1. Chest Pain

2. Goals
Review the pathophysiology, diagnosis and treatment of life threatening causes of chest pain.

3. The background:
Chest pain is one of the most common chief complaints of patients presenting to EDs annually.
8-10% of the 119 million annual ED visits are for chest pain and related symptoms
Accurate diagnosis remains a challenge

4. Visceral Pain
Visceral fibers enter the spinal cord at several levels leading to poorly localized, poorly characterized pain. (discomfort, heaviness, dull, aching)
Heart, blood vessels, esophagus and visceral pleura are innervated by visceral fibers
Because of dorsal fibers can overlap three levels above or below, disease of thoracic origin can produce pain anywhere from the jaw to the epigastrum

5. Parietal Pain
Parietal pain, in contrast to visceral pain, is described as sharp and can be localized to the dermatome superficial to the site of the painful stimulus.
The dermis and parietal pleura are innervated by parietal fibers.

6. always (look for conditions requiring immediate intervention)
Initial Approach
ABC’s first,
always (look for conditions requiring immediate intervention)
Aspirin for potential ACS
EKG
Cardiac and vital sign monitoring
Pain relief
Because of the wide differential, H+P will guide the diagnostic workup

7. Life Threatening Causes of Chest Pain
Acute Coronary Syndromes
Pulmonary Embolus
Tension Pneumothorax
Aortic Dissection
Esophageal Rupture
Pericarditis with Tamponade

8. CHEST PAIN there are a lot of importment data of the pain:
localisation
radiation
onset of the pain
the type (press, smart,cutting)
dinamic of the pain (continouosly, ongoing, undulaiting)
answer to the medical therapy

9. History O- onset P-provocation /palliation Q- quality/quantity
R- region/radiation
S- severity/scale
T- timing/time of onset

10. Initial Approach Triage Chest pain Significant abnormal pulse
Abnormal blood pressure
Dyspnoea
These pts need IV, O2, Monitor, ECG

11. The challenges:
Patients presenting with chest pain who have life threatening underlying disease often look well on initial presentation
It is estimated that 8-10% of patients presenting with ACS are discharged mistakenly from the ED
These patients have 30 day mortality of 2%

12. History Change in pain pattern
Associated symptoms: DOE, SOB, diaphoresis, vomiting, heart burn, food intolerance
PHx
Social history
FHx

13. Initial Approach Evaluation: Airway Breathing Circulation Vital Signs
Focused exam
Cardiac, pulmonary, vascular

14. Physical Exam General Appearance and Vitals (sick vs not sick)
Chest exam -Inspection (scars, heaves, tachypnea, work of breathing) -Auscultation (murmurs, rubs, gallops, breath sounds) -Percussion (dullness) -Palpation (tenderness, PMI)

15. Physical Exam Neck: JVD, crepitence, bruits Abdomen
Extremities: swelling, pulses, tenderness, Homan’s

16. Acute Coronary Syndromes - History
“Typical” Chest Pain Story (Pressure-like, squeezing, crushing pain, worse with exertion, SOB, diaphoresis, radiates to arm or jaw) The majority of patients with ACS DO NOT present with these symptoms!
Cardiac Risk Factors (Age, DM, HTN, FH, smoking, hypercholesterolemia, cocaine abuse)

17. Acute Coronary Syndromes – EKG Findings
STEMI - ST segment elevation (>1 mm) in contiguous leads; new LBBB
T wave inversion or ST segment depression in contiguous leads suggests subendocardial ischemia
5% of patients with AMI have completely normal EKGs

19. Acute Coronary Syndromes – Cardiac Markers
Initial Rise
Peak
Return to normal
Benefits
Troponin
2-4 hr hr
5 -10 days
Sensitive and specific
CK-MB
3-4 hr
10-24 hr
2 – 4 days
Unaffected by renal failure
LDH
10 hr hr
14 days
Myoglobin
1-2 hr
4 -8 hr
24 hours
Very sensitive, powerful negative predictive value

20. Acute Coronary Syndromes – Cardiac Markers

21. Echocardiogram Wall abnormalities occur within minutes
Will detect abnormalities in 80% of AMI
Normal resting echo in setting of chest pain gives low probability
Early screen for AMI complications: aneurysms, valve abnormalities, other structural destruction

22. Acute Coronary Syndromes - Treatment
Aspirin
Nitroglycerin
Oxygen
Analgesia

23. Treatment Beta-Blockers Anticoagulation Anti-Platelet Agents
Thrombolysis
Percutaneous Coronary Interventions (PCI)

24. Acute Coronary Syndromes - Treatment
STEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation, thrombolysis, PCI)
NSTEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation, PCI)
Unstable Angina (ASA, B-blocker, NTG, anticoagulation, risk stratification)

25. Acute Coronary Syndromes - Disposition
Mortality is twice as high for missed MI
Missed MI is the most successfully litigated claim against EP's. EP’s miss 3-5% OF AMI, this accounts for 25% of malpractice costs against EP’s

26. Acute Coronary Syndromes - Disposition
A single set of cardiac enzymes is rarely of use
Risk Stratification: goal is to predict the likelihood of an adverse cardiovascular event
Combination of H+P, EKG, Biomarkers
No single globally accepted algorithm
Mathematical models such as TIMI, GRACE, PURSUIT, and HEART can be helpful but are no substitute for clinical judgment

27. Case 1
46 yo M with DM, HTN, CAD and MI 1 year ago says “I think I am having a heart attack.”
What diagnostic test do you want NOW?
What are you looking for on this test?

28. Case 1 - ACS
EKG – This will differentiate what you must do now. (Specific but not sensitive)
ST elevation in 2 contiguous leads: STEMI
New LBBB
Ischemia/strain: ST depressions, new T wave inversions, Q waves
Nonspecific: T wave flattening/inversions or Q waves without old EKG

29. Case 1 – ACS What do you do if you see this?

30. Case 1 - ACS CXR Cardiac Enzymes
To look for failure and evaluate for other cause of chest pain
Cardiac Enzymes

31. What else can you do for the ACS patient?
Case 1 - ACS
What else can you do for the ACS patient?

32. Case 1 - ACS ASA Great benefit, little risk Give minimum of 182 mg NTG
Vasodilator, also reduces preload
Can give SL or IV
Heparin
Mild benefit, consider risks
Morphine?
Questionable benefit, reduces stress
B-Blocker?
May give oral, avoid if pt has symptoms of hear failure (includes HR <110)
Plavix? IIbIIIa inhibitor?
Very cardiologist dependent. A problem if pt needs CABG.

33. Case 2
30 yo M had an ORIF of ankle fx 2 weeks ago, c/o sudden onset of chest pain.
What are the signs/symptoms of this disease?
What are the risk factors for this disease?

34. Case 1 - ACS ASA Great benefit, little risk Give minimum of 182 mg NTG
Vasodilator, also reduces preload
Can give SL or IV
Heparin
Mild benefit, consider risks
Morphine?
Questionable benefit, reduces stress
B-Blocker?
May give oral, avoid if pt has symptoms of hear failure (includes HR <110)
Plavix? IIbIIIa inhibitor?
Very cardiologist dependent. A problem if pt needs CABG.

35. Pulmonary Embolus Risk Factors
Hypercoaguability
Malignancy, pregnancy, estrogen use, factor V Leiden, protein C/S deficiency
Venous stasis
Bedrest > 48 hours, recent hospitalization, long distance travel
Venous injury
Recent trauma or surgery

36. How will you confirm your suspicion?
Case 2 - PE
How will you confirm your suspicion?

37. PE Diagnosis D-dimer Very sensitive in low to moderate probability
Not sensitive enough for high probability
Not specific (Lots of false positives)
Spiral CT
Current gold standard
Quick and available
Caution if impaired creatinine clearance
V/Q
Many studies will be “Indeterminate”
PVL of LE
Surrogate maker, but DVT is treated in similar.

38. How will you treat this patient?
Case 2 - PE
How will you treat this patient?

39. PE Treatment IV fluid to maintain blood pressure
Heparin (Will limit propagation but does not dissolve clot)
Unfractionated: 80 u/kg bolus, 18 h/kg/hr
Fractionated (Lovenox): 1 mg/kg SC BID
Fibrinolytics
Consider with large if pt is unstable
No study has shown survival benefit, but very difficult to study.
Alteplase 50–100 mg infused over 2–6 hrs, (bolus in severe shock)

40. Case 3
35 yo M with sudden ripping pain radiating to back.

41. Aortic Dissection Blood violates aortic intimal and adventitial layers
False lumen is created
Dissection may extend proximally, distally, or in both directions

42. In whom should you suspect this disease?

43. Aortic Dissection Bimodal distribution Risk factors
Young: Connective tissue (Marfan) or pregnancy
Older: Most commonly > 50 (mean age 63)
Risk factors
Male: 66% of patients
Hypertension: 72% of patients
Connective tissue disease
30% of Marfan’s patients get dissections
Cocaine Use
Syphilis

44. What are the clinical features of this disease?

45. Aortic Dissection Presentation (Difficult clinical diagnosis)
85% have chest or back pain
“Ripping” or “tearing” in 50%
Neurologic symptoms in 20%
Hematuria
Asymmetric pulses

46. How do you confirm the diagnosis of this disease?

47. Aortic Dissection Diagnosis
CXR- Widened mediastinum, abnormal aortic knob, pleural effusions
Not sensitive (25% have wide mediastinums)
Chest CT- Very sensitive and specific
Quickly obtained
Must think about kidney + contrast
Angiography- Gold standard
Most reliable anatomy of dissection
Bedside US – evaluate aorta and look at heart to r/o tampanode.

48. How do you manage this disease?

50. Aortic Management Involve CT surgery early Blood pressure control
Goal SBP mmHg
Beta blockers are first line (Labetalol and Esmolol)
Can add vasodilators i.e. nitroprusside
Admission to ICU
Ascending dissections will need surgery
If dissection is only descending, management is only medical

51. Case 4
55 yo alcoholic with persistant vomiting presents with sudden onset of CP followed by hemetemisis.

52. What are the risk factors for this disease? What is the presentation?

53. Case 5
18 yo healthy male was lifting weights when he had sudden onset of sharp CP + SOB.
HR 122, RR 34, BP 70/P, Sat 88%
Decreased breath sounds on left.
What do you do first?

54. Needle Decompression

55. Where do you place the chest tube?

57. Thank You!
Questions?