Life Threatening Causes of

Chest Pain
By
Dr. Radwa Muhammad Ashour
Lecturer of Emergency Medicine
Patient 1 : Joe
Joe a 50-year-old male presents to the ED by ambulance
complaining the first time ever of severe chest pain that just
started while running on the treadmill. He immediately called
911. Vitals: BP = 140/90, P = 80, RR = 24, T = 98.3F, O2 sat =
98%.
Patient 2: Mary
Mary a 69-year-old female presents to the emergency department
via triage complaining of worsening shortness of breath, chest
and epigastric pain x 24 hrs. She has nausea/vomiting, weakness,
and fatigue. She “feels terrible.” Vitals: BP = 140/90, P = 80, RR
= 24, T = 98.3F, O2 sat = 98%.
Ches
t
 ILOS
Upon completion of this Lecture, you will be able to:

• Identify Life Threatening Causes of Chest Pain.

• Recognize Interpretation of Chest Pain.

• Explain Management of Acute Coronary Syndrome.

• Explain Management of Pulmonary Embolism.

What's Your
Greatest
Fear?
Life Threatening Causes
of Chest Pain
Life Threatening Causes of Chest Pain
Tension
Pneumothorax
DEATH

Aortic Dissection

Pulmonary
Embolism Acute coronary
syndrome
Pericardial
Tamponade
Mediastinitis e.g. Esophageal
Rupture (Hole)
Most Common Causes of
Chest Pain
 Most Common Causes of Chest Pain

Cardiac causes:
 Acute heart failure.
 Stable angina.
 Valvular heart disease: prolapse – stenosis.
 Pericarditis, myocarditis, and endocarditis.
 Arrhythmias.
 Most Common Causes of Chest Pain

Pulmonary causes:
 Infections: pneumonia.
 Asthma exacerbations.
 Pleural effusions.
Most Common Causes of Chest Pain

GIT causes:
 GERD.
 Esophageal rupture (Boerhaave's syndrome)
 Sliding hiatal hernia.
 Pancreatitis “referred”.
 Most Common Causes of Chest Pain

Musculoskeletal causes:
 Rib fractures.
 Intercostal muscle strains.
 Costochondritis
 Most Common Causes of Chest Pain

Psychiatric causes:
 Panic attack (diagnosis of exclusion).

Other conditions
 Herpes Zoster.
 Referred pain.
Interpretation of
Chest Pain
  Analyses of pain:
History
History
 Risk Factors of IHD:

Dyslipidemia Smoker
HTN Family History
DM Obesity

 Vitals  ECG
Examinatio
n  Monitor Investigation
 CXR
 IPPA
 Acute
Coronary
Syndrome
 Acute Coronary
Syndrome
ST-elevation MI Non-ST-elevation
(STEMI) ACS (NSTE-ACS)

Non-ST-elevation myocardial infarction Unstable

(NSTEMI). angina
W h e n to
ex c l u d e
A C S i n
E D?
Rule out
ACS:

 If serial troponins are negative and

 HEART score low ≤ 3

 Score 0-3: Discharge Home

 Score 4-6: Admit for Clinical Observation

 Score 7-10: Early Invasive Strategies

Acute Myocardial Infarction (4th Universal Definition of
MI)
1. Detection of a rise and/or fall of cTn +

2. At least one value above the 99th percentile +

3. At least one of the following: (1 of 5)

 Symptoms of acute myocardial ischemia.

 New ischemic ECG changes.

 Development of pathological Q waves.

Acute Myocardial Infarction (4th Universal Definition of
MI)
1. Detection of a rise and/or fall of cTn +

2. At least one value above the 99th percentile +

3. At least one of the following: (1 of 5)

 Imaging: new loss of viable myocardium or new SWMA.

 Identification of a coronary thrombus: by angiography or

by autopsy.
 Clinical
Presentation
1. Typical Presentation:

Chest Pain: SOCRATES

 Central retrosternal chest pain.

 Radiates to the arms, neck, or jaw.

 Sudden Onset, constant chest pain.

 Clinical
Presentation
1. Typical Presentation:

Chest Pain: SOCRATES

 Associated symptoms: sweating, nausea, vomiting, and

breathlessness.

 Similar to previous angina pectoris but is much more

severe, longer duration and unrelieved by GTN.

 Clinical
Presentation
2. Atypical Presentation: (common 1/3 patients)

Have a high level of suspicion

A. Shortness of breath without chest pain.
B. Epigastric abdominal pain or indigestion.
C. Fatigue or generalize weakness.
D. Mental status change - Collapse or syncope .
Be especially suspicious in: older, ♀, DM, Heart Failure.
 Examination

Direct examination towards searching for complications and

excluding alternative diagnoses.

1. Monitor: BP – HR – ECG Monitor (arrhythmia or

cardiogenic shock).

2. Listen to the heart (murmurs or third heart sound).

3. Listen to the lung fields (LVF, pneumonia, pneumothorax).

 Examination

4. Check peripheral pulses (aortic dissection).

5. Check legs for evidence of deep vein thrombosis (DVT) (PE).

6. Palpate for abdominal tenderness or masses (cholecystitis,

pancreatitis, perforated peptic ulcer).

 ECG Changes

The 12-lead ECG, which should be acquired and interpreted

within 10 minutes of arrival to a medical facility

Normal ECG on arrival doesn’t rule out MI.

If the initial ECG is normal, but symptoms are suspicious, repeat

the ECG after 15min and re- evaluate

Review old ECGs for comparison.

 ECG Changes
1. STEMI:
• ST elevation in ≥ 2 contiguous leads.
+/-
• Reciprocal ST-segment depression.
 ECG Changes
1. STEMI:
 ECG Changes
2. STEMI ECG Changes Over Time:
 ECG Changes

3. NSTEMI/UA:

• ST depression: New horizontal or down-sloping ≥ 0.5 mm

in 2 contiguous leads.

• T wave inversion: ≥ 1 mm in 2 contiguous leads with

prominent R wave or R wave > S wave.

 ECG Changes
4. Localization of MI:
 ECG Changes
4. STEMI Equivalent:

ST Elevation > 0.5mm V7-8-9

T wave
Pathological Q
Inversion
 ECG Changes
4. STEMI Equivalent: • Pathological R
• ST depression
• Upright T wave
A. Posterior MI
 Cardiac Markers

1. Troponin T (cTnT) and troponin I (cTnI):

 Proteins virtually exclusive to cardiac myocytes.

 ↑↑ within 2-3 h and normalize within 7 days.

2. CK-MB:

 The best alternative.

 ↑↑ within 2 h and normalize within 2 days.

 Management of
STEMI
1. ABCDE Approach.

2. Time = Muscle.

3. Monitor – Defibrillator.
 Management of
STEMI

4. MONA: M: Morphine Sulfate:

 Dose: 1-5 mg IV / 5 min “Max: 30 mg”

 ↓ Pain - ↓ Anxiety - ↓ Preload

 Avoid NSAID – Selective Cox II inhibitor.

O: Oxygen:

 Give O2 if needed maintain oxygen 94-98%.

 Management of
STEMI

4. MONA: N: Nitroglycerin:

 Dose: 0.4 mg SL or PO / 5 min “Max: 3 times” / 5-200

μg/min IVI.

 Avoid in hypotension, suspecting right ventricular

infarction, if phosphodiesterase inhibitor taken within 24

 Management of
STEMI

4. MONA: A: Antiplatelets: (DUAL)

 Aspirin: loading dose 300mg.

 P2Y12 receptor inhibitor: any of

a) Ticagrelor: loading dose 180mg PO.

b) Clopidogrel: loading dose 300-600 mg PO.

 Management of
STEMI

4. MONA: A: Anticoagulants

 Unfractionated heparin (UFH): 60 IU/kg (max 5000 IU). “if

PCI is likely”

 Enoxaparin: 30 mg IV bolus. “in Fibrinolytics not followed by PCI”

 Fondaparinux: 2.5mg SC “in Fibrinolytics not followed by PCI”.

 Management of
STEMI
Primary PCI
5. Reperfusion Therapy: (Door to Balloon 60-90 min)

 STEMI + Ischemic symptoms onset < 12 h.

 STEMI + Ischemic symptoms onset > 12 h + one of

“Cardiogenic Shock – hemodynamic instability - Heart

Failure – ongoing ischemia - life-threatening arrhythmia”.

 Management of
STEMI
Primary PCI
5. Reperfusion Therapy: (Door to Balloon 60-90 min)

 STEMI + evidence of failed reperfusion after fibrinolytic

therapy (Rescue PCI)

 Management of
STEMI
Fibrinolytic
5. Reperfusion Therapy: (Door to Needle 30 min)

 Primary PCI is not immediately available +

 Delay from hospital presentation to PCI is anticipated to be

> 120 minutes.

 Management of
STEMI
Fibrinolytic
5. Reperfusion Therapy: (Door to Needle 30 min)

 35% have failed reperfusion.

 10% have ineffective reperfusion.

 Management of
STEMI
Fibrinolytic
5. Reperfusion Therapy: (Door to Needle 30 min)

 Alteplase:

a) > 67 kg: 15 mg IV bolus - 50 mg over 30 min - 35 mg over 60

min.

b) < 67 kg: 15 mg IV bolus – 0.75 mg/kg over 30 min – 0.5 mg/kg

 Management of
STEMI
Fibrinolytic
5. Reperfusion Therapy: (Door to Needle 30 min)

 Streptokinase: 1.5 million IU over 60 min

 Management of
STEMI

6. Betablocker:

 Metoprolol tartrate “25 mg PO” - Atenolol.

 Avoid in signs/at risk of heart failure or signs of

hemodynamic compromise, bradycardia, or severe reactive

airway disease.
 Management of NSTE-
ACS
1. ABCDE Approach.

2. Monitor – Defibrillator.

3. MONA:

 M: Morphine Sulfate.  A: Antiplatelets: (DUAL)

 O: Oxygen.  A: Anticoagulants

 N: Nitroglycerin.
 Management of NSTE-
ACS

4. Reperfusion Therapy: PCI

 In all patients within 72 h.

 Immediate within 2 h if: Malignant ventricular arrhythmias –

Hemodynamic instability – Severe chest pain – severe heart failure.

 Early within 24 h if: High risk TIMI ≥ 4 – High Troponin –

Dynamic ECG changes – STE not meeting STEMI.

 Management of NSTE-
ACS

4. Reperfusion Therapy: PCI

 within 25-72 h if: Intermediate risk TIMI 2-3 – Recurrent angina

despite therapy – EF < 40% in DM, Renal insufficiency, Prior

CABG, PCI within 6 months.

5. Betablocker: avoid IV
Pulmonary
Embolism
 Pulmonary Embolism

Hemodynamically Hemodynamically
Stable Unstable

 Cardiac arrest.

 Obstructive shock.

 Persistent hypotension.
 Clinical
Presentation
Typical Presentation:  Tachycardia.

 Dyspnea.  Tachypnoea.

 Syncope with cyanosis.  Pyrexia following lung infarction.

 Chest Pain: pleuritic.  30% of all patients with PE have

 Hemoptysis. normal SpO2.

Always consider PE in patients with unexplained hypoxia or
 Assess Clinical Probability of
PE
Modified Wells Score for PE
Signs of DVT (minimum of objective leg swelling & tenderness) 3

PE is the most likely diagnosis 3

HR >100 1.5

Prior PE or DVT diagnosis 1.5

Immobilization > 3 days or surgery (within 4 weeks) 1.5

Active Cancer 1
 Investigation

ECG:

 Sinus tachycardia “most common”

 Non- specific ST- / T wave changes in anterior chest leads.

 The classical changes of acute corpulmonale: S1Q3T3,

RAD, or RBBB.

 Less common: atrial flutter or AF.

 Investigation

1. Laboratory Investigation

 ABG:

 Hypoxemia “↓ PaO2 - ↓ SaO2”.

 Respiratory alkalosis “↓ PaCO2” (due to tachypnoea)

 Metabolic acidosis (due to shock).

 Investigation

 CBC:

 Leukocytosis

 Cardiac Enzymes:

 Mildly elevated CK, troponin.

 Kidney Function Test.

 Investigation

2. Radiological Investigation

 CXR:

 Focal pulmonary oligemia

(Westermark’s sign)
 Investigation

 CXR:

 Palla’s Sign.

 Hampton's Hump.

 Normal CXR + severe respiratory compromise =

highly suggestive of PE.
 Investigation

 Echocardiography: (Exclude other causes)

 RV dilatation.

 Global hypokinesia, with apical sparing (McConnell’s sign).

 PA dilatation.

 Tricuspid/ pulmonary regurgitation.

 Thrombus in the PA may be visible.

 Investigation

 Duplex venous system

 Diagnostic Imaging

 CT pulmonary angiography (CTPA)

 Ventilation– perfusion (V/ Q) scanning.

 Pulmonary Embolism
Severity
Simplified pulmonary embolism severity index (PESI) score
Pulmonary Embolism
Severity
Management
 Management

 In patients with high or intermediate clinical probability of

PE, while diagnostic workup is in progress.

 LMWH or fondaparinux is recommended (over UFH) for

most patients.
 Management

 Enoxaparin: 1 mg/kg/12 h or 1.5 mg/kg/24 h. (SC)

 Fondaparinux: 5 mg (< 50kg) – 7.5 (50-100 kg) – 10 mg (>

100 kg) / 24 h. (SC)

 Unfractionated heparin: 80 units/kg bolus, then 18

units/kg/h.
 Management

 High-risk pulmonary embolism: (unstable)

Reperfusion “Fibrinolytics”:

 Streptokinase: 250000 IU loading over 30 min, then 100000

IU/h over 12-24 h. (Accelerated: 1.5 million IU over 2 h)

 rtPA: 100 mg over 2 h. (Accelerated: 0.6 mg/kg over 15

min (maximum 50 mg)

 Management

 Intermediate-risk pulmonary embolism

 Anticoagulation Therapy (either parenteral or oral).

 Management

 Treatment of RV Failure:
 Management

 Low-risk pulmonary embolism

 Early Discharge.

 Continuation of Anticoagulant Therapy.

 Consider if “Low risk - No conditions need hospitalization

- Proper outpatient care”

 Management

 Low-risk pulmonary embolism

 Rivaroxaban (Xarelto®): 15 mg BID for 21 d, then 20 mg/d.

 Apixaban (Eliquis®):10 mg BID for 7 days, then 5 mg BID.

 Dabigatran (Pradaxa®): 150 mg BID “require heparin

for 5–10 d”
Any Question?

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10
 Summary

 Life Threatening Causes of Chest Pain: DEATH = Dissection – Embolism – ACS –

Tension Pneumothorax – Tamponade – Hole “Mediastinitis”.

 Interpretation of Chest Pain: Analysis of pain – risk factors of IHD – examination

to exclude life-threatening causes – investigations including ECG & CXR.

 Exclude ACS if: low HEART score – negative serial troponin.

 Acute coronary syndrome: including STEMI – NSTE-ACS.

 Summary

 4th Universal Definition of MI: Detection of a rise and/or fall of cTn. + At least one

value above the 99th percentile. + At least one of the following: (Symptoms of acute

myocardial ischemia - New ischemic ECG changes - pathological Q waves –

Imaging of new loss of viable myocardium or new SWMA - Identification of

coronary thrombus).

 Typical Presentation of ACS: Sudden Onset - central retrosternal chest pain -

Radiates to the arms, neck, or jaw – associated with nausea, sweating.

 Summary

 STEMI: STE ≥ 1 mm in ≥ 2 contiguous leads except V2, V3.

 NSTE-ACS: STD ≥ 0.5 mm or TW inversion ≥ 1 mm in ≥ 2 contiguous leads.

 Management of ACS: ABCDE – Monitor – MONA – Reperfusion.

 Diagnosis of PE depending on: Hemodynamics – TTE - PE probability using Wells

Score – D Dimer – CTPA.

 PE severity depending on: Hemodynamics – PESI score – RV function – Troponin.

 Summary

 High risk PE: TTT with reperfusion.

 Intermediate risk PE: TTT with anticoagulants.

 Low risk PE: Discharge – oral anticoagulants.

Thank
You