Respiratory Acidosis

Also known as: Hypercapnia, Hypercapnic respiratory failure

Respiratory acidosis is a primary rise in PaCO₂ producing a fall in pH, resulting from alveolar hypoventilation: the lungs failing to clear CO₂ at the rate it is produced.

Renal compensation retains bicarbonate, but this takes 3–5 days to become fully established, which is why the distinction between acute and chronic matters so much.

Acute respiratory acidosis shows a markedly low pH with only a small rise in bicarbonate (roughly 1 mmol/L per 10 mmHg rise in PaCO₂), because compensation has not had time to develop.

Chronic respiratory acidosis shows a near-normal pH with a substantially raised bicarbonate (roughly 3.5–4 mmol/L per 10 mmHg), reflecting established renal compensation.

Causes include central respiratory depression (opioids, sedatives, brainstem pathology), neuromuscular disease (Guillain-Barré, myasthenia, motor neurone disease), chest wall and pleural disease, and airways and parenchymal disease, principally COPD, severe asthma and obesity hypoventilation.

Blood gas showing low pH with raised PaCO₂. An arterial sample is preferred where precise PaCO₂ matters, though venous CO₂ correlates well enough for screening
Distinguish acute from chronic by the bicarbonate, using the compensation rules above. A patient with PaCO₂ of 70 mmHg and bicarbonate of 26 is acutely decompensated and in danger; the same PaCO₂ with a bicarbonate of 38 reflects chronic adaptation. Mistaking chronic compensated hypercapnia for acute failure leads to unnecessary intervention, and mistaking acute failure for chronic leads to dangerous delay
Acute-on-chronic is common and is identified by a bicarbonate that is raised but insufficient for the degree of hypercapnia
Identify the cause: chest examination and imaging, drug chart review for opioids and sedatives, neurological assessment for neuromuscular weakness, and assessment for airway obstruction
Serial gases are more informative than a single measurement, since the trajectory determines management
In neuromuscular disease, forced vital capacity predicts respiratory failure earlier and more reliably than blood gases, which can remain normal until decompensation is imminent

Treat the underlying cause, which is the priority: bronchodilators, steroids and antibiotics for COPD exacerbation; naloxone for opioid-induced respiratory depression; treatment of the neuromuscular disorder
Controlled oxygen therapy in patients at risk of CO₂ retention, targeting saturations of 88–92% rather than normal values. The concern is real but is often misunderstood: the mechanism is principally increased ventilation-perfusion mismatch and the Haldane effect rather than simple loss of hypoxic drive. Critically, hypoxia kills before hypercapnia does, so oxygen should never be withheld from a hypoxic patient for fear of retention; it should be titrated
Non-invasive ventilation (BiPAP) is the key intervention in acute hypercapnic respiratory failure, particularly in COPD, where it has clear mortality benefit. Indications include a pH below 7.35 with PaCO₂ above roughly 45–50 mmHg persisting despite initial medical therapy
Invasive ventilation where non-invasive ventilation fails or is contraindicated: reduced consciousness with an unprotected airway, haemodynamic instability, copious secretions, facial trauma, or vomiting
Avoid over-correcting chronic hypercapnia: rapidly normalising PaCO₂ in a chronically compensated patient produces a post-hypercapnic metabolic alkalosis, since the raised bicarbonate persists after the CO₂ has fallen
Stop or reverse contributing sedatives and opioids
Discuss ceiling of care early in patients with advanced chronic lung disease, since decisions about escalation to invasive ventilation are best made before the patient deteriorates rather than during a crisis

Referral: respiratory medicine and critical care for acute hypercapnic failure; neurology for neuromuscular causes, with early critical care involvement given the speed of decompensation.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Pulmonary Embolism

Also known as: PE, Venous thromboembolism

Obstruction of pulmonary arterial circulation, most commonly by thrombus embolized from deep vein thrombosis of the lower limbs/pelvis (>90% of cases), causing ventilation-perfusion mismatch, increased pulmonary vascular resistance, and potential right ventricular strain/failure.

Classified by severity:

Low-risk (non-massive): hemodynamically stable, no RV dysfunction
Intermediate-risk (submassive): hemodynamically stable but with RV dysfunction (echo/CT) and/or elevated carintermediate; further subdivided intermediate-low/intermediate-high
High-risk (massive): hemodynamic instability (sustained hypotension SBP<90, requiring vasopressors, or pulseless); highest mortality, requires aggressive reperfusion

Sudden onset dyspnea (most common symptom), pleuritic chest pain, cough, hemoptysis (suggests pulmonary infarction)
Tachycardia, tachypnea, hypoxia; syncope/pre-syncope (suggests significant hemodynamic compromise; high-risk feature)
Examination: often unremarkable beyond tachycardia/tachypnea; signs of DVT present in a minority; signs of RV strain in massive PE ; raised JVP, loud P2, right-sided S3, hypotension
Risk factors (Virchow's triad): recent surgery/immobilization, malignancy, pregnancy/postpartum, estrogen therapy, prior VTE, inherited thrombophilia, long-haul travel, obesity, trauma, central venous catheter
Massive PE: shock, syncope, cardiac arrest ; PEA arrest should always prompt consideration of PE as a reversible cause

Clinical probability assessment first (Wells or Geneva score):
- Low/intermediate probability: D-dimer : if negative, PE effectively excluded; if positive, proceed to imaging
- High probability: proceed directly to imaging (D-dimer not useful for exclusion at high pre-test probability)
D-dimer: sensitive but non-specific (elevated in pregnancy, malignancy, infection, recent surgery, elderly) ; age-adjusted cutoffs improve specificity in older patients
CT pulmonary angiography (CTPA): investigation of choice; direct visualization of filling defect, also assesses RV size/strain (RV:LV ratio >1 suggests significant strain)
V/Q scan: alternative if CTPA contraindicated (renal impairment, contrast allergy) or in pregnancy
ECG: sinus tachycardia most common; S1Q3T3, right heart strain (T-wave inversion V1-4), RBBB ; classic but insensitive
Echocardiography: bedside assessment of RV strain in unstable patients when CTPA not immediately feasible
Troponin/BNP: elevated in RV strain, prognostic marker for risk stratification
Lower limb Doppler: confirms DVT source if positive, though normal doesn't exclude PE

Differentials: ACS, pneumonia, pneumothorax, pericarditis, musculoskeletal chest pain, anxiety, aortic dissection, COPD/asthma exacerbation.

Hemodynamically stable (low/intermediate-risk):

Anticoagulation : start promptly once diagnosis confirmed (or strongly suspected while awaiting imaging in high pre-test probability):
- DOAC (apixaban, rivaroxaban) : first-line for most; apixaban 10mg bd x7 days then 5mg bd; rivaroxaban 15mg bd x21 days then 20mg od
- LMWH (enoxaparin 1mg/kg bd) : preferred in pregnancy, severe renal impairment, active malignancy, or if intervention anticipated
- Warfarin: requires LMWH bridging until INR therapeutic (2-3), largely superseded except specific indications (mechanical valve, severe renal impairment, antiphospholipid syndrome)
Duration: minimum 3 months for provoked PE with reversible risk factor; longer/indefinite for unprovoked PE or ongoing risk factors ; individualized bleeding vs. recurrence assessment
Intermediate-high risk: closer monitoring, low threshold for escalation

Hemodynamically unstable (high-risk/massive PE) ; reperfusion indicated:

Systemic thrombolysis: alteplase 100mg IV over 2 hours (or accelerated regimens) : first-line for confirmed massive PE with shock
Catheter-directed thrombolysis/thrombectomy: alternative where contraindications to systemic thrombolysis exist or expertise available
Surgical embolectomy: for absolute contraindication to thrombolysis with appropriate surgical support
Supportive: cautious IV fluid (small boluses only : aggressive fluid worsens RV strain), vasopressor (noradrenaline) for hypotension, avoid excessive positive pressure ventilation if intubated
ECMO: bridge to definitive therapy in refractory cardiogenic shock/cardiac arrest

IVC filter: for absolute contraindication to anticoagulation with ongoing high VTE risk, or recurrent PE despite adequate anticoagulation.

Pregnancy-specific: LMWH is anticoagulant of choice (DOACs and warfarin contraindicated), continue through pregnancy and minimum 6 weeks postpartum, total duration ≥3 months.

Referral: respiratory/cardiology for risk stratification, hematology for thrombophilia workup if unprovoked/recurrent, ICU for massive PE.

Respiratory Acidosis

Overview

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management