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Cardiogenic Pulmonary Edema Treatment & Management

  • Author: Ali A Sovari, MD, FACP; Chief Editor: Henry H Ooi, MD, MRCPI  more...
 
Updated: Dec 28, 2015
 

Approach Considerations

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.[10, 11]  The use of noninvasive pressure support ventilation in acidotic patients with severe acute cardiogenic pulmonary edema does not appear to be associated with adverse outcomes (early mortality and intubation rates) in these patients.[12]

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

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.

Diet

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

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Ventilatory Support

Noninvasive pressure-support ventilation

Consider noninvasive pressure-support ventilation (NPSV) early when treating patients with severe CPE.

In NPSV, the patient breathes through a face mask against a continuous flow of positive airway pressure. NPSV maintains the patency of the fluid-filled alveoli and prevents them from collapsing during exhalation. As a result, the patient saves energy that would have been spent trying to reopen collapsed alveoli. NPSV improves pulmonary air exchange, and it increases intrathoracic pressure with reduction in preload and afterload.

Several studies suggest that NPSV is associated with decreased length of stay in the ICU, decreased need for mechanical ventilation, and decreased hospital costs. A few clinical trials showed that in patients with CPE—mainly defined as having severe dyspnea, oxygen saturation of less than 90%, and basal rales—early and prehospital NPSV treatment by paramedics is safe and associated with faster improvement of oxygen saturation.[13, 14] However, the mortality and the need for intensive care did not differ between the patients who were treated with NPSV and those who were treated with a Venturi face mask in most of those studies. Indeed, a more recent study that evaluated the safety and efficacy of implementing prehospital CPAP for the treatment of acute (CPE) and acute exacerbations of chronic obstructive pulmonary disease (AECOPD) found no benefit in morbidity, mortality, and length of hospital stay.[15]  

CPAP and BiPAP

Two types of NPSV are CPAP and BiPAP. In CPAP, a single airway pressure is maintained throughout all phases of the respiratory cycle. In BiPAP, high pressures can be applied during inspiration and low pressures, during expiration, increasing the patient's comfort.[10]

A randomized trial comparing CPAP, noninvasive intermittent positive pressure ventilation (NIPPV), and standard oxygen therapy in 1069 patients with acute cardiogenic pulmonary edema demonstrated no mortality benefit from noninvasive ventilation, but improvements were seen in symptomatology and oxygenation.[16]

Although CPAP improves the condition of patients with cardiogenic pulmonary edema and has been associated with a reduced need for tracheal intubation, its use fails to reduce short-term mortality in this setting.[17]

In one small study, researchers compared CPAP with BiPAP and found that BiPAP was associated with more rapid improvement in vital signs but also with an increased rate of MIs.[18] Moreover, patients who received BiPAP initially had more chest pain than did patients who received CPAP. Other randomized clinical trials, however, did not show an increased rate of MI in patients who received CPAP or BiPAP compared with those who received oxygen by means of a face mask.

As of now, the data are insufficient to compare the efficacy and safety of BiPAP with those of CPAP. Therefore, the authors suggest that CPAP be the preferred method employed when NPSV is used unless the patient has obstructive airway disease.

Mechanical ventilation

In general, use endotracheal intubation and mechanical ventilation when patients with CPE remain hypoxic despite maximal noninvasive supplemental oxygenation, when patients have evidence of impending respiratory failure (eg, lethargy, fatigue, diaphoresis, worsening anxiety), or when patients are hemodynamically unstable (eg, hypotensive, severely tachycardic).

Mechanical ventilation maximizes myocardial oxygen delivery and ventilation. Positive end-expiratory pressure is generally recommended to increase alveolar patency and to enhance oxygen delivery and carbon dioxide exchange.

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Preload Reduction

Nitroglycerin

Nitroglycerin (NTG) is the most effective, predictable, and rapidly-acting medication available for preload reduction. Several studies demonstrated greater efficacy and safety and a faster onset of action with NTG than with furosemide or morphine sulfate. The use of sublingual NTG is associated with preload reduction within 5 minutes and with some afterload reduction.

Topical NTG may be as effective as sublingual NTG in most patients with CPE, but it should be avoided in patients with severe LV failure, because of poor skin perfusion (manifesting as skin pallor or mottling) and resultant poor absorption.

Intravenous (IV) NTG at high dosages provides rapid and titratable preload and afterload reduction and is excellent monotherapy for patients with severe CPE. IV NTG can be started with 10mcg/min and then rapidly uptitrated to more than 100mcg/min. The other alternative is NTG given as 3 mg IV boluses every 5 minutes.

The antianginal dose of NTG of 0.4 mg every 5 minutes has the bioequivalence of an NTG IV infusion of less than 80 mcg/min. Therefore, the dosage of NTG for patients with CPE is higher than the standard antianginal dosage would be.

Considering the short half-life of nitrates, physicians should be comfortable with the high dosage for CPE, especially in most patients with CPE, who present with a hyperadrenergic state and moderately elevated blood pressure. However, nitrates should not be used in hypotensive patients, and they should be used with extreme caution in patients with aortic stenosis and pulmonary hypertension.

Diuretics

Loop diuretics have been considered the cornerstone of CPE treatment for many years. Furosemide is used most commonly. Loop diuretics are presumed to decrease preload through 2 mechanisms: diuresis and direct vasoactivity (venodilation).

In most patients, diuresis does not occur for at least 20-90 minutes; therefore, the effect is delayed. Loop diuretics affect the ascending loop of Henle; therefore, the diminished renal perfusion in CPE may delay the onset of effects of loop diuretics.

Many patients with CPE do not have fluid overload. Continued use of diuretics in these patients after their acute symptoms have resolved may be associated with adverse outcomes, including electrolyte derangements, hypotension, and worsening renal function (GFR) as a result of tubuloglomerular feedback.

The presumption that these medications have a direct vasoactive (venodilating) effect has been questioned. Some studies demonstrated initial adverse hemodynamic consequences (eg, elevations of PCWP, LV filling pressure, heart rate, and systemic vascular resistance) after the administration of IV furosemide, perhaps due to direct neurohormonal stimulation.

Premedication with drugs that decrease preload (eg, NTG) and afterload (eg, angiotensin-converting enzyme [ACE] inhibitors) before the administration of loop diuretics can prevent potential adverse hemodynamic changes.

Morphine sulfate

The use of morphine sulfate in CPE for preload reduction has been commonplace for many years, but good evidence supporting a beneficial hemodynamic effect is lacking. Data suggest that morphine sulfate may contribute to a decrease in cardiac output and that it may be associated with an increased need for ICU admission and endotracheal intubation.

Adverse effects (eg, nausea and vomiting, local or systemic allergic reactions, respiratory depression) may outweigh any potential benefit, especially given the availability of medications that are more effective than morphine in reducing preload (eg, NTG).

Any beneficial hemodynamic effect from morphine is probably due to anxiolysis, with a resulting decrease in catecholamine production and a decrease in systemic vascular resistance. An alternative can be low-dose benzodiazepines (eg, lorazepam 0.5mg IV) in patients who are extremely anxious. This alternative reduces the risk of respiratory depression in patients whose condition responded to initial therapy.

Nesiritide

Nesiritide is recombinant human BNP that decreases 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 has reduced ventricular ectopy and ventricular tachycardia. Heart-rate variability also improves with nesiritide.[19, 20, 21]

Most of the beneficial effects of nesiritide were shown in the landmark Vasodilation in the Management of Acute Congestive Heart Failure (VMAC) study. Investigators compared IV nesiritide with IV NTG. IV nesiritide was associated with some hypotension but was otherwise well tolerated.

However, the VMAC study also showed a trend toward increased mortality in the IV nesiritide group compared with the patients receiving IV NTG, although the difference was not statically significant (90-day mortality, 19% for nesiritide vs 13% for NTG). The most important limitation of this study was the use of suboptimal dosages of IV NTG (mean 30-40 mcg/min) because the dosage was based on physician's decision and not on a protocol.

A later meta-analysis of 3 randomized trials of 485 patients receiving nesiritide and 377 patients not receiving nesiritide showed a 7.2% 30-day mortality with nesiritide versus 4% without nesiritide.[22]

In most large clinical trials nesiritide has not had a significant effect on renal function. In one of the largest studies of nesiritide to date, the Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure (ASCEND HF), nesiritide had a neutral effect on survival and rehospitalization and a small effect on dyspnea when used in combination with other treatments.[23] In the study, which was powered to show the effects of the drug on survival and renal function, no association was found between use of nesiritide and deteriorating renal function, although use of this agent was associated with a slight increase in hypotension. The investigators recommended against the routine use of nesiritide in the broad population of patients with acute heart failure.[23]

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Afterload Reduction

ACE inhibitors

ACE inhibitors are generally considered the cornerstones for treating chronic CHF, and studies have demonstrated excellent results with ACE inhibitors for the treatment of acute decompensated CHF and CPE. The use of ACE inhibitors in CPE is associated with reduced admission rates to ICUs and decreased endotracheal intubation rates and length of ICU stay.

The hemodynamic effects of ACE inhibitors include reduced afterload, improved stroke volume and cardiac output, and a slight reduction in preload. The last effects happen when renal perfusion improves after cardiac output improves and diuresis occurs.

Enalapril 1.25 mg IV or captopril 25 mg, given sublingually, result in hemodynamic and subjective improvements within 10 minutes. Improvements occur much more slowly with the oral route.

Angiotensin II receptor blockers

Angiotensin II receptor blockers (ARBs) have comparable beneficial effects in heart failure. Studies have proposed a role for ACE inhibitors and ARBs in preventing structural and electrical remodeling of the heart, resulting in a reduced incidence of arrhythmias.

The Valsartan Heart Failure Trial (Val-HeFT) showed that valsartan reduces the incidence of atrial fibrillation (AF) by 37%. (BNP level and advanced age were the strongest independent predictors for AF occurrence.)[24] Similarly, the Candesartan in Heart Failure: Assessment in Reduction of Mortality and Morbidity (CHARM) trial showed a reduction in the onset of AF in patients who were treated with Candesartan compared with placebo, with a median follow-up period of 37.7 months.[25]

Nitroprusside

Nitroprusside results in simultaneous preload and afterload reduction by causing direct smooth-muscle relaxation, with an increased effect on afterload. Afterload reduction is associated with increased cardiac output. The potency and rapidity of onset and offset of effect make this an ideal medication for patients who are critically ill. It may induce precipitous falls and labile fluctuations in blood pressure; intra-arterial blood pressure monitoring is often recommended.

Nitroprusside should generally be avoided in the setting of acute MI. Its use is associated with the shunting of blood away from ischemic myocardium toward healthy myocardium (ie, coronary steal syndrome), which potentiates ischemia.

If nitroprusside is used, convert therapy to oral or alternative IV vasodilator therapy as soon as possible, because prolonged high-dose use is associated with thiocyanate and cyanide toxicity, particularly in patients with significant hepatic or renal dysfunction. Use in pregnancy is associated with fetal thiocyanate toxicity. Prolonged infusion can induce tolerance, and reflex tachycardia may occur.

Catecholamines

Inotropic support is usually used when preload- and afterload-reduction strategies are not successful or when hypotension precludes the use of these strategies. Two main classes of inotropic agents are available: catecholamine agents and phosphodiesterase inhibitors (PDIs). Calcium-sensitizer agents are a new class of medications that have notably beneficial effects in acute decompensated heart failure; these drugs are under investigation.

Dobutamine

Dobutamine, a catecholamine agent, mainly serves as a beta1-receptor agonist, though it has some beta2-receptor and minimal alpha-receptor activity. IV dobutamine induces significant positive inotropic effects, with mild chronotropic effects. It also induces mild peripheral vasodilation (decrease in afterload). The combination effect of increased inotropy with decreased afterload significantly increases cardiac output. Combination use with IV NTG may be ideal for patients with MI and CPE and mild hypotension to simultaneously reduce preload and increase cardiac output. In general, avoid dobutamine in patients with moderate or severe hypotension (eg, systolic BP < 80 mm Hg), because of the peripheral vasodilation.

Dopamine

The vascular and myocardial receptor effects of dopamine, a catecholamine agent, are dose dependent. Low dosages of 0.5-5 mcg/kg/min stimulate dopaminergic receptors in the renal and splanchnic vascular beds, causing vasodilation and increasing diuresis. Moderate dosages of 5-10 mcg/kg/min stimulate beta-receptors in the myocardium, increasing cardiac contractility and heart rate.

High dosages of 15-20 mcg/kg/min stimulate alpha-receptors, resulting in peripheral vasoconstriction (increased afterload), increased blood pressure, and no further improvement in cardiac output.

Moderate and high dosages are arrhythmogenic and increase myocardial oxygen demand (with the potential for myocardial ischemia). Therefore, use these dosages only in patients with CPE who cannot tolerate dobutamine because of severe hypotension (eg, systolic blood pressure 60-80 mm Hg)

Norepinephrine

Norepinephrine, a catecholamine agent, primarily stimulates alpha receptors, significantly increasing afterload (and the potential for myocardial ischemia) and reducing cardiac output. Norepinephrine is generally reserved for patients with profound hypotension (eg, systolic blood pressure < 60 mm Hg). After blood pressure is restored, add other medications to maintain cardiac output.

Phosphodiesterase inhibitors

PDIs increase the level of intracellular cyclic adenosine monophosphate (cAMP) by preventing the breakdown of cAMP to 5'AMP. This results in a positive inotropic effect on the myocardium, in peripheral vasodilation (decreased afterload), and in a reduction in pulmonary vascular resistance (decreased preload). Unlike the catecholamine inotropes, PDIs do not depend on adrenoreceptor activity. Therefore, patients are less likely to develop tolerance to PDIs than they are to other medications. (Tolerance to catecholamine inotropes can rapidly develop by means of a down-regulation of adrenoreceptors.)

PDIs are less likely than catecholamine inotropes to cause the adverse effects that are typically associated with adrenoreceptor activity (eg, increased myocardial oxygen demand, myocardial ischemia).

Several direct comparisons of PDIs (milrinone) to dobutamine in patients with CPE demonstrated that milrinone produced equal or greater improvements in stroke volume, cardiac output, PCWPs (preload), and systemic vascular resistance (afterload). However, milrinone was associated with the same or more tachycardia and with an increased incidence of tachyarrhythmias.

Furthermore, the use of milrinone in the Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) study did not reduce hospital length of stay and was associated with a significant increase in adverse events compared with placebo.[26]

All known IV inotropic agents are associated with an increased long-term mortality compared with placebo and therefore should be reserved for patients with heart failure and a markedly depressed cardiac index and stroke volume.

Calcium sensitizers

Levosimendan is a calcium sensitizer that is used in several European countries to manage moderate to severe heart failure. It has inotropic, metabolic, and vasodilatory effects. Levosimendan increases contractility by binding to troponin C. It does not increase myocardial oxygen demand, and it is not a proarrhythmogenic agent.[27, 28, 29]

Levosimendan opens potassium channels sensitive to adenosine triphosphate (ATP), causing peripheral arterial and venous dilatation. It also increases coronary flow reserve. Moreover, studies have shown levosimendan to have an anti-inflammatory effect.

Overall, levosimendan has been an effective and safe alternative to dobutamine. The most common adverse effects of levosimendan treatment are hypotension and headache. A randomized clinical study—the Survival of Patients With Acute Heart Failure in Need of Intravenous Inotropic Support (SURVIVE) trial—demonstrated no mortality benefit from levosimendan in comparison with dobutamine in patients with acute decompensated CHF.[30]

Tolvaptan

Tolvaptan is an oral vasopressin V2-receptor antagonist that was evaluated in a large (4133 patients), randomized, double-blind, placebo-controlled trial in patients with acute clinically decompensated CHF. This study, the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST), demonstrated no mortality or CHF hospitalization benefit at a median follow-up of 9.9 months. However, patients randomized to tolvaptan demonstrated early (1-7 d) improvements in body weight, dyspnea, serum sodium, and edema, as compared with placebo.[31, 32]

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Intra-Aortic Balloon Pumping

Kantrowitz initially described intra-aortic balloon pumping (IABP) in 1953, but IABP was first used clinically in 1969 in a patient with cardiogenic shock. Since the 1980s, IABP has been increasingly applied in various clinical situations as a life-saving intervention to achieve hemodynamic stabilization before definitive therapy. The IABP decreases afterload as the pump deflates, and it improves coronary blood flow as it inflates during diastole.

The intra-aortic balloon pump is inserted percutaneously through the femoral artery using a modified Seldinger technique. The distal end of the pump is placed just distal to the aortic knob and the origin of the left subclavian artery. Fluoroscopy may be used for correct positioning of the balloon, and a subsequent radiograph should be obtained to document satisfactory placement of the balloon. Helium, a low-density gas with minimal water solubility, is used to inflate the balloon.

Proper timing of counterpulsation is necessary for maximum hemodynamic support. The timing of balloon inflation and deflation are best evaluated and adjusted at a pump ratio of 1:2. Inflation of the balloon should occur in early diastole, just after the aortic valve closes, and it should correspond to the dicrotic notch of the aortic pressure waveform. Balloon deflation should occur in early systole, just before the aortic valve opens.

Proper inflation leads to an assisted peak diastolic pressure higher than the unassisted peak systolic arterial pressure. Proper deflation results in assisted aortic end-diastolic pressure of approximately 10mm Hg lower than the unassisted end-diastolic pressure.

Diastolic augmentation enhances perfusion of the coronary circulation and carotid arteries. The reduction in end-diastolic pressure decreases aortic impedance (afterload) and augments systole.

By reducing aortic impedance and systolic pressure, IABP leads to a 15-25% reduction in LV wall stress. This level of afterload reduction improves LV volume, LV emptying, and myocardial oxygen consumption.

Diastolic aortic pressure augmentation improves myocardial perfusion and coronary blood flow. The effects on coronary blood flow may be variable but generally consist of a boost of 10-20% in the ischemic territories.

IABP decreases LV filling pressures by 20-25% and improves cardiac output by 20% in patients with cardiogenic shock. Therefore, IABP substantially reduces myocardial oxygen demand, although increased oxygen supply to the myocardium may also be a beneficial effect in some clinical situations.

IABP is effective in providing temporary support to patients in cardiogenic shock and end-stage cardiomyopathy while definite therapies, such as angioplasty, cardiac bypass surgery, mechanical circulatory support, or cardiac transplantation, are undertaken. In this case, the use of IABP is considered a bridge to a definitive revascularization procedure or implementation of an LV-assist device.

IABP is effective in stabilizing patients with unstable angina refractory to medical therapy before a definitive revascularization procedure.

IABP may be a life-saving intervention in patients with acute mitral regurgitation secondary to papillary muscle rupture or in patients with ventricular septal defect as a complication of MI. IABP reduces afterload and thereby reduces the severity of mitral regurgitation. It enhances forward cardiac output, reduces LA pressure, and improves pulmonary edema. Furthermore, IABP decreases LV afterload and improves cardiac output.

IABP can also provide hemodynamic support in the perioperative and postoperative period in high-risk patients, such as those with severe coronary disease, severe LV dysfunction, or recent MI.

Contraindications

Absolute contraindications for IABP counterpulsation are a dissecting aortic aneurysm, severe aortic regurgitation, a large arteriovenous shunt, and severe coagulopathy. Relative contraindications are severe peripheral vascular disease, recent thrombolytic therapy, bleeding diathesis, and descending aortic and peripheral vascular grafts.

Complications

IABP can cause several complications, which should be monitored while the patient is receiving IABP support. In general, the patient’s platelet counts are mildly reduced; however, the counts usually do not fall below 100 x 109/L.

Complications also may occur during cannulation of the femoral artery. These include perforation, laceration, or dissection of the artery (1-6%). Thrombosis of the iliofemoral artery and distal emboli may also occur (1-7%), and limb ischemia is reported in up to 40% of patients. Limb ischemia is reversible by removing the intra-aortic balloon pump, unless thrombosis develops; if thrombosis does occur, embolectomy is required to save the limb.

The other complications are localized bleeding (3-5%), infection (2-4%), thrombocytopenia (< 1%), and intestinal ischemia (< 1%).

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Ultrafiltration

Ultrafiltration (UF) is a method of fluid removal that is particularly useful in patients with renal dysfunction and expected diuretic resistance.

The randomized Ultrafiltration Versus Intravenous Diuretics for Patients Hospitalized for Acute Decompensated Heart Failure (UNLOAD) trial demonstrated that ultrafiltration was superior to the use of IV diuretics in controlling net fluid loss and rehospitalization in hypervolemic patients with heart failure.[33] These results indicated that UF should be considered in patients with volume overload and acute CHF who have not responded well to moderate to large doses of diuretic treatment or in whom the adverse effects of such treatment (eg, renal dysfunction) do not allow initiation or continuation of the therapy. 

Use of ultrafiltration in patients with decompensated heart failure and worsening renal function compared to conventional stepwise pharmacotherapy (consisting of diuretics and inotropic agents) is associated with similar diuresis but more impaired renal function at 96 hours following the initiation of treatment.[34]  Therefore, use of ultrafiltration is generally considered after failure of pharmacologic options or when it is known in a particular patient that the clinical response to drugs will be inadequate.    

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Inpatient Care

After the patient's condition has been stabilized, further inpatient care depends on the underlying cause of the episode of CPE.

Admit patients to a telemetry unit to monitor for acute dysrhythmias. Pay strict attention to the patient's fluid balance and closely monitor fluid input and output. Maintain a negative fluid balance in patients who are fluid-overloaded by using diuretics or hemodialysis (in patients with renal failure).

Check cardiac enzyme levels to evaluate for MI. Stress testing or cardiac catheterization can also be performed during hospitalization to evaluate for reversible ischemia as the cause of pulmonary edema.

Consider echocardiography to evaluate for evidence of acute valvular dysfunction and wall-motion abnormalities and to assess the patient's ejection fraction. Patients with poor ejection fractions or severe dilated cardiomyopathies are often given digoxin.

In general, begin with oral vasodilator therapy, most commonly ACE inhibitors. If the patient was initially treated with inotropic medications, wean the patient off of these as soon as his or her condition is stable, to minimize adverse effects.

Patients in whom pulmonary edema is due to dietary factors or medication noncompliance need strict counseling and education to help prevent recurrences.

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Transfer

Transfer of patients to a tertiary receiving hospital is generally indicated if the initial hospital lacks adequate resources to care for the patient. Most patients with CPE can be treated well at community hospitals. However, if definitive surgery is required to stabilize the cause of CPE, transfer is often indicated.

Examples of patients who may require transfer include the following:

  • Patients with CPE due to acute valvular dysfunction requiring urgent valve replacement
  • Patients with acute MI that results in cardiogenic shock manifesting as CPE with hypotension (thrombolysis may be attempted at the initial hospital, but outcomes are generally poor without percutaneous coronary intervention or coronary artery bypass surgery)
  • Patients with CPE who require inotropic support or hemodialysis beyond the capabilities of the initial hospital

In severe cases of refractory cardiogenic shock, consider early transfer of appropriate patients to a tertiary medical center where, if clinically indicated, more advanced treatments, such as implantation of a left ventricular assist device may be performed.

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Consultations

Consultations with subspecialists depend on the underlying cause of the episode of CPE. If the acute episode is attributed to an acute MI, acute cardiac ischemia, or an acute dysrhythmia, consultation with a cardiologist is often warranted.

If the episode is attributed to fluid overload in a patient with renal failure, consultation with a nephrologist is indicated for emergency or urgent hemodialysis.

If CPE results from acute valvular dysfunction, consultation with a cardiothoracic surgeon (including a cardiologist) for urgent valve replacement may be indicated, depending on the integrity of the valve.

In patients who develop cardiogenic shock, consultation with a cardiologist and/or critical care specialist is generally indicated to assist with titrating inotropic medication and, in some cases, to place an intra-aortic balloon pump as a temporizing measure before surgery (eg, valve replacement or coronary revascularization).

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Contributor Information and Disclosures
Author

Ali A Sovari, MD, FACP Fellow in Clinical Cardiac Electrophysiology, Cedars Sinai Medical Center/Heart Institute

Ali A Sovari, MD, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Physician Scientists Association, American Physiological Society, Biophysical Society, Heart Rhythm Society, Society for Cardiovascular Magnetic Resonance

Disclosure: Nothing to disclose.

Coauthor(s)

Abraham G Kocheril, MD, FACC, FACP, FHRS Professor of Medicine, University of Illinois College of Medicine

Abraham G Kocheril, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Cardiology, Central Society for Clinical and Translational Research, Heart Failure Society of America, Cardiac Electrophysiology Society, American College of Physicians, American Heart Association, American Medical Association, Illinois State Medical Society

Disclosure: Nothing to disclose.

Arnold S Baas, MD, FACC, FACP Associate Professor of Medicine, Division of Cardiology, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Ronald Reagan UCLA Medical Center

Arnold S Baas, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Society of Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Amal Mattu, MD, FACEP, FAAEM, Program Director, Emergency Medicine Residency, Co-Director, Emergency Medicine/Internal Medicine Combined Residency Program, Department of Surgery, Division of Emergency Medicine, University of Maryland School of Medicine

Amal Mattu, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine.

Disclosure: Nothing to disclose.

Ari M Perkins, MD, Consulting Staff, Department of Emergency Medicine, Greenwich Hospital

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center

George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Radiograph shows acute pulmonary edema in a patient who was admitted with acute anterior myocardial infarction. Findings are vascular redistribution, indistinct hila, and alveolar infiltrates.
Radiograph shows acute pulmonary edema in a patient known to have ischemic cardiomyopathy. Findings are Kerley B lines (1mm thick and 1cm long) in the lower lobes and Kerley A lines in the upper lobes.
Radiograph demonstrates cardiomegaly, bilateral pleural effusions, and alveolar opacities in a patient with pulmonary edema.
Radiograph shows interstitial pulmonary edema, cardiomegaly, and left pleural effusion presenting at an earlier stage of pulmonary edema.
Lateral chest radiograph shows prominent interstitial edema and pleural effusions.
 
 
 
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