Lung Function Tests and ABG Interpretation Flashcards

1
Q

Notes on V/Q distribution in the normal lung

A
  • Both ventilation and perfusion increase from the lung apex to the base
  • Change in perfusion is greater than the change in ventilation (think of as blood sinking to the bottom quicker)
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2
Q

Causes of decreased FVC

A
  1. Lung -> resection (lobectomy, pneumonectomy), atelectasis, fibrosis, CHF (enlarged vessels, oedema), thickened pleura, tumour, airway obstruction (asthma, chronic bronchitis), emphysema
  2. Pleural cavity -> enlarged heart, pleural fluid, tumour
  3. Restriction of chest wall -> scleroderma, ascites, pregnancy, obesity, kyphoscoliosis, splinting due to pain
  4. Neuromuscular disease, old polio, paralysed diaphragm
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3
Q

Notes on FEV1/FVC ratio

A

Range 75-85% in normality - decreases with aging
Low = obstruction - curve looks concave or scooped
Normal/high = restriction - slope looks steeper
Low FEV1 with normal FEV1/FVC raio and low tlc = restriction

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4
Q

Grading of severity FEV1 decline

A
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5
Q

Flow volume loop restrictive lung disease

A
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6
Q

Notes on obstructing lesions of major airways - variable extrathoracic, variable intrathoracic, fixed lesions

A

**Variable extrathoracic lesions
**Vocal cord paralysis (thyroid op, tumour invading recurrent laryngeal nerve, ALS, post-radiotherapy)
Subglottic stenosis
Neoplasm (primary hypopharngeal or tracheal, metastatic from lung or breast)
Goitre

**Variable intrathoracic lesions
**Tumour or lower trachea
Tracheomalacia
Strictures
GPA

**Fixed lesions
**Fixed neoplasm in central airway
Vocal cord paralysis with fixed stenosis
Fibrotic stricture

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7
Q

Flow-volume loop obstructive disease

A
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8
Q

Changes in lung function in pregnancy

A
  • Inspiratory capacity increases
  • FRC and RV decreases
  • FEV1, FVC, PERF unchanged
  • TLC reduced slightly in last trimester
  • Minute ventilation increases - increased tidal volume (due to increased cirulating progesterone) -> normal pregnancy A/W compensated respiratory alkalosis
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9
Q

Notes on static lung volumes

A

RV + VC = TLC
Expiratory reserve volume - volume of air that can be exhaled after a normal expiration during quiet breathing
Tidal volume - volume used during normal breathing
Inspiratory reserve volume - volume of air that can be inhaled after a normal tidal inspiration
ERV + RV = FRC (functional residual capacity)
RV = remaining volume of air in lungs after maximal expiration
FRC = lung volume at which inward elastic recoil of lung is balanced by he outward elastic forces of the relaxed chest wall
- Normally 40-50% TLC
- Increased when lung elasticity reduced (emphysema) - lesser extend in aging
- Increased lung recoil in pulmonary fibrosis = FRC decreases

**Significance of RV and TLC
**TLC and RV often increased in COPD - especially emphysema - RV usually increased more than TLC - RV/TLC ratio increased
TLC reduce in restrictive disease, RV may also be decreased but not necessarily. Require reduced TLC to diagnose restricitve disease

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10
Q

Methods to measure lung volumes

A
  • Usually measure FRC
  • Methods:
    1. Nitrogen washout - underestimates FRC in obstruction (lung regions that are poorly ventilated)
    2. Inert gas dilution - also underestimates FRC in obstruction
    3. Plethysmography
  • Based on Boyle’s law - product of pressure and volume of a gas is constant under constant temperature conditions - more accurate in measuring volumes in obstruction
    4. Radiographic - more accurate than gas methods in COPD, also accurate in pulmonary fibrosis. Reserved for when above tests not available.
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11
Q

Notes on non-specific pattern PFTs - reduced FVC, normal FEV1/FVC, normal TLC

A

More often men
50% have evidence obstructive disease
Many have asthma
Many obese
Other -> heart failure, muscle weakness, cancer, chest wall abnormalities

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12
Q

Factors which affect diffusing capacity of lungs

A
  1. Area of alveolar-capillary membrane - greater the area greater the DLCO
  2. Thickness of the membrane - thicker membrane = lower DLCO
  3. Driving pressure - difference in oxygen tension between alveolar gas and venous blood
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13
Q

Notes on measuring DLCO

A
  • Measuring diffusing capacity of O2 technically difficult, carbon monoxide used as substitute - single breath method most commonly used
  • Normal values 20-30ml/min/mmHg
    • Decreases with age, slightly lower in women and shorter people
  • Helium included in test gives estimate of alveolar volume
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14
Q

Causes of decreased DLCO

A

**Note DLCO of <40% is a significant predictor of post-operative complications
Take note of KCO (DLCO/VA i.e measurement of effectiveness of each lung unit) in questions -> if given KCO (corrected for lung volume) use this to decide if DLCO high or low
Correct DLCO needs Hb measurement

  1. Conditions that decrease surface area
    - Emphysema
    - Bronchial obstruction e.g. tumour
    - Lung resection (can be near normal in setting of lobectomy but usually lowered following pneumonectomy)
    - Multiple pulmonary emboli
    - Anaemia
  2. Conditions that effectively increase wall thickness
    - Idiopathic pulmonary fibrosis
    - CHF
    - Asbestosis
    - Sarcoidosis
    - Collagen vascular disease - scleroderma, SLE
    - Hypersensitivity pneumonitis e.g. farmer’s lung
    - Pulmonary Langerhan’s histiocytosis
    - Alveolar proteinosis
  3. Miscellaneous
    - Smokers (decreases driving pressure of CO)
    - Pregnancy - variable effects on DLCO
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15
Q

Causes of increased DLCO

A

Usually not a matter of concern
- Asthma - ?more uniform distribution of pulmonary blood flow
- Obesity - increased pulmonary blood flow
- Supine position - increased blood flow to upper lobes
- Exercise or non-resting state - increased pulmonary blood flow
- Polycythaemia
- Intra-alveolar haemorrhage
- Left-to-right intracardiac shunt

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16
Q

Notes on diagnosis of diaphragmatic palsy

A

**Lying and standing spirometry
**10% decrease in VC when lying down normal
Up to 50% decrease in VC seen in bilateral diaphragmatic paralysis

**Sniff test
**AKA diaphram fluroscopy
Usually on sniff -> inspiration both hemi-diaphragms should move down
If unilateral phrenic nerve palsy -> affected hemidiaphragm won’t go down, can parodoxically go up

17
Q

Definition of bronchodilator reversibility in pulmonary function tests

A

-No SABA/SAMA for 6 hours, No LABA/LAMA for 12-24 hours
- Administer salbutamol via MDI/spacer and wait 15 minutes
- Improvement of >=12% and/or 200ml FEV1 = reversibility (in last 12 months updated to 10%)

18
Q

Notes on bronchoprovocation testing - indications, contraindications

A

**Indications
**Measure of airway hyperresponsiveness
Used to confirm asthma (when spirometry non diagnostic), assess degree of control/response to treatment in asthma, ensure absence of airway hyperresponsiveness in certain work environments

**Contraindications
**Pregnancy, lactation
Use of cholinesterase inhibitors (myasthenia gravis)
Recent MI/stroke (3 months)
Uncontrolled hypertension
Aortic aneursym
Recent eye surgery or increased ICP
Respiratory compromise

19
Q

Procedure for bronchial provocation testing

A

**Direct agents:
**Methacholine (cholinergic) , histamine - directly stimulate airway smooth muscle receptors
**Indirect
**Hypertonic saline, mannitol, adenosine

Measured as PD20 - dose that produces a 20% fall in FEV1
Bronchodilator given at end of test to reverse effects

First line test for diagnosis of exercise induced asthma would be saline rather than metacholine

20
Q

Role of exhaled nitric oxide in assessment of asthma

A
  • Exhaled nitric oxide correlates well with presence of eosinophilic mucosal inflammation in patients with asthma
  • > 50bbb = TH2 inflammation and sputum eosinophilia , <25 absence of inflammation responsive to steroid

Increased NO:
- Asthma (can be reduced by steroids)
- Viral respiratory tract infections
- SLE
- Hepatic cirrhosis
- Lung transplant rejection

Decreased/variable NO:
- COPD
- Cystic fibrosis
- HIV
- Pulmonary hypertension

21
Q

Notes on the oxygen dissociation curve

A

**Left shift
**Conditions that shift the curve to the left -> increase oxygen affinity; haemoglobin holds on more tightly to oxygen (at lower PO2) and delivers less oxygen to the tissues at a given arterial oxygen pressure. The left shifted curve fo Hb F is what allow transfer of oxygen from the maternal to foetal circulation

**Right shift
**Conditions that shift the curve to the right decrease oxygen affinity ; haemoglobin holds less tightly onto oxygen and delivers more oxygen to tssues at a given arterial oxygen pressure

22
Q

Notes on respiratory alkalosis

A

May cause tetay, confusion, or LOC if severe

**Hypoxic causes
**Acute - pneumonia, asthma, pulmonary oedema
Chronic - pulmonary fibrosis, cyanotic heart disease, high altitude, anaemia

**Non-hypoxic
**Anxiety, fever, sepsis, salicyclate intoxication, cerebral disease (tumour, encephalitis), hepatic cirrhosis, pregnancy, after correction of metabolic acidosis, excessive emchanial ventilation

23
Q

Calculation of A-a gradient

A

A-a gradient = PAO2 - PaO2
Alveolar o2 (PA02) = Fio2 X 713 - (pAco2 x1.25) [in mmHg]
Normal approx. 10mmHg - increases with age.
A-a gradient for age = (age in years/4) + 4
- Abnormal A-a gradient >20 -> indicates shunting rather than hypoventilation as cause for hypoxia

24
Q

Acid-base disturbances and expected compensation

A
25
Q

Calculation of anion gap and causes of metabolic acidosis

A

Na-(Cl + HCO3)
Normal = 8-16. Add 2.5 for every 10g drop in albumin

**Increased anion gap metabolic acidosis
**Lactic acidosis
Ketoacidosis (diabetic, alcohol)
Drugs -> methanol, salicylates, ethylene glycol, paraldehyde, toluene, isoniazid
Renal failure (late stage)

**Normal anion gap
**GI bicarbonate loss - diarrhoea, pancreatic or biliary drainage, urinary diversion
Renal bicarbonate loss - Type 2 RTA, ketoacidosis, post chronic hypocapnia
Impaired renal acid excretion - Type 1 and 4 RTA
Renal hypoperfusion

**Compensation for metabolic acidosis
**Hyperventilation - PCO2 should decrease as CO2 blown off.
- If not in predicted range - think co-existing respiratory disturbance
- Use Winter’s formula to calculate expected range of PCO2 for a metabolic acidosis
- Complete respiratory compensation for a metabolic acidosis does not occur - normal pH should raise suspicion for a concomitant alkalosis

26
Q

Notes on lactic acidosis

A

**Type A
**Shock
Severe hypoxaemia
Anaemia
Post-convulsion
Severe exercise
Sepsis

**Type B
**Sepsis
Drug induced - bguanides, ethanol, methanol, salicylates, sorbitol, fructose, paracetamol poisoning
Associated with other disease states - DM, renal failure, liver disease, infection, leukaemia, lymphoma, pancreatitis, thiamine deficiency, short bowel syndrome
Hereditary - G6PD deficiency, hepatic fructose 1,6 diphosphate deficiency

27
Q

Notes on metabolic alkalosis

A

**Volume/chloride depletion
**Vomiting/gastric drainage
Diuretic therapy

**Hyperadrenocorticoidism
**Cushing’s
Conn’s
Bartter’s
Secondary hyperaldosteronism
Steroid therapy

**Severe potassium depletion

**Excessive alkali intake
**Milk alkali syndrome

28
Q

Notes on respiratory acidosis

A

**Hypoventilation
** * Respiratory center depression
○ Drug, anaesthesia, head injury, encephalopathy
* Disruption of respiratory signal during transmission along the nerves to the respiratory muscles
○ Spinal cord injury, GBS, motor neurone disease
* NMJ
○ Paralytic agents, myasthenia gravis
* Dysfunction muscles of respiration
○ Myopathy, fatugie, malnutrition, dystrophy
* Chest wall abnormalities
○ Kyphoscoliosis, ank spond, plerual fibrosis

**Other
**Obstructive lung disease
Severe parenchymal lung disease
Pneumothorax, pleural disorders

29
Q

Notes on carbon monoxide exposure and methaemoglobinaemia

A

**CO exposure
**Standard pulse oximetry cannot distinguish between carboxy and oxy-haemoglobin and therefore gives normal readings
- Note diagnosis requires COHb level on VBG, >3% in non-smokers, >10% in smokers

**Methaemoglobinaemia
**A high methaemoglobin concentration causes the Spo2 to display at around 85%

In both cases - PO2 are normal, diagnosis is by co-oximetry of an ABG sample