Lung Function Tests and ABG Interpretation Flashcards
Notes on V/Q distribution in the normal lung
- 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)
Causes of decreased FVC
- Lung -> resection (lobectomy, pneumonectomy), atelectasis, fibrosis, CHF (enlarged vessels, oedema), thickened pleura, tumour, airway obstruction (asthma, chronic bronchitis), emphysema
- Pleural cavity -> enlarged heart, pleural fluid, tumour
- Restriction of chest wall -> scleroderma, ascites, pregnancy, obesity, kyphoscoliosis, splinting due to pain
- Neuromuscular disease, old polio, paralysed diaphragm
Notes on FEV1/FVC ratio
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
Grading of severity FEV1 decline
Flow volume loop restrictive lung disease
Notes on obstructing lesions of major airways - variable extrathoracic, variable intrathoracic, fixed lesions
**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
Flow-volume loop obstructive disease
Changes in lung function in pregnancy
- 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
Notes on static lung volumes
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
Methods to measure lung volumes
- 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.
Notes on non-specific pattern PFTs - reduced FVC, normal FEV1/FVC, normal TLC
More often men
50% have evidence obstructive disease
Many have asthma
Many obese
Other -> heart failure, muscle weakness, cancer, chest wall abnormalities
Factors which affect diffusing capacity of lungs
- Area of alveolar-capillary membrane - greater the area greater the DLCO
- Thickness of the membrane - thicker membrane = lower DLCO
- Driving pressure - difference in oxygen tension between alveolar gas and venous blood
Notes on measuring DLCO
- 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
Causes of decreased DLCO
**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
- 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 - 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 - Miscellaneous
- Smokers (decreases driving pressure of CO)
- Pregnancy - variable effects on DLCO
Causes of increased DLCO
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
Notes on diagnosis of diaphragmatic palsy
**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
Definition of bronchodilator reversibility in pulmonary function tests
-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%)
Notes on bronchoprovocation testing - indications, contraindications
**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
Procedure for bronchial provocation testing
**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
Role of exhaled nitric oxide in assessment of asthma
- 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
Notes on the oxygen dissociation curve
**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
Notes on respiratory alkalosis
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
Calculation of A-a gradient
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
Acid-base disturbances and expected compensation
Calculation of anion gap and causes of metabolic acidosis
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
Notes on lactic acidosis
**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
Notes on metabolic alkalosis
**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
Notes on respiratory acidosis
**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
Notes on carbon monoxide exposure and methaemoglobinaemia
**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
