Acute pulmonary oedema

Classify: wet (crackles) and warm (warm peripheries) — Nohria profile B, the largest profile in the 452-patient cohort; congested profiles carried a higher risk of death or urgent transplantation (HR 2.48).^[7] Oxygen and NIV: oxygen is indicated because SpO2 is under 90 percent (not routinely in non-hypoxaemic patients). Respiratory distress (RR over 25, SpO2 under 90 percent) means non-invasive positive pressure ventilation as soon as possible, monitoring BP because raised intrathoracic pressure reduces preload. 3CPO: NIV gave faster improvement in dyspnoea and metabolic disturbance than oxygen, with no difference in 7-day mortality. Intubate for progressive respiratory failure despite NIV.^[1][2] Vasodilator: SBP is over 110 mmHg, so an IV vasodilator may be considered — nitrate bolus then infusion, or repeated boluses (nitroglycerin 1–2 mg boluses in severely hypertensive acute pulmonary oedema). Cotter: the high-dose isosorbide dinitrate arm needed mechanical ventilation in 13 vs 40 percent.^[1][4] Diuretic: IV loop diuretic (oral absorption may be reduced by bowel oedema). DOSE: 1x vs 2.5x the previous oral dose and bolus vs infusion did not differ for the co-primary endpoints. Check the response: urine sodium under 50–70 mEq/L at 2 h and/or urine output under 100–150 mL/h in the first 6 h is insufficient — double the dose.^[5][3] Precipitant: in OPTIMIZE-HF the commonest identified were pneumonia/respiratory process, ischaemia and arrhythmia; non-adherence, hypertension and worsening renal function were also captured.^[8] Avoid routine morphine — in ADHERE it was an independent predictor of mortality after risk adjustment.^[6]