braunwald

1. Approach to the Patient with Chest Pain
DR RAMDHAN KR
KAMAT
PDT CARDIOLOGY
BMCH

2. Acute chest pain is one of the most common reasons for seeking
care in the emergency department (ED), accounting for
approximately 10% of all visits.
Although chest pain raises the possibility of an acute coronary
syndrome (ACS), after diagnostic evaluation only 10% to 15% of
patients with acute chest pain actually have ACS.
The diagnosis of ACS is missed in approximately 2% of patients,
which can lead to substantial consequences.

3. CAUSES OF ACUTE CHEST PAIN

5. Myocardial Ischemia or Infarction
The most common serious cause of acute chest discomfort is myocardial ischemia or
myocardial infarction (MI) , which occurs when the supply of myocardial oxygen is
inadequate for the demand.
Myocardial ischemia usually occurs in the setting of coronary atherosclerosis, but it may
also reflect dynamic component of vascular resistant.
Coronary spasm can occur in normal coronary arteries or, in patients with CAD, near
atherosclerotic plaque and in smaller coronary arteries.

6. Other, less common causes of impaired coronary blood
flow include syndromes that compromise the orifices or
lumina of the coronary arteries, such as coronary arteritis,
proximal aortitis, spontaneous coronary artery dissection,
proximal aortic dissection, coronary emboli from
infectious or noninfectious endocarditis or thrombus in
the left atrium or left ventricle, myocardial bridge, or a
congenital abnormality of the coronary arteries.

7. The classic manifestation of ischemia is angina, which is
usually described as a heavy chest pressure or squeezing,
a burning feeling, or difficulty breathing. The discomfort
often radiates to the left shoulder, neck, or arm. It
typically builds in intensity over a few minutes. The pain
may begin with exercise or psychological stress, but ACS
most frequently occurs without obvious precipitating
factors.

8. Atypical descriptions of chest pain reduce the likelihood that the symptoms represent
myocardial ischemia or injury. The American College of Cardiology (ACC) and American
Heart Association (AHA) guidelines list the following as pain descriptions uncharacteristic
of myocardial ischemia:
• Pleuritic pain (i.e., sharp or knifelike pain brought on by respiratory movements or
coughing)
• Primary or sole location of the discomfort in the middle or lower abdominal region
• Pain that may be localized by the tip of one finger, particularly over the left ventricular
apex
• Pain reproduced with movement or palpation of the chest wall or arms
• Constant pain that persists for many hours
• Very brief episodes of pain that last a few seconds or less
• Pain that radiates into the lower extremities

9. Clinicians should be mindful of “angina equivalents” such as jaw or
shoulder pain in the absence of chest pain; nausea or vomiting; and
diaphoresis. In particular, women, older persons, and individuals with
diabetes may be more likely to report atypical symptoms of myocardial
ischemia or MI
Not surprisingly, patients without chest pain had higher in-hospital
mortality.

11. Pericardial Disease
The visceral surface of the pericardium is insensitive to pain, therefore, noninfectious causes
of pericarditis (e.g., uremia) usually cause little or no pain.
In contrast, infectious pericarditis almost always involves the surrounding pleura, so patients
typically experience pleuritic pain with breathing, coughing, and changes in position.
Swallowing may induce the pain because of the proximity of the esophagus to the posterior
portion of the heart.
Because the central diaphragm receives its sensory supply from the phrenic nerve and the
phrenic nerve arises from the third to fifth cervical segments of the spinal cord, pain from
infectious pericarditis is frequently felt in the shoulders and neck.
Involvement of the diaphragm more laterally can lead to symptoms in the upper part of the
abdomen and back, and thus create confusion with pancreatitis or cholecystitis.
Pericarditis occasionally causes a steady, crushing substernal pain resembling that of AMI.

13. Vascular Disease
Acute aortic dissection usually causes a sudden onset of excruciating
ripping pain, the location of which reflects the site and progression of the
dissection. Ascending aortic dissection tends to manifest as pain in the
midline of the anterior aspect of the chest, and posterior descending
aortic dissection tends to cause pain in the back of the chest.
Aortic dissections are rare, usually occur in the presence of risk factors,
including Marfan and Ehlers-Danlos syndromes, bicuspid aortic valve,
pregnancy (for proximal dissections), and hypertension (for distal
dissections)

14. Pulmonary emboli often cause a sudden onset of dyspnea and pleuritic
chest pain, they may be asymptomatic .
Massive pulmonary emboli tend to cause severe and persistent substernal
pain, which is attributed to distention of the pulmonary artery.
Smaller emboli that lead to pulmonary infarction can cause lateral pleuritic
chest pain.
Hemodynamically significant pulmonary emboli may cause hypotension,
syncope, and signs of right-sided heart failure.
Pulmonary hypertension can result in chest pain similar to that of angina
pectoris, presumably because of right heart hypertrophy and ischemia.

16. Pulmonary Conditions
Pulmonary conditions that cause chest pain generally produce dyspnea and
pleuritic symptoms, the location of which reflects the site of pulmonary disease.
Tracheobronchitis tends to be associated with a burning midline pain, whereas
pneumonia can produce pain over the involved lung.
The pain of pneumothorax begins suddenly and is usually associated with
dyspnea. Primary pneumothorax typically occurs in tall, thin young men;
secondary pneumothorax occurs in the setting of pulmonary disease such as
chronic obstructive pulmonary disease (COPD), asthma, or cystic fibrosis. A
tension pneumothorax can be life-threatening.
Asthma exacerbations can cause chest discomfort, typically characterized as
tightness.

18. Gastrointestinal Conditions
Irritation of the esophagus by acid reflux can produce a burning discomfort that may be exacerbated by
alcohol, aspirin, and some foods. Assuming a recumbent position often worsens symptoms, and sitting
upright and acid-reducing therapies alleviate them.
Esophageal spasm can produce a squeezing chest discomfort similar to that of angina.
Mallory-Weiss tears of the esophagus can occur in patients who have had prolonged vomiting episodes.
Severe vomiting can also result in esophageal rupture (Boerhaave syndrome) with mediastinitis.
Chest pain caused by peptic ulcer disease usually occurs 60 to 90 minutes after meals and typically responds
rapidly to acid-reducing therapies. This pain generally localizes in the epigastrium but can radiate to the
chest and shoulders.
Cholecystitis produces a wide range of pain syndromes and generally causes right upper quadrant
abdominal pain, but chest and back pain caused by this disorder is not unusual. The pain is frequently
described as being aching or colicky.
Pancreatitis typically causes an intense, aching epigastric pain that may radiate to the back.

21. Musculoskeletal and Other Causes
Chest pain can arise from musculoskeletal disorders involving the chest wall (e.g.,
costochondritis), by conditions affecting the nerves of the chest wall (e.g., cervical disc
disease),
by herpes zoster, or following heavy exercise.
Chest pain due to musculoskeletal causes is often elicited by direct pressure over the
affected area or by movement of the patient’s neck. The pain itself can be fleeting, or it
can be a dull ache that lasts for hours.
Panic syndrome is a major cause of chest discomfort in ED patients. The symptoms
typically include chest tightness, often accompanied by shortness of breath and a sense
of anxiety, and generally last 30 minutes or longer.

22. INITIALDIAGNOSTICAPPROACHTOAPATIENTWITHCHESTPAIN

23. Clinical Evaluation
When evaluating patients with acute chest pain, clinicians must address a series of
issues related to prognosis and immediate management. Even before trying to arrive at
a definite diagnosis, high-priority questions include the following:
• Clinical stability: Does the patient need immediate treatment for actual or impending
circulatory collapse or respiratory insufficiency?
• Immediate prognosis: If the patient is currently clinically stable, what is the risk of a
life-threatening condition such as ACS, PE, or aortic dissection?
• Safety of triage options: If the risk for a life-threatening condition is low, is it safe to
discharge the patient for outpatient management, or should further testing or
observation to guide management be undertaken

24. History
Patients typically describe ACS discomfort as a diffuse substernal chest pressure that
starts gradually, radiates to the jaw or arms, worsens with exertion, and is relieved by rest
or nitroglycerin. Because angina tends to be manifested in the same way in a given
patient (at least if it is caused by ischemia in the same territory), it is useful to compare
the current episode with any previous documented episodes of angina.
THE RESPONSE TO NITROGLYCERIN MAY NOT RELIABLY DISCRIMINATE CARDIAC CHEST
PAIN FROM NON–CARDIAC-RELATED CHEST PAIN.
In contrast to the tempo of the chest discomfort in ACS, that of PE, aortic dissection, and
pneumothorax is usually sudden and severe in onset. Moreover, pain that is pleuritic or
positional in nature suggests PE, pericarditis, pneumonia, or a musculoskeletal condition.
Younger patients have a lower risk for ACS but should be screened with greater care for a
history of recent cocaine use.

25. Physical Examination
The initial examination of patients with acute chest pain should endeavor to identify potential
precipitating causes of myocardial ischemia (e.g., uncontrolled hypertension), important comorbid
conditions (e.g., COPD), and evidence of hemodynamic complications (e.g., congestive heart failure,
new mitral regurgitation, hypotension).
In addition to vital signs, examination of peripheral vessels should include assessment for the
presence of bruits or absent pulses, which suggest extracardiac vascular disease.
For patients whose clinical findings do not suggest myocardial ischemia, the search for
noncoronary causes of chest pain should focus first on potentially life-threatening issues (e.g.,
aortic dissection, PE) and then turn to the possibility of other cardiac diagnoses (e.g., pericarditis)
and noncardiac diagnoses (e.g., esophageal discomfort). Aortic dissection may produce blood
pressure or pulse disparities or a new murmur of aortic regurgitation accompanied by back or
midline anterior chest pain. A friction rub may accompany pericarditis. Differences in breath sounds
in the presence of acute dyspnea and pleuritic chest pain suggest pneumothorax. Tachycardia,
tachypnea, and an accentuated pulmonic component of the second heart sound (P2) may be the
major manifestations of PE on physical examination.

26. Electrocardiography
An ECG, should be obtained within 10 minutes after arrival for individuals with ongoing chest discomfort
and as rapidly as possible in those who have a history of chest discomfort consistent with ACS. Obtaining a
prehospital ECG decreases the door-to-diagnosis time and, for ST-segment elevation MI (STEMI), the door-
to-balloon time.
The ECG helps to define both diagnosis and prognosis.
New persistent or transient ST-segment abnormalities (≥0.05 mV) that develop during a symptomatic
episode at rest and resolve when the symptoms resolve strongly suggest acute ischemia and severe CAD.
Nonspecific, STsegment changes or T wave abnormalities of 0.2 mV or less are not as helpful for risk
stratification.
A completely normal ECG does not exclude ACS: the risk for AMI is approximately 4% in patients with a
history of CAD and 2% in those with no such history.
Patients with normal or near-normal findings on an ECG, however, have a better prognosis than those with
abnormal ECG at initial evaluation.
A normal ECG has a negative predictive value of 80% to 90%.

27. Diffuse ST-segment elevation and PR-segment depression suggest
pericarditis.
Tachycardia with right axis deviation, right bundle branch block, T wave
inversions in leads V1 to V4, and an S wave in lead I and Q wave and T
wave inversions in lead III suggest PE.
Posterior leads can help identify ischemia in the territory supplied by the
circumflex coronary artery, an otherwise relatively silent zone on ECGs.

28. Chest Radiography
All patients with chest pain typically have a chest radiograph. It is usually
nondiagnostic in patients with ACS but can show pulmonary edema
secondary to ischemia-induced diastolic or systolic dysfunction. It is
more useful for diagnosing or suggesting other disorders; for example, it
may show a widened mediastinum or aortic knob in patients with aortic
dissection. The chest radiograph generally has normal findings in PE but
can show atelectasis, an elevated hemidiaphragm, a pleural effusion, or
more rarely a Hampton hump or Westermark sign. The chest radiograph
can reveal pneumonia or pneumothorax.

29. Biomarkers
Patients with chest discomfort possibly consistent with ACS should undergo
measurement of biomarkers of myocardial injury. The preferred biomarker
is cardiac troponin T (cTnT) or I (cTnI); creatine kinase MB isoenzyme (CK-
MB) is less sensitive.
Diagnostic Performance
Studies of the diagnostic performance of cTnI, cTnT, and CK-MB indicate
that when any of these test findings is abnormal, the patient is highly likely
to have ACS. These assays aid indispensably the diagnosis of MI and have
excellent sensitivity and specificity when viewed as part of all the clinical
evidence.

30. TROPONINS.
Different genes encode troponins in cardiac muscle, therefore, assays for cardiac
troponins are more specific for myocardial injury than assays for CK-MB, and cardiac
troponin is the preferred diagnostic biomarker.
Myocardial damage may occur with direct forms of myocardial injury, such as in the
setting of myocarditis, myocardial contusion, or cardioversion or defibrillation.
Conditions that affect the pulmonary circulation, such as in PE or other causes of acute
pulmonary hypertension, can also lead to biochemically detectable right ventricular
injury.
Patients with renal disease may have elevated levels of cardiac troponins. (The exact
mechanism remains unclear.)
Elevated cTn levels can also occur in patients with severe sepsis.

31. Current U.S. guidelines recommend measurement at presentation and
then 3 to 6 hours after symptom onset Such a strategy yields a negative
predictive value (NPV) approaching 99%.
More recently, high-sensitivity troponin (hsTn) assays now enable even
lower limits of detection (e.g., 99% NPV. The generalizability of these
findings may also depend on the timing and nature of the presenting
syndrome, with patients with a very short time from symptom onset to
presentation needing serial sampling.
In centers without availability of high-sensitivity assays, serial testing at
presentation and after 3 to 6 hours remains the standard of care.

32. Creatine Kinase MB Isoenzyme.
CK-MB has less specificity than cardiac troponins because of its production by skeletal
muscle, tongue, diaphragm, small intestine, uterus, and prostate.
Use of the CK-MB relative index (ratio of CK-MB to total CK) partially addresses this
limitation for skeletal muscle as a source.
The amount of CK-MB in skeletal muscle, however, increases in patients with conditions
that cause chronic muscle destruction and regeneration (e.g., muscular dystrophy),
high-performance athletics (e.g., marathon running), and those with rhabdomyolysis.
One advantage of CK-MB is a shorter half-life in the circulation, which makes it useful
for gauging the timing of an MI (a normal CK-MB with an elevated troponin level could
represent a small MI or an MI that occurred several days ago) and for diagnosing
reinfarction in a patient who had an MI in the past week.
However, hsTn assays offer similar value.

33. Other Markers

34. Copeptin is secreted from the pituitary gland early in the course of MI. It has been investigated in combination
with troponin in patients presenting with suspected ACS. In the CHOPIN study, both a negative copeptin and a
sensitive troponin assay in patients presenting within 6 hours of symptom onset had NPV of 99.2%.
Myoglobin, heart-type fatty acid–binding protein, and ischemia-modified albumin (IMA) have been studied as
diagnostic biomarkers, but none is specific to myocardial tissue.
D-dimer testing is useful for patients with chest pain to help rule out PE, because a negative enzyme-linked
immunosorbent assay (ELISA) has NPV >99% in patients with a low clinical probability (patients with a higher
clinical probability should undergo an imaging study).
Similarly, a negative D-dimer has NPV of 96% for aortic dissection.
B-type natriuretic peptides (BNP and N-terminal pro-BNP) reflects increased ventricular wall stress. Natriuretic
peptides often aid in the diagnosis of heart failure. BNP levels can rise in the setting of transient myocardial
ischemia, and the magnitude of elevation in patients with ACS is related to prognosis.
Circulating microRNAs have been evaluated in small studies but have not yet been shown to provide
incremental diagnostic or prognostic value in patients presenting with suspected AMI.

35. Testing Strategy
The ACC/AHA and European Society of Cardiology (ESC) guidelines
recommend cTnI or cTnT as the preferred first-line marker, although CK-MB
(by mass assay) is an acceptable alternative.
The preference for cardiac troponins reflects the greater specificity of these
markers than CK-MB and the prognostic value of troponin elevations in the
presence of normal CK-MB levels.
If the initial set of markers is negative, another sample should be drawn 3 to
6 hours later; if a high-sensitivity assay is used, a 1-hour algorithm can be
considered.

36. Early Noninvasive Testing
Treadmill Electrocardiography
Treadmill exercise electrocardiography is inexpensive and available at many
hospitals every day, beyond traditional laboratory hours, and prospective
data indicate that early exercise test results provide reliable prognostic
information for low-risk patient populations.
Most studies have used the Bruce or modified Bruce treadmill protocol.
Multiple studies have demonstrated the safety of exercise testing in low-risk
patients, and a negative predictive value of typically greater than 99%,
although the positive predictive value is frequently less than 50%.

37. Patients with low clinical risk for complications can safely undergo
exercise testing after their second negative troponin test (typically 3 to 6
hours later) and no other evidence of myocardial ischemia.
In general, protocols for early or immediate exercise testing exclude
patients with electrocardiographic findings consistent with ischemia not
recorded on previous tracings, ongoing chest pain, or evidence of
congestive heart failure.
Analyses of pooled data have suggested that the prevalence of CAD in
populations undergoing early exercise testing averages approximately 5%
to 10%, the rate of adverse events is negligible, and fewer than 1%
ultimately proceed to angiography and revascularization.

39. Imaging Tests
Stress echocardiography and radionuclide scans are the
preferred noninvasive testing modalities for patients who
cannot undergo treadmill electrocardiographic testing
because of physical disability or who have resting ECGs that
confound interpretation. Imaging studies are less readily
available and more expensive than exercise
electrocardiography but have increased sensitivity for the
detection of CAD and the ability to quantify the extent of and
localize jeopardized myocardium.

40. In addition to stress imaging studies to detect provocable
ischemia, rest radionuclide scans can also help determine
whether a patient’s symptoms represent myocardial ischemia.
Rest myocardial perfusion imaging is most sensitive if performed
when a patient is experiencing ischemic symptoms, with its
sensitivity progressively diminishing thereafter. Imaging should be
performed within 2 hours of the resolution of symptoms,
although data support its use for up to 4 hours. It should be
noted that perfusion defects seen at rest could represent either
acute ischemia or previous MI, which can be differentiated on
subsequent pain-free rest imaging.

41. Echocardiography, with and without stress, can detect
wall motion abnormalities consistent with myocardial
ischemia or MI. The presence of induced or baseline
regional wall motion abnormalities is associated with a
worse prognosis. The sensitivity of stress
echocardiography appears comparable to that of
myocardial perfusion imaging (85% to 90%), and its
specificity is somewhat better (80% to 95% versus 75% to
90%).

42. As for myocardial perfusion imaging, the results are less
interpretable in patients with previous MI, in whom it is
difficult to exclude whether the abnormalities are preexisting
in the absence of a prior study. Myocardial contrast-
enhanced echocardiography using microbubble imaging
agents offers reasonable (77%) concordance with
radionuclide scanning, and the combination of regional wall
motion abnormalities and reduced myocardial perfusion has
a sensitivity of 80% to 90% and a specificity of 60% to 90% for
ACS.

43. Cardiac magnetic resonance imaging (MRI) may also aid the assessment of
patients with suspected ACS. A study that used cardiac MRI to quantify
myocardial perfusion, ventricular function, and hyperenhancement in
patients with chest pain showed sensitivity for ACS of 84% and specificity of
85%.
The addition of T2-weighted imaging, which can detect myocardial edema
and thus help differentiate acute from chronic perfusion defects, improves
the specificity to 96% without sacrificing sensitivity.
Stress MRI using adenosine, although more labor intensive, also shows
excellent sensitivity and specificity.

44. In contrast to the functional imaging data from stress testing, coronary
computed tomographic angiography (CTA) offers noninvasive anatomic
data. Using multidetector CT, coronary CTA has sensitivity of
approximately 90% and specificity of 65% to 90% for coronary stenosis
greater than 50%. In addition to diagnosis, coronary CTA can provide
calcium scores, giving prognostic information and potentially informing
the need for additional cardiac testing.
Another advantage of CTA is that it is often the test of choice for PE and
for aortic dissection and thus “triple-rule-out CTA” can evaluate for CAD,
PE, and aortic dissection.

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