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Pulmonary oedema is a broad descriptive term and is usually defined as an abnormal accumulation of fluid in the extravascular compartments of the lung parenchyma. This process leads to diminished gas exchange at the alveolar level, progressing to potentially causing respiratory failure.
Its etiology is either due to a cardiogenic process with the inability to remove sufficient blood away from the pulmonary circulation or non-cardiogenic precipitated by injury to the lung parenchyma.
It is an important pathologic feature in many disease processes
Determining the underlying disease process is crucial to guide its management.
Clinical features include progressive worsening dyspnea, rales on lung auscultation, and worsening hypoxia[1]
Image R: circled area on Xray showing region of pulmonary oedema
Clinical Presentation
The clinical presentation of pulmonary oedema includes:
Progressively worsening dyspnea, tachypnea, and rales (or crackles) on examination with associated hypoxia.
Cough, with pink foaming at the mouth (due to hypoxemia from alveolar flooding).
Distress
Auscultation - mainstay of bedside assessment in all patients with respiratory symptoms. Specifically, hearing of either fine or coarse crackles is very crucial to management.
Fine crackles are heard in cardiogenic pulmonary edema. They exclusively heard in the inspiratory phase when the small airways, which were shut during expiration, open abruptly[1][2]
Management
Therapeutic goals in patients with pulmonary edema include alleviation of symptoms and treatment of the underlying pathologic condition.
Management consists of the improvement of gas exchange by methods that range from supplemental oxygen administration to mechanical ventilatory support with PEEP, depending on the severity of the disturbance in lung function.
Diuretics remain the mainstay of treatment, and furosemide being the most commonly used medication. Higher doses are associated with more improvement in dyspnea, however, also associated with transient worsening of renal function.
Vasodilators can be added as an adjuvant therapy to the diuretics in the management of pulmonary edema.
IV nitroglycerin (NTG) is the drug of choice, and it lowers preload and pulmonary congestion. NTG should only be used when the systolic blood pressure (SBP) is > 110 mm Hg. The following lists the different formulations of nitroglycerin.
aerosol solution
packet
pumpspray
tablet
all above dissolve under the tongue#
apply to the skin - ointment or 24-hour patch
Nesiritide is a recombinant brain natriuretic peptide which has vasodilatory properties.
Newer drugs like serelaxin, or Clevidipine may also be used
Nifedipine has been utilized in the prophylaxis and treatment of high altitude pulmonary edema (HAPE). This calcium channel blocker counteracts the hypoxia-mediated vasoconstriction of the pulmonary vasculature.
Inotropes, such as dobutamine and dopamine, are used in the management of pulmonary congestion when associated with low SBP and signs of tissue hypoperfusion.
Significant adverse events include tachyarrhythmias, ischemia, and hypotension.
Ionotropes - Influence the force or speed of muscular contractility. Inotropic agents are used to improve the output of the heart in the treatment of eg heart failure[3].
Morphine reduces systemic vascular resistance and acts as an analgesic and anxiolytic. It has been used in the management of pulmonary edema secondary to acute coronary syndrome. However, it may cause respiratory depression needing intubation and generally not recommended.
Ventilatory support, both noninvasive and invasive, is used to improve oxygenation, direct alveolar, and interstitial fluids back into the capillaries, improve hypercarbia and hence reverse respiratory acidosis, and lastly, tissue oxygenation. It also aims at reducing the work of breathing.
The decision to provide ventilatory support is based on clinical improvement with a trial of the above-mentioned drugs, patient's mental status, overall energy, or lack of such.
In patients on invasive mechanical ventilation, continuous monitoring of hemodynamics is essential as a reduction in preload can lead to reduced cardiac output and thus a fall in SBP.
Noninvasive mechanical ventilation, when initiated early in the management of pulmonary edema, has been associated with lower occurrences of respiratory muscle fatigue and, thus, reduction in invasive ventilation[1]
Physiotherapy
Physiotherapists play an important role in the medical management of acute pulmonary oedema.
Monitor blood pressure and check medications taken as prescribed
Education
Sleeping positions eg Use foam wedges or elevate the head of bed (may help breathing while client are resting or sleeping). Prescribe a device that will tilt the whole body, or bend your body at the waist. The device should not bend the body at the upper back or neck.
Counselling on a low salt diet, regular exercise, and medication compliance must be emphasized.
Eating a healthy diet - Nutrition advice. Maintaining a healthy weight.
Cardiogenic pulmonary oedema can progress to respiratory failure requiring the utilization of a mechanical ventilator.
ARDS is a complication of acute lung injury with progressive hypoxemia, also requiring intubation and mechanical ventilation[1].
Similar Conditions
High-Altitude Pulmonary Oedema (HAPE) is a similar condition that can occur in individuals ascending altitude, especially greater than 2500m, in a short period of time. [5]
Feel free to read the linked page for more specific information.
