Pulmologic
Clinical Guide
A comprehensive guide for RT beginners from clinical perspective.
Respiratory Therapy (RT) is the specialty that manages breathing problems. As an RT, you help patients breathe better — whether that means giving oxygen, helping clear mucus, or running a breathing machine. The two most important numbers you'll watch are SpO₂ (oxygen in the blood, target 94–98%) and RR (breathing rate, normal 12–20 breaths/min). Think of the lungs as two zones: the conducting zone (pipes that move air — no gas exchange) and the respiratory zone (alveoli — where O₂ and CO₂ swap). CO₂ is your marker for ventilation; O₂ is your marker for oxygenation — they can fail independently.
Respiratory Therapy (RT) is a healthcare specialty focused on the assessment, treatment, and management of patients with disorders affecting the cardiopulmonary system. RTs work in ICUs, emergency departments, general wards, and outpatient settings.
| Care Goal | Clinical Objective |
|---|---|
| Maintain Oxygenation | Target SpO₂ 94–98% (88–92% for hypercapnic-risk patients) |
| Support Ventilation | Adequate CO₂ elimination; target PaCO₂ 35–45 mmHg |
| Airway Clearance | Mobilize secretions, prevent atelectasis, patent airway |
| Patient Education | Inhaler technique, breathing exercises, disease self-management |
| Monitoring | Continuous assessment of respiratory parameters and therapy response |
Extends from nose/mouth to terminal bronchioles (generations 0–16). Warms, humidifies, and filters air — no gas exchange occurs here. Constitutes anatomical dead space (~150 mL in adults).
- Trachea: ~10–12 cm long, supported by C-shaped cartilage rings
- Right main bronchus: shorter, wider, more vertical — aspirated objects lodge here more commonly
- Terminal bronchioles: no cartilage; held open by radial traction from lung parenchyma
Gas exchange begins at the respiratory bronchioles. Approximately 300–500 million alveoli in the adult lung — combined surface area of 50–100 m² (roughly a tennis court).
CO₂ diffuses ~20× more readily than O₂, which is why hypoxemia typically precedes hypercapnia in early lung disease.
| Parameter | Normal Value | Significance |
|---|---|---|
| Tidal Volume (Vt) | 500 mL (7 mL/kg) | Volume of one normal breath |
| Respiratory Rate (RR) | 12–20 breaths/min | Breathing frequency at rest |
| Minute Ventilation (Ve) | 6–8 L/min | RR × Vt; total volume exhaled per minute |
| Dead Space (Vd) | ~150 mL (30% of Vt) | Volume not participating in gas exchange |
| FRC | 2.0–2.5 L | Lung volume at end of normal expiration |
| Total Lung Capacity | 5.5–6.0 L | Total lung volume at full inspiration |
98.5% of O₂ is bound to hemoglobin; only 1.5% is dissolved in plasma. Anemia can cause tissue hypoxia even with normal SpO₂.
Oxygen is a drug — you prescribe a target range, not just "give O₂." The key device to know first: nasal cannula (1–6 L/min, mild cases) and non-rebreather mask (10–15 L/min, emergency). For COPD patients, be careful — target only 88–92% SpO₂ because too much oxygen can worsen their CO₂ retention. The Venturi mask is your friend here — it gives a precise, controlled FiO₂. HFNC (high-flow nasal cannula) is the modern upgrade for severe hypoxia — it can give up to 60 L/min and has a small PEEP effect. When weaning O₂, only reduce when SpO₂ is comfortably at the top of the target range for at least 30 minutes.
Prescribe with a specific target saturation range documented in patient notes. Indiscriminate high-flow oxygen causes hyperoxia — associated with increased mortality in COPD, AMI, and stroke (BTS 2017).
- SpO₂ < 94% (or < 88–92% in hypercapnic-risk patients)
- Acute hypoxemia: respiratory failure, pneumonia, pulmonary edema, ARDS
- Respiratory distress: dyspnea, increased WOB, accessory muscle use
- Shock states: septic, hemorrhagic, or cardiogenic — maximize O₂ delivery
- Carbon monoxide poisoning: high-flow 100% O₂ to displace CO from hemoglobin
- COPD exacerbation: titrate carefully to SpO₂ 88–92%
- Cardiac arrest / resuscitation: 100% O₂ during CPR, then titrate post-ROSC
| Device | Flow Rate | Approx FiO₂ | Best Used For |
|---|---|---|---|
| Nasal Cannula (NC) | 1–6 L/min | 24–44% | Mild hypoxemia, ambulatory, long-term O₂ |
| Simple Face Mask | 6–10 L/min | 40–60% | Moderate hypoxemia; min 6 L/min to flush CO₂ |
| Non-Rebreather Mask (NRB) | 10–15 L/min | 60–90% | Severe hypoxemia, CO poisoning, trauma |
| Venturi Mask | Variable by color | 24%, 28%, 31%, 35%, 40%, 50% | COPD — precise FiO₂ titration required |
| HFNC | Up to 60 L/min | 21–100% | Moderate–severe hypoxemia; reduces intubation need |
| CPAP/BiPAP (NIV) | Circuit-dependent | Up to 100% | OSA, hypercapnic failure, cardiogenic pulmonary edema |
HFNC delivers heated humidified gas at 20–60 L/min, meeting inspiratory demand. Benefits: dead-space washout, modest PEEP generation (2–5 cmH₂O), improved mucociliary clearance.
ROX > 4.88 at 12 hours → reduced intubation risk
65-year-old with known COPD, SpO₂ 88%, increased dyspnea, purulent sputum. Target SpO₂ 88–92%. Choose a 28% Venturi mask — not a non-rebreather mask. Driving SpO₂ above 92% risks worsening hypercapnia (Haldane effect + V/Q mismatch). Obtain ABG to guide management.
After surgery or during illness, sections of the lung can collapse (atelectasis) — like a deflated balloon. This causes fever, low SpO₂, and leads to pneumonia if not treated. Lung expansion therapy re-inflates those collapsed areas. The simplest tool: Incentive Spirometry (IS) — the patient takes slow, deep breaths using a visual feedback device, ideally 10 times per hour while awake. For patients who need more: CPAP provides constant positive pressure that physically stents airways open. The most important intervention overall? Get the patient sitting up and moving early. Pain control is essential — a patient who won't deep breathe because of pain gets atelectasis faster than anything else.
Lung expansion therapy prevents or treats alveolar collapse (atelectasis) — the leading cause of postoperative fever in the first 48 hours and a major contributor to postoperative pneumonia and prolonged stay.
| Technique | Mechanism | Best Indication | Evidence |
|---|---|---|---|
| Incentive Spirometry | Sustained maximal inhalation | Post-surgery (as part of bundle) | Moderate |
| CPAP | Constant positive pressure | OSA, pulmonary edema, post-extubation | Strong |
| PEP / Oscillating PEP | Expiratory resistance + oscillation | CF, bronchiectasis, COPD | Strong |
| IPPB | Pressure-assisted inhalation | Unable to cooperate with other methods | Low–Moderate |
| Early Mobilization | Gravity, diaphragm activation | All post-op patients | Strong |
Visual feedback for slow, deep sustained maximal inhalations. Hold breath 3–5 seconds for alveolar recruitment. Target: 10 breaths/hour while awake.
Note: Cochrane reviews suggest IS alone may not reduce pulmonary complications vs. early mobilization. Use as part of a respiratory care bundle.
Constant positive pressure stents open collapsed alveoli, improves FRC, reduces work of breathing. Cornerstone for OSA and highly effective in cardiogenic pulmonary edema.
Patient exhales against fixed resistance (10–20 cmH₂O), holding airways open and mobilizing secretions. Oscillating devices (Flutter, Acapella) add vibration to loosen mucus.
Positive pressure on inhalation only. Use has declined due to limited evidence. Reserved for patients unable to cooperate with other techniques.
58-year-old, day 1 after open cholecystectomy. SpO₂ 92% on 3 L NC, diminished breath sounds bilaterally, reluctant to deep breathe due to pain. Priority: Adequate analgesia first. Then hourly incentive spirometry, early sitting out of bed, consider CPAP if hypoxia persists. Atelectasis is the likely cause — not pneumonia at this stage.
An ABG is a blood test that tells you exactly what's happening with a patient's breathing at that moment. Think of it as a snapshot of the lungs and kidneys working together. Here's the quick cheat sheet: pH = is the blood acidic or alkaline? (normal 7.35–7.45) · PaCO₂ = how much CO₂ is in the blood? High = not breathing enough (hypoventilation) · HCO₃ = the kidney's response, takes days to change · PaO₂ = how much oxygen got into the blood. Your 4-step approach: (1) Is pH low (acidosis) or high (alkalosis)? (2) Does CO₂ match — high CO₂ + low pH = respiratory acidosis. (3) Is there compensation? (4) Is oxygenation okay? Common beginner mistake: confusing low SpO₂ with high CO₂ — they are different problems.
| Parameter | Normal Range | Critical Values | What It Tells You |
|---|---|---|---|
| pH | 7.35 – 7.45 | < 7.20 or > 7.60 | Overall acid-base balance |
| PaCO₂ | 35 – 45 mmHg | < 25 or > 60 mmHg | Adequacy of ventilation (CO₂ elimination) |
| PaO₂ | 80 – 100 mmHg | < 60 mmHg; severe if < 40 mmHg | Oxygen partial pressure in arterial blood |
| HCO₃⁻ | 22 – 26 mEq/L | < 10 or > 40 mEq/L | Renal/metabolic component of acid-base |
| SaO₂ | > 95% | < 90%; severe if < 85% | O₂ saturation of hemoglobin |
| Base Excess (BE) | −2 to +2 mEq/L | ≤ −10 or ≥ +10 mEq/L | Metabolic component; positive = alkalosis, negative = acidosis |
| Lactate | 0.5 – 1.6 mmol/L | ≥ 4 mmol/L | Tissue perfusion marker; elevated in shock/hypoxia |
| Disorder | pH | PaCO₂ | HCO₃⁻ | Main Problem | Common Causes | Quick Interpretation |
|---|---|---|---|---|---|---|
| Respiratory Acidosis | ↓ Low | ↑ High | Normal; ↑ if compensated | Hypoventilation / CO₂ retention | COPD exacerbation, opioid overdose, neuromuscular weakness, airway obstruction | The patient is not ventilating enough, so CO₂ builds up and makes the blood acidic. |
| Respiratory Alkalosis | ↑ High | ↓ Low | Normal; ↓ if compensated | Hyperventilation / excessive CO₂ removal | Anxiety, pain, pulmonary embolism, early sepsis, pregnancy | The patient is breathing off too much CO₂, making the blood alkalotic. |
| Metabolic Acidosis | ↓ Low | Normal; ↓ if compensated | ↓ Low | Bicarbonate loss or acid accumulation | DKA, lactic acidosis, renal failure, diarrhea | The metabolic system is causing acidosis, and the lungs may compensate by lowering CO₂. |
| Metabolic Alkalosis | ↑ High | Normal; ↑ if compensated | ↑ High | Bicarbonate excess or acid loss | Vomiting, diuretics, NG suction, hypokalemia | The metabolic system is causing alkalosis, and the lungs may compensate by retaining CO₂. |
| Primary Disorder | Compensation | Expected Formula |
|---|---|---|
| Respiratory Acidosis (acute) | HCO₃ rises | HCO₃ increases 1 mEq/L per 10 mmHg ↑ PaCO₂ |
| Respiratory Acidosis (chronic) | HCO₃ rises more | HCO₃ increases 3.5 mEq/L per 10 mmHg ↑ PaCO₂ |
| Respiratory Alkalosis | HCO₃ falls | HCO₃ decreases 2–5 mEq/L per 10 mmHg ↓ PaCO₂ |
| Metabolic Acidosis | PaCO₂ falls | PaCO₂ = 1.5 × HCO₃ + 8 (±2) — Winters formula |
| Metabolic Alkalosis | PaCO₂ rises | PaCO₂ increases 0.7 mmHg per 1 mEq/L ↑ HCO₃ |
SpO₂ alone is insufficient for managing COPD exacerbation or suspected respiratory failure. Order ABG when: (1) SpO₂ unexpectedly low despite O₂ therapy, (2) need to distinguish respiratory vs. metabolic acidosis, (3) titrating ventilator settings, or (4) patient deteriorating despite adequate oxygenation.
Want to see VCV, PCV, SIMV, and PSV actually behave differently on a live monitor? Try the interactive ventilator simulator → — pick a case, a severity, and a mode, and watch the waveforms and vitals respond.
A ventilator is a machine that breathes for the patient when they can't do it safely or effectively on their own. Picture it as a pump that pushes air into the lungs (inspiration) and lets it out (expiration) in a controlled, timed way. The three key settings to learn first: Tidal Volume (Vt) — how big each breath is (target ~6 mL/kg of ideal body weight) · Rate (RR) — how many breaths per minute (usually 12–20) · PEEP — a background pressure that keeps the lungs from fully collapsing between breaths (minimum 5 cmH₂O). The golden rule: always try non-invasive ventilation (BiPAP/CPAP) first before intubating. And once a patient is on the ventilator, start thinking about getting them off it — assess for extubation readiness every day using the SBT.
| Category | Examples | Key Indicator |
|---|---|---|
| Hypoxemic Respiratory Failure | ARDS, severe pneumonia, pulmonary edema | PaO₂/FiO₂ < 200 mmHg |
| Hypercapnic Respiratory Failure | COPD exacerbation, neuromuscular disease, OHS | ↑PaCO₂ + acidosis |
| Airway Protection | GCS < 8, massive hemoptysis, angioedema | Unable to protect airway |
| Apnea / Arrest | Cardiac arrest, drug overdose, CNS injury | Absent spontaneous breathing |
| Operative Ventilation | General anesthesia, thoracic surgery | Planned airway management |
For COPD exacerbation with hypercapnic acidosis (pH 7.25–7.35) and cardiogenic pulmonary edema, NIV/BiPAP should be first-line. NIV reduces intubation rates, ICU mortality, and hospital LOS. Avoid NIV if: coma, hemodynamic instability, unable to protect airway, or NIV failure.
Preset Vt delivered regardless of airway pressure. Guarantees minute ventilation. Risk: high pressures if compliance worsens.
Settings: Vt 6–8 mL/kg IBW, RR 12–20, PEEP 5 cmH₂O initial
Preset inspiratory pressure maintained per breath. Vt is variable. Reduces barotrauma risk. Useful in ARDS management.
Set mandatory breaths synchronized with patient effort + spontaneous breathing between. PSV can be added. Historically used for weaning.
Patient-triggered; every breath augmented with preset pressure. Vt and RR determined by patient. Ideal for weaning and SBTs.
The ARDSNet trial (NEJM 2000) demonstrated low-tidal-volume ventilation reduces ARDS mortality by 22%. This is now standard of care.
| Parameter | Target | Rationale |
|---|---|---|
| Tidal Volume (Vt) | 6 mL/kg IBW (max 8) | Prevent volutrauma and atelectrauma |
| Plateau Pressure | ≤ 30 cmH₂O | Surrogate for alveolar overdistension |
| Driving Pressure (Pplat − PEEP) | ≤ 15 cmH₂O | Independent predictor of ARDS mortality |
| PEEP | ≥5 cmH₂O; titrate by oxygenation | Prevent alveolar derecruitment at end-expiration |
| FiO₂ | Lowest to achieve SpO₂ 88–95% | Minimize oxygen toxicity |
| Permissive Hypercapnia | pH ≥ 7.20–7.25 acceptable | Accept CO₂ rise to protect lungs |
30–120 min on PSV 5–8 cmH₂O + PEEP 5 cmH₂O or T-piece.
Pass: RR <30, SpO₂ >90%, HR <140, no distress, stable BP
Fail: Increased WOB, desaturation, hemodynamic instability, diaphoresis, agitation
RSBI = RR ÷ Vt (L). RSBI < 105 breaths/min/L predicts successful extubation with ~80% sensitivity. Measure during 1–2 min T-piece or minimal PSV before the full SBT. High RSBI = rapid shallow breathing = respiratory muscle fatigue → delay extubation.
Most respiratory drugs are inhaled and work on the airways. The key groups: SABAs (Short-Acting Beta Agonists, e.g. Salbutamol) — your rescue inhaler, opens airways within minutes, lasts 4–6 hours. LABAs (Long-Acting, e.g. Salmeterol) — maintenance, lasts 12 hours, never use alone in asthma without ICS. SAMAs (e.g. Ipratropium) — anti-muscarinic bronchodilator, great for COPD. ICS (Inhaled Corticosteroids, e.g. Budesonide) — reduce airway inflammation, not for immediate relief. The easy mnemonic: SABA = Save (rescue), LAMA/LABA = Long-term, ICS = Inflammation control. In acute asthma: SABA + ipratropium + systemic steroids + O₂. In COPD: LAMA is first-line maintenance.
| Drug | Class | Onset | Duration | Use |
|---|---|---|---|---|
| Salbutamol (Albuterol) | SABA | 5–15 min | 4–6 hrs | Acute bronchospasm, asthma rescue |
| Terbutaline | SABA | 5–15 min | 4–6 hrs | Asthma, bronchospasm |
| Salmeterol | LABA | 10–20 min | 12 hrs | COPD, asthma (with ICS) |
| Formoterol | LABA | 1–3 min | 12 hrs | COPD, asthma (quick + long relief) |
| Indacaterol | LABA once daily | 5 min | 24 hrs | COPD maintenance |
Side effects: tachycardia, tremor, hypokalemia (esp. high doses), hyperglycemia. Monitor HR and potassium with frequent nebulized salbutamol.
| Drug | Class | Duration | Use |
|---|---|---|---|
| Ipratropium (Atrovent) | SAMA | 4–6 hrs | Acute COPD, acute severe asthma (add-on) |
| Tiotropium (Spiriva) | LAMA | 24 hrs | COPD maintenance; reduces exacerbations |
| Glycopyrronium | LAMA | 24 hrs | COPD maintenance |
| Umeclidinium | LAMA | 24 hrs | COPD (often in combination products) |
| Drug | Route | Dose (Adult) | Indication |
|---|---|---|---|
| Prednisolone | Oral | 30–40 mg/day × 5 days | COPD exacerbation, asthma exacerbation |
| Methylprednisolone | IV | 40–125 mg q6–8h | Acute severe asthma, severe COPD, ARDS |
| Hydrocortisone | IV | 100–200 mg q6h | Life-threatening asthma, adrenal insufficiency |
| Budesonide | ICS Inhaler/Neb | 200–1600 mcg/day | Asthma/COPD maintenance |
| Fluticasone | ICS Inhaler | 100–1000 mcg/day | Asthma maintenance |
Per GOLD 2024, ICS should not be used as monotherapy in COPD. Indicated in combination with LABA (ICS+LABA) for frequent exacerbators, blood eosinophils ≥300 cells/µL, or concurrent asthma. ICS increases pneumonia risk in COPD patients.
| Drug | Mechanism | Dose/Route | Indication |
|---|---|---|---|
| N-Acetylcysteine (NAC) | Breaks disulfide bonds; antioxidant | Inhaled or IV/oral | Thick secretions, CF, paracetamol overdose |
| Dornase Alfa (Pulmozyme) | Cleaves extracellular DNA in mucus | Nebulized 2.5 mg/day | Cystic fibrosis — reduces viscosity |
| Hypertonic Saline | Osmotic — draws water into airway lumen | Nebulized 3–7% | CF, bronchiectasis, atelectasis clearance |
| Carbocisteine | Reduces mucus viscosity | Oral 375–750 mg TID | Chronic productive cough, COPD |
Up to 70–80% of drug from an MDI deposits in the oropharynx without a spacer. A valved holding chamber (VHC) reduces oropharyngeal deposition, decreases oral candidiasis risk with ICS, and increases lung deposition. Always prescribe a spacer with MDIs for children, elderly, and acutely unwell patients.
Chronic inflammatory disorder with variable and reversible airflow obstruction, airway hyperresponsiveness, and inflammation. Affects ~300 million people worldwide. Managed per GINA 2023 strategy.
- Episodic wheeze, cough (worse at night/early morning), chest tightness, dyspnea
- Symptom variability — better with bronchodilators, worse with triggers
- Spirometry: FEV₁/FVC < 0.70 with significant bronchodilator reversibility (≥12% + 200 mL ↑ in FEV₁)
| GINA Step | Controller | Preferred Reliever |
|---|---|---|
| Step 1 — Mild Intermittent | None or low-dose ICS | Low-dose ICS-formoterol (MART) |
| Step 2 — Mild Persistent | Low-dose ICS daily | Low-dose ICS-formoterol (MART) |
| Step 3 — Moderate Persistent | Low-dose ICS-LABA | Low-dose ICS-formoterol (MART) |
| Step 4 — Severe | Medium/high-dose ICS-LABA | Low-dose ICS-formoterol (MART) |
| Step 5 — Uncontrolled | Add LAMA, anti-IgE, anti-IL5 | As above + specialist referral |
| Severity | SpO₂ | PEFR | Key Treatment |
|---|---|---|---|
| Mild–Moderate | ≥92% | >50% predicted | Salbutamol 4–8 puffs via spacer q20min ×3; oral prednisolone |
| Severe | 90–92% | 33–50% | Nebulized salbutamol + ipratropium; IV/oral steroids; O₂ to SpO₂ 94–98% |
| Life-Threatening | <90% | <33% | ICU; Mg sulfate IV; consider HFNC or intubation |
Absence of wheeze in acute severe asthma ("silent chest") indicates near-complete airway obstruction with minimal air movement. Requires immediate ICU escalation. Do not be reassured by quiet breath sounds — this is a life-threatening emergency.
Progressive, preventable, treatable disease with persistent irreversible airflow limitation. Third leading cause of death worldwide. ~80–90% of cases linked to tobacco smoking.
| GOLD Grade | Post-BD FEV₁ (% Predicted) | Severity |
|---|---|---|
| GOLD 1 | ≥ 80% | Mild |
| GOLD 2 | 50–79% | Moderate |
| GOLD 3 | 30–49% | Severe |
| GOLD 4 | < 30% | Very Severe |
- Controlled O₂: 28% Venturi mask; target SpO₂ 88–92%
- Bronchodilators: Salbutamol nebulizer + ipratropium nebulizer
- Steroids: Prednisolone 30–40 mg oral × 5 days (IV if unable to take oral)
- Antibiotics: If purulent sputum + increased dyspnea + sputum (Anthonisen criteria)
- NIV (BiPAP): If pH 7.25–7.35 after initial treatment
- Intubation: If NIV fails or contraindicated
Irreversible pathological dilation of the bronchi due to chronic infection and inflammation. Classic vicious cycle: retained secretions → infection → inflammation → further airway destruction.
- Airway clearance: chest physiotherapy, PEP, OPEP, AC nebulization daily
- Mucolytics: hypertonic saline (7%) nebulized; dornase alfa in CF only
- Exacerbation antibiotics: guided by sputum culture; 14 days (Pseudomonas coverage if colonized)
- Macrolide prophylaxis: azithromycin 250–500 mg 3×/week in frequent exacerbators
Chronic, progressive fibrosing interstitial pneumonia of unknown cause in adults typically >60 years. Median survival 2–5 years without treatment.
- Progressive exertional dyspnea + non-productive cough
- Bilateral fine inspiratory "Velcro" crackles at lung bases
- Restrictive PFTs: reduced FVC, TLC; preserved/elevated FEV₁/FVC
- HRCT: bilateral basal honeycombing with/without traction bronchiectasis (UIP)
- Clubbing in ~50% of patients
- Anti-fibrotics: Pirfenidone or Nintedanib — slow progression, reduce FVC decline ~50%
- O₂ therapy for rest, exertional, or nocturnal hypoxemia
- Pulmonary rehabilitation: improves exercise capacity and dyspnea
- Lung transplant: only curative option — refer early
Multisystem granulomatous disease of unknown etiology. Lungs and lymph nodes involved in >90% of cases. Most patients have self-limiting course; ~20–30% develop chronic or progressive disease.
| CXR Stage | Description |
|---|---|
| Stage 0 | Normal |
| Stage I | Bilateral hilar lymphadenopathy (BHL) |
| Stage II | BHL + parenchymal infiltrates |
| Stage III | Infiltrates without BHL |
| Stage IV | Fibrosis |
Diagnosis: Biopsy showing non-caseating granulomas + exclusion of other causes (TB, fungal).
Treatment: Prednisolone 20–40 mg/day for 6–12 months if symptomatic or progressive; methotrexate as steroid-sparing agent.
| Criterion | Points |
|---|---|
| Confusion (new onset) | 1 |
| Urea > 7 mmol/L (BUN > 20 mg/dL) | 1 |
| Respiratory Rate ≥ 30 breaths/min | 1 |
| Blood Pressure systolic <90 or diastolic ≤60 mmHg | 1 |
| Age ≥65 | 1 |
Caused by Mycobacterium tuberculosis. 10.6 million new cases and 1.3 million deaths in 2022 (WHO). Drug-sensitive TB is curable with structured 6-month regimen.
| Phase | Duration | Drugs |
|---|---|---|
| Intensive | 2 months | HRZE (Isoniazid + Rifampicin + Pyrazinamide + Ethambutol) |
| Continuation | 4 months | HR (Isoniazid + Rifampicin) |
Airborne precautions required — negative pressure room and N95 respirator for all staff. MDR-TB (resistance to H+R) requires 18–24 months with second-line drugs under specialist guidance.
| Severity | SpO₂ | Key Features | Respiratory Support |
|---|---|---|---|
| Mild | ≥94% | No hypoxemia, no dyspnea at rest | No supplemental O₂; home management |
| Moderate | 90–93% | Pneumonia, dyspnea on exertion | Supplemental O₂; hospital admission |
| Severe | <90% | RR ≥30, dyspnea at rest, bilateral infiltrates | HFNC or NIV; ICU level care |
| Critical ARDS | <88% | MV criteria met | Intubation + lung-protective MV; prone positioning |
- Antiviral: Nirmatrelvir-ritonavir (Paxlovid) — mild-moderate at-risk patients within 5 days of symptom onset
- Dexamethasone: 6 mg/day × 10 days for patients requiring supplemental O₂ (RECOVERY Trial)
- Anti-IL-6: Baricitinib or Tocilizumab for rapidly deteriorating patients on O₂/MV
- Prone positioning: Awake proning in non-intubated HFNC patients; mandatory in intubated ARDS (≥16 hrs/day)
- Anticoagulation: Prophylactic LMWH for all hospitalized; therapeutic dose if VTE confirmed
Clot (usually DVT) lodges in pulmonary vasculature causing V/Q mismatch, hypoxemia, and right heart strain. Massive PE can cause hemodynamic collapse and death.
- Wells Score: Pre-test probability; score >4 = PE likely
- D-Dimer: Highly sensitive, not specific; rules out PE if low probability
- CTPA: Gold standard imaging for PE diagnosis
- ABG: Hypoxemia, respiratory alkalosis, increased A-a gradient
- ECG: Sinus tachycardia (most common); S1Q3T3 in right heart strain
| PE Type | Hemodynamics | Treatment |
|---|---|---|
| Low-risk | Stable | DOAC (rivaroxaban, apixaban); outpatient management |
| Submassive | Stable but RV strain on echo/troponin | Anticoagulation; consider thrombolysis if deteriorating |
| Massive | Shock (SBP <90 mmHg) | Systemic thrombolysis (alteplase) or surgical embolectomy; vasopressors |
The classic S1Q3T3 pattern occurs in fewer than 20% of PE cases. The most common ECG finding is sinus tachycardia. New RBBB or right axis deviation also suggest right heart strain. A normal ECG does NOT rule out PE.
| Feature | Cardiogenic | Non-Cardiogenic (ARDS) |
|---|---|---|
| Mechanism | ↑PCWP >18 mmHg; LV failure | Capillary leak; inflammation |
| CXR | Bilateral fluffy opacities, Kerley B lines, cardiomegaly | Bilateral diffuse opacities; normal heart size |
| Fluid | Low-protein transudate | High-protein exudate |
| SpO₂ Response | Often improves well with O₂ | Often refractory (shunt physiology) |
| BNP / NT-proBNP | Markedly elevated | Usually normal or mildly elevated |
- Sit patient upright — reduces venous return
- CPAP (5–10 cmH₂O): reduces preload, afterload, WOB — reduces intubation rates (3CPO trial)
- IV furosemide: 40–80 mg IV; titrate to urine output
- IV nitrates: GTN infusion for BP and preload reduction
- Treat underlying cause: ACS, arrhythmia, hypertensive crisis
72-year-old with heart failure, SpO₂ 84%, severe dyspnea, bilateral crackles, pink frothy sputum. First intervention: apply CPAP (7.5–10 cmH₂O) immediately. This is the fastest way to reduce hypoxemia and WOB. Simultaneously give IV furosemide and IV GTN. Evidence shows CPAP reduces intubation need. If no CPAP available, high-flow O₂ via NRB while IV treatment is prepared.
PFTs are lung fitness tests. The most important is Spirometry — the patient blows hard into a tube and a machine measures the air. The two numbers that matter most: FEV₁ (how much you blow out in 1 second — tests airway speed) and FVC (total air blown out — tests lung size). The FEV₁/FVC ratio is the key: if it's below 70%, the airways are obstructed (COPD, asthma). If FVC is low but the ratio is normal, it's restrictive (stiff lungs, IPF, obesity). After a SABA puff, if FEV₁ improves by ≥12% + 200 mL, it's reversible obstruction → think asthma. DLCO measures how well gas crosses from air into blood — low DLCO + obstruction = emphysema; low DLCO + restriction = fibrosis.
Spirometry is the most widely used pulmonary function test, measuring the volume and flow of air during forced inhalation and exhalation. It is essential for diagnosing and monitoring obstructive and restrictive patterns.
| Parameter | Definition | Normal Value |
|---|---|---|
| FVC | Forced Vital Capacity — total air forcefully exhaled | ≥80% predicted |
| FEV₁ | Volume exhaled in the first second of FVC maneuver | ≥80% predicted |
| FEV₁/FVC | Ratio; key parameter for obstruction vs restriction | ≥0.70 (≥70%) |
| FEF 25–75% | Mean flow rate in mid-expiration; sensitive for small airway disease | ≥60% predicted |
| PEF | Peak Expiratory Flow — maximum expiratory flow rate | Varies by age/sex/height |
| MVV | Maximum Voluntary Ventilation — overall respiratory muscle endurance | ≈FEV₁ × 35–40 |
| Feature | Obstructive | Restrictive | Mixed |
|---|---|---|---|
| FEV₁/FVC | <0.70 ↓ | Normal or ↑ | <0.70 ↓ |
| FVC | Normal or ↓ | ↓ (<80%) | ↓ |
| FEV₁ | ↓ | ↓ proportionally | ↓↓ |
| TLC | Normal or ↑ (hyperinflation) | ↓ (<80%) | Variable |
| RV | ↑ (air trapping) | ↓ | Variable |
| Examples | COPD, Asthma, Bronchiectasis | IPF, Obesity, Pleural effusion | COPD + fibrosis |
Once FEV₁/FVC <0.70 confirms obstruction, severity is graded by FEV₁ % predicted: GOLD 1 ≥80% (mild), GOLD 2 50–79% (moderate), GOLD 3 30–49% (severe), GOLD 4 <30% (very severe). Post-bronchodilator values are used for COPD diagnosis.
Assess reversibility by repeating spirometry 15–20 minutes after 400 mcg salbutamol (4 puffs). A significant response suggests asthma rather than fixed obstruction.
Measures the ability of the lung to transfer gas across the alveolar-capillary membrane. Used when spirometry alone is insufficient to explain symptoms or hypoxemia.
| DLCO Finding | Pattern | Common Causes |
|---|---|---|
| ↓ DLCO + Obstruction | Emphysema pattern | COPD/emphysema (alveolar destruction) |
| ↓ DLCO + Restriction | Interstitial pattern | IPF, sarcoidosis, hypersensitivity pneumonitis |
| Normal DLCO + Obstruction | Airway disease | Asthma, chronic bronchitis |
| ↑ DLCO | Pulmonary haemorrhage / polycythaemia | Goodpasture syndrome, high Hb |
- TLC (Total Lung Capacity): Elevated in hyperinflation (COPD); reduced in restriction
- RV (Residual Volume): Air remaining after maximal expiration; elevated in air trapping
- FRC (Functional Residual Capacity): Resting lung volume; increased in emphysema
- RV/TLC Ratio: >40% indicates significant air trapping
- MIP (Maximum Inspiratory Pressure): Measures inspiratory muscle strength; normal >−80 cmH₂O (men), >−70 cmH₂O (women)
- MEP (Maximum Expiratory Pressure): Assesses expiratory/cough strength; normal >+90 cmH₂O
- Clinical use: Neuromuscular diseases (MND, GBS, myasthenia gravis), weaning from ventilation
PFT results are only valid with good patient effort and technique. ATS/ERS criteria require at least 3 acceptable and 2 reproducible maneuvers. Contraindications include recent MI (<1 month), active haemoptysis, unstable angina, and recent thoracic/abdominal/eye surgery.
Airway management is one of the most critical skills in respiratory therapy. Think of it in three parts: clearance (removing secretions), establishment (placing an artificial airway), and maintenance (keeping that airway patent and safe). The golden rule: no airway = no ventilation = no life. Before any airway procedure, always preoxygenate with 100% O₂. The most common artificial airway is the endotracheal tube (ETT) — passed through the mouth or nose into the trachea. For longer-term needs (>7–14 days), a tracheostomy tube (TT) is preferred — it's more comfortable, reduces work of breathing, and makes communication and weaning easier. Key number to memorize: keep the cuff inflated to 20–30 cmH₂O — too high damages the trachea, too low allows silent aspiration.
Retained secretions increase airway resistance, work of breathing, and can cause atelectasis and infection. Suctioning applies controlled negative pressure via a catheter to remove secretions from the large airways. It is a clinically indicated procedure — never performed on a preset schedule.
- Audible or palpable secretions (rhonchi on auscultation)
- Visible secretions in the artificial airway
- Increased peak inspiratory pressure (VCV) or decreased Vt (PCV) without another explanation
- Deteriorating SpO₂ or gas exchange
- Spontaneous coughing into the circuit
| Technique | Description | When to Use |
|---|---|---|
| Open Suction | Patient disconnected from ventilator; sterile single-use catheter | Tracheostomy patients not receiving mechanical ventilation |
| Closed (In-line) Suction | Sterile catheter permanently attached to ventilator circuit; no disconnection required | Preferred for all mechanically ventilated patients — especially PEEP ≥10 cmH₂O, FiO₂ ≥0.60, or patients at risk for derecruitment |
| Shallow Suctioning | Catheter advanced to a predetermined depth (end of artificial airway + adapter) | Recommended in all patients; reduces mucosal trauma and lung volume loss |
| Deep Suctioning | Catheter advanced until resistance met, then withdrawn ~1 cm before suction applied | Use with caution in adults — associated with lung volume loss and oxyhemoglobin desaturation |
Hypoxemia: Minimize by preoxygenating and using closed in-line suction. Cardiac dysrhythmias: Bradycardia (vagal stimulation) or tachycardia (hypoxemia/agitation) — stop suctioning and oxygenate. Mucosal trauma: Use shallow method and correct catheter sizing. Atelectasis: Limit suction pressure and duration; avoid circuit disconnection. Elevated ICP: Consider aerosolized lidocaine 15 minutes prior in at-risk patients. Bacterial colonization: Always use sterile technique; avoid routine normal saline instillation.
Indicated when the patient has retained secretions but no artificial airway. Place patient in the sniffing position (neck flexed, head extended) to align the larynx with the lower pharynx. Lubricate the catheter, advance through the nostril toward the nasal septum and floor of the nasal cavity without applying suction. Entry into the trachea is confirmed by a cough or a palpable increase in resistance. A nasopharyngeal airway (trumpet) can be left in place between sessions to protect the nasal mucosa in patients requiring repeated nasotracheal suctioning.
Artificial airways are inserted to relieve obstruction, facilitate secretion removal, protect against aspiration, and support positive pressure ventilation. They range from simple pharyngeal devices to surgically placed tracheal tubes.
| Airway Type | Route | Primary Use | Key Consideration |
|---|---|---|---|
| Nasopharyngeal Airway | Nose → pharynx | Repeated nasotracheal suctioning; post-facial surgery airway patency | Can be used in conscious patients; minimizes mucosal trauma; does not guarantee tracheal entry |
| Oropharyngeal Airway | Mouth → pharynx | Unconscious patients with tongue obstruction; bite block for oral ETT | Restricted to unconscious patients only — causes gagging and regurgitation in alert patients |
| Endotracheal Tube (ETT) | Oral or nasal → trachea via larynx | Acute airway management; short-to-medium term mechanical ventilation | Cuffed; Murphy eye for backup gas flow; radiopaque marker for X-ray verification |
| Tracheostomy Tube (TT) | Surgical neck stoma → trachea | Long-term artificial airway (>7–14 days); upper airway bypass; difficult weaning | Less work of breathing; improved comfort and communication; easier secretion removal |
| Laryngeal Mask Airway (LMA) | Oropharynx → over laryngeal opening | Difficult intubation; emergency airway bridge; unconscious patients only | No laryngoscope needed; does not protect against aspiration; ventilating pressure limited to <20 cmH₂O |
- 15-mm proximal adapter: Standard ventilator/BVM connection
- Centimeter markings: Monitor insertion depth (men: 21–23 cm at teeth; women: 19–21 cm)
- Beveled tip: Reduces mucosal trauma on insertion
- Murphy eye: Side port — backup gas flow if main port obstructed
- High-volume, low-pressure cuff: Target seal pressure 20–30 cmH₂O
- Pilot balloon: External cuff status indicator
- Radiopaque indicator: Confirms position on chest X-ray
- Outer cannula: Primary structural unit; attached to flange and cuff
- Flange: Prevents tube slippage; used to secure tube to neck
- Inner cannula: Removable for cleaning; prevents emergency tube change if obstructed
- Obturator: Rounded tip guide used during insertion only — remove immediately after placement
- Cuff (when present): High-volume, low-pressure; target 20–30 cmH₂O
- Correct sizing: Tube should occupy ²⁄₃ to ³⁄₄ of tracheal internal diameter
| Specialized ETT / TT | Feature | Clinical Indication |
|---|---|---|
| Double-Lumen ETT | Two lumens, two cuffs, two proximal connectors — each lung can be ventilated independently | Independent lung ventilation in unilateral lung disease; bronchoscopy must confirm placement |
| Subglottic Suction ETT/TT | Separate channel above cuff continuously aspirates secretions pooling above the cuff (at 20–30 cmH₂O) | VAP prevention; decreases aspiration-driven pneumonia when used with HOB elevation ≥30° |
| Combitube (Double-Lumen Airway) | Blind insertion; functions whether placed in trachea or esophagus; short-term only | Emergency airway when intubation is not possible |
| Fenestrated TT | Opening in posterior outer cannula above cuff; when inner cannula removed + cuff deflated, air passes to upper airway | Decannulation weaning; facilitates speech assessment — cannot suction with fenestrated inner cannula in place |
| Tight-to-Shaft (TTS) Cuff TT | Low-volume cuff collapses against tube when deflated; porous silicone material | Facilitates airflow around tube for speech; must be inflated with sterile water, not air |
| Metal Jackson TT | Stainless steel; no cuff; no 15-mm adapter | Long-term tracheostomy without ventilation or aspiration-protection needs |
| Age / Weight | ETT Size (mm ID) | Depth at Teeth/Lip |
|---|---|---|
| Premature <1 kg | 2.5 | 6.5–8 cm |
| Infant 2–3 kg | 3.5 | 8–9 cm |
| 6 months | 3.5–4.0 | 10–11 cm |
| 3 years | 4.5–5.0 | 12–14 cm |
| Women (average) | 7.5–8.0 oral; 7.0 nasal | 19–21 cm |
| Men (average) | 8.0–9.0 oral | 21–23 cm |
Orotracheal intubation is the preferred emergency tracheal airway route — the fastest and most accessible in most situations. No single intubation attempt should exceed 30 seconds. If unsuccessful, oxygenate for 3–5 minutes before the next attempt.
| Confirmation Method | What It Shows | Clinical Note |
|---|---|---|
| Bilateral Auscultation + Chest Rise | Air entry vs. esophageal or right mainstem placement | Always first-line bedside assessment |
| Waveform Capnography (EtCO₂) | Rising CO₂ waveform confirms tracheal placement; near-zero = esophageal | Gold standard; unreliable in cardiac arrest without effective compressions |
| Colorimetric CO₂ Detector | Color change on CO₂ exposure confirms tracheal placement | Inexpensive and portable; same limitation in cardiac arrest |
| Tube Depth (cm at Teeth) | Guide to approximate position | Cannot confirm tracheal vs. esophageal placement alone |
| Videolaryngoscopy | Real-time camera view of glottis during insertion | Especially valuable in anticipated difficult airways; camera at laryngoscope tip |
| Flexible Bronchoscopy / Laryngoscopy | Direct visualization of carina below tube tip | Definitively confirms tracheal placement; most precise depth measurement |
| Bedside Ultrasound | Tracheal ring visualization; rules out esophageal placement | Increasingly available; no ionizing radiation; real-time |
| Chest X-Ray | Final documentation of tube tip position (3–5 cm above carina) | Standard post-intubation; not a primary real-time confirmation tool |
In cardiac arrest without effective compressions, end-tidal CO₂ will read near zero even with correct tracheal placement — no blood is perfusing the alveoli to deliver CO₂. Never remove an ETT based on a flat capnogram alone in this setting. Once compressions begin and are effective, EtCO₂ will rise. A sudden significant rise in EtCO₂ during resuscitation can signal return of spontaneous circulation (ROSC).
Consider tracheotomy when an artificial airway is still required after approximately 7–14 days of translaryngeal intubation. Benefits over prolonged ETT use include elimination of laryngeal injury, reduced sedation requirement, improved patient comfort and communication, lower work of breathing, and easier ventilator weaning.
| Approach | Setting | Advantages | Contraindications |
|---|---|---|---|
| Percutaneous Dilation Tracheotomy | ICU bedside | Faster, fewer wound complications, better cosmetic result; bronchoscope can guide placement | Children <12 years; PEEP >15 cmH₂O; coagulopathy; poor landmarks; cervical spine limitations |
| Open Surgical Tracheotomy | Operating room | Can be done with poor anatomy; preferred in children; done emergently if needed | Stoma takes longer to stabilize (7–10 days) vs. percutaneous (5 days) |
Artificial airways that do not conform precisely to patient anatomy exert pressure on soft tissue, causing ischemia and ulceration. Tube movement creates friction-like injuries. Because injury cannot always be assessed while the airway is in place, careful evaluation after extubation is always required.
| Injury | Site | Key Cause | Presentation & Management |
|---|---|---|---|
| Glottic Edema / Vocal Cord Inflammation | Larynx | ETT pressure or intubation trauma; can worsen for 24 hrs post-extubation | Hoarseness and stridor; aerosolized epinephrine (racemic 2.25%) ± corticosteroid; IV steroids and/or diuretics 24 hrs before extubation in high-risk patients |
| Vocal Cord Ulcerations | Larynx | Prolonged ETT contact with posterior glottis | Hoarseness post-extubation; typically resolves spontaneously; no specific treatment required |
| Vocal Cord Polyps / Granulomas | Larynx | Develops slowly over weeks to months | Hoarseness, dysphagia, stridor; surgical removal if symptoms are severe or persistent |
| Laryngeal Stenosis | Larynx | Normal laryngeal tissue replaced by scar; does not resolve spontaneously | Stridor and hoarseness; surgical correction required; some patients require permanent tracheostomy |
| Tracheomalacia | Trachea | Sustained cuff pressure softens cartilaginous rings; trachea collapses during breathing | Variable obstruction on flow-volume loop (flattened inspiratory or expiratory limb); may require tube upsizing |
| Tracheal Stenosis | Trachea (cuff site, stoma, tube tip) | Fibrotic scarring from mucosal ischemia; symptoms appear when diameter reduced by 50–75% | Fixed obstruction on flow-volume loop (both limbs flattened); laser therapy (small lesions), resection, or stenting based on severity |
| Tracheoesophageal Fistula (TEF) | Trachea–esophagus | Cuff or nasogastric tube erosion; malnutrition and sepsis accelerate development | Recurrent aspiration; gastric distension during PPV; confirmed by endoscopy; requires surgical closure |
| Tracheoinnominate Artery Fistula | Trachea–innominate artery | TT erosion through artery; typically from too-low stoma placement or excess tube movement | Pulsating TT is the only early warning; massive hemorrhage follows; hyperinflate cuff as temporizing measure; surgical intervention required — only ~25% survive |
A tracheostomy tube that visibly pulsates with each heartbeat is a sentinel warning sign of impending fistula formation. When hemorrhage begins, maximally inflate the cuff as an immediate temporizing measure to compress the bleeding site. Call for immediate surgical intervention — this complication carries a very high mortality even with optimal management.
- Maintain cuff pressure at 20–30 cmH₂O — check regularly with a calibrated manometer; always re-adjust to target after measuring
- Select the correct airway size — ETT should occupy <50% of tracheal internal diameter
- Minimize tube movement — use swivel adapters on ventilator circuits, sedation, and stable tube holders
- Use nasotracheal intubation when prolonged intubation is expected (more stable, less likely to self-extubate)
- Do not change endotracheal or tracheostomy tubes unless clinically necessary
- Rotate ETT securing sites regularly to prevent skin breakdown; use foam dressings if drainage is present around stoma
- 1. Secure tube & confirm placement: Tape or commercial holder; document centimeter marking at teeth; confirm with CXR — tip 3–5 cm above carina. Note: neck flexion moves the tube toward the carina; extension moves it toward the larynx.
- 2. Patient communication: ETT patients — use letter, phrase, or picture boards. TT patients — speaking valve (e.g., Passy-Muir) with cuff fully deflated; confirm safety with transtracheal pressure <5 cmH₂O on exhalation. Fenestrated TT with inner cannula removed and cuff deflated also allows speech.
- 3. Adequate humidification: Artificial airways bypass the upper airway's warming and humidification functions — dry gas thickens secretions and impairs mucociliary clearance. Use active heated humidifier or heat and moisture exchanger (HME).
- 4. Minimize nosocomial infection: Closed suction system, sterile technique, consistent hand hygiene, head-of-bed elevation ≥30°, continuous subglottic suction, and stress ulcer prophylaxis.
- 5. Facilitate secretion clearance: Suctioning, physiotherapy, and adequate humidification. For patients with impaired cough (ALS, SMA, muscular dystrophy), use mechanical in-exsufflator (MIE/Cough Assist).
- 6. Cuff pressure management: Target 20–30 cmH₂O using a calibrated manometer. Always inflate to target after measuring — attaching the manometer evacuates a small volume from the cuff. Minimal occlusion volume and minimal leak techniques are no longer recommended due to increased aspiration risk.
- 7. Troubleshoot emergencies: Three key emergencies — tube obstruction, cuff leak, and unplanned extubation (see table below).
| Emergency | Clinical Signs | Stepwise Response |
|---|---|---|
| Tube Obstruction Causes: kinking, biting, herniated cuff, tube against tracheal wall, mucous plug |
Partial: ↓ breath sounds, ↑ PIP (VCV) or ↓ Vt (PCV). Complete: severe distress, absent breath sounds, no gas flow | (1) Reposition head and neck · (2) Deflate cuff · (3) Attempt to pass suction catheter through tube · (4) Remove inner cannula if TT · (5) Remove airway and provide BVM ventilation + oxygenation |
| Cuff Leak Causes: ruptured cuff, leaking pilot tube/valve, tube positioned too high in trachea |
Audible leak, decreasing delivered volumes, decreasing cuff pressure over time, airflow felt at mouth during PPV | Attempt reinflation; check pilot tube and valve for leaks. Ruptured cuff in ventilated patient → emergent ETT exchange using ETT exchanger. If tube is shallow, advance slightly and reassess before assuming cuff rupture |
| Unplanned Extubation Partial or complete displacement from trachea |
Decreased breath sounds, ability to pass catheter to full length without obstruction or eliciting cough, airflow from mouth or stomach with PPV | Remove tube completely; provide BVM ventilation; reintubate or reinsert TT once patient is oxygenated and stabilized. Document incident per institutional policy |
Cuff pressure >30 cmH₂O impedes tracheal mucosal capillary perfusion → ischemia → ulceration → stenosis or tracheomalacia. Cuff pressure <20 cmH₂O allows silent aspiration of subglottic secretions → a primary driver of ventilator-associated pneumonia (VAP). The target range of 20–30 cmH₂O is therefore both a safety floor and a ceiling. Combine cuff management with subglottic suction, HOB elevation ≥30°, and closed suction technique for a comprehensive VAP-prevention bundle.
The artificial airway should be removed as soon as it is no longer clinically needed. Premature removal risks respiratory failure and reintubation; delayed removal prolongs exposure to airway injury, infection, and sedation.
- Adequate spontaneous oxygenation and ventilation without mechanical support
- Low risk for upper airway obstruction: Perform the cuff-leak test — deflate cuff in VCV mode; a leak ≥15% of exhaled Vt (e.g., difference of ≥75 mL for a 500 mL breath) suggests no significant glottic edema. Most useful in women, children, and patients intubated >6 days.
- Airway protective reflexes intact: Gag reflex present; patient can follow commands (e.g., raise and hold head off bed)
- Adequate secretion clearance: Effective cough; acceptable secretion volume and consistency
| Decannulation Approach | Description | Use When |
|---|---|---|
| Direct Removal | Single-step TT removal; stoma closes in a few days | Upper airway obstruction resolved; patient otherwise stable; adequate cough (PEP >40 cmH₂O) |
| Fenestrated TT | Inner cannula removed + cuff deflated + cap or speaking valve → airflow through upper airway; suctioning still accessible by removing cap | Gradual upper airway reintroduction; speech testing; ventilator weaning — cannot suction with fenestrated inner cannula inserted |
| Progressively Smaller TTs | Sequential downsizing of tube diameter while maintaining stoma patency | When fenestrated tube unavailable or trachea too small; allows better stoma healing |
| Tracheal Button | Short device through skin to just inside tracheal wall — no cuff, no added resistance; maintains stoma for suctioning access | Patient tolerates upper airway breathing but stoma access still needed; avoids resistance of a full tube |
Laryngeal edema can worsen progressively for up to 24 hours after extubation — do not reduce monitoring prematurely. Extubation failure (need for reintubation) occurs most commonly within the first 8 hours, with aspiration and airway edema as the leading causes. Keep racemic epinephrine, suction equipment, and full reintubation supplies immediately at the bedside for at least 1–2 hours after extubation in high-risk patients.
When mucus gets stuck in the airways, it causes infections and blocks airflow. ACT helps patients move and cough out that mucus. The most important technique to learn first: ACBT (Active Cycle of Breathing) — it's three phases: relax and breathe normally → take 3–5 deep breaths → then do a "huff" (a forced breath out with mouth open, not a cough). This loosens and moves mucus up to where it can be coughed out. For patients who can't cooperate (e.g. intubated or very weak), we use suction — a thin tube that vacuums out secretions. In CF and bronchiectasis, patients use devices like Flutter or Acapella which add vibration to loosen thick mucus. Key rule: if a patient's peak cough flow is below 160 L/min, they can't clear secretions alone — consider mechanical cough assist (MI-E).
Airway Clearance Therapy (ACT) encompasses techniques to mobilize and remove secretions from the airways, reduce the risk of infection, and improve ventilation. Indicated when secretion retention is present or anticipated.
| Indication Category | Examples |
|---|---|
| Chronic hypersecretory conditions | Cystic fibrosis, bronchiectasis, chronic bronchitis |
| Acute respiratory failure | Pneumonia with retained secretions, post-extubation |
| Post-surgical | Thoracic/abdominal surgery, atelectasis prevention |
| Neuromuscular weakness | MND, GBS, high spinal cord injury, muscular dystrophy |
| Mechanical ventilation | Intubated patients with secretion retention |
A structured three-phase cycle performed independently by the patient or guided by a therapist. Evidence-based first-line technique for most ACT indications.
- Percussion (Clapping): Rhythmic cupped-hand percussion over lung segments to loosen secretions — typically 3–5 min per segment
- Vibration: Fine oscillatory pressure applied during expiration to assist mucus movement
- Postural Drainage (PD): Positioning the patient so gravity facilitates drainage from affected lung segments; combined with percussion/vibration for maximum benefit
| Device | Mechanism | Key Use |
|---|---|---|
| PEP (Positive Expiratory Pressure) | Resistance during expiration creates back-pressure that stents open small airways and assists collateral ventilation | CF, bronchiectasis, COPD |
| Oscillating PEP (Flutter / Acapella) | PEP + oscillations loosen mucus and stimulate cough; Acapella can be used in any position | CF, bronchiectasis |
| HFCWO (High-Frequency Chest Wall Oscillation) | Inflatable vest delivers rapid chest compressions (5–25 Hz) to thin and mobilise secretions | CF, neuromuscular disease |
| IPV (Intrapulmonary Percussive Ventilation) | Delivers high-frequency mini-bursts of gas into airway to mobilise secretions; can be used in ventilated patients | Ventilated patients, CF exacerbations |
| MI-E (Mechanical In-Exsufflation) | Applies positive pressure then rapidly switches to negative to simulate a cough; used when cough is ineffective (PCF <160 L/min) | Neuromuscular disease, high SCI |
Peak Cough Flow (PCF) <160 L/min indicates inability to clear secretions effectively — risk of respiratory failure with even mild chest infection. PCF <270 L/min warrants prophylactic use of MI-E. In MND and DMD, initiate before an acute crisis.
Indicated when patient cannot clear secretions independently despite other ACT. Used in intubated, tracheostomised, or obtunded patients.
| Route | Catheter Size | Suction Pressure | Max Duration |
|---|---|---|---|
| Nasopharyngeal / Oropharyngeal | 12–16 Fr (adult) | −80 to −120 mmHg | 15 seconds per pass |
| Endotracheal / Tracheostomy | ≤½ ETT internal diameter | −80 to −150 mmHg | 10–15 seconds per pass |
Hypoxemia, bronchospasm, arrhythmias, trauma, and haemodynamic instability. Pre-oxygenate with FiO₂ 1.0 before each pass. Limit passes to 3 per session. Closed-circuit suction systems preferred in intubated patients to maintain PEEP and minimise derecruitment.
| Condition | First-Line ACT | Notes |
|---|---|---|
| Cystic Fibrosis | ACBT or PEP + oscillating PEP; HFCWO vest | 2× daily minimum; increase during exacerbations |
| Bronchiectasis | ACBT, oscillating PEP, postural drainage | Target dependent lung segments; regular nebulised saline |
| COPD exacerbation | ACBT (huff), PEP if secretions copious | Avoid head-down positions; combine with NIV if hypercapnic |
| Post-operative | ACBT, incentive spirometry, early mobilisation | Splinted coughing (pillow support) for abdominal/thoracic incisions |
| Neuromuscular disease | MI-E (cough assist) ± manual assisted cough | Monitor PCF regularly; prophylactic MI-E if PCF <270 L/min |
| Mechanically ventilated | Positioning, closed-circuit suction, IPV | Lateral rotation therapy reduces VAP risk; saline nebulisation before suction |