Pulmonary edema is a broad descriptive term and is usually defined as an abnormal accumulation of fluid in the extravascular compartments of the lung 1. Acute pulmonary oedema is a medical emergency which requires immediate management. It is characterised by dyspnoea and hypoxia. Int J Tuberc Lung Dis. Feb;15(2), i. Pulmonary edema: pathophysiology and diagnosis. Murray JF(1). Author information: (1)University of California.
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Acute pulmonary oedema has a high mortality. It requires emergency management and usually admission to hospital. The goals of therapy are to improve oxygenation, maintain an adequate blood pressure for perfusion of vital organs, and reduce excess extracellular fluid.
The underlying cause must be addressed. There is a lack of high-quality evidence to guide the treatment of acute pulmonary oedema. The strongest evidence is for nitrates and non-invasive ventilation.
Pulmonary edema – Wikipedia
Diuretics are indicated for patients with fluid overload. Furosemide frusemide should be given by slow intravenous injection. Routine use of morphine is not recommended because of its adverse effects. Oxygen should only be administered in cases of hypoxaemia. Inotropic drugs should only be started when there is hypotension and evidence of reduced organ perfusion.
In these cases, dobutamine is usually first-line treatment. Acute pulmonary oedema is a medical emergency which requires immediate management.
Other causes include pulmonary embolus, anaemia and renal artery stenosis. There are no current Australian data on the incidence of acute pulmonary oedema or heart failure.
However, self-reported data from —12 estimated that 96 adults had heart failure, with two-thirds of these being at least 65 years old. There ede,a several different clinical guidelines for the management of acute pulmonary oedema. The goals of treatment are to provide symptomatic relief, improve oxygenation, maintain cardiac output and perfusion of vital organs, and reduce excess extracellular fluid.
Any underlying cause should be identified when starting treatment. The drugs used in treatment include nitrates, diuretics, morphine and inotropes.
Some patients will require ventilatory support. A working algorithm for the management of acute pulmonary oedema in the pre-hospital setting is outlined in the Figure.
Managing acute pulmonary oedema
Despite the widespread use of nitrates in acute pulmonary oedema, there is a lack of high-quality evidence to support this practice. When nitrates pulmoum 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. Pulmoum mechanism of nitrate action is smooth muscle relaxation, causing venodilatation and consequent preload reduction at low doses.
Specifically in the coronary arteries, this dilatation results in increased coronary blood flow. In general practice nitrates can be given sublingually. Hospitals may use efema as intravenous administration is preferred due to the speed of onset and the ability to titrate the dose Table 1. References 8 and Nitrates are associated with hypotension and therefore blood pressure monitoring is essential to ensure the systolic blood pressure is maintained above 90 mmHg.
Nitrates are generally well tolerated with the most common adverse effect being headaches. Other adverse oulmonum include reflex tachycardia and eedema bradycardia. 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.
Intravenous administration is preferred, with the dose of furosemide ranging from 40—80 mg Table 2. An initial bolus can be given slowly intravenously and repeated 20 minutes later if required.
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. References 128and Morphine has been part of the traditional treatment for acute pulmonary oedema as it can reduce dyspnoea.
The adverse effects of morphine include respiratory and central nervous system depression, pulmonumm cardiac output and hypotension. Morphine used for acute pulmonary oedema has been associated with adverse events such as significantly increased rates pulomnum mechanical ventilation, intensive care admissions and mortality.
Pulmonary oedema | Radiology Reference Article |
Morphine is therefore no longer recommended for routine use in acute pulmonary oedema. The first step in improving ventilation for patients with pul,onum pulmonary oedema is to ensure that they are positioned sitting up. Oxygen is not routinely recommended for patients without hypoxaemia as hyperoxaemia may cause vasoconstriction, reduce cardiac output and increase short-term mortality.
Depending on the clinical scenario, oxygen titration can occur using a number of oxygen delivery devices. If the patient has respiratory distress, acidosis or hypoxia, despite supplemental oxygen, non-invasive ventilation is indicated. If, despite non-invasive ventilation, there is persistent hypercapnia, hypoxaemia or acidosis, then intubation should be considered.
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. Intravenous inotropic drugs are indicated in acute pulmonary oedema when there is hypotension and evidence of reduced organ perfusion.
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. This includes reviewing their medicines to see if any drugs, such as non-steroidal anti-inflammatory drugs, verapamil or diltiazem, could have contributed to the problem. Additional monitoring including daily weights, and measurements of serum electrolytes and renal function is also recommended. Once the patient with cardiogenic acute pulmonary oedema has been stabilised the goal of therapy is to improve long-term outcomes.
If an echocardiogram shows a preserved left ventricular ejection fraction, the focus is to treat any associated conditions. This includes the management of hypertension with antihypertensive drugs, reduction of pulmonary congestion and peripheral oedema with diuretics, and rate control for atrial fibrillation.
If there is evidence of a reduced ejection fraction and chronic heart failure then an ACE inhibitor, beta blocker and mineralocorticoid receptor antagonist should be considered.
ACE inhibitors are best started at 24—48 hours after admission, provided the patient is haemodynamically stable. Mineralocorticoid receptor antagonist drugs, such as spironolactone, are best started soon after discharge with careful monitoring of blood pressure, serum potassium and renal function. Guidelines have highlighted that there is a lack of evidence to support the currently used therapies.
Additionally there are concerns regarding the efficacy and safety of these treatments for acute pulmonary oedema. There has therefore been a shift over the last few years to favour nitrates and non-invasive ventilation as first-line management. However, opioids and diuretics may have a role in some patients. National Center for Biotechnology InformationU. Journal List Aust Prescr v. Published online Apr 3. Author information Article notes Copyright and License information Disclaimer.
This article has been cited by other articles in PMC. Introduction Acute pulmonary oedema is a medical emergency which requires immediate management. Open in a separate window. Nitrates Despite the widespread use of nitrates in acute pulmonary oedema, there is a lack of high-quality evidence to support this practice. Diuretics There is a lack of controlled studies showing that diuretics are of benefit in acute pulmonary oedema.
Table 2 Recommended doses of furosemide frusemide. Morphine Morphine has been part of the traditional treatment for acute pulmonary oedema as it can reduce dyspnoea. Ventilatory support The first step in improving ventilation for patients with acute pulmonary oedema is to ensure that they are positioned sitting up. Inotropes Intravenous inotropic drugs are indicated in acute pulmonary oedema when there is hypotension and evidence of reduced organ perfusion.
Conclusion Guidelines have highlighted that there is a lack of evidence to support the currently used therapies. Footnotes Conflict of interest: Acute pulmonary oedema – management in general practice. Aust Fam Physician ; Treatment of acute decompensated heart failure: Updated 5 December Long-term prognosis of acute pulmonary oedema–an ominous outcome. Eur J Heart Fail ; 2: Flash pulmonary oedema and bilateral renal artery stenosis: Eur Heart J ; Australian Institute of Health and Welfare.
Cardiovascular disease, diabetes and chronic kidney disease: Krum H, Abraham WT. Eur J Heart Fail ; Acute cardiogenic pulmonary oedema. Therapeutic Guidelines Limited; Thoracic Society of Australia and New Zealand oxygen guidelines for acute oxygen use in adults: Pharmacotherapy for acute heart failure syndromes.