

Decreased

94
Q

Outline Causes of Metabolic Acidosis

A
  • Severe prolonged diarrhoea
  • Renal failure
  • Lactic Acidosis (due to sepsis/septic shock)
  • Diabetic Ketoacidosis
  • Aspirin Overdose (exogenous acid)
95
Q

Outline causes for Metabolic Alkalosis

A
  • Ingestion of exogenous alkali substances
  • Severe prolonged vomiting (due to GI loss of H+)
  • Use of loop / thiazide diuretics (Renal loss of H+)
96
Q

What would V/Q be in a Pulmonary Embolism?

A
  • High
  • Loss of perfusion to an area of ventilated alveoli resulting in dead space.
    V/Q would increase
97
Q

Describe Diabetic Ketoacidosis

A
  • Life-threatening complication of diabetes
  • Lack of insulin means glucose cannot be utilised for energy production and so ketone bodies are generated from fatty acids to use as alternative energy source.
  • Ketone bodies lead to metabolic acidosis and hyperglycaemia causes dehydration via osmotic diuresis
98
Q

Explain why testing lung function is useful

A
  • Detect if lung disease is present
  • Quantify severity of lung disease i.e. lung impairment
  • Look at extent of airways reversibility/hyperresponsiveness e.g. asthma
  • Assess effectiveness of intervention e.g. surgical, therapeutic, pharmacological
  • Pre-operative evaluation
99
Q

What is Peak Expiratory Flow Rate

A
  • PEFR - Maximum flow rate generated during a forceful exhalation, starting from full lung inflation
100
Q

Describe the principles and utility of peak flow measurement

A
  • Reflects the degree of resistance to flow in the airways and respiratory health.
  • Can be reduced by bronchial constriction/mucus secretion.
  • Useful in assessment and monitoring pt with asthma (underestimates effects on small airways though)
101
Q

Why are patients with suspected asthma asked to keep a PEFR diary? What is the GP looking for in the PEFR recordings?

A
  • Useful in aiding diagnosis as may reveal day-to-day fluctuations in peak flow outside of normal
  • NICE - Variations in excess of 20% over recordings made at least twice daily and for 2-4 weeks is regarded as positive
  • GP will be looking for fluctuations in PEFR diurnally (e.g. lower flow in morning) or linked to bouts of exercise
102
Q

Explain the principles and utility of Spirometry

A
  • Objective Measure of Lung function
  • Gives Dynamic Air Flow Measures:
  • Forced Vital Capacity (FVC): Total volume exhaled with maximal effort after a full inspiration
  • Forced Expiratory Volume in 1 second (FEV1): Volume of air expelled in the first second of a forced expiration, starting from full inspiration
  • Compared to predicted values based on height, age, sex
  • Normal FEV1:FVC ratio 80%
103
Q

How do you measure using Spirometry?

A
  • Nose clip on pt nose – To ensure only breathing out via mouth
  • Pt to take a deep breath in and asked to breathe out as hard and fast as possible and for as long as they can into mouthpiece with lips sealed around, connected to a machine (spirometer) which records and analyses the results.
  • Repeat 3 times
104
Q

How can Spirometry measurements be used?

A
  • Crude measure of lung size (vital capacity & forced vital capacity)
  • Measures airway calibre (FEV1)
  • Indicates airflow obstruction (FEV1:FVC)
  • Measures Flow (Peak Expiratory Flow Rate)
105
Q

Define total lung capacity and describe the lung volumes that contribute to it, including tidal volume, expiratory reserve volume, residual volume, inspiratory reserve volume.

A
  • Total Lung Capacity: After a full inspiration where lungs filled with air
  • Tidal volume: Volume of air breathed in/out during normal quiet breathing
  • Expiratory reserve volume: Extra Volume of air which can be expired after normal tidal expiration
  • Residual Volume: Air left in lungs at end of forceful expiration
  • Inspiratory Reserve Volume: Excess amount of air which can be breathed in from end of tidal volume to maximal inspiration
106
Q

What is Vital Capacity (L) - VC

A
  • Maximal volume of air that can be breathed in after a maximal expiration /
  • Maximal volume of air that can be exhaled after a maximal inspiration
  • = Tidal volume + Inspiratory reserve volume + expiratory reserve volume
107
Q

What is Forced Vital Capacity (L) - FVC

A

Maximum volume exhaled with maximum effort, following a full inspiration

108
Q

What is Forced Expiratory Volume in One Second (L) - FEV1

A

Volume of air exhaled in the first second of forced expiration

109
Q

What is Peak Expiratory flow rate (L/min or L/sec) - PEFR

A

Maximum flow rate generated during a forceful exhalation, starting from full lung inflation. Can be assessed by peak flow or spirometry

110
Q

Describe what is meant by Obstructive Lung Disorders

A
  • Used to describe conditions in which there is airway narrowing and increased resistance to airflow.
  • Most common disorders asthma and COPD, but also Cystic fibrosis and bronchiectasis.
111
Q

What are the mechanisms by which Obstructive disorders occur

A

o Inflammation and thickening of bronchial wall e.g. asthma
o Mucus obstructing airways e.g. asthma, COPD, Cystic Fibrosis
o Loss of elastic recoil and airway collapse e.g. COPD
o Bronchoconstriction e.g. Acute asthma
o Obstruction by a foreign body

112
Q

Explain how a combination of FVC and FEV1 can be used to in the assessment of lung function

A
  • FEV1 reduced
  • FVC can be normal or reduced to lesser extent
  • FEV1/FVC ratio reduced - Guidelines state <0.7 indicates obstruction
113
Q

Outline the Main Obstructive disease patterns shown on lung function testing

A
  • FEV1 reduced
  • FVC reduced or normal but lesser extent
  • FEV1/FVC ratio below <0.7
  • PEFR reduced
  • Concavity in effort-independent part of curve
  • Increased residual volume
114
Q

What is Bronchodilator Reversibility Testing

A
  • Administering of bronchodilator before and after lung function tests to see if it improves lung function and by how much. In adults with suspected asthma improvement in FEV1 of 12% or more is positive test
115
Q

Describe what is meant by Restrictive Lung Disorders

A
  • Used to describe conditions in which lungs are less able to expand. Means that the volume of air that can be breathed in and out is reduced.
  • May be due to stiffening of lung tissue (e.g. due to Pulmonary fibrosis), respiratory muscle weakness (e.g. neuromuscular disorders such as Duchenne muscular dystrophy) or other conditions that limit chest expansion e.g. scoliosis, obesity
116
Q

Outline the Main Obstructive disease patterns shown on lung function testing

A
  • FEV1 and FVC reduced, often in proportion to each other
  • FEV1/FVC ratio is normal / increased
  • May have reduced PEFR
117
Q

Outline the main differences between obstructive and restrictive disease patterns shown on lung function testing.

A
  • FEV1 and FVC both reduced
  • FEV1/FVC ratio - Reduced in Obstructive disorders
  • FEV1/FVC ratio - Normal or increased in Restrictive Disorders
118
Q

What is Inspiratory Capacity (IC)

A
  • Maximum volume of air that can be inspired from the end of a normal quiet expiration
  • Tidal volume + Inspiratory reserve volume
119
Q

What is Functional Capacity (FRC)

A
  • Volume of air remains in the lungs at the end of a normal expiration
  • Expiratory reserve volume + Residual volume
120
Q

What is Total Lung Capacity (TLC)

A
  • Total volume of air in the lungs after a maximal inspiration
  • Vital capacity + Residual volume
121
Q

Describe the Importance of Functional Residual Capacity (FRC)

A
  • Volume of air remains in lungs at end of normal expiration
  • Important:
  • Oxygen buffer - Allows gas exchange to continue between breaths
  • Prevent alveolar collapse
  • Optimal Lung Compliance
  • At FRC - Outward elastic forces of the chest wall are balanced by inward elastic recoil of the lungs
122
Q

Outline the effects of Obstructive Lung Disease on Lung Capacity Measures / Static Lung Volumes

A
  • Total Lung Capacity - Normal/increased
  • Residual volume - Increased
  • RV/TLC - Increased - % of residual volume to TLC should be <40%
  • Functional Residual Capacity - Increased: Outward pull of chest wall will be greater than inward recoil of lungs. Extra volume of air has to be added to balance.
  • Vital capacity - Decreased
123
Q

Outline the effects of Restrictive Lung Disease on Lung Capacity Measures / Static Lung Volumes

A
  • Total Lung Capacity - Decreased
  • Residual volume - Normal/Decreased
  • RV/TLC - Normal/Increased
  • Functional Residual Capacity - Decreased: Inwards collapsing force of lungs greater than outwards pull of chest wall, not balanced, so equilibrium occurs at lower lung volume
  • Vital capacity - Decreased
124
Q

Explain the effect of Emphysema on Functional Residual Capacity (FRC)

A
  • Obstructive disease, Destruction of elastic tissue means elastic recoil of lungs is reduced
  • Elastic recoil of chest wall is proportionally greater
  • Therefore, balance between the two opposing forces occurs at a higher lung volume
  • FRC is increased
125
Q

Explain the effect of Pulmonary Fibrosis on Functional Residual Capacity (FRC)

A
  • Restrictive Disease, Deposition of fibrotic tissue in the lungs mean they become stiffer
  • Elastic recoil is increased and is proportionally greater than chest wall elastic recoil
  • Balance between the two opposing forces occurs at a lower lung volume
  • FRC is decreased
126
Q

What Volumes can be measured using a spirometer? What Capacity can be calculated from these volumes?

A
  • Tidal volume, Inspiratory reserve volume, expiratory reserve volume can be measured
  • Vital capacity can be calculated
  • Residual volume, Functional residual capacity, and total lung capacity cannot be measured
127
Q

What methods are there for measuring Functional Residual Capacity and Residual Volume?

A
  • Helium Dilution
  • Nitrogen washout
  • Body Plethysmography
128
Q

What is Diffusing Capacity Measurement and What is it used for?

A
  • Examines ability of lungs to transfer gas between inhaled air and the capillary blood, and for that gas to combine with Hb in capillary RBCs
  • Useful in evaluation of dyspnoea (shortness of breath) and hypoxia + monitoring of disease progress
129
Q

How is Diffusing Capacity Measured?

A
  • Ability of lungs to transfer gas between inhaled air and capillary blood and for gas to combine with haemoglobin in capillary RBCs
  • Single Breath Test using Carbon Monoxide - Pt breathes in gas mixture with known [CO] and Helium from residual volume to TLC i.e. vital capacity.
  • Transfer of CO is diffusion-limited.
130
Q

What measures can be obtained from Diffusing Capacity / Single-breath test using carbon monoxide (CO)

A
  • Transfer factor/diffusing capacity of the lungs for carbon monoxide (TLCO/DLCO) – Total amount of CO transferred by unit time per unit of driving pressure CO
  • Alveolar volume (VA) – Single breath estimation of TLC using helium measurement which does not cross alveolar membrane
  • Transfer coefficient for CO (KCO) – Efficiency of alveolar transfer of CO
131
Q

Explain Abnormalities in Diffusing Capacity Measurement

A
  • Reduced diffusing capacity (TLCO) due to:
  • Reduced SA e.g. emphysema, pulmonary vascular disease
  • Increased thickness of membrane e.g. Pulmonary fibrosis/interstitial lung disease (chronic) or pulmonary oedema (acute)
132
Q

Why is it important to know a patient’s Haemoglobin concentration before the Single-breath test / diffusing capacity measurement?

A
  • As carbon monoxide has a very high affinity for haemoglobin and binds to it in the blood, the concentration of Hb will affect the amount of carbon monoxide transferred.
  • A lower Hb level will result in a lower TLCO
133
Q

Why may TLCO be raised following pulmonary haemorrhage (e.g., in vasculitis)?

A

Extra red cells in the lungs absorb CO and falsely elevate the TLCO. When Haemoglobin is broken down, TLCO levels return back to normal

134
Q

Which value measured on spirometry can be used to help assess the severity of airflow obstruction in COPD?

A

FEV1 % predicted

135
Q

What are features of a flow-volume loop of a person with COPD?

A
  • ‘Scooped out’ Appearance of the expiratory curve
  • Increased Functional Residual Capacity
  • Increased Residual volume
136
Q

Which lung volume cannot be measured using spirometry?

A

Residual Volume

137
Q

Which gas, which crosses the alveolar-capillary membrane, is used in the single-breath test for diffusing capacity?

A

Carbon Monoxide

138
Q

What other Atopic Conditions are associated with Asthma?

A
  • Eczema (Atopic Dermatitis)

- Hayfever (allergic rhinitis)

139
Q

Describe the Classifications of Asthma

A
  • Extrinsic asthma - Associated with atopy, typical childhood onset, maybe associated with sensitisers/exposure to pollutants
  • Intrinsic Asthma - No personal or family history of asthma/atopy, typical onset in middle age, often onset following upper airway infection
  • Often overlap
140
Q

What are the triad features in Pathogenesis of Asthma?

A
  • Airway obstruction - Reversible
  • Airway hyper-responsiveness
  • Airway inflammation
141
Q

Outline the pathophysiology of Asthma

A
  • Accumulation of mucus in bronchiole lumen, (plugging) restricting air flow. Increased mucus production due to increase in number of goblet cells + Hypertrophy of submucosal glands
  • Chronic inflammatory cells present in large numbers; eosinophils, mast cells, macrophages
  • Thickened basement membrane
  • Hypertrophy and hyperplasia of smooth muscle cells
  • Oedema and dilated blood vessels
142
Q

Which cell type release histamine during ‘degranulation’

A
  • Mast cells

- In presence of an allergen, IgE antibodies cause degranulation of mast cells

143
Q

Which T lymphocyte type is the most important in the response to allergens in asthma?

A
  • T-helper cells type 2 (TH2)

- Central to process of sensitisation and pathogenesis in asthma

144
Q

Describe the 3 phases of Asthma Pathogenesis

A
  1. Immediate/early phase - 0-60mins after allergen exposure, Allergen bound by IgE antibodies, Activated IgE binds mast cells, which degranulate, Chemical mediators e.g. histamine, leukotrienes, prostaglandins cause smooth muscle contraction, tightening the airway wall = Bronchoconstriction
  2. Late phase - 1-8hrs, chemical mediators from mast cells and TH2 cells cause:
    o Vascular leakage & Oedema
    o Infiltration of Eosinophils and Neutrophils (amongst other cells)
    o Mucus Secretion
  3. Chronic Remodelling phase - months to years if have repetitive exposure to same allergen/trigger: Smooth muscle hypertrophy, Smooth muscle and epithelial cell hyperplasia, Epithelial damage, Basement membrane thickening
145
Q

A 12 year-old boy is brought to A&E with an asthma attack. They are given some medication to dilate his bronchioles, and he improves dramatically over about 30 minutes. After being observed for 2 hours, he is ready to go home. However, just as he’s leaving, his asthma begins to get worse again and he doesn’t respond to the bronchodilator medication this time.

Explain why his asthma got worse after about 2 hours of observation. Why did his asthma not improve with a bronchodilator the second time?

A
  • Over first hour of asthma attack, main problem is bronchoconstriction, due to contraction of smooth muscle in bronchioles. Reversed by salbutamol (bronchodilator and Beta2-agonist)
  • 2-3 hrs late phase, mucosal oedema, vascular leakage, mucus secretion, inflammatory response. Further bronchoconstriction, less oxygen reaching blood, making him more breathless. Mucus may also begin blocking airways. Anti-inflammatory medications should have been given to reduce effect of late phase asthma (e.g. prednisolone steroid)
146
Q

Why can’t you diagnose asthma in children?

A
  • Asthma diagnosis requires tests such as peak flow/spirometry testing difficult in young children
  • If symptoms continue, or pt responds well to inhaler can continue treating and managing as ‘suspected asthma’
  • Can use peak flow diary at about 7/8 yo
147
Q

Outline the clinical signs and symptoms of Asthma

A

o Cough
o Wheeze
o Chest tightness
o Shortness of breath
o Diurnal variation (i.e. symptoms are often worse at night)
- In younger people ‘atopic asthma’ occur with other inflammatory/allergic symptoms such as hayfever or eczema.

148
Q

Why might reduced breath sounds indicate a more severe exacerbation?

A
  • Absence or reduced breath sounds likely suggests that very little air is getting in and out of the lungs. During an asthma exacerbation, could occur because of blockage of the airways by mucus - often called ‘mucus plugging’
149
Q

What clinical signs may a doctor find during an exacerbation of asthma?

A
  • Difficulty completing full sentences (i.e. needs to take a breath halfway through a sentence)
  • High respiratory rate (tachypnoea)
  • High heart rate (tachycardia)
  • Wheeze (may be audible without a stethoscope)
  • Use of accessory muscles of breathing
  • Reduced breath sounds - if severe
150
Q

A 9 year-old girl attends her GP describing a cough at night for the past year or more. Now that the weather is getting colder, she has been unable to play in the playground with her friends because she gets easily out of breath. On examination her chest is clear and no other abnormalities are found.

What is the most appropriate next step?

A

Give her a peak flow device and arrange a review in 2 weeks time

151
Q

Correlate the mechanism of action of the classes of drugs with the pathophysiology and basic management of the chronic obstructive airway diseases.

A
  • Beta2-agonist bronchodilators = Salbutamol – to treat bronchoconstriction
  • corticosteroids = Prednisolone orally/Hydrocortisone IV – to treat inflammatory component of asthma
  • Oxygen - to maintain oxygen saturations
  • Other treatments: Ipratropium bromide, Magnesium sulphate IV, Aminophylline IV, Antibiotics (if sign of infection)
152
Q

A 21 year-old man has had asthma since being a young child. He attends his university health centre and asks for a salbutamol inhaler. He is generally well, but he has been using his salbutamol inhaler every day, sometimes 2-3 times a day, for at least the past 3 months.

What is the most appropriate next course of action?

A
  • Arrange an asthma review with the nurse, who is likely to recommend a low-dose steroid inhaler
  • Useful to find out more about why his asthma might be worse now, as well as check inhaler technique, consider spacer. Very likely to benefit from ICS, as per BTS/SIGN guidance
153
Q

What is dyspnoea

A

Shortness of breath

154
Q

What is COPD

A
  • Chronic obstructive pulmonary disease - umbrella term for several different disease processes
  • Refers to chronic, mostly irreversible, obstructive airway changes
  • includes chronic bronchitis & emphysema
155
Q

Outline causes of COPD

A
  • Smoking - most common cause
  • Other pollutants
  • Alpha1-antitrypsin deficiency
156
Q

Describe Chronic Bronchitis

A
  • Most COPD - combination of bronchitis & emphysema
  • Inflammation of large upper airways (bronchus, larger bronchioles)
  • Mucus gland hypertrophy & Hyperplasia
  • Hypersecretion of mucus
  • Typically causes chronic productive cough
157
Q

Describe Emphysema

A
  • Smaller airways (Smaller bronchioles, alveoli)
  • Alveolar wall destruction
  • Air space enlargement -> Reduced gas exchange surface area
  • Typically causes shortness of breath (dyspnoea)
158
Q

Outline the Pathophysiology of Chronic Bronchitis - COPD

A
  • Squamous metaplasia + goblet cell and sub mucosal gland hyperplasia - Mucus hypersecretion
  • Airway wall infiltrated with macrophages + CD8+ T-lymphocytes
  • Neutrophils predominate in airway lumen and around submucosal glands
  • Airway smooth muscle and basement membrane minimally increased compared to findings in asthma
  • Severe COPD - Also lymphoid follicles, lumen filled with exudate + mucus, peribronchial fibrosis
159
Q

Outline the pathophysiology of Emphysema - COPD

A
  • Loss of elasticity in alveolar wall - Enlargement of alveoli
  • Alveolar wall destruction - Due too oxidative stress, inflammatory cells & mediators, Protease anti-protease imbalance.
  • Accumulation of inflammatory cells, predominantly macrophages and CD8+ lymphocytes
  • Destructive changes reduce the pulmonary capillary bed and so reduce the surface area over which gas exchange can take place
160
Q

What are the Different types of Emphysema

A
  • Centracinar emphysema – Typical of emphysema caused by smoking
  • Panacinar emphysema is more suggestive of alpha-1 antitrypsin deficiency (a relatively rare genetic condition)
161
Q

What are Bullae?

A
  • A Bulla is a distended acinus of >1 cm diameter
  • Extreme consequence of long-term emphysema, huge air-filled sacs that develop due to destruction of alveoli. Can burst and cause a pneumothorax, condition where air enters pleural space and causes collapse of lung.
162
Q

What are causes of Airflow Obstruction in COPD

A
  • Reversible: Accumulation of inflammatory cells, mucus, plasma exudate in bronchi, Smooth muscle contraction, dynamic hyperinflation during exercise
  • Irreversible: Fibrosis and narrowing of the airways, loss of elastic recoil due to alveolar destruction, Destruction of alveolar support that maintains latency of small airways
163
Q

Explain the clinical signs and symptoms of COPD in the context of changes that occur in the structure and functioning of the respiratory tract

A
  • Emphysematous changes: Breathless + Tachypnoeic as compensate for destruction of alveoli and reduced surface area for gas exchange
  • Chronic Bronchitis changes - Obstructive larger-airway changes, with accumulation of CO2 in airways, acid-base physiology changes to become more tolerant so become cyanotic and oedamotous, respiratory rate remains the same as CO2 changes very gradual
  • Most pt mixture
164
Q

What does a ‘reduced FEV1/FVC ratio’ mean?

A

Means that compared to someone with the same FVC, they are unable to breath out as much air in one second. Means that it takes them longer to empty their lungs of air during expiration, so outflow of lungs must be obstructed in some way – Obstructive airway problem.

165
Q

Why’s a chest x-ray an important test for someone presenting with suspected COPD?

A
  • Patients presenting with chronic cough and breathlessness, lung cancer should be ruled out before making any further diagnoses.
166
Q

What is the major management/treatment advice in COPD?

A
  • Smoking Cessation
  • FEV1 will have a rapid decline after ~40-50 years if susceptible to effects of smoke
  • Smoking at any point will improve life expectancy, often by several years.
167
Q

What drugs are used in the treatment of COPD?

A
  • Bronchodilators - Short-acting Beta2-agonists (e.g. salbutamol) and Short-acting anticholinergics (e.g. ipratropium)
  • Combination therapies - Long-acting Beta2-agonists + inhaled steroid (e.g. beclomethasone, fluticasone)/long-acting cholinergic
  • Oral theophylline - Only if bronchodilators ineffective
  • Mucolytic agents (e.g. carbocisteine)
168
Q

Compare the Pathophysiology of Asthma and COPD

A
  • Asthma
  • Causes: Asthma - Allergens and other env. triggers
  • Immune response: Asthma - IgE mediated mast cell degranulation, TH2 (CD4+) lymphocytes, Eosinophils
  • Pathological Findings: Bronchoconstriction due to smooth muscle hypertrophy & Hyperplasia. Airway hyper-responsiveness
  • Mostly reversible
  • COPD
  • Causes: Smoking
  • Immune response: Macrophages, Cytotoxic (CD8+) lymphocytes, Neutrophils
  • Pathological findings: Large and small airway narrowing, alveolar destruction
  • Mostly irreversible
169
Q

Compare the Clinical Presentation of COPD with Asthma

A
  • COPD
  • Smoking history - Nearly all
  • Chronic productive cough, Breathlessness persistent & progressive, Longitudinal observation - Deteriorates over time, Reversibility testing with Salbutamol, Inconsistent, not reproducible
  • Asthma
  • Possible smoking history
  • Symptoms often at <35yrs, Breathlessness variable, nocturnal waking with cough/breathlessness, significant diurnal variation in symptoms, longitudinal observation - Fairly consistent, Reversibility testing - Significant response
170
Q

A patient undergoes Fractional exhaled Nitric Oxide (FeNO) testing for suspected asthma.
This test looks for evidence of inflammation associated with which cell type?

A
171
Q

A 67-year-old man with severe pulmonary oedema has hypoxaemia. Which component of Fick’s Law regarding simple diffusion will be altered by the administration of oxygen?

A

Partial pressure difference of the gas

172
Q

What indicates Acute Severe Asthma

A

The patient has acute severe asthma based on: respiratory rate ≥25 breaths per minute, heart rate ≥110 bpm, and inability to complete sentences in one breath. The patient does not have any features of life-threatening asthma as they are alert, they are not hypotensive, they do not have a silent chest, their oxygen saturations are ≥92%, their PaO2 is ≥8kPa, and their PaCO2 is reduced secondary to hyperventilation (‘normal’ PaCO2 indicates the patient is tiring).

Block 2 (15 decks)

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