> Table of Contents > Pulmonary Edema
Pulmonary Edema
Timothy R. Takagi, MD
image BASICS
DESCRIPTION
  • Pulmonary capillaries leak fluid into the lung interstitium and alveoli, leading to hypoxia and respiratory distress.
  • Fluid accumulation results from cardiogenic causes (e.g., heart failure), leading to imbalanced hydrostatic and oncotic pressures within pulmonary capillaries or from noncardiogenic causes (e.g., acute lung injury) that increase alveolar membrane permeability.
EPIDEMIOLOGY
Incidence
  • Annual heart failure incidence: 650,000 cases
  • Heart failure incidence increases with age.
    • Age 35 to 64 years: 2 cases per 1,000
    • Age 65 to 69 years: 20 cases per 1,000
    • Age >85 years: >80 cases per 1,000
  • Disparities in heart failure incidence by race and sex
    • Blacks (16.3/1,000) versus whites (11.9/1,000)
    • Men (15.8/1,000) versus women (11.7/1,000)
  • Acute respiratory distress syndrome (ARDS): 190,000 cases annually in United States
Prevalence
Heart failure syndromes: 5.8 million U.S. adults
ETIOLOGY AND PATHOPHYSIOLOGY
  • Cardiogenic causes will increase hydrostatic pressure in the pulmonary capillaries, leading to increased transvascular filtration of a protein-poor fluid into lung interstitium.
  • Systolic dysfunction is due to decreased contractility of the left ventricle (LV), leading to decreased cardiac output, which in turn stimulates the renin-angiotensin system and increases fluid retention. Diastolic dysfunction is often due to decreased LV compliance secondary to hypertrophy.
  • Cardiogenic (left-sided heart failure)
    • Impaired contractility
      • Ischemic heart disease
      • Dilated cardiomyopathy
      • Myocarditis
      • Volume overload
      • Alcoholic cardiomyopathy
    • Increased LV afterload
      • Systemic hypertension (HTN)
      • Aortic stenosis
      • Cocaine abuse
    • Poor diastolic filling
      • LV hypertrophy
      • Hypertrophic cardiomyopathy
      • Mitral stenosis
      • Atrial fibrillation
    • Valvular dysfunction
      • Mitral regurgitation
      • Acute papillary muscle rupture
    • High cardiac output states
      • Thyrotoxicosis
      • Systemic arteriovenous fistulas
      • Anemia
    • Noncompliance with medications or diet
    • Medications with negative inotropic effects
  • Noncardiogenic causes will increase permeability of the lung vasculature, leading to accumulation of protein-rich fluid in the lung interstitium and air spaces. Many causes of this vascular permeability are associated with ARDS.
  • Noncardiogenic
    • ARDS
    • Acute lung injury
    • Transfusion-related acute lung injury
    • Preeclampsia
    • Rapid ascent to high altitude (>2,500 m)
    • Drug toxicity (salicylates, opiates)
    • Embolism (thrombus, fat, air, amniotic fluid)
    • Neurogenic (after head trauma/surgery)
    • Reexpansion (after pneumothorax/thoracentesis)
Genetics
Multifactorial
RISK FACTORS
  • Cardiogenic: HTN, valvular disease, hyperlipidemia, atherosclerosis, diabetes mellitus, obesity, excessive alcohol intake, physical inactivity, dietary choices, and smoking
  • Noncardiogenic: sepsis, aspiration, pneumonia, trauma, inhaled toxins, DIC
GENERAL PREVENTION
Early detection and treatment of risk factors, including high blood pressure, diabetes, alcohol intake, obesity, and tobacco abuse (1)[A]
COMMONLY ASSOCIATED CONDITIONS
See “Etiology and Pathophysiology.”
image DIAGNOSIS
PHYSICAL EXAM
  • Vital signs: tachypnea, tachycardia, and hypoxemia. Patients may be hypotensive or hypertensive.
  • General: respiratory distress, diaphoresis
  • HEENT (head, eyes, ears, nose, throat): frothy oral secretions, cyanosis
  • Cardiac: S3 or S4, jugular venous distension, murmurs suggestive of valvular disease
  • Pulmonary: crackles or wheezing
  • Extremities: edema, cyanosis, mottled skin
DIFFERENTIAL DIAGNOSIS
  • COPD
  • Pneumonia
  • Pulmonary embolism
  • Asthma/reactive airway disease
  • Pneumothorax
  • Cardiac tamponade
  • Asphyxiant or toxic gas exposure
  • Inhalational burns
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
  • CBC/differential to screen for anemia or infection
  • Chemistry panel to screen for acute kidney injury, hyponatremia (associated with severe heart failure), or electrolyte disturbances leading to dysrhythmias
  • Troponin may be elevated from recent infarction causing acute heart failure or from myocardial ischemia secondary to elevated ventricular strain. Elevated cardiac enzymes carry a strongly negative prognosis in heart failure.
  • In settings of clinical uncertainty, B-type natriuretic peptide (BNP), or N-terminal pro-BNP, can add to clinical judgment in patients with symptoms suggestive of heart failure (1,2)[A]. BNP >500 pg/mL suggests heart failure, and BNP <100 pg/mL suggests alternative causes. BNP may also be elevated due to atrial fibrillation, renal failure, severe valvular disease, or pulmonary HTN.
  • Liver function tests (LFTs) to check for elevated transaminases, which can suggest hepatic congestion from heart failure or may indicate heavy alcohol use contributing to cardiomyopathy
  • Drug levels (aspirin, opiates, cocaine, alcohol)
  • Arterial blood gas to measure PO2 and A-a gradient
  • Serum lipase if suspicious for pancreatitis
  • TSH if suspicious for thyrotoxicosis
  • Blood/urine cultures and lactic acid if concerned for severe sepsis or septic shock
  • Urinalysis to check for nephrotic syndrome or UTI
  • Chest x-ray to evaluate for the following:
    • Pneumothorax
    • Cardiomegaly
    • Infiltrate suggestive of pneumonia
    • Increased interstitial markings, perihilar alveolar edema, or pleural effusion
  • CT pulmonary angiography if concerned for pulmonary emboli
  • ECG to evaluate for ischemia or dysrhythmias
  • Echocardiography to assess ventricular function and size, valve function, and for presence of a pericardial effusion or wall motion abnormalities (2)[C].
Follow-Up Tests & Special Considerations
Emergent echocardiography if considering cardiogenic shock, tamponade, or papillary muscle rupture
Diagnostic Procedures
  • If cause of pulmonary edema is unknown, a pulmonary artery catheter (or Swan-Ganz) can be inserted to measure the pulmonary artery capillary wedge pressure. A wedge pressure <18 mm Hg favors acute lung injury over cardiogenic pulmonary edema.
  • Patients with new-onset or worsening heart failure (without determined cause) should have further evaluation for myocardial ischemia. The pretest probability of underlying ischemic cardiomyopathy should guide the decision on which testing modality to use (1)[C].
image TREATMENT
GENERAL MEASURES
  • Guide all treatment based on the suspected cause.
  • Start with supplemental oxygen.
MEDICATION
Cardiogenic pulmonary edema
P.883

First Line
  • Diuretics: reduce preload for acute cardiogenic edema; used in low doses daily for chronic heart failure to manage volume overload. If on chronic diuretics, start IV dose at or above home dose and titrate for acute cardiogenic edema. Onset is 15 to 30 minutes for IV loop diuretics. Monitor for electrolyte derangement and renal dysfunction. Use very carefully in patients with aortic stenosis.
    • Acute: furosemide 40 to 80 mg IV, torsemide 10 mg IV, or bumetanide 1 mg IV
    • Chronic: furosemide 20 to 80 mg q6-8h, torsemide 20 mg/day, or bumetanide 1 mg q12h
  • ACE inhibitors or angiotensin receptor blockers (ARBs): reduce afterload for systolic heart failure. Maintenance therapy may be cautiously continued during exacerbation. Avoid in acutely ill patients with hypotension, acute kidney insult, hyperkalemia, or poor diuresis. Use ARBs in patients who are ACE inhibitor-intolerant.
    • Target dose for chronic heart failure: lisinopril 20 to 40 mg/day, enalapril 10 to 20 mg q12h, captopril 50 mg q8h, candesartan 32 mg/day, valsartan 160 mg q12h, losartan 100 mg/day
  • &bgr;-Blockers: reduce afterload for systolic heart failure. Maintenance therapy may be continued for mild decompensation; hold or reduce dose for moderate to severe decompensation. Avoid if patients are hypotensive or recently received inotropic therapy. Do not initiate until recovery from acute exacerbation of heart failure.
    • Target dose for chronic heart failure: carvedilol 25 mg q12h, metoprolol ER 200 mg/day, bisoprolol 10 mg/day
  • Inotropes: Improve contractility in hypotensive patients with severe systolic heart failure and signs of systemic hypoperfusion (2)[B]. Inotropes increase myocardial oxygen demand and may damage the ischemic myocardium.
    • Dobutamine: 5 to 10 &mgr;g/kg/min IV, titrate
    • Milrinone: loading dose (optional): 50 &mgr;g/kg IV over 10 minutes, then infuse 0.375 to 0.750 &mgr;g/kg/min, titrate
    • Dopamine: 5 to 10 &mgr;g/kg/min IV, titrate
    • Norepinephrine: 2 to 4 &mgr;g/min IV for acute cardiogenic shock following acute MI; not for use in acute decompensated heart failure
  • Nitrates: Acute cardiogenic pulmonary edema use IV nitrate vasodilators. Rapid onset. Nitroglycerin IV 5 to 10 &mgr;g/min, titrate 5 to 10 &mgr;g/min q3-5min to max 200 &mgr;g/min until distress resolved or onset of hypotension. For severe HTN, consider IV nitroprusside 5 to 10 &mgr;g/min, titrate. Max 400 &mgr;g/min. Use <48 hours due to risk of cyanide toxicity.
    • For patients who are not tolerant of ACE inhibitors or ARBs, hydralazine and an oral nitrate should be started (1)[C].
  • Precaution: Monitor the additive hypotensive effects of diuretics, nitrates, and afterload reducers.
Second Line
  • Thiazide diuretics: hydrochlorothiazide (HCTZ) 25 to 50 mg/day PO, metolazone 2.5 to 10 mg/day PO
  • Spironolactone: 25 to 50 mg/day PO; recheck renal function and electrolytes in 7 to 10 days
  • Digoxin: 125 &mgr;g/day PO, titrate to serum concentration of 0.5 to 0.8 ng/mL
  • Noncardiogenic pulmonary edema
    • High-altitude pulmonary edema
      • Descent is the single best treatment (3)[A].
      • Adjunctive therapy: supplemental oxygen. Consider nifedipine ER 30 mg PO q12h or sildenafil 50 mg PO q8h or tadalafil 10 mg PO q12h (3)[C].
ISSUES FOR REFERRAL
  • Cardiology referral for underlying cardiac disease
  • Patients with ARDS should be carefully monitored in an ICU setting.
ADDITIONAL THERAPIES
  • Noninvasive positive pressure ventilation (NPPV) should be considered early for emergency department patients with acute respiratory distress from cardiogenic pulmonary edema/congestive heart failure (CHF). NPPV decreases preload and afterload, thereby alleviating symptoms and potentially avoiding intubation by allowing time for medications to work. Use cautiously if patients are hypotensive (4)[A].
  • Early invasive ventilation should be considered for patients with noncardiogenic pulmonary edema secondary to acute respiratory distress syndrome.
SURGERY/OTHER PROCEDURES
  • Extracorporeal membrane oxygenation (ECMO) for severe refractory hypoxia/ARDS
  • Intra-arterial balloon pump for cardiogenic shock
  • Implantable cardioverter defibrillator (ICD) for sudden cardiac death prevention in patients with prior cardiac arrest or ischemic/dilated cardiomyopathy and LVEF <30% (2)[B]
  • Cardiac resynchronization therapy (CRT) may be useful for LVEF ≤35%, sinus rhythm, and QRS >0.15 m/s (2)[B].
  • LV assist device (LVAD) for severe systolic dysfunction as bridge to a heart transplant (2)[B].
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
  • Hypotension
  • Acute kidney injury
  • Altered mental status
  • Dyspnea at rest
  • O2 saturation <90%
  • Acute coronary syndromes
  • Arrhythmias (i.e., new-onset atrial fibrillation)
  • Mild distress: oxygen by nonrebreather mask
  • Significant hypoxia
  • Intubation for patients with apnea, altered mental status, or hypoxia despite NPPV
IV Fluids
Use crystalloid infusions cautiously. Limit free water.
Nursing
  • Daily weights, strict input/output
  • Assess for functional improvement.
Discharge Criteria
  • Underlying condition treated, fluid status optimized
  • Started &bgr;-blocker and ACE inhibitor in patients with CHF (1)[B]
  • Patient and family educated about diet/medications
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
  • Strict input/output measurement, daily weights
  • Posthospitalization appointment in 7 to 10 days
DIET
Low-sodium diet (<2 g/day), fluid restriction (<2 L/day) (2)[C]
PATIENT EDUCATION
  • Dietary precautions
  • Early signs and symptoms of fluid overload
  • Adjust diuretic dose based on recent weight gain.
PROGNOSIS
Mortality: 30-60% for noncardiogenic edema/ARDS; up to 80% for cardiogenic causes
REFERENCES
1. Lindenfeld J, Albert NM, Boehmer JP, et al. HFSA 2010 comprehensive heart failure practice guideline. J Card Fail. 2010;16(6): e1-e194.
2. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013; 62(16):e147-e239.
3. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med. 2010;21(2):146-155.
4. Vital FM, Saconato H, Ladeira MT, et al. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Cochrane Database Syst Rev. 2008;(3):CD005351.
Additional Reading
&NA;
Putensen C, Theuerkauf N, Zinserling J, et al. Metaanalysis: ventilation strategies and outcome of the acute respiratory distress syndrome and acute lung injury. Ann Intern Med. 2009;151(8):566-576.
See Also
&NA;
Altitude Illness; Congestive Heart Failure: Differential Diagnosis; Respiratory Distress Syndrome, Acute (ARDS)
Codes
&NA;
ICD10
  • J81.1 Chronic pulmonary edema
  • J81.0 Acute pulmonary edema
Clinical Pearls
&NA;
  • Diagnosis of the underlying etiology is essential.
  • Initial treatment of acute cardiogenic edema among hypertensive/normotensive patients includes IV diuretics, IV nitrates, and NPPV.
  • Hypotensive patients with pulmonary edema due to CHF will require careful use of inotropes and vasopressor to improve hemodynamic stability.
  • Pulmonary edema from ARDS has very high mortality and requires ICU-level care. Home dietary and medication management are critical for long-term treatment of CHF.