Chronic Dyspnea – 1

Moving on to CHRONIC DYSPNEA, defined as SOB that has been going on for at least a few weeks, maybe months, possibly getting progressively worse.  We’ll assume that COUGH is NOT a prominent component of the picture (“Chronic Cough” comes later).

Again, as discussed previously, be sure we’re dealing with true SOB, not anxiety or other imitator.  Dyspnea by definition always gets worse during exertion.  Progressive deconditioning (out-of-shapedness, if that’s a word) also does, but it’s a diagnosis of exclusion.

Our differential for Chronic Dyspnea is much more limited.

TABLE  —  ORGANIC CAUSES OF CHRONIC DYSPNEA

CARDIAC

RESPIRATORY

 bold = common

Chronic dyspnea always occurs as dyspnea on exertion (DOE) [nobody has SOB at rest for a long time without seeking care].  The conditions listed in bold are “common” insofar as they are the most likely diagnoses for patients who complain only of DOE, without prominent cough.

HEART FAILURE —  Chronic congestive heart failure (CHF) is diagnosed as described previously.  Associated symptoms of orthopnea, paroxysmal nocturnal dyspnea, & edema are suggestive.  Physical findings include bibasilar rales, JVD, HJR (hepatojugular reflux), S3 or S4 gallops, and edema.  A serum BNP is useful, though sometimes not for right-sided CHF.  A CXR may show engorged vessels, cardiomegaly, or Kerly B lines; EKG may show non-specific abnormalities.  Or maybe not.

The main diagnostic test for CHF is the echocardiogram.  It estimates the strength of ventricular contraction, sometimes reported in terms of an ejection fraction (<40% is abnormal, <20% heads for transplant), or in terms of ventricular function (“severely diminished,” etc.).  The echo can:

  • distinguish left from right ventricular dysfunction;
  • estimate pulmonary artery pressure (for pulmonary hypertensive disease);
  • diagnose valvular lesions [possible causes of CHF];
  • distinguish wall thickening (hypertensive) from dilated cardiomyopathies.

The echo can also identify focal areas of decreased heart wall motion, possibly suggesting prior M.I. in that region.  However, this is better evaluated by a stress echo, since some focal wall motion abnormalities may be due to CHF alone.

Diastolic dysfunction, i.e. impaired relaxation of a ventricle, can also cause CHF.  However, many echo reports seem to note “Grade 1 diastolic dysfunction,” making it less specific or useful.

Diagnosing CHF isn’t hard, but don’t just give furosemide, whatever else, & be satisfied if the patient improves.  You have to identify the cause of CHF.  Some common etiologies include:

  • Hypertension (due to constant strain on myocardium)
  • M.I. (due to dead myocardium)
  • Dilated cardiomyopathy (due to prior myocarditis, current alcohol, etc., etc.)

Some less common & uncommon etiologies:

  • Anemia (which may itself be due to colon cancer, etc., etc.)
  • Thyroid Disorders
  • Amyloidosis (consider if CHF with low voltage on the EKG; you get bragging rights for nailing this, though probably not a raise)
  • Chagas Disease (worth considering in immigrants from Latin America)

Right-sided CHF may be due to pulmonary disease:

  • Chronic pulmonary emboli
  • Interstitial Lung Disease (of which there are many)

You can find these lists elsewhere.  Let’s go on to the lungs.

ASTHMA (EXERCISE-INDUCED)  —  Some asthmatics have their symptoms triggered by exercise, usually vigorous exercise.  This is most easily diagnosed by successful prophylactic use of an inhaled β-2 agonist shortly before exercise.  A daily leukotriene antagonist (e.g. monteleukast [Singulair]) can be added.  If this doesn’t work, & other diagnoses are ruled out, formal pulmonary function tests [see below] can be done after a treadmill session.

ASTHMA (PERSISTENT)  —  Some asthmatics don’t cough.  Lung auscultation often detects wheezes or rhonchi, or a prolonged expiratory phase, but sometimes not.  Symptoms will certainly be worse on exertion, but this is different from exercise acting as a trigger.  A therapeutic trial of asthma medication may be diagnostic, although pulmonary function testing (PFTs) may be needed.  The key finding is an obstructive pattern, which [usually] reverses with bronchodilator administration.  Methacholine challenge test is the gold standard.  We discuss these PFTs below.

Once again, a good clinical history elucidating chronology of illness can suspect the diagnosis.  If a patient has had similar episodes in the past, you’re far and away most likely dealing with recurrent asthma.  A therapeutic trial will help tell.  Pitfalls include “cardiac asthma” (CHF presenting with wheezes instead of rales), and Hypersensitivity Pneumonitis, which we’ll address at a different time under “Cough.”

COPD (EMPHYSEMA)  —  As opposed to Chronic Bronchitis, which presents with acute episodic exacerbations of cough and SOB [we’ll address this more under “Cough”], the Emphysema component of COPD does not generate a cough.  Its only symptom is dyspnea, initially occurring at a certain level of exertion, then with progressively less.  A simple glance at a patient may reveal the classic barrel-chest, and lung exam uncovers fine wheezes, certainly a long expiratory phase.

A chest x-ray may show hyperinflated lung fields, but diagnosis is best made by PFTs.  The latter reveal an obstructive pattern which doesn’t reverse after bronchodilator, and a diminished diffusing capacity (DLCO) indicating the degree of alveolar wall destruction.  COPD is almost always a smoker’s disease, with no other effective treatment.  Unfortunately, bad PFTs have been shown ineffective in motivating smokers to quit.  Non-smoker with emphysema needs a serum alpha-1-antitrypsin level.

Emphysema often presents when the insidious exertional dyspnea eventually interferes with an important activity of daily living (ADL).  The weekend sports enthusiast may be unable to keep up with friends.  A frenetic executive may find themselves slowing down.  Dyspnea during sex is often the unacceptable ADL infringement.  [We chart “DOE” = “Dyspnea On Exertion,” but there’s no “DDS” except for the dentist].

INTERSTITIAL LUNG DISEASE (ILD)  —  As opposed to obstructive airway disease, ILD involves surrounding parenchyma.  This is restrictive disease, as opposed to obstructive.  Fine rales may be heard at the posterior bases, especially the lateral aspects, though auscultation may well be unremarkable.  CXR may note “reticular” or “nodular” “opacities,” or “honeycombing,” usually bilaterally, but perhaps only in certain zones of each lung.

Pulmonary Hypertension (PHT)  is lumped in here because it’s the end result of ILD, & prominent in the mechanism of causing dyspnea.  PHT, primay or secondary, can present with a deceptively normal CXR.

PFTs are a key to diagnosis of ILD, revealing restrictive abnormalities and a decreased DLCO.  The image of choice is a high-resolution chest CT.  In terms of PHT, the echocardiogram reveals elevated Pulmonary Artery Pressure, & eventual Right Ventricular Hypertrophy.  But once you diagnose ILD or Pulmonary Hypertension, then comes the job of sorting through the myriad of etiologies, from environmental or occupational exposures, infections, and connective tissue disease, to that all-encompassing category “idiopathic.”  Find an appropriate on-line or textbook source.

ANEMIA  —  This can cause SOB on its own, but can also cause CHF to worsen things.  Order a CBC as part of your work-up of dyspnea, & you’ll be almost home [though not until you identify the cause of anemia].

MYOCARDIAL ISCHEMIA  —  We discussed this already.  The only puzzle when a patient presents with coronary artery ischemia after months of symptoms is, “Why’d you wait so long?”  Invariably it’s because the condition is progressing, which makes it unstable.

  • Never forget to ask all patients, with any chief complaint, “Over the last X period of time, is Symptom Y getting better, getting worse, or staying the same?”

Always query your patient with Chronic Dyspnea for telltale clues of Myocardial Ischemia:

  • Risk Factors: Hypertension, Smoking, Diabetes, Family History, Hyperlipidemia, Cocaine/Meth
  • Chest Pain occurring along with the SOB.  To rule-out denial, also ask about “pressure,” “heaviness,” squeezing,” or “tightness,” not only in the Chest, but also Left shoulder, upper arm, anterior neck, or lower jaw.
  • Anginal Equivalents — “At the same time you have SOB, do you also a) Get nauseous or vomit; b) Get lightheaded; c) Break out into a cold sweat on your forehead?

Get an EKG and work-up Ischemia as described in “Chest Pain – 1.”

As for the less likely etiologies of Chronic Dyspnea, you’ll find them during standard work-up:

Pleural Effusion  —  Easily visible on a CXR.

Morbid Obesity or Skeletal Deformities  —  Easily visible, though you need to R/O other causes of dyspnea.  PFTs will confirm the restrictive nature of these conditions.

Upper Airway Disorders —  Such as tracheal stenosis: identified by PFTs.

Neuromuscular Disorders  —  PFTs will alert you.

Pericardial disease  —  Dyspnea results from restricted movement of the heart, i.e., just like CHF.  Order the echo, & you’ll find the pericardial component.

Pulmonary Emboli (Chronic)  —  Up to 4% of acute PEs, many never identified, develop into chronic pulmonary thromboembolism.  Echocardiographic abnormalities such as pulmonary hypertension, or right ventricular dysfunction or hypertrophy, will commonly clue you in to this uncommon condition.  A ventilation-perfusion (V/Q) scan is more sensitive for chronic PEs than a CT.

We’ll conclude with Chronic Dyspnea – 2 next posting, summarizing our overall approach & briefly discussing PFTs specifically.

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