Clinical Management

The priorities are to relieve symptoms and to restore haemodynamic stability and tissue perfusion. The approach to management is summarised in Table 1.

Table 1: Emergency Management of CPO
Airway Positioning
Breathing High flow O2
Circulation Nitrates
Disability Morphine
Exposure Positioning


Allow the patient to find the best position for their airway and breathing.  If the airway is compromised intervene as required.  This may be due to (i) a reduction in conscious level due to hypoxia, hypercapnoea or excessive opiate administration, or (ii) due to pulmonary oedema fluid exuding from the lungs.


  • British Thoracic Society Guidelines suggest in acute heart failure, aim for an oxygen saturation of 94-98% [2].
  • High flow O2: 15L/minute with a reservoir bag is required for most patients, as hypoxia is frequently the key problem
  • Patients with coexistent COPD or otherwise at risk of hypercapnia need careful monitoring. When feasible the inspired O2 can be reduced to achieve target saturations of 88-92%.
  • Once non-invasive ventilation (NIV) is initiated, O2 supplementation will still be required

Non-invasive Ventilation (NIV)

The aim of NIV is to improve oxygenation, decrease the work of breathing and increase cardiac output.  Continuous Positive Airways Pressure (CPAP) provides a constant level of positive airways pressure preventing alveolar collapse.  Bi-level Positive Airways Pressure (BiPAP) enables increased CO2 clearance by providing a higher level of positive pressure on inspiration.

Evidence base for NIV in CPO

A Cochrane Review (2008) systematically reviewed the research data published prior to 2005 and concluded that NIV should be considered and implemented in all CPO patients early unless contraindicated.  The Review reported that:

(i) CPAP decreased intubations, mortality and length of ITU stay and that

(ii) BiPAP may be of use in CO2-retaining patients but that more research was required.  In order to avoid one death, the number needed to treat (NNT) with CPAP was 9 and to avoid 1 intubation the NNT with CPAP was 6 [3].

The 3CPO trial also published in 2008 is the largest multicentre RCT which compared standard medical therapy to BiPAP and CPAP [4].  This study found no reduction in mortality or intubation rates in either of the NIV groups but patients felt better more quickly. There was no evidence of additional harm.

The ESC recommends that all CPO patients should be considered for NIV early on in their management (unless contraindicated) [1].

Consider NIV early in the management of all patients with cardiogenic pulmonary oedema, unless contraindicated.

Practical aspects to NIV

Table 2: Practical aspects to NIV
Indications • Consider in all patients with CPO
• Particularly pH<7.35
• Respiratory rate >20/min
Cautions • Right ventricular failure
• Cardiogenic shock
• Severe obstructive airways disease
• Agitated patient
Contraindications • Immediate endotracheal intubation indicated
• Respiratory arrest or inadequate spontaneous ventilation
• Worsening life threatening hypoxia
• Unconscious patient – unable to protect own airway
How to deliver NIV • Correctly fitting mask
• Supplemental O2
• Commence PEEP at 5-7.5 cm H2O and increase to 10 cm as tolerated
• Continue for 30min/hr until reduction in dyspnoea and saturations are maintained off NIV
Complications • Intolerance due to anxiety, skin/eye discomfort, dry mouth
• Worsening right ventricular failure
• Hypercapnoea
• Pneumothorax
• Aspiration



Loop diuretics reduce preload by preventing sodium chloride reabsorption in the ascending Loop of Henle, which increases fluid excretion.  Preload is also reduced by their vasodilatory action. Both of these actions should be beneficial in a patient with CPO and fluid overload.

For decades diuretics have been the accepted mainstay of treatment in CPO despite a lack of randomised controlled trials demonstrating beneficial outcome; there is some evidence suggesting a detrimental effect at high doses [1,5-8]. Specifically, their use may dehydrate the euvolaemic patient and cause hyponatraemia and hypotension. Also, due to their effect on the renin/angiontensin/aldosterone system and stimulation of the sympathetic system, diuretics may increase afterload thereby decreasing stroke volume and cardiac output.

Patients with CPO generally have elevated systemic vascular resistance and reduced renal perfusion and consequently diuretic action may be delayed by up to 1 hour. It is probably only the vasodilatory action of diuretics that is initially beneficial and this can also be achieved with IV nitrates [5].

The ESC Guidelines advocate small intravenous boluses of furosemide at 20-40mg for patients with CPO and symptoms of fluid overload or congestion. In those with CPO already taking chronic diuretic therapy, the initial IV bolus should be at least equivalent to their usual oral dose [1].


These agents have positive physiological effects by off-loading the heart through their venous and/or arteriolar vasodilatory effects causing a reduction in pre-load and/or after-load. Vasodilators should not be used in patients with a systolic blood pressure of less than 90mmHg or in those with aortic stenosis (who are dependent on sufficient preload to force blood across the gradient).


The majority of patients with CPO have a high-end-of-normal blood pressure at presentation and are able to tolerate nitrates. Initially administer sublingual nitrates until intravenous access is established and then commence IV at a rate of 10-20mcg/min, increasing every 3-5 min by 5-10 mcg/min as needed and as BP allows, up to a maximum of 200mcg/min [1].


• This is an alternative vasodilator which reduces preload and afterload.  It is particularly useful in the rare cases of extreme hypertension precipitating CPO (ie. in a hypertensive emergency)
• It can precipitously drop the systolic blood pressure but tolerance is not an issue as it is with nitrates.
• The ESC 2016 guidelines suggest cautiously commencing an infusion at 0.3 mcg/Kg/min (titrated up to 5 mcg/Kg/min) with invasive blood pressure monitoring [1]


• This is a recombinant B-type natriuretic peptide with both a diuretic and natriuretic effect, as well as being a venous and arterial vasodilator.
• It is currently used in the USA but has limited licensing in the UK and Europe [1]


Inotropes should be considered if hypotension or signs of end organ hypoperfusion persist despite use of vasodilators/diuretics.

They should be commenced early once the need is recognised and stopped as soon as adequate tissue perfusion is achieved.

Their use is associated with increased mortality, as they increase cardiac oxygen demand and myocardial injury.
Dobutamine is probably the first choice agent.  Infusion is commenced at 2-3mcg/kg/min and increased as required [1]


Morphine should be given early for patients who are agitated and distressed or complaining of chest pain.

Opiates also provide a potential physiological benefit due to their vasodilatory effects and resultant reduction in pre-load.

Only small boluses of 2.5-5 mg are recommended as opiates may cause hypotension and/or respiratory depression [1]


Position the patient sitting upright supported with pillows as appropriate for their conscious level.

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