Concluding the topic “ACUTE (i.e. Recent-Onset”) DYSPNEA in the patient without obvious distress, and with normal vital signs and oxygen saturation. Once you determine that a patient indeed experiences SOB, or at least dyspnea on exertion (DOE), and not simply “fatigue,” anxiety, or another mimic which doesn’t truly impair oxygen exchange, take it very seriously. Causes of true dyspnea have guarded prognoses.
TABLE — CAUSES OF ACUTE DYSPNEA
CARDIAC
|
PULMONARY
|
UPPER AIRWAY
MISC. METABOLIC CAUSES |
bold = common
To review — the last 2 posts Acute Dyspnea – 2 and Acute Dyspnea – 3 we’ve:
** Sought risk factors & associated symptoms of coronary artery disease, either Acute M.I. or Ischemia:
- Send to ER if thinking MI
- Obtain EKG & order stress testing if suspecting ischemia.
** Thought about a Pulmonary Embolism, inquiring about very sudden onset of SOB, & about risk factors:
- Send to ER if suspicious.
** Looked for evidence of Congestive Heart Failure:
- Symptoms: orthopnea, PND.
- Signs: Bibasilar rales, JVD, Hepatojugular reflux, S3 or S4 gallops, edema.
- Obtain a BNP if it’s a possibility; Order an Echocardiogram if CHF seems likely.
** Considered Pneumonia:
- Fever, with cough and/or focal rales.
- Chest X-ray is easily diagnostic.
** Didn’t forget about Upper Airway Disease (stridor)
** Remembered the rare possibility of Anaphylaxis: wheezing or stridor, with specific criteria including hives, angioedema, itching, classic exposure, vomiting/abdominal pain, hypotension.
!!!! PROBABLY decided to diagnose Bronchospasm — i.e. Asthma / COPD Exacerbation, because:
- Patient is afebrile.
- We hear wheezes or rhonchi; AND / OR
- There’s a long expiratory phase.
- There’s some sort of cough.
If we diagnose “bronchospasm”, we treat as such — with inhalers, NOT antibiotics (unless a longtime smoker with new-onset green sputum).
BUT… for a patient with new-onset bona fide dyspnea who clinically does NOT convincingly seem to have bronchospasm, at a minimum order:
- CBC (for anemia) and chest X-ray (CXR).
- For older patients, add a BNP to rule out heart failure.
- A basic metabolic panel and TSH can screen for the variety of metabolic causes.
- An EKG might be helpful if abnormal (a normal EKG says nothing; it can be found in virtually any cardiac illness).
The CXR will easily identify pneumonia, pneumothorax, pleural effusion, and maybe even a pericardial effusion. Oftentimes you will have already suspected some of these on physical exam:
- Pneumothorax — unilaterally diminished breath sounds, resonant or hyperresonant to percussion.
- Pleural Effusion — unilaterally diminished breath sounds with signs of consolidation: dull to percussion, egophony (patient repeats “E-E-E,” sounds like “A-A-A,” chart “E → A”).
- Pneumonia — fever, cough, and focal rales. Possibly signs of consolidation as above.
Note that some of the entities in our table are not exactly diseases, but rather pathological manifestations with many possible etiologies. Pleural & pericardial effusions can be due to various infections, cancers, auto-immune diseases, etc. They require additional diagnostic work-up, too cookbook in nature (boring) to discuss here; many references are around, on- & off-line.
Even to say “pneumonia,” doesn’t tell us the specific bug (or drug), though we’ll discuss this one in more depth when we hit “cough.” The same with “heart failure,” which we’ll elaborate on next posting.
If these initial tests are unrevealing, symptoms persist, and we remain convinced that our patient is truly suffering from Dyspnea, next steps in the work-up are an echocardiogram and pulmonary function tests, maybe a high-resolution chest CT. We’ll discuss these more when we get to “Chronic Dyspnea”.
But a word about acute Myocarditis, usually viral, which presents as a form of heart failure. It’s uncommon, occurs mostly in young persons, and thus is often misdiagnosed as asthma (dyspnea and cough) or pulmonary infection (dyspnea with fever & myalgias). Any time you diagnose “New Onset Asthma” in a youngish person, at least think if myocarditis might be a possibility. If they don’t respond to nebulizers & other asthma treatment, question your diagnosis.
Clinical findings of acute myocarditis are similar to those of any cause of failure, but providers get fooled by the patient’s age. CXR often shows cardiomegaly. The best lab test is not the BNP but the common liver transaminase AST [an old “cardiac enzyme” used to diagnose M.I. before troponins or CK-MBs were invented]. An echocardiogram is definitive.
In the pre-antiretroviral days of AIDS 20 years ago, I missed a case of Pneumocystis carinii pneumonia (PCP) one evening, because my patient had normal vital signs and a normal O2-saturation. I hadn’t learned to recheck the “sat” after exercise. Fortunately his next-day CXR was diagnostic, but I should have sent him initially (for same-day film & blood gas). “Exercise” means enough to bump the heart rate — I have patients scurry up-&-down a flight of stairs (NOT if angina/MI is a possibility). The standardized maneuver is a 6-minute level walk.
Once Again — Take the complaint of acute DYSPNEA seriously — anything that threatens our oxygen supply can be fatal. Of course, determine that the patient’s “SOB” actually corresponds to what we mean by “Dyspnea” (best established by confirming that symptoms exacerbate with exertion). If not, we’re dealing with “Fatigue,” which has a completely different differential.
Today’s posting was brief. See also our previous postings Acute Dyspnea – 2 (pulmonary embolism, in depth) and Acute Dyspnea – 3 (CHF & other causes), as well as Acute Dyspnea – 1 (approach to Life-Threatening SOB). Next time we’ll go on to the work-up of Chronic Dyspnea.