Dyspnoea III – Pulmonary oedema EMC SDMH 2015
Define the pulmonary oedema syndrome and understand differing aetiologies Recognise predisposing and precipitating factors in cardiogenic pulmonary oedema Outline ED treatment modalities Objectives
Pulmonary oedema = fluid translocation into alveolar air spaces due to changes in pulmonary capillary properties Due to either altered capillary permeability(‘leakiness’) Altered transmembrane pressure gradient Two distinct groups – High (>20mmHg) pulmonary capillary pressure (‘Cardiogenic’) Low (<20mmHg) pulmonary capillary pressure (‘Non-cardiogenic’) Pathophysiology
Cardiogenic pulmonary oedema Progressive, accelerating cycle Accumulation of fluids alveolar collapse loss of lung capacity(FRC) increased work of breathing to inflate ‘waterlogged’ lung Cardiogenic pulmonary oedema
Cardiogenic pulmonary oedema = syndrome of ‘transient’ LV failure WHY does this individual have cardiogenic pulmonary oedema? ~40-60% will have normal LVEF; not oedematous NOT synonymous with ‘CHF’ Raises concept of ‘diastolic’ vs ‘systolic’ LV failure Cardiac failure?
Systolic/Diastolic failure
Other acute causes APO may have several other acute causes -’Pump failure’ - Valve failure RVF in isolation (eg chronic pulmonary disease) does not cause APO Overlaps possible Other acute causes
Precipitants Frequently an acute triggering event Coronary event Needs to be sought and corrected if possible Mnemonic – ‘CHIVE MAN’ Coronary event Hypertensive episode Infection Volume overload/Valve Embolism Medication changes Arrhythmia(AF) Non-compliance Precipitants
Management Principles of treatment -Reverse hypoxia -Reduce WoB -Decrease SVR -Improve cardiac output -Seek and remove triggering factors Management
Breathing High flow O2 to keep Sats >95% NIPPV as soon as available PEEP recruits collapsed alveoli Reduces WoB and restores FRC with each breath cycle CPAP/BiPAP equally efficacious at reducing need for intubation Potential for hypotension 10-30% mask intolerance Breathing
Circulation Aim to reduce preload and afterload to assist failing LV PEEP reduces both by instituting intra-thoracic pressure Effect can be increased by use of nitrates GTN SL or by infusion. GTN 600mcg SL q 5 equivalent to 60mcg/min infusion Action primarily by venodilation + preload reduction May cause hypotension. Avoid in Aortic Stenosis Circulation
Diuretics Mainstay of treatment for 40 + yrs Primarily useful in volume overload APO Utility in hypertensive diastolic LVF? Postulated to have venodilating and diuretic effect Frusemide should produce diuresis in 15-20mins Diuretics
CXR – Confirmatory for diagnosis; exclude other causes of severe dyspnoea ECG – ACS; arrhythmia FBC – Check for anaemia UEC – Na, K and renal parameters. Consider checking Mg Troponin – ACS ; beware high sensitivity results BNP ?- Clinical APO more sensitive and specific. ABG? – Not required Investigations
Challenging scenarios APO in the Dialysis patient APO with rapid AF APO with hypotension Challenging scenarios
APO and the dialysis pt Often true volume overload Prone to all other causes of LVF however!! Unable to remove salt/H2O Often respond well to NIPPV/nitrates Require emergent transfer to acute dialysis centre/ICU APO and the dialysis pt
Check for background history of AF and if rate appropriate New onset AF requires control Avoid –ve inotrope Amiodarone 5mg/kg q 60min If fails with clinical deteriorationcardioversion Digoxin unlikely to help acutely APO and rapid AF
APO and hypotension Potentially = cardiogenic shock Check to ensure PEEP correct Assess cause and prognosis Senior intervention with Cardiology and ICU STEMI/ACS Retrieve to Cath. Centre (?Cardiothoracic) Dobutamine 2.5-20 mcg/kg/min OR Adrenaline .01-1 mcg/kg/min Consider early intubation (high risk) APO and hypotension
Questions?
Summary APO = syndrome, not a diagnosis APO is due to LV failure which may be either due to systolic or diastolic failure NIPPV improves both oxygenation and cardiac performance Seek precipitating causes and treat Beware the hypotensive APO patient Summary