BY JOHN BRAY
Aortic weakness and rupture claimS the lives of more than 13,000 people each year, making it the 18th leading cause of death.1 Despite this, aortic aneurysms are often misdiagnosed because signs and symptoms can be subtle and easily confused with other conditions. In addition, patients are apprehensive and may be afraid to explain their complaints. This dilemma crosses over all social and economic borders, as in the case of actor John Ritter, whose complaints of chest pain and weakness were initially diagnosed as acute coronary syndrome (ACS). The fire-EMS provider can take the following steps to help ensure proper diagnosis.
PATIENT SIZE-UP
It all starts with the initial patient contact. When interviewing a patient complaining of chest pain, take the time to ask the deeper questions that will help you discover some hidden clinical gems that might otherwise be obscured or overlooked.
PATHOPHYSIOLOGY
Aortic aneurysms begin with a weakening of the connective tissue making up the innermost lining of the vessel known as the tunica intima. Men are three times more likely than women to suffer from this disease. A variety of conditions crossing over different age groups can trigger aortic aneurysms. The tunica intima is comprised of squamous cells that can become brittle as a result of hyperlipidemia, atherosclerosis, or chronic hypertensionall common issues with the elderly. Younger patients suffering from congenital problems such as Marfan and Ehlers-Danlos syndromes or abusers of cocaine or ecstasy can develop a weakened inner lining.
The forceful flow of blood created with each cardiac cycle eventually tears through the weakened tunica intima and enters the middle lining, known as the tunica media. This portion of the vessel is comprised of smooth muscle that is not very resilient to high-pressure flow. As the blood enters this layer, it begins to burrow a tunnel known as a false lumen, which creates a dissection. As blood diverts into this new pathway, it extends the tunneling downward toward the abdominal aorta. The outermost lining, known as the tunica adventitia, is comprised of tough, elastic collagen tissue capable of withstanding the high pressures in this new lumen for hours or even days, but, ultimately, rupture is inevitable.
CLASSIFICATION OF AORTIC ANEURYSMS
During the initial tear and subsequent dissection, 96 percent of all patients will complain of a “tearing” pain. The location of this pain is determined by the area of initial dissection. The location of aortic aneurysms is broken into two regions, known as the Stanford Classification System. This “mapping” of the initial entry point and creation of the false lumen is based on the original classification system created by Dr. Michael DeBakey, among whose many accomplishments include the conception and development of Mobile Army Surgical Hospitals (MASH units). Dr. DeBakey (1908-2008) was a pioneer in cardiac surgery and performed the first surgical repair of an aortic aneurysm in 1955. Ironically, in 2005, at the age of 97, Dr. DeBakey, himself, went under the knife to repair an aortic aneurysm, undergoing the very surgical intervention he created.
 Figure 1. Anatomy of the Aorta Figure 1. Type A dissections originate in the ascending aorta. Type B originates in the descending thoracic aorta. |
Stanford Type A aneurysms originate in the ascending aorta, just past the coronary arteries. The dissection continues up and around the aortic arch. High blood pressure extends the dissection down the length of the thoracic aorta to the abdominal aorta. This is the most common type, affecting about 75 percent of diagnosed patients, and has the highest probability of having the longest false lumen dissection.
Stanford Type B aneurysms originate in the descending aorta just distal from the left subclavian artery. About 25 percent of patients with aortic aneurysms have this origination point, which can extend down into the thoracic region.
LOCATION, LOCATION, LOCATION
Type A aneurysm patients are likely to experience sudden pain in the chest, while Type B patients will have similar pain originating in the abdomen. Unlike cardiac chest pain, which begins slowly and is dull and diffuse, pain from an aortic aneurysm is maximal at the outset, sharp and pinpointed. The pain often begins to subside and, as the dissection tears further and begins to enlarge, becomes more dull and diffuse. This explains why typical aortic aneurysm patients arriving in the Emergency Department are initially triaged as suspected myocardial infarction (MI) patients. Their complaints at that time are very similar to typical MI chest pain. After a full cardiac workup, which includes 12-lead ECG and blood panels, comes back normal, patients are sometimes down-triaged and advised to follow up with their primary care provider.
ROLE OF THE FIRST RESPONDER
The medical community is very interested in knowing exactly what happened at the very start of a medical or traumatic event. Understand that fire-EMS responders play an important role in patient outcomes through observation, initial management, and hospital transport decisions.
ASSESSMENT OF THE ANEURYSM PATIENT
It’s not uncommon for patients with chest pain to downplay their symptoms. Close observation is required to see what others might miss. Look for signs of apprehension; patients who just felt this incredible tearing pain are stoic, sitting quietly and sometimes afraid to move. Consider the increase in the size of the aorta and the effects this expansion will have on other organs in the thoracic and mediastinal regions. Patients may display shortness of breath as the lungs are compressed, as well as hoarseness and nonproductive cough as pressure in the mediastinum increases and begins to affect the trachea. In addition, the dissection will create a loss of circulating blood volume; this drop in cardiac output will be immediately felt by baroreceptors in carotid arteries, resulting in a compensatory tachycardia. Typically, patients will have mild tachycardias (heart rates greater than 100 but less than 120) with a normal blood pressure. This reflects a normal response to a five- to 10-percent blood loss.
 Figure 2. Aortic Dissection Figure 2. Aortic dissection. Notice the separation of the tunica intima and the tunica media with blood flowing through the false lumen. |
As the dissection continues, blood loss increases, and you can expect to see compensatory signs like diaphoresis, nausea, and thirst. As the dissection extends into the abdomen, you may feel pulsatile masses, but absence of a pulsating mass does not mean an aortic aneurysm does not exist. While checking for pulsations in the abdomen, be sure to check each extremity for distal pulses. Patients suffering from an aneurysm will almost always develop asymmetrical pulses; some patients will lose lower extremity perfusion and have cool, grayish or cyanotic feet, so don’t forget to pull off those socks!
PUTTING IT ALL TOGETHER
You are dispatched to a sick person call. On arrival, you find a 67-year-old male sitting bolt upright on the living room couch. The patient complains of a sudden onset of sharp chest pain followed by shortness of breath, hoarseness, and nonproductive cough. Vital signs are pulse 110 and regular, respirations 28 and unlabored, and blood pressure 120/90. A 12-lead ECG shows no abnormalities. Oxygen saturation on room air is 92 percent. History includes hypertension and COPD. He has a social history of smoking and a family history of his father dying of a heart attack at the age of 60. Medications include home O2 at 2 LPM, nifedipine, and clonidine. He has no allergies. Physical exam reveals mild diaphoresis, clear lung sounds bilaterally, no stridor, and no JVD or peripheral edema. Further exam shows diminished pulses to the right radial and popliteal arteries. The feet are bluish and cold; the patient has a puzzled look as he stares at his feet.
IN-DEPTH INTERVIEW SKILLS
This patient complained of sudden onset of chest pain, followed by shortness of breath. Sudden is bad; most respiratory infections are gradual. The hidden gem in the clinical assessment is the timeline of symptoms. Sudden onset of chest pain, followed by shortness of breath and ending with hoarseness and cough, is the opposite of a respiratory infection, which usually starts with a cough and progresses to chest pain. See if the patient is aware of his normal blood pressure; share your finding, and ask him if this is normal. The tachycardia and narrow pulse pressure may be compensatory Stage 1 shock. Next, the diaphoresisnot what you would expect from an inflammatory response caused by an infection. Finally, the asymmetrical pulses and poor distal perfusion, coupled with the social history of smoking, COPD, and hypertension, should make this patient a prime candidate for an aortic aneurysm.
FIELD TREATMENT
Field treatment is limited; beta blockers such as lopressor or labetolol are effective in managing the diastolic blood pressure, while nitroprusside can address the systolic pressures. Because the pathology of an aortic aneurysm involves tearing a major artery, do not use vasodilator agents (such as nitroglycerine or nitroprusside) until adequate beta blockade is onboard. Premature use of dilator agents can exacerbate the dissection. Few EMS systems have a protocol to address an aortic aneurysm. Consider IV access with a large bore needle (16-18), and be prepared to intubate if the patient’s condition suddenly deteriorates. Having the rupture while en route is the last thing you want, so rapid transport to a hospital with imaging and surgical capabilities is paramount.
HOSPITAL PRESENTATION
We make a real difference in patient treatment in the hospital; just the act of bringing a patient in on a stretcher with a cardiac monitor and IV attracts attention. During the initial report to hospital staff, it’s important to stress the timeline of the pertinent positive findings. Emphasize especially the sudden onset of sharp chest pain followed by shortness of breath and ending with hoarseness and cough. Making a generic statement of findings without a timeline will make this patient appear to have an upper respiratory infection (URI). Stress the fact that the patient has diminished pulses on one side, and lift the sheet to expose the blue feet. While blood work is being processed, tests such as a chest X-ray or CT scan can reveal the ticking time bomb hiding in this patient. Once recognized, new surgical interventions are able to repair or rebuild the weakened aorta, restoring circulation and improving the patient’s quality of life. Some patients can be treated less invasively by having a stent-like device placed into the aorta through the femoral arteries.
We can easily discover aortic dissection, but only if we are diligent in our most important role in patient carethe initial contact. Thorough, in-depth interview skills, early detection, and sharing the evidence with the appropriate receiving facility can make all the difference in the patient’s outcome.
Reference
1. Centers for Disease Control, CDC 2005 survey. On line: http://webappa.cdc.gov/sasweb/ncipc/leadcaus10.html.
JOHN BRAY, BS, NREMT-P, CCEMTP, is the paramedic education coordinator at Saint Vincent’s Hospital-Manhattan and director of the Institute of Emergency Care. He has been involved in EMS since 1986; he began his career in NYC*EMS in the Bronx. He is a hazardous materials technician and a member of the West Haverstraw (NY) Volunteer Hose Company.
