CHEST PAIN David Griffen, MD, PhD Southern Illinois School of Medicine.

CHEST PAIN

David Griffen, MD, PhDSouthern Illinois School of Medicine

Chest Pain• Acute Coronary Syndrome• Aortic Dissection• Pulmonary Embolus• Pneumothorax• Boerhaave syndrome• Myocarditis• Pericarditis• Trauma• Peptic ulcer, cholecystitis, pancreatitis• Pleurisy • GERD• Herpes Zoster• Hyperventilation• Costochondral pain• Chest wall strain

Differential DiagnosisLIKELY NOT LIKELY

SERIOUS

NOT SERIOUS

Chest Pain

• Acute Coronary Syndrome• Aortic Dissection• Pulmonary Embolus• Pneumothorax• Boerhaave syndrome• Myocarditis• Pericarditis

Patient #1

• This is a 47 year old male with a history of hypertension presenting to the ED with complaint of chest pain beginning 11 hours prior to arrival.

• The pain is now better but was located in the lower chest and did not radiate. It has been intermittent through the day, at times associated with some mild diaphoresis but no other symptoms.

Patient #1

• The patient did have one episode of transient paresthesias of her left hand and had a brief episode of paresthesia of his left leg without any weakness.

• He stated that this rapidly resolved when she “walked it off”.

• No extremity weakness. • Other than the hypertension, PMH is

unremarkable.

Patient #1• EKG with rate of 64, sinus rhythm, no diagnostic ST

or T wave changes• Laboratory testing negative including cardiac

markers. • The patient had some epigastric discomfort on

palpation which was completely relieved with Mylanta and Viscous xylocine.

• The patient was hypertensive in the ED.• As a precaution he was placed in the chest pain

protocol to have myocardial infarction ruled out and a stress dobutamine echocardiogram performed.

Patient #1

• Four hours after arrival, the patient complained of chest and epigastric pain. A repeat EKG showed marked bradycardia at 45. The patient was taken out of the chest pain protocol and Cardiology consulted. The patient’s pain became more intense and moved to the upper abdomen, a CT scan of the abdomen with IV and oral contrast was obtained.

Differential?

Patient #1

• The CT showed a dissection of the lower thoracic and abdominal aorta with extension of the dissection into the origin of the superior mesenteric artery and with extensive dissection into the left common iliac artery.

1000 Words

Chest Pain

• Aortic Dissection

THORACIC AORTIC DISSECTION

• Commonest aortic emergency• Can occur at any age• Males and females


• Tear in the intima layer of the artery

• Dissection occurs in the media layer of the artery

• False lumen and a true lumen• Blood from the false lumen

may enter the true lumen again through another tear in the intima, or may escape through a rupture of the adventitia


• Risk Factors– Hypertension present in 2/3 of cases– Connective tissue disorders

• Marfan’s• Ehlers-Danlos

– Cocaine– Pregnancy– Associated with congenital cardiovascular

abnormalities• Coarctation of aorta• Patent ductus arteriosis• Bicuspid aortic valve


• Classification– DeBakey Classification• Type I – ascending and descending aorta involved• Type II – only ascending aorta involved• Type III – only descending aorta involved

– Stanford Classification• Type A – involves ascending aorta (DeBakey Types I

and II)• Type B – involves descending aorta only (DeBakey

type III)


• Complications– Aortic valve incompetence– Rupture• Into pericardium with pericardial tamponade• Into left chest

– Any tributary artery can be occluded by dissection


• Symptoms– Pain is usually present

• May migrate as dissection extends• May be absent

– May have episode of syncope– Stroke symptoms– Symptoms consistent with myocardial infarction– Ischemic limb (may mimic arterial embolus)– Abdominal pain– Neurologic symptoms


• Signs– May have pulse variations between limbs which may wax

and wane– Murmur of aortic insufficiency may be present (soft

diastolic murmur)– May have left pleural effusion seen on CXR– May see widening of the aorta on CXR– Paraparesis or parapalegia on exam– Cold leg– EKG changes

DIAGNOSIS

• CT WITH CONTRAST• Transesophageal ultrasonography (TEE)• Aortography


• Treatment– Blood pressure control

• Nitroprusside plus a beta blocker• Labetalol

– Surgery if the ascending aorta is involved– Medical management if only the descending aorta is

involved

• Prognosis– 75% mortality in 2 weeks if not treated– 60% survival in 5 years if treated

Difficult to Diagnose

• Viljanen, et al 1986– Delay > 24 hours in 31% proximal TAD– Delay > 24 hours in 53% distal TAD

• Bickerstaff, et al 1989. 38% missed.• 1-2% mortality per hour delay in diagnosis.

Januzzi, JL, Sabatine, MS, Eagle, KA, et al. Iatrogenic aortic dissection. Am J Cardiol 2002; 89:623.

6.4 % of patients with TAD had no pain

Litigation in nontraumatic aortic diseases--a tempest in the malpractice maelstrom. - Elefteriades JA - Cardiology - 01-JAN-2008; 109(4): 263-72

SymptomsKlompis, M. 2002 Jama

• Ripping pain LR 10.8• Sudden onset pain LR 1.6• Migrating pain LR 7.6• Pulse deficit LR 5.7• Focal neurologic deficit LR 33• Diastolic murmur LR 1.8

• 12.7 % present with syncope (IRAD study)

D-dimer and TAD?

D-Dimer and TAD

• Controversial• Cutoffs?• Acute intramural hemorrhage

Consider aortic dissection when “north-south” symptoms (above and below diaphragm) are present

Patient #2

Chest Pain

• Aortic Dissection• Acute Coronary Syndrome

ACS

• Cardiac ischemia• Acute coronary syndrome covers the

spectrum of clinical conditions ranging from unstable angina to non-Q-wave myocardial infarction and Q-wave myocardial infarction

Role of ECG in ACS

Classify patients with acute ischemic chest pain into 1 of the 3 groups above within 10 minutes of arrival.

• ST elevation or new or presumably new LBBB:

strongly suspicious for injury

• ST-elevation AMI

• ST depression or dynamicT-wave inversion:

strongly suspicious for ischemia

• High-risk unstable angina/non–ST-elevation AMI

• Nondiagnostic ECG:absence of changes in ST segment or T waves

• Intermediate/low-riskunstable angina

12-Lead ECG Variations in AMI

Baseline

Ischemia—tall or inverted T wave (infarct),ST segment may be depressed (angina)

Injury—elevated ST segment, T wave may invert

Infarction (Acute)—abnormal Q wave,ST segment may be elevated and T wavemay be inverted

Infarction (Age Unknown)—abnormal Q wave,ST segment and T wave returned to normal

LATERAL LEADS = I and AVL, V5 and V6

INFERIOR LEADS = II, III and AVF

ANTERIOR LEADS = V1, V2, V3 and V4

Paper is cheap

Patient #3

• Triage note: “Dyspnea with severe distress”• Presented at noon. Dyspnea and CP started

the previous evening.• VS– RR 48– Pulse rate 36– BP 156/115

• Taken straight back and ED physician called into room

Patient #3

History from husband– PMH positive for “blood clot” in brain (cavernous sinus

thrombosis)– Patient on Lovenox QD– Under treatment for infertility

• Patient mottled, gasping, cyanotic• Becames apneic shortly after arrival• Intubated and ventilated without problems• CT Surgeon consulted and CVOR notified shortly after

patient arrived• Despite ACLS interventions, patient deteriorates to asystole

Patient #3

• CT surgeon arrives but patient in asystole.• Declared expired 1 hour after arrival• Coroner case: autopsy showed bilateral

pulmonary artery thrombosis occluding the pulmonary arteries.

Chest Pain

• Acute Coronary Syndrome• Aortic Dissection• Pulmonary Embolus

Pulmonary Embolism• Notoriously hard to Diagnosis• Symptoms– Dyspnea at rest or with exertion (73 percent) (ONSET USUALLY

WITHIN SECONDS OR MINUTES)– Pleuritic pain (44 percent)– Cough (34 percent)– Orthopnea (28 percent)– Calf or thigh pain (44 percent)– Calf or thigh swelling (41 percent)– Wheezing (21 percent)

Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. AU Stein PD; Beemath A; Matta F; Weg JG; Yusen RD; Hales CA; Hull RD; Leeper KV Jr; Sostman HD; Tapson VF; Buckley JD; Gottschalk A; Goodman LR; Wakefied TW; Woodard PK SO Am J Med. 2007 Oct;120(10):871-9.

Pulmonary Embolism

• Signs– Tachypnea (54 percent)– Tachycardia (24 percent)– Rales (18 percent)– Decreased breath sounds (17 percent)– Accentuated pulmonic component of the second heart

sound (15 percent)– Jugular venous distension (14 percent)

Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. AU Stein PD; Beemath A; Matta F; Weg JG; Yusen RD; Hales CA; Hull RD; Leeper KV Jr; Sostman HD; Tapson VF; Buckley JD; Gottschalk A; Goodman LR; Wakefied TW; Woodard PK SO Am J Med. 2007 Oct;120(10):871-9.

Pulmonary Embolism Caveats

• Syncope is a well documented presentation of pulmonary embolus– Syncope as an emergency department presentation of pulmonary embolism. AU Wolfe TR; Allen

TL SO J Emerg Med. 1998 Jan-Feb;16(1):27-31.

• May have elevated troponins in PE• Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes.

AU Ammann P; Maggiorini M; Bertel O; Haenseler E; Joller-Jemelka HI; Oechslin E; Minder EI; Rickli H; Fehr T SO J Am Coll Cardiol 2003 Jun 4;41(11):2004-9.

• Wells and PERC Criteria, and D-dimers, may be useful in non-pregnant patients

Include TAD and PE in your differential for syncope

Chest Pain

• Acute Coronary Syndrome• Aortic Dissection• Pulmonary Embolus

Thank you

CHEST PAIN David Griffen, MD, PhD Southern Illinois School of Medicine.

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