Assessing Respiratory Distress

One of the first things they teach you in EMT school is that air should go in and out. So when patients report feeling short of breath, it's time to get serious. Differentiating between the many cases of respiratory distress is far from simple, but using your clinical acumen, being diligent and paying attention to detail can lead you down the path to the right conclusion, facilitating the right treatment plan and doing right for the patient.

First, remember that shortness of breath can be primary or secondary. That is, something might be wrong with the lungs or elsewhere, prompting the lungs to compensate. Primary problems would include asthma, COPD, pulmonary edema, anaphylaxis, pneumonia, pleural effusion and pneumothorax. Secondary problems would include metabolic acidosis, stroke, head trauma, toxicological overdose, sepsis and diabetic ketoacidosis. Figuring out which path to go down requires a careful physical exam, including vital signs, the incident history and patient symptoms.

PHYSICAL EXAM

Focusing on the lungs, auscultation is key. Crackles aren't just crackles, and wheezes aren't just wheezes. Crackles that are coarse, thick and sound "junky" can indicate mucus or infection, while crackles that are fine and "gurgley"-sounding can indicate edema. Wheezes indicate bronchoconstriction, but not necessarily from asthma or COPD. A cardiac wheeze brought on by heart failure is probably more common than we realize, and is often misinterpreted by EMS providers (and emergency physicians, for that matter). Careful, purposeful auscultation is key to understanding what is wrong with your patient and how you can fix it. To get more clues from auscultation, listen intently with your stethoscope on the patient's skin at the left and right apex, hilum and bases.

Air goes in and out, but when is extra respiratory effort required? The inspiratory and expiratory phases of respiration can shed more light on why your patient is in distress. Is your patient working hard to breathe in or trying to force air out? Inspiratory problems are likely caused by compliance pathologies, like pulmonary edema and pneumonia, while expiratory problems are likely caused by resistance pathologies, like asthma and emphysema. Of course, some pathologies are mixed: Anaphylaxis creates mucus that requires more inspiratory effort, as well as bronchoconstriction, which requires increased expiratory pressure. Just staring at the chest to see which phase of respiration is delayed may be a valuable exercise that enlightens your clinical decisions.

Other clues on physical exam include signs of cardiogenic right-sided heart failure, like JVD, ascites and peripheral edema. But remember that these are also signs of cor pulmonale, which is right-sided heart failure caused by pulmonary hypertention, usually the result of lung pathologies like COPD. Further, in flash cardiogenic pulmonary edema, the left heart failure leading to edema may not have affected the right side of the heart just yet, so these signs may be absent altogether. It's important to conduct a careful physical assessment, as your treatment decision could teeter on your findings.

INCIDENT HISTORY

The usual OPQRST works well here, along with a careful understanding of past episodes of shortness of breath. Has this patient been hospitalized for such? Intubated? Does he sleep with CPAP? Does he take his puffers every once in awhile, or every day? Is his chest pain in addition to the breathing problem? Has he had any air travel, operations, or pain in his calves? What about exposure to sick people, hospitals, nursing homes or daycares? Is he compliant with his medications, and have the medications been changed at all recently? The answers to these questions will start to paint a picture that can guide you to the right conclusion.

VITAL SIGNS

When was the last time you actually counted a respiratory rate? Often, we just glance at the chest and guess--16 per minute. But a proper 30-second count can often reveal markedly high respiratory rates. As the body compensates for poor ventilation, heart rate will also increase. Tachycardia is never a good sign. Level of awareness and GCS may start to drop, as will the oxygen sats. Be sure you have a waveform with your saturation value; if the waveform isn't good, don't even consider the value. Pupils may start to slow in reaction time, and skin may become pale and cool with delayed capillary refill. The hands and feet are a good place to check initially, as the shunting of blood during the sympathetic response starts here. If there is poor cap refill centrally, we know we have a huge problem. Watch for trending to see if your treatments are having any effect. Vital signs are just part of the puzzle, but they are an important piece.

TREAT OR NOT TREAT?

You are called at 1:30 am for a 56-year-old female complaining of shortness of breath. On arrival, you find her sitting in a chair in her bedroom, pale, dry and in severe respiratory distress with one-word dyspnea. Her husband tells you she woke up to go the bathroom, and as she came back, he could hear her gasping for air. She couldn't even make it back to bed and sat down in the reading chair, so he immediately called 911. Your physical exam reveals no JVD or ascites and normal peripheries. Her lungs are mostly quiet; you hear nothing in the bases and a very tight, high-pitched wheeze in the apices. Her vitals are not encouraging, with a heart rate of 122, respiratory rate of 50 and O2 saturation at 80%. She seems to be having trouble breathing in. She denies chest pain and indicates that this is the worst shortness of breath she has ever had. Her husband tells you that her asthma gets very bad sometimes, but not usually at night. Last week, her doctor told her to start taking only half of her water pills because of some test result the lab found after drawing blood. Her past history includes asthma, MI, NIDDM, HTN, COPD and CHF. She also has an irregular heart beat, but the medicine has done its job and her heart beats normally now. She has a grocery bag full of medications for all of the above, including nitro spray and blue, orange, purple and brown puffers. She appears fearful. What would you do?

The stakes are high. If she is having an asthma exacerbation, Ventolin (albuterol) is a good start, but given the severity, a call to your physician for SC or IM epinephrine could save her life by relaxing her bronchioles. If she is in acute heart failure, nitroglycerin and CPAP are the treatments of choice; epinephrine might kill her. So which path would you choose? This is perhaps the toughest kind of case paramedics have to make a judgment call on. You probably want some more answers before going ahead with treating her, but hurry-–her GCS is starting to drop. Prehospital providers must be diligent, thorough and accurate to provide this patient with the best care possible. Her life depends on it.

TIP FOR THE STREET

Sometimes, you can be diligent, thorough and accurate and still not know what is wrong with your patient. Whenever I'm on the fence about treating with nitro or Ventolin, I start with nitro. Whether or not these patients have already used their inhalers, a few shots of nitro tends to make a big difference quickly. If I'm wrong, that's all part of paramedicine: There is no rule saying I can't change paths and switch to Ventolin.

Blair Bigham, ACP, MSc, is an advanced care flight paramedic and prehospital science investigator in Toronto. When not roaming the streets and skies practicing clinical paramedicine, he studies resuscitation and patient safety related to EMS and transport medicine. Trained at Sunnybrook Health Sciences Centre and the University of Toronto, he now studies lifesaving interventions at Rescu, the world-renowned prehospital research program at St. Michael's Hospital and U.T. Contact Blair at bighamb@smh.ca.