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Emergency Medicine 1 > Evaluation of the Adult with CP in the ED > Flashcards

Evaluation of the Adult with CP in the ED Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

2nd most common complaint in ED

A

chest pain

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2
Q

percent of adults with chest pain

A

~5%

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3
Q

Exclude life-threatening causes

A
  • Acute Coronary Syndrome
  • Pulmonary Embolism
  • Aortic Dissection
  • Esophageal Rupture
  • Tension Pneumothorax
  • Pericardial Tamponade
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4
Q

Acute coronary syndrome

A
  • Unstable Angina
  • ST segment elevation MI
  • Non-ST segment elevation MI
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5
Q

Angina

A
  • sensations in chest of squeezing, heaviness, pressure, weight, vise-like aching, burning, tightness
  • radiation to shoulder, neck, jaw, inner arm, epigastrum (can occur without chest component); band like discomfort
  • relatively predictable
  • lasts 3-15 min
  • abates when stressor is gone or nitro is taken
  • Angina: metabolic demand for the heart is higher than what we can get there
  • EXERTION related pain that is consistent
  • You cant necessarily have no sxs yesterday and then have severe sxs today with angina
  • Chest pain, exertional component, fixed component
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6
Q

Unstable angina

A
  • Class I: no angina with ordinary physical activity, angina with strenuous or prolonged exertion
  • Class II: Early-onset limitation of ordinary activity, angina may be worse after meals, in cold temp, or with emotional stress
  • Class III: marked limitation of ordinary activity
  • Class IV: inability to carry out any physical activity without chest discomfort, angina occurs during rest
  • Unstable angina – when the CP gets more severe
  • Chronic progressive problem that occurs over decades
  • Unstable is class 3 or class 4 angina
  • If you have anginal sxs with less than two blocks or two flights of stairs, that’s REALLY concerning
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7
Q

ST segment elevation MI

A
  • Occlusive myocardial infarction resulting in abrupt cessation of coronary flow distal to site of thrombosis
  • ECG is characterized by ST segment elevation in an anatomic distribution
  • Troponin increase is a marker of myocardial infarction
  • ST elevation MI: occlusive MI is when the vessel is completely occluded and the myocardium distal to the occlusion suffers and dies
  • For the most part, occlusion happens when you have ST segment elevation MI, but sometimes it happens with NSTEMI
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8
Q

Non-ST segment elevation MI

A
  • Troponin increase in the absence of strict ECG criteria for STEMI
  • 2/3rd of the time, this occur in the setting of demand ischemia (i.e. situation where myocardial blood demand outstrips blood supply)
  • 1/3rd of the time, this occurs with occlusive myocardial infarction without clear STEMI on ECG
  • NSTEMI is a spectrum of disease. Diagnosed by troponin and EKG
  • Two different causes: EKG just doesn’t show the elevation
  • The vast majority of the Mis are supply and demand mishaps
  • Example: severe sepsis – hypotensive, cool, clammy, shock, there is global hypoperfusion to the whole body including the heart – this can result in a troponin leak. This is an MI that was caused by sepsis
  • If anemia is causing the problem, the fix is fixing the anemia. Same with sepsis, fix the sepsis!
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9
Q

Cardiogenic Shock

A
  • Inadequate tissue perfusion in the setting of profound cardiac dysfunction
    • Hypotension (SBP < 80-90 mmHg or MAP < 30 mmHg compared to baseline)
    • Cardiac index < 1.8 L/min per m2
    • Adequate or elevated filling pressures

-Cardiogenic shock: if you’ve had an MI in the past and then you have another MI later on, then the total damage to the heart can be around 40%!

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10
Q

CAD risk factors

A
  • male >45, female >55
  • trans fats and cholesterol
  • family hx
  • smoking
  • high blood pressure
  • diabetes
  • Obesity, sedentary lifestyle, mental stress, depression, insomnia
  • Amphetamine/Cocaine use
  • ESRD
  • Connective tissue disorders (e.g. SLE, RA)
  • Vasculitis
  • HIV and HAART medications
  • Trauma
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11
Q

AMI risk factors

A
  • Being alive
  • Not being dead
  • Having a heart
  • Risk increases after age 40 in men and after age 50 in women
  • Troponin is better than your history!
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12
Q

Myocardial infarction

A
  • pain - sudden onset, substernal, crushing, tightness, severe, unrelieved by nitro, may radiate to back, neck, jaw, shoulder, arm
  • dyspnea
  • syncope (decreased BP)
  • nausea
  • vomiting
  • extreme weakness
  • diaphoresis
  • denial is common
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13
Q

atypical populations

A
  • women
  • elderly
  • DM
  • ESRD
  • demetia
  • psych
  • language barrier
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14
Q

Atypical symptoms of MI without chest, arm, neck, or jaw discomfort

A
  • N/V
  • cold sweats
  • SOB
  • fatigue
  • syncope
  • cold, clammy skin
  • back pain
  • palpitations
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15
Q

Nitro administration

A

-Cannot be used by itself to determine CAD bc It can relieve non ischemic pain too

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16
Q

Low risk chest pain

A
  • Pleuritic pain (i.e., sharp or knifelike pain brought on by respiratory movements or cough)
  • Pain reproduced with movement or palpation of the chest wall or arms
  • Primary or sole location of discomfort in the middle or lower abdominal region
  • Pain that may be localized at the tip of 1 finger, particularly over the left ventricular apex or a costochondral junction
  • Very brief episodes of pain that last a few seconds or less
  • Pain that radiates into the lower extremities
17
Q

Who needs an ECG

A

-CART analysis of >3 million chest pain ED visits

  • Age >30 with chest pain
  • Age >50 with dyspnea, AMS, upper extremity pain, syncope, weakness
  • Age >80 with abdominal pain, nausea/vomiting
  • Use clinical judgment

-SEN 92% for STEMI, NPV 99.98%

18
Q

Troponin

A
  • Specific for cardiac muscle
  • Rise within hours of symptoms and remain elevated for up to 1-2 weeks
  • Be familiar with lowest level of detection and lowest level of AMI
    • Assay can detect 0.04 ng/mL
    • Lab reports values ≥ 0.10 ng/mL
    • AMI diagnostic at ≥ 0.30 ng/mL

-Current Gold Standard for AMI

19
Q

Best test for diagnosing unstable angina?

A

Nuclear imaging

20
Q

initial ED tx of ACS

A
  • IV – establish 1-2 large bore peripheral IV’s
  • O2 – provide supplemental O2 by nasal cannula if hypoxia is present
  • Cardiac monitor with automated HR and BP recording
21
Q

Medical therapy

A
  • Aspirin – 162mg, non-enteric coated, chewed
    • Significant mortality benefit 2.4%-5.2%
  • Other antiplatelet agents
    • Clopidogrel preferred*
  • LMWH/heparin
    • Small benefit when used as a bridge to more definitive intervention

-Analgesia – opiates

  • Nitrates
    • Avoid if SBP < 90 mmHg, suspected RV infarct, recent phosphodiesterase inhibitor
  • Statins
    • ?attenuation of inflammatory response that occurs with ACS
  • Beta-blockers
    • Avoid IV beta-blockers in first 24 hours; improved mortality when PO given on day #2
  • ACE inhibitors
    • Administer when hemodynamics stabilize
22
Q

Life-threatening causes of chest pain

A
  • Acute Coronary Syndrome
  • Pulmonary Embolism
  • Aortic Dissection
23
Q

Pulmonary Embolism

A
  • Obstruction of pulmonary artery or one its branch by clot/fat/air/tumor
    • Typically clot originates in deep veins or the leg, pelvis, or arm
  • Clinical presentation is related to timing and location of pulmonary embolism
    • Timing: acute, subacute, or chronic
    • Location: saddle, lobar, segmental, or subsegmental
24
Q

Risk factors for PE

A
  • Prolonged immobilization (e.g. long distance travel)
  • Surgery (especially orthopedic surgery of the lower extremity)
  • Central venous catherization
  • Trauma
  • Pregnancy and immediate post-pregnancy period
  • Cancer
  • Personal or family history of hypercoagulability
  • Exogenous estrogen or testosterone

-A significant number of patients with PE have no identifiable risk factors at the time of diagnosis

25
Q

Clinical Presentation of PE: sxs

A
  • Dyspnea at rest or with exertion (73%)
    • Onset is seconds to minutes (72%)
  • Pleuritic chest pain (66%)
  • Cough (37%)
  • Unilateral leg swelling or pain (44%)
  • Wheezing (21%)
  • Hemoptysis (13%)

-Rarely, patients present with shock, arrhythmia, or syncope

26
Q

Clinical Presentation of PE: signs

A
  • Tachypnea (70%)
  • Unilateral leg swelling or tenderness (47%)
  • Tachycardia (30%)
  • Pulmonary rales (51%)
  • Decreased breath sounds (17%)
  • Jugular venous distension (14%)
  • Hypotension (8%)
  • Fever (3%)
27
Q

PE rule-out criteria

A
  • age <50yo
  • pulse <100 bpm
  • SaO2 >/= 95% on room air
  • no hemoptysis
  • no exogenous estrogen use
  • no prior venous thromboembolism
  • no surgery or trauma requiring hospitalization within the past 4 weeks
  • no unilateral leg swelling
28
Q

Diagnostic evaluation of PE

A

-Use PERC and Wells criteria to risk stratify

  • Wells Score
    • PE unlikely (0-4 pts): PERC score or d-dimer (Overall 12% incidence of PE, Use age-adjusted d-dimer in patients > 50yrs)
    • PE likely: CT PE chest (Overall 37% incidence of PE)
  • If you sent a d-dimer to evaluate for PE, and the d-dimer is (+), then CT PE chest
  • Hemodynamically unstable patients – consider bedside ECHO for RV size and treat accordingly
29
Q

Treatment of PE

A

-Treatment depends on clinical severity of PE, location of the clot, and underlying coagulation state

  • Options
    • Heparin or low molecular weight heparin
    • Coumadin or novel oral anticoagulant
    • Thrombolytics for massive PE (Sustained hemodynamic instability (SPB < 90 mm Hg for 15 min or requirement for vasopressors))

-Prognosis: recurrent thromboembolism, chronic embolic pulmonary hypertension, death

  • Disposition
    • PESI or sPESI score
    • In general, hemodynamically stable patients can be treated as outpatients
30
Q

Aortic dissection

A
  • Tear in aortic intima creates a false aortic lumen – which can lead to aortic rupture
  • Chronic HTN is the most important predisposing factor
  • Stanford classification
    • Type A: ascending aorta
    • Type B: descending aorta

Variants

  • Aortic intramural hematoma
  • Intimal tear without hematoma
  • Penetrating atherosclerotic ulcer
31
Q

AD detection: High risk conditions

A
  • marfan syndrome
  • connective tissue disease
  • family hx of aortic disease
  • known aortic valve disease
  • recent aortic manipulation
  • known thoracic aortic aneurysm
32
Q

AD detection: high risk pain features

A

-chest, back, or abdominal pain described as the following: abrupt in onset/severe in intensity AND ripping/tearing/sharp or stabbing quality

33
Q

AD detection: high risk exam features

A
  • evidence of a perfusion deficit (e.g. pulse deficit, systolic BP differential, focal neurologic deficit - in conjunction with pain)
  • murmur of aortic insufficiency (new or now known to be old - in conjunction with pain)
  • hypotension or shock state
34
Q

Clinical presentation of AD

A
  • Abrupt-onset, severe chest or back pain
    • Sharp, knife-like
    • Ripping or tearing
  • Syncope
  • On exam, a pulse deficit may be appreciated
  • New diastolic heart murmur (aortic regurgitation)
  • Focal neurologic deficit (e.g. stroke, ALOC, Horner syndrome, hoarseness, acute paraplegia from spinal cord ischemia)
  • Hypotension
    • May be related to cardiac tamponade, aortic valve regurgitation, acute myocardial infarction/complete heart block, hemothorax or hemoperitoneum
35
Q

Diagnostic evaluation of AD

A
  • CXR – wide mediastinum in 60-70% of cases
  • D-dimer – use a cutoff of 500 ng/mL
    • SEN 97%, SPE 56%, NPV 96%
  • ADD Risk Score: 0-1pts
    • Send d-dimer – CTA chest only if d-dimer > 500 ng/mL
  • ADD Risk Score: 2-3pts
    • CTA chest
  • The finding of wide mediastinum on CXR + 1pt by ADD – CTA chest
  • Hemodynamically unstable patients – consider bedside ECHO for detection of aortic dissection
36
Q

Treatment of AD

A

Goals:

  • HR < 60 bpm, SBP 100-120 mmHg
    • Esmolol or labetalol preferred
    • Nicardipine is 2nd line therapy
  • Use opiates for pain control

-Type A Aortic Dissection – keep patient alive by decreasing BP and HR until patient can be evaluated by thoracic surgery

  • Type B Aortic Dissection – medical management +/- thoracic surgery consult
    • If no perfusion deficit, then admit to ICU
    • If perfusion deficit is present, then thoracic surgery

-Know that you want to get HR less than 60 and BP less than 100-120

37
Q

ACS summary

A
  • Know typical and atypical symptoms
  • Have a low threshold for sending a troponin

-CAD risk factors are helpful to determine if a patient has angina/unstable angina

  • The ECG is key
  • Trop don’t lie!
  • Cath lab
  • Medical management: ASA, NTG, heparin, b-blockers, statin, etc.
38
Q

PE summary

A
  • Hypoxia and/or tachycardia are more likely associated with PE
  • Use PERC and Wells criteria to risk stratify patients
  • A (-) d-dimer rules out PE in low risk patients
  • CT PE protocol
  • Use sPESI to risk stratify
  • Start anticoagulation if uncomplicated
  • Thrombolytics if shock is present
39
Q

AD summary

A
  • Abrupt onset of severe vascular pain – patient looks uncomfortable
  • Use AD detection risk score and CXR to stratify patients
  • A (-) d-dimer rules out AD in low risk patients
  • CTA Chest
  • Keep the patient alive until surgery
  • HR goal: < 60 bpm
  • BP goal: 100-120 mm Hg

Emergency Medicine 1 (8 decks)

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