My notes for the tutorial in the Preparatory Course for Pre-Interview Assessment in Emergency Medicine MMed Intake (PIAEM) 2015

1. Pre-Interview Assessment For Emergency
Medicine Preparatory Course 2015
Chest Pain Evaluation in Emergency Department
LECTURER: DR. CHEW KENG SHENG
cksheng74@usm.my
Learning Objectives
By the end of this lecture, participants should achieve the following objectives:
1. Understand the five life-threatening causes of chest pain that must be considered
in emergency department, i.e., acute coronary syndrome, acute pulmonary
embolism, pneumothorax, pericarditis/myocarditis, aortic dissection
2. Understand the values and pitfalls of chest pain history in each of these five
conditions
3. Understand the specific approaches in the initial evaluations of each of these five
conditions in emergency department
4. Understand the characteristics of a non-life threatening cause of chest pain
(musculoskeletal chest pain) that may be commonly present in emergency
department besides the five life threatening causes of chest pain
● Go to my post in Storify.com for more collated resources from the internet.
https://storify.com/cksheng74/introduction-to-cardiovascular-emergencies
1

2. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
Chest Pain Evaluation In Emergency Department
1. Main focus of chest pain (CP) evaluation in emergency department (ED) - ​rule out
life threatening causes
2. Life threatening causes of CP (mnemonic: ‘​PA-PA Hook’​’)
a. P = Pericarditis/myocarditis
b. A = Acute coronary syndrome
c. P = Pneumothorax
d. A = Acute pulmonary embolism
e. Hook =Aortic dissection (shape of aorta looks like a hook)
3. Differential Diagnosis of CP:
a. Non life threatening: Chest wall pain (musculoskeletal causes)
i. typically not life-threatening although can present concomitantly
with ACS
ii. usually sharp, localized to a specific area (such as the xiphoid, lower
rib tips, or midsternum)
iii. positional or exacerbated by deep breathing (pleuritic), turning, or
arm movement
iv. occurs more frequently among women than men (69% in study by
Disla et al, 1994)1
v. majority of cases have diffuse but regional pain syndrome (i.e.,
multiple areas of tenderness with reproducible CP)
vi. Areas of tenderness are not accompanied by heat, erythema, or
localized swelling.
vii. Upper costal cartilages at the costochondral or costosternal
junctions are most frequently involved2
viii. Bösner et al (2010),​N = ​1212 patients in outpatient setting:
1. presence of at least 2 of 4 of the following features:
a. localized muscle tension
1
Disla E, Rhim HR, Reddy A, et al. Costochondritis. A prospective analysis in an emergency department setting.
Arch Intern Med 1994; 154:2466.
2
Wolf E, Stern S. Costosternal syndrome: its frequency and importance in differential diagnosis of coronary
heart disease. Arch Intern Med 1976; 136:189; Fam AG, Smythe HA. Musculoskeletal chest wall pain. CMAJ 1985;
133:379.
2

3. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
b. stinging pain
c. pain reproducible by palpation, and
d. absence of cough
ix. has 63% sensitivity, 79 percent specificity to diagnose chest wall
syndrome3
b. Life-threatening:
c. Acute coronary syndrome
i. Less than 15 to 30% of non-traumatic CP patients to ED actually
have ACS
ii. Due to conditions that causes increased oxygen demand and/or
decreased oxygen supply to myocardium.
iii. Examples:
1. Atherosclerotic plaque rupture and thrombus formation via
the adhesion, activation, and aggregation of platelets
2. oxygen supply-demand mismatch from coronary artery
spasm causes
3. coronary artery embolus
4. anemia
5. arrhythmia
6. hypertensive crisis
7. left ventricular hypertrophy and strain
iv. History:
v. Remember: ​NO ONE SINGLE ELEMENT FROM CP HISTORY IS
POWERFUL ENOUGH TO PREDICT ACS FROM NON-ACS ​that would
allow a clinician to make a diagnosis from history alone
vi. Radiation
1. In Panju et al (1998) classic paper:
a. CP radiation to
i. left shoulder: LR 2.3 95% CI (1.7 to 3.1)4
3
Bösner S, Becker A, Hani MA, et al. Chest wall syndrome in primary care patients with chest pain:
presentation, associated features and diagnosis. Fam Pract 2010; 27:363.
4
LR = Likelihood ratio, it describes the relative likelihood that a positive test (in this case, presence of
left shoulder radiation of pain) would be expected in a patient with the disease (in this case, myocardial
infarction compared to its presence in a patient without the disease.
3

4. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
ii. right shoulder: LR 2.9 (1.4 to 6.0)
iii. both shoulder: LR 7.1 (3.6 to 14.2)
b. Nature of CP that reduces the LR of MI
c. Mnemonic: 3Ps: ​p​leuritic, ​p​ositional, ​p​roducible (or
re-producible) with ​p​alpation
i. pleuritic: LR 0.2 (0.2 to 0.3)
ii. stabbing: LR 0.3 (0.2 to 0.5)
1. Beware of cultural differences.
2. In a study by Summers et al (1999), the
word “sharp” may be used to as a
descriptor of acuity/severity rather than
or nature in certain parts of US
iii. positional LR 0.3 (0.2 to 0.4)
iv. pain reproduced by palpation: LR 02 (0.2 to 0.4)
vii. Location of pain
a. In general, region of infarct has no correlation with CP
location except maybe for inferior MI - more often
present with abdominal pain or GI symptoms than
anterior MI.
b. Everts et al (1996) - pain location at central or
mid-chest region has little value in predicting AMI
c. Esophageal pathology also produces pain at this
region
viii. Relief of pain
1. Relief of pain following the administration of sublingual
nitroglygerin ​does ​not​reliably distinguish between cardiac vs
noncardiac origin of CP (Grailey et al, 2012)
2. This is because nitroglycerin can also relaxes esophageal
muscle, thus relieve esophageal-related pain as well
ix. Risk factors
1. Cocaine use: A history of cocaine use may increase the
suspicion of myocardial infarction and, less commonly, aortic
4

5. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
dissection, pulmonary hypertension, and acute pulmonary
syndrome
x. In one study by Mittleman et al (1999) involving 3946 patients with
an acute myocardial infarction, the risk of a myocardial infarction
was increased 24 times over baseline in the 60 minutes after cocaine
use.
xi. Troponins
1. is a highly sensitive biomarker that aids in the detection of
myocardial cell damage
2. while highly specific for myocardial injury, it is not specific for
ACS as the cause.
3. As a result, if troponin testing is applied indiscriminately in
broad populations with a low pretest probability of
thrombotic disease, the positive predictive value for ACS is
greatly diminished
4. Causes of elevated troponin​can be divided into the
following broad categories:
5. Myocardial ischemia
a. Acute coronary syndrome
b. Other coronary conditions beside ischemia
i. Arrhythmia: tachy- or brady-
ii. Cocaine/methamphetamine use
iii. Coronary intervention - PCI, cardiothoracic
surgery)
iv. Coronary artery spasm (variant angina)
v. Severe hypertension
vi. Aortic dissection
vii. Coronary artery vasculitis (SLE, Kawasaki's)
c. Non-coronary ischemia conditions
i. Shock (hypotension)
ii. Hypoxia
iii. Hypoperfusion
iv. Pulmonary embolism
5

6. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
6. Myocardial injury but without ischemia:
a. Trauma: cardiac contusion
b. Extreme exertion
c. Burns >30% BSA
d. Cardiotoxic meds: anthracyclines, herceptin
e. Electrical shock
f. Carbon monoxide exposure
g. Apical ballooning (Takotsubo)
h. Myocarditis
i. Myopericarditis
j. Rhabdomyolysis involving cardiac muscle
k. Hypertrophic cardiomyopathy
l. Peripartum cardiomyopathy
m. Heart failure, malignancy, stress cardiomyopathy
7. In the population-based Dallas Heart Study to evaluate the
prevalence of cardiac troponin T (cTnT) elevations in the
general population, the data strongly support the concept
that normal individuals have very low (in this study
undetectable) levels of troponin.
8. Nonetheless, troponin T elevations primarily occurred in
individuals with heart failure, left ventricular hypertrophy,
chronic kidney disease, or diabetes
9. These associations were seen even with minimal elevations in
cTnT (0.01 to 0.029 microg/L).
10. Elevations in cTnT were rare in individuals without these
underlying disorders, who were more similar to a normal
population.
11. In a study using high-sensitivity assay for cTnT (hs-TnT), it
shows an increase in the prevalence of detectable troponin to
25% vs 0.7% when using the standard assay. The prevalence
of a hs-cTnT concentration of 0.014 ng/mL or above (the 99th
percentile cut-point for diagnosis of myocardial infarction
[MI]) was 2.0%. After adjustment for traditional risk factors,
6

7. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
chronic kidney disease, and other biomarkers (C-reactive
protein, and N-terminal pro-brain-type natriuretic peptide),
hs-cTnT remained independently associated with all-cause
mortality (adjusted hazard ratio, 2.8 [95% CI, 1.4-5.2]) .5
12. Therefore, troponin elevation in the absence of an ACS still
has significant prognostic value. Troponin elevations in a
variety of settings predict worse short- and long-term
survival. The reasons for this increase in mortality are
currently poorly understood, but may be related to several
factors, including myocardial necrosis with myocyte loss, or
underlying undetected coronary artery disease.
xii. HEART score
1. Recently, the HEART risk score was developed for risk
stratification of chest pain patients presenting to the ED.
2. The HEART score is composed of five parameters of clinical
judgement: H = History, E = ECG, A = Age, R = Risk factors and
T = Troponin. By appreciating each of these five elements
with 0, 1 or 2 each patient patients will receive a score of 0-10
3. The HEART score divides patients into low (0-3), intermediate
(4-6) or high risk groups (7-10), with mean risks of a MACE
event of 0.9%, 12% and 65%, respectively .6
d. Pulmonary embolism
i. The most common presenting symptom is dyspnea followed by
pleuritic pain, cough, and symptoms of deep venous thrombosis.
ii. Hemoptysis is actually an unusual presenting symptom in PE.
iii. For example, in the Prospective Investigation of Pulmonary
Embolism Diagnosis II (PIOPED II) study :7
1. Dyspnea at rest or with exertion (73%)
5
de Lemos JA, Drazner MH, Omland T, et al. Association of troponin T detected with a highly sensitive
assay and cardiac structure and mortality risk in the general population. JAMA 2010; 304:2503.
6
Backus B, Six A, Kelder J, Gibler W, Moll F, Doevendans P. Risk Scores for Patients with Chest Pain:
Evaluation in the Emergency Department. Current Cardiology Reviews. 2011;7(1):2-8.
7
Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, et al. Clinical characteristics of patients
with acute pulmonary embolism: data from PIOPED II. Am J Med 2007;120(10):871-9.
7

8. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
2. Pleuritic pain (44%)
3. Cough (37%)
4. Orthopnea (28%)
5. Calf or thigh pain and/or swelling (44%)
6. Wheezing (21%)
7. Hemoptysis (13%)
iv. Common presenting signs on examination include [6]:
1. Tachypnea (54%)
2. Calf or thigh swelling, erythema, edema, tenderness (47%)
3. Tachycardia (24%)
4. Rales (18%)
5. Decreased breath sounds (17%)
6. An accentuated pulmonic component of S2 (15%)
7. Jugular venous distension (14%)
8. Fever, mimicking pneumonia (3%)
v. Troponins - are neither sensitive nor specific diagnostically in PE
1. Troponins can be elevated in up to 30 - 60% in moderate to
large PE as a marker of right ventricular dysfunction, troponin
levels are elevated in 30 to 50%8
vi. ECG
1. simultaneous T-wave inversions in the anterior and inferior
leads is predictive of right ventricular strain/hypertrophic
conditions including PE and can be used to differentiate ACS
2. Kosuge et al (2007) for example, have shown that
simultaneous inversion in III and V1 are diagnostically
significant as they were observed in only 1% of patients with
ACS vs 88% of patients with Acute PE (p less than 0.001). The
sensitivity, specificity, positive predictive value, and negative
predictive value of this finding for the diagnosis of PE were
8
Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB. Cardiac troponin I elevation in acute pulmonary
embolism is associated with right ventricular dysfunction. Journal of the American College of
Cardiology. 2000;36(5):1632-6.
8

9. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
88%, 99%, 97%, and 95%, respectively. In conclusion, the
presence of negative T waves in both leads III and V1 allows
PE to be differentiated simply but accurately from ACS in
patients with negative T waves in the precordial leads.” (Ref:
Kosuge M, Kimura K, Ishikawa T, Ebina T, Hibi K, Kusama I,
Nakachi T, Endo M, Komura N, Umemura S.
Electrocardiographic differentiation between acute
pulmonary embolism and acute coronary syndromes on the
basis of negative T waves. Am J Cardiol. 2007 Mar
15;99(6):817-21.)
3. Remember: The ECG changes described above are not unique
to PE. A similar spectrum of ECG changes may be seen with
any disease that causes right ventricular strain/hypertrophy
like cor pulmonale9
vii. Wells criteria can be applied as a diagnostic algorithm for
non-pregnant patients
1. If Wells criteria shows PE unlikely (score ≤4)
a. then apply PERC score
b. If ALL eight PERC rule criteria is fulfilled, no further
testing is required
c. If patient does not fulfill all PERC rule criteria, do
D-dimer or proceed with imaging
d. The PE rule-out criteria ("PERC rule") is an alternative
to D-dimer testing in patients with a low pre-test
probability for PE
e. The PERC rule has eight criteria (mnemonic:10
BREATHSS​)
i. B​= No hemoptysis (blood in sputum)
ii. R​= Oxyhemoglobin saturation ≥95% at room air
iii. E​= No estrogen use
9
The ECG in Pulmonary Embolism. In: Life In The Fast Lane. Available at URL:
http://lifeinthefastlane.com/ecg-library/pulmonaryembolism/​Accessed 18 September 2015
10
Kline JA, Courtney DM, Kabrhel C, Moore CL, Smithline HA, Plewa MC, et al. Prospective multicenter
evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost 2008;6(5):772-80.
9

10. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
iv. A​= Age <50 years
v. T​= No prior DVT or PE
vi. H​= Heart rate <100 beats/minute
vii. S​= No unilateral leg swelling
viii. S​= No surgery/trauma requiring hospitalization
within the prior four weeks
f. PERC rule is only valid in clinical settings with a low
prevalence of PE (<20%). In clinical settings with a
higher prevalence of PE (>20 percent), the PERC-based
approach has been shown to have a substantially
poorer predictive value .11
g. D-dimer: Generally, D-dimer is useful for its negative
predictive value. For patients in whom PE is thought to
be ​unlikely​, a normal D-dimer (<500 ng/mL)
effectively excludes PE, and, therefore, no further
testing is required, including in 1) patients who have
had a prior PE 2) those with a delayed presentation,
and 3) women who are pregnant. In contrast, an
elevated D-dimer (>500 ng/mL) should raise the
suspicion for PE and prompt further testing in patients
who have a low clinical probability of PE.
2. If Wells criteria show PE likely, for most nonpregnant patients,
CTPA is the imaging modality of first choice
3. V/Q scan is reserved for patients in whom the CTPA is
contraindicated (eg, pregnant, severe nondialysis requiring
chronic kidney disease, contrast allergy, or morbid obesity), is
inconclusive, or is negative.
viii. Bedside ultrasound:
1. Echocardiography cannot definitively diagnose PE
11
Hugli O, Righini M, Le Gal G, Roy PM, Sanchez O, Verschuren F, et al. The pulmonary embolism
rule-out criteria (PERC) rule does not safely exclude pulmonary embolism. J Thromb Haemost
2011;9(2):300-4.
10

11. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
2. About 30 to 40% of patients with PE have echocardiographic
abnormalities indicative of RV strain :12
a. Increased RV size
b. Decreased RV function
c. Tricuspid regurgitation
3. Other echo findings:
a. RV thrombus – The incidence of PE among ​patients
with an RV thrombus​appears to be >35% .13
However, only 4% of patients with PE have a RV
thrombus .14
b. Regional wall motion abnormalities that spare the
right ventricular apex (​"McConnell's sign"​) –
McConnell’s sign is insensitive (77%) for the diagnosis
of PE, but, in those with this sign, it is useful to
distinguish patients with acute PE from those with
pulmonary hypertension, who tend to have global RV
dysfunction .15
c. Compression ultrasound to diagnose DVT (to support
diagnosis of PE):
i. Prospective studies have demonstrated that
lack of compressibility of a vein with the
ultrasound probe is highly sensitive (>95%) and
specific (>95%) for proximal vein thrombosis .16
12
Kucher N, Rossi E, De Rosa M, Goldhaber SZ. Prognostic role of echocardiography among patients
with acute pulmonary embolism and a systolic arterial pressure of 90 mm Hg or higher. Archives of
internal medicine. 2005;165(15):1777-81.
13
Ogren M, Bergqvist D, Eriksson H, et al. Prevalence and risk of pulmonary embolism in patients with
intracardiac thrombosis: a population-based study of 23 796 consecutive autopsies. Eur Heart J 2005;
26:1108.
14
Torbicki A, Galié N, Covezzoli A, et al. Right heart thrombi in pulmonary embolism: results from the
International Cooperative Pulmonary Embolism Registry. J Am Coll Cardiol 2003; 41:2245.
15
McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by
echocardiography in acute pulmonary embolism. Am J Cardiol 1996; 78:469.
16
Lensing AW, Prandoni P, Brandjes D, et al. Detection of deep-vein thrombosis by real-time B-mode
ultrasonography. N Engl J Med 1989; 320:342; Mattos MA, Londrey GL, Leutz DW, et al. Color-flow
duplex scanning for the surveillance and diagnosis of acute deep venous thrombosis. J Vasc Surg 1992;
15:366; Monreal M, Montserrat E, Salvador R, et al. Real-time ultrasound for diagnosis of symptomatic
11

12. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
e. Aortic Dissection
i. Typically begins with a tear in the inner layer of the aortic wall
allowing blood to track between the intima (inner layer) and media
(middle layer). Pulsatile blood flow causes propagation of the
dissection with subsequent obstruction of branch arteries and
ischemic injury to areas perfused by those vessels.
ii. In approx 13 percent of cases, no intimal tear is identified.
iii. Typically present with severe, sharp or "tearing" posterior chest or
back pain
iv. But in the ​International Registry of Acute Aortic Dissection (​IRAD) review ,17
73% of patients described the CP as typically abrupt in onset and
was more often sharp rather than “tearing”.
v. CP was significantly more common in patients with type A
dissections (79% vs 63% in type B dissections), while both back pain
(64% vs 47%) and abdominal pain (43% vs 22%) were significantly
more common with type B dissections.
vi. In the IRAD review, widened mediastinum is present in only 63%
with type A dissections, while 11% of patients had no abnormality on
chest radiography. The comparable values in patients with type B
dissections were 56% and 16% respectively.
f. Pericarditis
i. In healthy individuals, the pericardial cavity contains 15 to 50 mL of
an ultrafiltrate of plasma.
ii. Viral pericarditis may be preceded by “flu-like” respiratory or
gastrointestinal symptoms.
iii. The vast majority of patients with acute pericarditis present with CP
(>95% of cases)18
venous thrombosis and for screening of patients at risk: correlation with ascending conventional
venography. Angiology 1989; 40:527.
17
Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection
(IRAD): new insights into an old disease. JAMA 2000; 283:897.
18
Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a management
program for outpatient therapy. J Am Coll Cardiol 2004; 43:1042.
12

13. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
iv. CP may be minimal or absent in uremic pericarditis or pericarditis
associated with a rheumatologic disorder
v. CP is typically sudden in onset, sharp and pleuritic in nature,
aggravated by inspiration or coughing
vi. The distinctive feature is the relief of CP intensity when the patient
sits up and leans forward19
vii. The presence of a pericardial friction rub on physical examination is
highly specific for acute pericarditis
1. Pericardial rubs have a superficial scratchy or squeaking
quality that is best heard with the diaphragm of the
stethoscope. They may be localized or widespread, but are
usually loudest over the left sternal border20
viii. The diagnosis of acute pericarditis is usually suspected based on a
history of characteristic pleuritic chest pain, and confirmed if a
pericardial friction rub is present.
ix. Pericarditis should also be suspected in a patient with persistent
fever and pericardial effusion or new unexplained cardiomegaly.
x. ECG
xi. Typically described is the four stages:
1. Stage 1 – widespread STE and PR depression with reciprocal
PR elevation in aVR (occurs during the first two weeks)
a. PR depression (primarily in V5 - V6) is due to an atrial
current of injury
b. The ST/T ratio can be used to differentiate pericarditis
from BER21
c. If ST/T >0.25, suggestive of pericarditis
2. Stage 2 – normalization of ST changes; generalized T wave
flattening (1 to 3 weeks)
19
Spodick DH. Acute pericarditis: current concepts and practice. JAMA 2003; 289:1150.
20
Spodick DH. Pericardial rub. Prospective, Multiple observer investigation of pericardial friction in 100
patients. Am J Cardiol 1975; 35:357.
21
Ginzton LE, Laks MM. The differential diagnosis of acute pericarditis from the normal variant: new
electrocardiographic criteria. Circulation 1982; 65:1004.
13

14. PIAEM 2015 Chest Pain Evaluation In Emergency Department (version 1)
3. Stage 3– Flattened T waves become inverted (3 to several
weeks)
4. Stage 4 – ECG returns to normal (several weeks onwards)
xii. PR depression is not specific and in fact, can be a normal finding,
and only if greater than 0.8 mm is it specific for pericarditis22
xiii. Spodick's sign​, the downsloping TP segment, is said to be specific.
However, so far, there is no original study mentions about this yet .23
g. Pneumothorax
i. Can occur following trauma, pulmonary procedures or
spontaneously.
ii. If occurs spontaneously, common in patients with underlying lung
disease (secondary pneumothorax) and without (primary
pneumothorax).
iii. Patients with primary spontaneous pneumothorax tend to be
younger males who are tall and thin.
iv. Secondary spontaneous pneumothorax occurs with greatest
frequency in patients with chronic obstructive pulmonary disease,
cystic fibrosis, and asthma.
v. Usually with unilateral history and physical findings
vi. ipsilateral chest pain, sharp and pleuritic; but may become dull or
achy over time
22
Charles MA, Bensinger TA, Glasser SP. Atrial injury current in pericarditis. Arch Intern Med
1973;131(5):657-62.
23
Smith, S. Diffuse ST Elevation and Chest Pain, What is it? In: Dr. Smith’s ECG Blog. Available at URL:
http://hqmeded-ecg.blogspot.my/2015/07/diffuse-st-elevation-and-chest-pain.html​Accessed 18
September 2015
14