Continuing with our discussion of ACUTE DYSPNEA, onset within 1-2 weeks (often just days). Remember, we’re not talking here about the person in obvious distress, as we had earlier. This topic now pertains to patients who look fine, with normal O2 sats. Last posting (Acute Dyspnea – 2) we covered Pulmonary Embolism; on to the rest.
TABLE — CAUSES OF ACUTE DYSPNEA
MISC. METABOLIC CAUSES
bold = common
** HEART FAILURE (CHF) — Dyspnea is the cardinal symptom of pump dysfunction, especially left-sided heart failure. Ask about other Symptoms:
- paroxysmal nocturnal dyspnea (PND, waking up suddenly at night with acute SOB)
- pedal edema
- chest pain (“pressure” / “tightness” / “discomfort”) — failure is often precipitated by an M.I.
Bibasilar Rales — The cardinal sign of CHF, crackles at both bases during inspiration. Beware of spurious sounds which mimic rales. Hairy chests can generate confusion, as can gas in the GI tract. The most common imitator of rales is upper airway noise. I may have to take the stethoscope out of one of my ears and listen to the mouth/nose simultaneously with the lungs, to determine where sounds originate. Sometimes I ask a patient to “take deep, quiet breaths,” demonstrating myself how I’d like them to breathe for me to auscultate.
Signs of CHF include:
- Bibasilar Rales
- Jugular venous distention (JVD)
- Hepatojugular reflux [transient JVD when you press on the liver, with patient at 45° recumbency]
- S3 or S4 Gallop
- Pedal edema.
A word about Gallops. These are low-pitched diastolic sounds. You must roll the patient slightly onto their left side & listen at the apex (PMI) with your bell (being sure you have a good seal). Otherwise, you can’t chart “no gallop.”
Listen carefully for a soft, momentary sound right after S2 (which would be an S3). Listen carefully for a soft, momentary sound right before S1 (for the S4). If you think you hear one, press hard with the bell “converting” it into a “diaphragm” — the gallop should disappear (it’s low-pitched). Ease up, it becomes a bell again, the sound should return. Do this a few times to confirm the finding for yourself. Gallops can be normal in young people.
Auscultating the heart, also search for arrhythmias and murmurs which may suggest the source of failure.
Brain-type Natriuretic Peptide (BNP), the key blood test for CHS [it’s associated with ventricular stretch]. Many patients with new, mild failure may have no physical findings, and no symptoms other than dyspnea on exertion. The BNP is much more accurate than chest x-ray or EKG. Values >400 pg/ml are quite specific, except in renal failure. Values <100 pg/ml are quite sensitive in ruling out CHF. The BNP is about as good as an echocardiogram, except in young people with myocarditis, or cardiomyopathies.
I’ve had a rare patient inquire what “BNP” means. Be careful when you mention “brain.” Once you get to “natriuretic,” they’ll probably be satisfied at least you know what it’s all about.
Causes of CHF — there are many, including worn out myocardium from long-standing hypertension, dead myocardium from prior M.I., valvular heart disease, arrhythmias, renal failure, various cardiomyopathies (due to alcohol / toxins, collagen-vascular or metabolic diseases, etc.), viral myocarditis (affecting young people), and more. Look these up.
Maybe the failure is due to anemia, which is due to colon cancer. If you diagnose CHF, always ask yourself, “why?”!
** MYOCARDIAL INFARCTION — Don’t miss this one. We discussed it before (Chest Pain – 1), but a little review in terms of the patient whose chief complaint is “SOB.”.
Identify Risk Factors. If there aren’t any, the likelihood of an M.I. is quite low, especially the younger the age. If there are risks, with new onset SOB, it’s hard to dismiss.
Inquire about Chest Pain. If present, determine if it is pleuritic [occurs predictably with each inspiration or cough]. If clearly pleuritic, think pulmonary, NOT coronary. Adjectives for the pain of cardiac ischemia: dull, achy, heavy, pressing, squeezing.
Cardiac ischemic pain is usually in mid- or left-chest, but may only be felt in the epigastrium, or in the left shoulder, upper arm, or jaw. Sometimes it’s the dentist who makes the diagnosis, when a patient seeks care for “toothache.”
Beware of DENIAL, common with an M.I. I ask my patients, “At the same time you feel short-of-breath, do you also have chest pain?” [‘No!’] “What about a little pressure, or ache, or heavy feeling?” [‘no…’] “How about in the top of your belly, or your shoulder or arm, or jaw?”
Inquire about Angina Equivalents: “At the same time you feel short-of-breath, do you also feel:
- Cold sweat on your forehead?
- Dizzy or lightheaded?
The more positives, the more you think “coronary.”
Physical exam is invariably normal in the midst of an M.I. There may be signs of heart failure, like bibasilar rales, but typically not. Cardiac auscultation might reveal a murmur of papillary muscle dysfunction, but those patients look pretty sick. Usually, everything sounds fine.
Get an EKG if you or someone else on site know how to read them [don’t rely on computer interpretations]. The most important changes are exactly that: changes from past tracings. Never chart “changes” unless you have an old comparison. But if you’re thinking that M.I. is possible [a judgment call], don’t send your patient off-site for the EKG. Call 911 for transport to an E.D.
NEVER FORGET that an EKG can be stone-normal in the midst of an M.I. The more suspicious the history, the less useful the tracing — send them to the E.D.
NEVER order cardiac enzymes in an out-patient setting. An attorney’s bonanza. The only rationale for that test is to R/O M.I. Do it in the E.R.
** MYOCARDIAL ISCHEMIA — Seek the same history as you would for a possible M.I. (see “Chest Pain – 1):
- Risk Factors
- Chest pain (or especially chest ‘pressure’) occurring along with the SOB
- Other angina equivalents occurring along with the SOB
The difference between suspecting ischemia vs. infarction depends on chronology. Consider ischemia when symptoms aren’t occurring at the moment. They probably haven’t even occurred today; if they did, they were associated with exertion, and similar to past episodes.
The dyspnea associated with myocardial ischemia, with or without chest pain, is intermittent. Each episode last less than 5 minutes, usually only 2-3 minutes, but at least 1 minute. Symptoms which last seconds are never ischemic.
As you can see, the diagnosis of myocardial ischemia is made by history. So is unstable angina: exertional dyspnea precipitated by progressively less exertion.
If your patient has risk factors and symptoms suggestive of stable ischemia, but feels fine now, obtain a baseline EKG. Institute maximal medical therapy for coronary artery disease while work-up is pending (aspirin, high dose statin for target LDL <70 mg/dL, perhaps a beta-blocker). Then order stress testing (see “Chest Pain – 1”).
** ANEMIA — A very common reason for new-onset dyspnea. Loss of oxygen-carrying capacity causes SOB depending on a combination of how fast the hemoglobin falls, and how severely. A rapid decline from 14 gm to 11 gm can be quite symptomatic, while in the 3rd World, people work hard in the fields, asymptomatic despite their chronic hemoglobin of 9-10 gm.
You may not find textbook signs of anemia — pale conjunctiva don’t occur until the hemoglobin drops to around 8 gm. Skin pallor becomes noticeable under 7 gm. Always order a CBC in your work-up of dyspnea. Of course, if you find anemia, you have to identify type and etiology [another time for that one].
In the ER, I had a young woman present with new-onset dyspnea. The diagnosis was easier because she was also in shock. Not another symptom. Her hematocrit was 38%, I ran 2 liters of saline rapidly and repeated it — dropped to 28%. Pregnancy test was positive: a ruptured ectopic, without any complaint except new-onset SOB.
** PNEUMONIA — This is not a tricky diagnosis when a patient complains of dyspnea. There’s usually a cough and fever. Symptoms may develop within hours, invariably during the first day. Physical exam may show focal rales, but may well be normal.
A chest x-ray is almost 100% sensitive for community-acquired bacterial pneumonias, certainly in adults, also in children >5. Be very skeptical of “pneumonia” with a normal film.
Watch out in terms of temperature. Low-grade fevers also occur with DVT & PE, and resultant pulmonary infarction can cause a small infiltrate, though not a large consolidation, nor bilateral interstitial infiltrates. We’ll discuss pneumonia more when we come to “Cough.”
** ANAPHYLAXIS — This is not common, but should always be considered in the patient with very new-onset SOB, because there’s life-saving immediate treatment available. As discussed in a prior post, when a patient presents with a few hours of acute dyspnea, diagnosis “Anaphylaxis” if EITHER of the following bulleted criteria:
- generalized itching, hives, flushing; OR swollen lips, tongue, or uvula
- history of exposure to a likely allergen; PLUS either persistent vomiting / abdominal cramps, or hypotension
Common culprit allergens: meds, bees, nuts or shellfish (also milk, eggs, soy in children). If you diagnosis anaphylaxis, give IM epinephrine, repeat 1-2 times every 5-15 minutes as needed. Observe the patient for a number of hours; have a low threshold for allowing an E.D. to take this responsibility.
Anaphylaxis can cause either upper airway obstruction or bronchospasm, with stridor or wheezing, respectively.
Up to 25% of patients with anaphylaxis have a biphasic reaction — a relapse occurs within 72 hours. High-dose daily prednisone for 3 days may be protective; a take-home EpiPen is nice. Antihistamines probably don’t help. See posting “Acute Dyspnea – 1”.
NEVER delay epinephrine when diagnosing anaphylaxis that causes acute dyspnea. Of course, for patients with urticaria alone, an antihistamine alone is completely appropriate.
** ASTHMA / COPD EXACERBATION — i.e. Bronchospasm. Perhaps the most likely cause of acute dyspnea, especially in younger persons, and an easy diagnosis if you have a nebulizer in your office or clinic. Sometimes you’ll read about “Reactive Airways Disease” (RAD); I prefer to define “RAD” as “Reversible Airways Disease.” You give nebulized Albuterol, the patient feels lots better, abnormal lung findings disappear, & that’s “RAD.”
Albuterol can be administered 3 times, 10-15 minutes between each treatment, before assessing absence of response. Pre- and post- peak flow rates can also be obtained.
Obviously, obtain a history & perform an exam before rushing to Albuterol, assuming no severe distress is noted. Asthma usually presents under 40-years-old, but not necessarily. There’s invariably an associated cough, such that I’m cautious with the diagnosis if no cough is present. But “exercised-induced asthma” may lack it. An exacerbation of COPD (i.e. of Chronic Bronchitis) is a smoker’s disease, and always includes a cough. We’ll discuss it at a later date when we come to “Cough.”
Undiagnosed asthmatics commonly describe similar previous episodes, though there’s always a first time. I ask for a history of frequent bouts of “acute bronchitis” [probably treated with antibiotics]. Acute bronchitis is viral, & nobody gets repeated lower respiratory tract viruses several times a year. Not even annually. “Recurrent bronchitis” is invariably asthma.
Wheezing — I don’t ask about it, because the word can mean almost anything to patients, including sounds of mucus in the nose or pharynx. But I certainly auscultate for it. Wheezes, once again, are long-duration expiratory sounds, usually (not always) high-pitched. “Rhonchi” are the shorter-duration squeaks and gurgles. The difference is useful but not important, because both are diagnostic of bronchospasm PROVIDED THAT you also hear a long expiratory phase.
The long expiratory phase is key. Look at a healthy person breathing: inspiration doesn’t seem as long as the time from expiration to the next breath. But on auscultation, a normal inspiratory phase always lingers longer, while the expiratory phase is brief. They’re not even close to equal. If lungs are clear, I still diagnose “bronchospasm” in a patient with new-onset of symptoms and a prolonged expiratory phase. Always make this part of your routine exam. On patients without respiratory complaints, I still chart “Lungs clear, I>E” (i.e. inspiration longer than expiration).
** UPPER AIRWAY OBSTRUCTION — Stridor is a key finding. Don’t confuse it with wheezing or rhonchi:
- Stridor: Long, high-pitched inspiratory sound, heard best over trachea.
- Wheeze: Long high-pitched expiratory sound, with expiratory phase longer than inspiratory.
- Rhonchi: Maybe a high-pitched inspiratory lung sound, but definitely short. Squeaks or gurgles, not a whistle. May come & go. Accompanied by a long expiratory phase.
Drooling may herald complete obstruction (e.g. epiglottitis, peritonsillar or retropharyngeal abscesses, floor-of-mouth infections or angioedema), but such patients look truly sick.
We’ll wrap up our discussion of Acute (i.e. “Recent-Onset”) Dyspnea the next time, outlining a summary approach, & touching on Myocarditis in specific (see Acute Dyspnea – 4).