Approach to chest pain

Dr R. Lamour
 Overview
 Why is chest pain important?
 Differential diagnosis of chest pain
 Types of chest pain
 Acute coronary syndrome:
 Definition
 Epidemiology
 Risk factors
 Mechanisms of myocardial injury
 Pathophysiology
 History
 Physical examination
 Investigations
 Management
 Complications
 Aortic dissection
 Pulmonary embolus
 Tension pneumothorax
 Pericardial tamponade
 Mediastinitis
 Other common causes of chest pain
 References
 Why is chest pain important?
 Chest pain accounts for approximately 7,6 million
visits to the ED in the US annually
 Second most common complaint in the ED
 It is important to recognise signs and symptoms
distinguishing life threatening causes of chest pain
from non-life threatening causes of chest pain
 There are patients which present with life threatening
causes pf chest pain, but appear deceptively well
 Discussion: common causes of chest pain and
recognition and management of ACS
 DDx of chest pain
 Life threatening causes:
 Acute coronary syndrome
 Acute aortic dissection
 Pulmonary embolism
 Tension pneumothorax
 Pericardial tamponade
 Mediastinitis (eg. oesophageal rupture)
 Types of chest pain
 Cardiac origin:
 Angina: retrosternal chest
discomfort/tightness/pressure due to heart
muscle hypoperfusion, radiating to neck
shoulder or arm (mainly left arm)
 Stable vs Unstable Angina
Stable Angina Unstable Angina
 Occur during  Pain at rest or
physical exertion minimal activity
 Pain lasting 5-  Pain lasting
15minutes >20minutes
 Relieved by rest or  Pain more severe
SL nitrates within 3- than stable angina
5minutes  Pain occurring with
increased frequency
 Types of chest pain
 Characteristics of non-ischaemic chest
pain
 Pleuritic pain, sharp or knife-like pain related to respiratory
movements or cough
 Primary or sole location in the mid or lower abdominal region
 Any discomfort localized with one finger
 Any discomfort reproduced by movement or palpation
 Constant pain lasting for days
 Fleeting pains lasting for a few seconds or less
 Pain radiating into the lower extremities or above the
mandible
 Examples of non-ischaemic
causes of chest pain
 Pleurisy: sudden and intense sharp, stabbing, or burning pain
in the chest when inhaling and exhaling
 Stent chest pain: sharp and localised not related to physical
activity, post-coronary artery stent placement.
 Pericarditis pain: pain that is worse when supine and relieved
when leaning forward, It is also worse on inspiration
 GERD chest pain: burning in nature, worse after eating
 Anxiety-related chest pain: non-specific but often over
exaggerated with near normal vital signs
Acute Coronary Syndrome
 Definition
 Acute coronary syndrome:
 ACS is the umbrella term for clinical signs and
symptoms of myocardial ischemia
 It consists of:
 Unstable Angina – No ST elevation and normal troponin
blood levels
 Non-ST segment Elevation myocardial infarction (NSTEMI)
– No ST elevation but raised troponin blood levels
 ST segment Elevation Myocardial infarction (STEMI) – ST
elevation with raised blood troponin levels
 Important to note: stable angina does not form part
of ACS
 Epidemiology
 In the 2022 Journal of the American Heart Disease
Association, a systematic review was done, focussing on ACS
in Sub-Saharan Africa
 Epidemiology
 In the 2022 Journal of the American Heart Disease Association,
a systematic review was done, focussing on ACS in Sub-
Saharan Africa
 Sharp increase in ACS in recent years
 Reasons attributed to:
 Uncontrolled cardiovascular risk factors
 Rapid urbanisation
 Changes in lifestyle and diet
 Aging population
 1 of 3 leading causes of death in Sub-Saharan Africa
 Increase in health expenditure
 Epidemic of Coronary Heart Disease was declared 30 years
ago
 Epidemiology
 According to the 2016 Heart Disease and
Stroke Statistics update of the American
Heart Association (AHA)
 The prevalence of MI is higher in men than
women
 Age 40 years - the lifetime risk of developing
CHD was 49% in men and 32% in women
 Age 70 years - the lifetime risk was 35% in men
and 24% in women
 Risk Factors
 Modifiable factors
 Dyslipidemia/diet
 Physical inactivity
 Cigarette smoking
 Alcohol
 Obesity
 Diabetes Mellitus
 Hypertension
 Metabolic Syndrome
 PVD
 Recent cocaine use or other sympathomimetic
 Risk Factors
 Non-modifiable factors
 Age >65
 Male
 Family history of CHD
 Previous history of ACS
 Mechanisms of myocardial
injury
 Decreased oxygen supply to the
myocardium
 Coronary artery occlusion:
 Decreased coronary artery perfusion pressure

 Increased myocardial oxygen demand

 Pathophysiology
 Atherosclerosis is present in most patients with ACS
 Early manifestations include fatty streaks and intimal
thickening of the coronary arteries
 A more advanced plaque is called pathological intimal
thickening which is characterised by extracellular lipid
pools containing proteoglycans without necrosis
 Many histological characteristics are seen on post-
mortems
 Most importantly, early calcifications are observed in
areas of lipid pools and death of smooth musculature
 Pathophysiology cont.
 Plaque rupture
 Most ACS results from the loss of integrity of the
protective covering of the plaque covering
 This occurs with plaque rupture when the fibrous cap
overlying the plaque gets disrupted or with erosion when
the endothelial lining of the plaque is disturbed
 This disruption of the protective covering allows blood to
come in contact with the highly thrombogenic contents of
the necrotic core (including tissue factor)
 At the rupture site, a thrombus forms and occlusion of the
coronary artery occurs
 Pathophysiology cont.
 Sometimes ACS can be secondary to vasospasm
with or without underlying atherosclerosis
 The result of coronary artery occlusion or
vasospasm > decreased blood flow to a part of
heart musculature > ischemia > infarction of that
part of the heart
 Diagnosis of ACS

History
 Physical examination
 Investigations
 Management
 Complications
 Symptoms of ACS
 Angina pectoris (cardiac chest pain)
 Nausea and vomiting
 Shortness of breath/orthopnea/PND (symptoms of acute
heart failure)
 Palpitations
 Anxiety
 Sudden collapse
 Epigastric pain(atypical presentation)
 Symptoms of ACS – atypical
presentation
 Vague symptoms in elderly, pregnant or diabetic
patients
 Dizziness
 Syncope
 Confusion
 Symptoms of peripheral emboli
 Unexplained hypotension
 These symptoms may represent silent ischemia
without chest pain
 Patients can present with atypical or pleuritic chest
pain
 Diagnosis of ACS
 History

 Physical examination
 Investigations
 Management
 Examination of a patient with
ACS
 Responsiveness, airway, breathing, circulation
 Evidence of systemic hypoperfusion – impending cardiogenic shock
 Hypotension
 Tachycardia
 Impaired cognition
 Cool, clammy, pale
 Signs of acute heart failure
 Raised JVP
 Bibasal pulmonary crackles
 Hypotension
 Tachycardia
 New S3
 New or worsening MR
 Focused neurological examination
 GCS
 Focal neurological fallout or cognitive deficits
 Any contraindication to thrombolytic therapy
 Diagnosis of ACS
 History
 Physical examination

Investigations
 Management
 Investigations

 ECG – NB! NB! NB!

 Cardiac biomarkers
 Blood work up
 Chest X-ray
Normal ECG – no ischaemic
changes
 ECG in ACS
 Clinicians must be aware that the initial ECG is often not diagnostic
in patients with ACS
 41% percent of patients with NSTEMI do not have the typical ST-
depression or T-wave inversion
 In patients at intermediate to high risk for ACS without a clear
diagnosis, ECGs should be repeated at frequent intervals until the
patient's chest pain resolves or a definitive diagnosis is made
 The ECG should be repeated at least every 15 to 30 minutes
 Patients whose repeat ECGs are diagnostic for or strongly suggestive
of either STEMI or NSTEMI should be managed for those diagnoses
 Some clinicians assume that an ECG obtained while the patient is
experiencing chest pain that fails to show evidence of ischemia rules
out the possibility of ACS – this is a false statement
 ECG in ACS: STEMI
 New or presumed new ST elevation at the J
point in two anatomically contiguous leads
using the following diagnostic thresholds:
 ≥0.1 mV (1 mm) in all leads other than V2 to V3,
where the following diagnostic thresholds apply:
 ≥0.2 mV (2 mm) in males ≥ 40 years
 ≥0.25 mV (2.5 mm) in males <40 years
 ≥0.15 mV (1.5 mm) in females
ECG in ACS: STEMI
12 lead ECG in ACS: STEMI
12 lead ECG in ACS: STEMI
 12 lead ECG in ACS: STEMI
Anterior wall STEMI: Two or more of the
precordial leads (V1 to V6)
 12 lead ECG in ACS: STEMI
Anteroseptal STEMI: Leads V1 to V3
 12 lead ECG in ACS: STEMI
Apical or lateral STEMI: Leads aVL and I,
and leads V4 to V6
 12 lead ECG in ACS: STEMI
Anterolateral STEMI
 12 lead ECG in ACS: STEMI
Inferior STEMI: Leads II, III, and aVF
ECG in ACS: Right Ventricle
MI
In patients with inferior STEMI, right
ventricular infarction is suggested by:
 ST elevation in V1
 ST elevation in V1 and ST depression in V2
(highly specific for RV infarction)
 Isoelectric ST segment in V1 with marked ST
depression in V2
 ST elevation in III > II
Diagnosis is confirmed by the presence
of ST elevation in the right-sided leads
(V3R-V6R)
ECG in ACS: Right Ventricle
MI
ECG in ACS: Right Ventricle
MI
ECG in ACS: Posterior MI
12 lead ECG in ACS: Posterior MI
 Septal precordial leads (V1 to V2) and
posterior precordial leads
 Posterior STEMI suggested by:
 Prominent R waves in V1 and V2
 T-wave depressions in leads V1 and V2
ECG in ACS: Posterior MI
 ECG in ACS: NSTEMI
 New or presumed new horizontal or down-sloping
ST depression ≥0.05 mV (0.5 mm) in two
anatomically contiguous leads and/or

 T wave inversion ≥0.1 mV (1 mm) in two

anatomically contiguous leads with prominent R
wave or R/S ratio >1
12 lead ECG in ACS: NSTEMI
12 lead ECG in ACS: NSTEMI
ECG: other things to look out for
 New LBBB
 New LBBB with T-wave inversions
 Pathological Q-waves – late
presentation or old MI
ECG in ACS: New LBBB
 ECG in ACS: Existing BBB
and new MI
 RBBB does not usually interfere with the diagnosis of an
acute ST-elevation MI (STEMI)
 The reason is that MI most often involves the left ventricle
(LV) and therefore affects the initial phase of ventricular
depolarization, sometimes producing abnormal Q waves
 In contrast, RBBB primarily affects the terminal phase of
ventricular depolarization, producing a wide R' wave in the
right chest leads and a wide S wave in the left chest leads
 These changes are due to delayed depolarization of the RV,
while depolarization of the LV is not substantially affected
 ECG in ACS: Existing RBBB
and new MI
 There may be some diagnostic difficulties in interpreting the
ECG in patients with RBBB who have a non-ST-elevation MI
 RBBB is typically associated with secondary ST-T changes
due to abnormal RV repolarization
 This leads with an R' wave (leads V1, V2, and sometimes V3)
will show T-wave inversions
 In contrast, ST depressions or T-wave inversions in leads with
a terminal S wave (leads V5 and V6) cannot be attributed to
the RBBB alone
 Such ST-T changes may be due to ischemia or non-ST-
elevation MI, or to other factors such as drug effects (digoxin)
or electrolyte abnormalities, such as hypokalemia
 ECG in ACS: Existing LBBB
and new MI and pacing
 Sgarbossa criteria applies:
 The three original ECG criteria with independent value in the
diagnosis of acute infarction and the score for each were:
 ST-segment elevation of ≥1 mm in the same direction as the QRS
complex (concordant) in any lead: score 5.
 ST-segment depression of ≥1 mm in any lead from V1 to V3:
score 3.
 ST-segment elevation of 5 mm or more that is discordant with the
QRS complex (ie, associated with a QS or rS complex): score 2
 Cabrera sign: prominent (about 0.05 s in duration) notching in
the ascending limb of the S wave in leads V3 and V4
 Chapman’s sign: prominent notching of the ascending limb of
the R wave in lead V5 or V6
ECG in ACS: existing LBBB
with new MI and pacing –
Sgarbossa criteria
ECG in ACS: existing LBBB
with new MI and pacing –
Modified Sgarbossa criteria
ECG in ACS: existing LBBB
with new MI – Cabrera’s sign
 Investigations
 ECG

 Cardiac biomarkers
 Blood work-up
 Chest X-ray
 Cardiac biomarkers
 High-sensitivity Troponin levels:
 Preferred test whenever available
 Rises 2-3 hours after MI
 A troponin must be above the 99th percentile of the upper
reference limit (URL) for the normal range of the assay being used
 For a diagnosis of STEMI, there must be:
 A rise and/or fall of troponin along with at least one other criterion for
STEMI
 Patients who present late after the onset of ACS, there may be on
the downslope of the time-concentration curve - difficult to
appreciate a changing pattern over a short period of time
 For a diagnosis of NSTEMI, there must be:
 A rise and/or fall of troponin and other criterion for NSTEMI
 Cardiac biomarkers
 Troponin levels:
 The conventional method of assessing troponin concentrations is
via central laboratory testing with a turnaround time ranging from
1-6hours
 False positives:
 Renal failure
 Neuromuscular diseases
 Acute myocarditis
 Stress cardiomyopathy
 PE with acute right heart overload
 Trauma
 CPR
 Electrical cardioversion
 Implantable defribrillator
 Cardiac Biomarkers
 Point of Care Troponin Testing
 Shorter turn around time
 10-20 minutes
 More expensive
 Beneficial to emergency departments
 Cardiac Biomarkers

 Point of Care Troponin Testing

 Cardiac biomarkers
 Creatine kinase-MB
 Rises 4-6 hours after MI
 Less sensitive and specific than troponin
 Longer turn around time than troponin
 No point of care testing available
 Investigations
 ECG
 Cardiac biomarkers
 Blood work-up
 Chest X-ray
 Cardiomegaly

 Pulmonary oedema

 Identify other causes for chest pain

 Investigations
 Basic electrolyte concentrations
 Keep potassium and magnesium levels within
normal limits
 Kidney function
 Complete blood count
 Anemia can exacerbate myocardial
ischemia – crossmatch may be required
 Coagulation studies if coagulopathy
suspected
 Investigations
 ECG
 Cardiac biomarkers
 Blood work-up
 Chest X-ray
 Cardiomegaly
 Pulmonary oedema
 Identify other causes for chest pain
 Other investigations – not in
the ED
 Echocardiography – can be done in
the ED if available and if the patient is
stable
 CT coronary angiography
 Cardiac catheterisation
 Stress ECG
 Diagnosis of ACS
 History
 Physical examination
 Investigations

 Management
 Complications
 Management in ACS
 Goals of management
 Decrease the size of infarct
 Increase blood flow and oxygen delivery to heart
 Decrease oxygen consumption by heart
 Reduce chest pain
 Reduce morbidity
 Prevent mortality
 Prevent further damage and future attacks
 Prevent complications
 Management in ACS – initial
management
 Airway, breathing, and circulation assessed
 Preliminary history and examination obtained
 12-lead electrocardiogram (ECG) interpreted
 Resuscitation equipment brought to the bedside
 Cardiac monitor attached to patient
 Oxygen given as necessary (if sats < 94%)
 Intravenous access and blood work including
troponin
 Management in ACS – stat
medication
 Aspirin 300mg chewed – unless known allergy
 Clopidogrel 300mg orally
 Clexane: can be given IV or S/C
 The approach to the use of clexane depends on the choice of reperfusion strategy and other patient
characteristic
 Nitrates SL
 Contraindications to nitrates
 severe aortic stenosis
 hypertrophic cardiomyopathy
 suspected right ventricular infarct, hypotension
 marked bradycardia or tachycardia
 recent use of phosphodiesterase 5 inhibitor (eg, Viagra])
 Atenolol 25-50mg orally
 Contraindications to atenolol
 Shock
 Heart failure
 Bradycardia
 Heart block
 Cocaine-induced ischemia
 High dose statin
 Give morphine with caution
 ACE-I in the first 24hours if haemodynamically stable
 Management in ACS
THEN….
TRANSFER PATIENT TO APPROPRIATE DEPARTMENT

(whether it is Unstable Angina/NSTEMI/STEMI)

DO NOT WAIT FOR BLOOD RESULTS

ACS IS A CLINICAL DIAGNOSIS WITH

ASSISTANCE OF ECG
Management in ACS - STEMI
 Options:
 Percutaneous coronary intervention (PCI)
 Fibrinolysis
 Conservative management
IDEAL Management in ACS –
STEMI
Management in ACS - STEMI
 PCI is the preferred method if available
 Factors to consider between choosing the ideal
management
 Time delay between first medical contact and
performance of PCI
 Time from symptom onset to presentation
 Presence of cardiogenic shock
 Diagnostic uncertainty
 Contraindications to PCI or fibrinolysis
 High-risk factors that favour no reperfusion
 Management in ACS -STEMI
 Alteplase preferred fibrinolytic agent in our
setting
 Know the contraindications
 Absolute:
 Previous ICH or stroke
 Ischemic stroke in last 6months
 Cerebral vascular lesion
 Intracranial haemorrhage
 Recent major trauma/head injury/surgery < 3 weeks
 GI bleeding within the last month
 Dissecting aortic aneurysm
 Active bleeding or bleeding disorder
 Non-compressible punctures in past 24hours eg lumbar
puncture
Management in ACS -STEMI
 Alteplase preferred fibrinolytic
 Know the contraindications
 Relative
 Chronic severe poorly controlled HPT
 Refractory hypertension
 TIA < 6 months ago
 Major surgery within previous 3 weeks
 Advanced liver disease
 Active peptic ulcer
 Current use of anticoagulants
 Pregnancy or within 1 week postpartum
Management in ACS - STEMI
 Conservative management
 Indicated when:
 Contraindications to PCI or fibrinolysis
 Lack of resources
 The acute management consists of:
 Monitoring for complications
 Continuing medical therapy
Management in ACS – NSTEMI
and UA
 The same initial management and stat
medications apply
 Early risk stratification is necessary
 Choice of management strategy
 Early PCI
 Conservative management
 Fibrinolysis not indicated
Management in ACS – NSTEMI
and UA
 Early risk stratification
 To identify those patients at risk of further cardiac
events
 TIMI risk score most often used
 Age ≥65 years.
 Presence of at least three risk factors for coronary heart
disease ●Prior coronary stenosis of ≥50 percent.
 Presence of ST segment deviation on admission
electrocardiogram.
 At least two anginal episodes in prior 24 hours.
 Elevated serum cardiac biomarkers.
 Use of aspirin in prior seven days
 Impact of missed diagnosis of
ACS
 With careful evaluation using effective risk scores, serial
ECGs and appropriate diagnostic testing, only a very
small percentage of patients with an ACS are mistakenly
discharged from the emergency department
 Consequences of missed diagnosis lead to increase in
short-term mortality
 Possible reasons for patients mistakenly discharged are
mainly in atypical presentations:
 Females less than 55 years of age
 Not White Americans
 Shortness of breath as the major presenting symptom
 Normal or non-diagnostic ECG
 Diagnosis of ACS
 History
 Physical examination
 Investigations
 Management

 Complications
 Complications of ACS
 Arrhythmias
 Heart failure
 Cardiac arrest
 Cardiogenic shock
 Death
 DDx of chest pain
 Life threatening causes:
 Acute coronary syndrome
 Acute aortic dissection
 Pulmonary embolism
 Tension pneumothorax
 Pericardial tamponade
 Mediastinitis (eg. oesophageal rupture)
 Aortic dissection
 Defined as a “tear” in the inner layer of the aortic wall
allowing blood to pool between the layers of the aortic
wall
 Incidence is underestimated – often missed
 Risk factors: hypertension, >69 of age, connective tissue
disorders, aortic valvular disease
 Characteristics of chest pain:
 Ripping/tearing/sharp pain

 Sometimes painless especial in DM

 Abrupt onset of chest pain (ascending aorta)

 Back pain (descending aorta)

 Pulmonary Embolism
 Defined as a dislodged venous clot migrates through the right
side of the heart and migrates and lodges in the pulmonary
arteries > pulmonary hypertension > RV dysfunction > poor gas
exchange > pulmonary infarction
 Common occurrence in SA – often missed
 Mortality depends on comorbid conditions and size of embolus
 Risk factors: same as DVT (Virchow’s triad)
 Characteristics of chest pain:
 SOB followed by chest pain
 Non-specific sudden onset chest pain
 Chest pain worsens over time
 May be painless
 Tension Pneumothorax
 A tension pneumothorax develops from a normal
pneumothorax which results in the accumulation of air in
the pleural space > compression of the mediastinal
space > rapid clinical deterioration > death
 Spontaneous/traumatic/iatrogenic
 Characteristics of chest pain:
 Sudden onset non-specific chest pain

 Ipsilateral pain

 Associated SOB

 Non-traumatic pneumothoraces occur suddenly at

rest
 Pericardial Tamponade
 Defined as the accumulation of fluid in the
pericardial space under pressure > impaired cardiac
filling > cardiogenic shock requiring immediate
pericardiocentsis
 Some causes: aortic dissection, acute pericarditis,
malignancy, uremia
 Characterestics of chest pain:
 Non-specific left sided chest pain

 Asocciated symptoms: SOB, fatigue, syncope

 Mediastinitis
 Defined as the swelling and irritation in the
mediastinum. Anything abnormal in the
mediastinum.
 Some causes:
 Spread of odontogenic and deep neck infections

 Oesophageal perforation

 Iaotrogenic eg complications of cardiac surgery

or upper GI or airway procedures

 Other common causes of
chest pain
 Cardiac causes:
 Acute heart failure
 Aortic stenosis
 Pericarditis/myocarditis/endocarditis
 Some cardiac arrhythmias
 Pulmonary causes:
 LRTI
 Bronchospasm
 Exacerbation of cor pulmonale
 Pleural effusions
 Other common causes of
chest pain cont.
 GIT causes:
 GERD/sliding hiatal hernia
 Oesophageal spasm
 Referred pain from acute pancreatitis
 MSK cause:
 Rib fractures
 Costochondritis
 Non-specific muscle spasm
 Psychiatric causes:
 Anxiety attack
 Other causes:
 Shingles referred pain
 SLE
 Takayasu arteritis
Chest pain causes and
features
 References
 Pathophysiology of acute coronary syndrome – Carlos Santos Gallego
 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/ SCMR Guideline for the
Evaluation and Diagnosis of Chest Pain: A Report of the American
College of Cardiology/American Heart Association Joint Committee on
Clinical Practice Guidelines
 National Heart Foundation of Australia & Cardiac Society of Australia
and New Zealand: Australian Clinical Guidelines for the Management
of Acute Coronary Syndromes 2016
 Acute Coronary Syndrome: Diagnostic Evaluation – Craig Barstow
and Matthew Rice
 Talley O’Connor
 Acute Coronary Syndromes in Sub‐Saharan Africa: A 10‐Year
Systematic Review from the Journal of American Heart Association
 https://www.uptodate.com/contents/initial-evaluation-and-
management-of-suspected-acute-coronary-syndrome-myocardial-
infarction-unstable-angina-in-the-emergency-department?
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