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Pathophysiology of cardiogenic pulmonary edema

Authors: Duane S Pinto, MD, MPH, Robb D Kociol, MD

Section Editor: Wilson S Colucci, MD
Deputy Editor: Susan B Yeon, MD, JD, FACC

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 2017. | This topic last updated: Mar 04, 2016.

INTRODUCTION Cardiogenic pulmonary edema is a common and potentially fatal cause of acute
respiratory distress. Cardiogenic pulmonary edema is most often a result of acute decompensated heart
failure (ADHF). The clinical presentation is characterized by the development of dyspnea associated with the
rapid accumulation of fluid within the lung's interstitial and/or alveolar spaces, which is the result of acutely
elevated cardiac filling pressures [1].

ADHF is most commonly due to left ventricular systolic or diastolic dysfunction, with or without additional
cardiac pathology, such as coronary artery disease or valve abnormalities. However, a variety of conditions or
events can cause cardiogenic pulmonary edema in the absence of heart disease, including primary fluid
overload (eg, due to blood transfusion), severe hypertension, renal artery stenosis, and severe renal disease.

Noncardiogenic pulmonary edema is a distinct clinical syndrome associated with diffuse filling of the alveolar
spaces in the absence of elevated pulmonary capillary wedge pressure [1]. Focused history, physical
examination, echocardiography, laboratory analysis and, in some cases, direct measurement of pulmonary
capillary wedge pressure can be used to distinguish cardiogenic from noncardiogenic pulmonary edema, as
well as from other causes of acute respiratory distress. (See "Evaluation of acute decompensated heart
failure" and "Noncardiogenic pulmonary edema".)

Flash pulmonary edema is a term that is used to describe a particularly dramatic form of cardiogenic
alveolar pulmonary edema. In flash pulmonary edema, the underlying pathophysiologic principles, etiologic
triggers, and initial management strategies are similar to those of less severe ADHF, although there is a
greater degree of urgency to the implementation of initial therapies and the search for triggering causes. (See
'Precipitating factors' below.) Often, flash pulmonary edema is related to a sudden rise in left-sided
intracardiac filling pressures in the setting of hypertensive emergency, acute ischemia, new onset
tachyarrhythmia, or obstructive valvular disease. In addition to standard therapies for cardiogenic pulmonary
edema, this condition responds well to combined venous and arterial vasodilators.

General issues related to the pathophysiology and etiology of cardiogenic pulmonary edema will be reviewed
here. The evaluation and treatment of ADHF and the evaluation of the clinically stable patient with suspected
HF are presented separately. (See "Evaluation of acute decompensated heart failure" and "Treatment of
acute decompensated heart failure: General considerations" and "Evaluation of the patient with suspected
heart failure".)

PATHOPHYSIOLOGY Cardiogenic pulmonary edema is characterized by increased transudation of

protein-poor fluid into the pulmonary interstitium and alveolar spaces. The primary etiologic factor is a rapid
and acute increase in left ventricular filling pressures and left atrial pressure.

Fluid transudation Fluid transudation is mediated by a rise in pulmonary capillary pressure that results
from an increase in pulmonary venous and left atrial pressure. This occurs in the absence of a primary
change in the permeability or integrity of the endothelial and epithelial layers of the pulmonary capillaries. The
net result is filtration of protein-poor liquid across the pulmonary endothelium into the pulmonary interstitium
and alveolar spaces, leading to decreased diffusing capacity, hypoxia, and shortness of breath [2].
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The Starling relationship Fluid balance between the interstitium and vascular bed in the lung, as in other
microcirculations, is determined by the Starling relationship, which predicts the net flow of liquid across a
membrane [3,4]. This can be expressed in the following equation:

Net filtration = Kf x ( hydrostatic pressure - oncotic pressure)

= Kf x [(Pc - Pi) - (c - i)]

where:

Kf is the filtration coefficient = Lp x S

Lp is the hydraulic conductivity
S is the surface area available for fluid movement.
Pc and Pi are the capillary and interstitial fluid hydrostatic pressures.
c and i are the capillary and interstitial fluid oncotic pressures; the interstitial oncotic pressure is
derived primarily from filtered plasma proteins and to a lesser degree proteoglycans in the interstitium.
represents the reflection coefficient of proteins across the capillary wall (with values ranging from 0 if
completely permeable to 1 if completely impermeable).

In normal microvessels, there is ongoing filtration of a small amount of low protein liquid. In cardiogenic
pulmonary edema, the increase in transcapillary filtration is generally attributed to elevation in pulmonary
capillary pressure, although permeability of the capillary wall may also be affected. (See 'Pulmonary capillary
stress failure' below.)

Compensatory mechanisms, particularly activation of the renin-angiotensin and sympathetic nervous

systems, result in tachycardia and an elevation in systemic vascular resistance (SVR) that may be
deleterious in this setting:

Tachycardia, which shortens the duration of diastole, impairs the ability of the left ventricle to fill.

An elevated SVR with or without an increase in left ventricular chamber dimension increases left
ventricular afterload (wall stress), increasing myocardial oxygen demand.

These changes can lead to a further increase in left ventricular end-diastolic pressure and more edema
formation. To the degree that pulmonary edema results in hypoxia, there may be a further worsening of
myocardial function.

Pulmonary capillary stress failure Although cardiogenic pulmonary edema is generally attributed to
transudation of low protein fluid in response to high pulmonary capillary pressure, experimental studies have
demonstrated that severe elevation in pulmonary capillary pressure can lead to increased permeability of the
capillary wall and eventually stress failure of the blood-gas barrier at the capillary endothelial and/or alveolar
epithelial layer [5]. Stress failure of pulmonary capillaries is manifest as high-permeability edema and/or
alveolar hemorrhage. Pulmonary capillary stress failure may occur in some patients with flash pulmonary
edema with abrupt severe increases in pulmonary capillary pressure [6]. (See 'Precipitating factors' below.)

Role of lymphatics The rate of accumulation of lung liquid at a given elevation in pulmonary capillary
pressure is related to the functional capacity of the lymphatic vessels to remove the excess fluid, which varies
from patient to patient and with the duration of disease [7]. With acute rises in pulmonary capillary pressure,
the pulmonary lymphatics cannot rapidly increase the rate of fluid removal; as a result, pulmonary edema
occurs at pulmonary capillary pressures as low as 18 mmHg. In contrast, patients with chronic heart failure,
in whom the pulmonary capillary wedge pressure is persistently elevated, have increased lymphatic capacity
and do not develop pulmonary edema until significantly higher pulmonary capillary pressures are reached.

PREDISPOSING CONDITIONS When considering the etiologies of cardiogenic pulmonary edema, it is

useful to distinguish the chronic cardiac conditions that predispose to episodes of pulmonary edema from the
triggers that precipitate pulmonary edema.
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The chronic conditions that predispose to heart failure (HF) are presented in detail separately. For the
purposes of this discussion, some of the more common conditions leading to HF and cardiogenic pulmonary
edema (eg, left ventricular [LV] systolic and diastolic dysfunction) are reviewed briefly here. (See
"Epidemiology and causes of heart failure", section on 'Predisposing conditions for HF'.)

Systolic dysfunction Impaired LV contractility, resulting in reduced cardiac output, is the most common
predisposing condition leading to cardiogenic pulmonary edema. LV systolic dysfunction itself has many
causes, including the following (see "Causes of dilated cardiomyopathy"):

Coronary heart disease

Hypertension
Valvular heart disease
Idiopathic dilated cardiomyopathy.
Toxins (eg, anthracyclines)
Metabolic disorders (eg, hypothyroidism)
Viral myocarditis (eg, Coxsackie B virus or echovirus infection).

The decrease in forward flow caused by systolic dysfunction leads to activation of the renin-angiotensin-
aldosterone and sympathetic nervous systems. The compensatory renal sodium and water retention induced
by these adaptations ultimately result in pulmonary edema. (See "Pathophysiology of heart failure:
Neurohumoral adaptations".)

Diastolic dysfunction Diastolic dysfunction refers to an increase in ventricular stiffness (reduced

compliance) and impaired relaxation that impedes ventricular filling during diastole. It can be induced by
chronic disorders, such as left ventricular hypertrophy of any etiology or hypertrophic and restrictive
cardiomyopathies, and acutely with ischemia and acute hypertensive crisis. The net effect of diastolic
dysfunction is an increased end-diastolic pressure for any given end-diastolic volume. (See "Clinical
manifestations and diagnosis of heart failure with preserved ejection fraction".)

In addition to the elevated end-diastolic pressure, additional factors that may promote the development of
pulmonary edema in patients with diastolic dysfunction include concurrent systolic dysfunction, reduced
diastolic coronary blood flow (resulting in subendocardial ischemia), and tachycardia (eg, atrial fibrillation with
rapid ventricular response). (See "Pathophysiology of heart failure with preserved ejection fraction".)

Not all cases of cardiogenic pulmonary edema in patients with normal ejection fraction are due primarily to
intrinsic abnormalities of LV diastolic function. Other causes include volume overload (as in renal failure) and
increased afterload (as in hypertensive crisis) [8]. (See 'Volume overload' below and 'Renovascular
hypertension' below.)

Left ventricular outflow obstruction LV outflow obstruction can be the result of critical aortic stenosis
(including supravalvular and subvalvular stenosis), hypertrophic cardiomyopathy, and/or severe systemic
hypertension. Chronic LV outflow obstruction is associated with a hypertrophied LV wall, which can produce
diastolic and, over time, systolic dysfunction. (See "Clinical manifestations and diagnosis of aortic stenosis in
adults" and "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".)

Mitral stenosis Mitral stenosis is generally the result of rheumatic heart disease. It is now less often seen
in the United States, but is still a major cardiac problem in the third world. The chronic obstruction to atrial
outflow leads to elevated left atrial pressures. (See "Clinical manifestations and diagnosis of mitral stenosis".)
Mitral annular calcification is a rare cause of symptomatic mitral stenosis. (See "Mitral annular calcification".)

The typically slow progression of the disease allows gradual adaptation to the increased pressures and
patients with mild to moderate degrees of stenosis are not typically symptomatic. (See 'Role of lymphatics'
above.) However, conditions that cause an elevated heart rate and decreased diastolic filling time, such as

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poorly rate-controlled atrial fibrillation or exercise, can lead to acute elevations of left atrial pressures, and
pulmonary edema. (See "Pathophysiology and natural history of mitral stenosis".)

Renovascular hypertension Renovascular disease, particularly chronic hypertension due to renal artery
stenosis, is associated with predisposing conditions as well as precipitating factors for pulmonary edema [8-
12]. Patients with renovascular disease may be predisposed to pulmonary edema because of chronic
hypertension and secondary diastolic dysfunction and also from excess sodium and water retention
secondary to activation of the renin-angiotensin system and associated renal dysfunction, resulting in
chronically elevated filling pressures [8,13]. (See "Establishing the diagnosis of renovascular hypertension".)

An association between recurrent pulmonary edema and renovascular hypertension was first described by
Pickering et al. who reported pulmonary edema in 13 of 55 patients with renovascular hypertension and
azotemia [9]. Flash pulmonary edema appears to be more common in patients with bilateral renal artery
stenosis as compared to those with unilateral disease (eg, 41 versus 12 percent) [9,14]. The combination of
bilateral renal artery stenosis and flash pulmonary edema has been named the Pickering syndrome [15,16].
Limited evidence is available on the efficacy of revascularization for this condition. (See "Treatment of
bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney" and "Treatment of
acute decompensated heart failure: Components of therapy".)

PRECIPITATING FACTORS In the presence of pre-existing systolic or diastolic dysfunction, other disease
entities or physiologic conditions may precipitate hemodynamic decompensation and promote the
development of pulmonary edema (table 1) [17].

Flash pulmonary edema is a term that is used to describe a particularly dramatic form of acute
decompensated heart failure (ADHF) caused by acute increases in left ventricular (LV) diastolic pressure with
rapid fluid accumulation in the pulmonary interstitial and alveolar spaces [6]. This may occur in some patients
with myocardial ischemia with or without myocardial infarction, acute severe mitral regurgitation, hypertensive
crisis, acute aortic regurgitation, and stress-induced (takotsubo) cardiomyopathy. (See "Treatment of acute
decompensated heart failure in acute coronary syndromes" and "Acute mitral regurgitation in adults" and
"Acute aortic regurgitation in adults" and "Clinical manifestations and diagnosis of stress (takotsubo)
cardiomyopathy" and "Evaluation and treatment of hypertensive emergencies in adults", section on 'Cardiac
emergencies'.)

Bilateral renal artery stenosis is a risk factor for flash pulmonary edema. (See 'Renovascular hypertension'
above.)

Hypertensive crisis Patients presenting with cardiogenic pulmonary edema commonly present with
systemic hypertension, which may be severe [18]. Many of these patients have a preserved (normal or near
normal) LV ejection fraction. Excess afterload, instead of or in addition to fluid overload, may precipitate
decompensation in these patients. (See "Moderate to severe hypertensive retinopathy and hypertensive
encephalopathy in adults".)

Myocardial ischemia/infarction Patients with ADHF commonly have coronary artery disease with or
without an acute coronary syndrome [19]. The acute onset of severe myocardial ischemia can lead to a
sudden impairment in systolic and diastolic function, resulting in a decreased cardiac output, elevated filling
pressures and the development of pulmonary edema. (See "Overview of the acute management of unstable
angina and non-ST elevation myocardial infarction" and "Overview of the acute management of ST elevation
myocardial infarction".)

With systolic dysfunction, there is less forward ejection, leading to increases in diastolic volume and
diastolic pressure.

With diastolic dysfunction, the enhanced stiffness of the myocardium raises diastolic pressure at any
given diastolic volume. Even transient ischemia can exacerbate pre-existing diastolic dysfunction, which

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is a common finding in patients with coronary artery disease. (See "Pathophysiology of heart failure with
preserved ejection fraction".)

Myocardial ischemia may also precipitate acute valvular pathology, particularly mitral regurgitation. (See
'Acute mitral regurgitation' below.)

Acute aortic regurgitation The abrupt onset of acute aortic regurgitation leads to a rapid rise in cardiac
filling pressures due to the inability of the left ventricle to quickly adapt to the rapid increase in end-diastolic
volume caused by the regurgitant blood. Acute valvular dysfunction can be seen in cases of endocarditis,
aortic root dissection, complications associated with prosthetic valves and surgical technique, and
spontaneous or traumatic rupture of the aortic leaflets. (See "Acute aortic regurgitation in adults".)

Acute mitral regurgitation The most common cause of isolated, severe acute mitral regurgitation in
adults is chordal rupture with or without associated myxomatous disease. Other causes of acute mitral valve
incompetence include myocardial ischemia or infarction, resulting in papillary muscle rupture or papillary
muscle displacement (previously known as papillary muscle dysfunction); endocarditis, which can lead to
chordal rupture; and prosthetic valve dysfunction. (See "Acute mitral regurgitation in adults".)

In patients who do not have chronic mitral regurgitation, the left atrium is usually not compliant. Regurgitant
flow into a noncompliant left atrium leads to an increase in pressure that is conducted to the pulmonary
circulation.

Some patients with ischemic heart disease and LV systolic dysfunction develop acute pulmonary edema
without apparent cause. Some of these patients have mitral regurgitation, which may be mild at rest but is
made substantially worse with exercise, often leading to dyspnea that requires cessation of exercise [20].
This change can occur in the absence of detectable ischemia. (See "Clinical manifestations and diagnosis of
chronic mitral regurgitation", section on 'Stress testing'.)

Acute left atrial outflow obstruction Acute impairment of outflow from the left atrium to the LV can cause
increased pulmonary pressures. Although uncommon, this can precipitate pulmonary edema. Causes of
acute left atrial outflow impairment include the following:

Left atrial tumors (eg, myxoma) (see "Cardiac tumors", section on 'Left atrial tumors')

Thrombosis of a prosthetic valve

In chronic left atrial outflow impairment (eg, mitral stenosis or cor triatriatum), pulmonary edema is often
precipitated when an elevated heart rate decreases the time for LV filling. Pulmonary edema may also be
precipitated by an increased intravascular volume, as occurs with pregnancy or an increase in salt intake.

Volume overload Volume overload of the LV can be induced by any cause of increased intravascular
volume (eg, primary sodium retention), and also by ventricular septal rupture or aortic insufficiency. Acute
ventricular septal rupture is a complication of acute myocardial infarction (both anterior and inferior). Rupture
occurs within five to seven days after the infarct. (See "Mechanical complications of acute myocardial
infarction", section on 'Rupture of the interventricular septum'.)

SUMMARY

Cardiogenic pulmonary edema is characterized by the development of dyspnea associated with the rapid
accumulation of fluid within the lung's interstitial and alveolar spaces, which is the result of acutely
elevated cardiac filling pressures (cardiogenic pulmonary edema). (See 'Pathophysiology' above.)

Cardiogenic pulmonary edema is characterized by increased transudation of protein-poor fluid into the
pulmonary interstitium and alveolar spaces. The primary etiologic factor is a rapid and acute increase in
left ventricular filling pressures and left atrial pressure, usually associated with a reduction in cardiac
output. Fluid exchange between the interstitium and vascular bed in the lung, as in other

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microcirculations, is determined by Starling forces, which govern the net flow of liquid across a
membrane. (See 'Pathophysiology' above.)

Chronic conditions that predispose to acute decompensated heart failure (ADHF) and resultant
pulmonary edema include disorders causing systolic dysfunction, those causing diastolic dysfunction,
causes of left ventricular outflow obstruction, and causes of mitral stenosis. (See 'Predisposing
conditions' above.)

Precipitating factors that promote development of cardiogenic pulmonary edema include myocardial
ischemia or infarction, acute aortic regurgitation, acute mitral regurgitation, renovascular hypertension,
acute left atrial outflow impairment, and other causes of volume overload. (See 'Precipitating factors'
above.)

Flash pulmonary edema is a term that is used to describe a dramatic form of ADHF, caused by an
acute increase in left ventricular diastolic pressure as may occur with myocardial ischemia with or
without myocardial infarction, acute severe mitral regurgitation, hypertensive crisis, acute aortic
regurgitation, and stress-induced (takotsubo) cardiomyopathy. (See 'Precipitating factors' above.)

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REFERENCES

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3. Chua TP, Coats AJ. The lungs in chronic heart failure. Eur Heart J 1995; 16:882.
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5. West JB, Mathieu-Costello O. Vulnerability of pulmonary capillaries in heart disease. Circulation 1995;
92:622.
6. Rimoldi SF, Yuzefpolskaya M, Allemann Y, Messerli F. Flash pulmonary edema. Prog Cardiovasc Dis
2009; 52:249.
7. Szidon JP. Pathophysiology of the congested lung. Cardiol Clin 1989; 7:39.
8. Gandhi SK, Powers JC, Nomeir AM, et al. The pathogenesis of acute pulmonary edema associated with
hypertension. N Engl J Med 2001; 344:17.
9. Pickering TG, Herman L, Devereux RB, et al. Recurrent pulmonary oedema in hypertension due to
bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. Lancet 1988;
2:551.
10. Messina LM, Zelenock GB, Yao KA, Stanley JC. Renal revascularization for recurrent pulmonary edema
in patients with poorly controlled hypertension and renal insufficiency: a distinct subgroup of patients
with arteriosclerotic renal artery occlusive disease. J Vasc Surg 1992; 15:73.
11. Missouris CG, Belli AM, MacGregor GA. "Apparent" heart failure: a syndrome caused by renal artery
stenoses. Heart 2000; 83:152.
12. Planken II, Rietveld AP. Rapid onset pulmonary edema (flash edema) in renal artery stenosis. Neth J
Med 1998; 52:116.
13. Vasan RS, Benjamin EJ. Diastolic heart failure--no time to relax. N Engl J Med 2001; 344:56.
14. Bloch MJ, Trost DW, Pickering TG, et al. Prevention of recurrent pulmonary edema in patients with
bilateral renovascular disease through renal artery stent placement. Am J Hypertens 1999; 12:1.

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15. Messerli FH, Bangalore S, Makani H, et al. Flash pulmonary oedema and bilateral renal artery stenosis:
the Pickering syndrome. Eur Heart J 2011; 32:2231.
16. Pelta A, Andersen UB, Just S, Bkgaard N. Flash pulmonary edema in patients with renal artery
stenosis--the Pickering Syndrome. Blood Press 2011; 20:15.
17. Heart Failure Society of America, Lindenfeld J, Albert NM, et al. HFSA 2010 Comprehensive Heart
Failure Practice Guideline. J Card Fail 2010; 16:e1.
18. Weintraub NL, Collins SP, Pang PS, et al. Acute heart failure syndromes: emergency department
presentation, treatment, and disposition: current approaches and future aims: a scientific statement
from the American Heart Association. Circulation 2010; 122:1975.
19. Flaherty JD, Bax JJ, De Luca L, et al. Acute heart failure syndromes in patients with coronary artery
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20. Pirard LA, Lancellotti P. The role of ischemic mitral regurgitation in the pathogenesis of acute
pulmonary edema. N Engl J Med 2004; 351:1627.

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GRAPHICS

Common and uncommon precipitating factors associated with hospitalization for

ADHF

Dietary and medication related causes

Dietary indiscretion - excessive salt or water intake

Nonadherence to medications

Iatrogenic volume expansion

Progressive cardiac dysfunction

Progression of underlying cardiac dysfunction

Physical, emotional, and environmental stress

Cardiac toxins:

Alcohol

Cocaine

Right ventricular pacing

Cardiac causes not primarily myocardial in origin

Cardiac arrhythmias:

Atrial fibrillation with a rapid ventricular response

Ventricular tachycardia

Marked bradycardia

Conduction abnormalities

Uncontrolled hypertension

Acute myocardial infarction

Myocardial ischemia

Valvular disease:

Progressive mitral regurgitation

Non-cardiac causes
Pulmonary disease - pulmonary embolus, COPD

Anemia, from bleeding or relative lack of erythropoietin or bone marrow suppression

Systemic infection; especially pulmonary infection

Thyroid disorders

Adverse cardiovascular effects of medications

Cardiac depressant medications

Nondihydropyridine calcium antagonists

Type Ia and Ic antiarrhythmic agents

Sodium retaining medications

Steroids

Nonsteroidal anti-inflammatory drugs

Medications that reduce contractility

Anthracyclines and other chemotherapeutic agents

Reproduced with permission from: Heart Failure Society Of America. Evaluation and management of patients with acute
decompensated heart failure. J Card Fail 2006; 12:e86. Copyright 2006 Elsevier.

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Contributor Disclosures
Duane S Pinto, MD, MPH Grant/Research/Clinical Trial Support: Medtronic [Stents/TAVR
(Resolute/Evolut)]; Medicines [ACS (Bivalirudin/Cangrelor)]; Medicure [ACS (Tirofiban)]; Boston Scientific
[Coronary stents]; Amarin [Clinical trial event adjudication]. Consultant/Advisory Boards: Abiomed [Circulatory
support]; Boston Scientific [Coronary stents]. Robb D Kociol, MD Nothing to disclose Wilson S Colucci,
MD Consultant/Advisory Boards: Novartis [Heart failure (Valsartan, sacubitril/valsartan)], Merck [Heart failure
(Enalapril)], Amgen [Heart failure (Ivabradine)]. Susan B Yeon, MD, JD, FACC Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.

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