2. Everyone has one
Very common
Acute management. Mostly benign, AND
rarely **life-threatening **
Therefore concentrate on the work-up and
treatment of those
4. Epidemiology
Up to 30% cardiac catheterizations are
negative for CAD*
3.15 million to 1.8 billion $/yr
Low mortality and high morbidity, i.e. the
cause and effect of your hard work
Nevens, F, Janssens, J, Piessens, J, et al. Prospective study on prevalence of esophageal chest pain in patients referred
on an elective basis to a cardiac unit for suspected myocardial ischemia. Dig Dis Sci 1991;36:229–235.
Achem, S, DeVault, K. Recent developments in chest pain of undetermined origin. Curr Gastroenterol Rep 2000;2:201–
209.
9. Likelihood of ACS
Framingham Cardiac Risk Factors
(intermediate)
History*
ECG (ST deviations)*
Cardiac Biomarkers*
* Any ONE connotes high probability
2002 AHA/ACC USA guidelines
10. The Lung
Pneumonia, URI
- rhonchi
PTX
- absent breath sounds
COPD, sarcoid, pulmonary fibrosis,
pulmonary htn, i.e. increased pulmonary
resistance
- no air movt, wheeze, velcro rales
11. The Upper GI Tract
Boerhaave (esophageal rupture): fever, shock,
odynophagia, tachypnea, hypoxia
EMD and GERD, esophagitis
- Burning, odynophagia, dysphagia,
- POSITIONAL, TEMPORAL
- bad breath in am, or vomit in mouth
- NO RADIATION
- non-exertional
- PILLS: especially clinda, tetracycline,
bisphosphonates
12. GERD, esophagitis
• Can account for >20-65% of UCP
• Diagnostic and Therapeutic: Antacids
- PPI
- H2-blockers
- sucralfate
35. ECG findings: RV infarct
V1-V3 turn over
and upside down or
ST-depression, R: S
is >1, R may be
broad
V7-V9: place leads
V4-V6 horizontally
at level of V6 (post
axillary, mid
scapula)
37. Cardiac Biomarkers
AST: first test, not specific
CK-MB: 6-12 hours (artifactual if skelatal
muscle is present). Disappears quickly but good
for extension of infarction
troponin: 12 hours, persists up to 7 days. Can
correlate to size of infarct but can take up to 3
days to result
LDH: 72 hours, not specific
41. Armamentarium
Beta- blockers – decrease O2 demand
- no CHF
- can give iv: metoprolol 5mg q5min x 3
Statins (PROVE-IT trial): atorvastatin 80mg
(decreased mortality)
ACEI – if HTN persists, and renal fxn ok
Cardiac catetherization: superior to thrombolysis if
STEMI and w/in 90 minutes of symptom onset.
Ovoid thrombolysis in NSTEMI
- use plt glycoprotein IIb/IIIa inhibitor upfront
(shown to reduce ischemic events by 25%, ISAR-REACT 2)
42. Special Considerations
Cocaine/vasospasm
- NTG/CCB/Ativan, can also have
thrombotic occlusion – clinical/resolution of
CP suggests spasm
RV Infarct: preload dependent
- R sided ECG V3R V4R
- hypotension with NTG/BB – Rx with
volume/inotropes
45. Conclusions
Chest Pain does not necessarily = Acute
Coronary Syndrome
Recognize DDx and clinical manifestations
PE, Aortic Dissection, PTX, Boerhaave’s, (SVC
syndrome)
Angina/ACS – myocardial 02 supply
insufficient to meet demand; recognize
“secondary angina” and treat correctable
causes
Shock: contractility agents (dobutamine), IVF,
reperfusion,
Call for help if needed
Notas do Editor
TTE: underfilled LA and “D-sign” from large RV
T wave abnormalities
– hyperacute: hyper K, early MI
– inversions: DDx: ischemia, pericardial dz, myocarditis, CNS, drugs (TCA, phenothiazine)
• Q waves
– pathologic: >.04 wide, 25% of total qrs height
– precordial R wave progression (should increase V1-V5/6)
• Special
– – – –
Posterior MI: early transition (tall R V1 or V2, ST depression)
RV infarct: ST elevation V3R V4R new LBBB
less than 50% of acute MI have clear ECG findings on 1st ECG, 10% of pt with MI may not show ECG changes
T wave abnormalities
– hyperacute: hyper K, early MI
– inversions: DDx: ischemia, pericardial dz, myocarditis, CNS, drugs (TCA, phenothiazine)
• Q waves
– pathologic: >.04 wide, 25% of total qrs height
– precordial R wave progression (should increase V1-V5/6)
• Special
– – – –
Posterior MI: early transition (tall R V1 or V2, ST depression)
RV infarct: ST elevation V3R V4R new LBBB
less than 50% of acute MI have clear ECG findings on 1st ECG, 10% of pt with MI may not show ECG changes
T wave abnormalities
– hyperacute: hyper K, early MI
– inversions: DDx: ischemia, pericardial dz, myocarditis, CNS, drugs (TCA, phenothiazine)
• Q waves
– pathologic: >.04 wide, 25% of total qrs height
– precordial R wave progression (should increase V1-V5/6)
• Special
– – – –
Posterior MI: early transition (tall R V1 or V2, ST depression)
RV infarct: ST elevation V3R V4R new LBBB
less than 50% of acute MI have clear ECG findings on 1st ECG, 10% of pt with MI may not show ECG changes
T wave abnormalities
– hyperacute: hyper K, early MI
– inversions: DDx: ischemia, pericardial dz, myocarditis, CNS, drugs (TCA, phenothiazine)
• Q waves
– pathologic: >.04 wide, 25% of total qrs height
– precordial R wave progression (should increase V1-V5/6)
• Special
– – – –
Posterior MI: early transition (tall R V1 or V2, ST depression)
RV infarct: ST elevation V3R V4R new LBBB
less than 50% of acute MI have clear ECG findings on 1st ECG, 10% of pt with MI may not show ECG changes