emergency department evaluation of chest pain
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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?
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