Chest Pain Patient - @ JEMS.com


Chest Pain Patient

 

 
 
 

Christopher Suprun, NREMT-P, CCEMT-P | | Monday, November 10, 2008


You're enjoying a relatively quiet summer weekend when your unit is dispatched to a middle-aged woman with difficulty breathing. As you arrive, you find a 38-year-old woman sitting upright who is having trouble breathing and coughing up blood. She describes sudden chest tenderness, rating it a 9 on a scale of 10. Her pain is reproducible on palpation, and she describes a stabbing sensation that just started an hour ago.

Her history is relatively benign. She has no allergies, takes a daily multivitamin and oral contraceptive and has no medical history -- though her doctor always tells her to stop smoking. Her husband says she's just under stress because they are going back to work Monday from a two-week vacation overseas. They returned earlier this morning and were on the plane for eight hours.

You and your partner start vital signs and oxygen therapy by non-rebreather mask. You ask your partner to add the nasal cannula with capnography attachment. Your patient's vitals are:

RR: 28 with SpO2 of 98% on room air

HR: 130 in a sinus tachycardia with occasional ectopy

BP: 110/60

You also perform a field 12-lead ECG (Figure 1), which yields ST abnormality but no obvious STEMI indication. Your capnogram (Figure 2) shows a normal waveform, though with lower-than-expected carbon dioxide release. You start a large-bore IV catheter run at a "to keep open" (TKO) rate. The patient says the oxygen isn't helping.

While you prepare to transport the patient to the hospital, her husband says he thinks this is likely just a muscular problem from their travel. He notes she had leg pain earlier, which made her leg very warm and made it hard to move her foot, but she was able to rub the pain away with a calf massage.

With the latest information, you suspect a pulmonary embolism (PE), though field confirmation is often difficult and must be treated more as a suspicion than a known quantity.

Pulmonary embolism isn't a disease but a complication of underlying venous thrombosis, which causes 600,000 plus episodes per year in the U.S. and 200,000 deaths. (1) It's suspected to cause one third of all in hospital deaths. Deep vein thrombosis is usually thought of in relation to the calf but also occurs in the axillary and subclavian veins. Thrombus formation can also occur from indwelling catheters as well.

One of the difficulties with PE is that the symptoms are significant for other disease processes. The classic triad PE is known by (hemoptysis, dyspnea and chest pain) are not sensitive nor specific, occurring in fewer than 20% of PE cases. (2)

Although our primary suspicion of PE must come from history taking and understanding of the many contributing factors, two available diagnostic resources may help us consider PE in our patients.

The first is dynamic waveform capnography monitoring. Using waveform capnography, negative changes in exhaled carbon dioxide levels with traditional waveforms should indicate to the provider a negative change in perfusion. Additionally, persons with lower-than-normal carbon dioxide exhalation should also be suspected for poor perfusion levels.

The normal waveform would be indicative of appropriate exhalation without rebreathing or airtrapping from such conditions as bronchospasm, but the decline or lower level of exhaled carbon dioxide would indicate that oxygen isn't being burned up at the cellular level, producing carbon dioxide as a waste product.

In most cases where capnography is discussed from a perfusion standpoint, it's the other end of the spectrum where we see dramatic and sharp increases in carbon dioxide in patients in cardiac arrest situations where perfusion is occurring at the cellular level and good CPR and ACLS is returning perfusion to the organs. However, the same is true in PE, or dead space ventilation, from the opposite side. The patient is breathing in good levels of oxygen but because of the embolis blocking gas exchange, the patient's end-tidal carbon dioxide levels will diminish as lower levels of oxygen are used by the body. This may occur dynamically or have already occurred when EMS responders arrive on scene.

Again, it's important to understand that a downward trend of carbon dioxide indicates decreasing perfusion, not a PE. In this case, it helps us toward consideration of PE as the culprit, but could easily indicate lack of perfusion in a major trauma patient who isn't perfusing because of an injury that hasn't been found yet. Ultimately, the capnogram tells us there is less perfusion going on. Coupling that with our history and physical exam, we might use this as an additional resource in considering PE -- not definitively diagnosing PE because of it.

Similarly, another tool that might assist in the consideration of PE is the S1Q3T3 pattern on a 12-lead. S1Q3T3 is characterized by an S wave signifying a complete or more often incomplete RBBB in Lead 1 and a Q wave with a slight ST elevation and an inverted T wave in Lead III. These findings are due to the pressure and volume overload over the right ventricle, which can cause repolarization abnormalities. S1Q3T3 may be evident in as few as 12% of PE cases to perhaps as many as one in five cases. (4,5) Again, S1Q3T3 isn't an indicator of pulmonary embolism by itself, because it can also indicate other conditions causing right ventricular strain, such as cor pulmonale, acute bronchospasm and pneumothorax.

Because of the significant nature of pulmonary embolism and the possibility of fatal complication, PE must be considered carefully when treating patients. Sound clinical decision-making and investigation, combined with such tools as 12-lead and waveform capnography, can assist in treating patients as best possible.

References

1. Lee LC, Shah K: "Clinical manifestation of pulmonary embolism." Emerg Med Clin N Am. 19(4):925-942, 2001.

2. Feied CF: "Pulmonary Embolism." eMedicine: http://www.emedicine.com/emerg/topic490.htm

3. Harrigan RA, Jones K: "ABC of clinical electrocardiography. Conditions affecting the right side of the heart." BMJ (Clinical research ed.) 324(7347):1201-1204, 2002.

4. Ferrari E, Imbert A, Chevalier T, et al: "The ECG in pulmonary embolism: predictive value of negative T waves in precordial leads: 80 case reports." Chest. 111:537-543, 1997.




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