by Khalid Mohammed Ali, Shirley Ooi – Singapore
A 46 years old man with a past medical history of hypertension and hyperlipidemia developed central crushing chest pain associated with sweating and shortness of breath while driving. He presented to the emergency department 1 hour after the onset of chest pain. On physical examination, his vital signs were as follows; pulse rate: 60 beats/min, blood pressure: 100/50 mm Hg, respiratory rate: 20/min, SpO2 98% on room air. Patient has no leg edema, new murmur or features of heart failure.
His ECG is as follows:
What are the ECG features? What is the diagnosis?Answer
ECG features are ST elevation more than 2 mm in inferior leads (II, III, AVF) with reciprocal changes (deep ST depression in lateral leads of I, AVL) and ST depression in lead V1, V2 which indicate the involvement of posterior wall.
The ECG is diagnostic of inferior and posterior wall ST elevation MI.
Acute coronary syndromes (ACS) include conditions that share the same pathophysiology of myocardial ischaemic states, i.e., unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI).
History and Physical Examination Hints
The patient may experience the following symptoms:
- Chest pain described as pressure, squeezing or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either or both arms.
- Shortness of breath especially exertional dyspnoea
- Diaphoresis from sympathetic stimulation
- Nausea from vagal stimulation
- Decreased effort tolerance
It is important to ascertain the onset of chest pain as it will affect the management of STEMI. Other important questions to ask are the chest pain character, radiation, associated symptoms, relieving and exacerbating factors, especially exertion.
Do not forget to ask about the risk factors. You can use the TIMI score.
TIMI (Thrombolysis in Myocardial Infarction) investigators have developed a 7-variable risk stratification tool that predicts the risk of death, re-infarction, or urgent revascularization at 14 days after the presentation:
- ≥ 65 years of age
- Presence of ≥ three cardiac risk factors
- Prior coronary artery stenosis of ≥ 50%
- >= two angina events in the preceding 24 hours
- Aspirin use in the previous seven days
- ST-segment deviations of ≥ 0.5 mm on ECG at presentation
- Positive cardiac biomarkers
Patients are considered to be high risk if their TIMI risk score is ≥ 5 and low risk if the score is ≤ 2. High-risk patients have a more significant benefit from early percutaneous coronary intervention and use of adenosine phosphate inhibitor and low molecular weight heparin than lower risk patients.
Most of the cases with ACS have a normal cardiovascular examination. In a busy emergency department where time is of an essence, targeted physical examination in the patient with ACS is important to rule out complications and possible differential diagnosis.
The following are essential components:
- Differential pulse and BP between both arms, which if present may indicate the possibility of aortic dissection
- Tachypnoea, pitting leg edema and raised jugular venous pressure with crackles in the base of the lung or only crackles in the base of the lung may indicate either existing heart failure or an acute one secondary to acute myocardial ischemia
- A new cardiac murmur may indicate acute valvular insufficiency or rupture interventricular septum
- Distant heart sound on auscultation of precordium may indicate acute pericardial effusion secondary to rupture of a free ventricular wall or acute aortic dissection with extension to precordium.
In addition to the above, it is essential to check the vital signs carefully. If the patient has hypotension with acute myocardial ischemia, this may indicate cardiogenic shock. Tachycardia may range from sinus tachycardia to ventricular tachycardia; bradycardia, on the other hand, may range from sinus bradycardia to third-degree heart block.
There are many critical differential diagnoses when we consider A.C.S. Please look for all in the given table. However, Unstable angina, Acute myocardial infarction, Acute pulmonary embolism, Acute aortic dissection, Tension pneumothorax, Oesophageal rupture (Boerhaave’s syndrome) are the life-threatening ones. We advise you to read these chapters form multiple resources to feel confident.
See the following table:
ACS/Chest Pain Differential Diagnosis
|Life threatening||Cardiovascular||Respiratory||Gastrointestinal||Referred pain|
Acute myocardial infarction
Acute pulmonary embolism
Acute aortic dissection
Oesophageal rupture (Boerhaave’s syndrome)
|Stable angina |
|Sub phrenic abscess / inflammation
The acute complication which we may see in the emergency department includes the following:
- Acute pulmonary edema due to acute myocardial ischemia which leads to decrease effective ejection fraction and heart failure
- Mechanical complications include rupture of papillary muscles, free left ventricular wall, and interventricular septum
- Arrhythmias include tachyarrhythmias and bradyarrhythmias
- Cardiogenic shock
- Cardiac arrest in the form of ventricular fibrillation
Decision Making Process and Reaching The Diagnosis
There are three pillars of diagnosis: history, ECG, and cardiac enzymes.
Clinical features of unstable angina include the following:
- Unstable angina differs from stable angina in that the chest pain is usually more intense, easily provoked, more prolonged, more frequent and more severe. All first presentation of angina should be regarded as unstable. In unstable angina typically there is either no ECG changes or non-specific ECG changes, the patient is usually chest pain-free on presentation to the emergency department, and the cardiac enzymes will be normal.
- NSTEMI should be diagnosed in any patient whose cardiac enzymes are raised without evidence of ST elevation MI. An NSTEMI does not need to have ECG changes at the time of presentation. The ECG may show the following:
- ST-segment depression
- The transient ST-segment elevation that resolves spontaneously or after glyceryl trinitrate treatment
- T-wave inversion
- Evidence of previous myocardial infarction
- Left bundle branch block
- Minor non-specific changes
The ECG can also be normal. It should not show persistent acute ST-segment elevation.
- STEMI (ST-segment elevation MI) is a true cardiac emergency. The criteria of diagnosing ST-segment elevation MI on ECG are: New ST elevation at the J point in at least two contiguous leads of ≥ 2 mm in leads V2–V3 and/or of ≥ 1 mm in other contiguous chest leads or the limb leads.
ST Segment Changes And Its Anatomical Relation In Acute Myocardial Infarction
|Location||Leads||ST segment changes|
|Anterior wall||V1 -V4||Elevation|
|Inferior wall||II, III, aVF||Elevation|
|Posterior wall||V8 and V9|
|Right Ventricular wall MI||V4R, V5R, V6R||Elevation|
|Lateral wall||I, aVL, V5 and V6||Elevation|
There are other causes of ST elevation should be known to differentiate it from the ST elevation of myocardial infarction. These are;
- Acute pericarditis
- Benign early repolarization
- Brugada’s Syndrome
- Left Bundle Branch Block
- Left ventricular aneurysm
- Left ventricular hypertrophy
- Normal variant
- Osborn wave of hypothermia
- Prinzmetal’s angina
- Ventricular paced rhythm
In general, the difference between unstable angina and NSTEMI/STEMI is an absence of cardiac enzymes abnormalities.
Cardiac enzymes (CKMB, Troponin T or I) are highly sensitive to cardiac muscle injury. Another lab investigation is full blood count, urea, and electrolyte. A chest x-ray may give clues to acute pulmonary congestion or indicate the diagnosis of other conditions like pneumothorax or acute aortic dissection.
Emergency Treatment Options
In typical emergency medicine room, once a patient presents with chest pain suspecting of acute myocardial ischemia should be seen in the monitored area, the patient should remain under continuous cardiac monitoring, HR, BP, and SpO2.
The proper approach will consist of all following:
- ECG should be done immediately or within the first 10 minutes by the emergency room staff nurse, which should be interpreted by a senior doctor.
- Targeted history of onset of chest pain, associated symptoms and risk factors.
- Targeted examination to exclude potential differential diagnosis and complications of acute myocardial ischemia.
- IV cannula will be set, and blood will be sent for full blood count, urea and electrolytes, cardiac enzymes (CKMB, troponin I or T).
- Radiological examination of the chest will be required only to diagnosis acute pulmonary edema, rule out possible differentials like pneumothorax or aortic dissection.
- Antiplatelet typically aspirin 300 mg and either Ticagrelor 180 mg or Prasugrel 60 mg.
- GTN sublingually or spray to relieve chest pain, if chest pain persists after two sublingual GTN tablet, proceed with GTN infusion especially if the patient has concomitant hypertension or heart failure.
- IV morphine with anti-emetic if chest pain persisted and titrated according to the response of the patient.
- Oral beta blocker if no contraindication within 24 hours.
- Definitive treatment depends on which condition within the acute coronary syndrome is diagnosed.
- STEMI should undergo reperfusion therapy preferably percutaneous coronary intervention (PCI) or intravenous thrombolytic therapy
- Unstable angina and NSTEMI: medical therapy of antiplatelet, anticoagulant and beta blocker followed by admission to hospital and arranging of urgent PCI
- For STEMI, time is muscle, the sooner the PCI or thrombolysis, the better prognosis is.
Advantages And Disadvantages Of Thrombolysis Versus PCI
|Better clinical efficacy i.e. superior vessel patency, TIMI grade 3 flow rates and reduced occlusion rates
Early definition of coronary anatomy allows tailored therapy and more efficient risk stratification
|Disadvantages||Patency ceiling, i.e. infarct-related artery is restored in only 60-85% of patients, with a normal TIMI grade 3 epicardial coronary flow in only 45-60% of patients|
Less clinical efficacy, i.e. optimal reperfusion is not achieved in more than
50% of patients, and re-occlusion of infarct vessel occurs in 5-15% of patients at week 1 and 20-30% within 3 months
Risk of haemorrhage
|Delay limits efficacy
Less widely available
In the absence of PCI, thrombolysis is alternative, and the following should present for the patient to be a candidate of thrombolysis:
- Typical chest pain of AMI
- ST-segment elevation fulfilling the criteria stated above
- Chest pain <12 hours from onset
- Patients <75 years of age
Contraindications Of Intravenous Thrombolysis
|History of intracranial haemorrhage|
History of ischaemic stroke in the past 3 months (except acute ischaemic stroke within 3 hours)
Presence of cerebral vascular malformation or intracranial malignancy
Suspected aortic dissection
Bleeding diathesis or active bleeding (except menses)
Significant head trauma or facial trauma in the past 3 months
|Severe hypertension (blood pressure > 180/ 110 mm Hg)
History of ischaemic stroke >3 months
Presence of dementia
Known intracranial disease that is not an absolute contraindication
Traumatic or prolonged cardiopulmonary resuscitation (CPR) that lasted more than 10 minutes
Major surgery within 3 weeks
Presence of active peptic ulcer
Internal bleeding within the last 2 to 4 weeks
Non-compressible vascular punctures.
On warfarin therapy
For streptokinase, prior exposure (more than 5 days ago) or history of allergic reaction
In the acute management of acute coronary syndromes, please take note of the following:
If the patient is in shock, always look for precipitating causes:
- Do a gentle rectal examination to look for gastrointestinal bleeding.
- Is the patient bradycardic? Treat according to ACLS guidelines.
- Is the patient tachycardic? Treat according to ACLS guidelines.
- Does the patient have a right ventricular infarct?
- Do right-sided leads in the presence of ST elevation in II and III and aVF as in inferior AMI (Look for at least 1 mm ST elevation in V4R, V5R, and V6R.
- If so, give the fluid challenge of 100-200 ml normal saline over 5 to 10 minutes and assess response.
- This can be repeated if the patient does not become breathless and there are no clinical signs of pulmonary edema.
- Start inotropes (IV dobutamine/dopamine 5-20 µg/kg/min) if the blood pressure remains low despite IV fluid administration of 500 ml.
- Is the patient in cardiogenic shock because of mechanical complications, e.g., papillary muscle dysfunction or rupture, septal rupture or cardiac tamponade from free wall rupture?
- Call the cardiologist and cardiothoracic surgeon.
- Meanwhile, start inotropic support, e.g. IV dobutamine/dopamine 5-20 µg/kg/min
- Catheterize the patient to measure the urine output.
- Admit to the coronary care unit or send the patient to the cath lab.
References and Further Reading
- Kuan Win Sen, Shirley Ooi. Coronary syndromes, acute. In: Shirley Ooi, Peter Manning, eds. Guide to the essentials in emergency medicine, 2nd Ed, Singapore: McGraw-Hill; 2015:239-249.
- David L Coven; Chief Editor: Eric H Yang, MD, Acute coronary syndrome, http://emedicine.medscape.com/article/1910735-overview
- Robert E. O’Connor, Chair; Abdulaziz S. Al Ali, William J. Brady, et al.
Acute Coronary Syndromes 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
- Michael C. Kurz, Amal Mattu, and William J. Brady. Acute coronary syndrome. In: John A. Marx, Robert S. Hockberger, Ron M. Walls, eds. Rosen’s emergency medicine concepts and clinical practice, 8th Ed, USA: Elsevier Saunders; 2014: 997-1033.
- Acute Coronary Syndrome: Practice Essentials, Background .., http://emedicine.medscape.com/article/1910735-overview (accessed July 07, 2016).
Links To More Information
- CDEM Curriculum – Patwari R. Acute Coronary Syndromes (2008). https://cdemcurriculum.com/cardiovascular/acute-coronary-syndromes/ Accessed July 2018. – Link
- REBEL EM – Tag Archive for ACS. http://rebelem.com/tag/acute-coronary-syndrome/ Accessed July 2018. – Link
- Flipped EM Classroom – ACS. https://flippedemclassroom.wordpress.com/2013/10/20/acute-coronary-syndrome/ Accessed July 2018. – Link