Cardiogenic Pulmonary Edema Clinical Presentation

  • Author: Ali A Sovari, MD, FACP; Chief Editor: Henry H Ooi, MBBCh   more...
 
Updated: Feb 3, 2012
 

History

Patients with cardiogenic pulmonary edema (CPE) present with the dramatic clinical features of left heart failure. Patients develop a sudden onset of extreme breathlessness, anxiety, and feelings of drowning. Clinical manifestations of acute CPE reflect evidence of hypoxia and increased sympathetic tone (increased catecholamine outflow).

Patients most commonly complain of shortness of breath and profuse diaphoresis. Patients with symptoms of gradual onset (eg, over 24 h) often report dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea.

Cough is a frequent complaint and may provide an early clue to worsening pulmonary edema in patients with chronic LV dysfunction. Pink, frothy sputum may be present in patients with severe disease. Occasionally, hoarseness may be present as a result of recurrent laryngeal nerve palsy from mitral stenosis or pulmonary hypertension (Ortner sign).

Chest pain should alert the physician to the possibility of acute myocardial ischemia/infarction or aortic dissection with acute aortic regurgitation, as the precipitant of pulmonary edema.

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Physical Examination

Physical findings in patients with CPE are notable for tachypnea and tachycardia. Patients may be sitting upright, they may demonstrate air hunger, and they may become agitated and confused. Patients usually appear anxious and diaphoretic.

Hypertension is often present, because of the hyperadrenergic state. Hypotension indicates severe LV systolic dysfunction and the possibility of cardiogenic shock. Cool extremities may indicate low cardiac output and poor perfusion.

Auscultation of the lungs usually reveals fine, crepitant rales, but rhonchi or wheezes may also be present. Rales are usually heard at the bases first; as the condition worsens, they progress to the apices.

Cardiovascular findings are usually notable for S3, accentuation of the pulmonic component of S2, and jugular venous distention. Auscultation of murmurs can help in the diagnosis of acute valvular disorders manifesting with pulmonary edema.

Aortic stenosis is associated with a harsh crescendo-decrescendo systolic murmur, which is heard best at the upper sternal border and radiating to the carotid arteries. In contrast, acute aortic regurgitation is associated with a short, soft diastolic murmur.

Acute mitral regurgitation produces a loud systolic murmur heard best at the apex or lower sternal border. In the setting of ischemic heart disease, this may be a sign of acute MI with rupture of mitral valve chordae. (See the image below.)

Radiograph shows acute pulmonary edema in a patienRadiograph shows acute pulmonary edema in a patient who was admitted with acute anterior myocardial infarction. Findings are vascular redistribution, indistinct hila, and alveolar infiltrates.

Mitral stenosis typically produces a loud S1, opening snap, and diastolic rumble at the cardiac apex.

Another notable physical finding is skin pallor or mottling resulting from peripheral vasoconstriction, low cardiac output, and shunting of blood to the central circulation in patients with poor LV function and substantially increased sympathetic tone. Skin mottling at presentation is an independent predictor of an increased risk of in-hospital mortality.

Patients with concurrent right ventricular (RV) failure may present with hepatomegaly, hepatojugular reflux, and peripheral edema.

Severe CPE may be associated with a change in mental status, which can be caused by hypoxia or hypercapnia. Although CPE is usually associated with hypocapnia, hypercapnia with respiratory acidosis may be seen in patients with severe CPE or underlying chronic obstructive pulmonary disease (COPD).

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Contributor Information and Disclosures
Author

Ali A Sovari, MD, FACP  Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois College of Medicine; Staff Physician and Hospitalist, St John Regional Medical Center, Cogent Healthcare, Inc

Ali A Sovari, MD, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Physiological Society, and Heart Rhythm Society

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, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, and Illinois State Medical Society

Disclosure: Nothing to disclose.

Arnold S Baas, MD, FACC, FACP  Assistant Professor of Medicine, Division of Cardiology, University of California, Los Angeles School of Medicine; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital

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, and American Society of Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MBBCh  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.

Additional Contributors

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

References

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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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