Chest Pain Dr. Mohannad F Allehyani Emergency Medicine Demonstrator KAUH – Faculty of Medicine

Chest Pain

Dr. Mohannad F AllehyaniEmergency Medicine Demonstrator

KAUH – Faculty of Medicine

Goals

Review the pathophysiology, diagnosis and treatment of life

threatening causes of chest pain.

Epidemiology

5% of all ED visits

Approximately 5 million visits per year

Visceral Pain

Visceral fibers enter the spinal cord at several levels leading to poorly localized,

poorly characterized pain. (discomfort, heaviness, dull, aching)

Heart, blood vessels, esophagus and visceral pleura are innervated by visceral

fibers

Because of dorsal fibers can overlap three levels above or below, disease of thoracic

origin can produce pain anywhere from the jaw to the epigastrum

Parietal Pain

Parietal pain, in contrast to visceral pain, is described as

sharp and can be localized to the dermatome superficial to the site

of the painful stimulus.

The dermis and parietal pleura are innervated by parietal fibers.

Initial ApproachABC’s first, always (look for conditions

requiring immediate intervention)

Aspirin for potential ACS

EKG

Cardiac and vital sign monitoring

Pain relief

Because of the wide differential, H+P will guide the diagnostic workup

History

O- onset

P-provocation /palliation

Q- quality/quantity

R- region/radiation

S- severity/scale

T- timing/time of onset

History

Change in pain pattern

Associated symptoms: DOE, SOB, diaphoresis, vomiting, heart

burn, food intolerance

PHx

Social history

FHx

Physical ExamGeneral Appearance and Vitals (sick vs

not sick)

Chest exam-Inspection (scars, heaves, tachypnea,

work of breathing)-Auscultation (murmurs, rubs, gallops,

breath sounds)-Percussion (dullness)

-Palpation (tenderness, PMI)

Physical Exam

Neck: JVD, crepitence, bruits

Abdomen

Extremities: swelling, pulses, tenderness, Homan’s

Cardiovascular Acute myocardial infarction,  Acute coronary ischemia,  Aortic dissection,  Cardiac tamponade, Unstable angina, Coronary spasm, Prinzmetal's angina, Cocaine induced, Pericarditis, Myocarditis,  Valvular heart disease,  Aortic stenosis,  Mitral valve prolapse,  Hypertrophic cardiomyopathy

Pulmonary Pulmonary embolus,  Tension pneumothorax, Pneumothorax,  Mediastinitis, Pneumonia,  Pleuritis,  Tumor, Pneumomediastinum

Gastrointestinal Esophageal rupture (Boerhaave), Esophageal tear (Mallory-Weiss),  Cholecystitis,  Pancreatitis, Esophageal spasm,  Esophageal reflux,  Peptic ulcer,  Biliary colic

Musculoskeletal Muscle strain,  Rib fracture,  Arthritis, Tumor,  Costochondritis,  Nonspecific chest wall pain

Neurologic Spinal root compression,  Thoracic outlet,  Herpes zoster,  Postherpetic neuralgia

Other Psychologic,  Hyperventilation

Differential Diagnoses

Life Threatening Causes of Chest Pain

Acute Coronary Syndromes

Pulmonary Embolus

Tension Pneumothorax

Aortic Dissection

Esophageal Rupture

Pericarditis with Tamponade

Acute Coronary Syndromes - Epidemiology

In a typical ED population of adults over the age of 30

presenting with visceral-type chest pain, about 15 percent will

have AMI and 25 to 30 percent will have UA

Acute Coronary Syndromes - History

“Typical” Chest Pain Story (Pressure-like, squeezing, crushing pain, worse with

exertion, SOB, diaphoresis, radiates to arm or jaw) The

majority of patients with ACS DO NOT present with these

symptoms!

Cardiac Risk Factors (Age, DM, HTN, FH, smoking,

hypercholesterolemia, cocaine abuse)

Acute Coronary Syndromes – EKG Findings

STEMI - ST segment elevation (>1 mm) in contiguous leads;

new LBBB

T wave inversion or ST segment depression in contiguous leads

suggests subendocardial ischemia

5% of patients with AMI have completely normal EKGs

Marker Initial Rise

Peak Return to normal

Benefits

Troponin 2-4 hr 10 -24 hr 5 -10 days Sensitive and specific

CK-MB 3-4 hr 10-24 hr 2 – 4 days Unaffected by renal failure

LDH 10 hr 24 -72 hr 14 days

Myoglobin 1-2 hr 4 -8 hr 24 hours Very sensitive, powerful negative predictive value

Acute Coronary Syndromes – Cardiac Markers

Acute Coronary Syndromes – Cardiac Markers

Echocardiogram

Wall abnormalities occur within minutes

Will detect abnormalities in 80% of AMI

Normal resting echo in setting of chest pain gives low probability

Early screen for AMI complications: aneurysms, valve

abnormalities, other structural destruction

Echo

Acute Coronary Syndromes - Treatment

AspirinNitroglycerin

OxygenAnalgesia

Treatment

Beta-BlockersAnticoagulation

Anti-Platelet AgentsThrombolysis

Percutaneous Coronary Interventions (PCI)

Stress echocardiograms

Sensitivity 60-90%

Specificity 75% ?

Should be employed with moderate to high risk

stratification

Limitations of reader, image quality, and previous functional

impairment

Negative test has time limited value

Acute Coronary Syndromes - Treatment

STEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation,

thrombolysis, PCI)

NSTEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation,

PCI)

Unstable Angina (ASA, B-blocker, NTG, anticoagulation, risk

stratification)

Acute Coronary Syndromes - Disposition

Mortality is twice as high for missed MI

Missed MI is the most successfully litigated claim

against EP's. EP’s miss 3-5% OF AMI, this accounts for 25% of

malpractice costs against EP’s

Acute Coronary Syndromes - Disposition

A single set of cardiac enzymes is rarely of use

Risk Stratification: goal is to predict the likelihood of an

adverse cardiovascular eventCombination of H+P, EKG,

BiomarkersNo single globally accepted

algorithmMathematical models such as TIMI, GRACE, PURSUIT, and

HEART can be helpful but are no substitute for clinical judgment

Pulmonary Embolism - Pathophysiology

Thrombosis of a pulmonary artery

>90% arise from DVT

Clot from a DVT travels through the venous system and lodges in

the pulmonary vasculature creating a ventilation/perfusion

mismatch

Pulmonary Embolism – History

Dyspnea is the most common symptom, present in 90% of

patients diagnosed with PE

Sharp pleuritic chest pain, syncope,

Prolonged immobilization, neoplasm, known

hypercoagulable disorder

Pulmonary Embolism – Physical Exam

Tachycardia, tachypnea, diaphoresis, hypotension,

hypoxia, low grade fever, anxiety, cardiovascular collapse, right

ventricular heave

Pulmonary Embolism – Diagnostic Testing

Sinus Tachycardia is the most frequent EKG finding

Classic S1,Q3,T3 finding is seen in less than 20%

ABG plays no role in ruling out PE

D-Dimer in a low risk patient can be used to rule out PE

Pulmonary Embolism – Wells Criteria

Clinical Signs and Symptoms of DVT? Yes +3PE is #1 Diagnosis, or Equally Likely? Yes +3

Heart Rate > 100? Yes +1.5Immobilization at least 3 days, or Surgery in the

Previous 4 weeks? Yes +1.5Previous, objectively diagnosed PE or

DVT? Yes +1.5Hemoptysis? Yes +1

Malignancy w/ Treatment within 6 mo, or palliative? Yes +1

<2 = Low risk, 2.5-6 = moderate risk, >6 = high risk

Pulmonary Embolism – Diagnostic Imaging Algorithm

Pulmonary Embolism – Treatment/Disposition

Unfractionated heparin vs low molecular weight heparin (some

studies suggest superiority of LMWH)

Thrombolysis (for cardiovascular collapse)

Floor vs ICU

PE CXR

Aortic Dissection - Pathophysiology

Intimal tear of the aorta leads to dissection of the layers of the aorta

creating a false lumen

Aortic Dissection - Diagnosis

Tearing chest pain radiating to the back

Risk Factors: HTN, connective tissue disease

Exam: HTN, pulse differentials, neuro deficits

Radiology: Wide mediastinum on CXR, CT angio chest, echo

Aortic Dissection - Classification

De Bakey system: Type I dissection involves both the ascending and

descending thoracic aorta. Type II dissection is confined to the ascending aorta. Type III dissection is confined to

the descending aorta.

The Daily system classifies dissections that involve the ascending aorta as type

A, regardless of the site of the primary intimal tear, and all other dissections as

type B.

Aortic Dissection - Treatment

Patients with uncomplicated aortic dissections confined to the descending thoracic aorta (Daily

type B or De Bakey type III) are best treated with medical therapy.

Medical Therapy: Goal to decrease the blood pressure and the velocity of left ventricular

contraction, both of which will decrease aortic shear stress and minimize the tendency to further

dissection. Acute ascending aortic dissections (Daily type A or

De Bakey type I or type II) should be treated surgically whenever possible since these patients

are a high risk for a life-threatening complication such as aortic regurgitation, cardiac tamponade, or

myocardial infarction.

Tension Pneumothorax - Pathophysiology

Collection of air in the pleural space causes collapse of the

ipsilateral lung and then cardiovascular collapse as

intrathoracic pressures increase.

Tension Pneumothorax - Diagnosis

 Risk factors: COPD; connective tissue disease, trauma, recent

instrumentation, positive pressure ventilation

Absent breath sounds unilaterally, hypotension,

distended neck veins, tracheal deviation

Tension Pneumothorax - Treatment

Needle decompression

Tube thoracostomy

Esophageal Rupture - Pathophysiology

Tear in the esophagus leads to leaking of gastrointestinal

contents into the mediastinum

Inflammation followed by infection cause rapid

deterioration, sepsis and death

Esophageal Rupture - Diagnosis

Rare but devastating

Risk Factors: Iatrogenic, heavy retching, trauma, foreign bodies,

toxic ingestion

Radiology: Mediastinal air on plain films or CT scan

Subtle

Not so subtle

Imaging

Esophageal Rupture - Treatment

Antibiotics

Supportive Care

Small tears with minimal extraesophageal involvement can

be managed conservatively

Surgical consult for all regardless of size

Take Home Points

ABC’s first

History is key

Have a low threshold for missed MI