Chest Pain

Hosam Hasan El-Araby,

MD, PhD, FACC, FESC
Professor of Cardiovascular Medicine
Assiut University
 Basic concepts in chest pain analysis
• Chest pain is one of the most common presenting complaints.

• It has a diversity of causes that range from benign myoskeletal pain to life threatening
illnesses like myocardial infarction and aortic dissection.

• In evaluating chest pain:

o the focus should be on excluding serious causes.

o History is often more useful than clinical examination in diagnosing the cause of chest pain.

o Assessment of the settings at which chest pain occurred is very important (age, concominant
risk factor profile, precipitating circumstances)
 Differential Diagnosis of Chest Pain

Cardiac neurosis
 When to suspect IHD?
Chest pain or severe epigastric pain, non-traumatic in origin, with components typical of myocardial ischemia :
•Location: Typically retrosternal (central pain), Atypically in radiation sites
• Radiation: Any combination of the following sites: One or both sides of the chest, shoulders, arms especially to the left, more on the
ulnar side and may be down to the wrist. May be also to the epigastrium, neck, lower jaw and to the back especially the inter-scapular
region.
•Character:
• Pressure, compression, heaviness, oppressive, crushing chest pain
• Tightness, girdle like
• Cramping, burning, boring, aching sensation
• Unexplained indigestion, belching, chocking, viselike, chocking, epigastric pain
• Atypical: stabbing, knife like ( when paint can pinpoint to the painful site and/or change with movement are less likely ischemic.
•Precipitated by any physical (exertion, emotional stress, heavy meals, cold weather, sexual activity) and/or emotional stress
• Relieved by rest and/or sublingual nitrates (esophageal spasm also is improve by nitrates. Esophageal reflux may worsen with nitrates).
•Duration: usually 3-5 min and in severe cases 10-15 min. If >20-30 min suspect MI
•Associated symptoms: dyspnea, nausea/vomiting, diaphoresis (increase suspicion esp. in inferoposterior wall ischemis and
may be associated with bradycardia, hypotension, dizziness and fainting due to vagal stimulation)
Walk through angina (2nd wind angina): Pt has angina on walking or exertion that is relieved by rest and doesn't reappear on
resuming walking or exercise
Angina equivalent: Dyspnea rather than pain in women, DM, elderly
Clinical Presentation (cont.)

Levine sign
 Canadian Cardiovascular Society Classification

Class I: Angina on extraordinary work.

Ordinary physical activity does not cause angina, such as walking, climbing stairs (no
limitation of ordinary physical activity).
Class II: Angina at ordinary physical activity
Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill,
walking or stair climbing after meals, or in cold, or in wind, or under emotional stress, or
only during the few hours after awakening. Walking more than two blocks on the level
and climbing more than one flight of ordinary stairs at a normal pace and in normal
conditions
Class III: Angina at less than ordinary physical activity
Marked limitation of ordinary physical activity. Walking one or two blocks on the level
and climbing one flight of stairs in normal conditions and at normal pace
Class IV: Angina at rest or minimal activity
Inability to carry on any physical activity without discomfort—anginal symptoms at rest.
 Physical Examination
One of the most important parts in a chest pain examination is the “initial
impression.”
• Diaphoresis, tachypnea, and anxious expression should alert you to a potentially
life-threatening process.
• Tachycardia and tachypnea are both nonspecific but occur in almost all cases of
pulmonary embolism.
• Check BP in both arms: a difference >20 mm Hg systolic suggests aortic dissection
(present in >70% of cases).
• Hypotension may suggest massive pulmonary embolism or cardiac shock.
• Fever may suggest pneumonia or mediastinitis (esophageal rupture) as the cause
of chest pain.
• Evidence of atherosclerosis (corneal lipid rings, narrowed retinal arteries, and
pigment and hair changes in the legs) is commonly seen in patients with coronary
syndromes.
Inspection & Palpation: of chest wall for

• Tender areas. If the tender area corresponds to the location of the

patient’s pain and palpation exactly reproduces the pain, consider
musculoskeletal chest pain as the cause of chest pain.

• Respiratory motion, respiratory retractions, or accessory muscle use.

Cardiac Auscultation:
• Wide physiologic splitting of the second heart sound (splitting wider with inspiration)
can be found in right bundle branch block or in right ventricular infarction.

• New paradoxical splitting is most often due to left bundle branch block (LBBB), or
anterior or lateral infarction.

• A new fourth heart sound can occur with angina or infarction.

• An S3 is more likely due to underlying heart failure.

• A new murmur may be significant: aortic regurgitation occurs in over half of patients
with aortic dissection, while mitral regurgitation can occur in patients with angina or
infarction and is due to papillary muscle dysfunction.
Lung Auscultation:

• The lungs should be auscultated for crackles and asymmetrical breath

sounds.

• Asymmetry of breath sounds may be found in patients with

spontaneous pneumothorax.

• Absent lung sounds also may occur in pneumothorax and pleural

effusions.
The extremities should be examined for

Pulses, edema, and signs of atherosclerotic vessel disease.

• Absence of pedal pulses may occur in aortic dissection.

• Calf swelling or edema raises the odds of pulmonary embolism as the

cause of chest pain.
Aortic dissection:

• The pain is sharp/tearing/very severe; typically radiates to the back,

and a loss of pulses or aortic insufficiency often develops.

• On chest x-ray, mediastinum is widened

• MI may occur if dissection extends into coronary artery

• Diagnosis confirmed by MRI, CT scan, or transesophageal

echocardiogram
Pulmonary embolism:

• Dyspnea, tachycardia, and hypoxemia are prominent;

• pain is usually pleuritic, especially when pulmonary infarction

develops.

• ECG is usually nonspecific but may show S wave in lead I, Q wave in

lead III, or inverted T wave in lead III (S1Q3T3)

• Diagnosis confirmed by CT angiogram

Chest disorders:
• Pneumothorax:
o Onset abrupt with sharp pleuritic chest pain and dyspnea;
o breath sounds absent;
o chest x-ray confirms.
• Pleuritis:
o Pain is sharp and increases on inspiration;
o friction rub or dullness may be present;
o other respiratory symptoms and underlying pulmonary infection usually
present.
Pericarditis:

• May be preceded by viral illness;

• Pain is sharp, positional, pleuritic, and relieved by leaning forward.

• Pericardial rub often present

• Diffuse ST elevation occurs without evolution of Q waves

• CK level usually normal

• Responds to anti-inflammatory agents

Myocarditis:

• May be preceded by viral illness;

• pain is generally vague and mild if present;

• total CK and MB fraction of CK (CK-MB) are often elevated;

• conduction abnormalities and Q waves may occur.

 GI disorders:
• Esophageal reflux is often made worse with recumbency or after meals; may be associated with
regurgitation, relieved by antacids; may worsen by nitrates. Diagnosis may be confirmed by upper
endoscopy or esophageal manometry

• Episodes of esophgeal spasm may be brought on by cold liquids, relieved by nitroglycerin, and
may closely resemble angina or infarction. Diagnosis may be confirmed by upper endoscopy or
esophageal manometry

• Peptic ulcer disease, pancreatitis, and cholecystitis may occasionally mimic infarction;
o abdominal tenderness is present, with radiation to back

o elevated amylase in pancreatitis;

o upper endoscopy diagnosis peptic ulcer and sonography can confirm cholecystitis.
Musculoskeletal disorders:

• Most common cause of chest pain.

• Includes costochondritis, cervical osteoarthritis, radiculitis;

• pain is atypical, stabbing, localized, may be pleuritic; reproduced by

motion or palpation;

• ECG changes absent.

• Responds to antiinflammatory analgestics

:ECG -1
- The most important test to evaluate the cause and must be done for all patients with chest pain.
It should be done immediately after initial stabilization and taking of vital signs.
- In patients with acute coronary syndromes, the ECG is the sole test required to select patients
for emergency reperfusion.
- Interpretation:
o 50% with acute MI will have diagnostic findings (ST elevation, new LBBB, or Q waves)
o 35% will have findings consistent with ischemia (ST depression and/or T wave inversion)
o acute chest pain with normal ECG → the chance of acute MI is much less than 10% (in some
studies 1–2.6%).
o An abnormal ECG can be seen in many non-cardiac conditions
Make every effort to obtain a previous ECG for comparison. Any ECG finding is assumed to be new unless
proven otherwise by an old ECG (if one is available).
DD of ischemic ECG changes
1. Non-specific ST-T changes (normal individuals esp females, MVP).
2. Digitalis effect.
3. Hypokalemia.
4. Evolving phase of pericarditis
5. Subarachnoid hemorrhage.
6. Ventricular strain pattern with ventricular hypertrophy.
7. Associated with BBB.
8. Myocarditis
9. WPW.
10. Post-tachycardia T wave inversion
2- Chest x-ray: should be obtained on patients with chest pain.

• May show pneumothorax, pneumomediastinum (i.e., from esophageal rupture), pleural

effusion, or infiltrates

• Aortic dissection can cause widening of the mediastinum

• Subtle findings such as loss of lung volume or unilateral decrease in vascular markings

may suggest PE
3- Cardiac Enzymes:
play a vital role in the evaluation of acute chest pain and the diagnosis of
acute MI
A. CK-MB isoenzyme (typically measured upon ED admission and
repeated 6–12 hours later)
 Cardiac-specific; useful for early diagnosis of acute myocardial infarction

 Typically detectable in serum 4–6 hours post-onset of ischemia, peaks in 12–24

hours and normalizes in 2–3 days
 Peak CK-MB level can be useful for detecting early reinfarction since it
normalizes 2-3 days post-initial MI (does not predict infarct size)
 CK-MB subforms/isoforms (not routine): CK-MB1 is found in plasma, while CK-
MB2 is found in myocardial tissue
B. Cardiac troponins (admission and repeated 6–12 hours later )
• Troponins (T-I-C) are found in striated and cardiac muscle; because the cardiac and skeletal
muscle isoforms of troponin T and I differ, they are known as the “cardiac troponins”
• Troponins T and I (preferred in most settings) have similar preferred markers) (typically
measured upon ED admission and repeated 6–12 hours later )
• Troponins (T-I-C) are found in striated and cardiac muscle; because the cardiac and skeletal
muscle isoforms of troponin T and I differ, they are known as the “cardiac troponins”
• Troponins T and I (preferred in most settings) have similar sensitivity for the detection of
myocardial injury, but T (unlike I) may be elevated with renal disease, polymyositis, and
dermatomyositis
• Elevated T or I is helpful for identifying those at increased risk of death or of developing
acute myocardial infarction. "Increased risk" relates to the high serum troponin level.
• Troponins also can help identify those at low risk who may be sent home with close follow-
up; those with a normal (or nearly normal) ECG and a normal troponin I test 6 hours post-
admission have a very low risk of major cardiac events during the next 30 days
o Normal CK-MB and elevated troponin = minor myocardial damage, or microinfarction
o Elevated CK-MB and elevated troponin = acute myocardial infarction
• — May remain elevated up to 2 weeks after symptom onset, which makes them useful as
late markers of recent acute MI
C. Myoglobin:
• begins to rise as early as 1–4 hours after the onset of pain.
• Normal myoglobin at 4 hours has a very high negative predictive
value.
• Especially if a noncardiac diagnosis is suspected, arterial blood gases,
BNP, and CT angiogram may be helpful for evaluating acute chest
pain.

Some markers are no longer used in cardiac disease testing, due to low
specificity.
Serum markers such as aspartate transaminase, lactate dehydrogenase, and
lactate dehydrogenase subforms Total creatine kinase (CK), found in striated
muscle and tissues of the brain, kidney, lung, and GI tract
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