Block 3: Respiratory investigations, Airway obstruction Flashcards

1
Q

Types of respiratory investigations

A
  • ABG
  • Pulmonary function tests: Spirometry, flow volume loops, lung volume, gas transfer
  • Imaging: CXR, CT scan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ABG: normal values

A
  • pH: Acidaemia < 7.35 – 7.45 >Alkalaemia
  • Pa02:10.7 – 13.3 (on room air)
  • PaCO2:4.7 – 6.0
  • HCO3:22 – 26
  • Base excess -2 - +2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ROME mnemonic

A
  • Respiratory opposite= if the pH is up and Pco2 is down then its respiratory alkalosis. If the pH is down and the Pco2 is up then its respiratory acidosis.
  • Metabolic equal= If the pH and HCO3 are up then its metabolic alkalosis. If the pH and HCO3 are down then its Metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ABG: rule of thumb CO2

A
  • Metabolic problems PH and PCO2 move in the same direction i.e. both go up
  • In Respiratory Problems they tend to move in opposite directions
  • Problem is mixed defect – both respiratory and metabolic acidosis etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Respiratory acidosis

A
  • Acute respiratory acidosis= pH goes down, pCo2 goes up, Bicarbonate doesn’t change
  • Chronic respiratory acidosis= pH doesn’t change, pCo2 goes up, Bicarbonate goes up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ABG: alkalosis

A
  • Acute respiratory alkalosis= pH goes up, pCo2 goes down, Bicarbonate doesn’t change
  • Chronic respiratory alkalosis= pH doesn’t change, pCo2 goes down, Bicarbonate goes down
  • Metabolic alkalosis: If there is an excess of HCO3- compared to H+ due to loss of H+ with severe vomiting then this may cause an alkalosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Blood gas: giving oxygen

A
  • Rule of thumb to check for hypoxemia is “the Pao2 should be 10-15 kpa less then the FiO2”
  • Example= on room air(Fio2 21%) you would expect the Pao2 to be -> 21-10= 11 Kpa (normally 10-14 kpa)
  • If someone is on oxygen with a 40 % Venturi mask(FIo2 is 40%) , there PaO2 should be -> 40-15= 25 Kpa( 25-30 Kpa)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

The two systems that control pH

A
  • Respiratory system– controlling ventilation and the amount of CO2 in the blood.
  • ‘Metabolic’ system– predominantly controlling the production of HCO3 by the kidneys.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hypoxia and respiratory failure

A
  • Hypoxia is present if PaO2 < 10.7 whilst breathing air (oxygen content 21%, FiO2 0.21).
  • Respiratory failurewould be defined as a PaO2 < 8 whilst breathing air.
  • Problem with oxygen being transferred from the alveoli into the bloodstream e.g. due to pulmonary fibrosis – may lead to type 1 respiratory failure. If PaO2 is <8 and the PaCO2 is normal or low
  • Problem with oxygen being transferred from the air into the lungs e.g. ventilation problems in neuromuscular disease – may lead to type 2 respiratory failure. If PaO2 is <8 and the PaCO2 is high
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Step wise approach to ABG interpretation

A

1.Is there:- An acidaemia (low pH) < 7.35 or an alkalaemia (high pH) > 7.45

  1. Determine the respiratory component: If the pH is low, is the PaCO2 high (>6.0) – this is a respiratory acidosis. If the pH is high, is the PaCO2 low (<4.7) – this is a respiratory alkalosis
  2. Determine the metabolic component: If the pH is low, is the HCO3 low (< 22) – this is a metabolic acidosis. If the pH is high, is the HCO3 high (>26) – this is a metabolic alkalosis
  3. Is there an oxygenation problem? Is the patient hypoxic – PaO2 < 10.7 breathing air. Is the patient in respiratory failure – PaO2 < 8 breathing air
  4. If present, which type of respiratory failure: PaCO2 is normal/low in T1RF. PaCO2 is high in T2RF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ABG: mixed cause

A
  • Patients may have a mixed cause of an acid-base problem e.g. a mixed respiratory and metabolic acidosis. pH is low, PaCO2 is high and HCO3 is low.
  • The body may have compensated for an acid-base problem, and corrected the pH into normal range whilst the PaCO2 and HCO3 are within abnormal ranges
  • In compensated T2RF: pH is normal, PaCO2 is mildly high and HCO3 is high
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Spirometry measurements

A
  • Forced vital capacity – the total volume of air that a patient has expired at the end of maximal forced expiration (following maximal inspiration)
  • Forced expiratory volume in 1 second (FEV1) –the volume of air that a patient can forcefully expire in 1 second (following maximal inspiration)
  • The FEV1/FVC ratio – helps us to identify whether the patient has an obstructive or restrictive pathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Obstructive vs restrictive pattern

A
  • Obstructive: FEV1/FVC <70%. The FEV1 is reduced more than the FVC. For example: COPD, asthma
  • Restrictive: FEV1/FVC >70% is maintained. The FEV1 and FVC are reduced by the same amount. For example, interstitial lung disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Flow volume loops

A
  • A maximum inspiration followed by a maximum expiration. Records flow at any given volume
  • The result is plotted on a graph, with a positive expiratory component (above the x axis) and a negative inspiratory component (below the x axis).
  • Used to measure peak expiratory flow rate
  • Obstructive: have reduced expiratory flow in the small airways. There is a reduction in the peak expiratory flow and a concave (often compared to a church steeple) appearance to the descending portion of the expiratory limb.
  • Restrictive: reduced volume in lungs. Normal appearance but reduced expiratory and inspiratory volumes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Large airway abnormalities: extra-thoracic and intra-thoracic

A
  • The extra-thoracic (upper or above the thoracic inlet) airways which go from the nasal cavity to the cervical trachea i.e. vocal cord paralysis, goitre, malignancy
  • The intra-thoracic (lower or below the thoracic inlet) airways which go from the thoracic trachea to the bronchi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Large airway abnormalities: flow volume loops and fixed upper airway obstruction

A

Flow volume loops:

-In variable extra-thoracic obstruction: limitation in the inspiratory flow
- In fixed upper airway obstruction: present in inspiration and expiration, both components of the flow volume loop are reduced. I.e. tracheal stenosis, endotracheal malignancy and foreign body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

TLC

A
  • Measured with a whole body plethysmography in an air tight box
  • Total lung capacity (TLC)is the total volume of air in the lungs after maximal inspiration. May be increased in patients with obstructive lung disease such as COPD. May be decreased in patients with restrictive lung disease such as kyphoscoliosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Residual volume

A

Residual volume (RV)is the amount of air remaining in the lungs after a maximal expiration. May be increased in patients with obstructive lung disease such as COPD where there is air trapping. If excessively raised can have lung volume reduction surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Transfer capacity of the lung for carbon monoxide (TLCO)

A
  • A test of functionality of the alveolar-capillary membrane, when reduced there is reduced surface area for gas exchange
  • CO is rapidly inspired and held for a short period of time then expired: remaining CO is then measured and compared with inspired amount
  • Reduced TLCO: Interstitial lung disease, COPD, obesity, Thoracic abnormality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Transfer co-efficient (KCO)

A

Is TLCO corrected for alveolar volume. So is gas exchange measured per unit volume of lung. If you only have a half a lung but its functioning perfectly it will be 100%. Is disproportionately high in obesity and neuromuscular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Values for KCO and TLCO

A
  • Reduced TLCO and KCO: COPD/emphysema, ILD, Pulmonary hypertension
  • Reduced TLCO and normal/high KCO: obesity, kyphoscoliosis and thoracic cage abnormalities, Neuromuscular disease, Pneumonectomy, Pleural disease. Because more blood is diverted to the ventilated areas
  • Normal TLCO and high KCO: asthma (increased pulmonary blood flow to certain areas of the heart) and alveolar haemorrhage
22
Q

Chest x-ray

A
  • A (airway): Trachea (central), Carina, Bronchus and Hilar
  • B (breathing): lung fields, opacities
  • C (circulation): heart size, boarders
  • D (diaphragm): costophrenic angle, anything under the diaphragm
  • E (everything else): bones, soft tissue, drains/pacemakers
23
Q

CT of the chest

A
  • A cross sectional evaluation of the heart, airway, lungs, mediastinum and associated bones and soft tissue
  • Standard CT with contrast: useful for evaluation of nodules or masses identified on CXR, staging of lung cancer and detection of metastasis
  • CT pulmonary angiogram: acute or chronic PE
  • High resolution CT: interstitial lung disease, bronchiectasis and cystic lung disease. Thin slice images allowing lots of lung detail
24
Q

Obstructive sleep apnoea

A

Reduced tone in the soft palate, tongue and tonsils causes collapse and complete airway obstruction during sleep. Cause oxygen dip and subconscious arousal. Co-exists with COPD and obesity.

25
Q

OSA signs and symptoms

A

Unrefreshing sleep, daytime sleepiness and snoring - aren’t typically breathless or stridorous in the daytime

26
Q

ILO/vocal card dysfunction

A

Inducible laryngeal obstruction (ILO)/vocal cord dysfunction: increased muscle tension and paradoxical movement of the vocal cords causes airflow obstruction at the level of the larynx. Diagnosed through flow volume loops

27
Q

ILO signs and symptoms

A

Exertional breathlessness and wheeze similar to asthma, stridor, triggered by emotional distress, cough or irritant smells. Throat tightness, hoarse voice and difficulty swallowing. Can co-exist with lower airway disease

28
Q

Tracheal obstruction

A
  • causes: stenosis or a mass such as a large goitre or mediastinal tumour
  • Signs and symptoms: fixed stridor and breathlessness. Unlike laryngeal obstruction its likely to be fixed and not episodic, onset may be more gradual. Diagnosed through flow volume loops
29
Q

Neuromuscular weakness

A
  • For example due to motor neuron disease, polio, diaphragmatic palsy or inherited muscular dystrophy
  • Under breathe at night: unrefrehing sleep, daytime sleepiness, weak cough, prone to chest infection and orthopnoea
  • FVC will be reduced in supine position compared to standing, mouth pressures are reduced
  • Inspiratory pressure tends to measure intercostal strength whilst expiratory pressure measures diaphragmatic strength.
  • Ultrasound/fluoroscopy: reduced or paradoxical movement of the diaphragm
  • Static CXR: loss of volume/scoliosis or an elevated diaphragm
30
Q

Pneumothorax versus pleural effusion

A
  • A pneumothorax presents suddenly and is associated with chest pain, pleural effusions develop more gradually, both have reduced breath sounds
  • Pneumothorax signs- hyperresonance to percussion and subcutaneous emphysema
  • Pleural effusion signs-’stony dullness’ on percussion an fluid overload elsewhere i.e. oedema and ascites
31
Q

Conditions affecting the lung parenchyma and alveoli

A
  • Pneumonia, pulmonary oedema, alveolar haemorrhage (vasculitits or drugs) and inflammatory interstitial lung disease
  • On CXR there will be airspace opacification
  • Breathless because no gas exchange in the affected lung so there’s a reduction in A-a gradient
32
Q

Interstitial lung disease

A
  • Experience exertional breathlessness with marked hypoxia
  • Type 1 respiratory failure with a decline in gas transfer (TLCO and KCO) and reduced FVC caused by stiffening of the lungs
  • Normally develop gradually
33
Q

Obstructive sleep apnoea factors

A
  • Strongly associated with obesity but 1/4 of patients arent obese
  • Co-exists with asthma/COPD and causes night time hypoxia due to recurrent dips, shouldn’t cause hypercapnia i.e. type 2 respiratory failure
  • If you have identified hypercapnia in a patient with daytime sleepiness, consider either 1) comorbid COPD or 2) obesity hypoventilation syndrome.
34
Q

Hypoventilation

A

Minute ventilation is less than that required for effective gas exchange. There’s raised carbon dioxide and low oxygen

35
Q

Definition: Tidal volume and Minute ventilation

A
  • Tidal volume: volume of gas inhaled or exhaled per respiratory cycle (breath), normally 400-500ml
  • Minute ventilation= volume of gas inhaled or exhaled per minute. Respiratory rate x tidal volume
36
Q

Respiratory failure

A
  • Hypoxia is normally due to a V/Q mismatch, the blood in the pulmonary capillaries is not meeting the ventilated alveoli
  • Hypercapnia is normally due to hypoventilation where the waste CO2 is not being blown off
  • Type 1 respiratory failure: pH normal, PaO2 low, PaCO2 is normal, Bicarbonate is normal
  • Type 2 respiratory failure: pH is normal/low, PaO2 is low, PaCO2 is high, Bicarbonate is normal or high. If on supplemental oxygen the PaO2 might be normal
37
Q

Causes of hypoventilation

A
  • Central drive: sedating drugs like opioids or benzodiazepine
  • Respiratory muscle weakness: primary problem with muscles (motor neurone disease) or due to lung mechanics i.e. in COPD where lungs are damaged
  • Obstruction: i.e. obstructive sleep apnoea
  • Reduced thoracic cage compliance: kyphoscoliosis (spine and rib cage are mal shaped) or old polio
38
Q

Signs and symptoms of hypercapnia

A
  • Sleepiness / drowsiness
  • Confusion or low conscious level
  • Poor concentration
  • Early morning/wakening headaches
  • Palmar erythema/flushing
  • Twitching (CO2 retention flap)
  • Cyanosis
  • Unrefreshing sleep
  • Breathlessness
39
Q

Causes of hypoventilation/hypercapnia

A
  • Respiratory: COPD, bronchiectasis, cystic fibrosis
  • Neuromuscular disease: MND, Duchennes, Beckers, Spinal muscular atrophy
  • Obesity hypoventilation syndrome: inspiratory muscles are not strong enough to shift the diaphragm down against the weight of the abdomen, coexistent with OSA
  • Thoracic cage compliance: Kyphoscoliosis, post polio
  • Central drive/; drugs (alcohol, opioids), brainstem stroke
40
Q

Hypoventilation: investigations 1

A
  • ABG: generally shows daytime respiratory failure, if you do an early morning ABG you can see nocturnal respiratory failure
  • Obstructive diseases= Low FEV1, low-normal FVC, low FEV1/VC ratio
  • Restrictive diseases= Low FEV1, low FVC, normal ratio
  • Lung volumes= Big – think obstruction. Mainly COPD. Small – think obesity hypoventilation or neuromuscular. CXR
41
Q

Hypoventilation investigations 2

A
  • Gas exchange= COPD or ILD - low. OHS/Neuromuscular – preserved or high gas transfer (reduced TLCO)
  • Positional changes= Erect/Supine spirometry– changes are common in muscular weakness like MND, drop when going from erect to supine. VC drops when gravity eliminated
  • MIPS/MEPS/SNIPS= Low in muscle weakness. MIPS and MEPS measure mouth pressure, SNIPS measures nose pressure.
42
Q

Hypoventilation history 2

A
  • Smoking history
  • BMI/recent changes in weight
  • Morning headache, poor sleep quality/waking unrefreshed
  • Dozing through the day
  • Changes in cognition or alertness- ‘brain fog’
43
Q

TOSCA

A
  • Transcutaneous measurement of CO2 (plus sats and heart rate)= Attached to ear, forehead, forearm. Heated probe to vasodilate
  • Really only used in outpatient setting for home ventilation assessment and monitoring. Shows people with nocturnal hypoventilation but not daytime respiratory failure.
  • Also to check if patients on ventilators are being adequately oxygenated
  • No real role in acute treatment = Some use in research
44
Q

Hypoventilation: obstructive sleep apnoea

A
  • Most common sleep related breathing disorder
  • Obstruction of the upper airway= Hypopnoeas – partial obstruction. ≥10 seconds duration with a ≥30% reduction of flow and desaturation of ≥4%. Apnoeas – complete obstruction
  • Continued muscular efforts= (as distinct from central sleep apnoea)
  • Excessive sleepiness
  • When there is a dip in oxygen adrenaline is released causing you to wake up a little so you can breathe again- causes tachycardia and changes to blood pressure increasing CVD risk
  • Associated with AF, CVD, Stroke, Hypertension
45
Q

OSA: symptoms

A
  • Excessive daytime sleepiness
  • Snoring or ‘stops breathing overnight’
  • Can drop off during normal activities, takes naps
  • Associated with increased being male, BMI, larger neck sizes: Craniofacial abnormalities or narrow nasopharynx
  • Can get 40-50 episodes an hour meaning they never get to deep sleep
46
Q

Detecting OSA

A
  • Epworth sleepiness scale: has to be really high in OSA, helps measure treatment effect
  • STOP BANG questionnaire is more specific to OSA
  • Polysomnography- sleep study that has ECG, EMG, oxygen saturations, heart rate, airflow. Complex, in hospital
  • Can have more simple sleep studies that are done at home. Would measure oxygen saturations, pulse rate, nasal airflow and body movement. In OSA likely to get a drop in nasal airflow followed by an increase in body movement, pulse rate and a dip in oxygen.
47
Q

Treatment of OSA

A
  • Weight loss
  • Wean opiares/benzos
  • CPAP
  • Mandibular advancement devices: done by dentists
48
Q

NIV versus CPAP

A
  • Non-invasive ventilation (NIV): two pressures IPAP (high pressure, inspiration), EPAP (lower pressure, expiration). Ventilatory support as reduces work of breathing. As you breathe in the device detects this and helps deliver a breath giving your muscles a rest. Sometimes called BiPAP
  • Continuous positive airways pressure (CPAP): one pressure throughout both inspiration and expiration, similar to the EPAP alone on NIV. Helps splint airway open and can improve oxygenation. Does not assist musculature so does not deliver ventilatory support.
  • NIV is used to treat hypoventilation and hypercapnia, CPAP is used to treat OSA. CPAP is not a ventilator
49
Q

Oxygen and hypoventilation

A
  • Oxygen can worsen hypoventilation= Target lower saturations – 88-92% is acceptable. COPD, Neuromuscular disease, Obesity hypoventilation, anyone on a ventilator at home
  • Mechanism; loss of hypoxic pulmonary vasoconstriction. In reduced oxygenated areas there is vasoconstriction to maintain V/Q. Increases blood flow to healthy alveoli. When you give oxygen the unhealthy alveoli become oxygenated so the vessels dilate. However the alveoli are still not ventilated and contain lots of CO2 so you get a V/Q mismatch and CO2 retention
  • Other mechanisms= loss of hypoxic drive, Haldane effect, Absorption atelactasis, high O2 density, rebreathing at low flow rates
50
Q

COPD and acute exacerbation: hypoventilation

A
  • Arterial blood gas – can have decompensated T2RF: High CO2, Low pH (Acidaemia).Often not hypoxic on gas as patient on supplemental O2
  • Noninvasive ventilation if T2RF
  • Appropriate oxygen therapy (target sats 88-92%)
  • Medical management: Bronchodilators, Prednisolone, Physiotherapy, ?antibiotics, Smoking cessation, flu jabs
  • Most commonly due to exacerbation and T2RF resolves alongside exacerbation