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Timing of Release of Various Biomarkers After Acute Myocardial Infarction. The biomarkers are plotted showing the multiples of the cutoff for acute myocardial infarction (AMI) over time. The dashed horizontal line shows the upper limit of normal (ULN; defined as the 99th percentile from a normal reference population without myocardial necrosis; the coefficient of variation of the assay should be 10% or less) The earliest rising biomarkers are myoglobin and CK isoforms (leftmost curve). CKMB (dashed curve) rises to a peak of 2 to 5 times the ULN and typically returns to the normal range within 2 to 3 d after AMI. The cardiac-specific troponins show small elevations above the ULN in small infarctions (e.g., as is often the case with NSTEMI) but rise to 20 to 50 times the ULN in the setting of large infarctions (e.g., as is typically the case in STEMI). The troponin levels may stay elevated above the ULN for 7 d or more after AMI. Modified from Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3rd ed. Rochester, MN: Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007: 773–80.70 Used with permission of Mayo Foundation for Medical Education and Research. CK = creatine kinase; CKMB = MB fraction of creatine kinase; CV = coefficient of variation; MI = myocardial infarction; NSTEMI = non–ST-elevation myocardial infarction; UA/NSTEMI = unstable angina/non–ST-elevation myocardial infarction.
Chest pain cardiac or not Dr Yasser Diab
By Yasser Diab
Farwanyia hospital Emergency department
Emergency department clinicians have a difficult task, identifying which patients
to admit and which patients to discharge home.
Chest pain is one of the most common causes for referral to emergency
departments (ED), accounting for several million visits annually. (S.Goodacre et al
Cardiac disease accounts for only 8-18% of all cases of chest pain and the
majority of chest pain seen in primary care is due to more benign conditions -
e.g. gastrooesophageal reflux disease (GORD), muscle sprains, panic disorder or
shingles. (Ruigomez et al 2006)
GORD is the most common cause of non-cardiac chest pain.(Flooket al 2007)
The evaluation of patients with acute chest pain in emergency rooms is time
consuming and expensive, and it often results in uncertain diagnosis (Hamm et al
Aetiologies of patients over 35 years of age, admitted to hospital from the
emergency department with a chief complaint of non-traumatic chest pain: Kohn
MA et al 2005
acute myocardial infarction (10.7%)
angina/coronary artery disease (22.5%)
atypical chest pain (29.4%)
aortic dissection (0.3%)
other cardiac causes, primarily CHF and atrial fibrillation, (13.8%)
pulmonary embolus (0.4%)
non-PE pulmonary causes, primarily bacterial pneumonia, (11.2%) but also spontaneous pneumothoraces (0.6%)
abdominal causes (1.6%)
Percentage of patients presenting to the emergency
department with acute chest pain (Nawar et al 2007)
In one insurance industry—based study, the physician group most likely to be
sued for missed myocardial infarction (MI) was Family practitioners (32%),
followed by General internists (22%) and ED physicians (15%). (Rockville 1996)
Meanwhile, an increase in overcrowding in emergency departments was
associated with a substantial increase in the system response interval and the
ambulance transport interval for patients with chest pain. (Michael et al 2003)
In the US, an estimated 5 million patients per year present to the Emergency Department
with chest pain, but accurate diagnosis remains a challenge (Rosamond et al 2008).
More than 50% of patients presenting to emergency facilities with unexplained chest pain
will have coronary disease ruled out.
About 1.5 million patients/ year are admitted for workup of acute coronary syndrome
Approximately 8 billion dollars/year are spent to evaluate complaints related to chest
Chest pain means pain at the anterior thorax, between xiphoid and
suprasternal notch and between the right and left midaxillary lines.
It is classified into
1. Visceral chest pain: Originates from deep thoracic structures (heart, blood
vessels, oesophagus) and is often (but not always) described as dull, heavy or
aching in nature. It is transmitted via the autonomic system (so usually
associated with anorexia,sweating, nausea, vomiting, palpitations, dizziness,
and syncope) but may be referred via an adjacent somatic nerve - e.g. referred
cardiac pain felt in the jaw or left arm.
2. Somatic chest pain: arises in the chest wall, pericardium and parietal pleura
and is characteristically sharp in nature and more easily localised (usually
Differential diagnosis of chest pain
Potentially life-threatening causes Common non-life-threatening causes
1. Acute coronary syndromes
• Acute myocardial infarction
ST segment elevation MI
Non-ST segment elevation MI
• Unstable angina
2. Pulmonary embolism
3. Aortic dissection
4. Myocarditis (most common cause of sudden
death in theyoung)
5. Tension pneumothorax
6. Acute chest syndrome (in sickle cell disease)
8. Boerhaave’s syndrome (perforated esophagus)
• Biliary colic
• Gastroesophageal reflux
• Peptic ulcer disease
3. Chest wall syndromes
• Musculoskeletal pain
• Thoracic radiculopathy
• Texidor’s twinge (precordial catch syndrome)
Step-by-step diagnostic approach
& exclusion of
• A rapid and accurate history is the first step in the ED diagnosis of chest pain and is the key to right diagnosis.
• The pain should be analyzed into its usual characteristics: site and radiation, quality, intensity,
duration, onset and offset, precipitating and relieving factors, and associated symptoms.
• The character of chest pain should be determined, as this can help differentiate between cardiac,
respiratory, musculoskeletal, and other causes.
• Association with serious medical problems such as diabetes, Marfan syndrome, thyroid illness,
anemia and SLE should be kept in mind.
• The ability to take a detailed history will obviously be limited with severe acute pain.
• Associated symptoms may include:
Syncope: Consider myocardial infarction, pulmonary embolus and dissecting aneurysm.
Pain on inspiration: Consider pleurisy, pericarditis, pneumothorax and musculoskeletal (chest wall pain).
Thoracic back pain: Consider spinal dysfunction, myocardial infarction, angina, aortic dissection,
pericarditis and gastrointestinal disorders such as a peptic ulcer, cholecystitis and oesophageal spasm.
• Patient age is helpful in evaluating chest pain. Chest pain in children and young adults (< 30 yr) is less likely
to result from myocardial ischemia, although MI can occur in people in their 20s. Musculoskeletal and
pulmonary disorders are more common causes in these age groups.
Duration of pain : can provide clues to the severity of the disorder.
Long-standing pain (ie, for weeks or months) is not a manifestation of a disorder
that is immediately life threatening. Such pain is often musculoskeletal in origin.
Similarly, brief (< 5 sec), sharp, intermittent pains rarely result from serious
Serious disorders typically manifest pain lasting minutes to hours, although episodes may
be recurrent (eg, unstable angina may cause several bouts of pain over 1 or more days).
Exacerbation and relief like exercise and rest, emotional stress, movement and
respiration, or specific posture can point to the cause.
Nitroglycerin may relieve pain of both myocardial ischemia and noncardiac smooth
muscle spasm (eg, esophageal or biliary disorders); its efficacy or lack thereof should not
be used for diagnosis.
Associated findings may also suggest a cause, the presence or absence of specific
risk factors can point to etiology of the pain.
Fever is nonspecific but, if accompanied by cough, suggests a pulmonary cause.Patients
with Raynaud syndrome or migraine headaches sometimes have coronary spasm.
Meets three of the following characteristics
1.Substernal chest discomfort of
CHARACTERISTIC quality and duration.
2.Provoked by exertion or emotional stress.
3.Relieved by rest and/or GTN spray.
Meets two of these characteristics
Meets one or none of these
• The history is often influenced by the patient’s own reluctance to seek care for chest pain. In fact, the
average patient waits 2 hours before seeking care for chest pain. (Welsh et al 2003).
• According to the Rapid Early Action for Coronary Treatment (REACT) study, patients with chest pain do
not seek timely care for the following reasons:
• A lack of knowledge about symptoms, especially atypical or minor symptoms.
• A wait-and-see attitude that assumes the pain is self-limiting and will go away.
• A false assessment of personal risk factors.
• A lack of knowledge about the importance of rapid and timely interventions.
• The fear of causing a false alarm. (Finnegan et al 2000).
• Description of chest pain alone cannot be used to rule out a cardiac event,
however. In a landmark study, Lee et al evaluated the symptoms and ECG results of 596 patients
presenting with chest pain to the ED and found that patients with characteristics of chest pain usually
thought to indicate a noncardiac cause may indeed be suffering from cardiac ischemia. For instance,
o approximately 7% of patients with an MI or UA had pleuritic chest pain,
o up to 20% of patients with an MI or UA had pain reproduced by chest wall palpation
o 13% had positional chest pain.
• Additionally, they determined that no single clinical factor could be used to
eliminate cardiac ischemia from the differential diagnosis. (Lee et al 1985).
Cardiac pain Non-cardiac causes of chest pain
Often heavy, pressing and tight. Symptoms that may
indicate ACS include: (NICE Guidelines 2010)
• Pain in the chest and/or other areas (eg, the arms, back
or jaw) lasting longer than 15 minutes.
• Chest pain with nausea and vomiting, marked sweating
and/or breathlessness, or haemodynamic instability.
• New-onset chest pain, or abrupt deterioration in stable
angina, with recurrent pain occurring frequently with little
or no exertion and often lasting longer than 15 minutes.
However, clinical features are not completely reliable in the
diagnosis of acute, undifferentiated chest pain:
The site and nature of pain, the presence of nausea and
vomiting and diaphoresis were not found to be predictive of
ACS in one study.(Goodacre et al 2002)
• ACS is often atypical (without chest pain). There is
some evidence to suggest that this occurs more
frequently in women, particularly premenopausal
women (Methot et al 2004)
• ACS pain can be intermittent and appear to 'settle',
providing false reassurance.
Response to nitrates or antacids does not prove the
diagnosis as angina and GORD may appear to be relieved by
Consider it when recent trauma, past medical history, and
Pleuritic pain (pain is aggravated during inspiration and
when coughing) may indicate a respiratory or
musculoskeletal cause of pain.
Musculoskeletal pain is usually associated with tenderness
of the chest wall.
Gastrointestinal chest pain may be very difficult to
distinguish from cardiac chest pain, especially in patients with
Screen for Panic disorder:
A positive screen ('yes' to either question) is highly sensitive for
panic disorder but should not preclude cardiac testing in patients
with risk factors: (Cayley et al 2012)
• 'In the past six months, did you ever have a spell or
an attack when you suddenly felt anxious or
frightened or very uneasy?'
• 'In the past six months, did you ever have a spell or
an attack when for no apparent reason your heart
suddenly began to race, you felt faint or couldn't
catch your breath?'
1) Where exactly do you get the pain?
2) Does the pain travel anywhere?
3) Can you give me a careful description of the pain?
4) How long did the pain last and could you do anything to relieve it?
5) Is the pain brought on by exertion and relieved by rest?
6) Do cold conditions bring it on?
7) Do you have any other symptoms, such as breathlessness, faintness, sweating or back pain?
8) Is the pain made worse by breathing or coughing, or by movement or pressing on that area?
9) Is there any blood in any sputum you bring up?
10) Is your pain associated with what you eat and drink? Or with a bitter taste in your mouth?
11) Do you get the pain on stooping over and after lying in bed at night?
12) Do antacids relieve your pain?
13) Have you noticed a rash where you get the pain?
14) Have you had a blow to your chest or an injury to your back?
Assessment using OLD CARTS framework: Seidel et al 2003
Discription Location Radiation Associations
squeezing, or a
anterior chest or
R or L shoulder,
R or L arm/hand,
Whole chest (massive)
or Focal chest
none Dyspnea, unstable
vital signs, feeling
of impending doom if massive
or just Tachycardia,
Tachypnea if segmental
Aortic dissection Ripping, tearing Midline,
area of back
Pneumothorax Sudden, sharp,
One side of
Shoulder, back Dyspnea
Substernal none Fever, pericardial
Substernal back Dyspnea,
diaphoresis, signs of sepsis
The examination should focus on the following areas:
1. General appearance: evidence of atherosclerosis (senile arcus, thickened vessels), pale and sweating (myocardial
infarction, dissecting aneurysm or pulmonary embolus), hemiparesis(? aortic dissection)
2. Pulses: both radial and femoral, check for nature of pulse and absence of femoral pulses
3. Blood pressure: hypotension or shock in MI, pneumothorax ,PE or dissection, hypertension in Aortic dissection
4. Temperature: high in pneumonia , low in shock.
Of chest wall, lower cervical spine and thoracic spine, look for evidence of localized tenderness, pathological fracture,
spinal dysfunction, herpes zoster
Palpation of legs: check for evidence of deep venous thrombosis.
6. Examination of chest: check for evidence of pneumothorax.
Reduced breath sounds, hyper-resonant percussion note and vocal fremitus → pneumothorax.
Friction rub → pericarditis or pleurisy.
Basal crackles → cardiac failure.
Apical systole murmur → mitral valve prolapse.
Aortic diastolic murmur → proximal dissection (aortic regurgitation).
7. Upper abdominal palpation: check for tenderness suggestive of gall bladder disease or peptic ulceration.
In Myocardial infarction, the examination may be normal but the patient, apart from being cold, clammy or shocked, may have
muffled heart sounds, a gallop rhythm, a systolic murmur. With a Aortic dissection the patient may also appear cold, clammy
and shocked, but may show absent femoral pulses, hemiparesis and a diastolic murmur of aortic regurgitation.
Certain findings raise suspicion of a more serious etiology of chest pain:
1. Abnormal vital signs (tachycardia, bradycardia, tachypnea, hypotension)
2. Signs of hypoperfusion (e.g., confusion, ashen color, diaphoresis)
3. Shortness of breath
4. Hypoxemia on pulse oximetry
5. Asymmetric breath sounds or pulses
6. New heart murmurs
7. Pulsus paradoxus > 10 mm Hg
• The initial ECG is the easiest, simplest, most important tool for early diagnosis and risk stratification.
• Current recommendations indicate that it should be performed within 10 minutes of ED presentation
for all patients with chest discomfort or other symptoms suggestive of ACS (ACC/AHA 2007), and may
best be considered one of the “vital signs” for patients with chest pain. (Anderson et al 2007)
• This may be diagnostic for ischemia and myocardial infarction, although it is important to bear in mind
that it may be normal with both, including the early minutes to hours of an acute infarction.
• The presence of ST-segment elevation or new LBBB should prompt consideration for immediate
reperfusion therapy. ST-segment depression is associated with a marked increase in risk of MI and
• As little as 0.5 mm of ST-segment depression predicts increased risk; the greater the extent of
depression, the higher the likelihood of MI and death. (Kaul et al 2003)
• T-wave inversion and Q waves are markers of ischemia but less predictive than ST-segment depression
(Savonitto et al 1999).
• It can be helpful to differentiate between myocardial infarction, pulmonary embolism and pericarditis.
• The ECG in pulmonary embolism may show right axis deviation. Pericarditis is characterised by low
voltages and saddle-shaped ST segment elevation.
Typical ECG pattern for
specific possible causes
of acute chest pain:
(a) Acute pulmonary embolism
(B) Acute pericarditis
(C) Acute inferolateral myocardial
Pitfalls To Avoid
1. “But the ECG was normal.” While a normal or near normal ECG reduces
the likelihood of MI and the likelihood of a complication should an MI develop,
it does not exclude this diagnosis. (Howell et al 1994), Rouan et al. found that
3% of MI patients had completely normal presenting ECG and another 7% of MI
patients had non-specific ECG.
2. “Normal cardiac enzymes exclude an Ml diagnosis” : Cardiac
enzymes have a characteristic time-related release, so all patients with
suspected ACS should undergo serial cardiac biomarker sampling.
3. I know the troponin was elevated, but the patient has renal
failure.” Recent data show that the troponin T level retains its prognostic
value in all degrees of renal dysfunction.
4. “I know that he had persistent tearing back pain, but the chest x-ray
was negative.” This is a difficult diagnosis to make and may be fatal
when treated inappropriately.
5. “He had ECG changes and severe chest pain; why did I need a chest
Because he had an aortic dissection. Nearly half of all patients with dissection have some
ECG changes. Almost 10% have dissection involving the coronary arteries, in which the
ECG may show an AMI.
6. “I only did one set of enzymes because his pain was atypical.”
If your suspicion is high enough to get enzymes in the first place, it should be high enough
to do them right—serial levels over a six- or eight-hour period (or delta levels over a
shorter period). One negative set drawn more than six hours after pain onset
accompanied by a normal ECG may be an exception to this rule.
7. “The pain wasn’t ripping or tearing; it didn’t even radiate to the back.”
Aortic Dissection may not fit the “classic” description. Perform a detailed physical
examination looking for a pulse deficit or neurologic abnormalities, CXR for mediastinal
changes, and order CT angiography when the diagnosis remains in doubt.
8. “But the left bundle branch block was old—I even got a prior ECG to prove
It is very difficult (almost impossible) to diagnose AMI in the presence of a left bundle—
and individuals with a left bundle branch block have underlying cardiac disease in the first
place. Use cardiac markers and be liberal in admission or observation in such patients
with chest pain.
9. We must be careful not to place words in the patient's mouth:
Rephrasing of the patient's description may help clarify misunderstandings, try not to ask
10. “Young patients cannot have an Ml”:
Studies found that patients with missed MIs were generally younger than those correctly
diagnosed as having an MI at the same hospital. (Rusnak et al 1989).
11. Indigestion symptoms exclude an Ml diagnosis:
indigestion-like symptoms occurred in 10% of MI patients (Lee et al 1985).While the
administration of antacids with or without topical anaesthetic agents may soothe
oesophageal or gastric irritation, pain relief does not prove the absence of cardiac
12.Sharp pain or chest wall tenderness excludes the diagnosis of Ml:
8% of MI patients complained of a 'sharp or stabbing' pain
19% pleuritic' discomfort,
8% chest wall tenderness,
11% of MI patients had pain that was positional in nature (Tierney et al 1986).
13.Do not assess symptoms of an ACS differently in ethnic groups.(NICE
2010) There are no major differences in symptoms of an ACS among different
14.Do not routinely administer oxygen, (NICE 2010) only offer supplemental
• oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory
failure, aiming for SpO2 of 94–98%.
• chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to
achieve a target SpO2 of 88–92% until blood gas analysis is available.
15.Do not use people's response to (GTN) to make a diagnosis. (NICE
16.Referred pain from spinal disorders, especially of the lower cervical spine—
one of the great pitfalls in medical practice
17.Over-Labelling chest pain as psychological in an anxious patient presenting
with acute chest pain.
18.Being unaware that up to 20% of myocardial infarctions are silent,
especially in elderly patients, and that pulmonary embolism is often painless.
The diagnosis of NSTE-ACS may be easy to confirm but is often hard to be
excluded (Hollander et al 2003)
Of the patients presenting to the emergency department for chest pain, 55 to 85
percent do not have a cardiac cause for their symptoms. (Hollander et al 2007)
Of those admitted for chest pain, more than 60 percent do not have acute
coronary syndromes. (Hoffmann et al 2006) and unnecessary admissions for chest pain
in the U.S. alone cost billions of dollars annually. (Hoffmann et al 2006)
But ACS still the most important and the most mistaken
cause of chest pain
Clinical presentation: (Canto et al 2002,ESC 2011)
• Angina can be felt anywhere between the ear and the umbilicus.
• The typical clinical presentation of angina is retrosternal pressure or heaviness
radiating to the left arm, neck, or jaw, which may be intermittent (usually lasting for several
minutes) or persistent.
• These complaints may be accompanied by other symptoms such as diaphoresis, nausea,
abdominal pain, dyspnoea, and syncope.
• However, atypical presentations are not uncommon. These include epigastric pain,
indigestion, stabbing chest pain, chest pain with some pleuritic features, or increasing
• Atypical complaints are more often observed in older (>75 years) patients, in women, and in
patients with diabetes, chronic renal failure, or dementia.
• Anginal equivalents:
Anginal equivalents are exertional pain in the jaw, neck, ear, arm, shoulder, back, or epigastric
area; exertional dyspnea; nausea and vomiting; diaphoresis; and fatigue.
Features that Suggest ACS: (Guidelines And Protocols Advisory Committee, ACC/AHA 2011)
1) Cardiac chest “pain” is usually described as an unpleasant sensation in the chest:
“pressing”, “squeezing”, “constricting”, “bursting”, “burning”, “a band around the chest”, “a
weight in the centre of the chest” or a “vise tightening around the chest”.
Clenching the fist in front of the sternum (Levine’s sign) is a strong indication of an ischemic
origin of the pain.
2) Acute coronary syndrome may present with acute shortness of breath with or without
evidence of chest pain
3) May radiate or be completely isolated to:
the neck, jaw, teeth, epigastrium, shoulder or arms (most commonly the left). It is frequently
associated with shortness of breath, diaphoresis, weakness, nausea and vomiting, and
occasionally associated with gas, belching or “indigestion”.
4) The discomfort may be partially or fully relieved by nitroglycerine
but may not respond to nitroglycerine at all. There may or may not be a prodrome of the
discomfort precipitated by exercise, cold weather or emotional stress relieved by rest or nitro-glycerine.
5) Chest discomfort that lasts for more than 10 minutes or occurs at rest suggests unstable
angina; but chest discomfort that lasts for more than 20 minutes suggests acute myocardial
Features of Chest Pain that do not Suggest ACS:
1) Pleuritic pain (i.e., sharp or knifelike pain brought on by respiratory movements
2) Pain or discomfort that is localised to the skin or chest wall and can be
reproduced by localised pressure. Pain that is localised to a small area of the
chest (< 3 cm in diameter), or pain that radiates to the right lower chest.
3) Pain that is sharp, stabbing or knifelike and aggravated by deep breathing or
rotating the chest.
4) Pain that lasts for less than 15 seconds is rarely ischemic in origin.
5) Pain that radiates into the lower extremities.
6) Pain that is worse in the supine position and relieved by sitting up or leaning
forward is suggestive of pericarditis.
7) Dissection of the aorta often causes pain in the back in addition to the front of
Historical Factors that Increase the Likelihood of Acute
Historical and Exam Factors that Decrease the
Likelihood of Acute Myocardial Infarction
Radiation to right arm or shoulder.
Radiation to both arms or shoulders.
Associated with exertion.
Radiation to left arm.
Associated with diaphoresis.
Associated with nausea or vomiting.
Worse than previous angina or similar to
previous myocardial infarction.
Described as pressure.
Described as pleuritic.
Described as positional.
Described as sharp.
Reproducible with palpation.
Not associated with Exertion.
Risk factors that increases the probability of
Identify potential precipitating causes of
Age >40 years old.
A positive family history.
Known atherosclerosis in non-coronary
territories, such as peripheral or carotid
Past medical history of CAD: the most
predictive risk factor for cardiac ischemia
such as uncontrolled hypertension,
thyrotoxicosis, anemia, or gastrointestinal
• Aim (Anderson et al 2011, ACC/AHA 2011)
1. To exclude non-cardiac causes of chest pain and non-ischaemic cardiac disorders (e.g.
Pulmonary embolism, aortic dissection, pericarditis, valvular heart disease) or potentially
extracardiac causes such as acute pulmonary diseases (e.g. Pneumothorax, pneumonia,
or pleural effusion).
2. Comorbid conditions that could impact therapeutic risk and decision making, such as
pulmonary disease and malignancies.
3. Assess the hemodynamic impact of the ischemic event.
• Patients with evidence of LV dysfunction on examination (rales, S3 gallop) or with
acute mitral regurgitation have a higher likelihood of severe underlying CAD and
are at a high risk of a poor outcome.
• Examination of the peripheral vessels can also provide important prognostic
information. The presence of bruits or pulse deficits that suggest extracardiac
vascular disease identifies patients with a higher likelihood of significant CAD
should be obtained within 10 min after first medical contact (ESC 2011, ACC/AHA 2007)
Patients whose current ECG suggests ischemia can be Other
assessed with greater
diagnostic accuracy or LBBB
if a prior ECG is available for comparison
ST-segment elevation :
occurs within minutes and may last for up to 2 weeks. ST elevation of ≥2 mm in adjacent chest leads and ≥1 mm in
adjacent limb leads.
New LBBB: denotes LAD , if no old baseline ECG, Sgarbosa crieteria can be used with >90% specifity
Sgarbossa's criteria: identify acute myocardial infarction in the presence of a left bundle branch block (LBBB) or a
paced rhythm (Sgarbossa et al 1996)
≥3 points = 90% specificity of STEMI (sensitivity of 36%)
Posterior extension is suggested by:
Horizontal ST depression in V1-3
Tall, broad R waves (> 30ms) in V2-3
Dominant R wave (R/S ratio > 1) in V2
Upright T waves in V2-3
Right ventricular infarction is
ST elevation in V1
ST elevation in lead III > lead II
• Changes can be transient and/or fixed, especially if a diagnosis of NSTEMI is
• ST-segment depression of ≥0.05 mV is highly specific of myocardial ischemia
(unless isolated in V1–V3, suggesting a posterior STEMI).
• T-wave inversion is sensitive but nonspecific for acute ischemia unless very deep
• Rarely, Q waves may evolve or there may be transient or new LBBB.
Electrocardiograms Demonstrating Normalization Of Prior Negative T-Wave In Patient With NSTE-ACS:
Limitations of ECG as a diagnostic tool of ACS:
1. Relatively low diagnostic sensitivity for ACS, especially for unstable angina;
ischemic changes are apparent at the time of presentation in only 20% to
30% of patients who have an acute MI (kontos et al 2009).
2. Conversely, 5% to 10% of patients with MI have normal findings on ECG at
3. The sensitivity of ECG is affected by the anatomic location of the culprit
vessel and is less likely to be diagnostic in patients with left circumflex
lesions. (Huey et al 1988 ).
How to overcome these limitations:
1. Serial assessment (every 15-30 minutes) should be performed routinely in
patients with ongoing symptoms or ECG findings that are suggestive but not
diagnostic of ischemia. (Anserson et al 2008)
2. Addition of posterior leads and multilead ECG devices. Results have been
mixed for routine use of posterior leads however, the cost-effectiveness of
routine use is unclear. (Zalenski et al 1993)
• Current recommendations advise that all patients with suspected ACS should undergo
serial cardiac biomarker sampling. (Morrow et al 2007).
• If baseline data are negative, further sampling should be obtained 6 to 8 hours later
depending on symptom onset.
• Current recommendations indicate troponin as the preferred biomarker, and considered as
the “GOLD STANDARD” for diagnosis of AMI. (ACC/ESC)
• Troponin is a complex of three regulatory proteins (troponin c, troponin i, and troponin t)
that is integral to muscle contraction in skeletal muscle and cardiac muscle, but not smooth
• Cardiac troponins T and I are the preferred markers for myocardial injury as they have the
highest sensitivities and specificities for the diagnosis of acute myocardial infarction (nice
guidelines March 2010)
• Elevation is defined as >10% of 99th percentile or CV upper reference limit in the
appropriate clinical setting. (ACC/ESC guidelines 2011)
1. 99th percentile is the the upper limit of what can be expected in a normal.
2. CV is coefficient of variation: is the percent variation in assay results that can be
expected when the same sample is repeatedly analyzed.
TEST Advantages Disadvantages Comment
1. Powerful tool for risk stratification.
2. Greater sensitivity and specificity
3. Detection of recent MI up to 2
weeks after onset.
4. Useful for selection of therapy.
5. Detection of reperfusion.
1. Low sensitivity in very early phase
of MI (less than 6 h after symptom
onset) and requires repeat
measurement at 8 to 12 h, if negative
2. Limited ability to detect late minor
Useful as a single test to efficiently
diagnose NSTEMI (including minor
myocardial damage),with serial
Clinicians should familiarize
themselves with diagnostic
“cutoffs” used in their local
CK-MB 1. Rapid, cost-efficient, accurate
2. Ability to detect early reinfarction.
1.Loss of specificity in setting of
skeletal muscle disease or injury,
2. Low sensitivity during very early MI
(less than 6 h after symptom onset) or
later after symptom onset (more than
36 h) and for minor myocardial
damage (detectable with troponins).
Prior standard and still acceptable
diagnostic test in most clinical
Myoglobin 1. High sensitivity
2. Useful in early detection of MI
3. Detection of reperfusion
4. Most useful in ruling out MI
1. Very low specificity in setting of
skeletal muscle injury or disease
2. Rapid return to normal range limits
sensitivity for later presentations.
More convenient early marker
than CK-MB isoforms because of
greater availability of assays for
Causes Of Elevated Troponin
• Renal impairment or failure.
• Trauma to chest.
• Congestive heart failure.
• Aortic valve disease.
• Pulmonary embolism.
• Septic shock.
• In the literature, several risk scores for NSTE-ACS have been
published. The most reputed are the TIMI, PURSUIT, GRACE and
HEART risk scores.
• They are a good predictive indicators for death or MI at 1 year
and enabled the identification of high-risk subsets of patients
who will benefit most from myocardial revascularization
performed during initial hospital stay (De Araújo et al 2005).
Advantages of the HEART score as a stratification tool in ED (A.J. Six et al 2008)
The HEART score is an easy, quick and reliable predictor of outcome in chest pain
patients and can therefore be used for Triage.
Facilitates communication between doctors with figures:
1. A score of 0-3 points holds a risk of 1.6% and therefore supports a policy of early
2. A score of 4-6 points, indicates a risk of 13%, immediate discharge is not an option and
should be admitted for clinical observation, treated as an ACS awaiting final diagnosis and
subjected to noninvasive investigations, such as repeated troponin, exercise testing and
possibly advanced ischemia detection.
3. A score ≥7 points, with a risk of 50%, implies early aggressive treatment including invasive
Guidelines for the Identification of ACS Patients by ED
Registration Clerks or Triage Nurses (ACC/AHA 2011)
Chest pain can be triaged into traumatic and atraumatic etiologies.
The evaluation of atraumatic chest pain requires an algorithmic
approach that first excludes potentially life threatening conditions before
working through the various aetiologies of chest pain.
Patients with the following chief complaints require immediate assessment
by the triage nurse and should be referred for further evaluation:
o Chest pain, pressure, tightness, or heaviness; pain that radiates to neck, jaw,
shoulders, back, or 1 or both arms
o Indigestion or “heartburn” nausea and/or vomiting associated with chest discomfort
o Persistent shortness of breath.
o Weakness, dizziness, lightheadedness, loss of consciousness
Patients with the following symptoms and signs require immediate
assessment by the triage nurse for the initiation of the ACS
• Chest pain or severe epigastric pain, non-traumatic in origin, with components
typical of myocardial ischemia or MI.
• Central / substernal compression or crushing chest pain.
• Pressure, tightness, heaviness, cramping, burning, aching sensation.
• Unexplained indigestion, belching, epigastric pain.
• Radiating pain in neck, jaw, shoulders, back, or 1 or both arms.
• Associated dyspnea.
• Associated nausea and/or vomiting.
• Associated diaphoresis.
If these symptoms are present, obtain immediate ECG.
The triage nurse should take a brief, targeted, initial history
with an assessment of current or past history of:
• CABG, PCI, CAD, angina on effort, or MI.
• GTN use to relieve chest discomfort.
• Risk factors, including smoking, hyperlipidemia, hypertension, diabetes
mellitus, family history, and cocaine or methamphetamine use.
• Regular and recent medication use.
The brief history must not delay entry into the ACS protocol.
o Women may present more frequently than men with atypical chest pain
o Diabetic patients may have atypical presentations due to autonomic
o Elderly patients may have atypical symptoms such as generalized
weakness, stroke, syncope, or a change in mental status.
History (Runyon MS vol6) Examination Investigation
o Classic presentatioin:
The PIOPED study :Worsley et al 1995
Pleuritic chest pain (66%)
Symptoms may vary from sudden
collapse to gradually progressive
Suspected in patients with
unexplained by an
Syncope, Abdominal pain, Fever,
Productive cough, Hemoptysis Wheezing,
Decreasing level of consciousness, New
onset of atrial fibrillation,, Flank pain,
Delirium (in elderly patients).
o Tachypnea (respiratory rate >16/min) -
o Crepitations- 58%
o Accentuated second heart sound -
o Tachycardia (heart rate >100/min) -
o Fever (temperature >37.8°C) - 43%
o Diaphoresis - 36%
o S3 or S4 gallop - 34%
o Clinical signs and symptoms
suggesting thrombophlebitis - 32%
o Lower extremity edema - 24%
o Cardiac murmur - 23%
o Cyanosis - 19%
• Nonspecific ST-T wave abnormalities
• S1 Q3 T3 pattern
• P pulmonale
o CXR: may normal or Westermark sign.
o Angiography: The gold standard for
diagnosis of segmental and sub
• RV condition (strain, dilatation).
• Pulmonary artery pressure.
• Pericardial effusion
• May show the emboli if central.
o D-Dimer: useful in low or moderate
pretest probability patients.
(Wells score of ≤4 with a negative
qualitative D-dimer test exclude
pulmonary embolism Geersing et al 2012)
o Troponin: high in 50% (Konstantinides 2008).
Modified Wells Score for Pretest Probability of
Clinical Characteristic Score
Previous pulmonary embolism or deep vein thrombosis + 1.5
Heart rate >100 beats per minute + 1.5
Recent surgery or immobilization (within the last 30 d) + 1.5
Clinical signs of deep vein thrombosis + 3
Alternative diagnosis less likely than pulmonary embolism + 3
Hemoptysis + 1
Cancer (treated within the last 6 months) + 1
Clinical Probability of Pulmonary Embolism Score
Massive PE Submassive PE Low-risk PE
Acute PE with
(systolic blood pressure [SBP]
< 90 mm Hg for at least 15
minutes or requiring
inotropic support, not due to
a cause other than PE such as
sepsis, or left ventricular [LV]
or persistent profound
bradycardia (heart rate < 40
beats per minute with signs
or symptoms of shock).
Acute PE without systemic hypotension (SBP ≥ 90 mm
Hg) but with either RV dysfunction or myocardial
RV dysfunction means the presence of at
least 1 of the following:
• RV dilation or RV systolic dysfunction on
• RV dilation on CT
• Elevation of BNP (> 90 pg/mL)
• Elevation of N-terminal pro-BNP (> 500 pg/mL) or
• Electrocardiographic changes (new complete or
incomplete right bundle-branch block, anteroseptal ST
elevation or depression, or anteroseptal T-wave
Defined as either of the following:
• Elevation of troponin I (> 0.4 ng/mL) or
• Elevation of troponin T (> 0.1 ng/mL)
Acute PE and the
absence of the clinical
markers of adverse
prognosis that define
American Heart Association Proposed Definitions
History Findings Investigations
Character sharp or stabbing precordial
or retrosternal chest pain, pain become
dull with dyspnea and orthopnea in
Pericardial friction rub: A triphasic
(systole, diastole and atrial systole) best
Onset is sudden or gradual onset and
heard with the diaphragm of the
Radiates to the back, neck, left
stethoscope at the lower left sternal
shoulder, or arm.
border or apex when the patient is sitting
Referral of pain to the left trapezial
and leaning forward.
ridge (due to inflammation of the joining
Signs of tamponade:
diaphragmatic pleura) is a particular
Beck’s triad: hypotension,
raised JVP, and quiet heart sounds
Aggravated by inspiration or
Pulsus paradoxus >10mmhg drop during
movement. Typically, chest pain is most
severe when the patient is supine and is
relieved when the patient sits up and
Associated symptoms include
fever, dyspnea due to accentuated pain
with inspiration, and dysphagia from
irritation of the esophagus by the
ECG: diagnostic in most cases:
Sinus tachycardia: from pain or
Widespread concave ST elevation,
especially in I, V5, and V6
ST amplitude: T wave amplitude:
• A ratio of > 0.25 suggests
• A ratio of < 0.25 suggests BER
PR segment depression throughout
most of the limb leads.
Chest X ray: for tamponade.
Lab investigations: for diagnosis of
the cause i.e. CBC, kidney functions,
ESR, serologic studies, bacterial work
up and thyroid functions.
Features suggesting pericarditis in ECG:
1. Generalised ST elevation of concave manner.
2. Presence of PR depression, elevation in aVR.
3. Normal T wave amplitude.
4. ST segment / T wave ratio > 0.25
5. Absence of “fish hook” appearance in V4
6. ECG changes evolve slowly over time
Benign Early Repolarisation
•ST segment height = 1 mm
•T wave height = 6 mm
•ST / T wave ratio = 0.16
•The ST / T wave ratio < 0.25
•ST segment height = 2 mm
•T wave height = 4 mm
•ST / T wave ratio = 0.5
•The ST / T wave ratio > 0.25
History Examination Invstigations
• Recent history (≤1-2 wk) of flulike
symptoms of fevers, arthralgias, and
malaise or pharyngitis, tonsillitis, or
upper respiratory tract infection (viral
• Mild symptoms of chest pain (in
concurrent pericarditis), fever, sweats,
• Palpitations, syncope, or sudden
cardiac death due to underlying
ventricular arrhythmias or AV block
especially in giant cell myocarditis (in
young adults, myocarditis causes up to
20% of all cases of sudden death).
Signs of acute decompensation of heart failure
like tachycardia, gallop, mitral regurgitation,
edema) and, in those with concomitant
pericarditis, with pericardial friction rub.
•Sarcoid myocarditis: lymphadenopathy, also
with arrhythmias, sarcoid involvement in other
organs (up to 70%)
•Acute rheumatic fever - usually affects heart
in 50-90%; associated signs, such as erythema
marginatum, polyarthralgia, chorea, subcutaneous
nodules (jones criteria)
pruritic maculopapular rash and history of using
•Giant cell myocarditis - sustained ventricular
tachycardia in rapidly progressive heart failure.
•Peripartum cardiomyopathy - heart failure
developing in the last month of pregnancy or within
5 months following delivery.
• ECG: often nonspecific eg,
nonspecific ST- or T-wave
heart block (AV block or
arrhythmia, or injury
• Elevated ESR and CRP
• Rheumatologic screening
- To rule out systemic
• Elevated cardiac enzymes
– CK or cardiac troponins
• Serum viral antibody titers
- For viral myocarditis
1. Rate / Pressure Control: Titrate to heart rate < 60
IV beta blockade Labetalol (If contraindication, substitute diltiazem or
BP Control if high by IV vasodilator to titrate to BP< 120 mmHg
2. Pain Control: I.V. opiates & titrate to pain control.
3.If hypotensive or shocked: IV fluid bolus Titrate to MAP of 70 mm
4. Urgent surgical consultation.
History Examination Investigation
Sudden acute or subacute one-sided, sharp,
lancinating, pleuritic chest pain and sudden onset
dyspnea. exacerbated by deep respiration and
coughing, alleviated by shallow breathing and
sometimes with irritative cough
Associated with Hypotension, hypoxia, chest pain,
No clinical signs or symptoms
If a bleb ruptures results in classic picture
similar to those of spontaneous pneumothorax, depending on
patient’s age, presence of underlying lung disease, and extent of
Catamenial pneumothorax: (Korom et al 2004)
Women aged 30-40 years with onset of symptoms within 48 hours
Tachypnea and Respiratory distress.
Tracheal shift to the contralateral side
with a large tension pneumothorax.
Unilateral distant or absent breath
Hyperresonance on percussion
Ipsilateral crackles or wheezes
Tachycardia: if more than 135 bpm,
tension pneumothorax is likely.
Pulsus paradoxus and Hypotension
Jugular venous distention: seen in
tension pneumothorax, may be absent
if hypotension is severe.
Cardiac apical displacement.
Pleural line (D.D. scapular
line) no lung parenchyma
beyond, usually upper lobe.
recommended for uncertain
or complex cases.
Emergency treatment: Needle Thoracostomy
Classical management of tension pneumothorax is emergent chest decompression with needle
A 14-16G intravenous cannula is inserted into the second rib space in the mid-clavicular line.
The needle is advanced until air can be aspirated into a syringe connected to the needle.
The needle is withdrawn and the cannula is left open to air.
An immediate rush of air out of the chest indicates the presence of a tension pneumothorax.
The manoeuver essentially converts a tension pneumothorax into a simple pneumothorax.
Boerhaave syndrome means spontaneous rupture usually results from transient increase in
intraesophageal pressure (coughing, straining, seizures, and childbirth have been reported as
causing perforations), common in alcoholic males.
The pain is acute, severe, unrelenting, and diffuse, in the chest, neck, and abdomen.
Pain can radiate to the back and shoulders, exacerbated by swallowing, associated with
dysphagia, dyspnea, hematemesis, and cyanosis can be present as well
Examination may be normal or ill-appearing, dyspneic, and diaphoretic patient and may reveal
evidence of pneumothorax or subcutaneous air. Fever, hemodynamic instability, septic
complication occure lately.
CXR findings includes: unilateral effusion, usually on the left. pneumothorax,
pneumomediastinum, pneumoperitoneum, and/or subcutaneous air.
Diagnosed by: Esophagram or CT scan.
Mainstays of therapy include the following:
1. Intravenous volume resuscitation.
2. Administration of broad-spectrum antibiotics.
3. Prompt surgical intervention.
Musculoskeletal “chest wall pain syndromes”
• It is important to rule out visceral causes of chest pain, including cardiac, esophageal,or
pulmonary causes, such as angina, myocardial infarction, malignancies, or pulmonary
embolism, before definitively diagnosing musculoskeletal chest pain. (Proulx & Zryd
• Pain is characterized by highly localized, sharp, positional chest pain and completely
reproducible by light to moderate palpation of a discrete area of the chest wall,
although chest wall tenderness occurs in some patients with pulmonary embolism and
myocardial ischemia as mentioned.
Pain related to bony and
cartilaginous structures of
the chest wall
-Fractures related to trauma
•Slipping rib syndrome
Pain related to
strains 2)Injuries to
Pain related to thoracic
of chest wall pain
Causes of musculoskeletal chest pain
Peptic ulcer disease
History and presentation:
“Classic" history, including epigastric burning pain; relief of pain with ingestion of milk, food,
or antacids; and night pain, also history of upper endoscopy, NSAIDS intake, or H.pylori
Pain is characterized as a postprandial, dull, boring pain in the midepigastric region.
Patients often describe being awakened from sleep by discomfort.
Duodenal ulcer pain is usually relieved after eating food, in contrast to gastric ulcer Symptoms,
which are often exacerbated by eating.
Symptomatic relief is usually provided by antacid medications.
Acute pancreatitis and biliary tract disease present with right upper quadrant or epigastric pain
and tenderness but also can cause chest pain.
Epigastric tenderness (neither sensitive nor specific for the diagnosis).
Findings indicative of complications: a rigid abdomen consistent with peritonitis in perforation;
abdominal distention or a succussion splash due to obstruction; occult or gross rectal blood or
blood in the nasogastric aspirate signaling ulcer bleeding.
Acute chest syndrome
The acute chest syndrome (ACS) is an acute pulmonary illness that occurs in patients with sickle cell disease.
ACS is currently defined as a new infiltrate on chest radiograph in conjunction with 1 other new symptom or
sign: chest pain, cough, wheezing, tachypnea, and/or fever (> 38.5°C).
1. Serial chest radiographs
2. Consider ventilation and perfusion imaging
3. Serial hematologic testing
• Complete blood count
• Reticulocyte count
4. Secretory phospholipase A2 measurement,
5. Arterial blood gas with co-oximetry
6. Blood cultures
7. Consider bronchoscopy
The patient's age, presenting symptoms, time course of symptom development and
resolution, and lack of other identifiable medical causes are often helpful in considering the
differential diagnosis of a panic attack.(Zauble et al 1998)
One screening question that has been shown to rapidly identify patients who are suffering
from panic attacks is: "Have you experienced brief periods for seconds or minutes of an
overwhelming panic or terror which was accompanied by racing heart, shortness of breath,
or dizziness? (Ballenger et al 1998)
1. Cognitive Behavioral Therapy (CBT).
selective serotonin reuptake inhibitors (SSRIs), serotonin/norepinephrine reuptake
inhibitors (SNRIs), TCAs, monoamine oxidase inhibitors (MAOIs), and
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