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#14. Admission Pathways of ACS Patients


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    Dr. Nicola Cosentino
    Dr. Nicola Cosentino

The ECG provides critical information that assists in establishing the diagnosis of acute coronary syndrome and determining the treatment strategy. In acute coronary syndrome, common ECG abnormalities include T-wave tenting or inversion, ST-segment elevation or depression (including J-point elevation in multiple leads), and pathologic Q waves

Show Notes

ECG risk stratification allows appropriate referral of patients to a chest pain center or, even, to a catheterization laboratory.

Thus, in this podcast Dr. Cosentino aims at improving your confidence in the interpretation of ECG during a suspected or confirmed acute coronary syndrome. A systematic approach to ECG analysis is essential for identifying an early and appropriate management for patients with acute coronary syndrome.

This podcast is ideal for those required to interpret ECGs during suspected or confirmed acute coronary syndrome within their clinical role and who wish to quickly develop a reliable method for ECG interpretation in this clinical setting.

Learning objectives:

  • learn how to use a systematic and solid approach when interpreting an ECG during ACS
  • identify coronary lesion site responsible for the ACS by ECG monitoring
  • be able to quickly recognize ECG patterns most closely associated with a worse prognosis during ACS

Who should attend?

Healthcare professional, Consultant, Electrophysiologist, General Practitioner/Physician, Neurologist, Nurse, Surgeon, Anesthesiologists, Cardiology Professionals, Clinical Engineers, Intensivists, ED physicians and nurses

Hello, I am Dr. Nicola Cosentino. Welcome to this podcast series on ECG monitoring, sponsored by GE Healthcare. Today´s topic will be on Admission Pathways of acute coronary syndrome (ACS) patients.

The term acute coronary syndrome (ACS) is applied to patients in whom there is a confirmation of acute myocardial ischemia or infarction and usually occurs when an atherosclerotic plaque disrupts, resulting in platelet and coagulation factor activation and thrombus formation. Non-ST-elevation myocardial infarction (NSTEMI), ST-elevation MI (STEMI), and unstable angina are the three traditional types of ACS.

From a practical point of view, and with relevant therapeutic implications, ACS are subdivided into STE-ACS and NSTE-ACS. All ACS which exhibit persistent ST-segment elevation (lasting >20minutes/especially if more than 30 minutes) on ECG are classified as STE-ACS and it is usually caused by a complete coronary artery occlusion and virtually all patients will develop MI, which is classified as STEMI. NST-ACS includes all ACS without significant and persistent ST-segment elevation and is usually caused by partial occlusion of the artery and encompasses NSTEMI and unstable angina. NSTE-ACS, typically, presents with ST-segment depression and/or T-wave abnormalities (inversion) or may have non-diagnostic alterations or, even, normal ECG.

Any patient presenting to the emergency department with chest pain or chest pain equivalent (dyspnea, jaw or neck discomfort, epigastric discomfort, back [interscapular] discomfort, left and/right shoulder, elbow, or arm discomfort) should have an ECG performed within 10 minutes. Non-ACS chest pain should be urgently excluded, such as aortic dissection, pericarditis and pericardial effusion, pulmonary embolism, tension pneumothorax, acute perforation of peptic ulcer or esophageal tear or rupture. Other causes of chest pain are aortic stenosis and hypertrophic cardiomyopathy. If any of these emergency conditions is suspected, immediate echocardiogram or CT scan should be requested. Patients with chest pain or chest pain equivalent lasting longer than 20-30 minutes are prioritized according to their ECG findings.

STEMI patients are those with one of the following ECG criteria for acute MI:

  • >1 mm ST-elevation in two contiguous leads, especially if there is a concomitant reciprocal ST-segment depression
  • new left bundle branch block
  • acute posterior wall MI (ST-segment depression in leads V1-V3 and ST-segment elevation in posterior leads V7 to V9, in posterior leads the cut-off for the clinical significance is 0.5 mm).

These patients should be referred for emergent coronary angiography and primary percutaneous intervention.

In STEMI patients, it is important to define the AMI culprit vessel by ECG. In anterior STEMI, look at the ST-segment elevation in V1, V2, and V3.

  • If the ST-segment elevation in V1 is more than 2.5 mm or if there is de novo right bundle branch block with Q wave or both, the lesion is at ostial/proximal left anterior descending artery (proximal to S1)
  • if there is ST-segment depression (reciprocal depression) more than 1 mm in II, III, and aVF the lesion is at proximal left anterior descending artery (proximal to D1)
  • if ST-segment depression (reciprocal depression) in inferior leads is < 1 mm or there is ST-segment elevation in II, III, aVF, the level of the coronary lesion is at distal left anterior descending artery.

In inferior STEMI, always perform posterior and right precordial leads while in lateral STEMI always perform posterior leads.

In inferior STEMI, if the ST-segment elevation in III is greater than ST-elevation in II and ST-segment depression in I, aVL, or both (reciprocal depression) is greater than 1 mm, the lesion is at the right coronary artery. In this case, if there is ST-segment elevation in V1, V4R, or both, the occlusion is at proximal right coronary artery with right ventricular infarction. If ST-segment elevation in III is not greater than ST elevation in II and ST-segment depression in I, aVL, or both (reciprocal depression) is less than 1 mm, then look at ST-segment in left precordial leads and if there is ST-segment elevation in I, aVL, V5 and V6 and ST-segment depression in V1,V2, V3, the culprit lesion is the left circumflex coronary artery.

Finally, if a patient comes with acute chest pain and the ECG shows hyperacute T wave (that is the amplitude of the T wave is greater than 2/3 of the corresponding R wave), then this is a myocardial ischemia and T wave are usually tall, symmetrical, broad-based and not pointed in the leads involved by the AMI.

Do not forget all the situations that can mask AMI, i.e. left bundle branch block, ventricular pre-excitation, ventricular pacing, and ventricular tachycardia. Notably, the ECG patterns most frequently responsible for human errors in ACS are left ventricular hypertrophy, LBBB, RBBB, and pacemaker. In all these situations, if there is a clinical suspicious of acute myocardial ischemia, still monitor the patient, repeat several ECG and ask for troponin and echocardiogram. However, there is a quick rule to follow. In LVH and BBB, ST-segment is discordant from the major deflection of the QRS complex (i.e, positive QRS complex, ST-segment depression; negative QRS complex ST-segment elevation). In the setting of acute ischemia and LBBB or LVH,

  • if we find an ST-elevation > 1 mm in a lead with upward QRS complex (concordant), then think on acute MI;
  • if there is ST-depression is > 1 mm in leads V1, V2 or V3 (concordant) think on acute MI, or if there is ST elevation > 5 mm in a lead with downward QRS complex (discordant) think on acute MI.

If the patient does not have a STEMI, then she or he might have a NSTE-ACS. Typically, these patients present with prolonged chest pain (>20 minutes) relieved by

  • nitroglycerine
  • rest
  • new onset prolonged chest pain at rest, or
  • with accelerated chest pain within 48 hours

If ACS patients have dynamic ST changes (mainly horizontal or downsloping depression) on the ECG (> 0.5mm) and/or evolving T wave (negative T wave, more than 1 mm), they are at advanced risk. Among the NSTE-ACS, ECG can identify those patients at very high risk who should be referred for immediate invasive approach (<2 hrs). In particular, if ECG shows ST-segment depression > 1mm/6 leads plus ST-segment elevation in aVR and/or V1 the patient is classified at very high-risk. Why is that? Because if you find such an ECG pattern this means that the angiographic pattern will be a left main or left main equivalent or severe and proximal three vessel disease.

Another important point is to distinguish between T wave inversion (more than 1 mm) due to myocardial ischemia or LVH with strain. In LVH with strain, we see voltage criteria for LVH (often with left atrial enlargement), T wave inversion is asymmetrical with the ascending limb of T wave steep and with the overshoot of the terminal positivity of the T wave over the baseline. On the other hand, in myocardial ischemia, voltage criteria for LVH may be present or not, T waves are symmetrical with the ascending limb of the T wave less steep and, usually, T wave do not overshoot the baseline.

Finally, another rule is that T wave inversion in V6 is less pronounced in myocardial ischemia as compared to V3, while in LVH, T wave inversion in V6 may be pronounced, and even more pronounced than the T wave inversion in V3. Last two things: if we see T wave inversion in antero-septal leads (V1-V3) and the clinical picture does not really convince for ACS, always think of pulmonary embolism and look for simultaneous T wave inversion in inferior and anteroseptal leads, right axis deviation/RBBB, and the SIQIIITIII pattern. These features strongly suggest acute pulmonary embolism.

Finally, T wave alterations (specifically biphasic T wave) may be associated with myocardial ischemia or hypokalemia. However, in myocardial ischemia T waves go up and then down; in hypokalemia, T waves go down and then up and are often associated with long QT interval.

Finally, do not forget that in up to 8-10% of the patients, ECG may be normal and in up to 30% of patients ECG may show non-specific ST-T alterations. Therefore, always pay the correct attention to any patient presenting with acute chest pain or chest pain equivalent and if we are in doubt, closely monitor the patient, repeat ECG several times, wait for high-sensitivity troponin, and ask for transthoracic echo or even a thoracic CT.

 Thanks for listening to this podcast on Admission Pathways for ACS patients. 

Dr. Nicola Cosentino

Dr. Nicola Cosentino

Dr. Nicola Cosentino, a member of the AHA/ASA and of the Royal Society of Medicine, is a practicing clinician at the Monzino Cardiology Center in Milan, Italy, who specializes in the treatment of patients with acute cardiovascular diseases.

Dr. Cosentino is a member of the PhD program in Translational Medicine at the University of Milan, Italy and has been the receiver of several grants since 2014. He is a member of the editorial board of the Journal of Clinical Medicine, Frontiers of Cardiovascular Medicine, and has reviewed several scientific journals. In addition to his clinical practice,

Dr. Cosentino teaches Cardiology in the University of Medicine; as well as, the Cardiology Medical School of Milan, Italy. Dr. Cosentino is the author of over one hundred scientific publications and has written several medical book chapters.

  • Circulatory
  • ECG
  • Cardiac care
  • Clinical