Cardiac & Resuscitation, Patient Care, Trauma

Chest Pain Call Turns Complex

Issue 2 and Volume 37.

It’s 10 a.m. on Monday: the first day of the week for most people but the second day of your tour. You and your paramedic partner are dispatched to assist a 62-year-old male complaining of chest pain. As the ambulance heads in the direction of the call, the causes of chest pain parade through your head. Myocardial infarction (MI) is toward the top of the list, but there are several other causes of chest pain that must also be considered.

Arrival on Scene
You arrive on the scene and are met by an EMT first responder, who reports that your patient is complaining of substernal chest pain radiating to his left shoulder and back. The patient says it began while he was moving furniture. The patient rates the pain as a 7 on a scale of 10.

As you enter the patient’s living room, you see a healthy-looking male wearing a non-rebreather oxygen mask placed by the first responding EMTs. The patient appears anxious and is in obvious distress. His skin appears diaphoretic but not pale.

One of the EMTs is obtaining vital signs, and another reports the history and medications he has gathered from the patient’s wife. The patient’s medications include Hyzaar, Crestor and Actos.

He has also recently completed a prescription of an antibiotic to treat a case of pneumonia, but his wife can’t recall the name of the drug. She also reported a history of hypertension, heart “troubles” and diabetes, and she said he takes garlic and hawthorn as supplements.

His pulse is 75 beats per minute, and his blood pressure is 82/60. The presentation fits the description of an MI, but you’re cautious not to jump at the most commonly thought-of cause for chest pain. His history of hypertension and hyperlipidemia put him at risk for a thoracic aortic dissection. And with his history of pneumonia, you realize his pain could be caused by pleurisy, muscle skeletal pain from coughing or a return of the pneumonia. The possibility of a pulmonary embolism or tension pneumothorax must also be considered, especially with the sudden onset of his symptoms.

As you begin your assessment, you notice the patient keeps removing the oxygen mask. His pulse oximeter reading is 98% on room air, and he isn’t short of breath, so you remove the oxygen. Physical inspection of his chest reveals equal chest excursion with no intercostal retractions or noted deformities. Palpation of his chest wall and abdomen doesn’t increase or decrease the pain, and the pain isn’t reproduced with breathing or movement. His breath sounds are clear in all fields and his capnogram is a normal waveform with an end-tidal carbon dioxide (EtCO2) of 38 mmHg. An S4 sound can be heard when listening to heart sounds.

The patient remains in obvious distress, appearing anxious and telling you repetitively that “something isn’t right.” You and your partner, recognizing the potential severity of the patient’s condition, establish an IV and place a 12-lead ECG while you perform the initial assessment.

With the initial blood pressure of 82/60, you begin to administer a fluid bolus of 250 mL. A quick glance at the ECG shows a regular sinus rhythm with ST-segment and T-wave changes. As you prepare the patient for transport, you have him chew and swallow four 81 mg aspirin tablets after finding no contraindications.

En route to the hospital, you reevaluate his vital signs. His pulse remains regular at 75 beats per minute; his pulse oximeter reading and capnogram are unchanged, but his blood pressure is now 178/90. You retake the BP to verify your findings and then remember that the EMT in the house was taking vital signs on the patient’s right arm. In the ambulance, you’re now positioned at the patient’s left side. You move to verify the EMT’s findings and discover the blood pressure in the patient’s right arm is 88/68. You quickly turn the first IV line to a TKO rate and establish a second IV line set at a TKO rate as well.

Your standing orders for pain control allow for the administration of 100 mcg of fentanyl, which results in the patient relaxing and reporting his pain is down to a 4 out of 10. Closer evaluation of the 12-lead ECG indicates ventricular hypertrophy and not ischemia. Your radio report to the receiving emergency department (ED) alerts them to prepare to receive a patient with a possible thoracic aortic dissection.

The ED team is ready on your arrival and the lead physician commends you for recognizing the differing blood pressures. After a brief assessment, he sends the patient for a CAT scan, which confirms the presence of a thoracic aneurysm. The ED physician orders the administration of labetalol and continued pain control, and he requests a surgical consultation.

Thoracic aortic dissections can be easily missed on assessment or misdiagnosed because of their ability to cause or mimic other conditions, such as MIs or strokes. Patients experiencing a thoracic aortic dissection will commonly have an underlying history of hypertension and hyperlipidemia. The interior lining—or intima—of the aorta tears, which allows blood to move between the layers of the aorta. This then creates a false lumen, which then creates an aneurysm.

As this tissue separates or dissects, the false lumen is enlarged, and the patient experiences pain. Symptom onset is rapid and commonly includes chest pain and anxiety. It should be noted, however, that some patients will have no pain.

Two common classification systems are used to identify the location of the aneurysm: the DeBakey and Stanford systems.

The DeBakey system classifies aortic dissections into three types as follows:
>> Type I: Originates in the ascending aorta, progresses to the aortic arch and further;
>> Type II: Originates in and is confined to the ascending aorta; and
>> Type III: Originates in the descending aorta and extends distally.

The Stanford system uses the two following classifications:
>> Type A: Ascending aorta involvement; and
>> Type B: Descending aorta involvement.

Depending on the location of the aneurysm, the blood supply can be partially occluded to one or both arms. Interarm blood pressure variants greater than 20 mmHg should be considered significant. The aneurysm can also occlude blood supply to nerves, causing a stroke appearance. Or it can occlude the coronary arteries, which results in the patient presenting with an MI. Because of the sympathetic response associated with the pain, the patient’s blood pressure can increase, which can extend the dissection or cause a rupture of the aneurysm.

Hypotension suggests rupture of the aneurysm or dissection into the pericardial sac, causing a tamponade. Thoracic aortic dissections are treated surgically or pharmacologically. They can be fatal if left untreated.

The ECG changes and the heart sounds discovered on exam are secondary to left ventricular hypertrophy (LVH), which is common in patients with chronic hypertension.

Ventricular Strain Pattern
The ST-segment sloping and T-wave inversion are referred to as strain patterns and suggest heart chamber enlargement. The other noted finding is the increased amplitude of the QRS complexes. QRS axis will be normal or left.

The S4 sound can be heard in patients with LVH, but it’s not specific to LVH, nor does the absence of the sound rule out LVH.

Case Summary
The paramedics completed a thorough assessment to rule in and out other possible etiologies of the chest pain. Obtaining the prescription medications helped confirm the wife’s statements about her husband’s history.

This patient was taking garlic and hawthorn supplements, which are used to treat heart and vascular disease. Although they didn’t play a role in this case, supplements must be taken into account when evaluating patients. Hawthorn has been shown to interact with prescription antihypertensive medications, resulting in hypotension. Supplements may affect patient presentation and the response to our treatment.

The patient’s breath sounds were clear, and the discomfort wasn’t reproducible with respiration or palpation, suggesting the pain wasn’t caused by pneumonia or musculoskeletal pain. There were no strong risk factors for pulmonary embolism, and the EtCO2 values were within normal limits. Not all ST and T-wave changes on the ECG represent myocardial ischemia or infarction.

The paramedics identified chamber enlargement rather than ischemia. And the large variance between blood pressures from left to right arm was a significant finding. Appropriate assessment and prehospital treatment and early notification and recognition by the ED staff all allowed for appropriate patient disposition and a good outcome. The patient made a full recovery. JEMS

>> Marx J, Hockberger R, Walls R. Rosen’s Emergency Medicine, Concepts and Clinical Practice 6th Edition. Mosby: Philadelphia, 2006.
>> Mancini MC. (Nov. 3, 2011). Aortic Dissection In Medscape. Retrieved from
>> Skidmore-Roth L. Mosby’s Handbook of Herbs & Natural Supplements 3rd Edition. Elsevier Mosby: St. Louis, 2006.

This article originally appeared in February 2012 JEMS as “More Complex than Chest Pain: Providers treat patient with thoracic aortic dissection.”