Emergency Department Evaluation of Chest Pain

Emergency Department

Evaluation of Chest Pain

Indiana University SOMDepartment of Emergency Medicine

MS-IV Lecture Series

Why this is important• Many of the causes of chest pain are

imminently or potentially life threatening

• Therapy for many of these conditions can be lifesaving and must be started in the ED

• Failure to recognize and treat serious causes of chest pain will be costly to your patients and to you.

Caring for Chest Pain:Two Major Goals

• Distinguish serious from non-serious causes

• Institute appropriate interventions

Causes of Chest Pain• Imminently life threatening:

– MI/ACS, aortic dissection, pulmonary embolus

• Potentially life threatening:– Pneumothorax, Boehaave’s, pericarditis,

pneumonia, others

• Non-emergent:– Chest wall pain, GERD, many others

Case #1• 54 yo F presents with SSCP. She is

being placed into the bed as you walk in. She looks sweaty and uncomfortable.

• What do you want the nurses to begin doing as you start your H&P?

Chest Pain: Initial Interventions

• Vitals, including pulse oximetry• EKG

– Within 10 minutes after arrival to the ED

• “Safety net”– IV– *02– Monitor

*ACLS 2010: “there is insufficient evidence to support its (supplemental oxygen’s) routine use in uncomplicated ACS. If the patient is dyspneic, hypoxemic, or has obvious signs of heart failure, providers should titrate therapy, based on monitoring of oxyhemoglobin saturation, to <94%”

Chest Pain: Initial Interventions

• ASA– Cheap, little downside, 23% reduction in

mortality in AMI.

– Give it to (almost) everyone with CP and give it early

Case #1 (continued)• You begin to ask your patient about

her pain.• What type of pain typifies the

following:

– Myocardial ischemia?– Aortic Dissection?– Pulmonary Embolism?

Case #1 (continued)• Your patient has been having

intermittent episodes of sub-sternal squeezing pressure for one day, with radiation to both arms. Episodes last 10-15 minutes. Currently, the pain is more severe and has been ongoing for one hour.

• The nurse hands you the EKG…

What does the EKG show?

What therapies need to be instituted?

Acute MI: Treatment• Reperfusion Therapy

– Primary angioplasty (Percutaneous Coronary Intervention - PCI) or thrombolytics

– PCI generally preferred (better outcomes), but not available 24/7 in most hospitals

– Time is critical• Door-to-lytic time should be < 30 minutes• Door-to-balloon time should be < 90 min• “Time is tissue”

Acute MI: TreatmentReperfusion Therapy

• Thrombolytics– Convert plasminogen to plasmin, which is

fibrinolytic– Coronary artery thrombus is lysed,

allowing myocardial reperfusion– Marked reduction in mortality (~20%)– Many agents now available:

streptokinase, alteplase (t-PA), retevase, tenecteplase (TNK)

Acute MI: TreatmentReperfusion Therapy

Thrombolytics – eligibility criteria:H&P consistent with AMI

+Symptom duration < 12 hours

+1. ST elevation > 1mm in two or more contiguous

limb or precordial leads, or2. New or presumed new LBBB

Decision to reperfuse based on H&P and EKG, not labs

Acute MI: TreatmentOther therapies

• Aspirin• Nitrates

– Decrease preload (and thus myocardial O2 demand) and cause some direct vasodilatation of the coronary arteries

– Sublingual or IV in setting of STEMI– Avoid if PDE inhibitor (e.g. sildenafil)

taken in past 24-48 hrs (intractable hypotension)

Acute MI: TreatmentOther therapies

• Beta blockers – Controversial– Decrease myocardial 02 demand– Increase risk of cardiogenic shock– Routine use currently not recommended– Contraindications:

• Hypotension• Bradycardia• AV block• Heart failure• Cocaine intoxication

Acute MI: TreatmentOther therapies

• Heparin– Unfractionated or Low Molecular Weight

(enoxaparin)– Used in addition to thrombolytics or PCI

• Direct thrombin inhibitors– Bivalirudin (Angiomax)– An alternative to heparin/LMWH– Does not cause thrombocytopenia– Exact role still emerging

Acute MI: TreatmentOther therapies

• Platelet inhibitors– Clopidogrel (Plavix)– Prasugrel (Effient)– Inhibit platelet aggregation by a different

mechanism than ASA (irreversibly inhibit platelet ADP receptor)

Acute MI: TreatmentOther therapies

• Morphine– Efficacy not adequately studied– No known mortality benefit– Analgesic and anxiolytic effects may be

beneficial– Consider if patient’s pain not relieved with

nitrates

What if your patient’s EKG had looked like this?

Acute Coronary Syndrome

• ACS = a spectrum of clinical disease that includes AMI and unstable angina– It is not always possible to distinguish

between these entities in the ED

• The Acute Coronary Syndromes share a common pathophysiology: a ruptured or eroded atheromatous plaque

The spectrum of ACS

STEMI

Non-ST elevation MI

Unstable Angina with EKG changes

Unstable angina without EKG changes

Treatment of ACS• ASA• Nitrates• Heparin/enoxaparin• Clopidogrel• Beta-blockers*• GP IIb-IIIa receptor inhibitors*

*Controversial/evolving role

Treatment of ACS

• +/- Cath lab– Depending on clinical picture

(ongoing pain, etc.)

• Thrombolytics only for STEMI– Worsen outcome if no acute STE

Acute Coronary Syndromes Algorithm

The management of ACS is complex, rapidly changing, and constantly evolving

What if your patient’s EKG had looked like this?

(normal)

Risk stratification of CP patients

• Most CP patients do not have acute EKG changes, but still may have underlying myocardial ischemia causing their CP.

• Risk stratification of these patients determines whether or not they require admission and what therapies are appropriate.– Higher risk patients require more aggressive

therapy

Risk stratification of CP patients for CAD

• The history and EKG are, by far, the most important factors

• Other less important factors:– Classic cardiac risk factors– Cardiac markers (CK and troponin)

• Normal markers do not rule out ACS– Response to therapy (NTG)– Physical exam findings

A difficult patient

• The patient with CP somewhat suggestive of myocardial ischemia, but with a normal EKG, normal cardiac markers and no apparent alternative dx.

• What are your disposition options?

A difficult patient• Discharge/outpatient stress

– Low risk, pain free patients only

• Rapid (12-24 hr) rule out and stress– Often done in ED CP unit

• Admit– High risk patients, known CAD,

concern for ACS

Case #2• 57 yo M presents with abrupt onset

sharp CP that radiates to his upper back. The pain is constant and not exacerbated by exertion or cough.

• PMHx: HTN• Meds: Non-compliant with BP meds x

3 yrs• Vitals: 985F 22 102 224/108

What diagnosis are you concerned about?

Aortic Dissection• Separation of the intima and media,

creating a false lumen• Type A: Any involvement of the

ascending aorta• Type B: Involves descending aorta

only

Aortic DissectionWhat complications can occur?

• Aortic regurgitation• Tamponade• Hemothorax • MI• CVA• Limb/renal/intestinal ischemia• Overall mortality 27%

Aortic Dissection

• What exam findings are suggestive?

– Pulse deficit (present in 15%)– Murmur of AI (32%)– Neuro findings (5%)– Hypertension (49%)

Aortic Dissection

• What CXR findings are suggestive?

– Widened mediastinum (62%)– Abnormal aortic contour (50%)– Pleural effusion (19%)

If dissection is suspected, it cannot be ruled out by exam findings or CXR

Aortic DissectionDiagnostic Tests

• CT• MRI• TEE• Aortography

Aortic DissectionED Management

• BP control is the cornerstone of ED management

• Nitroprusside + beta-blocker– May alternatively use labetalol as single

agent

• Definitive management– Type A: surgical– Type B: medical or surgical

Case #3• 46 yo F presents with 8 hours of left-sided

chest pain that is worse “every time I breathe.” The pain began suddenly at rest. It is associated with SOB.

• PMHx is unremarkable• No meds or allergies• Vitals: 989F 24 106 138/88 97% RA• You order IV/O2/Monitor/EKG/ASA as you

continue your H&P• The nurse hands you the EKG:

Case #3

Case #3S1

Q3 T3

Pulmonary Embolus• Can be difficult to diagnose• Important clues:

– Hx– DVT/PE risk factors

• Work-up: controversial• Non-specific tests are rarely helpful

– EKG– CXR– ABG

Pulmonary EmbolusPERC rule• “Pulmonary Embolism Rule-out Criteria”• When applied to low-risk patients, the absence of

any of the criteria predicts a very low (<2%) risk of PE, obviating the need for further testing.

• Criteria:-Age < 50 -Pulse < 100-SaO2 > 94% -No unilateral LE swelling-No recent trauma or surgery -No hemoptysis-No prior DVT or PE -No hormone use

Am J Emerg Med 2008; 26:181-5 J Thromb Haemost 2004; 2:1247-55

Pulmonary Embolus• Diagnostic studies

– D-dimer• Sensitive, but not specific• Helpful in low risk patients

– V/Q scan• PIOPED probabilities

– CT• May miss small peripheral emboli• Most commonly used imaging test

– Pulmonary Angiography• The Gold Standard, but rarely done

Pulmonary Embolus• Treatment

– Anticoagulation (Heparin or LMWH)

– IVC filter if anticoagulation contraindicated

– Thrombolytics if hemodynamic instability• Surgical embolectomy if contraindicated

NEJM 2008;358:1037-52

Case #4• 44 yo M presents with 10 hours of

constant, sharp, pleuritic, sub-sternal chest pain that is exacerbated by lying supine.

• Vitals: 992F 18 102 112/78

Diagnosis?

Pericarditis

Pericarditis: Diagnosis

• History– Sharp pleuritic pain, worse when supine

• Exam– Pericardial friction rub

• EKG– Diffuse ST elevation and PR depression

• Echo

Pericarditis• Many etiologies

– Idiopathic most common– Infectious– Neoplastic– Post MI / Post CABG– Autoimmune– Uremic

Pericarditis: Treatment• Treatment depends on cause

– NSAIDS– Antimicrobials– Dialysis

Case 4 (continued)• The patient becomes hypotensive

(80/38)• Repeat EKG

• Electrical alternans• What diagnostic and therapeutic

steps would you consider?

Case 4 (continued)

Pericardial effusion/tamponade

• IV fluids• Pericardiocentesis vs. pericardial

window• Treat underlying cause

Case #5• 48 yo M developed vomiting and

severe chest pain that is worse with swallowing after competing in a pizza eating contest.

• Vitals: 1013F 24 116 98/58• On cardiac auscultation, there is a

systolic crunching sound (Hamman’s crunch)

• What diagnosis do you suspect?

Boerhaave’s Syndrome• Esophageal rupture, often preceded

by vomiting• Results in mediastinitis• May see pleural effusion or pneumo-

mediastinum on CXR• Diagnostic studies: CT, esophogram,

endoscopy• Treatment: NPO, fluids,

antimicrobials, surgery

Questions?