Restrictive lung disease Dr Duncan Powrie Consultant Chest Physician Southend University Hospital December 2018 Simple spirometry FEV1 = Forced Expiratory Volume in 1 second (how much you can blow out in the first second of a forced blow) FVC = Forced Vital Capacity (how much you can breathe out
altogether in a forced blow) VC = Vital Capacity (how much you can sigh out altogether in a full, steady blow) FEV1/FVC ratio = a calculation using the above measurements (% of total that can be forced out in the first second ) 2 Performing spirometry
1 Record the patients sex age and height to find their predicted normal values Ask the patient to: breathe in as deeply as possible blow out forcibly as hard and fast as possible until there is nothing left to expel* Repeat * severe patients
may take up to twice 15 seconds the procedure This should give 3 readings, with at least 2 within 100ml or 5% of each other Consistent result Inconsistent result 3
Obstructive vs.restrictive patterns If the ratio FEV1/FVC <70%, obstruction is present If this ratio is normal but FEV1 and FVC are both reduced, restrictive pattern is present A restrictive pattern should be referred to the doctor to check for lung fibrosis, pleural disease, chest wall disease. Obstructive disorder Restrictive disorder e.g COPD
e.g. Fibrosing alveolitis, pleural disease FEV1 reduced (<80%) reduced (<80%) FVC normal or reduced reduced (<80%) FEV1/FVC ratio reduced (<70%) normal (>70%) 5
Assessment of a patient with restrictive spirometry Pulm fibrosis (severe), neuromuscular disease, obesity , chest wall disease History Examination CXR Full PFTs (inc tests of resp muscle function) Oximetry Blood gases
Sleep study Pulmonary fibrosis Progressive exertional breathlessness Dry cough Arthralgia 20% Weight loss
Finger clubbing in 50% End inspiratory velcro crackles Cyanosis Cor pulmonale Epidemiology 6-28/ 100 000yr M:F 1.7:1
Median age of diagnosis 70 Uncommon before 50 Risk factors
Exposure to metal or wood dust Organic solvents Mycotoxins EBV, Hepatitis C Cigarette smoking Family history Management No really effective evidence based
treatment Information provision and supportive management is key Monitor lung function if minimal symptoms If deteriorating lung function consider triple therapy Pirfenidone Anti- inflammatory and anti-fibrotic
action Inhibits fibroblast proliferation GI side effects May reduce decline in lung function Consider if FVC between 80 and 50% predicted Breathlessness Hypoxia is common as is desaturation on exercise
LTOT if pO2 < 7.3 kPa or <8 if signs of pulmonary hypertension Ambulatory oxygen if desaturates on exertion Cough
Treat reflux Consider simple linctus Oral codeine Consider oramorph or MST in end stage disease Pulmonary rehabilitation No randomised controlled studies But strong evidence base in COPD
Improves QoL, reduces breathlessness Deconditioning, breathlessness, nutritional deficit, fatigue and social isolation Oxygen may be required to allow exercise Other measures
Opioids Anxiolytics Relaxation and distraction techniques Breathlessness clinic Causes of acute
Lung transplantation Patients <65 TLCO <40% 70-80% 1 year survival and 50% 5 yr survival Prognosis Variable Median survival 2.5-3.5 years
Improved survival associated with young age, female sex, less honeycombing and better lung function at diagnosis Death from respiratory failure or infection Lung cancer common Ventilatory pump failure Myopathies- myotonic dystrophy
C. Ca2+14.3 2.02 Neut1.711.9 INR Plt 255 Immediate treatment
Nebulised salbutamol and atrovent Steroids Pabrinex and vitamin B Regular chlordiazepoxide stopped BiPAP commenced
Respiratory review Recent increase in alcohol consumption Recent rapid weight gain Daytime somnolence, falling asleep at work Epworth score 14/24 Continue nocturnal BiPAP
Sleep study as inpatient Sleep study
Low sats throughout- down to 70% Multiple hypopnoeas Some apnoeas Lots of paradox AHI- 29 Compatible with OSAHS Discharge ABG pH 7.417
pCO2 5.61 pO2 8.30 HCO3- 26.3 BE 1.5 Follow up Weight loss 106.5kg No alcohol since discharge No daytime sleepiness
Epworth score 0/24 ABG continue to improve BiPAP stopped Obesity hypoventilation syndrome Definition Severe obesity BMI > 30 kg/m2 and diurnal
PaCO2 > 45 mmHg (6 kPa) In the absence of other known cause of hypoventilation Olson et al Am J Med 2005 Obesity hypoventilation syndrome Clinical presentation
Prez de Llano Chest 2005 Morbid obesity OSA dyspnoea daytime hypersomnolence
PREVALENCE Increases with BMI; Prevalence >25% for BMI>40 kg/m2 and >50% for BMI>50 kg/m2 Stable state OSA Hospitalised patients 15% in the general population of ambulatory obese patients?
Mokhlesi B, CHEST 2007 Nowbar, Am J Med 2004 Mechanisms underlying hypercapnia in obesity Neurohormonal 3 abnormalities 2
1 4 Mokhlesi et al. Proc Am Thorac Soc Obesity hypoventilation syndrome igh prevalence of associated cardiovascular morbidity in observational cohorts
Compared with obese control subjects, patients with OHS were statistically much more likely to have been diagnosed with: Congestive heart failure (OR 9; 95% CI, 2.335) Angina pectoris (OR, 9; 95% CI, 1.457.1) Cor pulmonale (OR, 9; 95% CI, 1.457.1) Berg Chest 2001 Mokhlesi Proceedings ATS 2008
Treatment Weight loss CPAP BiPAP besity hypoventilation syndrome home message Highly prevalent and easy to diagnose but underdiagnosed
Non invasive ventilation (NIV) improves blood gases, sleep, daytime sleepiness and mortality Impact of NIV on cardiovascular morbidity? Assessment and treatment of cardiovascular and metabolic risk recommended in OHS patients in association with NIV Mr CB 75 male Raised PSA normal bone scan, CT
CAP unremarkable General deterioration Wgt loss, lethargy, poor appetite 2 weeks dyspnoea unable to sleep No wheeze, no crackles Sats 84% on air Nil to find on examination CXR small volume lungs
pH 7.24 pCO2 13.41 pO2 18.31 HCO3 42.5 BE 9.8
Confused Minimal history available Dysarthric Generally wasted Poor respiratory effort Thoraco-abdominal paradox Multiple fasciculations
MND and respiratory failure Respiratory failure in MND is common and a frequent cause of death It may be the cause of presentation Deterioration may be rapid Multidisciplinary involvement is key There is some evidence that NIV improves survival and quality of life
Mrs JT 45 female Kyphoscoliosis from birth
Spinal fusion aged 14 Married 2 teenage chidren Nil else in PMH 4-6 week history of dyspnoea on exertion 1 week history of ankle oedema and new onset confusion Started on salbutamol and frusemide
by GP Wheezy JVP raised, oedema to knees WCC 12 CRP 50 Na 115 pH 7.307 pCO2 14.75 pO2 11.7 HCO3 54.1 Commenced on BiPAP
Deteriorating conscious level and worsening acidosis Intubated Echo- pulm hypertension, PAP 65mm Hg Weaned to BiPAP 4/52 post discharge
Using BiPAP all night 15:5 Exercise tolerance improved to half a mile Oedema resolved No daytime somnolence pH 7.42 pCO2 8.16 pO2 7.32 HCO3 38.4 Commenced on LTOT
IPAP increased 18 2 years Unlimited ET BiPAP 24:5 pH 7.45 pCO2 5.33 pO2 9.77 HCO3 27.2 Echo PAP 35mm Hg Differential diagnosis of restrictive spirometry
How to assess for respiratory muscle weakness The importance of OHS
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