Elizabeth arrives in your ED gasping for air with pink, frothy sputum. She was skiing on the highest peak and developed difficulty breathing.

Richard, a confused patient, has labored respirations of 36, and his lungs reveal crackles three-fourths of the way up. The paramedics were unable to obtain any medical history; however, they did report his bedroom contained paraphernalia used to inject heroin.

Brandon, a pool maintenance man, was overcome with chlorine gas fumes in a closed storage room. He is tachypnic at 40 breaths per minute and is visibly struggling to breathe.

While riding without a helmet, Alice fell off her bicycle. She arrives on a backboard with a cervical collar in place and has profuse bleeding from her scalp and an obvious depressed skull fracture. Suddenly she develops difficulty breathing and attempts to sit up to ease her respiratory distress.

Does this sound like four totally different patients, or will closer observation reveal they all have developed the same underlying disorder — pulmonary edema?

A drowning sensation

Acute PE develops rapidly with a dramatic clinical picture. Air hunger develops along with tachypnea and a productive cough with copious pink, frothy sputum, leading to an impending sense of doom and panic. Often the bubbling “wet” secretions, combined with labored breathing that inadequately satisfies the demand for air, leave the patient feeling as if he or she is “drowning from the inside out.” To compensate, the patient prefers an upright position and uses accessory muscles to assist respiration. The patient is clearly in acute distress and needs the sharpest assessment, diagnostic, and treatment skills the ED has to offer.

PE occurs when pressure within the pulmonary capillaries drives fluid into the pulmonary interstitial tissues. Interstitial edema results, leading to hypoxia, which causes damage and chemical changes to the endothelial cells that line the blood vessels in the lungs.¹ If not corrected rapidly by lymphatic system absorption, this interstitial edema is forced into the alveolar air spaces, reducing oxygenation by obstruction. Small pulmonary vessels rupture, leading to areas of pulmonary hemorrhage — hence the pink-tinged sputum.²

Dyspnea is often the most distressing symptom when PE develops. The increased ventilatory effort, combined with increased use of typical and accessory muscles for respiration, produces an uncomfortable sensation. Combine the physical distress and fatigue of breathing with the emotional awareness and urgency that one simply cannot “get enough air,” and you have the recipe for an intensely anxious patient who needs immediate attention.

Other physical findings can include hypertension; jugular venous distention; laterally displaced apical pulse; lower extremity edema, especially in the early phase; cold, gray, cyanotic, diaphoretic skin; tachypnea; and, depending on the causative factor, pulsus alternans (pulses that alternate between weak and strong intensity that suggest depressed left ventricular function).

Crackles will be audible, and wheezes may also be heard. While dyspnea is present with both cardiogenic- and noncardiogenic-caused PE, some distinct differences exists between the two types. S3 is common with cardiogenic-caused PE. Patients with cardiogenic PE also usually have left ventricular heaves and gallops and cool, cyanotic, diaphoretic skin. Patients with noncardiogenic PE typically present with warm skin.²

The inside story

Pulse oximetry reveals markedly decreased oxygen saturation with PE. Arterial blood gases drawn early will initially reveal a decreased PO2 and PCO2 as the rapid respiratory rate and effort attempt to increase oxygenation. Without rapid intervention, the ability to blow off carbon dioxide is also affected, and the PCO2 increases.

Chest x-ray films will typically reveal bilateral hilar infiltrates (at the root of the lungs at the level of the fourth and fifth vertebrae) that may have a characteristic butterfly shape. Be wary of impending PE, especially in patients who have a previous history of decompensated congestive heart failure (CHF). These patients may actually show negative chest x-ray findings and lack early warning signs until they are in severe distress.³

Now often used as a diagnostic and treatment marker for CHF, B-type natriuretic peptide (BNP), a protein marker released during cardiac dysfunction, is a powerful diagnostic tool for identifying PE, even when readings fall within the medium range of 100 pg/mL to 500 pg/mL. A point-of-care bedside test for BNP is available that provides results in 15 minutes. While helpful, BNP testing is not exclusively diagnostic for CHF or PE. Other circumstances may produce elevated BNP levels within this range, including end-stage renal failure, cirrhosis, hormone replacement therapy, primary pulmonary hypertension, and pulmonary embolism.⁴

Risks to consider

Cardiogenic PE is the most severe manifestation of CHF and the most frequent type of PE in most EDs. Cardiogenic PE represents an imbalance in cardiac pump function in which the heart cannot adequately maintain circulation. But don’t be fooled: PE has many noncardiogenic causes, and being able to differentiate cardiogenic and noncardiogenic causes is important because the subsequent treatments, beyond ensuring the ABCs (airway, breathing, and circulation), may differ significantly.²

The most common cause of CHF that can lead to cardiogenic PE is coronary artery disease that leads to myocardial infarction, especially when the left ventricle is damaged. Hypertension, congenital heart disease, infectious endocarditis, myocarditis, cardiomyopathies, hyperthyroidism, and valvular heart disease are also contributing factors for PE.

Pregnancy may also precipitate cardiogenic PE, often signaling undiagnosed cardiac disease or cardiomyopathies that existed before the pregnancy; the excess fluid volume and cardiac demand associated with pregnancy may be too much for the woman’s heart to effectively manage.²

When pulmonary capillary pressure increases, PE can develop from cardiac and noncardiac causes. Cardiac causes can include mitral stenosis, left ventricular failure from any cause, and bacterial endocarditis. Noncardiac causes include congenital pulmonary vein stenosis, pulmonary venous fibrosis, pulmonary venoocclusive disease, and acute respiratory distress syndrome (ARDS). Probably the most common cause of PE associated with increased pulmonary pressure that many nurses are familiar with is the overinfusion of intravenous fluids.²

Thinking outside the heart …

PE resulting from altered capillary permeability can also be caused by infection (viral or bacterial), inhaled toxins, vasoactive substances (histamine and kinins released after exposure to an allergen), disseminated intravascular coagulation, immunologic reactions, exposure to radiation, uremia, near drowning, aspiration pneumonia, and smoke inhalation.²

When albumin levels drop from nutritional, renal, or hepatic causes, oncotic pressure drops and PE can develop.

Other causes of PE with varied pathophysiology include neurogenic insult or injury, high altitude, narcotic overdose, eclampsia, and cardioversion. PE also can occur after cardiopulmonary bypass surgery and the administration of anesthetics.

With the shifting of care to more community settings, patients are also at a greater risk for experiencing treatment- or diagnostic-procedure-related acute PE that requires immediate transport to the ED. For example, a patient having a CT scan with contrast media may experience a reaction that precipitates PE by increasing intravascular volume, increasing left ventricular diastolic pressure, and congesting pulmonary vasculature with fluid shifting into the alveoli.² Consider also the multitude of patients at oncology treatment clinics who are at risk for transfusion-associated PE, related not only to fluid overload but also to the transfer of antibodies that provoke a reaction.

Patients who opt to have elective surgical procedures like breast implants or liposuction outside the country may also be at increased risk for developing PE both outside the country and when they return to recover in the U.S. Inadequate fluid volume management and varied — or absent — limitations on the volume of fat removed during procedures performed in other countries may contribute to the complications.⁵

Physically active lifestyles and travel to high-altitude locations also lead to a greater risk for PE. In coastal areas, there is a risk of PE from salt-water aspiration during swimming, boating, or other water sports.⁶ In fact, any body of water can pose a PE risk following a near-drowning event — fresh water stream, lake, backyard pool, or bathtub. Aspiration of fresh water is actually much more dangerous than aspiration of salt water because of the profound electrolyte imbalances, sudden increase in blood volume, and hemolysis that occur. Water temperature is also an important factor: The colder the water, the better the potential outcome because the oxygen demands of the body decrease with lower temperatures. In less domesticated environments, envenomation from scorpions can also provoke PE.⁷

PE may also be a result of high-altitude exposure. High altitudes, typically above 8,000 feet, cause increased microvascular permeability and a ventilation/perfusion mismatch. Fluid accumulates in the lung’s interstitial tissues and accumulates more rapidly than the lymphatic system is able to remove it. High altitudes also decrease platelet counts and increases platelet aggregation, especially in the pulmonary microcirculation.⁸ Symptoms of high-altitude pulmonary edema (HAPE) typically develop 24 to 96 hours after a rapid ascent. When HAPE develops at lower levels, underlying pulmonary artery pathology or old pulmonary embolism should be suspected, affecting treatment and diagnostic decisions.⁹

People who are exposed to chemicals and gases at work are at high risk for PE. Exposure to substances such as nitrogen dioxide used by welders produces a subtle onset of symptoms and may not cause severe respiratory distress for as long as 12 hours. But even the do-it-yourself homeowner is at risk for developing chemical-exposure-related PE. Many consumer products pose extreme pulmonary risk if not handled and stored properly. Some gases, such as chlorine and ammonia, cause immediate mucous membrane irritation and respiratory symptoms. Some unusual causes of PE include illicit drug use, airway obstruction and rapid reexpansion of a pneumothorax, or rapid resolution of a pulmonary effusion (see chart, “Pulmonary Edema Causes and Contributing Factors,” on facing page).

Treatment options

Because PE can result from multiple causes, it’s important to identify and treat the underlying cause. All patients should receive continuous ECG and pulse oximetry monitoring. Cardiogenic and noncardiogenic PE require different therapeutic treatment approaches. Lab markers help identify renal and hepatic abnormalities. A 12-lead ECG and serial cardiac enzymes can confirm or reduce suspicion of myocardial ischemia; ventilation/perfusion scans can identify pulmonary embolisms; the CBC can confirm suspicions of infection; and echocardiograms, especially when performed transthoracically, can identify cardiac tamponnade, valvular heart disease, and cardiac wall motion abnormalities.

When fluid overload is a contributing factor, the patient receives diuretics to reduce circulating blood volume — but not for all instances of PE, and that’s why identifying the cause first will help guide the most appropriate treatment.

The treatment of near drowning may vary based on the fluid aspirated. Fresh water passes rapidly across the lung membranes, reducing the usefulness of suctioning. Salt water, because of its hypertonic properties, draws plasma into the lungs, making drainage a desirable treatment option. A Trendelenburg position while suctioning and maintaining positive pressure may be helpful.¹⁰

Morphine is often given to reduce dyspnea, promote vasodilatation, and calm an anxious patient.^9,10 Vasodilatation is desirable because it reduces preload and afterload. An upright position is preferred to reduce venous return and decrease preload.

When chest pain is present without severe hypotension, sublingual nitroglycerine may be a first-line choice. IV nitroglycerin and nitroprusside may be instituted for the patient who is hemodynamically stable. Expect to titrate infusions to keep the blood pressure on the low side, but maintain systolic pressure above 90 mm Hg, especially when diastolic dysfunction is present, to reduce myocardial workload.²

Nesiritide (Natrecor) infusion may be considered. Nesiritide is a recombinant DNA form of human BNP that causes venous and arterial vasodilation, including dilation of the coronary arteries. It’s also a neurohormonal antagonist that helps prevent reflex tachycardia and decreases myocardial oxygen consumption. It leads to rapid vasodilation and a reduction in pulmonary capillary wedge pressure, so congestive symptoms, especially dyspnea, rapidly improve.¹¹ While BNP monitoring is a sensitive diagnostic tool, it’s not helpful in monitoring patients receiving nesiritide therapy. They must be monitored with a test that monitors a BNP precursor, proBNP, instead.

Once stabilized, the patient receives ACE inhibitors, such as lisinopril (Zestril) and enalopril (Vasotec), to help reduce preload and afterload and reverse hemodynamic instability — and reduce the risk for future episodes of PE.¹²

Breathing easier

A patient struggling for air requires immediate oxygenation with a 100% nonrebreather mask, a nonrebreather mask with high-flow oxygen, or a bag-valve-mask device until a more definitive airway and ventilation method are chosen.

Noninvasive positive-pressure ventilation is typically the most effective initial treatment option that can reduce the need for intubation in patients who have acute cardiogenic PE.¹³ Noninvasive ventilation methods include continuous positive airway pressure (CPAP) and bilevel noninvasive pressure support ventilation (NIPSV), methods that have been shown to reduce PE mortality by as much as 45%.¹⁴

The use of CPAP and bilevel positive airway pressure (BiPAP) systems in the ED often averts endotracheal intubation in patients experiencing acute respiratory failure from PE.¹² But this modality is not a viable option for patients with acute facial trauma or airways of questionable intactness or for those who have an altered mental status or are combative or uncooperative.

Positive airway pressure, when combined with pressure support, eases the effort of respiration. Patients receiving this type of oxygen therapy require close supervision and plenty of reassurance — having a mask strapped to one’s face may provoke a claustrophobic feeling and worsen the fear of smothering.

Remember that maintaining positive pressure is important. If you suction patients who require intubation and have copious secretions, remember to suction thoroughly, yet in short intervals to minimize negative pressure.

While treating “wet with wet” may sound odd, humidification during respiratory support is important when PE is related to chemical exposure and lung irritation.

Patients requiring intubation, CPAP, BiPAP, or NIPSV require careful observation for signs of gastric distention, pulmonary aspiration, and respiratory deterioration.

In the future

Researchers are exploring the usefulness of inhaled nitric oxide to improve oxygenation by decreasing ventilation-perfusion mismatches. This treatment option has been found useful in treating PE caused by high-altitude exposure.

Despite new diagnostic and treatment options, the ED nurse must rely on basic physical assessment skills to detect subtle changes that can suggest a worsening clinical picture or a suboptimal response to therapy. Because of facility closures, at-capacity ICUs, and staffing shortages, many ED nurses have to observe patients with PE for longer periods of time, providing care typically given by critical care nurses. Because of the many underlying causes and treatment strategies, PE is one emergency diagnosis that most certainly cannot be treated by a single routine treatment protocol.