Sympathetic Crashing Acute Pulmonary Oedema

Sympathetic crashing acute pulmonary oedema (flash pulmonary oedema, or acute hypertensive heart failure) is a sudden, severe form of pulmonary oedema driven by extreme sympathetic activation, with high blood pressure (often systolic over 180 mmHg), tachycardia and respiratory failure. The problem is redistribution of fluid into the lungs from vasoconstriction, and not total body fluid overload.

Epidemiology. It is a recognised presentation of acute heart failure in older adults, women and those with hypertension, diastolic dysfunction or renal artery stenosis. Intubation and intensive care admission can often be avoided with prompt vasodilator and ventilatory support.

Causes and associations. Hypertensive crisis, acute coronary syndrome, acute valve regurgitation, bilateral renal artery stenosis, non-compliance with antihypertensives, sympathomimetic drugs and poor diastolic function.

Pathophysiology. Surge in catecholamines raises systemic vascular resistance and shifts blood from the periphery to the chest. Left ventricular afterload rises, stroke volume falls, left atrial pressure increases and the lungs fill, causing hypoxia that drives further sympathetic output.

Presentation is extreme breathlessness, inability to speak, sweating, agitation, pink frothy sputum, cool clammy skin, hypertension (often over 180 mmHg), tachycardia, hypoxia, diffuse crackles and wheeze, and tripod posture. Peripheral oedema may be absent.

Red flags.

• Saturation under 90%, exhaustion or drowsiness.
• ST elevation or ongoing chest pain.
• Systolic pressure falling to under 100 mmHg.

Diagnosis is clinical. Use bedside ultrasound (B lines, left ventricular function, valves), ECG, troponin, natriuretic peptide, chest radiograph, arterial gas and lactate, and creatinine. Do not delay treatment for tests.

Differential diagnosis. Acute coronary syndrome, severe asthma or COPD exacerbation, pneumonia, pulmonary embolism, aortic dissection, acute valvular regurgitation, and negative pressure or non-cardiogenic oedema.

Sit upright and give oxygen to keep saturation 94 to 98%.

Positive pressure support. Continuous positive airway pressure 5 to 10 cmH2O, or bilevel support, started at once and titrated to comfort and saturation. This reduces preload and afterload and often avoids intubation. Intubate for exhaustion, hypoxia, acidosis or reduced consciousness despite support.

High dose nitroglycerin (first line).

• Sublingual glyceryl trinitrate 400 to 800 microgram (1 to 2 sprays or tablets) every 5 minutes while IV access is established.
• IV infusion starting at 100 microgram/min and increasing by 50 to 100 microgram/min every 3 to 5 minutes to a usual maximum of 400 microgram/min as blood pressure allows, with reduction when pressure falls. Some centres give an initial IV bolus of 400 to 1000 microgram over 2 to 3 minutes with close monitoring (evidence is limited). Conventional doses (10 to 200 microgram/min) are insufficient for this presentation.
• Avoid with right ventricular infarction, severe aortic stenosis and recent phosphodiesterase-5 inhibitor use (sildenafil within 24 hours, tadalafil within 48 hours).

Alternatives. Nicardipine 5 mg/h IV, titrated by 2.5 mg/h every 5 to 15 minutes (maximum 15 mg/h), or nitroprusside 0.3 to 0.5 microgram/kg/min (maximum 10 microgram/kg/min, short term), or enalaprilat 1.25 mg IV over 5 minutes (avoid in acute infarction, renal artery stenosis and renal failure).

Diuretic. Furosemide 40 mg IV only if there is clinical fluid overload (previous diuretic use, oedema, weight gain), because many patients are not volume overloaded and may become hypovolaemic.

Avoid morphine (associated with worse outcomes), beta blockers in acute decompensation, and fluid boluses.

Treat the cause. Coronary reperfusion for infarction, valve surgery for acute regurgitation, antihypertensive control, and treatment of arrhythmia.

Monitoring. Continuous ECG, oximetry, blood pressure every 5 minutes at first, respiratory rate, urine output and arterial gas.

Referral and escalation. Cardiology and intensive care if there is no response within 30 to 60 minutes, or for ischaemia, valve disease or renal artery stenosis.

Special groups. In pregnancy, give nitroglycerin, furosemide cautiously and treat the cause (including peripartum cardiomyopathy and pre-eclampsia). In renal impairment, avoid nitroprusside accumulation and enalaprilat.