Approach to chest pain

An approach to chest pain
Dr.Manish Patil

Introduction
 Chest discomfort is one of the most common
challenges in the OPD or Casualty.
 Differential diagnosis includes conditions affecting
organs throughout the thorax and abdomen, with
prognostic implications that vary from benign to life-
threatening.
 Failure to recognize potentially serious conditions such
as acute ischemic heart disease, aortic dissection,
tension pneumothorax, tamponade or pulmonary
embolism can lead to serious complications, including
death.

History matters!
 Location: Central, left, or right
 Associated symptoms: SOB, sweating, nausea
 Provocation: What makes worse or better?
 Quality: Visceral vs somatic
 Radiation: Back, neck, arm
 Severity.
 Timing: Gradual or sudden onset

Location and radiation
 Location: Retrosternal or slightly to the left of the
midline.
 Ischemic chest pain radiate to neck, jaw, teeth,
arms, or shoulders, reflecting the common origin in
the posterior horn of the spinal cord of sensory
neurons supplying the heart and these areas.
 One or two clenched fists held by the patient over
the sternal area (Levine sign) is much more
indicative of ischemic pain.
 Highly localized pain are unlikely angina episode.

Location and radiation
 Esophageal disorders most commonly present with
substernal pain .
 Severe pain radiating to back should suggest aortic
dissection.
 Radiation to ridge of trapezius is charecteristic of
pericarditis.
 Hepatobilliary, Pancreatic and peptic ulcer pains are
predominantly epigastric.

Duration & pattern of disappearance:
 Stable Angina : last for 2 min to 10 minutes, begins
gradually and reaches its maximal intensity over a
period of minutes before dissipating (usually within
10 min) with rest or nitroglycerin.
Unstable Angina: self limited, anginal pain that is
exertional but occurs at increased frequency with
progressive lower intensity of physical activity or even
at rest, lasting for <20 minutes.

 Chest discomfort associated with MI is prolonged
(>30 min) and not relieved by rest.
 Short lasting migratory pain unlikely to be ischemic
origin.
 Constant and prolonged pain are also unlikely to
represent ACS, more likely to be hepatobilliary or
pancreatic in origin.

Aggravating and relieving factor
 Classically, Stable Angina discomfort:
induced by exercise, emotion, eating (after meals),
or cold weather and relieved by rest.
 Similar discomfort at rest, suggest life threatening
ACS.
 Post prandial angina suggest severe underlying
CAD.

Aggravating and relieving factor
 Alteration in severity of pain with change in position
or movement, more likely to be musculo skeleton
pain .
 Pain getting worsened in supine and relieved by
sitting upright or leaning forward suggest
pericarditis.
 GERD symptoms aggravates in supine position and
relieved in sitting.

Associated symptoms
 Diaphoresis, dyspnoea, nausea , Fatigue, syncope
may accompany Angina chest pain.
 Pulmonary embolism is associated with dyspnoea
and /or syncope.
 Hemoptysis suggest parenchymal pathology,
pulmonary edema, Pulmonary embolism.
 Predominant nausea, vomiting , generally indicate
gastro intestinal pathology.

Physical examination
• Pt. with ACS or other acute cardiopulmonary
disorders are anxious, uncomfortable, pale,
diaphoretic.
• Peripheral signs of shock are hallmark of severe
organic pathology and needs emergent attention
• Hypertension and pulse asymmetry noted in
aortic dissection.
• Hypoxemia indicating severe nature , may occur
both in pulmonary and cardiac conditions.

• CVS:
• JVP : often normal in ACS , may reveal
characteristic pattern in pericardial tamponade
or acute right ventricular dysfunction.
• 3rd or 4th heart sound sound reflecting
systolic or diastolic dysfunction.
• Murmur of aortic insufficiency may be a
complication of proximal aortic dissection.

• Chest:
• pleural rub(pleurisy), bronchial breathing
(pneumonia), absent lung sound
(pneumothorax), basal rales (pulmonary edema).
• Pericardial friction rub indicates pericarditis.
• Evidence of DVT should arose strong suspicion
of pulmonary embolism.
• Hyperventilation is sign of psychological origin.

Investigations
 ECG: should be obtained within 10 minutes after
presentation in pts with ongoing chest discomfort.
 Excellent tool to identify Acute coronary syndrome
specially STEMI.
 ST and T wave changes may be seen in variety of non
ischemic condition :
Pericarditis, myocarditis, metabolic abnormality,
Pulmonary embolism, Ventricular hypertrophy etc.

The J point
 J point is the
the junction
between the
termination of
the QRS
complex and the
beginning of the
ST segment

Benign Early Repolarization
 ECG pattern most commonly seen in young,
healthy patients < 50 years of age.
 Up to 10-15% of patients presenting with chest
pain will have BER on their ECG .
 Normal variant, that is not indicative of underlying
cardiac disease
 widespread ST segment elevation that may mimic
pericarditis or acute MI.

 Concave ST elevation is
commonly seen in leads V2 to
V6 and also in leads II,III,aVF.
 Prominent notch at terminal
portion of QRS complex in leads
with ST elevation.
 The T wave in V6 are usally tall
when compared with the height
of ST segment, thus the ratio
between height of ST segment
and that of T wave is usually <
25%

ELECTROCARDIOGRAPHIC MANIFESTATIONS OF ACUTE
MYOCARDIAL INFRACTION (IN THE ABSENCE OF LBBB)
 ST Elevation MI
 New ST elevation at the J point in two contiguous
leads with the following cut points:
• ≥0.1 mV in all leads (except V2-V3)
 • In leads V2-V3 the following cut points apply:
• ≥0.2 mV in men ≥40 years. ≥0.25 mV in men <40
years
• ≥0.15 mV in women

ELECTROCARDIOGRAPHIC MANIFESTATIONS OF
ISCHEMIA IN THE SETTING OF(LBBB)
 Electrocardiographic Criterion
Points
 ST-segment elevation ≥1 mm and
concordant with the QRS complex
(5)
 ST-segment depression ≥1 mm in
lead V1, V2, or V3 (3)
 ST-segment elevation ≥5 mm and
discordant with the QRS complex
(2)
 A score of ≥3 had a specificity of
98% for acute MI

Morphology Of ST Depression
 ST depression can be either
upsloping, downsloping, or
horizontal.
 New horizontal or down-sloping ST
depression ≥0.05 mV in two
contiguous leads and/or T inversion
≥0.1 mV in two contiguous leads
with prominent R wave or R/S ratio
>1.
 Up sloping ST depression is non-
specific for myocardial ischaemia.

Chest Radiograph
 Chest pain due to pulmonary cause, may reveal
pneumonia, pneumothorax, pleural effusion.
 Mediastinal widening present in acute aortic
syndrome.
 Pericardial calcification seen in chronic pericarditis.

In pulmonary embolism,
Focal oligemia
(Westermark sign)
indicates massive central
embolic occlusion.
peripheral wedge-shaped
density above the
diaphragm (Hampton
hump) usually indicates
pulmonary infarction.

Cardiac biomarkers
 D-dimer assesment is useful in evaluation of
suspected pulmonary embolism, very high negative
predictive value.
 NT-pro BNP is useful in diagnosis and
prognostication in heart failure.
 Elevated biomarkers indicates myocardial injury
and rise is proportional to degree of injury.

Cardiac specific Troponin T and I ; preferred in
evaluation of ACS.
•An increased value for cardiac troponin is defined as, a
measurement exceeding the 99th percentile of URL.
•Detection of a rise and/or fall of the measurements is
essential to the diagnosis of acute myocardial infarction
•cTnI and cTnT may remain elevated for 7-10 days after
STEMI. CK-MB rises within 4-8 hrs and returns to
normal by 48 – 72 hours.

Echocardiography
 TTE :
to assess overall ventricular function, valvular
morphology, presence of regional wall motion
abnormality, Pericardial effusion etc.
 TEE :
can accurately detect acute aortic syndrome,
mechanical complications of MI like MR, VSD,
Cardiac Tamponade.
 Right sided chamber assesment can reveal
possibility of pulmonary embolism

CT angiography
 CT coronary angiography can detect presence or
absence of significant obstructive coronary disease.
 CT pulmonary angiography can identify pulmonary
embolism.
 CT angiography is useful in evaluating aortic
dissections.
 CT scan can detect other pulmonary and pleural
pathology.

MRI
 Cardiac MRI can accurately predict structural and
functional abnormalities of heart and vasculature.
 Gadolinium enhanced CMR can provide early
detectionn of MI.
 MR angiography is very accurate in detecting Aortic
dissections.

 1. Angina pectoris/myocardial infarction
 2. Other cardiovascular causes
 a. Likely ischemic in origin
 (1) Aortic stenosis
 (2) Hypertrophic cardiomyopathy
 (3) Aortic regurgitation
 (4) Severe anemia/hypoxia
 b. Nonischemic in origin
 (1) Aortic dissection
 (2) Pericarditis
 (3) Mitral valve prolapse
 3. Gastrointestinal
 a. Esophageal spasm/ Reflux/Rupture
 b. Peptic ulcer disease

 4. Psychogenic
 5. Neuromusculoskeletal
 a. Thoracic outlet syndrome
 b. Degenerative joint disease of cervical/thoracic spine
 c. Costochondritis (Tietze syndrome)
 d. Herpes zoster
 e. Chest wall pain and tenderness
 6. Pulmonary
 a. Pulmonary embolus with or without pulmonary infarction
 b. Pneumothorax
 c. Pneumonia with pleural involvement
 7. Pleurisy

Chest Pain
 Foremost manifestation of myocardial ischemia.
 An increase in myocardial oxygen consumption
(MVO2) (demand ischemia) or
 Decrease in or inadequate blood flow(supply
ischemia), or their combination, can be
responsible for anginal chest pain
 Most common causes are :
coronary atherosclerosis, coronary
vasoconstriction, and coronary artery thrombosis.

 Classically, the discomfort is induced by exercise,
emotion, after meals or cold weather or spontaneously at
rest
 Walk-through phenomenon :- Occasionally, angina will
dissipate despite continued exercise.
 Warm up phenomenon:- chest discomfort will not occur
when a second exercise effort is undertaken that
previously produced.
 Due to opening of functioning coronary arterial collaterals
during the initial myocardial ischemia. This is consistent
with ischemic preconditioning
`

 Ischemic episode stimulate chemo sensitive and mechano
receptive receptor. Stimulate release of adenosine, bradykinin
that activate the sensory ends of sympathetic and vagal afferent
fiber.
 Afferent fibers traverse the nerves that connect to the upper 5
thoracic sympathetic ganglia and upper 5 distal thoracic root of
spinal cord. Impulse are transmitted to the thalamus.
 Within spinal cord, cardiac sympathetic afferent impulse may
converge with impulses from somatic thoracic structure(basis for
referred cardiac pain).
 Cardiac afferent fiber synapse in nucleus tractus solitarius of
medulla and then descend to the upper cervical spinothalamic
tract, contribute to anginal pain experienced in neck and jaw.
Mechanism of cardiac pain

 Chest pain or discomfort ("tightness," "pressure,"
"burning," "heaviness," "aching," "strangling," or
"compression.") of cardiac origin.
 Results from a temporary imbalance between
myocardial oxygen supply and demand.
 Angina pectoris should be considered a symptom
and not a specific disease.
 Location: Retrosternal, tends to radiate to the neck,
jaw, teeth, arms, or shoulders,
Angina pectoris

 NSTE-ACS: characteristics
1. Relatively new onset chest pain (within the prior 2 weeks)
2. Exertional pain but occurs at increased frequency with
progressive lower intensity of physical activity or even at
rest. Lasting for less than 20 min.
3. crescendo pattern
 Unstable ischemic heart disease classified as unstable
angina when there is no detectable myocardial injury
with 1 of the 3 above mentioned features and non ST
elevation MI when acute atherothrmobosis occurs ,
intracoronary thrombus may be partially obstructive ,
leading to myocardial ischemia in the absence of ST
segment elevation.

Pathophysiology of UA/NSTEMI
(1) Rupture of unstable atheromatous plaque or erosion leads to
formation of superimposed thrombus (typically non occlusive
in NSTE-ACS) along with subsequent impaired myocardial
perfusion, which if persistent, leads to myocardial necrosis
(2) Coronary arterial vasoconstriction (dynamic obstruction
result of intense focal spasm of a segment of an epicardial
coronary artery (Prinzmetal or variant angina. )
(3) Imbalance between the supply and demand of
myocardium for oxygen.
(4) Gradual intraluminal narrowing of an epicardial coronary
artery because of progressive atherosclerosis or post stent
restenosis.

Factors that increase the probability of NSTE-ACS
 Older age
 male sex
 positive family history of CAD
 Presence of peripheral arterial disease
 Diabetes mellitus
 Renal insufficiency.
 Prior MI, and prior coronary revascularization.
 Traditional risk factors for atherosclerosis.

In Acute myocardial infarction :
chest pain more severe and longer-lasting.
•often associated with nausea, vomiting, and diaphoresis
•accompanied by sustained LVdysfunction (dyspnea,
orthopnea) and autonomic nervous system
hyperactivity (tachycardia, diaphoresis).
Painless or atypical presentations of MI, occur in up to
40 % of patients, particularly in diabetic and elderly
patients.

Ischemia is caused by hemodynamic changes
associated with an inadequate CBF in relation to a
normal or increased myocardial oxygen demand.
Conditions are:
Aortic stenosis, hypertrophic cardiomyopathy, and
systemic arterial hypertension, in which LV systolic
pressure and LV wall tension are greatly increased,
or LV hypertrophy is present.
Cause of likely ischemic cardiac chest pain

Chest pain -
 Severe aortic regurgitation (AR) :
large LV volume load
augmented MV O2
reduced diastolic perfusion pressure resulting
in inadequate CBF.
 Severe RV systolic hypertension (in pulmonic
stenosis or pulmonary hypertension), can cause
exertional angina, presumably on the basis of RV
subendocardial ischemia.

Severe anemia or hypoxia – can produce myocardial
ischemia : inadequate oxygen supply even in the absence
of associated CAD. Both also can increase angina in the
presence of obstructive CAD.
Acute myocarditis : chest discomfort may either
originate with inflammatory injury of myocardium or due
to severe increase in wall stress related to poor
ventricular performance

DIAGNOSIS
History
ECG
Cardiac biomarkers
Echocardiography

HEART Score for Chest Pain Patient (UA/NSTEMI)
History Highly suspicious 2
Moderately suspicious 1
Slightly suspicious 0
ECG Significant ST-depression 2
Non specific repolarisation
disturbance
1
Normal 0
Age ≥ 65 year 2
45 – 65 year 1
≤ 45 year 0
Riskfactors ≥ 3 risk factors or history
of atherosclerotic disease
2
1 or 2 risk factors 1
No risk factors known 0
Troponin ≥ 3x normal limit 2
1-3x normal limit 1
≤ normal limit 0
The HEART score divides patients into low (0-3),
intermediate (4-6) or high risk groups (7-10), with mean
risks of an event of 0.9%, 12% and 65%, respectively.
Total

CHEST PAIN SCENARIO
A 40-YEAR-OLD FEMALE HAS PRESENTED TO THE EMERGENCY
DEPARTMENT WITH CHEST PAIN AND SHORTNESS OF BREATH FOR 12
HOURS. THE PAIN IS LOCATED AROUND THE RIGHT SIDE OF HER
CHEST AND IS MADE WORSE ON DEEP INSPIRATION. SYMPTOMS HAD
COME ON SUDDENLY AT REST. SHE DENIES ANY SYMPTOMS OF
COUGH OR FEVER. HER HISTORY IS SIGNIFICANT FOR TWO
MISCARRIAGES AND A DVT IN HER LEFT LEG.
ON EXAMINATION,
BP 100/60mm Hg, PULSE 120 bpm, RR 32 BPM,
OXYGEN SAT 88% AT ROOM AIR.
ECG SHOWS……

ECG in Pulmonary embolism
 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 inversion in lead
III suggest pulmonary
embolism

Clinical manifestation
 Symptoms
 Unexplaned dyspnea- Present in 90%
 Chest pain - 66% of patients with PE
 Cough
 Sudden onset
 Signs
 Tachycardia > 100 beats per minute
 Tachypnea > 20 breaths per minute
 Hypoxia < 95% on RA (no other cause)
 Lower extremity swellings
 Jugular venous distension
 Tricuspid regurgitant murmur
 Accentuated P2
 Hemoptysis

 Massive pulmonary emboli cause
 Severe and persistent substernal pain
Distention of the pulmonary artery.
 Smaller emboli 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.

Classic Wells Criteria
 To Assess Clinical Likelihood of Pulmonary Embolism
 CRITERION SCORING*
 DVT symptoms or signs 3
 An alternative diagnosis is less likely than PE 3
 Heart rate > 100 beats/min 1.5
 Immobilization or surgery within 4 weeks 1.5
 Previous DVT or PE 1.5
 Hemoptysis 1
 Cancer treated within 6 months or metastatic 1
 *>4 score points = high probability; ≤4 score points = non–
high probability.

CHEST PAIN SCENARIO
•A 28-YEAR-OLD YOUNG MALE PRESENTS TO EMERGENCY
DEPARTMENT WITH SUDDEN ONSET OF RIGHT SIDED CHEST PAIN.
THE PAIN STARTED AS SHARP BUT NOW DULL BUT INCREASES
WITH INSPIRATION.
•HE HAS COUGH AND SHORTNESS OF BREATH WHICH HE RELATES
WITH HIS SMOKING.
•ON EXAMINATION,
PULSE 102 bpm, BP 120/80 mm Hg,
RR 26 bpm. OXYGEN SATURATION IS 97% AT ROOM AIR.
•CHEST AUSCULTATION DEMONSTRATED DECREASED AIR ENTRY
ON RIGHT SIDE .
• ECG IS REPORTED AS NORMAL..
• WHAT IS THE NEXT INVESTIGATION…….

Primary spontaneous pneumothorax(Ptx)
 Occurs in the absence of underlying lung disease.
 Typically results from apical pleural blebs .
 Risk factors : male sex, smoking, family history and
marfan’s syndrome.
 Symptoms are sudden in onset and dyspnea may be
mild.
 Simple aspiration may be adequate treatment for an
initial primary spontaneous Ptx.
 Recurrence typically requires thoracoscopic
intervention.

Secondary pneumothorax
 Occurs in the setting of pulmonary disease such
as chronic obstructive pulmonary disease, asthma,
or cystic fibrosis
 Chest tube placement is typically required for
secondary spontaneous Ptx; thoracoscopy and/or
pleurodesis also be considered.

Tension Pneumothorax:-
Result from trauma or mechanical ventilation.
Positive pleural pressure in mechanical ventilation can
rapidly lead to a tension Ptx with reduced cardiac
output.
Urgent treatment :
either with a chest tube or, if not immediately available,
with a large-bore needle inserted into the pleural space
through the second anterior intercostal space.

Other Pulmonary causes of chest pain
 Pneumonia and malignancy,
because of involvement of pleura and surrounding
structures.
 Pleurisy is typically described as a knifelike pain
that is worsened by inspiration or coughing
 Chronic pulmonary hypertension, suggesting right
ventricular myocardial ischemia in some cases.

 Inflammation of pericardium due to infectious or
non infectious cause.
 Visceral surface of the pericardium is insensitive
to pain, as is most of the parietal surface.
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.
Pericarditis

 Chest pain: Positional, Sharp and penetrating in
quality.
 Cardinal diagnostic feature because of pleural
association is, worsening by changes in body
position (relieved by leaning forward); during deep
inspiration.
 Central diaphragm receives its sensory supply from
the phrenic nerve ( C3 to C5 segments of the spinal
cord), pain from infectious pericarditis is frequently
felt in the shoulders and neck.
Clinical feature

 Physical Examination:-
Rapid or irregular pulse, coarse pericardial friction rub,
which may vary in intensity and is loudest with pt sitting
forward.
 ECG:-
Diffuse ST elevation (concave upward) usually present in
all leads except aVR and V1; PR-segment depression
(and/or PR elevation in lead aVR) may be present.
 Echocardiogram :- Most readily available test for
detection of pericardial effusion, which commonly
accompanies acute pericarditis.

Aortic Dissection
 Presentation (Difficult clinical diagnosis)
 85% have chest or back pain(commonly
interscapular region)
 Sudden onset , “Ripping” or “tearing” in 50%
 Acute aortic syndrome involving ascending aorta
tend to cause pain in midline of anterior chest
while descending aortic syndrome present with
pain in back
 Neurologic symptoms in 20%(if involve cerebral
arteries)
 Asymmetric pulse.

•Proximal aortic dissection that involve ascending aorta
are at high risk for major complication:
1) compromising aortic ostia of coronary arteries-
resulting in MI.
2) Disruption of aortic valve - acute aortic insufficiency,
3) Rupture of hematoma in pericardial space- leads to
pericardial tamponade.
• Risk factor for dissection:
Long standing hypertension,
Increasing age,
Inherited diseases(e.g. Marfan’s syndrome, Ehlers-
Danlos syndrome type IV,
Infection (syphilis)
Previous cardiovascular surgery etc.

Aortic Dissection
 Blood violates aortic intimal and
adventitial layers
 False lumen is created
 Dissection may extend
proximally, distally, or in both
directions.
 Penetrating ulcer : Ulceration of
an aortic atheromatous plaque
that extends through the intima
and into aortic media , with the
potential to initiate an intra
medial dissection or rupture
into adventitia.
 Intra mural hematoma: due to
rupture of vasa vasorum

Aortic Dissection Diagnosis
 CXR- Widened mediastinum, abnormal aortic
knob, pleural effusions
 Not sensitive (25% have wide mediastinum)
 Chest CT- Very sensitive and specific
 Quickly obtained
 Angiography- Gold standard
 Most reliable anatomy of dissection
 Bedside Echo – evaluate aorta and look at heart to
r/o tampanode.

Diffuse esophageal spasm
 Neuromuscular motor disorder of the esophagus.
 Age : more common in 50- 60 yrs old individuals.
 Pain is retrosternal; can be burning, squeezing, or
aching in quality; often radiates to the back, arms,
and jaw.
 Pain as a result of dysphagia, and regurgitation of
gastric contents, can last for minutes or hours, can be
relieved by TNG, which also relaxes esophageal
smooth muscle
 Diagnosis: based on the history, and abnormal
motility by esophageal manometry

Reflux esophagitis
 Mucosal irritation :- failure of the lower esophageal
sphincter to prevent regurgitation of highly acidic
gastric contents.
 Heartburn and regurgitation occur after meals or
ingestion of coffee or after postural changes.
 Dysphagia due to stricture formation secondary to
long-standing esophageal reflux.
 Esophagoscopy and esophageal biopsy: to
demonstrate mucosal lesions and for assessing the
severity of inflammation.

 Recurrent chest pain .
 Difficult to separate from angina pectoris, particularly when it
occurs in patients with multiple risk factors for CAD or in
otherwise asymptomatic patients of CAD.
 Most common psychogenic cause of chest discomfort : anxiety.
 Quality of Pain : sharp or stabbing, localized to the left infra
mammary area(sharply circumscribed), extremely short duration
(<1 min). At times, pain can persist for many hours.
 Associated symptoms- air hunger, circumoral paresthesias,
globus hystericus, and multiple somatic complaints- suggest a
neurasthenic personality or hyperventilation syndrome.
Psychogenic chest discomfort

Tietze syndrome, or idiopathic costochondritis
Anterior chest-wall pain, aggravated by movement and
deep breathing.
Reproducing the chest pain syndrome by direct pressure
over the involved costochondral junction or the relief of
pain after local infiltration with lidocaine, is a helpful
diagnostic maneuver.

 Commonest symptom for attending emergency department.
 Can be manifestation of a life threatening situation, can also
be a manifestation of insignificant cause.
 Clinical (detail history, physical examination), biochemical
and other investigations should be used for rapid
identification, triage and treatment of high risk cardio-
pulmonary conditions.
 Early initiation of targeted therapy reduces mortality and
morbidity.
 Protocol driven evaluation of chest pain, to control costs and
not to overuse of testing , unnecessary hospitalizations and
resultant psychological stress.
conclusion

Approach to chest pain

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