Learn — Respiratory

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PCWP (pulmonary capillary wedge pressure)

Pulmonary capillary wedge pressure is the pressure recorded when the balloon at the tip of a pulmonary artery catheter is inflated until it occludes a branch of the pulmonary artery, so that the tip sees the pressure transmitted backwards from the pulmonary veins and the left atrium. It is therefore an indirect measure of left atrial pressure and left ventricular end-diastolic pressure, which makes it the bedside estimate of left ventricular preload and the number that separates cardiogenic from non-cardiogenic pulmonary oedema.

The normal wedge pressure is about 4 to 12 mmHg, read at end-expiration with the transducer levelled and zeroed at the phlebostatic axis, which lies at the fourth intercostal space in the mid-anteroposterior plane of the chest.
Pulmonary congestion begins as the wedge pressure passes about 18 mmHg and frank pulmonary oedema appears above about 25 mmHg, so the number tracks exactly what is heard in the chest.
Cardiogenic pulmonary oedema has a high wedge pressure, while acute respiratory distress syndrome and other non-cardiogenic oedema have a wedge pressure of 18 mmHg or less; that contrast is the classic examination discriminator and the reason the measurement was invented.
The wedge pressure rises in left ventricular failure, mitral stenosis or regurgitation, fluid overload and cardiac tamponade, and falls in hypovolaemia and in distributive shock before fluid resuscitation.
The balloon is inflated only for the measurement, for no more than two respiratory cycles or about 15 seconds, and is then allowed to deflate passively until a pulmonary artery waveform returns; a catheter left wedged causes pulmonary infarction and over-inflation causes pulmonary artery rupture.
Mitral stenosis raises the wedge pressure without a corresponding rise in left ventricular end-diastolic pressure, so in that one lesion the wedge overestimates left ventricular filling; high levels of positive end-expiratory pressure also falsely raise the reading.
In the classification of pulmonary hypertension a wedge pressure of 15 mmHg or less defines pre-capillary disease, while a value above 15 mmHg indicates post-capillary disease from left heart disease.
The measurement is only as good as the set-up: a transducer left at the wrong height changes the reading by about 0.7 mmHg for every centimetre of error, so it is re-levelled after every change of patient position.

Pulmonary artery catheter

The pulmonary artery or Swan-Ganz catheter is a balloon-tipped, flow-directed catheter introduced through a central vein and carried by the blood stream through the right atrium and right ventricle into the pulmonary artery. It measures right atrial, right ventricular, pulmonary artery and wedge pressures, samples mixed venous blood for oxygen saturation and measures cardiac output by thermodilution, so it gives the full haemodynamic profile that distinguishes hypovolaemic from cardiogenic from distributive shock at the bedside.

Normal values: right atrial or central venous pressure 2 to 6 mmHg, right ventricular 15 to 25 over 0 to 8 mmHg, pulmonary artery 15 to 25 over 8 to 15 mmHg, wedge pressure 4 to 12 mmHg, cardiac output 4 to 8 litres per minute, cardiac index 2.5 to 4.0 litres per minute per square metre, and mixed venous oxygen saturation 60 to 80 percent.
The waveform tells you where the tip is: a low-amplitude atrial trace becomes a ventricular trace with a systolic step up and a diastolic near zero, then a pulmonary artery trace with the same systolic pressure but a raised diastolic and a dicrotic notch, and finally a damped wedge trace.
The balloon is inflated with air only, never fluid, to a maximum of about 1.5 mL, inflated before advancing the catheter from the right atrium so that flow carries it forward, and always deflated before it is withdrawn.
Shock patterns are the reason the catheter is floated: hypovolaemic shock gives a low central venous pressure, low wedge pressure, low cardiac output and high systemic vascular resistance; cardiogenic shock gives a high wedge pressure, low cardiac output and high resistance; septic or distributive shock gives a high cardiac output with low resistance and a low or normal wedge pressure.
Insertion complications are ventricular ectopy and ventricular tachycardia as the tip crosses the right ventricle, new right bundle branch block, and complete heart block if the patient already has left bundle branch block, so external pacing must be available during the float.
Later complications are pulmonary infarction from a persistently wedged catheter, pulmonary artery rupture presenting as sudden haemoptysis, balloon rupture with air embolism, knotting, thrombosis, valve injury and catheter-related bloodstream infection.
Nursing care: level and zero the transducer at the phlebostatic axis after every change of position, read all pressures at end-expiration, keep the pressurised flush bag at 300 mmHg delivering about 3 mL per hour, watch the trace continuously for spontaneous wedging, and keep the balloon port locked and syringe removed between measurements.
Mixed venous oxygen saturation falls when oxygen delivery falls or consumption rises, so a fall below 60 percent points to a low cardiac output, anaemia, hypoxaemia, fever, shivering or pain before the blood pressure changes.
Routine use of the catheter has not been shown to improve survival in shock or acute respiratory distress syndrome, so it is now reserved for selected patients such as those with pulmonary hypertension, complex or mixed shock and transplant assessment, and echocardiography with less invasive cardiac output monitors has replaced it in most units.

Normal respiratory rate

The respiratory rate is the number of complete breathing cycles in one minute, counted by watching the rise and fall of the chest or, in an infant, of the abdomen, over a full 60 seconds while the patient is calm. It matters more than any other vital sign because it is the earliest to change in deterioration, sepsis and shock and the one most often left uncounted, and because in a child the single number decides whether the breathing is fast enough to be called pneumonia.

Normal ranges by age: newborn 30 to 60 a minute, infant under 1 year 30 to 50, toddler 1 to 3 years 24 to 40, preschool child 3 to 6 years 22 to 34, school-age child 6 to 12 years 18 to 30, adolescent 12 to 20 and adult 12 to 20. The rate falls steadily with age while tidal volume rises.
The IMNCI fast-breathing cut-offs are the ones the exam and the field both use: 60 breaths a minute or more in an infant under 2 months, 50 or more from 2 to 12 months, and 40 or more from 12 months to 5 years, counted twice if the first count is at the borderline.
Count for a full minute in infants and children because their breathing is normally irregular, count when the child is quiet and not crying or feeding, and watch the abdomen rather than the chest because infants are diaphragmatic breathers.
Fast breathing plus chest indrawing in a child under 5 is pneumonia in the IMNCI classification, and fast breathing with any general danger sign — inability to drink or breastfeed, vomiting everything, convulsions, lethargy or unconsciousness — is severe pneumonia needing referral and oxygen.
In adults a rate above 20 is tachypnoea and below 12 is bradypnoea; a rate of 22 a minute or more is one of the three qSOFA items alongside altered mentation and a systolic pressure of 100 mmHg or less, and in the National Early Warning Score a rate of 8 or less or 25 or more scores the maximum of 3 points.
Recognise the abnormal patterns: Kussmaul breathing is deep and rapid in metabolic acidosis such as diabetic ketoacidosis, Cheyne-Stokes breathing waxes and wanes with apnoeic pauses in heart failure and raised intracranial pressure, and apneustic or ataxic breathing indicates brainstem damage.
In the newborn, periodic breathing with pauses of under 20 seconds and no colour or heart rate change is normal, whereas apnoea is a pause of more than 20 seconds or any shorter pause with bradycardia, cyanosis or desaturation, and it must be reported.
Fever, pain, anxiety, crying, exercise, anaemia, acidosis and a full stomach all raise the rate, while opioids, sedatives, raised intracranial pressure, exhaustion and neuromuscular weakness lower it, so a rate is interpreted with the temperature, the drug chart and the child's state of activity beside it.
Count the rate without telling the patient you are counting — keep your fingers on the pulse and observe the chest, because a person who knows they are being watched changes the rate.

Respiratory distress signs

Respiratory distress is the set of signs that appear when a patient has to work harder than normal to move air and keep gas exchange going, and it is a compensated state in which the effort is still succeeding. Respiratory failure is the decompensated state that follows, when the effort fails and hypoxaemia, carbon dioxide retention, exhaustion and a falling conscious level take over, so the whole purpose of recognising distress is to intervene while the patient is still compensating.

Tachypnoea is the earliest and most sensitive sign, and it must be counted over a full minute against the normal range for the age before anything else is concluded.
Increased effort shows as nasal flaring, suprasternal, intercostal and subcostal retractions, sternal recession, tracheal tug, head bobbing in an infant, use of the sternocleidomastoid and other accessory muscles, and the tripod position in an older child or adult who sits leaning forward on the arms.
Grunting is an expiration against a partly closed glottis by which the patient generates his own positive end-expiratory pressure to keep alveoli open; in a newborn or infant it means alveolar collapse and is an ominous sign that should never be dismissed as a noise.
Sound localises the obstruction: stridor is upper airway, wheeze is lower airway, and a silent chest in a previously wheezy patient means so little air is moving that the wheeze has disappeared, which is worse and not better.
Cyanosis is a late and unreliable sign because central cyanosis needs about 5 g/dL of deoxygenated haemoglobin to be visible, so a severely anaemic child can be profoundly hypoxic and never look blue, while a polycythaemic one looks blue easily.
The Silverman-Anderson score grades neonatal distress on five items — upper chest movement, lower chest retraction, xiphoid retraction, nasal flaring and expiratory grunt — each scored 0 to 2, where 0 means no distress and a total of 7 or more means severe distress with impending respiratory failure.
The signs of impending failure are the opposite of the signs of distress: a falling respiratory rate, decreasing effort, a silent chest, see-saw or paradoxical abdominal breathing, bradycardia, sweating, agitation giving way to drowsiness, and apnoea. Any of these means immediate airway and ventilatory support.
In an adult, judge severity by how much the patient can say in one breath, by the ability to lie flat, and by oxygen saturation, aiming for 94 to 98 per cent in most acutely ill patients but 88 to 92 per cent in a patient at risk of hypercapnic respiratory failure such as chronic obstructive pulmonary disease.
Nursing management is oxygen, an upright position of comfort, minimal handling, nothing by mouth when the respiratory rate is very high because of the aspiration risk, continuous monitoring of rate, effort, saturation and conscious level, gentle suction only when needed, and preparation for continuous positive airway pressure or intubation; a child with stridor and drooling is left undisturbed on the parent's lap and the throat is not examined, because that can precipitate complete obstruction.

Mantoux test

The Mantoux or tuberculin skin test is the intradermal injection of purified protein derivative into the volar aspect of the forearm to provoke a delayed type IV hypersensitivity reaction, read as induration at 48 to 72 hours. It detects sensitisation to tuberculous protein, which means infection, and it can never by itself say whether that infection is latent or active — a distinction that under the National Tuberculosis Elimination Programme is settled by a rapid molecular test on a clinical specimen, not by the skin test.

Technique: 0.1 mL of purified protein derivative is injected strictly intradermally with a tuberculin syringe and a fine needle held bevel upwards, raising a pale wheal of 6 to 10 mm; if no wheal forms the dose has gone subcutaneously and the test is repeated at a site at least 5 cm away. The strength is 5 tuberculin units of PPD-S internationally and 2 tuberculin units of PPD RT23 with Tween 80 in Indian practice.
Read the test between 48 and 72 hours and measure the transverse diameter of the palpable induration in millimetres, not the erythema; the ballpoint pen technique, in which a line is drawn towards the reaction until the pen stops at the raised edge, marks the margins reliably.
The cut-off changes with the person, not with the test: 5 mm or more is positive in people living with HIV, recent close contacts of an infectious case, those with fibrotic changes on chest radiograph and patients on transplant immunosuppression or the equivalent of 15 mg of prednisolone a day for a month; 10 mm or more is positive in children under 5, in people from high-burden settings, health-care workers and those with diabetes, chronic kidney disease, silicosis or malignancy; 15 mm or more is needed in a person with no risk factor at all.
False negatives are common and dangerous to over-read: advanced HIV, miliary or severe tuberculosis itself, severe malnutrition, measles or another recent viral illness, a live viral vaccine given in the preceding 4 to 6 weeks, corticosteroids, sarcoidosis, the very young infant, and faulty technique or badly stored antigen.
False positives come from previous BCG vaccination, which usually gives an induration under 10 mm and wanes over about 10 years, and from infection with non-tuberculous mycobacteria; the interferon-gamma release assay is not affected by BCG and is used where the history confuses the reading.
The test cannot diagnose or exclude active tuberculosis. Under the National Tuberculosis Elimination Programme the diagnosis of active disease is made by a rapid molecular nucleic acid amplification test such as CBNAAT or Truenat on sputum or another specimen, supported by chest radiography, with universal drug susceptibility testing on every diagnosed patient.
Where the Mantoux still earns its place is in children and in contact investigation: a positive test with a contact history, weight loss or failure to thrive and a suggestive chest radiograph supports childhood tuberculosis, and it is used with clinical assessment when deciding on tuberculosis preventive treatment.
Tuberculosis preventive treatment under the programme is offered to household contacts of a pulmonary tuberculosis patient and to people living with HIV only after active disease has been ruled out, using 6 months of daily isoniazid or a shorter rifamycin-based regimen such as 3 months of weekly isoniazid with rifapentine or 3 months of daily isoniazid with rifampicin.
Store the antigen at 2 to 8 degrees Celsius protected from light, never freeze it, draw it up immediately before use, and record the exact site, date, time, batch and the millimetres of induration with the date and time of reading, because an unread or wrongly read test has to be repeated.

Tuberculin test interpretation

The tuberculin skin test injects purified protein derivative into the dermis and measures the delayed type IV hypersensitivity wheal it provokes, so a positive result means only that the person has been sensitised to tuberculous protein. It cannot say whether that sensitisation is latent infection, active disease, an old healed infection or BCG, which is why interpretation reads the induration against the patient's risk group and why the diagnosis of active tuberculosis under NTEP rests on NAAT, smear and culture rather than on this test.

Technique: 0.1 mL of 2 TU PPD RT23 with Tween 80 is injected intradermally into the flexor aspect of the forearm to raise a pale 6 to 10 mm wheal, and the result is read at 48 to 72 hours.
Only the transverse diameter of induration is measured in millimetres, felt with the fingertips or outlined by the ballpoint-pen method; erythema without induration is recorded as 0 mm and is not a positive test.
Cut-offs move with risk: 5 mm or more is positive in HIV infection, other immunosuppression including long-term corticosteroids, and recent close contacts of a sputum-positive case; 10 mm or more is the general cut-off used in Indian practice; 15 mm or more is required in a person with no risk factor at all.
False negatives (anergy) occur in miliary and advanced tuberculosis itself, HIV with a low CD4 count, severe malnutrition, measles and other viral illness, live vaccination in the previous 4 to 6 weeks, corticosteroids and other immunosuppressants, sarcoidosis, and at the extremes of age.
False positives come from previous BCG and from non-tuberculous mycobacteria; a repeat test some weeks later can also recall a waned response (the booster phenomenon) and be mistaken for a new conversion.
A positive test proves infection, not disease, and a negative test never excludes tuberculosis, so in an adult with cough for 2 weeks or more the tuberculin test has no place in the diagnostic pathway.
IGRA (QuantiFERON, T-SPOT) measures interferon-gamma release to the MTB-specific antigens ESAT-6 and CFP-10, which BCG and most non-tuberculous mycobacteria do not carry, so BCG does not confound it; it needs a single visit and no return reading, but it still cannot separate latent infection from active disease.
Under NTEP, active disease is confirmed microbiologically: upfront NAAT (CBNAAT or Truenat) on sputum reports MTB and rifampicin resistance in about 2 hours, smear microscopy needs roughly 5,000 to 10,000 bacilli per mL to turn positive, and culture is the gold standard but takes weeks; rifampicin resistance moves the patient onto the drug-resistant pathway, not the standard 6-month course.
A positive test with active disease excluded means latent infection: NTEP offers TB preventive treatment to household contacts and to people living with HIV once the four-symptom screen (cough, fever, weight loss, night sweats) is negative, using daily isoniazid for 6 months or the shorter weekly isoniazid with rifapentine for 3 months.

Pulmonary oedema

Pulmonary oedema is the accumulation of fluid in the pulmonary interstitium and alveoli, which floods the gas-exchange surface and produces sudden severe breathlessness with hypoxaemia. It is cardiogenic when a failing left ventricle drives capillary hydrostatic pressure up (pulmonary capillary wedge pressure above 18 mmHg) and non-cardiogenic when the alveolar-capillary membrane itself leaks at a normal wedge pressure, as in ARDS, sepsis, aspiration, near-drowning, high altitude and neurogenic causes.

Cardiogenic causes are acute left ventricular failure after myocardial infarction, hypertensive crisis (flash pulmonary oedema), acute mitral or aortic regurgitation, tachyarrhythmia, fluid overload and stopping diuretics; the fluid is a transudate driven by pressure, not by leak.
The picture is orthopnoea, paroxysmal nocturnal dyspnoea, agitation and a sense of drowning, respiratory rate above 30, accessory muscle use, fine crackles rising from the bases, wheeze (cardiac asthma), a third heart sound, raised jugular venous pressure and cold sweaty skin; pink frothy sputum is a late sign of alveolar flooding.
Chest X-ray shows upper-lobe blood diversion, Kerley B lines, perihilar bat-wing shadowing, cardiomegaly and pleural effusions; in ARDS the shadowing is patchy and bilateral with a normal heart size and a normal wedge pressure.
BNP or NT-proBNP is raised in cardiogenic oedema and a low value makes acute heart failure unlikely; bedside echocardiography and lung ultrasound B-lines settle the question in minutes.
Immediate treatment is to sit the patient upright with the legs dependent, give oxygen titrated to a saturation of 94 to 98% (88 to 92% if she retains carbon dioxide), start non-invasive ventilation early in severe distress because CPAP or BiPAP reduces the need for intubation, give intravenous furosemide 40 mg or one to two and a half times the usual home dose, and add a nitrate infusion when the systolic pressure is above 110 mmHg.
Nitrates are the drug that unloads flash pulmonary oedema with a high blood pressure, but they are withheld if the systolic pressure is below 90 mmHg, in severe aortic stenosis, in right ventricular infarction, and within 24 hours of sildenafil or 48 hours of tadalafil.
Morphine is no longer routinely recommended in acute heart failure because it causes respiratory depression, vomiting and more intensive care admissions, so the old LMNOP mnemonic is a memory aid rather than a prescription.
Hypotension with cold peripheries, oliguria and altered sensorium is cardiogenic shock, not simple pulmonary oedema: stop the nitrate, do not chase it with more diuretic, and prepare inotropes or vasopressors while the cause is treated.
Monitoring is continuous saturation and cardiac rhythm, hourly urine output through a catheter, strict fluid balance, daily weight (a change of 1 kg is about 1 litre of fluid), and daily potassium and creatinine while high-dose loop diuretic is running.

Obstructive sleep apnoea

Obstructive sleep apnoea is repeated collapse of the pharyngeal airway during sleep, so that breathing effort continues against a closed airway until an arousal reopens it; each event ends in a desaturation and a surge of sympathetic activity. It is defined by an apnoea-hypopnoea index of 5 or more events per hour with daytime symptoms, or 15 or more regardless of symptoms, and it matters because those nightly surges drive resistant hypertension, atrial fibrillation, stroke and road traffic accidents.

An apnoea is cessation of airflow for 10 seconds or longer; a hypopnoea is a fall in airflow of at least 30% for 10 seconds or longer with a 3% desaturation or an arousal. Severity by apnoea-hypopnoea index: mild 5 to 15, moderate 15 to 30, severe above 30.
The history is loud habitual snoring, apnoeas witnessed by the partner, choking or gasping arousals, unrefreshing sleep, morning headache, nocturia and daytime sleepiness; the Epworth Sleepiness Scale scores the sleepiness and a score above 10 is abnormal.
STOP-BANG screens with eight yes-or-no items — Snoring, Tiredness, Observed apnoea, high blood Pressure, BMI above 35 kg/m2, Age above 50, Neck circumference above 40 cm, and male Gender; 3 or more is high risk and 5 or more predicts moderate to severe disease.
Attended overnight polysomnography is the diagnostic standard; a home sleep apnoea test is acceptable in a patient with a high pre-test probability and no cardiorespiratory comorbidity.
CPAP is first-line for moderate and severe disease and it works only if it is worn — the nurse's job is mask fit, humidification for a dry nose, ramp settings and follow-up of the adherence data, with a usual target of at least 4 hours a night on most nights.
Adjuncts and alternatives: weight reduction (about 10% of body weight gives a clinically useful fall in the apnoea-hypopnoea index), avoiding alcohol and sedatives in the evening, avoiding the supine position, treating nasal obstruction, a mandibular advancement device for mild to moderate disease or CPAP intolerance, and surgery such as tonsillectomy in children or uvulopalatopharyngoplasty in selected adults.
Untreated disease causes resistant hypertension with a non-dipping night-time pattern, atrial fibrillation, coronary disease, stroke, pulmonary hypertension and cor pulmonale, insulin resistance and secondary polycythaemia.
The discriminator from obesity hypoventilation syndrome is the daytime blood gas: obesity hypoventilation has a BMI of 30 kg/m2 or more with a daytime arterial carbon dioxide above 45 mmHg, and needs bilevel ventilation rather than plain CPAP.
Perioperative care is a nursing flashpoint: opioids and benzodiazepines abolish the arousal that ends each apnoea, so these patients need their own CPAP machine in hospital, continuous pulse oximetry after surgery, opioid-sparing analgesia and no sedation on an unmonitored ward.
In children, adenotonsillar hypertrophy is the usual cause and the presentation is mouth breathing, restless sleep, bed-wetting, poor growth and inattention that is mistaken for a behaviour problem; adenotonsillectomy is first-line, not CPAP.

Lung cancer

Lung cancer is a malignant tumour arising from the bronchial or alveolar epithelium and it is the leading cause of cancer death worldwide, with tobacco smoking behind the great majority of cases. It divides for treatment purposes into small-cell carcinoma, which is aggressive, usually disseminated at diagnosis and treated chemotherapeutically, and non-small-cell carcinoma, where surgery is possible when the disease is caught early and where molecular testing now decides the drug.

Small-cell carcinoma is about 15% of cases, is central, is almost always related to smoking, spreads early, and produces the paraneoplastic syndromes — SIADH with hyponatraemia, ectopic ACTH causing Cushing syndrome, and Lambert-Eaton myasthenic syndrome; surgery has little place and chemotherapy with radiotherapy is the treatment.
Non-small-cell carcinoma is about 85%: adenocarcinoma is now the commonest type overall and the usual type in non-smokers and in women and sits peripherally; squamous cell carcinoma is central, cavitates, and causes hypercalcaemia through PTH-related peptide; large-cell carcinoma is poorly differentiated.
Risk factors are smoking including bidis (the dominant cause, with risk falling but never returning to baseline after quitting), second-hand smoke, indoor air pollution from biomass cooking fuel which matters greatly in Indian women, asbestos (which multiplies the risk of smoking), radon, silica, arsenic, chromium and previous tuberculosis scarring.
The presentation is a new or changed cough, haemoptysis, breathlessness, chest pain, recurrent pneumonia in the same lobe, hoarseness from recurrent laryngeal nerve involvement, weight loss and clubbing; a cough that changes character in a smoker is the sentence that should trigger imaging.
Local invasion syndromes: a Pancoast (superior sulcus) tumour causes shoulder and ulnar arm pain with Horner syndrome (ptosis, miosis, anhidrosis); superior vena cava obstruction causes facial and arm swelling with distended neck veins; phrenic nerve involvement raises a hemidiaphragm; malignant pleural effusion makes the disease unresectable.
Diagnosis is by tissue: bronchoscopic biopsy for central lesions, CT-guided needle biopsy for peripheral lesions, EBUS or mediastinoscopy for nodes, and pleural fluid cytology; staging uses contrast CT chest and abdomen, PET-CT and brain imaging, with pulmonary function tests to decide fitness for resection.
Treatment follows type and stage: lobectomy with nodal dissection for early non-small-cell disease, chemoradiotherapy for locally advanced disease, and for advanced disease targeted therapy where a driver mutation is present (EGFR, ALK, ROS1) or immunotherapy where PD-L1 is expressed, so molecular testing must be requested on the biopsy at the outset.
Screening is annual low-dose CT for adults aged 50 to 80 years with a 20 pack-year history who still smoke or quit within the past 15 years; India has no national screening programme, and the public-health effort is tobacco control under COTPA and the National Tobacco Control Programme with opportunistic screening under the NCD programme.
Supportive and palliative care runs alongside from diagnosis: pain control on the WHO analgesic ladder, breathlessness management with a fan, positioning and opioids, nutrition, pleurodesis for recurrent effusion, and honest discussion of goals of care.

Occupational lung disease — bagassosis, Monday fever/byssinosis

Occupational lung diseases are respiratory disorders caused by inhaled dusts, fumes and organic antigens at work, and they divide into the pneumoconioses, in which mineral dust is deposited and fibrosis follows, and the hypersensitivity reactions, in which organic dust provokes an immune response in the small airways and alveoli. They matter to the nurse because the diagnosis is made largely from an occupational history that nobody else will take, and because the treatment that works is removal from exposure rather than any drug.

Silicosis follows free silica exposure in stone quarrying and crushing, sandblasting, agate and slate-pencil grinding, foundry work and mining; the chest X-ray shows upper-zone nodules with egg-shell calcification of the hilar nodes, and progressive massive fibrosis develops in advanced disease.
Silicosis multiplies the risk of tuberculosis several times over (silicotuberculosis), so every silica-exposed worker with new cough, fever, haemoptysis or weight loss is screened for tuberculosis, and periodic screening is part of surveillance.
Asbestosis follows asbestos in shipbreaking, insulation, brake linings and cement sheeting; it causes lower-zone fibrosis with pleural plaques, and the long-latency malignancies are mesothelioma (20 to 40 years after exposure, and not related to smoking) and bronchogenic carcinoma, whose risk is multiplied by smoking.
Coal workers' pneumoconiosis produces upper-zone nodules and progressive massive fibrosis; when it occurs with rheumatoid arthritis and rheumatoid nodules in the lung it is called Caplan syndrome.
Byssinosis is caused by cotton, flax, hemp and jute dust; its signature is chest tightness and breathlessness on the first working day after a break in exposure, which is why it is called Monday fever or Monday chest tightness, with symptoms easing through the week and, in chronic disease, persisting into later days and finally becoming fixed airflow obstruction.
Bagassosis is a hypersensitivity pneumonitis caused by mouldy sugarcane bagasse containing thermophilic actinomycetes; fever, dry cough, chills and breathlessness begin 4 to 8 hours after exposure and settle away from work, so the story is one of recurrent illness that improves on holidays.
The other hypersensitivity pneumonitides follow the same 4 to 8 hour pattern with different antigens: farmer's lung from mouldy hay, bird fancier's lung from avian proteins, malt worker's lung from Aspergillus, and humidifier lung; repeated attacks lead to irreversible fibrosis.
Occupational asthma is distinguished by symptoms that worsen at work and improve on days off and on holidays, confirmed by serial peak flow readings kept for at least 2 weeks at work and 2 weeks away.
Prevention follows a hierarchy: substitute the hazardous material, enclose or automate the process, use wet methods and local exhaust ventilation, then personal protective equipment; add pre-placement and periodic medical examination with spirometry, dust-level monitoring, and worker education. These pneumoconioses are notifiable occupational diseases under the Factories Act 1948, and affected workers are entitled to ESI benefits and compensation.
Treatment is removal from exposure first; then bronchodilators and, in hypersensitivity pneumonitis, corticosteroids for acute episodes, influenza and pneumococcal vaccination, smoking cessation, pulmonary rehabilitation and long-term oxygen in advanced disease. No drug reverses established fibrosis.

Apnoea

Apnoea is the cessation of airflow at the mouth and nose, and it is defined by duration and by consequence rather than by appearance alone — in an adult a pause of 10 seconds or more, and in a newborn a pause of 20 seconds or more, or a shorter pause accompanied by bradycardia, cyanosis or desaturation, or hypotonia. It matters because the newborn brain tolerates it very poorly and because the cause, not the pause, determines the treatment: apnoea in the first 24 hours of life or in a term baby is a sign of sepsis or another acute illness and never of prematurity.

Types: central apnoea is absent respiratory effort and absent airflow; obstructive apnoea is continued or increased effort against a closed airway with no airflow; mixed apnoea begins central and ends obstructive and is the commonest pattern in preterm infants.
Apnoea of prematurity affects infants born before 37 weeks (and almost all born before 28 weeks), typically starts on day 2 to 7 of life, and resolves as the infant approaches term-corrected age; it is a diagnosis of exclusion.
Secondary causes to exclude before accepting apnoea of prematurity: sepsis and meningitis, hypoglycaemia, hypocalcaemia, hyponatraemia, anaemia, hypothermia or overheating, intraventricular haemorrhage, seizures, necrotising enterocolitis, patent ductus arteriosus, gastro-oesophageal reflux, airway obstruction from neck flexion, and maternal or infant drugs.
Immediate management at the cot follows a fixed order: gentle tactile stimulation of the back or soles, position the neck in neutral (a rolled towel under the shoulders, never a flexed or hyperextended neck), suction only if secretions are visible, and if there is no response within seconds give positive pressure ventilation with bag and mask with oxygen and call for help.
Caffeine citrate is the drug of choice for apnoea of prematurity: a loading dose of 20 mg/kg followed by a maintenance dose of 5 to 10 mg/kg once daily; the citrate dose is twice the caffeine base dose, so the two must never be confused, and side effects are tachycardia, jitteriness, feed intolerance and diuresis.
Nasal CPAP at about 5 to 6 cm H2O splints the pharynx and is added for obstructive and mixed apnoea; persistent apnoea despite caffeine and CPAP is an indication for mechanical ventilation.
Continuous cardiorespiratory and saturation monitoring is mandatory, with every episode documented for duration, lowest heart rate, lowest saturation, colour, tone and the intervention needed, because a change in the pattern is what signals a new illness such as sepsis.
Preterm infants may be nursed prone or side-lying in hospital only while continuously monitored; healthy infants at home are placed supine to sleep, because supine sleep is the single strongest measure against sudden infant death.
In adults, apnoea is most often obstructive sleep apnoea, opioid or sedative-induced respiratory depression, or a sign of exhaustion in respiratory failure; opioid-induced apnoea is reversed with naloxone while ventilation is supported by bag and mask.
Apnoea in the newborn is never treated as an isolated event in the first 24 hours of life or in a term infant — a full septic screen, blood glucose and neurological assessment come first.

Pulmonary function test

Pulmonary function testing measures how much air the lungs hold and how fast it can be moved, and spirometry is the part of it that a ward nurse will most often prepare a patient for. It separates the two great patterns of lung disease — obstructive, where air cannot get out fast enough, and restrictive, where the lungs cannot fill — and it grades their severity, so it decides both the diagnosis and the fitness of a patient for lung surgery.

Spirometry measures the volumes a patient can move, so it cannot measure residual volume, functional residual capacity or total lung capacity; those need helium dilution, nitrogen washout or body plethysmography.
Normal values in an average adult: tidal volume about 500 mL, inspiratory reserve volume about 3000 mL, expiratory reserve volume about 1100 mL, residual volume about 1200 mL, vital capacity about 4600 mL and total lung capacity about 6000 mL; anatomical dead space is about 150 mL.
Obstruction is defined by a post-bronchodilator FEV1/FVC ratio below 0.70; severity is then graded on the FEV1 as a percentage of predicted — GOLD 1 mild at 80% or more, GOLD 2 moderate 50 to 79%, GOLD 3 severe 30 to 49%, GOLD 4 very severe below 30%.
Restriction shows a normal or high FEV1/FVC ratio with both FEV1 and FVC reduced, and it is confirmed by a total lung capacity below 80% of predicted; the causes are interstitial fibrosis, kyphoscoliosis, obesity, neuromuscular weakness, pleural disease and large effusions.
Reversibility testing is the discriminator between asthma and COPD: an improvement in FEV1 of 12% or more and at least 200 mL after a short-acting bronchodilator supports asthma, and a peak flow diurnal variability of more than 20% supports it too.
The transfer factor DLCO separates diseases with the same spirometry: it is low in emphysema and in interstitial lung disease, low in pulmonary embolism and pulmonary hypertension, but normal or high in asthma and in alveolar haemorrhage.
Preparation: withhold short-acting bronchodilators for about 4 to 6 hours and long-acting ones for 12 to 24 hours as instructed, no smoking for at least an hour, no heavy meal or vigorous exercise beforehand, loosen tight clothing, seat the patient upright with a nose clip and a tight lip seal, and coach a maximal inspiration followed by a hard, fast, sustained blow.
Quality matters more than the number: at least three acceptable manoeuvres are recorded and the two best FEV1 and FVC values should agree within 150 mL; the largest FEV1 and the largest FVC are reported even if they come from different blows.
Spirometry is deferred after a recent myocardial infarction, in unstable angina, with an untreated pneumothorax, with active haemoptysis, with a known thoracic, abdominal or cerebral aneurysm, and after recent eye, chest or abdominal surgery, because the forced manoeuvre raises intrathoracic, intracranial and intraocular pressure.
A flow-volume loop shows the pattern at a glance: a scooped-out expiratory limb in obstruction, a small narrow loop in restriction, and flattening of the inspiratory limb, the expiratory limb or both in upper airway obstruction.

Cheyne-Stokes respiration

Cheyne-Stokes respiration is a periodic breathing pattern in which the depth of breathing waxes and wanes in a smooth crescendo and then decrescendo, ending in a central apnoea of 10 to 30 seconds before the cycle starts again. It arises when the respiratory control loop becomes unstable — the chemoreceptors overreact to carbon dioxide and the circulation carries the blood to them too slowly — so it is a physical sign of left ventricular failure, of a damaged brain or of high altitude, and its appearance in a ward patient signals deterioration rather than comfort.

Mechanism: an exaggerated ventilatory response to carbon dioxide overshoots and blows the carbon dioxide below the apnoeic threshold, breathing stops, carbon dioxide rises again, and the prolonged circulation time of a failing heart delays the feedback so the oscillation continues; that delay is why the cycle length is longer in severe heart failure.
Causes: congestive cardiac failure with a low ejection fraction, in which it is common and marks a worse prognosis; stroke, raised intracranial pressure and other bilateral cerebral lesions; uraemia; opioids and sedatives; high altitude, where periodic breathing is a normal acclimatisation phenomenon; and the last days of life.
The neighbouring patterns are separate answers: Kussmaul breathing is deep, sighing and regular with no apnoea and signals metabolic acidosis such as diabetic ketoacidosis or uraemia; Biot (ataxic) breathing is irregular in both rate and depth with irregular pauses and signals medullary damage, raised intracranial pressure or meningitis; apneustic breathing is a prolonged inspiratory pause from a pontine lesion; agonal gasping is terminal.
Assessment at the bedside is to observe and count for a full 2 to 3 minutes without the patient knowing, record the cycle length and the apnoea duration, note the lowest oxygen saturation during the apnoea, and correlate the pattern with the conscious level, the pupils and the blood pressure.
Treatment is treatment of the cause: optimise heart failure with guideline-directed therapy and diuresis, manage the stroke or raised intracranial pressure, review opioids and sedatives, and correct uraemia; nocturnal oxygen may reduce the oscillation in heart failure.
Adaptive servo-ventilation must not be used for predominantly central sleep apnoea in heart failure with an ejection fraction of 45% or less, because a large trial found increased mortality; CPAP and oxygen are the options that remain.
In the dying patient, Cheyne-Stokes breathing is expected and is not distressing to the patient; the nursing task is to explain it to the family, who find it frightening, to position the patient and give mouth care, and to avoid futile suctioning and oxygen escalation.
New Cheyne-Stokes breathing in an acutely ill patient is documented and reported rather than merely charted, because in heart failure it means decompensation and in head injury it means a rising intracranial pressure.

Pneumonia

Pneumonia is acute infection of the lung parenchyma in which the alveoli fill with inflammatory exudate, so that the affected lung is consolidated and no longer exchanges gas. It is classified by where it was acquired, because that determines the likely organism and therefore the antibiotic — community-acquired pneumonia, hospital-acquired pneumonia appearing 48 hours or more after admission, ventilator-associated pneumonia appearing 48 hours or more after intubation, and aspiration pneumonia — and it remains one of the leading causes of death in Indian children under 5 years and in the elderly.

Community-acquired pneumonia is most often Streptococcus pneumoniae; the atypicals are Mycoplasma pneumoniae (young adults, dry cough, headache, cold agglutinins), Chlamydophila and Legionella (hyponatraemia, diarrhoea, confusion, contaminated water systems); influenza and other viruses precede or accompany many cases.
Hospital-acquired and ventilator-associated pneumonia are caused by Klebsiella, Pseudomonas, Acinetobacter, Escherichia coli and MRSA, so the antibiotic is chosen from the unit's own antibiogram rather than from a textbook list.
Aspiration pneumonia involves oral anaerobes and goes to the dependent segments — the posterior segment of the right upper lobe and the superior segment of the right lower lobe in a supine patient, the basal segments when upright — and the right lung is hit more often because the right main bronchus is wider, shorter and more vertical.
Signs of consolidation on examination are dullness to percussion, bronchial breath sounds, increased vocal resonance and whispering pectoriloquy with crackles; a pleural effusion gives the opposite — a stony dull percussion note with reduced breath sounds and reduced vocal resonance.
CURB-65 scores one point each for new Confusion, blood Urea above 7 mmol/L, Respiratory rate of 30 or more, Blood pressure below 90 systolic or 60 or less diastolic, and age 65 years or more: 0 to 1 can usually be managed at home, 2 needs admission, and 3 to 5 needs admission with assessment for intensive care.
Investigations are chest X-ray, pulse oximetry and blood gas if hypoxic, full blood count, urea and electrolytes, blood cultures and sputum culture before the first antibiotic dose, and blood glucose and HIV testing where relevant; procalcitonin and C-reactive protein help track the response rather than make the diagnosis.
Treatment of community-acquired pneumonia: amoxicillin for a well outpatient, amoxicillin-clavulanate or a cephalosporin with a macrolide for admitted patients so that atypicals are covered, and antipseudomonal cover for hospital-acquired disease; the first dose is given within an hour when sepsis is suspected, and the usual course is 5 to 7 days continued until the patient has been afebrile for 48 to 72 hours.
In children the WHO and IMNCI approach counts the breathing for a full minute: fast breathing is 60 or more per minute under 2 months, 50 or more from 2 to 11 months, and 40 or more from 1 to 5 years; chest indrawing or fast breathing alone is pneumonia treated at home with oral amoxicillin (a dispersible tablet, about 40 mg/kg per dose twice daily) while any general danger sign — inability to drink, persistent vomiting, convulsions, lethargy or unconsciousness, stridor at rest, or severe malnutrition — makes it severe pneumonia needing referral and injectable antibiotics with oxygen.
Nursing care is semi-Fowler's or upright positioning, oxygen to a saturation of 94 to 98% (88 to 92% in a carbon dioxide retainer), adequate hydration to loosen secretions, deep breathing and incentive spirometry, early mobilisation, chest physiotherapy where indicated, temperature control, and mouth care.
Prevention: pneumococcal conjugate vaccine in the Universal Immunization Programme at 6 weeks, 14 weeks and a booster at 9 months, annual influenza vaccine and pneumococcal vaccination for the elderly and those with chronic disease, exclusive breastfeeding for the first 6 months, reduction of indoor smoke, smoking cessation, hand hygiene, and the ventilator bundle in the intensive care unit.

COPD — emphysema vs chronic bronchitis

Chronic obstructive pulmonary disease is a preventable and treatable lung disease with persistent respiratory symptoms and airflow limitation that is not fully reversible, confirmed by a post-bronchodilator FEV1/FVC ratio below 0.70 on spirometry. Emphysema, which is destruction of alveolar walls with loss of elastic recoil, and chronic bronchitis, which is a productive cough on most days for at least 3 months a year in 2 consecutive years, are its two clinical faces, and most patients have some of both. In India it is caused as often by biomass smoke from indoor cooking fires — which is why women who have never smoked develop it — as by tobacco.

The diagnosis is spirometric and cannot be made on symptoms alone: a post-bronchodilator FEV1/FVC below 0.70 is required, and the severity grade then comes from the FEV1 percentage predicted, with GOLD 1 at 80% or more, GOLD 2 at 50 to 79%, GOLD 3 at 30 to 49% and GOLD 4 below 30%.
The GOLD groups that choose the drugs are A, B and E: group A has no more than one moderate exacerbation with few symptoms (mMRC 0 to 1 or a COPD Assessment Test score under 10), group B has the same exacerbation history with more symptoms (mMRC 2 or more or a CAT score of 10 or more), and group E has 2 or more moderate exacerbations or 1 exacerbation needing hospital admission.
Initial treatment is a bronchodilator for group A and a LABA plus LAMA combination for groups B and E, with an inhaled corticosteroid added in group E when the blood eosinophil count is 300 cells/µL or higher; an inhaled corticosteroid is not first-line in COPD as it is in asthma, and it raises the risk of pneumonia.
Emphysema is the pink puffer — thin, barrel-chested, pursed-lip breathing, quiet breath sounds, hyperinflated lungs with flattened diaphragms on the film, a reduced diffusing capacity and carbon dioxide held near normal until late; chronic bronchitis is the blue bloater — overweight, productive cough, cyanosis, secondary polycythaemia, right heart failure with oedema and a normal diffusing capacity.
Panacinar lower-zone emphysema in a young non-smoker, particularly with liver disease, is alpha-1 antitrypsin deficiency, whereas smoking-related emphysema is centriacinar and upper-zone.
Long-term oxygen therapy for at least 15 hours a day is prescribed for a resting PaO2 of 55 mmHg or less or an SaO2 of 88% or less, or for a PaO2 of 55 to 60 mmHg with cor pulmonale, peripheral oedema or polycythaemia, and it is one of the few measures that prolongs survival in COPD.
In an exacerbation the oxygen target is a saturation of 88 to 92% delivered through a controlled device such as a 24 to 28% Venturi mask, because uncontrolled high-flow oxygen in a carbon dioxide retainer worsens hypercapnia and causes narcosis; the correct response to a rising carbon dioxide is to titrate the oxygen down to target, never to withdraw it from a hypoxic patient.
Exacerbation treatment is short-acting salbutamol with ipratropium by nebuliser or spacer, oral prednisolone 40 mg daily for 5 days, and an antibiotic when there is increased sputum purulence together with increased dyspnoea or increased sputum volume, or when the patient is being ventilated.
Non-invasive ventilation is first-line ventilatory support in acute hypercapnic respiratory failure, defined as an arterial pH below 7.35 with a PaCO2 above 45 mmHg, and it reduces intubation, length of stay and mortality.
Stopping smoking is the only intervention that slows the accelerated fall in FEV1; annual influenza vaccination, pneumococcal vaccination and a structured pulmonary rehabilitation programme reduce exacerbations and admissions, and the nurse teaches pursed-lip and diaphragmatic breathing, controlled coughing and energy conservation.

Asthma — nursing management adult

Asthma is a chronic inflammatory disease of the airways with variable expiratory airflow limitation, which is why the same patient can have normal spirometry between attacks and a life-threatening obstruction an hour later. The bedside picture is wheeze, cough, chest tightness and breathlessness that vary in time and intensity and are typically worse at night and in the early morning or after a trigger such as cold air, exercise, dust, pollen, a viral infection, aspirin or a beta-blocker.

The diagnosis needs documented variable airflow limitation and not symptoms alone: a reduced FEV1/FVC with a rise in FEV1 of more than 12% and more than 200 mL measured 10 to 15 minutes after 200 to 400 µg of inhaled salbutamol, or an average daily peak flow variability above 10% in an adult.
Current GINA practice has abandoned treatment with a short-acting beta-2 agonist alone at every step, because SABA-only treatment increases exacerbations and asthma death; every adult and adolescent receives an inhaled corticosteroid, and the preferred reliever throughout is as-needed low-dose ICS-formoterol.
The stepwise ladder runs as-needed low-dose ICS-formoterol at steps 1 and 2, low-dose maintenance-and-reliever ICS-formoterol at step 3, medium-dose maintenance-and-reliever at step 4, and at step 5 the addition of a long-acting muscarinic antagonist with referral for phenotyping and biologic therapy.
Control is assessed by four questions covering the last 4 weeks — daytime symptoms more than twice a week, any night waking from asthma, reliever use more than twice a week, and any activity limitation; none of them means well controlled, one or two partly controlled, three or four uncontrolled.
Before stepping up the drug, check the three things that fail more often than the drug does: inhaler technique, adherence, and continuing exposure to a trigger such as smoke, a pet, an occupational agent, untreated allergic rhinitis or reflux.
Acute severe asthma in an adult is a peak flow of 33 to 50% of predicted or personal best, a respiratory rate of 25/min or more, a pulse of 110/min or more, or an inability to complete a sentence in one breath.
Life-threatening features are a peak flow below 33%, a saturation below 92%, a silent chest, cyanosis, feeble respiratory effort, bradycardia, arrhythmia, hypotension, exhaustion or confusion — together with a normal or rising PaCO2, which in a tiring asthmatic means the patient can no longer blow it off.
Acute treatment is oxygen titrated to a saturation of 93 to 95% in adults, salbutamol repeated every 20 minutes through the first hour (4 to 10 puffs by metered-dose inhaler with a spacer, or 2.5 to 5 mg by nebuliser) with ipratropium added in severe attacks, and a systemic corticosteroid within the first hour — prednisolone 40 to 50 mg orally for 5 to 7 days, or intravenous hydrocortisone if the patient cannot swallow.
Intravenous magnesium sulfate 2 g over 20 minutes is the add-on for a severe attack that has not responded to the first hour of standard treatment, and it is not part of routine care.
Sedatives and anxiolytics are contraindicated in an acute attack, while non-selective beta-blockers, aspirin and other NSAIDs can precipitate one; the combination of aspirin sensitivity, nasal polyps and asthma is Samter's triad. Every patient goes home with a written action plan, a demonstrated inhaler technique using a spacer, and a review appointment within 2 to 7 days.

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