ECG Monitoring Podcast Series

Hi, I am Dr. Nicola Cosentino. Welcome to this podcast series on COVID-19 and ECG, sponsored by GE Healthcare. Today’s topic will be on clinical evidence on COVID and ECG.

After two and half years of facing cardiovascular patients with COVID-19, we have more and more appreciated the close association between COVID-19 and ECG. I would start from two points.

Thus far, the medical evidence show that cardiovascular patients have not an increased risk of SARS-CoV2 infection but, when they have the SARS-Cov2 infection, they have a significantly higher risk of complications as compared to those patients without a history of cardiovascular disease. So, the next question is: does COVID-19 affect the myocardium? And the answer is yes: COVID-19 can cause myocardial injury through several mechanisms both ischemic and non-ischemic, including cytokine storm effects and direct myocardial injury. When myocardial injury occurs, as assessed by the increase in high-sensitivity troponin levels in these patients, early mortality increases up to 10 times. The mechanisms underlying the association between COVID-19 and acute myocardial injury are the same responsible for ECG alterations. Indeed, thus far no specific ECG changes have been described in COVID-19 patients so that we might assume the infection does not translate into characteristics ECG manifestations in the majority of patients; however, in severe COVID-19 patients, ECG acute changes may occur and they reflect the mechanisms underlying the ongoing acute cardiac injury.

Several studies have been published focusing on ECG manifestations during SARS-CoV2 infection. Indeed, the QRS complex is wider in COVID-19 patients with elevated troponin or brain-natriuretic peptide values and this is the same for the QTc interval which has been shown to be longer in patients with elevated troponin or brain-natriuretic peptide values. So that when myocardial injury occurs during SARS-CoV2 infection, the QRS complex becomes wider and the QTc interval longer. Importantly, the more severe is the clinical picture in terms of respiratory and hemodynamic impairment, the longer is the QTc. Not only the QTc correct is associated with the clinical picture and with the ongoing acute myocardial injury, but also QTc dispersion does. QTc dispersion is the difference between the longest and shortest QTc interval in the 12-lead ECG.

In COVID-19 patients, the more severe is the clinical picture and the longer is the QTc dispersion; moreover, QTc dispersion is greater in non-surviving patients and this ECG parameter is a critical prognostic marker especially in younger patients (<65 years) hospitalized with COVID-19. QTc dispersion mainly depends on the difference in T wave morphology across the 12 leads. Interestingly, about 5% of hospitalized COVID-19 patients show a new T wave inversion in the ECG. If T wave inversion occurs, mortality is about 25%, while the need of invasive mechanical ventilation is 30%. In addition, when ECG alterations occur with simultaneous increase in troponin value, overall survival may be only 50% in COVID-19 hospitalized patients, so that ECG and troponin have a synergist prognostic effect. In particular, if new T wave inversion occurs in all leads and troponin levels are increased, in-hospital mortality may rise up to 80%.

Finally, it is important to repeat ECG along hospitalization: in particular, ECG at 7 day is critical as the cytokine storm occurring during COVID-19 usually is present between day 5 to day 15. If ECG at 7 days is abnormal, especially if it shows an increase in heart rate > 20% or a new acquired wide QRS complex, the rate of in-hospital mortality and the need of oro-tracheal intubation is very high. Similar data have been observed when investigating the prognostic impact of new ST-segment alterations. Of note, the presence of ST-segment deviation is associated with higher troponin values and with a worse prognosis, particularly if this occurs later during hospitalization (again at 7 days since hospital admission), as it reflects the ongoing oxygen supply/demand imbalance due to arterial hypotension, hypoxemia, sepsis, and anemia, or less frequently, due to coronary plaque activation, disruption, and thrombosis

Not only ECG may be acutely abnormal but also the risk of arrhythmia is common among COVID-19 patients. Indeed, 20% of hospitalized COVID-19 patients have cardiac arrhythmias (atrial or ventricular) and a higher incidence has been observed among those requiring ICU admission (nearly 50%) with malignant ventricular arrhythmias (ie, ventricular tachycardia/fibrillation) occurring in 6% of COVID-19 patients requiring ICU admission. All spectrum of arrhythmias has been observed in hospitalized COVID-19 patients (ICU and non-ICU wards), but the most frequent ones are sinus tachycardia (about 40% of patients), premature ventricular complex (about 25%), atrial fibrillation (about 12%, new-onset Atrial fibrillation about 6%), and non-sustained VT (nearly 15%). However, the most dangerous arrhythmias, most closely associated with a worse prognosis, are: new onset high-degree AV block, new-onset atrial fibrillation with rapid ventricular rate; polymorphic VT, and sinus tachycardia with new LBBB. If these arrhythmias are encountered, the risk of invasive mechanical ventilation and the risk of needing ECMO or even dying during hospitalization may be high.

Regardless of the underlying arrhythmia, faster heart rates are always an ominous sign as they reflect the ongoing respiratory and hemodynamic impairment. Therefore, ECG is very useful when managing COVID-19 patients as any ECG alterations, by reflecting the ongoing acute cardiac injury, identify those patients at higher risk of complications who need to be closely monitored and urgently treated.

Thank you for listening to this podcast on clinical evidence in ECG and COVID. The next podcast of this series will be on who to ECG monitor in COVID patients.

References:

Cho JH, Namazi A, Shelton R, Ramireddy A, Ehdaie A, Shehata M, Wang X, Marbán E, Chugh SS, Cingolani E. Cardiac arrhythmias in hospitalized patients with COVID-19: A prospective observational study in the western United States. PLoS One. 2020 Dec 28;15(12):e0244533.

Kang Y, Chen T, Mui D, Ferrari V, Jagasia D, Scherrer-Crosbie M, Chen Y, Han Y. Cardiovascular manifestations and treatment considerations in COVID-19. Heart. 2020 Aug;106(15):1132-1141.

Poterucha TJ, Elias P, Jain SS, Sayer G, Redfors B, Burkhoff D, Rosenblum H, DeFilippis EM, Gupta A, Lawlor M, Madhavan MV, Griffin J, Raikhelkar J, Fried J, Clerkin KJ, Kim A, Perotte A, Maurer MS, Saluja D, Dizon J, Ehlert FA, Morrow JP, Yarmohammadi H, Biviano AB, Garan H, Rabbani L, Leon MB, Schwartz A, Uriel N, Wan EY. Admission Cardiac Diagnostic Testing with Electrocardiography and Troponin Measurement Prognosticates Increased 30-Day Mortality in COVID-19. J Am Heart Assoc. 2021 Jan 5;10(1):e018476.

Romero J, Alviz I, Parides M, Diaz JC, Briceno D, Gabr M, Gamero M, Patel K, Braunstein ED, Purkayastha S, Polanco D, Valencia CR, Della Rocca D, Velasco A, Yang R, Tarantino N, Zhang XD, Mohanty S, Bello J, Natale A, Jorde UP, Garcia M, Di Biase L. T-wave inversion as a manifestation of COVID-19 infection: a case series. J Interv Card Electrophysiol. 2020 Dec;59(3):485-493.

Bergamaschi L, D'Angelo EC, Paolisso P, Toniolo S, Fabrizio M, Angeli F, Donati F, Magnani I, Rinaldi A, Bartoli L, Chiti C, Biffi M, Pizzi C, Viale P, Galié N. The value of ECG changes in risk stratification of COVID-19 patients. Ann Noninvasive Electrocardiol. 2021 May;26(3):e12815

Hi, I am Dr. Nicola Cosentino. Welcome to this podcast series on COVID-19 and ECG, sponsored by GE Healthcare. Today’s topic will be on what to look at in the ECG of COVID-19 patients and which patients with COVID-19 should be continuously monitored.

SARS-CoV2 infection may cause acute myocardial injury and this injury may be associated, in turn, with ECG alterations. Many ECG alterations and many kind of arrhythmias have been described in COVID-19 patients. Yet, there are some ECG patterns that must be closely monitored and, if detected, identify very-high risk COVID-19 patients, as these ECG acute changes mainly reflect the ongoing left ventricular ischemia/stiffness and/or right ventricular distention/dysfunction.

Notably, the following alterations are the ones most closely associated with a worse prognosis, in terms of in-hospital mortality and need of invasive mechanical ventilation:

• de-novo T wave inversion (especially if involving several leads)
• new ST-segment deviation >0.5 mm, new intra-ventricular conduction delay  (i.e. LBBB or RBBB) or QRS prolongation more than 25% from baseline
• QTc interval is >500 msec (or any acute increase of >60 msec or >25% from baseline)
• de-novo right bundle branch block and right axis deviation.

On the other hand, although all types of arrhythmias have been observed in hospitalized COVID-19 patients, there are some that, again, are most strongly associated with an ominous clinical outcome. These are:

• de-novo atrial fibrillation with rapid ventricular rate
• new atrio-ventricular block
• torsades de pointes
• sinus tachycardia with new left bundle branch block.

Regardless of the underlying arrhythmic disorder, faster heart rates are always associated with a more complicated in-hospital clinical course, by mirroring the hemodynamic and respiratory impairment.

Therefore, a 12 lead-ECG should be performed in all patients at admission, and at day 3 and 7 of hospitalization and before discharge. Moreover, ECG should be performed anytime there is an increase in troponin and/or brain natriuretic peptide circulating level or if the patient experiences chest pain or dyspnea, in order to exclude the presence of ECG ischemic alterations.

Furthermore, due to the high risk of serious arrhythmias, potentially life-threating, there are some COVID-19 patients that need to be continuously monitored by the ECG with the aim to rapidly detect any complex arrhythmias and to identify early any progressive clinical deterioration.

So, which COVID-19 patients should be continuously monitored?

• Patients admitted to ICU need to be continuously monitored
• For those not admitted to the ICU, continuous ECG monitoring for at least 48, and if possible, 72 hours, should be reserved for
  • hospitalized patients with pre-existing cardiovascular disease
  • those having elevation in cardiac biomarkers, that is, troponin and/or brain natriuretic peptide
  • those with de novo ECG changes, especially if de novo wide QRS complex or de-novo diffuse T wave inversion, or prolonged QTc interval
  • those with severe COVID-19 disease, in particular if dyspnea, tachypnea, and hypoxia persist after 7-10 days of symptoms’ onset, despite treatment

There are still some subsets of COVID-19 patients who should be continuously monitored, despite not meeting the prior criteria. In particular:

• Those with bradycardia (heart rate <40) or tachycardia (heart rate >120 bpm)
• Those with ventricular arrhythmia (>6 VEB/min, non-sustained ventricular tachycardia, sustained ventricular tachycardia) and/or sustained supraventricular arrhythmia
• Those with de-novo left ventricular disfunction (left ventricular ejection fraction <50%, especially if <40%) and/or de-novo right ventricular distention or dysfunction
• Those with altered mental status or severe electrolyte abnormality
• Those in whom chest CT scan shows >30/40% lung involvement.

There are two additional electrocardiographic issues that deserve attention in COVID-19 patients. One critical issue in COVID-19 patients is represented by QTc prolongation, as it can lead to polymorphic ventricular tachycardia (torsades de pointes [TdP]). Patients with a baseline QTc >500 msec (>550 msec if bundle branch block or ventricular pacing) are at risk of developing TdP or sudden death. Briefly, the following steps are required to reduce the risk of drug-induced TdP:

1. Identify non-modifiable risk factors associated with QTc prolongation (congenital LQTS, QTc prolongation on known QT prolonging drugs, female sex, age >65 years, structural heart disease, renal impairment, and liver impairment)
2. Identify and correct modifiable risk factors in all patients (correct hypocalcaemia, hypokalaemia, hypomagnesaemia, stop non-necessary concomitant use of QTc-prolonging medications, and avoid bradycardia [the concomitant use of beta-blockers, CCBs, ivabradine and digoxin should also be evaluated])
3. Perform a baseline ECG (12-lead or single strip, depending on resource availability) before initiating therapy;
4. Perform ECG once on treatment (after 1 day if no risk factors are present and after 4 hours of treatment if risk factors or prolonged QTc are known).

If the patient has a QTc >500 ms or shows an increase in QTc >60 ms (or >25%), switching to a drug with lower risk of QTc prolongation, reduction of the administered dose, or continuing treatment plan are the options to consider. Close surveillance of QTc interval (preferably including telemetry for arrhythmia monitoring) and electrolyte balance are mandatory.

Finally, Brugada syndrome may represent an important issue in COVID-19 patients and the main concern is fever-triggered malignant ventricular arrhythmia. COVID-19-induced fever may uncover the type 1 Brugada pattern and lead to symptomatic Brugada syndrome in previously unsuspected cases. Therefore, in all COVID-19 patients with Brugada syndrome, fever should be aggressively treated with paracetamol. Continuous ECG monitoring should be considered if antipyretic therapy is ineffective, and the temperature remains >38.5C in higher-risk Brugada syndrome patients (those with sodium channel mutation carrier, < 26-years old > 70-years old, spontaneous and/or known fever induced type-1 ECG pattern).

In conclusion, 12-lead ECG and continuous ECG monitoring are critical aspects in the treatment of COVID-19 patients, as they may help to early identify very-high risk patients who may deserve a close follow-up and more intensive therapeutic strategies. And I believe that what we have learned during COVID-19 on the clinical benefit derived from ECG and continuous ECG monitoring may be translated to most acute illness and should be a lesson to keep always with us when we face critical patients.

Thank you for listening to this podcast on what to look at when ECG monitoring is implemented in COVID-19 patients. The next podcast of this series will be on ECG monitoring in non-cardiac areas.

References:

Sandau KE, Funk M, Auerbach A, Barsness GW, Blum K, Cvach M, Lampert R, May JL, McDaniel GM, Perez MV, Sendelbach S, Sommargren CE, Wang PJ; American Heart Association Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Council on Cardiovascular Disease in the Young. Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings: A Scientific Statement From the American Heart Association. Circulation. 2017 Nov 7;136(19):e273-e344.

Kochav SM, Coromilas E, Nalbandian A, Ranard LS, Gupta A, Chung MK, Gopinathannair R, Biviano AB, Garan H, Wan EY. Cardiac Arrhythmias in COVID-19 Infection. Circ Arrhythm Electrophysiol. 2020 Jun;13(6):e008719.

Task Force for the management of COVID-19 of the European Society of Cardiology. ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic: part 2-care pathways, treatment, and follow-up. Eur Heart J. 2022 Mar 14;43(11):1059-1103.

Hi, I am Dr. Nicola Cosentino. Welcome to this podcast series on ECG monitoring, sponsored by GE Healthcare. Today´s topic will be on ECG monitoring in non-cardiac areas.

Since the introduction of ECG monitoring in hospital units >60 years ago, the goals of monitoring have expanded from simple tracking of heart rate and basic rhythm to the diagnosis of complex arrhythmias, the detection of myocardial ischemia, and the identification of a prolonged QT interval. During the same six decades, major improvements have occurred in cardiac monitoring systems, including computerized arrhythmia detection algorithms, ST-segment/ischemia monitoring software, improved noise-reduction strategies, multi-lead monitoring, and reduced lead sets for monitoring-derived 12-lead ECGs with a minimal number of electrodes.

All these technical advances have led to the implementation of continuous ECG monitoring not only in cardiac and cardiac-surgery patients but also in a variety of other critical and non-critical care hospital settings. Notably, although cardiovascular complications in the acutely ill “non-cardiac” patients are small in number, they are associated with a high mortality and morbidity rate. This makes it essential for physicians to continuously monitor ECG in these patients.

In particular, continuous ECG monitoring should be recommended for:

• non-cardiac patients with major trauma
• acute respiratory failure
• sepsis
• shock
• acute pulmonary embolus
• major non-cardiac surgery (especially in older adult patients with a history of coronary artery disease or coronary risk factors)
• renal failure with electrolyte abnormalities (e.g. hyperkalaemia)
• drug overdose (especially from known arrhythmogenics, e.g., digoxin, tricyclic antidepressants, phenothiazines, antiarrhythmic).

The first goal of continuous ECG monitoring in these patients is to aid in immediate recognition of sudden cardiac arrest to improve time to defibrillation. In particular, nearly 2/3 of the life-threating ventricular arrhythmias ultimately leading to cardiac arrest occur unexpectedly (out of the blue, without the so-called warning arrhythmias), although most of them develop in patients with known cardiovascular disease. In addition, continuous ECG monitoring may help recognizing deteriorating arrhythmic conditions such as non-sustained arrythmias that may lead to a life-threatening arrhythmia. Of note, in all these acute “non-cardiac” patients, the chance of a new-onset arrhythmia can be high, as high as 1 patient out of 5.

However, there are other several goals of continuous ECG monitoring in these non-cardiac clinical settings. It may assist clinicians in early detecting any serious cardiac, respiratory, or neurologic impairment as assessed by the increase in heart rate or increase in ventricular ectopic beats. In the hospitalized patient, heart rate helps monitor deterioration and therapy response as patient’s heart rate increases before their arterial pressure drops so heart rate is vital to monitor continuously, especially in the acutely-ill patient.

Take, for example, gastrointestinal bleeding. In order to know if the patient needs to be transferred immediately for endoscopy, you look at vital parameters, mainly heart rate and arterial pressure, as well as arterial blood gases and hemoglobin levels. If we detect a progressive increase in heart rate, probably our patient is keeping bleeding and heart rate will tell us the presence of an active bleeding earlier than hemoglobin levels or arterial pressure drop. This notion can be actually applied to almost all hospitalized patients. Indeed, an old adage says: tachycardia, especially progressively increased tachycardia, is always a bad sign. Continuous ECG monitoring is not only complex arrhythmia and heart rate, it means also myocardial ischemia (ST-segment) and QTc interval. Any progressive change in ST-segment deviation or QT interval length can be detected earlier by continuous ECG monitoring before the “clinical picture becomes overt” and this will let us have more time to act or counteract the ongoing clinical issue. Indeed, hypoxia, arterial hypotension, or anemia may all lead to ST-segment changes (especially ST-segment depression) and/or QT interval prolongation. Therefore, in patients hospitalized for clinical reasons beyond acute cardiac issues, continuous ECG monitoring helps clinicians with arrhythmia detection and, probably more importantly, with clinical decision making by anticipating deterioration, evaluating if the therapy is working, and driving any further diagnostic tests.

Thank you for listening to this podcast on ECG monitoring in non-cardiac areas. The next podcast of this series will be on how to prioritize which patients should be monitored with ECG.

References:

Sandau KE, Funk M, Auerbach A, Barsness GW, Blum K, Cvach M, Lampert R, May JL, McDaniel GM, Perez MV, Sendelbach S, Sommargren CE, Wang PJ; American Heart Association Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Council on Cardiovascular Disease in the Young. Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings: A Scientific Statement From the American Heart Association. Circulation. 2017 Nov 7;136(19):e273-e344.

Drew BJ, Califf RM, Funk M, Kaufman ES, Krucoff MW, Laks MM, Macfarlane PW, Sommargren C, Swiryn S, Van Hare GF; American Heart Association; Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young. Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young: endorsed by the International Society of Computerized Electrocardiology and the American Association of Critical-Care Nurses. Circulation. 2004 Oct 26;110(17):2721-46.

Hello, I am Dr. Nicola Cosentino. Welcome to this podcast series on ECG monitoring, sponsored by GE Healthcare. Today´s topic will be on how to prioritize which patients should be monitored with ECG.

Continuous ECG monitoring was first introduced nearly 60 years ago for critically ill patients, but today is used increasingly to monitor patients with a variety of conditions. Early monitoring focused on heart rate measurement and fatal arrhythmia detection. Today, monitoring has expanded to include diagnoses of complex arrhythmias, acute myocardial ischemia, and prolonged QT intervals and, hence, it is currently applied in a variety of critical and non-critical care hospital settings.

When a patient is hospitalized, the first rule is to perform a 12-lead ECG; this will allow to have a baseline ECG for any comparison during hospitalization. Then, we should decide who deserves to be monitored? A basic rule is that, regardless of the underlying acute condition leading to hospitalization, if the patient is in hemodynamic, respiratory, or neurologic distress then of course you need to continuously monitor them. It must be included for every one of these patients in order to promptly evaluate rapid deterioration or to immediately detect life-threatening arrhythmias. So, as a general rule, all patients admitted to intensive care unit need to be continuously monitored.

 

Among “acute cardiac” patients, those during their early-phase acute coronary syndrome should be immediately monitored (STEMI patients for at least 48hrs and intermediate-high risk NSTEMI patients for at least 24hrs). It is also reasonable to perform continuous ST-segment monitoring in patients in whom there is the suspicion of ongoing myocardial ischemia. All patients with ventricular tachycardia (VT, ventricular fibrillation, or hemodynamically unstable VT should be monitored until a ICD is implanted or underlying problem resolved. For all arrhythmias, add ST-segment monitoring if ischemic origin is suspected. Moreover, patients with non-sustained VT, new or recurrent atrial fibrillation (AF), or hemodynamically unstable or symptomatic AF should be monitored until treatment strategy is determined or during ongoing rate control management and during initiation of a new antiarrhythmic agent. For sinus bradycardias, an indication for continuous ECG monitoring are symptomatic sinus bradycardia (<50 bpm), significant bradycardia (<40 bpm) regardless of symptoms, symptomatic atrio-ventricular (AV) block or asymptomatic second- or third degree AV block caused by distal conduction system disease (as suggested by a wide QRS complex). For WPW, Brugada, or LQTS, continuous ECG monitoring is recommended in the case of hemodynamic instability, or if recurrent syncope or recurrent VT until appropriate therapy is delivered or until QTc returns to baseline. In particular, patients with a baseline QTc >500 msec (>550 msec if bundle branch block or ventricular pacing) or those showing an increase in QTc >60 ms (or >25%) from baseline, are at risk of developing torsade de pointes or sudden death and need to be continuously monitored.

Continuous ECG monitoring is also recommended for non-cardiac patients with major trauma, acute respiratory failure, sepsis, shock, acute pulmonary embolus, renal failure with electrolyte abnormalities (e.g. until normalization of electrolytes of hyperkalaemia), and drug overdose (especially from tricyclic antidepressants and/or antiarrhythmic, until patients are free of the influence of the drug(s) and clinically stable). In addition, in patients with acute stroke, continuous ECG monitoring for 24-48hrs is recommended or for longer time periods if cryptogenic stroke and occult atrial fibrillation is suspected.

Patients undergoing major cardiac interventions should be monitored 48–72 hrs, if uncomplicated. After non-cardiac major thoracic surgery (such as pulmonary resection) ECG monitoring should be performed for 48/72 hrs to identify AF. In any case, for all major non-cardiac surgeries (especially in older patients with a history of coronary artery disease or coronary risk factors), continuous ECG monitoring may be beneficial during the first post-operative 48/72 hrs.

If a patient is required to leave the monitored unit for diagnostic or therapeutic procedures, then cardiac monitoring should be continued with a portable, battery-operated monitor-defibrillator. Continuous ECG monitoring is also indicated in patients undergoing diagnostic/therapeutic procedures requiring conscious sedation or anesthesia and should be continued until patients are awake, alert, and hemodynamically stable.

In summary, the first rule is to perform a 12 lead ECG at admission in all hospitalized patients; secondly, if you have a clinical doubt, monitor the patient as this may help you save time and lives. Thirdly, documentation with a “stat” standard 12-lead ECG if the monitored rhythm modifies. Any patient acutely unwell is at risk of life-threating arrythmias and/or may quickly deteriorate and evolve towards overt shock so she/he should be continuously ECG monitored. Last, but not least, hospitalized patients should be assessed daily for the appropriateness of cardiac monitoring.

Thanks for listening to this podcast on how to prioritize which patients should be monitored with ECG. The next podcast of this series will be on admission pathways of ACS

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.