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It is essential to have in mind that acute pulmonary edema is one of the most common medical emergency and very lifetreathing. The intervention must be done as soon as the diagnosis was suspected. It can be difined as the signs and symptoms that grossly represent the tranference of fluids from intravascular compartment to interstitium and consequently to the alveolu. Since both cardiac and non-cacdiac disease can produce pulmonary edema, the physician should be aware of underlyieng conditions that can be precipitating the problem. The clinical problem is complicated due to patients have frequently cardiac and pulmonary disease concurrently.
The physiopathology of Acute Pulmonary Edema is similar to that in which subcutaneous tissues are involved ; an imbalance in Starlin Forces is the key point to fluid accumulation in interstitium and alveolus.
The mechanism responsable to keep the interstitium and alveolus dry are three : 1-Plasma oncotic pressure (25mm Hg) higher than pulmonary capillary pressure (7-12 mmHg) 2-Connective tissue and cellular barriers relatively impermeable to plasma proteins 3-Extensive lymphatic system
The opposing forces that most likely are responsable for fluid transference to interstitium are : 1-Pumonary capilar pressure 2- Plasma oncotic pressure
When normal mechanisms to keep the lung dry either malfunction or are overwhelmed by excess fluid, edema tends to accumulate through a predictable sequence of steps. This process has been divided into three stages :
Stage 1 - Fluid transfer is increased into the lung interstitium; because lymphatic flow also increases, no net increase in interstitial volume occurs.
Stage 2 - The capacity of the lymphatics to drain excess fluid is exceeded and liquid begins to accumulate in the interstitial spaces that surround the bronchioles and lung vasculature (which yields the roentgenographic pattern of interstitial pulmonary edema).
Stage 3 - As fluid continues to build up, increased pressure causes it to track into the interstitial space around the alveoli and finally to disrupt the tight junctions of the alveolar membranes. Fluid first builds up in the periphery of the alveolar capillary membranes and finally floods the alveoli . During stage 3 the roentgenographic picture of alveolar pulmonary edema is generated and gas exchange becomes impaired.In addition to the processes occurring at the level of each alveolus, gravity also exerts an important influence on the fluid mechanics of the lung. Because blood is much denser than air and air-containing tissue, the effect of gravity on it is most pronounced. Under normal circunstances more perfusion occurs at the lung bases than at the apices; however, when pulmonary venous pressures rise and when fluid begins to accumulate at the lung bases the blood flow begins to be redistributed toward the apices.
The most likely causes of Acute Pulmonary Edema are cardiacs ones. The identification of primary cause can be lifesaving. Bellow are listed the main causes for pulmonary edema.
I. Altered capillary permeability
A. Infectious pulmonary edema (viral or bacterial)
B. Inhaled toxins
C. Circulating toxins
D. Vasoactive substances (histamine, kinins)
E. Disseminated intravascular coagulation
F. Immunologic reactions
G. Radiation pneumonia
H. Uremia
I. Near-drowning
J. Aspiration pneumonia
K. Smoke inhalation
L. Adult respiratory distress syndrome
II. Increased pulmonary capillary pressure
A. Cardiac causes
1. Left ventricular failure from any cause
2. Mitral stenosis
3. Subacute bacterial endocarditis
B. Noncardiac causes
1. Pulmonary venous fibrosis
2. Congenital stenosis of the origin of the pulmonary veins
3. Pulmonary venoocclusive disease
C. Overinfusion of fluids
III. Decreased oncotic pressure
A. Hypoalbuminemia from any cause (renal, hepatic, nutritional, or protein-losing enteropathy)
IV. Lymphatic insufficiency
V. Mixed or unknown mechanisms
A. High-altitude pulmonary edema
B. Neurogenic pulmonary edema (CNS trauma, subarachnoid bleeding)
C. Heroin overdose (also other narcotics)
D. Pulmonary embolism (very rare)
E. Pulmonary parenchymal disease
F. Eclampsia
G. Cardioversion
H. Postanesthetic
I. Cardiopulmonary bypass
Modified from E. D. Robin, C. E. Cross, and R. Zelis,Pulmonary edema. N. Engl. J. Med. 288:239, 292, 1973.
The clinical signs and symptoms of acute pulmonary edema can start as a primary manifastation of certain pathology or as an evolution of an already installed disease.
The patients presents dyspnea, tachypnea, orthopnea, tachycardia, hypertension, thoracic oppression, cold extemities with cyanosis or not, cough with a frothy or pink sputum, extensive use of accessory muscles of respiration, moist rales with or without wheezing .
At the beginig of the process , when edema is only in the interstitium, patients can present only tachydyspnea and dry cough. It is necessary that pulmonary fluid reachs 3 times more the normal value for the instalation of rales. On the other hand, dramatics situations can be found . When the pulmonary fluid accumulation is very intense and fastly installed , patients present an intense dyspnea, cyanosis, and elimination of large amount of frothy pink sputum.
In order to establish the diagnosis of pulmonary edema we should first ask about previous history of cardiac or pulmonary desease, previous episodes of pulmonary edema or cardiac failure and the use of any medicines. Physical examination must be done seeking for signs of ventricular failure, manifestations of dyspnea, signs of hypoxia and fluids in the lungs. Laboratory tests and image exams may be helpful in establishing the diagnosis and assessing cardiac, respiratory and renal functions. The usually required tests and their common findings are:
1- Blood studies: CBC with differencial, eletrolyte, BUN, creatinine and serum protein concentrations.
2- Urianalysis and microscopic examination of urine: proteinuria may be noted.
3- Room air arterial blood gas concentrations: we can first note a decrease in PO2 and PCO2. As the desease develop, PO2 is yet reduced while PCO2 is increased. PO2 values < 50 mmHg and PCO2 > 50 mmHg denotates severity and the need of mecanic ventilation.
4- PA and lateral chest x-ray films: the early signs of pulmonary edema (intersticial edema) are the Kerley B lines, horizontal lines seen laterally in the lower zones, 2 cm long at last, that, on the contrary of blood vessels, reach the lung edge. As the edema progress alveolar edema is observed with its "butterfly" pattern, caracterized by the central predominance of shadows with a clear zone at periphery lobes. Other feature that may be seen is cardiac enlargement, in case of cardiac failure previously present. It is important to remember that the inicial stages of ARDS may resemble cardiac pulmonary edema. It, though, becomes more widespread and uniform over 24 to 48 hours after the onset of tachypnea, dyspnea and hypoxia. A helpful feature in distinguishing cardiac pulmonary edema from non cardiac pulmonary edema and from widespread exudates, such as pneumonia, is the speed with which the edema appears and disappears. Substantial improvement in a 24 hour period is virtually diagnosis of cardiac pulmonary edema.
5- ECG: if there is any cardiac abnormality, which may be causing the edema, the ECG may show its signs.
6-Further tests: In selected patients, in which the underlying cause of the edema is not clear, right heart catheterization may be done to measure pulmonary capillary wedge pressure, which is universally elevated (> 25 mmHg) in cardiac pulmonary edema, while it is normal or even low in non cardiac pulmonary edema. Echocardiography may show valvular lesions or cardiomyophaty if they are present. Blood cultures and pulmonary function tests (obtained several days after clinical situation is stabilized) can be helpful too.
We must remenber that acute pulmonary edema is a dynamic medical emergency and, as such, treatment must be set up as soon as the diagnosis is suspected, and the patient must be frequently examined. The proposed approach to treatment is:
1- A brief history, physical examination and laboratory tests (see diagnosis) should be done to possibly establish the underlying cause of the pulmonary edema. In this case, the cause must be treated with specific measures.
2- The patient must be placed in a sitting position with legs dangling over the side of the bed in order to make respiration easier and to reduce venous return.
3- 100% oxygen should be delivered by mask to ensure sufficient oxygenation.
4- Morfine is administered to reduce anxiety, decrease sympathetic outflow and cause venodilation and decreased preload, which helps relieve the pulmonary edema. It should not be given to patients with decreased sensorium or respiratory drive, as it may bring about respiratory arrest. In case it happens, naloxone (0.8 to 2.0 mg IV bolus) should be given to the patient. The inicial dosage of morfine is 2 to 5 mg IV bolus, which may be repeated up to a maximum of 15 mg.
5- Furosemide (40 to 100 mg IV bolus) should be administered as it causes instant venodilation and then diuresis, mobilizing fluid from the lungs into circulation, which is then expelled in urine, reducing venous return.
6- Nitroglycerine should be administered in sublingual tablets or in an IV drip (0.4 mg), as it relieves pumonary edema by producing venodilation. It also dilates the epicardial coronaries and, therefore, is a treatment for ischemia, which can be the underlying cause of the pulmpnary edema. NTG may be repeated twice at five minute intervals, as long as there is no important fall in blood pressure, and it should not be given to any patient with a systolic blood pressure <120 mmHg, unless an IV line is in place.
7- Digoxin (0.25 mg in a slow IV push) can be administered if atrial fibrilation and a rapid ventricular response is a contributing factor, as it slows ventricular rate. The total dosage may bring near 1 to 1.5 mg IV in the first 24 hours.
8- Inhaled beta-adrenergic agonists or aminophylin IV may be administered to treat the bronchospasm that may occur in response to pulmonary edema and, then, increase the severity of hypoxemia and dyspnea. Aminophylin still increase renal plasmatic flow, excretion of sodium, cardiac contracion and provoke venodilation, thus decreasing peripheral vascullary resistance.They both may, however, induce tachycardia and supraventricular arrhythmias.
9- Other measures to help reduce ventricular preload are phlebotomy of approximatelly 500 ml of blood and plasmapheresis.<\p>
10- If these measures are not enough, tourniquets may be used in the limbs (3 at a time for 15 to 20 minutes) if there is no arterial obstructions.
In case of a non cardiac pulmonary edema we should treat the underlying cause, maintain respiratory function and consider the use of NSAIDS.
1- Cecil , Textbook of Medicine. Bennett, Plum. Saunders 20th edition.
2-Harrison's Principles of internal Medicine , MacGraw Hill 13th edition.
3-Manual de urgencias em pronto Socorro. Guilherme Erazo, Marco Pires . MEDSI, 4 edição.
4-D. Robin, C. E. Cross, and R. Zelis,Pulmonary edema. N. Engl. J. Med. 288:239, 292, 1973.
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