Today we’ll begin to address the patient who complains of ACUTE DYSPNEA, but does not appear in such distress as to require immediate E.D. care. We’ll define this as new-onset SOB within the last 2-3 weeks. However, SOB being what it is, patients may present earlier.
TABLE — CAUSES OF ACUTE DYSPNEA
MISC. METABOLIC CAUSES
bold = common
Step #1 — Define. Be sure we’re dealing with true dyspnea. As you see from the differential diagnosis, true SOB is almost always due to a disorder of the lungs or heart [upper airway obstruction means air can’t reach the lungs, & metabolic causes are uncommon]. However, patients may say “I can’t breathe,” when they really mean their nose is all stuffed up, or a coughing spell feels suffocating, or now-&-then they feel an urge to take a deep sighing breath.
The most common mimic of true dyspnea is anxiety, especially if there’s also hyperventilation. Imagine the sensation of a full-blown panic attack. Yet this can be ruled-out with one basic question — “When you walk up stairs, climb a hill, or run for a bus, does your SOB get better, get worse, or stay the same?” Other clues to hyperventilation include tingling in the hands / lips.
True dyspnea ALWAYS gets worse with exertion, by definition. If not, I chart “no SOB,” regardless of what words a patient uses to describe their complaint. Imagine a tornado approaching — you might hyperventilate or panic, but you’d sure dash to the shelter. If you’re in heart failure, you ain’t gonna make it.
Physiologic Deconditioning (plain old out-of-shape) also gets worse with exertion. If I, myself, try to run a mile, I’ll be quite short of breath, but the reason will be obvious, & I won’t seek care. But sometimes a person finds themselves in a new setting, with new exertional necessities they didn’t think of. Maybe they have to walk up new flights of stairs, for example. Still, if a patient complains of “SOB,” deconditioning is a diagnosis of exclusion.
Brief note for Spanish speakers — in Central America at least, maybe Mexico & elsewhere, the word “cansado” is used interchangibly for “SOB,” “fatigued” (worn out), and “sleepy.” It’s real important to distinguish, since these complaints have completely different differentials.
Step #2 — Quantitate the dyspnea. Identify a common activity for the patient that provokes SOB, e.g. a flight of stairs at work, a hill near their home, hurrying a block for a bus, walking 3 blocks at a normal pace. This helps define progression, like “Last week SOB at 2 flights, this week 1 flight.” But most importantly, it confirms that the patient does have true dyspnea — a patient who can’t relate to this line of inquiry may not. Dyspnea at rest, or en route to TV when remote is lost, is most severe.
Step #3 — Determine the chronology. Inquire how long they have felt SOB with that specific activity. Was the onset abrupt, or did they notice the dyspnea over a gradual period of time. Try hard to assess progression; if the patient doesn’t have steps to climb, find whatever place they get dyspneic (e.g. 1 block), & ask if when before had they been able to walk 2 blocks without trouble
Other questions to ask emerge from the differential. Thinking angina? Ask about chest pain. Heart failure? Try orthopnea and paroxysmal nocturnal dyspnea. Asthma? There ought to be a cough. We’ll explore these more disease by disease.
In terms of exam, obviously focus on lungs & heart. Vital signs & pulse oximetry are usually normal when the patient is comfortably at rest in your office. But if the history is convincing, & there’s no obvious diagnosis like asthma or heart failure, consider rechecking the O2 saturation after exertion.
Have the patient walk somewhat briskly for up to 6 minutes, and repeat the oximetry if they feel symptomatic [you can have an assistant do this while you catch up with administrative burdens or squeeze in another patient]. To save time in relatively younger patients in whom coronary artery disease is not a consideration, I have them walk up & down a staircase, enough to reproduce dyspnea. If O2 saturation drops to ≤92%, they’re sicker than you thought. If it remains normal, you haven’t proved anything, but feel more comfortable.
The differential of Acute (i.e. recent) Dyspnea is similar to that of our previous posting (Dyspnea – 1), minus those entities which always present in some sort of distress. Consider the highlighted diagnoses first; the others are pretty obscure. Let’s start with the toughest diagnosis of all, perhaps among the potentially lethal entities that are most frequently missed…
** Pulmonary Embolism (PE) — A very tricky disease. Chest x-ray and EKG are usually normal with a PE. And when they’re abnormal, they can mimic other conditions like pneumonia or cardiac ischemia. The main error clinicians make is simply failure to “Think PE.”
When thinking “PE,” focus on two key diagnostic parameters:
- Acute Onset: Dyspnea begins within seconds 46% of the time, within minutes another 26%. It makes sense — an asymptomatic clot sits in the legs or pelvis, a piece dislodges, floats happily up the vena cava to the right heart, gets stuck in a pulmonary artery, & Bingo, there’s SOB.
- Risk Factors: The main one is a clinical picture compatible with deep venous thrombosis (DVT). This includes pain, tenderness or rarely swelling near a femoral vein (medial thigh), or new unilateral pedal edema.
Other big risk factors are:
- Immobilization for ≥3 days
- Anesthesia within the past 4 weeks
- Active cancer
- Prior history of either DVT or PE.
- HIV infection, though not usually listed, predisposes to a hypercoagulable state.
Clinical findings of concern, in addition to suggestions of lower-extremity DVT, include:
- Loud S2 heart sound
- Also worry about obese hypertensive women who smoke.
Another key parameter in assessing the chance of a PE, equally predictive as concurrent DVT symptoms, is, “does another diagnosis appear likely?” Not “guessed,” but likely. New-onset dyspnea is a serious symptom. If there’s no obvious explanation, think PE.
A brief word about tachycardia; literature often suggests that it’s the most common sign. Maybe true, compared to the other objective findings listed, but it’s not very sensitive. Most patients with PEs have normal pulse rates. I’ve seen the diagnosis missed by clinicians dismissing the possibility because, “he’s not tachycardic.” Tachycardia is useful when found, but not for its absence.
Estrogen use, like oral contraceptives? They increase the relative risk 2- to 4-fold, but absolute risk remains very low. DVT or PE occurs in 1 of 500 pregnancies (often post-partum). And in terms of airplanes, a healthy traveler who flies 4 hours has a 1 in 6000 risk. These risks are not factored into clinical scoring tools, because they’re way too low. But they raise eyebrows among the public, & among health professionals, who in our own personal lives may relate more easily to plane flights & birth control than to cancer or leg casts.
For a good review of PEs, see Am J Med 2007;120:871.
Send patients with new-onset dyspnea to an E.D. to R/O PE if:
- Their symptoms began very suddenly, & there’s no other explanation for them.
- They have risk factors for PE, and there’s no other obvious diagnosis.
- There’s no other obvious diagnosis.
The E.D. will order a D-dimer, generate a clinical probability score [e.g. JAMA 2006; 295:171], & decide if the case warrants a CT or ventilation/perfusion [V/Q] scan. Never order a D-dimer as an out-patient; it’s analogous to cardiac enzymes. If you think PE, think E.D.
That’s enough for today. Next time we’ll cover other causes of acute dyspnea (see Acute Dyspnea – 3).