Cardiac Pulmonary Edema

Pulmonary alveolar edema ( Fig 15.3 ) is a classic example of a diffuse air space filling process ( Chart 15.1 ). The presence of alveolar edema, however, does not imply the absence of interstitial edema. Cardiac pulmonary alveolar edema is always preceded by interstitial edema, but the extensive alveolar consolidation obscures the fine reticular opacities of the interstitial process. Radiologic documentation of the underlying interstitial process entails examination of areas not significantly involved by the alveolar filling process. When alveolar pulmonary edema is secondary to congestive heart failure, the alveolar edema often has a perihilar distribution, and Kerley B lines may be present in the costophrenic angles.

Pulmonary edema is one of the most common causes of diffuse bilateral confluent air space opacities. Associated pleural effusions and cardiac enlargement should confirm the diagnosis of pulmonary alveolar edema resulting from congestive heart failure.

The latter sign confirms the underlying interstitial process. Other radiologic signs that may be associated with cardiopulmonary edema and can be helpful in suggesting the diagnosis include: (1) prominence of the upper lobe vessels ⁴⁵⁴ ; (2) indistinctness of vessels ²⁹¹ ; (3) peribronchial cuffing ³⁹⁰ ; (4) increased width of the vascular pedicle ³⁹⁰ ; (5) pleural effusion, frequently with fluid in the fissures; and (6) cardiac enlargement with a left ventricular prominence. Correlation of the radiologic findings with clinical findings usually confirms the diagnosis. An electrocardiogram indicating cardiac enlargement or an old or acute myocardial infarction is also supportive evidence, whereas an S3 heart sound, neck vein distention, hepatomegaly, or peripheral edema usually confirm the diagnosis of congestive failure. Also, auscultation over the lungs usually reveals characteristic basilar rales.

Occasionally, alveolar edema is not distributed uniformly. As a result of gravity, when the patient is upright, the edema fluid has a predominantly lower lobe distribution, but when the patient is supine, the fluid tends to have a more posterior distribution. When the patient favors one side, the fluid tends to gravitate to the dependent side. The resolution of pulmonary edema is often not uniform, so that serial chest radiographs reveal a change in the distribution from diffuse perihilar opacities to a pattern of more uneven multifocal opacities. Other causes for atypical or nonuniform distribution of pulmonary edema are usually of pulmonary origin. The best known of these is severe emphysema, which results in a patchy distribution of the alveolar edema. Presumably, loss of vasculature in the emphysematous areas of the lung results in the development of edema in the more normal areas. Pulmonary embolism is a complication of pulmonary edema that may result in a nonuniform or patchy distribution of the alveolar edema. Two factors may determine the distribution of the air space edema following pulmonary embolism: (1) abrupt interruption of perfusion to an area of lung may prevent the development of typical pulmonary edema; and (2) severe ischemia of the lung may give rise to pulmonary hemorrhage. Clinical suspicion of pulmonary embolism in a patient with congestive heart failure will usually require computed tomography angiography (CTA).

Concomitant infection is another cause of uneven distribution of pulmonary edema. Like the diagnosis of pulmonary embolism, this requires correlation with the clinical history. An elevated temperature, leukocytosis, or purulent sputum should prompt a bacteriologic study to rule out superimposed pneumonia.

Cardiac enlargement in combination with diffuse alveolar opacities that are otherwise characteristic of pulmonary edema is not always a reliable indicator that the patient’s primary problem is a cardiac disorder. For instance, chronic renal failure with uremia can cause pulmonary edema (uremic pneumonitis) as well as hypertension and associated heart disease, with the result of cardiac enlargement. Not only does uremia cause true cardiomegaly, which is probably related to chronic hypertension, but it also may cause pericardial effusion. Thus, the pulmonary edema that results from chronic renal failure and uremia is typically associated with enlargement of the cardiac silhouette. Correlation with the clinical history should readily identify uremic pneumonitis.

In contrast to pulmonary alveolar edema and cardiac enlargement, the presence of a normal-sized heart might suggest a noncardiac form of pulmonary edema, but there are situations in which such patients may actually have cardiac pulmonary edema. These include acute cardiac arrhythmias and acute myocardial infarction, which result in pulmonary edema before dilation of the heart. Thus, there are at least two mechanisms for cardiac pulmonary edema with a normal-sized heart.

Noncardiac Pulmonary Edema

The preceding discussion suggests that the radiologic appearance of noncardiac pulmonary edema is similar to that of cardiac pulmonary edema. ⁵⁴⁶ In general, the most helpful radiologic feature for distinguishing the two is the presence or absence of cardiac enlargement. Accurate assessment of heart size is often difficult. Technical factors—including supine and anteroposterior positioning, especially when done with portable units—may all contribute to cardiac magnification. Patient condition may also lead to inaccurate cardiac size estimation. Patients with emphysema often have cardiac enlargement, although the chest radiograph is suggestive of a normal or even small heart size. Aggressive intravenous (IV) fluid resuscitation may actually enlarge the heart and cause pulmonary edema. The evaluation of serial radiographs is especially useful for distinguishing a number of the causes of noncardiac edema because the evolution of the edema may be strikingly different. Many of the entities listed in Chart 15.2 may result in acute alveolar edema in the absence of the pulmonary vascular and interstitial changes that precede the edema because of either renal failure or cardiac failure. These entities tend to occur in very acute cases of pulmonary edema and are often best diagnosed by clinical correlation, ⁵ as is shown in the following discussions of acute toxic inhalations, near-drowning, acute airway obstruction, drug reactions, and ARDS.

Chart 15.2

• I.
  

  Chronic renal failure

  
  
• II.
  

  Toxic inhalations

  
  
  
  
  • A.
    

    Nitrogen dioxide (silo filler’s disease)

    
    
  • B.
    

    Sulfur dioxide ⁷⁴

    
    
  • C.
    

    Smoke 285 , 446

    
    
  • D.
    

    Beryllium

    
    
  • E.
    

    Cadmium

    
    
  • F.
    

    Silica (very fine particles; silicoproteinosis) ²⁹⁹

    
    
  • G.
    

    Carbon monoxide ⁵⁴⁹

  
  
  
  
• III.
  

  Anaphylaxis (e.g., penicillin, transfusion, ⁶² radiologic contrast medium ²⁰⁵ )

  
  
• IV.
  

  Narcotics (e.g., morphine, methadone, cocaine, heroin) 201 , 473 , 671

  
  
• V.
  

  Drug reaction (e.g., interleukin-2 therapy, 90 , 518 β-adrenergic drugs ³⁹¹ )

  
  
• VI.
  

  Acute airway obstruction ⁴²² (e.g., foreign body)

  
  
• VII.
  

  Near-drowning ⁴⁴⁸

  
  
• VIII.
  

  High altitude ²⁵⁴

  
  
• IX.
  

  Fluid overload

  
  
• X.
  

  Cerebral (trauma, stroke, tumor) ⁴⁶⁷

  
  
• XI.
  

  Hypoproteinemia

  
  
• XII.
  

  ARDS (early stages) 277 , 291

  
  
• XIII.
  

  Pancreatitis ⁴⁹⁴

  
  
• XIV.
  

  Amniotic fluid embolism ⁵³⁷

  
  
• XV.
  

  Fat embolism

  
  
• XVI.
  

  Re-expansion following treatment of pneumothorax or large pleural effusion

  
  
• XVII.
  

  Organophosphate insecticide ingestion ³³⁹

  
  
• XVIII.
  

  Hanta virus pulmonary syndrome ²⁹¹

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related posts:

Introduction Shift of the Mediastinum Anterior Mediastinal Mass Atelectasis Hyperlucent Thorax Multiple Lucent Lesions

Stay updated, free articles. Join our Telegram channel

Join