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Published byJeremiah Daugherty Modified over 11 years ago
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Approach to the ED Patient with Chest Pain
University of Utah Medical Center Division of Emergency Medicine Medical Student Orientation
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The Stats 5.4% of all ED visits
High volume High risk $$$ malpractice claims Misdiagnosis Delay in treatment < 1/3 have myocardial ischemia or infarction Chest pain accounts for over 5% of all ED visits. It is a high volume and high risk presentation, resulting in 20% of malpractice claims in dollars. These are often the result of misdiagnosis (missed MI) and a delay in treatment. Of all the patients who present to the ED with chest pain, less than 1/3 of them actually have myocardial ischemia or infarct. However, there is a broader differential for chest pain which holds significant morbidity and mortality.
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Common Etiologies of Life-threatening Chest Pain
Acute MI Unstable angina Aortic Dissection Pulmonary Embolism Spontaneous Pneumothorax Esophageal Rupture (Boerhaave’s Syndrome) Ask students to list the differential diagnosis for life threatening causes of chest pain.
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Acute MI
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Acute MI HPI Onset Palliates/Provokes Quality Radiation Severity
Time course Undo (what have they done to “undo” their pain) PMHx Med Hx HTN DM Cholesterol Meds FHx Immediate relatives CAD Social Hx Tobacco Drugs Exercise Stressors Typical Symptoms Crescendo pain Crushing Pressure Tightness Radiation Arms Jaw Neck Associated Symptoms Nausea Vomiting Diaphoresis Shortness of breath Risk Factors HTN Diabetes High cholesterol Obesity Male Family history Smoker Sedentary Post-menopausal We will talk about the “typical’ signs and symptoms – but remember there are many patients who fall outside of this realm. You must keep your differential open and broad. (The McDonald’s man is something that showed up on google.com)
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Acute MI But don’t be fooled Atypical symptoms Atypical demographics
Stridor Tooth pain Headache/neck pain Atypical demographics Young Female Cocaine use Dissection Aorta Coronary arteries Again, many folks can present with atypical symptoms – especially those that are young and female. Cocaine use puts you at risk for early atherosclerosis Not only can the aorta dissect back into the coronary arteries, causing MI, but the coronary arteries themselves can spontaneously dissect, leading to MI.
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Initial Work-up ECG/repeat ECG CXR Labs
before you even step foot in the room! CXR Labs Get an ECG before you step foot in the room! Remember, this is only a 12 second snapshot of something that is very dynamic. It is important to repeat the ECG during the patients stay, when their symptoms change (i.e. chest pain resolves, pain returns). CXR is important to help you rule out other etiologies of chest pain, i.e. PTX, PNA, aortic dissection etc. We now use CKMB (absolute value) and troponin for our labs. Remember, the troponin does not approach 100% sensitivity until 12 hours out from the onset of pain. Enzymes indicated myocardial damage. Could your patient be having unstable angina and not necessarily an MI? Thus, enzymes must be used in the context of the patient presentation. Just because the enzymes are negative, does not mean that the patient is safe for discharge home. Enzyme Rise Peak Baseline Myoglobin 1-2 h 4-6 h 24 h Troponin 3-6 h 12-24 h 7-10 d CKMB 12-36 h 3-4 d LDH 12 h 24-48 h 10-14 d
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ECG STEMI Ischemia 1mm ST elevation in 2 limb leads
2mm ST elevation in two contiguous anterior leads Reciprocal changes Ischemia ST flattening ST depression
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Treatment Anti-platelet Heparin Analgesia B-blockade Oxygen
ASA Plavix Heparin Analgesia Nitrates Narcotics B-blockade No longer recommended in STEMI patients Oxygen Thrombolytics vs. Cath Lab According to the new guidelines, B-blockers are not longer recommended in acute STEMI! Lytics vs. cath lab depends on the type of facility you are working in. Here, patients will go to the cath lab. If all are busy, lytics will be administered. If you are working in a “sending” hospital, it depends upon the time it will take you to transport the patient to a tertiary care facility with cath ability.
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Missed MI ~ 2% missed infarction rate 25% had missed ST elevation
15% had Hx of nitroglycerin use 25% died or potentially lethal outcome! As conservative as we are, we still miss up to 2% of MIs. We discharge them from our EDs. Of these 2%, a quarter of them had missed ST elevation on their ECG. And 25% had a bad outcome!
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Unstable Angina
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Angina vs. MI Heart muscle Stable vs. Unstable Angina death in MI
Ischemia in angina Stable vs. Unstable Angina
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Presentation of Angina
Established character, timing, duration of CP Transient, reproducible, predictable Easily relieved by rest or SL NTG Reduced coronary flow through fixed atherosclerotic plaques Unstable Angina Angina deviating from normal pattern Rest angina > 20 min New-onset angina, previously undiagnosed Increasing angina or change in class Discuss difference between stable and unstable angina
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Evaluation Detailed history Physical ECG/repeat ECG CXR Labs
BP in both arms helps with aortic dissection in the differential; similar w/u to MI as you don’t know if the angina is progressing to MI.
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Risk Stratify While this is recommended, exactly how to do it is controversial. There are several scoring systems. They each pros and cons. How risk stratification is will vary from institution to institution. TIMI score GRACE Braunwald Risk Stratification
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Risk Stratify High/Moderate = admission to r/o MI
ASA SL NTG for pain x3 then paste if pain free NTG gtt if pain continues IV heparin B-blockade Low = provocative testing From department Low-risk obs pathway With patients with Angina, we must risk stratify them. First of all, do we think this is cardiac chest pain? Is it MI/angina? If patients are deemed high to moderate risk, they get the full work up and admission; if they are low risk (where we really do not think this is cardiac chest pain, but cannot be sure), we have 2 options here at UMC – admit to ECU as low risk observation pathway (<24 admit for serial cardiac enzymes followed by provocative testing) or provocative testing right from our department (during daylight hours)
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Aortic Dissection
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Aortic Dissection 25-50% mortality in 24 hours
Morbidity and mortality can be quite high in these patients – we must keep this in our differential for chest pain!
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Aortic Dissection-Typical Symptoms
Onset Palliates/provokes Quality Radiation Severity Time course Undo sudden, chest/back nothing! intense ripping, tearing, cutting chest to back, flank, extremities 10/10! Constant nothing These are the “typical” symptoms. Though I have seen patients present with chest pain relieved by nitrates without radiation to their back, not a severe pain etc. have a dissection. Often it is SUDDEN in onset, this should raise a red flag!
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Aortic dissection-caveat
Only about 30% present typically This can be a great mimicker Neurologic sx’s + CP = think about dissection
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Aortic Dissection Risk Factors Trauma (high velocity) HTN Men 3:1
Congenital abnormal aortic valve Coarctation of aorta Turner’s Syndrome Cocaine Pregnancy Connective tissue d/o Marfan’s Ehlers-Danlos Vascular damage Card cath, CABG, IABP There are many risk factors for dissection and you should think of all of these as you evaluate your patient.
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Aortic Dissection Physical Exam
Aortic regurgitation (diastolic murmur) Loss/decreased pulse Sternoclavicular heave/pulsation JVD tamponade On physical exam, you may notice a new diastolic murmur or aortic regurgitation if the dissection involves the root – these patients may present hypotensive and in frank shock. Evaluate BP in both arms, evaluate peripheral pulses, if JVD, think about an aortic root dissection that has dissected into the pericardium, causing tamponade.
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Aortic Dissection Evaluation CXR ECG TEE MRI CT
Select an image by clicking on the blue button. Continue with slides until you see a blue house button in the lower right hand corner. Click the house and it will return you to this home slide. When you have gone through the imaging, click the button in the lower right hand corner to move you onto the subject, management of aortic dissection.
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CXR findings Dilated ascending aorta Dilated aortic knob
Apical pleural cap Depression of L mainstem bronchus Displacement of trachea to R Widened mediastinum Various findings you are looking for on a CXR to evaluate for aortic dissection); 12-20% of those with aortic dissection will have a normal CXR Sensitivity of 67%
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Normal mediastinum
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Review findings of this traumatic dissection: wide mediastinum, loss of aortic knob, L pleural apical cap, trachea deviated to right
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Impressive aortic knob; aortic aneurysm patient
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93% Sensitivity 87% Specificity
CT scan with IV contrast has 93% sensitivity for aortic dissection; depends on technique/timing of contrast. 93% Sensitivity 87% Specificity
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Here you can see bleeding outside of the calcifications of the aorta.
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98% Sensitivity 97% Specificity
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97% Sensitivity 77% Specificity
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Aortic dissections can dissect into the coronary arteries, causing infarction
LVH, Infarct, Ischemia
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Aortic Dissection Initial Management Cardiothoracic Surgery Consult
Control HTN and shear forces = IV infusions B-blocker + Nitroprusside Labetalol Cardiothoracic Surgery Consult For dissections involving the aortic root Start beta blocker first and then add alpha blockade to lower pressure; if you lower pressure first, you will get a reflex tachycardia, which will increase the shear forces across the aortic wall.
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Stick to Type A (involving ascending aorta) or Type B (descending aorta only);Who has survived an aortic dissection: Dr. Michael E. DeBakey, who devised the surgery to correct aortic dissection (as well as other cardiovascular and vascular techniques). Dr. DeBakey was also noteworthy for being the oldest patient ever to receive his own operation: he was 97 at the time of his surgery on February 9 and 10 of He survived and, though he worked with physical therapists to walk on his own again after suffering muscle deconditioning from prolonged physical inactivity during recovery, retained all of his mental faculties and was back to working nearly a full day until his death of natural causes on July 11, 2008 Type 1: ascending & descending; Type 2: ascending only; Type 3: Descending only; Type A: Ascending aorta; Type B: Descending aorta
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Aortic Dissection Suggested reading (IRAD):
“The International Registry of Acute Aortic Dissection: New Insights Into an Old Disease” JAMA Feb 16, 2000 Vol 283 No 7.
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To be discussed in another lecture
Pulmonary Embolism To be discussed in another lecture Will be addressed in the dyspnea lecture.
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Spontaneous Pneumothorax
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Spontaneous Pneumothorax
Absence of trauma Primary = no lung disease Secondary = underlying lung disease A primary spontaneous ptx occurs in patients without any underlying lung disease.
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Pneumothorax Presentation may vary Sudden onset Gradual symptoms
Sharp, pleuritic pain, radiates to shoulder Gradual symptoms Progressive dyspnea over weeks…
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Spontaneous Pneumothorax
Risk Factors Smoker:Non-smoker 120:1 COPD/asthma Malignancy Infectious Abscess TB PCP Pulmonary infarction Pneumonoconiosis Silicosis Berylliosis Congenital disease Cystic fibrosis Marfan’s Diffuse lung disease Idiopathic Pulm fibrosis Eosinophilia granuloma Scleroderma Rheumatoid Sarcoid Etc.
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Spontaneous Pneumothorax
Physical exam Absence or decreased breath sounds Tension pneumothorax Cyanosis Tachypnea Tachycardia Hypotension JVD Watch out for referred sounds from the good lung. It is best to listen in the axillary region.
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Spontaneous Pneumothorax
Imaging CXR Visceral pleural line +/- Expiratory film CT Scan Help w/size Cause
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Visceral pleural line
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R sided PTX, no pulmonary markings present, at all!
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This patient actually drove himself to the ED from home after having an outpatient CXR for progressive SOB over a month….Actually shows a tension ptx by film with L ptx and shift of mediastinum to the right…but he was stone cold STABLE! Arrow points to collapsed lung parenchyma.
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s/p chest tube an re-inflation of the lung.
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L PTX
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Pneumothorax Treatment oxygen <15% = observation
>15% = chest tube vs. aspiration Recurrence is common ~ up to 50% in 2-3 yrs.
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Esophageal Rupture
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Esophageal Rupture Boerhaave’s Syndrome
Complete tear Esophageal contents leak into mediastinum Mediastinitis SICK!
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Esophageal Rupture Presentation Chest and neck pain
Often recent instrumentation of esophagus Hx of forceful vomiting
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Esophageal Rupture Evaluation & Diagnosis Subcutaneous emphysema
Hammon’s Sound Pleural effusion CXR CT Esophagram
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Elderly female presented with severe chest and back pain after forceful vomiting. 1. air in mediastinum 2. air in pericardium 3. subcutaneous emphysema.
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Progressive worsening
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non=-operative, perimortum CXR of same patient
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Esophageal Rupture Management Surgical!
80-90% survival if fixed within 24 hours
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Chest Pain Summary High index of suspicion Broad differential
Risk stratification Evidence-based medicine Do what is right for your patient
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