Features:
- tachypnoea – acutely breathless
- anxious, cold, sweaty
- productive cough – pink, frothy (wheeze)
- tachycardia – raised JVP, gallop rhythm
- crackles and rhonchi
CXR
- fine diffuse haziness: blurring (interstitial) vessel margins: Pcap > 20 mmHg
- Kerley ‘B’ lines
- Perihilar (alveolar) haziness (“bat-wing” appearance): Pcap > 30 mmHg
Causes
- Left Ventricular Failure (LVF)
- Mitral Stenosis (MS)
- precipitating factors for decompensation: e.g., arrhythmia, infection, etc.
Treatment
- identify and treat precipitating causes
- arrhythmia
- infarction
- infection
- patient sitting up: reduces the ventilation–perfusion mismatch and assists with their work of breathing
- high FiO2 (~ 60%)
- ECG
- CCU
- morphine IV: reduce anxiety (and avoid neurogenic / primary pulmonary oedema)
- frusemide 20-80 mg slow IV bolus (at 4 mg/min) q 20 min x 1
- glyceryl trinitrate: 600 mcg buccal q5 min x 3
- 5–10 microgram per min infusion, double every 5 min to max. 200 microgram per min.
- continue digoxin
- Non-Invasive Ventilation:
- CPAP: 10 cm water pressure
- BiPAP: 10/4 cm water pressure
In “Managing acute pulmonary oedema,” Purvey and Allen discuss the role of each of the therapeutics:
Nitrates: The mechanism of nitrate action is smooth muscle relaxation, causing venodilatation and consequent preload reduction at low doses. Higher doses cause arteriolar dilatation, resulting in reduced afterload and blood pressure. Specifically in the coronary arteries, this dilatation results in increased coronary blood flow. These actions collectively improve oxygenation and reduce the workload of the heart. In general practice nitrates can be given sublingually. Hospitals may use infusions as intravenous administration is preferred due to the speed of onset and the ability to titrate the dose. Despite the widespread use of nitrates in acute pulmonary oedema, there is a lack of high-quality evidence to support this practice. When nitrates have been compared to furosemide (frusemide) and morphine, or furosemide alone, there has been no difference in efficacy for outcomes such as the need for mechanical ventilation, change in blood pressure or heart rate, and myocardial infarction. Nitrates are associated with hypotension and therefore blood pressure monitoring is essential to ensure the systolic blood pressure is maintained above 90 mmHg. They should not be given if the systolic blood pressure is less than 90 mmHg or the patient has severe aortic stenosis, as these patients are preload dependent. If the patient has recently taken a phosphodiesterase inhibitor, such as sildenafil, nitrates are contraindicated. Nitrates are generally well tolerated with the most common adverse effect being headaches. Other adverse effects include reflex tachycardia and paradoxical bradycardia. Nitrates are also associated with tachyphylaxis, with tolerance developing within 16–24 hours of continuous administration.
Furosemide: Intravenous administration is preferred, with the dose of furosemide ranging from 40–80 mg. The higher doses in the range are used for patients already taking oral diuretics or with chronic kidney disease. An initial bolus can be given slowly intravenously and repeated 20 minutes later if required. After the bolus, a continuous intravenous infusion may be considered, commencing at a rate of 5–10 mg per hour. A small randomised controlled trial did not find any difference in outcomes between bolus and continuous infusion. Higher doses have been associated with greater improvement in dyspnoea. They are also associated with worsening of renal function and increased admissions to intensive care, but this association is likely to reflect more severe disease. In hospital, insertion of an indwelling catheter helps to monitor urine output. There is a lack of controlled studies showing that diuretics are of benefit in acute pulmonary oedema. However, diuretics are indicated for patients with evidence of fluid overload. Loop diuretics such as furosemide reduce preload and should be withheld or used judiciously in patients who may have intravascular volume depletion. The oral bioavailability of furosemide (frusemide) is approximately half that of the intravenous formulation, less with splanchnic congestion.
Morphine: In the absence of high-quality randomised trial data, the best current evidence suggests that morphine may cause harm. Morphine is therefore no longer recommended for routine use in acute pulmonary oedema. It may be beneficial if there is ongoing chest pain resistant to nitrates. Low doses of morphine (1–2.5 mg) can be useful to facilitate the tolerance of non-invasive ventilation but the patient needs to be monitored for sedation. The adverse effects of morphine include respiratory and central nervous system depression, reduced cardiac output and hypotension. Morphine used for acute pulmonary oedema has been associated with adverse events such as significantly increased rates of mechanical ventilation, intensive care admissions and mortality. Morphine has been part of the traditional treatment for acute pulmonary oedema as it can reduce dyspnoea. This effect was presumed to be secondary to venodilatation, resulting in venous pooling and preload reduction. However, this mechanism of action is now being questioned. Morphine also reduces sympathetic nervous activity and can reduce the anxiety and distress associated with dyspnoea.
Ventilatory support: Oxygen is not routinely recommended for patients without hypoxaemia as hyperoxaemia may cause vasoconstriction, reduce cardiac output and increase short-term mortality. There is a risk that prescribing oxygen for a breathless patient in the absence of hypoxaemia may mask clinical deterioration and hence delay appropriate treatment. Supplemental oxygen and assisted ventilation should only be used if the oxygen saturation is less than 92%. If required, oxygen should be administered to achieve a target oxygen saturation of 92–96%. Depending on the clinical scenario, oxygen titration can occur using a number of oxygen delivery devices. These include up to 4 L/minute via nasal cannulae, 5–10 L/minute via mask, 15 L/minute via a non-rebreather reservoir mask or high-flow nasal cannulae with fraction of inspired oxygen greater than 35%. For patients with chronic obstructive pulmonary disease, the target oxygen saturation is 88–92% and the use of a Venturi mask with inspired oxygen set at 28% is recommended. If the patient has respiratory distress, acidosis or hypoxia, despite supplemental oxygen, non-invasive ventilation is indicated. There is no significant clinical benefit of bi-level positive airway pressure ventilation (BiPAP) over continuous positive airway pressure ventilation (CPAP), so the modality chosen should be guided by local availability. Non-invasive ventilation should be commenced at 100% oxygen with recommended initial settings of 10 cm of water pressure for CPAP and 10/4 cm water pressure (inspiratory positive airway pressure/expiratory positive airway pressure) for BiPAP. Contraindications to non-invasive ventilation include hypotension, possible pneumothorax, vomiting, an altered level of consciousness or non-compliance. If, despite non-invasive ventilation, there is persistent hypercapnia, hypoxaemia or acidosis, then intubation should be considered. Other indications for intubation include signs of physical exhaustion, a decreasing level of consciousness or cardiogenic shock. Endotracheal intubation is only indicated in a very limited number of cases and carries inherent risks and challenges. The rapid sequence induction needs to be modified to account for the haemodynamic compromise of the patient. After intubation constant suctioning is usually required and ventilation can be very challenging. Additionally, positive pressure ventilation is likely to potentiate any hypotension.
Inotropic support: Intravenous inotropic drugs are indicated in acute pulmonary oedema when there is hypotension and evidence of reduced organ perfusion. Their use is limited to this clinical situation in critically ill patients as they are associated with a longer length of hospital stay and increased mortality. In cases of impaired left ventricular function and hypotension, first-line therapy is an intravenous infusion of dobutamine. As well as its positive inotropic actions, dobutamine has peripheral vasodilatory effects that can result in worsening hypotension, which may require management with a vasopressor. Dobutamine can cause arrhythmias and is contraindicated if the patient has ventricular arrhythmias or rapid atrial fibrillation. Another inotrope that may increase cardiac output and improve peripheral perfusion is milrinone. It should only be used for the short-term management of severe heart failure that has not responded to other treatments. Milrinone may increase mortality in acute exacerbations of chronic heart failure. It can be considered in patients with chronic beta blockade.
Chioncel, Ovidiu et al. “Pulmonary Oedema-Therapeutic Targets.” Cardiac failure review vol. 1,1 (2015): 38-45. doi:10.15420/CFR.2015.01.01.38.
Iqbal MA, Gupta M. Cardiogenic Pulmonary Edema. [Updated 2020 Dec 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK544260/.
Purvey M, Allen G. Managing acute pulmonary oedema. Aust Prescr 2017;40:59-63. https://doi.org/10.18773/austprescr.2017.013.
