Chronic Dyspnea – 2

Last posting (Chronic Dyspnea – 1) we surveyed the possible causes of SOB lasting >3-4 weeks — primarily noted only upon exertion, in particular WITHOUT a prominent COUGH — and discussed six in some detail.  Today, we’ll summarize our overall approach.  Once again, our differential:

TABLE  —  ORGANIC CAUSES OF CHRONIC DYSPNEA

CARDIAC

RESPIRATORY

bold = common

First, decide if Myocardial Ischemia is a possibility, by risk factors, setting, & associated symptoms [chest pain/pressure & other angina equivalents] as we discussed.  If so, work it up with EKG & stress testing [see posting Chest Pain – 1].

But let’s assume it’s not a consideration.  Then focus on the Lung Exam:

**  Bibasilar rales (with normal inspiratory : expiratory phases) suggests CHF, especially in the older (elder?) patient.  Edema, maybe even JVD/HJR, clinches it.

**  Bilateral wheezes with expiration longer than inspiration (“E>I”) suggests Asthma or COPD:

  • If non-smoker, it’ll certainly be asthma, especially if they also cough.
  • If long smoking history, bet on emphysema (& chronic bronchitis if also coughs).
  • Though unlikely, keep “cardiac asthma” in mind (i.e. CHF that happens to sound like asthma).

If asthma seems likely, go for a therapeutic trial.

If not, or if symptoms remain unchanged after a trial, Order:

  • Chest X-Ray (CXR)
  • CBC
  • BNP if CHF is a possibility (EKG too)
  • Metabolic panel & thyroid tests if you can’t completely rule out “fatigue” vs. “SOB.”

No diagnosis?  And you’re convinced the patient has true dyspnea?  We’re probably heading for an echocardiogram [not a stress echo, which is only to R/O ischemia] and/or PFTs.

  • The echo will define Left Ventricular Function (decreased in CHF), identify pericardial disease, and find Pulmonary Hypertension (right ventricular hypertrophy, decreased right ventricular function, and/or increased pulmonary artery pressure).
    • If chronic Pulmonary Emboli are a consideration because of Pulm HTN, a V/Q Scan is more sensitive than the CT used for acute PEs
  • PFTs are especially important in diagnosing restrictive disease, particularly Interstitial Lung Disease (ILD).

Pulmonary Function Tests:  PFTs measure:

  1. Flow Rates [how fast one can exhale];
  2. Volumes [how much air one can & can’t exhale]; &
  3. Diffusing Capacity (DLCO) [how much oxygen crosses the alveoli into the blood].

“Spirometry,” often available in primary care settings, only measures flow rates, though this is usually the most useful.  With spirometry alone, you can diagnose asthma and COPD.  But office-based spirometry requires both high-level upkeep of equipment, and well-trained staff.

Whoever assists with spirometry must be well-versed in patient coaching.  Professional respiratory technicians in pulmonary labs are excellent at helping patients through maneuvers, & commenting to you upon any lack of cooperation or effort which may affect results.  Children <6 may not be suitable for testing unless techs are exceptionally able.  Another advantage to ordering PFTs through a pulmonary lab is that you get complete testing, and an expert interpretation.  But you can’t bill, as you could with your own in-house spirometer.

Always tell patients NOT to use albuterol inhalers for at least 4 hours before testing.  Then you can test before & after bronchodilator administration, to see if values improve [“reversibility”].  Results are reported both as raw numbers, and also as “percent predicted,” based on a patient’s age, gender, height, & perhaps waist circumference.  “Percent predicted” is what counts.

PFTs distinguish obstructive vs. restrictive disease.  The former comprises primarily asthma & COPD [duh] (chronic bronchitis & emphysema).  Restrictive includes everything else, especially ILD.  Results include a myriad of values, most of which can be ignored.  The important ones are:

  • FVC (forced vital capacity)  —  Total air you force out.  Normal = no restrictive disease.
  • FEV1 = Forced Expiratory Volume that’s exhaled in 1 second
  • FEV1 : FVC ratio  —  If low, there’s obstructive disease.

In plain speech, a low FEV1 : FVC means a patient can’t exhale well.  Old air stays trapped in the airways, “obstructing” fresh air entering with each new breath.  With restrictive disease, patients exhale fine.  But lung volumes are small, so the total amount of air inhaled (& exhaled) is “restricted.”

If you find obstructive disease which gets better after bronchodilators (“reversible”), it’s asthma.  The FEV1 should increase by at least 12%.  Lack of reversibility doesn’t exclude asthma, but in a smoker, certainly points to emphysema.  If PFTs are normal, the gold standard for diagnosing asthma is a methacholine challenge test, mostly used for patients not responding to aggressive asthma therapy, in whom you still suspect the diagnosis.  A squirt of methacholine provokes a drop in the FEV1 [safely done in a pulmonary lab, with nebulizers & trained techs on hand].

Peak expiratory flow rate (PEFR) derived from cheap peak flow meters is a poor-guy’s version of an FEV1.  They’re very inaccurate overall, but useful for changes in a given patient; improvement after bronchodilator suggests asthma (“reversibility”).

For good PEFR testing: a) perform standing; b) patient’s lips must make a good seal; c) tell patient not to put tongue in the mouthpiece; d) do lots of coaching for good effort; e) report the best of 3 tries (not the average).

Restrictive Disease — Decreased lung volumes, from testing in a formal PFT lab.  But the most important measurement is the diffusing capacity (DLCO).  Only look at the plain DLCO on report, not the “corrected” or the “DLCO/VA,” which aren’t useful.

  • Normal FEV1 : FVC and decreased DLCO = restrictive disease
  • Reduced FEV1 : FVC & decreased DLCO = COPD with emphysema
  • DLCO <40% of predicted = severe disability: 1/3 of patients will be dead in 4 years.  However, Social Security requires <30% predicted to qualify for disability payments.
  • Restrictive disease by flows & volumes, with normal DLCO = non-pulmonary disease such as neuromuscular conditions, or obesity.

It took me 30 years before I realized what the “L” meant in “DLCO” — the original phrase was “Diffusing Capacity of the Lung for Carbon Monoxide.  In terms of the carbon monoxide (CO), don’t be scared: an infinitesimally-tiny amount is used to make measurements during the test.

If PFTs diagnose restrictive disease, ILD is the major concern.  The list is long, some treatable, others preventable, a few transplantable.  The next step in diagnosis is a high-resolution chest CT (HRCT).  Then comes referral to pulmonology for probable biopsy.  One key ILD not to miss is hypersensitivity pneumonitis, which we’ll address another time under “COUGH.”

STOP  —  WAIT !!!

Deconditioning or Anxiety as the cause of chronic “dyspnea” are diagnoses of exclusion.  However, I’ve occasionally identified hyperventilation right on the first visit, obviating the need for any additional work-up.  Perform an exhaustive lung exam, listening to all lung fields, as the patient takes deep breaths.  If the patient slows down, acknowledging that this reproduces their “SOB” [& they also deny worsening of “dyspnea” upon exertion], you’ve saved a lot of trouble & $$$.

We’re done with DYSPNEA.  Next topic, covering similar subject matter [though avoiding repetition] — COUGH.

Advertisements

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google+ photo

You are commenting using your Google+ account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s