1. Chest Pain William Beaumont Hospital Department of Emergency Medicine
Shanna Jones, MD

2. The Things That Kill… Acute MI Pulmonary Embolus (PE)
Pneumothorax (PTX)
Aortic Dissection
Esophageal Rupture (Boerhaave’s)

3. Let’s dive right in…

4. Chest Pain: What is it?
65 y/o male complains of substernal chest pressure and tightening that radiates to his left arm, shortness of breath, diaphoresis, and nausea that started while working in the yard.
PMHx: HTN, high cholesterol
Soc: + tobacco
FHx: father died at 62 of MI

5. Chest Pain: What is it?
86 y/o female presents with generalized weakness, mental status changes, vomiting, epigastric pain, and syncope after her last episode of vomiting.
There is no other history as the NH did not feel it was necessary to send her records.

6. Chest Pain: What is it?
36 y/o obese, diabetic male presents with weakness, fatigue. shortness of breath whenever he gets off the couch, and “just not feeling right, doc.”
PMHx: diabetes since his teens, HTN, high cholesterol
FHx: Mom – HTN; Dad – “had a bad heart”

7. Acute Coronary Syndrome (ACS)
Includes USA, NSTEMI, STEMI
Leading cause of death among adults in the US (about 1 million, 2006)
6 million people present to the ER per year with chest pain
2 million of these receive the diagnosis of ACS
Cost of doing business: $ billion

8. Risk Factors for CAD – Typical
Male
Older Age
Tobacco
HTN DM
High Cholesterol
FHx
Cocaine
Artificial/early menopause

9. Risk Factors for CAD – AtypicalDM
Elderly
Female
Nonwhite
Dementia
No history of MI
No history of high cholesterol
CHF
CVA

10. Unstable Angina (USA) Defined
New onset angina occurring with minimal exertion or at rest, worsening of previous angina, increased frequency or duration of attack, and resistance to previous treatment
ECG: normal/unchanged, nonspecific ST segment changes, or T wave inversions

11. Acute Myocardial Infarction (AMI) Definition
Rise and fall of cardiac biomarkers with the following
Ischemic symptoms (critical vessel stenosis with increased myocardial work load or plaque rupture)
Development of Q waves on ECG
ST segment elevation or depression (STEMI & NSTEMI)
Coronary artery intervention (lytics or cath lab)

12. NSTEMI Definition
Positive cardiac enzymes in the appropriate clinical scenario without ST elevation on the ECG
ECG – normal, T wave inversions, ST segment depressions

13. ECG Findings of ACS Hyperacute T waves ST segment elevation of 1 mm
ST segment depression – NSTEMI vs reciprocal changes
T wave inversions – initial presentation or evolving infarct
Q waves – may emerge in the initial hour, but usually develop at 8-12 hours
Normal ECG

14. Injury Patterns on the ECG
Anterior wall MI: ST segment elevation V1-V4
Vessel: LAD

15. Injury Patterns on the ECG
Anterior wall MI: ST segment elevation V1-V4

16. Injury Patterns on the ECG
Lateral Wall MI: I, aVL, V5, V6
Vessel: variable perfusion of LAD, RCA, LCx

17. Injury Patterns on the ECG
Anterolateral with reciprocal changes
Vessels: LAD and 1st diagonal branch

18. Injury Patterns on the ECG
Inferior wall MI: II, III, aVF
Vessel: 90% RCA, 10% LCx

19. Injury Patterns on the ECG
Posterior Wall MI: V1-V3 depression, tall upright T, tall wide R wave, R/S ratio greater than 1
Vessel: RCA, PDA, LCx

20. Injury Patterns on the ECG
Inferior Wall MI with Posterior Wall MI: V1-V3 depression, tall upright T, tall wide R wave, R/S ratio greater than 1
Vessel: RCA, PDA, LCx

21. Moving on…
What do you want to order in addition to an ECG for a patient presenting with chest pain, suspected ACS?

22. Initial Evaluation IV, O2, monitor Focused H&P CBC Chem 7
CK-MB, troponin, myoglobin
CXR
PT/PTT
Possible D-dimer
? Repeat ECG

23. Treatment in the ED: STEMI
Activate the acute MI page and cath lab
ASA 325mg PO – proven to save lives
NTG SL and gtt – reduces preload>afterload, dilates coronary arteries
Heparin 60 U/kg bolus then 16 U/kg/hour
? Beta Blocker
– decrease catecholamine driven tachycardia and contractility, therefore decreasing myocardial oxygen demand

24. Treatment in the ED: STEMI
Morphine – for persistent pain or anxiety to reduce O2 need, weak sympathetic blocker, preload reducer through venous dilation
Glycoprotein IIb/IIIA inhibitors – started in the EC or cath lab for those patients undergoing mechanical coronary intervention
Plavix – in consultation with the cardiologist as it prohibits CABG for 5 days

25. Treatment in the ED: STEMI Reperfusion Therapy
PCI – 90 minute rule
Most people are eligible
Decreased risk of bleeding and stroke
Higher initial reperfusion rates
Defines coronary vasculature and allows for treatment vs. surgical referral
t-PA – when PCI cannot be achieved in 90 minutes or is not available
0-12 hours after symptom onset

26. NTG When to think twice?

27. NTG: Be cautious… Bradycardia Hypotension
Inferior or posterior wall MI with RV INFARCT
Decreased preload will cause sudden hypotension and increase infarct size
These patients need fluids to increase preload and help fill the malfunctioning/weakened ventricle

28. Treatment in the ED: USA/NSTEMI
Basically the same, but without the cath lab or fibrinolytics
IV, O2, monitor
ASA, heparin, NTG, ? beta blocker, morphine
Plavix and GIIb/IIIa inhibitors potentially after discussion with cardiology
Admit to a monitored unit

29. Chest Pain: low risk, but risky enough
Patients who are low risk with risk factors (silly isn’t it?), chest pain free, and have a normal ECG and enzymes
Observation unit for serial cardiac enzymes and ECG
Stress test vs. CTA
Cardiology consult variable

30. Chest Pain: What is it?
38 y/o female presents with sudden onset of chest pain and shortness of breath after retrieving her bags at the baggage claim from a flight home from Hawaii. She states that it is worse when she takes a deep breath. She also complains of this aching pain in her right leg when walking.

31. Chest Pain: What is it?
80 y/o bedridden patient sent from the NH with mental status changes and hemoptysis. She is pleasant during the conversation, but has no idea why she is here. She is actively coughing and appears to have increased work of breathing.
PMHx: positive for almost everything (she is 80)
Vitals: HR 110, BP 90/60, RR 28, sPO2 88% RA
Lungs: bibasilar rales with right mid lung rhonchi

32. Pulmonary Embolism – 2006 Stats
Approximately 1 in every EC patients has a PE
EM MDs correctly diagnose about 50%
10% of EC patients with PE die within 30 days even when PE is promptly diagnosed and treated

33. PE – Risk Factors Carcinoma Immobility
Trauma or surgery in the last 4 weeks
Smoking
Estrogen/OCP
Pregnancy/PP
Thrombophilia
Connective Tissue Dz
Prior PE or DVT

34. PE – Signs and Symptoms Chest Pain Dyspnea Hemoptysis Splinting
Syncope
HR > 100
Pulse ox < 95%
Unilateral arm or leg swelling

35. PE – Diagnosis Basic Labs – CBC and Chem 7
? Labs – CK-MB, troponin, PT/PTT
D-dimer – low risk patients only with low pretest probability
CXR
Exclude other diagnosis – CHF, PNA, PTX
Unilateral basilar atelectasis increases the probability of PE
Hamptom’s hump – wedge shaped infarction
Westermark’s sign – unilateral lung oligemia

36. PE – Hampton’s Hump

37. PE – Westermark’s Sign

38. PE – Diagnosis
ECG
Again to exclude other diagnosis
Most common finding is sinus tachycardia
T wave inversions V1-V4
McGinn-White Pattern – S1Q3T3
New incomplete or complete RBBB
Chest CT – moderate to high risk patients or pre-test probability, positive D-dimer

39. PE – ECG

40. PE – ECG

41. PE – Treatment LMWH 1 mg/kg SQ q12 hours
Heparin unfractionated 80 U/kg bolus then 18 U/kg/hr
LMWH 1 mg/kg SQ q12 hours
Coumadin – usually started on the floor

42. PE – Treatment
IVC filter – for pts who failed anticoagulation or have contraindications
Thrombolytics – consider in high risk pts such as systolic hypotension, persistent hypoxemia, elevated troponin or BNP (early shock or shock)
Surgery – large clot burden, refractory hypotension, floating emboli in the R heart

43. Chest Pain: What is it?
18 y/o tall, thin healthy male c/o sudden onset L sided CP with shortness of breath. The pain started while he was inhaling on a marijuana cigarette. It hurts more to breathe.
Vitals: HR 110, RR 28, BP 110/70, sPO2 96%

44. Chest Pain: What is it?
60 y/o male with a history of severe COPD c/o increasing shortness of today that is not relieved with his home inhalers.
Vitals: HR 110, RR 28, BP 110/70, sPO2 90%
Heart: distant, tachycardic and regular
Lungs: diffuse wheezing, decreased breath sounds on the right

45. Pneumothorax
Primary Spontaneous – occurs in people without clinically apparent lung disease
More common in men
Associated factors = tall, smoking, changes in ambient atmospheric pressure, genetics, MVP, Marfan’s syndrome
Disruption of the alveolar-pleural barrier is thought to occur when a bleb or bulla ruptures into the pleural space

46. Pneumothorax
Secondary Spontaneous – occur with known underlying pulmonary disease
More common in men
Associated with any underlying pulmonary disease including infection, ILD, neoplasms, COPD, asthma, etc…
Weakening of the alveolar-pleural barrier occurs secondary to the underlying lung disease either from inflammation or development of bullae

47. Pneumothorax Iatrogenic
Complication of intubation or aggressive BVM, central line placement, or any endoscopic procedure involving the trachea or esophagus
Consider in any stable patient with acute deterioration, hypoxia, or increased difficulty with ventilation

48. Tension Pneumothorax
Positive intrapleural pressure causes compression of the mediastinum and the contralateral lung
Pressure exceeding 15 to 20 mm Hg impairs venous return to the heart
Leads to cardiovascular collapse if not treated immediately  this is a clinical diagnosis not a radiographic one!

49. Pneumothorax – Symptoms
Ipsilateral sharp CP
Dyspnea
Pleuritic pain
Cough

50. Pneumothorax – Signs Sinus tachycardia Hyperresonance
Decreased breath sounds
Unilateral enlargement of the hemithorax
Splinting
Hypoxia

51. Pneumothorax: Diagnosis
Clinically for tension PTX
CXR
Radiolucent band devoid of lung markings
Inspiratory/expiratory views
Lateral decubitus views in sick patients
Supine CXR may have deep sulcus sign
Thoracic ultrasound
Chest CT

52. Pneumonthorax

53. Pneumothorax - Tension

54. Pneumothorax – Deep Sulcus Sign

55. Pneumothorax: Management
Tension – needle decompression
Tube thoracostomy  F for air, 32F at least if fluid is present
Observation – for PTX < 20% collapse
Reabsorption Rate
1-2% per day
4-8% if on 100% NRB

56. Chest Pain: What is it?
60 y/o male complains of sudden onset tearing chest pain that went up into his jaw, through to his back, and then down into his abdomen. He also vomited once, is diaphoretic, and appears very anxious.
Vitals: BP 190/120, HR 110, RR 22, sPO2 95%

57. Aortic Dissection Occurs more often in men older than 40
HTN is the most common risk factor
Associated with cardiac surgery, bicuspid aortic valve, stimulant use, and trauma
Age<40, associated with congenital heart disease, Marfan, Ehlers-Danlos, and giant cell arteritis
44% of pts with Marfan’s will develop an aortic dissection

58. Aortic Dissection Type A – 62% Type B – 38%
Involve the ascending aorta  more lethal
Type B – 38%
Do not involve the ascending aorta
Pt more likely to be older, smoke, have chronic lung disease, HTN, or atherosclerosis

59. Aortic Dissection - Diagnosis
Labs – CBC, chem7, PT/PTT, type & cross, CK-MB, troponin
ECG – exclude other dx, 15% may have ischemic changes  3% dissect back and most commonly involve the RCA, may have LVH or nonspecific ST or T wave changes
CXR – abnormal in 80% but nonspecific findings

60. Aortic Dissection - Diagnosis
CT scan – test of choice
TEE – limited by availability and operator
Aortography – no longer the test of choice
MRI – excellent test but limited by availability and instability of the patient

61. Aortic Dissection - Management
Opioids – decrease pain and sympathetic tone
Beta blockers – esmolol and labetalol
Decrease BP and HR to decrease shearing forces
Should be started first unless the pt is bradycardic
Nipride – vasodilator, used in conjunction with a beta blocker to maintain SBP

62. Aortic Dissection - Management
Hypotensive pts – measure BP in all 4 extremities to make sure it is real, IVF, blood, immediately to OR
Type A  OR (27% mortality if treated surgically vs. 56% if treated medically)
Type B uncomplicated – 10% mortality when treated medically (32% mortality if complicated)

63. Chest Pain – What is it?
22 y/o healthy male complains of chest and back pain after forcing himself to vomit. He states he had food stuck in his chest while eating at Mongolian BBQ and then forced himself to vomit for relief. He now says that his voice is hoarse, it hurts to breathe deep, and he is still very nauseated. He tried to drink some water, but this only intensified the pain.
Vitals: HR 120 BP, 130/90, RR 25, sPO2 97%

64. Esophageal Rupture – Boerhaave’s
15% are spontaneous with the remainder being iatrogenic from endoscopy, NGT, ETT, combitube, foreign body…
90% of spontaneous ruptures occur in the distal esophagus
DX – CXR, gastrograffin swallow, CT
Management
IV antibiotics
NPO and likely NGT
Surgery consult

65. Chest Pain: What is it?
26 y/o male c/o retrosternal, sharp CP, difficulty breathing, pain when breathing deeply, and worsening dyspnea tonight when he laid down to sleep. He states that for the last week he has had URI symptoms and low grade fever, but now feels that it has moved into his chest with the increasing pain and difficulty breathing.
Vitals: HR 110, BP 110/80, RR 24, sPO2 98%
Heart: Tachycardic and regular, (+) pericardial rub
Lungs: CTA
Bedside TTE is negative for effusion

66. Pericarditis

67. Pericarditis
Causes – infectious, injury/trauma, metabolic, systemic (RA), carcinoma, or aortic dissection
DX – clinical suspicion, ECG, echo
Echo – pericardial effusion and tamponade are worrisome complications  pts should be put in obs or hospitalized
Treatment – NSAIDS, steroids for pts who cannot tolerate NSAIDS

68. THE END!