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Chest Pain

Chest Pain. Goals Review the pathophysiology, diagnosis and treatment of life threatening causes of chest pain. The background:. Chest pain is one of the most common chief complaints of patients presenting to EDs annually.

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Chest Pain

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  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. 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

  18. Acute Coronary Syndromes – Cardiac Markers

  19. Acute Coronary Syndromes – Cardiac Markers

  20. 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

  21. Acute Coronary Syndromes - Treatment • Aspirin • Nitroglycerin • Oxygen • Analgesia

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

  23. 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)

  24. 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

  25. 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

  26. 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?

  27. 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

  28. Case 1 – ACSWhat do you do if you see this?

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

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

  31. 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.

  32. 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?

  33. 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.

  34. 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

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

  36. 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.

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

  38. 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)

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

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

  41. In whom should you suspect this disease?

  42. Aortic Dissection • Bimodal distribution • 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

  43. What are the clinical features of this disease?

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

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

  46. 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.

  47. How do you manage this disease?

  48. Aortic Management • Involve CT surgery early • Blood pressure control • Goal SBP 120-130 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

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