Important questions when managing cardiogenic acute pulmonary oedema ?

What are we talking about  ?

APE is usually defned by the sudden increase in pulmonary capillary wedge pressure as a result of acute and fulminant left ventricle (LV) (systolic and/or diastolic) failure or acute severe mitral regurgitation . Among the various clinical phenotypes of acute heart failure (AHF), four major clinical presentations can be described with possible overlaps between them and APE represents 30–80% of AHF clinical phenotypes . Clinical criteria  :

related to lung 

• congestion include dyspnea with orthopnea. 
• increased respiratory rate.
•  increased work of breathing and respiratory failure .
•  Hypoxia is a mandatory feature of APE.  potential overlap between ARDS and APE since ARDS defnition includes “Respiratory failure not completely explained by excessive volume loading or cardiac failure.

How about pathophysiology?

Pathobiology of APE is more complex than the hydrostatic vs. the permeability dichotomy previously used . 

Alveolar oedema is generated by a rapid increase in the hydrostatic pressure in the pulmonary capillaries and has a low protein concentration compared to plasma . Resolution of this APE is usually rapid, mainly because the alveolar-epithelial barrier is not damaged . Sustained pulmonary injury might happen in relation with disruption in alveolar capillary units leading to acute infammation. 

Organ cross talk: which actors?

 APE leads to a cascade sequence of inter-organ crosstalk, including lungs and kidneys, but also liver, intestine, brain, neuro-endocrine and vascular system . Congestion is an essential pathophysiological mechanism leading to organ dysfunction. 

Hypoperfusion can also contribute in cases of cardiogenic shock .Neurohormonal and infammatory response to systemic congestion and/or peripheral hypoperfusion, may further contribute to organ injury. However, all the pathophysiological mechanisms remain incompletely understood. 

How to recognise it ? 

Early diagnosis of APE is dependent on history, clinical exam, and few diagnostic modalities . Natriuretic peptide measurements should be integrated into the interpretation of clinical signs and symptoms, since they are accurate to confIrm heart wall stressor and rule out APE.

 They must be completed with :

• chest X-Ray, bedside lung and cardiac ultrasonography. 
• When APE is suspected, an integrative approach is recommended, including determination of cardiopulmonary instability, evaluation of congestion and determining underlying causes/precipitants .

What are the goals of management?

 Goals of APE management  are to improve oxygenation, maintain an adequate blood pressure and reduce excess extracellular fluid .  whilst addressing the underlying cause . Due to the challenges of undertaking high-quality research in the field, many recommendations that underline management decisions are largely based on expert consensus rather than robust evidence .

How to ensure adequate oxygenation? 

Pulmonary oedema increases up to 20-fold the work of breathing and oxygen consumption . This major physiological stress on the heart can be partially relieved by noninvasive ventilation (NIV), either continuous positive airway pressure (CPAP) or pressure support ventilation with positive end-expiratory pressure, which improves oxygenation and ventilation. 

NIV decreases cardiac preload and LV afterload, increases right ventricule (RV) afterload and finally facilitates cardiac function . NIV should be used in patients with APE in order to reverse respiratory failure faster, avoid endotracheal intubation and, with lower evidence, potentially reduce mortality in high-risk patients . Of note, 50%  of APE require invasive ventilation . 

High fow oxygenation (HFO) may improve oxygenation and respiratory rate in APE patients and may potentially be an alternative to NIV. However, initiation of invasive ventilation should not be delayed if APE patients do not improve under HFO .

How to use loop diuretics?

Intravenous (IV) loop diuretics to achieve decongestion is the cornerstone of APE therapy . They act as immediate venodilator and subsequent diuretic agent (i.e. increasing renal sodium and water output), usually rapidly relieving symptoms . High diuretic doses induce a faster improvement of dyspnea, change in weight and net fluid loss, however, they may cause greater neuro-hormonal activation, electrolyte abnormalities and are associated with poorer outcomes . It may be appropriate, to start IV diuretic treatment using low doses and to assess the diuretic response (hourly urine output and urine sodium content) .

 Of note respiratory improvement is the goal of the treatment and monitoring diuresis in patient for whom we did not reach yet that goal may help to adjust treatment. If there is an insufficient diuretic response , the loop diuretic dose can be increased, followed by concomitant administration of thiazides Impaired diuretic response is associated with increased rehospitalization and mortality compared with patients having normal diuretic response .

How to avoid readmission? 

Persistent congestion before discharge is associated with a higher risk of readmission and mortality . Once respiratory and hemodynamic stabilization is achieved, treatment should be optimized before discharge. Treatment optimization has three major aims; 

• (1) to relieve congestion; 
• (2) to treat comorbidities .
• (3) to initiate, or restart oral medications . In this way, the question of the early introduction of ACE-inhibitors should be addressed in APE with LV systolic and diastolic dysfunction . Beta-blockers are potentially dangerous if used acutely when the patient is unstable but should be restarted in patients already on beta-blockers. The cardiologist should be involved and follow these patients .