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Differential Diagnosis of PULMONARY EDEMA

Myocardial ischemia
High-altitude pulmonary edema
Neurogenic pulmonary edema
Pulmonary embolism
Respiratory failure

Neurogenic pulmonary edema

Neurogenic pulmonary edema (NPE) is a relatively rare form of pulmonary edema caused by an
increase in pulmonary interstitial and alveolar fluid. Neurogenic pulmonary edema develops within a
few hours after a neurologic insult, and diagnosis requires exclusion of other causes of pulmonary
edema (eg, high-altitude pulmonary edema).

Pneumothorax is defined as the presence of air or gas in the pleural cavity (ie, the potential space
between the visceral and parietal pleura of the lung), which can impair oxygenation and/or ventilation.
The clinical results are dependent on the degree of collapse of the lung on the affected side. If the
pneumothorax is significant, it can cause a shift of the mediastinum and compromise hemodynamic
stability. Air can enter the intrapleural space through a communication from the chest wall (ie, trauma)
or through the lung parenchyma across the visceral pleura.

Pulmonary embolism
Pulmonary emboli usually arise from thrombi that originate in the deep venous system of the lower
extremities; however, they rarely also originate in the pelvic, renal, upper extremity veins, or the right
heart chambers. After traveling to the lung, large thrombi can lodge at the bifurcation of the main
pulmonary artery or the lobar branches and cause hemodynamic compromise.
Pulmonary thromboembolism is not a disease in and of itself. Rather, it is a complication of underlying
venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets,
and fibrin) are formed and lysed continually within the venous circulatory system.

Myocardial infarction
Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle
secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and
demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel,
resulting in an acute reduction of blood supply to a portion of the myocardium.

High altitude pulmonary edema

High-altitude pulmonary edema (HAPE) generally occurs 1-4 days after rapid ascent to altitudes in
excess of 2500 m (8000 ft). Young people and previously acclimatized people reascending to a high
altitude following a short stay at low altitude seem more predisposed to HAPE. Cold weather and
physical exertion at high altitude are other predisposing factors.The earliest indications are decreased
exercise tolerance and slow recovery from exercise.The person usually notices fatigue, weakness,
and dyspnea on exertion.The condition typically worsens at night, and tachycardia and tachypnea
occur at rest. Periodic breathing during sleep is almost universal in sojourners at high altitude.
Cough, frothy sputum, cyanosis, rales, and dyspnea progressing to severe respiratory distress are
symptoms of the disease.

A low-grade fever, respiratory alkalosis, and leukocytosis are other common features.
In severe cases, an altered mental status, hypotension, and death may result.


The initial management of patients with cardiogenic pulmonary edema (CPE) should address the
ABCs of resuscitation, that is, airway, breathing, and circulation. Oxygen should be administered to all
patients to keep oxygen saturation at greater than 90%. Any associated arrhythmia or MI should be
treated appropriately.
Methods of oxygen delivery include the use of a face mask, noninvasive pressure-support ventilation
(which includes bilevel positive airway pressure [BiPAP] and continuous positive airway pressure
[CPAP]), and intubation and mechanical ventilation. Which method is used depends on the presence
of hypoxemia and acidosis and on the patient's level of consciousness. For example, intubation and
mechanical ventilation may become necessary in cases of persistent hypoxemia, acidosis, or altered
mental status.[3, 4]
Following initial management, medical treatment of CPE focuses on 3 main goals: (1) reduction of
pulmonary venous return (preload reduction), (2) reduction of systemic vascular resistance (afterload
reduction), and, in some cases, (3) inotropic support. Preload reduction decreases pulmonary
capillary hydrostatic pressure and reduces fluid transudation into the pulmonary interstitium and
alveoli. Afterload reduction increases cardiac output and improves renal perfusion, which allows for
diuresis in the patient with fluid overload.
Patients with severe LV dysfunction or acute valvular disorders may present with hypotension. These
patients may not tolerate medications to reduce their preload and afterload. Therefore, inotropic
support is necessary in this subset of patients to maintain adequate blood pressure.
Patients who remain hypoxic despite supplemental oxygenation and patients who have severe
respiratory distress require ventilatory support in addition to maximal medical therapy.

Ultrafiltration is a fluid removal procedure that is particularly useful in patients with renal dysfunction
and expected diuretic resistance.

Intra-aortic balloon pumping

Intra-aortic balloon pumping (IABP) can be employed to achieve hemodynamic stabilization in the
patient before definitive therapy. The IABP decreases afterload as the pump deflates; during diastole,
the pump inflates to improve coronary blood flow.

Patients admitted with heart failure or pulmonary edema should be given a low-salt diet to minimize
fluid retention. Closely monitor their fluid balance.


Loop diuretics have long been the cornerstone of cardiogenic pulmonary edema (CPE) treatment,
with furosemide being the most commonly used of these drugs. Premedication with drugs that
decrease preload (eg, nitroglycerin [NTG]) and afterload (eg, angiotensin-converting enzyme [ACE]
inhibitors) before the administration of loop diuretics can prevent adverse hemodynamic changes.
Nesiritide is recombinant human brain-type natriuretic peptide (BNP); it reduces pulmonary capillary
wedge pressure (PCWP), pulmonary artery pressure, RA pressure, and systemic vascular resistance
while increasing the cardiac index and stroke volume index. Therapy with nesiritide has decreased
plasma renin, aldosterone, norepinephrine, and endothelin-1 levels and reduced ventricular ectopy
and ventricular tachycardia. Heart-rate variability also improves with nesiritide.

Inotropic support is usually used following unsuccessful attempts at preload and afterload reduction or
when hypotension precludes the use of these strategies. The 2 main classes of inotropic agents that
are available are catecholamine agents and phosphodiesterase inhibitors (PDIs).