ORIGIN OF THE PAIN

• Heart
• Lungs
• Oesophagus
• Musculoskeletal structures of thorax or
shoulder
• Abdomen
• Anxiety
DIFFERENTIAL DIAGNOSIS OF
CHEST PAIN
 ISCHEMIC CARDIAC PAIN V/S NON-CARDIAC PAIN

LOCATION CENTRAL, PERIPHERAL

DIFFUSE LOCALIZED
RADIATION JAW/NECK/SHOULDER/ OTHER OR
ARM (OCCASIONALLY NO RADIATION
BACK)
CHARACTER TIGHT SHARP
SQUEEZING STABBING
CHOKING CATCHING
PRECIPITATION EXERTION SPONTANEOUS
EMOTION NOT RELATED TO EXERTION
PROVOKED BY POSTURE,
RESPIRATION OR PALPATION
RELIEVING REST NOT RELIEVED BY REST
FACTORS NITRATES SLOW OR NO RESPONSE BY
NITRATES
ASSOCIATED BREATHLESSNESS RESPI, GIT, LOCOMOTOR,
FEATURES OR PSYCHOLOGICAL
Cardiac causes of chest
pain
1. Myocardial ischemia (angina)
2. AMI
3. Pericarditis
4. Aortic dissection
5. Aortic aneurysm
6. Mitral valve prolapse
 MYOCARDIAL ISCHEMIA (ANGINA)
 Angina is a clinical syndrome characterized by :
 Discomfort in chest, jaws, shoulder, back or arms.
 Typically aggravated by exertion or emotional stress.
 Relieved by rest or nitroglycerin (GTN).

 Angina is caused by an imbalance between myocardial

oxygen supply and demand which most commonly due to
atherosclerosis.

 There are many types of angina, including microvascular

angina, variant (Prinzmetal) angina, stable angina/angina
pectoris and unstable angina.
 RISK FACTORS

 Unhealthy cholesterol levels

 High blood pressure
 Smoking
 Diabetes
 Overweight or obesity
 Metabolic syndrome
 Inactivity
 Unhealthy diet
 Older age (The risk increases for men after 45 years of age
and for women after 55 years of age.)
 Family history of early heart disease
 STABLE ANGINA

 Pathophysiology : Fixed stenosis

 Clinical features :
 Demand-led ischemia
 Symptoms at exertion,
relieved by rest
 Lasts 2-5 minutes

 Risk assessment :
 Symptoms on minimal exertion
 Exercise testing (Duration, degree of ECG changes, abn
BP response)
 ACUTE CORONARY SYNDROME
 Is a spectrum of disease ranging from UA/NSTEMI to
STEMI depending on the acuteness and severity of the
coronary occlusion.
 Pathogenesis :
 ACS occurs due to atherosclerotic plaque rupture, fissure
or ulceration with superimposed thrombosis and coronary
vasospasm.
 3 criterias for STEMI :
 Chest pain (ischemic type)
 ECG changes (new onset ST elevation/presumed new LBBB)
 Cardiac biomarkers elevated (injury/necrosis)
 3 criterias for UA/NSTEMI :
 Chest pain (ischemic type)
 ECG changes (ST depression, T inversion, etc)
 Cardiac biomarkers elevated (Troponin T, CK, CK-MB)
 UNSTABLE ANGINA
 Pathophysiology :
Dynamic stenosis
 Clinical features :
 Supply-led ischemia
 Symptoms at rest
 Unpredictable
 Lasts > 10 minutes
 Risk assessment :
 ECG changes at rest
 ECG changes with
symptoms
 Elevation of troponin
 UNSTABLE ANGINA/NSTEMI
◦ NSTEMI is similar with UA with addition to Myocardial necrosis
(elevated cardiac biomarkers)
 Class of UA:
 New onset severe angina, no rest pain
 Angina at rest within 1 hour but not within 48 hours (angina
at rest, subacute)
 Angina at rest (>20 mins) within 48 hours (acute angina)
 Further classified into :
 Primary (develop in absence of extracardiac disease)
 Secondary to extracardiac disease :
 Increase myocardial oxygen demand (eg in fever,
thyrotoxicosis)
 Reduced coronary blood flow (due to hypotension)
 Reduced myocardial oxygen delivery (eg in anaemia,
hypoxemia)
HISTORY
◦ Chest pain
◦ Site (retrosternal, central)
◦ Onset (sudden/gradual)
◦ Character (burning, squeezing, pressing, crushing,
tightness)
◦ Radiation (jaw, upper limbs)
◦ Association (profuse sweating, N/V, SOB, palpitation,
PND, orthopnea, swelling, syncope)
◦ Time (>20 mins indicates STEMI)
◦ Exacerbation/relieving factor (rest low stress activity)
◦ Severity (pain score)
 EXAMINATION
◦ Normal or diaphoresis
◦ Pale cool skin
◦ Tachycardia Cardiac biomarkers :
◦ S4
◦ Basilar rales
• CK-MB elevated
 ECG : • Cardiac specific
 ST depression
troponins elevated
 T-wave inversion
 STEMI
◦ History :
◦ Symptoms :
◦ Chest pain (similar to angina)
◦ Nausea/vomiting
◦ Weakness
◦ Light headedness with syncope
◦ Sweating

◦ 25% are insidious and silent.

◦ Other significant history :
◦ Prev history of IHD/PCI/CABG
◦ Risk factors for atherosclerosis
◦ Prev TIA/CVA
◦ Family history of IHD/CVA/DM/HTN
◦ Social (smoker, alcoholic, occupation)
PHYSICAL EXAMINATION
◦ Physical examination :
◦ Pallor
◦ Diaphoresis
◦ Tachycardia
◦ S4 heart sound
◦ Dyskinetic cardiac impulses

◦ In MI + CHF :
◦ Rales
◦ S3
◦ Jugular venous extension
INVESTIGATIONS
◦ ECG : ST elevation, new LBBB
◦ CXR : TRO pneumothorax, aortic dissection, etc
◦ Serum Cardiac markers highly specific (These
serum should
be assess at presentation of chest pain, 6-9
hours after attack, and at 12-24 hours) :
◦ Troponin T/Troponin I (Remain elevated for 7-10 days)
◦ Creatine phosphokinase
◦ Rise within 4-8 hours
◦ Peaks at 24 hours
◦ Normalize by 48-72 hours
*CK-MB is more specific for MI but elevated in
myocarditis.
 MANAGEMENT
 GOALS :
 Pain relief
 Early perfusion
 Treat complications

 Pre-Hospital management
 At home : 1 tab GTN every 5 mins (3x)
 At GP :
 Chew/swallow 1 tab aspirin
 Sublingual GTN
 Oxygen if hypoxia
 ECG (if ischemic changes) -> 300 mg Clopidogrel
 IV access -> IV morphine 3-5 mg slowly
 To hospital
In Hospital Management :
◦ Admit to RED ZONE
◦ Quick history and vital signs
◦ Confirm diagnosis by ECG
◦ Sublingual GTN if pain persist, cont ECG
monitoring, Aspirin, Clopidogrel, O2, IV access.
◦ Reperfusion strategy (fibrinolytic/PCI)
COMPLICATIONS
1. Arrythmias.
◦ Ventricular arrythmias
◦ Ventricular tachycardia
◦ Ventricular fibrillation
◦ Supraventricular arrythmias
◦ Bradyarrythmias and AV block
2. Heart failure
3. Cardiogenic shock
4. RV infarction - hypotension, clear lung field, raised JVP
5. Pericarditis - pain worsen on deep inspiration, relieve
on sitting and leaning forward, pericardial
rub
6. Ventricular aneurysm
7. Recurrent angina
 PERICARDITIS

 Is the inflammation of pericardial sac.

 More common in men.
 Between 20-50 years old.
 Etiology :
 Viral illness (Coxsackie, Echovirus, mumps etc)
 AMI
 Bacterial infection
 Tuberculous, fungal pericarditis
 Malignant pericarditis
Clinical presentation
◦ Sharp central chest pain.

◦ Exacerbated by movement, respiration and lying down.

◦ Relieved by sitting forward

◦ Dyspnea

◦ fever
 PERICARDITIS

• Investigations :
 Lab investigations (ESR, CBC, cardiac profiles- CK-MB,

troponins TRO AMI, rheumatoid factors)

 ECG (ST elevation, PR interval depression, ST depression in

aVR and V1)

 CXR (cardiac silhoutte enlarged, heart appears globular)

 Echocardiogram

• Management :
 NSAIDs

 Analgesia

• Complications :
 Pericardial effusion

 Cardiac tamponade

 Constrictive pericarditis
AORTIC ANEURYSM

◦ Abnormal dilatation of the abdominal or thoracic aorta.

◦ Defined as permanent dilatation of the artery to twice its normal

diameter.

◦ Primarily due to atherosclerosis.

HISTORY

◦ Maybe clinically silent.

◦ Thoracic aortic aneurysm – deep diffuse chest pain radiating to upper back.

◦ Rupture – associated with hypotension, tachycardia.

◦ Stridor – compressed bronchial tree

◦ Hoarseness – compression of recurrent laryngeal nerve

◦ Hemoptysis – aortobronchial fistula

◦ Dry cough

◦ Abdominal aortic aneurysm – abdominal pain

PHYSICAL EXAMINATION :

◦ Abdominal aortic aneurysym often palpable in periumbilical area.

◦ Ascending thoracic aneurysm features of Marfan Syndrome.

INVESTIGATION :

◦ Thoracic AA CXR – enlarge aortic shilouette.

◦ Confirm by echocardiogram.

◦ AAA – plain film – rim of calcification.

Treatment

◦ Control hypertension (Beta blocker)

◦ If aneurysm is >6cm then operative surgical repair or stenting

may be appropriate.

◦ Endovascular aneurysm repair is the choice of treatment for

descending thoracic aneurysms.
 AORTIC DISSECTION
INTRODUCTION
◦ Potentially life threatening.
◦ Disruption or aortic intima allows dissection of blood into vessel
walls.
◦ Ascending aorta (type II)
◦ Descending aorta (type III)
◦ Both (type I)

◦ Another classification :
Type A – ascending aorta. Most lethal.
Type B – transverse or descending aorta.
 AORTIC DISSECTION
PREDISPOSING FACTORS

• HTN
• AORTIC ATHEROSCLEROSIS
• NON-SPECIFIC AORTIC ANEURYSM
• AORTIC COARCTATION
• COLLAGEN DISORDERS MARFANS SYNDROME
• FIBROMUSCULAR DYSPLASIA
• PREVIOUS AORTIC SURGERY CABG AV REPLACEMENT
• PREGNANCY(3RD, TRIMESTER)
• TRAUMA
• IATROGENIC
 AORTIC DISSECTION
CLINICAL FEATURES

• CENTRAL CHEST PAIN

• TEARING PAIN
• ABRUPT ONSET
• RADIATES TO BACK AND ARM
• COLLAPSE
• PT APPEARS TO BE IN SHOCK
• BP---NORMAL OR reduced
• ASYMMETRY OF PULSES
• ABSENT PERIPHERAL PULSES
• MI
• PARAPLEGIA(SPINAL)
• ACUTE ABDOMEN(MESENTERIC
CAELIAC)
• RENAL FAILURE
• ACUTE LIMB ISCHEMIA(LEGS)
Physical examination :
◦ Sinus tachycardia
◦ Cardiac tamponade (hypotension, pulsus paradoxus, pericardial rub)

Lab :
◦ CXR – widening of mediastinum.
◦ Confirm by CT, MRI and Transesophageal echocardiography
Treatment :
◦ Reduce cardiac contractility.
◦ Reduce hypertension.
◦ Maintain systolic BP 100-120 mmHg (sodium nitroprusside + beta
blocker)
**if contraindicated use verapamil

◦ Avoid direct vasodilator (hydralazine) increase shear stress.

◦ Type B can be medically stabilized by oral hypertensive.

 Respiratory causes of
chest pain

Pulmonary
1
embolism
Tension
2
pneumothorax

3 Pneumonia

4 Pleuritis or pleurisy
Pulmonary embolism
(venous thromboembolism)
◦ Cause : from venous thrombosis, clots break off and pass
through the veins and the right side of the lung.
◦ blood clot becomes lodged in a lung (pulmonary) artery, blocking
blood flow to lung tissue, causes SOB and increase HR.
◦ Inflammation of the tissue can cause pleuritic chest pain.
 Features of pulmonary
thromboembolism

◦ Clinical presentation varies,depending on

number,size & distribution of emboli.

Symptoms : acute breathlessness, pleuritic chest

pain, hemoptysis, dizziness, syncope.
Signs : pyrexia, cyanosis, tachypnoea, tachycardia,
hypotension, raised JVP, pleural
rub, pleural effusion.
Pneumothorax

◦ Definition: is when there is

air builds up in the pleural
sac, between the outside
of the lung and the inside
the chest wall. The air
can come from the lung
or from outside the body
if there is a chest injury.
Classification of
Pneumothorax
a) Based on general terms :
i. Closed – no opening from ext. chest ( in crashes, falls,
MVAs)
ii. Open – opening from external chest wall into pleura
(stabbing, gunshots)
iii. Tension
b) Based on origin :
i. Spontaneous - Primary
- Secondary
i. Iatrogenic – puncture or laceration of visceral pleural
during medical treatment.
Clinical Manifestations of
Pneumothorax
Symptoms Signs
sudden-onset Reduced expansion
unilateral pleuritic
chest pain
Dyspnea Hyperresonance
Diminished breath
sounds
Pleuritic chest Cyanosis
pain/pleurisy : Sharp
chest pain,
aggravated by
Tracheal Deviation
deep breathing or
coughing. On
examination, chest
expansion may be
Investigation
CXR-sharply defined
edge of the deflated
lung with complete
translucency(absenc
e of lung marking).It
also can show the
extent of any
mediastinal
displacement and
reveal any pleural
fluid or underlying
pulmonary disease.
CT scan-for small
pneumothorax that
CXR can miss exact
location
 Management
* depends on whether it is a primary or secondary
pneumothorax
◦ General mx : - high fowlers position
- O2 therapy if needed
- rest to decrease O2 demand
◦ Evacuate the air : - chest tube insertion
- surgery (thoracotomy)
◦ Promote pleural symphysis : - chemical or medication is
injected into
the chest cavity
- produces inflammatory reaction
between lungs and inner
chest cavity
 PNEUMONIA
DEFINITION:
◦ Acute lower respiratory tract illness associated with
fever, symptoms and signs in the chest.
◦ Pneumonia is also an inflammation of the
parenchyma of the lung.
◦ It is usually caused by bacteria but can also be
caused by viruses and fungi.
TYPES OF PNEUMONIA
CLINICAL FEATURES
1. Chest pain:
This is commonly pleuritic in nature and is due to
inflammation of pleura. A pleural rub may be heard
early on in this illness.
pain is usually at the mid chest.
 Sharp or stabby chest pain ( might feel it more when cough or take a
deep breath.)

2. Cough
3. Breathlessness
4. Fever
5. Extrapulmonary features:
◦ Myalgia, arthralgia and malaise are common,
particularly infections are caused by Legionella
and Mycoplasma.
6. Abdominal pain, diarrhea and vomiting are common.
Investigations
1. Full blood count
2. Blood C&S
3. Sputum culture and gram stain.
4. Pulse oximetry and ABG analysis
General management
ofpneumonia
1. Antibiotic – 3 gen. cephalosporin
rd

2. IV fluids – if dehydration, shock

3. Oxygen in Paco2
4. Bed rest with patient sitting up
5. Analgesia

Complication:
1. general:
◦ Respiratory failure
◦ Sepsis-multisystem failure

2. local:
◦ Pleural effusion
◦ Empyema
◦ Lung abscess
 PLEURISY / PLEURITIS
• The pleura becomes inflamed
• usually the lung slides along the chest wall
when a deep breath is taken.
• On occasion, viral infections can cause the
pleura to become inflamed
• Instead of sliding smoothly, the 2 linings
scrape each other, causing pain.
 GI causes of chest pain

1 GERD

2 Oesophageal spasm

3 Pancreatitis

4 Peptic ulcer
4 Oesophagitis

5 Mallory –Weiss syndrome

6 Hiatal hernia

7 Achalasia

7 Common bile duct obstruction

 Gastro-oesophageal reflux
◦ Is(GERD)
digestive disorder that affects the lower
esophageal sphincter(LES) lead to abnormal
reflux of gastric contents into the esophagus
causing mucosal damage.
◦ Often chronic and relapsing
Symptoms
1. Esophageal:
◦ Heartburn
◦ Dysphagia
◦ Odynophagia
◦ Regurgitation
◦ Belching

2. Extraesophageal:
◦ Cough
◦ Wheezing
◦ Hoarseness
◦ Sore throat
◦ Globus sensation
◦ Non-cardiac chest pain(NCCP)
(Burning pain behind the sternum associated with epigastric pain, dull in
nature or sharp and related to meals)
INVESTIGATIONS
◦ Barium swallow
◦ Endoscopy
◦ Ambulatory pH monitoring
◦ Impedance-pH monitoring
◦ Esophageal manometry
TREATMENT
NON-PHARMACOLOGICAL:
◦ Weight reduction if overweight
◦ Avoid clothing that is tight around the waist
◦ Modify diet – Eat more frequent but smaller meals – Avoid
fatty/fried food, peppermint, chocolate, alcohol, carbonated
beverages, coffee and tea, onions, garlic.
◦ Stop smoking
◦ Elevate head of bed 4-6 inches
◦ Avoid eating within 2-3 hours of bedtime

PHARMACOLOGICAL:
1. Antacid
2. Proton pump inhibitor
3. Histamine H2-Receptor Antagonists
4. Anti-reflux surgery
 Peptic Ulcer Disease
Pathophysiology:
1. H Pylori - increases acid
secretion
2. NSAIDs - impairs mucosal
defences
3. Smoking - Increase risk & cause
complication and slow healing of
ulcer
Clinical features:
1. Burning epigastric pain - patient can point the pain to the
epigastrium
2. Nausea & vomiting
3. Anorexia & weight loss
 Investigations:
1. Non invasive
• Serology
• C-urea breath tests
• Fecal antigen test

2. Invasive – biopsy
• Histology
• Rapid urease tests
• Microbiological culture
Management:
1. H. Pylori Eradication
2. General measures: Avoid smoking, NSAIDs, & aspirin should
be avoided
3. Maintenance treatment: Not needed in successful
eradication
4. Surgical treatment: partial gastrectomy
Complication:
◦ Perforation
◦ Gastric outlet obstruction: The presentation is with nausea,
vomiting and abdominal distension. Large quantities of gastric
content are often vomited, and food eaten 24 hours or more
previously may be recognised.
 Acute Pancreatitis:
Common causes:
1. Gallstones
2. Alcohol
3. Idiopathic
4. Post endoscope retrograde cholangio-
pancreatography (ERCP)
Clinical Features:
Typical Feature:
In severe case:
◦ Severe and constant upper abdominal • Hypoxic
pain of increasing intensity. • Grey Turner's sign
◦ Radiates to the back • Cullen's sign
◦ Associated with nausea and vomiting
◦ Epigastric tenderness
Investigations:
*Raised serum amylase
*Raised serum lipase
*U/S or CT – pancreatic swelling, gallstones,
biliary obstruction
*X-ray – to exclude other causes
Management:
1. Opiate analgesics should be given to treat pain and hypovolaemia
should be corrected using normal saline or other crystalloids.
2. Hyperglycaemia should be corrected using insulin, but it is not
usually necessary to correct hypocalcaemia by intravenous calcium
injection, unless tetany occurs.
3. Nasogastric aspiration is only required if paralytic ileus is present.
4. Enteral feeding, if tolerated, should be started at an early stage in
patients with severe pancreatitis because they are in a severely
catabolic state and need nutritional support
5. Patients who present with cholangitis or jaundice in association with
severe acute pancreatitis should undergo urgent ERCP to diagnose
and treat choledocholithiasis
 Esophageal Motility
Disorders
◦ Impaired esophageal motility occurs when the muscle contractions of
the esophagus (peristalsis) which is responsible for pushing food into
the stomach is either too weak or too strong, delayed or
uncoordinated.
◦ It may also be hampered by partial or complete obstruction of the
esophagus.
◦ In terms of slow motility, the ball of food (bolus) causes prolonged
stretching of the esophagus and this triggers pain.
◦ Some of the causes of impaired esophageal motility :-
- achalasia
- diffuse esophageal spasm
- esophageal cancer or compressions from surrounding structures
like the heart, aorta or tumors outside of the esophagus.
 Musculoskeletal causes of chest pain

1 Costochondritis

2 Trauma (Rib fracture,

intercostal muscle
injury )
 COSTOCHONDRITIS
• Acute inflammation of the costal cartilage.
• Associated with scoliosis, ankylosing spondylitis,
rheumatoid arthritis and infection of the costoternal
joint.
• CF : Pain/tenderness on the sides of the sternum,
worsened with coughing/deep breathing/exercise.
Severe inflammation associated with painful swelling is
referred to as TIETZE'S SYNDROME.
• Treated with NSAIDs (ibuprofen) or analgesics
(acetaminophen), opioids, TCA or corticosteroids if
patient is unresponsive to NSAIDs.
 Neurogical causes of chest pain

1 Herpes zoster (Shingles)

2 Thoracic outlet syndrome

 HERPES ZOSTER

 Shingles can present as acute

chest pain.
 The pain is usually burning
and unilateral, following the
dermatomes.
 Chest pain from Shingles can
occur before the onset of
vesicles thus making a
reliable diagnosis difficult.