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Pulmonary Edema
Ryan Malek; Shadi Soufi.

Author Information and Affiliations

Last Update: April 7, 2023.

Continuing Education Activity

Pulmonary edema is defined as an abnormal accumulation of extravascular fluid in the lung
parenchyma. Two main types are cardiogenic and noncardiogenic pulmonary edema. This
activity highlights the role of the interprofessional team in the diagnosis and treatment of this
condition.

Objectives:

Outline the signs and symptoms of different types of pulmonary edema.

Review the pathophysiology of different types of pulmonary edema.

Describe the management of different types of pulmonary edema.

Summarize the importance of an interprofessional approach for effective management of

patients with pulmonary edema.

Access free multiple choice questions on this topic.

Introduction
Pulmonary edema can be defined as an abnormal accumulation of extravascular fluid in 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, and hence learning the underlying disease process is crucial to guide its
management. Clinical features include progressive worsening dyspnea, rales on lung
auscultation, and worsening hypoxia.[1]

Etiology
Pulmonary edema can be broadly classified into cardiogenic and noncardiogenic pulmonary
edema.

Cardiogenic or volume-overload pulmonary edema arises due to a rapid elevation in the

hydrostatic pressure of the pulmonary capillaries. This is typically seen in disorders involving
left ventricular systolic and diastolic function (acute myocarditis including other etiologies of
non-ischemic cardiomyopathy, acute myocardial infarction), valvular function (aortic/mitral
regurgitation and stenosis in the moderate to the severe range), rhythm (atrial fibrillation with a
rapid ventricular response, ventricular tachycardia, high degree, and third-degree heart block).[2]

Noncardiogenic pulmonary edema is caused by lung injury with a resultant increase in

pulmonary vascular permeability leading to the movement of fluid, rich in proteins, to the
alveolar and interstitial compartments. Acute lung injury with severe hypoxemia is referred to as
acute respiratory distress syndrome (ARDS) and is seen in various conditions directly affecting
the lungs, such as pneumonia, inhalational injury, or indirectly, such as sepsis, acute pancreatitis,
severe trauma with shock, multiple blood transfusions.[3]
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Epidemiology
More than 1 million patients are admitted each year with a diagnosis of pulmonary edema
secondary to cardiac causes (heart failure).[4] An estimated 190,000 patients are diagnosed with
acute lung injury each year.[5] About 1.5 to 3.5 cases/100,000 population are diagnosed with
ARDS.

Pathophysiology
The resultant pathology of increased extravascular fluid content in the lung remains common to
all forms of pulmonary edema. However, the underlying mechanism leading to the edema arises
from the disruption of various complex physiologic processes, maintaining a delicate balance of
filtration of fluid and solute across the pulmonary capillary membrane. This imbalance can be
from one or more of the following factors:

Increase in intravascular hydrostatic pressure transmitted in a retrograde fashion to the

pulmonary microvasculature

Increase in interstitial hydrostatic pressure

Endothelial injury and disruption of epithelial barriers

Decrease in oncotic pressure due to underlying hepatic, renal, malnutrition, and other
protein-losing states.

Lymphatic insufficiency

Increased negative interstitial pressure

The relationship between hydrostatic and oncotic forces in relation to net fluid filtration is best
explained by Ernest Starling’s equation. The rate of fluid filtration is determined by the
differences in the hydrostatic and oncotic pressures between the pulmonary capillaries and
interstitial space.[1][3][6]

History and Physical

Progressively worsening dyspnea, tachypnea, and rales (or crackles) on examination with
associated hypoxia are the clinical features common to both cardiogenic and noncardiogenic
pulmonary edema.

Cough with pink frothy sputum noted due to hypoxemia from alveolar flooding and auscultation
of an S3 gallop could suggest cardiogenic edema. Similarly, the presence of murmurs, elevated
jugular venous pressure, peripheral edema may point towards a cardiac etiology.

In patients with non-cardiogenic pulmonary edema, the symptoms of infections such as fever,
cough with expectoration, dyspnea pointing to likely pneumonia, recent trauma, blood
transfusions should be carefully assessed as these patients may progress to acute respiratory
distress syndrome.

Auscultation remains the mainstay of bedside assessment in all patients with respiratory
symptoms. More specifically, hearing of either fine or coarse crackles is crucial to determine the
next steps in the management. Fine crackles are heard in cardiogenic pulmonary edema. They are
exclusively heard in the inspiratory phase when the small airways, which were shut during
expiration, open abruptly.[7]

Evaluation
In addition to a thorough history and physical examination, electrocardiogram assists in
diagnosing cardiac ischemia or myocardial infarction. It is a quick, inexpensive, and relatively

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less specialized test that can be done at the bedside.

Following are a variety of diagnostic tools utilized to help diagnose pulmonary edema and, more
importantly, differentiate between its different types.

Laboratory Testing

Brain-type natriuretic peptide (BNP) is secreted by the cardiac myocytes of the left ventricles in
response to stretching caused by increased ventricular blood volume or increased intracardiac
pressures. Elevated BNP levels correlate with left ventricular end-diastolic pressure as well as
pulmonary occlusion pressure and can be seen in patients with congestive heart failure.[3] BNP
levels less than 100 pg/ml suggest heart failure is less likely, and levels greater than 500 pg/ml
suggest a high likelihood of heart failure. Levels between 100 and 500 pg/ml do not help in the
diagnosis of heart failure and are often seen in critically ill patients.[3]

Troponin elevation is commonly noted in patients with damage to myocytes, such as acute
coronary syndrome. They, however, are also noted to be elevated in patients with severe sepsis.
[3]

Hypoalbuminemia (≤3.4 g/dL) is an independent marker of increased in-hospital and post-

discharge mortality for patients presenting in acute decompensated heart failure.[8] Low albumin
in isolation does not lead to pulmonary edema as there is a concurrent drop in pulmonary
interstitial and plasma albumin levels preventing the creation of a transpulmonary oncotic
pressure gradient.[9]

Obtaining serum electrolyte levels, including renal function, serum osmolarity, toxicology
screening, help in patients with pulmonary edema due to toxic ingestion. Obtaining lipase and
amylase levels help diagnose acute pancreatitis.

Radiographic Testing

Both posteroanterior and lateral views in standard imaging or anteroposterior views in portable
imaging are utilized. Cardiogenic pulmonary edema is characterized by the presence of central
edema, pleural effusions, Kerley B septal lines, peribronchial cuffing, and enlarged heart size. In
noncardiogenic etiologies, the edema pattern is typically patchy and peripheral that can
demonstrate the presence of ground-glass opacities and consolidations with air bronchograms.
[10] Pleural effusions are more commonly seen in the cardiogenic type.[1]

Echocardiography

Assists in the diagnosis of left ventricular systolic dysfunction and valvular dysfunction. Through
modalities, including tissue Doppler imaging of the mitral annulus, the presence and degree of
diastolic dysfunction can be assessed.[3]

Lung Ultrasound

A newer technique that is non-invasive and does not involve radiation exposure. It is most
commonly used in intensive care units, emergency rooms, and operating rooms. It helps detect
the accumulation of extravascular lung water (EVLW) ahead of the clinical manifestations.[10]

Pulmonary Artery Catheterization

Often considered a gold standard in the determination of the etiology of pulmonary edema, it is
an invasive test that helps monitor systemic vascular resistance, cardiac output, and filling
pressures. An elevated pulmonary artery occlusion pressure over 18 mm Hg is helpful in the
determination of cardiogenic pulmonary edema.[3]

Transpulmonary Thermodilution

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It is an invasive testing modality performed in patients typically undergoing major cardiac,

vascular, or thoracic surgeries. They are also used in septic shock and monitors several
hemodynamic indices such as cardiac index, mixed venous oxygen saturation, stroke volume
index, and EVLW.[10]

Treatment / Management
Therapeutic goals in patients with pulmonary edema include alleviation of symptoms and
treatment of the underlying pathologic condition.

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.[11]

Vasodilators can be added as an adjuvant therapy to the diuretics in the management of

pulmonary edema.[12] 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. Nesiritide is a recombinant brain natriuretic peptide that has vasodilatory properties.
It has been shown to reduce pulmonary capillary wedge pressure (PCWP) and filling pressures
significantly, but no subsequent improvement in dyspnea has been noted.[13] Newer drugs like
serelaxin, a recombinant human form of relaxin, induced nitric oxide activation, which causes
vasodilation. Clevidipine is an ultra-short-acting calcium channel blocker, initiated very early in
the presentation, has been associated with reduced length of stay, improved dyspnea, and less
frequent ICU admission.[14]

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. This leads to the lowering of the pulmonary arterial pressure with
subsequent improvements in gas exchange, exercise capability, and chest radiography.
[15] Nifedipine is only used as a prophylactic strategy when altitude acclimatization cannot be
achieved in high-risk individuals and situations, including a rapid rate of ascent, extreme
physical exertion, recent respiratory tract infection, and low altitude of native place of residence.
[16]

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. Milrinone is an IV inotrope with
vasodilatory properties but is associated with an increase in post-discharge mortality.[17]

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.[11]

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.[11]

Differential Diagnosis

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Immersion pulmonary edema from drowning, neurogenic pulmonary edema from stroke, head
trauma, medication hypersensitivities or toxic ingestions, blood transfusions leading to
transfusion-related acute lung injury (TRALI), liver disease, pulmonary embolism or infarct, and
uremia.[18]

Prognosis
Pulmonary edema is an acutely decompensated state due to either cardiac or noncardiac
etiologies. Temporizing measures such as supplemental oxygenation, diuretics, nitrates, and
morphine help manage dyspnea, hypoxemia. However, definitive management of the underlying
causes is necessary to prevent its recurrences. Prognostic predictions are difficult to quantify,
given the vast number of cardiogenic and non-cardiogenic etiologies of pulmonary edema and
their individual mortality data. Pulmonary edema's advanced state in ARDS has had
progressively improved outcomes. Hospital mortality has decreased from 60% from 1967
through 1981 to the range of 30% to 40% in the 1990s.[19] Furthermore, analysis of ARDS
mortality studies demonstrated a decline in overall mortality of about 1.1% per year from 1994 to
2006. Prognosis utilizing mortality data is largely variable and depends on the precipitating
process of ARDS.[20]

Complications
Since pulmonary edema is a result of complex physiologic derangements, be it cardiac, hepatic,
multiorgan system involvement, toxic stimuli, the complications arising from it are generally
secondary to the aforementioned pathophysiologic processes. Cardiogenic pulmonary edema 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.

Deterrence and Patient Education

Patients with a history of ischemic or valvular cardiac disease must be educated on the symptoms
of pulmonary edema on every clinic visit with their doctors. Counseling on a low salt diet,
regular exercise, and medication compliance must be emphasized.

Enhancing Healthcare Team Outcomes

Pulmonary edema can be a result of multiorgan involvement, and hence the involvement of an
interprofessional team such as internists, cardiology, pulmonology early in the course is
recommended for timely initiation of targeted therapy to improve patient outcomes. Education to
the nurses, medical students, nursing students on the signs of respiratory failure must be provided
regularly for earlier identification of patients with an impending respiratory decompensation.
Good history-taking skills must be practiced to identify factors such are medication non-
compliance, a poor socioeconomic situation, illicit drug use to avoid recurrences or readmissions.
[Level 5]

Review Questions

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Comment on this article.

References
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Disclosure: Ryan Malek declares no relevant financial relationships with ineligible companies.

Disclosure: Shadi Soufi declares no relevant financial relationships with ineligible companies.

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