Acute Myocardial Ischaemia Terminology, Pathophysiology and Recognition

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Acute Myocardial Ischaemia Terminology,
Pathophysiology and Recognition
Table of Contents
 Preface
 Introduction
 Terminology
 Unstable Angina (UA)
 Myocardial Infarction
 Myocardial infarction with non obstructive coronary arteries (MINOCA)
 Myocardial infarction in the Intensive Care Unit
 Pathophysiology Of AMI
 Understanding the underlying mechanisms
 Pathophysiology of the complications and sequelae of Myocardial
Infarction
 Understanding normal coronary artery anatomy
 Cardiogenic Shock
 Recognition of AMI
 Clinical features of ischaemic chest pain
 Triage and early risk stratification
 Immediate management of ACS
 On going physical examination
 Investigations
 Risk Scoring Systems
 Conclusion
 
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https://collaboration.esicm.org/Acute+Myocardial+Ischaemia%3A+Terminology%2C+Pathophysiology+and+Recognition%3A+Introduction?page_ref_id=3153
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Terminology?page_ref_id=3154
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Terminology%3A+Unstable+Angina+%28UA%29?page_ref_id=3155
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Terminology%3A+Myocardial+Infarction?page_ref_id=3156
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Terminology%3A+Myocardial+infarction+with+non+obstructive+coronary+arteries+%28MINOCA%29?page_ref_id=3157
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Terminology%3A+Myocardial+infarction+in+the+Intensive+Care+Unit?page_ref_id=3158
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Pathophysiology+Of+AMI?page_ref_id=3189
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Pathophysiology+Of+AMI%3A+Understanding+the+underlying+mechanisms?page_ref_id=3190
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https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Pathophysiology+Of+AMI%3A+Understanding+normal+coronary+artery+anatomy?page_ref_id=3192
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Pathophysiology+Of+AMI%3A+Cardiogenic+Shock?page_ref_id=3193
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Recognition+of+AMI?page_ref_id=3182
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Recognition+of+AMI%3A+Clinical+features+of+ischaemic+chest+pain?page_ref_id=3183
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Recognition+of+AMI%3A+Triage+and+early+risk+stratification?page_ref_id=3184
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Recognition+of+AMI%3A+Immediate+management+of+ACS?page_ref_id=3185
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Recognition+of+AMI%3A+On+going+physical+examination?page_ref_id=3186
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Recognition+of+AMI%3A+Investigations?page_ref_id=3187
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Recognition+of+AMI%3A+Risk+Scoring+Systems?page_ref_id=3188
https://collaboration.esicm.org/Acute+Myocardial+Ischaemia%3A+Terminology%2C+Pathophysiology+and+Recognition%3A+Conclusion?page_ref_id=3194
Acute myocardial ischaemia Terminology,
Pathophysiology and Recognition
 
Current Status 2019
Completed 
This module is updated and maintained by the Cardiovascular Dynamics section
Latest Update
First Edition
Cardiovascular Dynamics
Chair
Thomas Scheeren MD, PHD, University Medical Centre Groningen, Department
of Anaesthesiology, Groningen, The Netherlands; Chair Cardiovascular Dynamics
Section, ESICM
Deputy
Jan Bakker Prof. Dr., Department of Intensive Care Adults, Erasmus MC
University Medical Center, Rotter-dam, The Netherlands. Division of Pulmonary,
Allergy, and Critical Care, Columbia University College of Physicians and
Surgeons/New York-Presbyterian Hospital, New York, NY, USA. Department of
Pulmonary and Critical Care, Langone Medical Center, New York University, New
York, USA. Department of Intensive Care, Pontificia Uni-versidad Catholica de
Chile, Santiago, Chile.
Section Editor
Jan Bakker Prof. Dr., Department of Intensive Care Adults, Erasmus MC
University Medical Center, Rotter-dam, The Netherlands. Division of Pulmonary,
Allergy, and Critical Care, Columbia University College of Physicians and
Surgeons/New York-Presbyterian Hospital, New York, NY, USA. Department of
Pulmonary and Critical Care, Langone Medical Center, New York University, New
York, USA. Department of Intensive Care, Pontificia Uni-versidad Catholica de
Chile, Santiago, Chile.
ELearning Committee
Chair
Kobus Preller Dr., Consultant, John Farman ICU, Cambridge University Hospitals
NHS Foundation Trust, Cambridge, UK
Deputy
Mo Al-Haddad MD, Consultant in Anaesthesia and Critical Care, Queen Elizabeth
University Hospital; Honorary Clinical Associate Professor University of Glasgow,
Glasgow UK
Project Manager
Estelle Pasquier , European Society of Intensive Care Medicine
First Edition 2019
Module Authors
Jose Alfonso Rubio Mateo Sidron MD, Intensive Care Unit. Hospital
Universitario 12 de octubre, Madrid.
Patricia Marquez Lozano MD, Cardiology Service. Hospital Infanta Cristina.
Badajoz. Spain
Sara Helena De Miguel Martin MD, Intensive Care Unit. Hospital de Villalba.
Madrid. Spain
Eduardo Morales Sorribas MD, Intensive Care Unit. Hospital Sanitas-La
Moraleja. Madrid. Spain
Module Reviewers
Daniel Caeiro MD, Cardiac Intensive Care Unit. Centro Hospitalar Vila Nova de
Gaia/Espinho, Porto, Portugal
Robert von Arx MD, University Hospital Bern, Switzerland
Section Editor
Jan Bakker Prof. Dr., Department of Intensive Care Adults, Erasmus MC
University Medical Center, Rotter-dam, The Netherlands. Division of Pulmonary,
Allergy, and Critical Care, Columbia University College of Physicians and
Surgeons/New York-Presbyterian Hospital, New York, NY, USA. Department of
Pulmonary and Critical Care, Langone Medical Center, New York University, New
York, USA. Department of Intensive Care, Pontificia Uni-versidad Catholica de
Chile, Santiago, Chile.
CoBaTrICE Mapping Contributors
Cristina Santonocito MD, Dept. of Anesthesia and Intensive Care, IRCSS-
ISMETT-UPMC, Palermo, Italy
Victoria Anne Bennett MD, St George’s Hospital, London, United Kingdom
Co-Ordinating Editor
Joana Berger Estilita MD, Consultant in Anaesthesia and Intensive Care
Department of Anaesthesia and Pain Therapy, Bern University Hospital, University
of Bern, Switzerland
Executive Editor
Mo Al-Haddad MD, Consultant in Anaesthesia and Critical Care, Queen Elizabeth
University Hospital; Honorary Clinical Associate Professor University of Glasgow,
Glasgow UK
Update Info 
Intended Learning Outcomes
Acute myocardial ischaemia Terminology, Pathophysiology
and Recognition: Introduction
1. Review the latest definition, causes and pathophysiology of acute coronary
syndrome
2. Recognise how to confirm a diagnosis of acute coronary syndrome with the
use of the contemporary detection strategies
3. Demostrate how to manage acute coronary syndrome with the latest
strategies
4. Recognise the evidence based secondary prevention strategy in acute
coronary syndrome.
5. Distinguish between myocardial injury and myocardial infarction (MI)
Acute myocardial ischaemia Terminology, Pathophysiology
and Recognition: Terminology
1. Distinguish between myocardial injury and myocardial infarction (MI)
2. Distinguish between acute myocardial injury with/without myocardialischaemia and chronic myocardial injury
3. Define and differentiate UA, NSTEMI, and STEMI.
4. Distinguish between acute myocardial injury related to either acute coronary
athero-thrombosis (MI type 1) or to an imbalance between myocardial
oxygen supply/demand secondary to underlying stressor(s) (MI type 2)
5. Distinguish between procedural related myocardial injury and procedural
related myocardial infarction (MI types 4a or 5)
Acute myocardial ischaemia Terminology, Pathophysiology
and Recognition: Pathophysiology
https://collaboration.esicm.org/tracker75
1. Discuss the pathophysiology of acute coronary syndromes describing the
role of atherosclerotic plaque, platelets, and the coagulation system.
2. Describe the therapy for acute coronary syndromes (aspirin, thrombolytic
therapy, etc.) in terms of the underlying pathophysiology
3. Explain the complications of acute myocardial infarction
4. Define the mechanisms of heart failure and cardogenic shock in coronary
artery disease
Acute myocardial ischaemia Terminology, Pathophysiology
and Recognition: Recognition
1. Triage, identify and activate immediate management strategies of patients
with suspected ACS
2. Apply algorithm diagnostic to rule in/out ACS (ECG, biomarkers and
imaging techniques) and confirm a diagnosis of AMI
3. Distinguish ST-segment elevation MI (STEMI) and non-STEMI by different
prognosis and treatment strategy
4. Detect ACS and distinguish the types of myocardial infarction that can occur
in critically ill patients
5. Discuss the role of primary PCI in the management of AMI and appropriate
pharmacotherapy
6. Establish risk stratification models (clinical, ischemic and bleeding) of
STEMI and non-SETMI
eModule Information
Relevant Competencies from CoBaTrICE
Acute myocardial ischaemia Terminology, Pathophysiology
and Recognition: Introduction
Adopts a structured and timely approach to the recognition, assessment and
stabilisation of the acutely ill patient with disordered physiology
Undertakes timely and appropriate investigations
Manages the care of the critically ill patient with specific acute medical
conditions
Collaborates and consults; promotes team-working
Critically appraises and applies guidelines, protocols and care bundles
Ensures continuity of care through effective hand-over of clinical information
Acute myocardial ischaemia Terminology, Pathophysiology
and Recognition: Terminology
Obtains a history and performs an accurate clinical examination
Performs electrocardiography (ECG / EKG) and interprets the results
Integrates clinical findings with laboratory investigations to form a differential
diagnosis
Acute myocardial ischaemia Terminology, Pathophysiology
and Recognition: Pathophysiology
Define the Pathophysiology of cardiovascular disorders including: unstable
angin, acute myocardial infarction, left and right ventricular failure, arrhythmias
and conduction disturbances and cardiogenic shock.
Basic science. Anatomy of the Cardiovascular System:
Heart: chambers, valves, conducting system, arterial blood supply and
pericardium
Physiology and biochemistry of the heart and circulation:
Cardiac muscle contraction.The cardiac cycle.Regulation of cardiac
function. Characteristics of coronary circulation. Electrocardiogram and
arrhythmias.Peripheral circulation: capillaries, vascular endothelium and
arteriolar smooth muscle. Neurological and humoral control of systemic
blood pressures, blood volume and blood flow.
Acute myocardial ischaemia Terminology, Pathophysiology
and Recognition: Recognition
Adopts a structured and timely approach to the recognition, assessment and
stabilisation of the acutely ill patient with disordered physiology.
Triages and prioritises patients appropriately, including timely admission to ICU.
Obtains a history and performs an accurate clinical examination.
Undertakes timely & appropriate investigations.
Performs electrocardiography (ECG / EKG) and interprets the results.
Monitors and responds to trends in physiological variables.
Integrates clinical findings with laboratory investigations to form a differential
diagnosis.
Manages the care of the critically ill patient with specific acute medical
conditions.
Recognises and manages the patient with circulatory failure.
Prescribes drugs and therapies safely.
Administers oxygen using a variety of administration devices
Communicates effectively with members of the health care team
Communicates effectively with patients and relatives
Maintains accurate and legible records / documentation
Involves patients (or their surrogates if applicable) in decisions about care and
treatment
Faculty Disclosures: 
The authors of this module have not reported any disclosures.
Copyright©2019. European Society of Intensive Care Medicine. All rights reserved.
1. Introduction
The most obvious effect of coronary artery disease (CAD) is the compromise on the
oxygenation of the myocardial cells, which leads to an entity known as ischemic heart
disease. CAD cause approximately one third of all deaths in persons above 35 years
old.
In its acute form, it initially presents as a particularly serious condition known as acute
coronary syndrome (ACS) and represents a group of medical conditions with different
stages of a continuum that may be indistinguishable at presentation to emergency
departments. They share similar pathogenic mechanisms, being the common link the
rupture of a vulnerable coronary atherosclerotic plaque and the formation of the
intracoronary thrombus.
ACS account for nearly 2 million hospitalizations annually in the United States, and if
patients who die before reaching the hospital are included, the mortality may be as
high as 25%.
The ACS is a major challenge time-dependent process where time is muscle. The
existence of a well-organized network for rapid assistance from the moment it occurs
and transfers to the appropriate hospital is essential. The monitoring of the diagnostic
and therapeutic process based on guidelines of clinical practice, following local
protocols and applied by a multiprofessional team of doctors, nurses and technicians,
where ICU staff should participate, are the best guarantee of the best results.
After being treated in the Emergency Department, and some of them go through the
hemodynamics laboratory, many of these high risk patients are in current practice
finally admitted to the Intensive Care Unit (ICU) / Coronary Care Unit under the
responsibility and direct supervision of the intensivist physician depending on the local
health organization.
 Note
The management of acute coronary syndromes (ACS) is evolving rapidly
The management of patients with ACS is changing and evolving rapidly. The advances
achieved in recent years in the knowledge of pathophysiological mechanisms of the
ACS have meant in practice to have new drugs and procedures that have improved
the diagnostic process and treatment, achieving better short and long term results. At
the same time, the intensivist doctor is faced with new complex situations and difficult
decisions to obtain the best risk/benefit ratio that requires an updated knowledge of
the disease and its management. This is generally drawn from multicentre studies of
patients presenting to emergency departments or chest pain/coronary unit. In patients
already admitted to the ICU, ACS is a difficult diagnosis to make as there are often
multiple possible causes for a raised troponin or ECG changes and there is often a
lack of clinical history to put these results into context. In addition, establishing the
type of myocardial infarction and reason for the troponin rise is especially important in
patients admitted to the ICU for its implications in the treatment and prognosis.
 Note
Patients with ACS are at high risk
In text References
(Reed, Rossi and Cannon 2017; Werns 2019; Carroll, Mount and Atkinson 2016;
Fuster et al. 1992)
 References
Reed GW, Rossi JE, Cannon CP, Acute myocardial infarction., 2017,
PMID:27502078
Werns S, Acute Coronary Syndromesand Acute Myocardial Infarction.,
Elsevier, 2019, Philadelphia, ISBN: 9780323446761
Carroll I, Mount T, Atkinson D, Myocardial infarction in intensive care units:
A systematic review of diagnosis and treatment., 2016, PMID:28979516
Fuster V, Badimon L, Badimon JJ, Chesebro JH., The pathogenesis of
coronary artery disease and the acute coronary syndromes (1)., 1992,
PMID:1727977
https://www.ncbi.nlm.nih.gov/pubmed/27502078
https://www.ncbi.nlm.nih.gov/pubmed/28979516
https://www.ncbi.nlm.nih.gov/pubmed/1727977
2. Terminology
ACS has evolved as a useful operational term that refers to a spectrum of conditions
compatible with acute myocardial ischemia and/or infarction that are usually due to an
abrupt reduction in coronary blood flow.
These syndromes are almost always caused by acute rupture or erosion of pre-
existing coronary artery atherosclerotic plaque, leading to acute thrombus formation,
closure of coronary arteries and impaired myocardial oxygen supply.
The underlying rationale is that regional myocardial hypoperfusion and ischaemia lead
to a cascade of events including myocardial dysfunction and cell death, early
releasable cytosolic pool biomarkers (troponin -cTn- and creatine kinase MB isoform -
CK MB-) into the blood stream from stressed cardiomyocytes.
ACS has traditionally been classified into Q-wave or transmural myocardial infarction,
non-Q-wave or no transmural myocardial infarction (NQMI), and unstable angina (UA).
This classification refers to a later phase in the evolution of the clinical process.
In initial assistance it is more useful to use the classification based on the initial
electrocardiogram. Patients are divided into three groups:
(1) those with ST– elevation (STEMI) on the presenting or subsequent 12-lead
ECGs
(2) those without ST elevation on the presenting or subsequent 12-lead ECGs but
with enzyme evidence of myocardial damage (non–ST elevation MI or NSTEMI),
and
(3) those with UA.
The importance of this classification lies in the fact that the initial ECG changes
coincide with current treatment strategies: STEMI benefit from immediate reperfusion.
In contrast fibrinolytic agents should not be used in NSTEMI.
2. 1. Unstable Angina (UA)
UA is considered to be present in patients with ischemic symptoms suggestive of an
ACS and no elevation in troponins, with or without electrocardiogram changes
indicative of ischemia (eg, ST segment depression or transient elevation or new T
wave inversion).
Myocardial infarction differs from unstable angina, which is usually precipitated by
increased myocardial oxygen demand (e.g. exertion, fever, tachycardia) with
background coronary artery narrowing (limitation of oxygen supply).
Stable exertional angina results from an imbalance in myocardial oxygen supply and
demand, in this case brought on by increased demand (e.g. exertion, fever,
tachycardia) with a limitation oxygen supply (coronary artery narrowing).
In UA ischaemic type chest pain, which is of recent origin, is more frequent, severe, or
prolonged than the patient’s usual angina; is more difficult to control with drugs; or is
occurring at rest or on minimal exertion.
In text References
(Ford, Corcoran and Berry 2018) 
 References
Ford TJ, Corcoran D, Berry C, Stable coronary syndromes:
pathophysiology, diagnostic advances and therapeutic need., 2018,
PMID:29030424
2. 2. Myocardial Infarction
An updated classification of myocardial infarction has been recently published that
takes into account the setting in which ACS has been diagnosed (see table 1). This
differentiation is extremely important in severe acute illness or postoperative settings
admitted to the ICU, as trial data obtained in different settings may or may not be fully
applicable.
Detection of an elevated cTn value above the 99th percentile upper reference limit
(URL) is defined as myocardial injury. The injury is considered acute if there is a rise
and/or fall of cTn values.
Although elevated cTn values reflect injury to myocardial cells, they do not indicate the
underlying pathophysiological mechanisms, and myocardial ischaemic or non-
ischaemic conditions associated with increased cTn values are presented in Table 1.
This is important in ICU setting because many causes of myocardial injury are
common in critical ill patients.
Table 1: Causes of Myocardial Injury. Reproduced from: Thygesen K,
Alpert JS, Jaffe AS, et al., 2018
https://www.ncbi.nlm.nih.gov/pubmed/29030424
Myocardial injury related to acute myocardial ischaemia
Atherosclerotic plaque disruption with thrombosis
Myocardial injury related to acute myocardial ischaemia
because of oxygen supply/demand imbalance
Reducer myocardial perfusion, e.g.
Coronary artery spasm, microvascular dysfunction
Coronary embolism
Coronary artery dissection
Sustained bradyarrhythmia
Hypotensive or shock
Respiratory failure
Severe anaemia
Increased myocardial oxygen demand, e.g.
Sustained tachyarrhythmia
Severe hypertension with or without left ventricular
hypertrophy
Other causes of myocardial injury
Cardiac conditions, e.g.
Heart failure
Myocarditis
Cardiomyopathy (any type)
Takotsubo syndrome
Coronary revascularization procedure
Cardiac procedure other tan revascularization
Catheter ablation
Defibrillator shocks
Cardiac contusion
Systemic conditions, e.g.
Sepsis, infectious disease
Chronic kidney disease
Stroke, subarachnoid haemorrhage
Infiltrative disease, e.g. amyloidosis, sarcoidosis
Chemotherapeutic agents
Critically ill patients
Strenuous exercise
 
The clinical definition of AMI denotes the presence of acute myocardial injury in the
setting of evidence of acute myocardial ischaemia.
The diagnosis of AMI relies on criteria established by a committee grouping the
European Society of Cardiology (ESC), the American College of Cardiology (ACC), the
American Heart Association (AHA), and the World Heart Federation (WHF). Indeed,
according to the Fourth Universal Definition, AMI is a clinical event consequent to the
death of cardiac myocytes (myocardial necrosis) that is caused by ischemia (as
opposed to other aetiologies). According to this definition, spontaneous myocardial
infarction (also known as Type 1) occurs in cases of detection of a rise and/or fall of
cardiac biomarker values (preferably cardiac troponin) with at least one value above
the 99th percentile upper reference limit (URL) and with at least one of the following:
symptoms of ischemia, ischemic ECG changes, identification of an intracoronary
thrombus by angiography, or imaging evidence of new loss of viable myocardium or a
new regional wall motion abnormality.
The other types of myocardial infarction identified according to the Fourth Universal
Definition are as follows: Type 2, myocardial infarction due to ischemic blood
supply/demand imbalance; Type 3, cardiac death presumed to be caused by
myocardial infarction when markers of myocardial injury are unavailable; Type 4a,
myocardial infarction associated with percutaneous coronary intervention (arbitrary
defined by elevation of biomarker values higher than five times 99th percentile URL in
patients with normal baseline values or a rise of values over 20% if the baseline values
are elevated but stable or falling); Type 4b, myocardial infarction related to stent
thrombosis; Type 4c, caused by restenosis associated with percutaneous coronary
intervention and Type 5, myocardial infarction associated to coronary artery bypass
grafting (arbitrary defined by elevation of biomarker values over 10 times the 99th
percentile URL in patients with normal baseline values) (Table 2).
Table 2: Clinical classification of different types of myocardial
infarction
Type Classification Description
Type 1
Myocardial infarction (MI) caused by
atherothrombotic coronary artery
disease and usually precipitated by
atherosclerotic plaque disruption.
Type 2
MI in a context of a mismatch between
oxygen supply and demand (eg.
Coronary artery spasm, anaemia,
arrhythmias or hypotension).
Type 3
Sudden cardiac death with symptoms
suggestiveof myocardial ischaemia
accompanied by presumed new
ischemic changes or ventricular
fibrillation, but die before biomarkers
can be obtained. Is detected by
autopsy examination.
Type 4a
MI after percutaneous coronary
intervention (< 48 h).
Type 4b
MI associated with stent thrombosis as
documented by angiography or
autopsy.
Type 4c
MI associated with restenosis after
percutaneous coronary intervention.
Type 5
MI associated with coronary artery
bypass grafting (<48h).
Differentiating between Type 1 and 2 MI is very important in Critical Care setting: dual
antiplatelet therapy is only indicated in Type 1 MI. Factors that point to a diagnosis of
Type 2 MI include presence of another definitive diagnosis known to be associated
with an increase in troponin levels.
A conceptual model to facilitate the clinical distinction between acute ischaemic
myocardial injury with or without an acute atherothrombotic event (Type 1 or Type 2
MI) vs. conditions without acute ischaemic myocardial injury is displayed in Figure 1
Figure 1: A model for interpreting myocardial
injury. Reproduced from: Thygesen K, Alpert JS,
Jaffe AS, et al., 2018.
Figure 1: A model for interpreting myocardial injury. Ischaemic thresholds vary
substantially in relation to the magnitude of the stressor and the extent of underlying
cardiac disease. MI = myocardial infarction; URL = upper reference limit. (a) Stable
denotes ≤ 20% variation of troponin values in the appropriate clinical context. (b)
Ischaemia denotes signs and/or symptoms of clinical myocardial ischaemia.
In text References
(Thygesen et al. 2018) 
 
 References
Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, White
HD; ESC Scientific Document Group., Fourth universal definition of
myocardial infarction (2018)., 2018, PMID:30165617
https://collaboration.esicm.org/dl1536?display
https://www.ncbi.nlm.nih.gov/pubmed/30165617
2. 3. Myocardial infarction with non obstructive coronary
arteries (MINOCA)
It is increasingly recognized that there is a group of MI patients with no angiographic
obstructive CAD (≥ 50% diameter stenosis in a major epicardial vessel), and the term
myocardial infarction with non-obstructive coronary arteries (MINOCA) has been
coined for this entity.
 Note
For MINOCA keep in mind that other aetiologies for the symptoms and changes
in ECG and cardiac biomarkers must be evaluated.
In text References
(Pasupathy et al. 2015; Agewall et al. 2017) 
 References
Pasupathy S, Air T, Dreyer RP, Tavella R, Beltrame JF, Systematic review of
patients presenting with suspected myocardial infarction and nonobstructive
coronary arteries., 2015, PMID:25587100
Agewall S, Beltrame JF, Reynolds HR, Niessner A, Rosano G, Caforio AL,
De Caterina R, Zimarino M, Roffi M, Kjeldsen K, Atar D, Kaski JC, Sechtem
U, Tornvall P, WG on Cardiovascular Pharmacotherapy., ESC working
group position paper on myocardial infarction with non-obstructive coronary
arteries., 2017, PMID:28158518
2. 4. Myocardial infarction in the Intensive Care Unit
The pathophysiology of infarction in many ICU patients is probably different to that of
ACS. Studies suggest that, in the presence of severe ischaemia, left main disease and
triple-vessel disease are common and that ischaemia is secondary to oxygen supply
and demand problems (Type 2 MI) rather than thrombosis.
Some elevation of cTn values may reflect Type 2 MI due to underlying CAD and
increased myocardial oxygen demand, whereas in other patients, Type 1 MI may occur
because of plaque disruption leading to thrombosis in a coronary artery. However,
other patients may have elevated cTn values and marked decreases in ejection
fraction (EF) due to sepsis caused by endotoxin, with myocardial function recovering
completely with normal EF once the sepsis is treated.
https://www.ncbi.nlm.nih.gov/pubmed/25587100
https://www.ncbi.nlm.nih.gov/pubmed/28158518
It is frequently challenging for the clinician caring for a critically ill patient to decide on
a plan of action when the patient has elevated cTn values.
Furthermore the clinical presentation is often different and establishing the diagnosis
and weighting the relevance of elevated biomarkers can be challenging. Clinical
judgement should be employed to decide whether further evaluation for CAD or
structural heart disease is indicated.
 Note
in association with ECG an serial cTn consider the use of echocardiography to
identify 
regional wall motion abnormality (RWMA) for diagnosis of AMI in ICU setting.
In text References
(Mazzarelli and Hollenberg. 2017; Bradley P. Sppelt. 2019) 
 References
Mazzarelli J, Hollenberg S., Acute Coronary Syndromes: Therapy., 2017,
ISBN:9780323376389
Bradley P. Sppelt I., Acute cardiac syndromes, investigations and
interventions., 2019, ISBN:97807020722215
3. Pathophysiology Of Acute Myocardial Ischaemia,
Infraction and Cardiogenic Shock
The majority of patients with acute MI have coronary artery atheroma. ACS usually
results from the formation of either totally or partially occluding thrombus upon
disrupted, fissured or eroded atheromatous plaque.
3. 1. Understanding the underlying mechanisms
MI is caused mainly by atherothrombotic of a coronary artery disease (CAD) and
usually precipitated by atherosclerotic plaque disruption (rupture or erosion) of a major
epicardial vessel. 
Often termed vulnerable plaques, atherosclerotic plaque tend to have a thin fibrous
cap over a central core of foam cells, lipids, and necrotic debris is designated as a
type 1 MI. Exposed subendothelial matrix to circulating blood leads to platelet
adhesion and activation, thrombin generation, thrombus formation and myocardial cell
death due to prolonged ischaemia. 
The first ultrastructural changes are seen as early as 10–15 min after the onset of
ischaemia. It can take hours before myocyte necrosis evolves and progresses from the
subendocardium to the subepicardium. The time course may be prolonged by
increased collateral flow and reduced determinants of myocardial oxygen
consumption. Timely implementation of reperfusion therapy, when appropriate,
reduces ischaemic injury to the myocardium. 
The exact cause of plaque rupture or fissuring is unknown. Inflammatory processes
with activation of metalloproteinases that degrade collagen in the fibrous cap and
inhibit synthesis of new collagen and acute hemodynamic stress are synergistically
associated with increased adrenergic tone and are considered important triggers of
plaque rupture. 
Lipid-lowering agents may stabilise plaque not only by lowering plaque cholesterol but
also through lipid independent (‘pleiotropic’) anti-inflammatory effects.
3. 1. 1. Pathophysiology correlated with presenting syndrome
The relative burden of atherosclerosis and thrombosis in the culprit lesion varies
greatly, and the dynamic thrombotic component may lead to total occlusion of an artery
supplying a substantial volume of myocardium typically leading to ST-segment
elevation myocardial infarction (STEMI) or partial non-occlusive thrombus of the vessel
determines leading to non–ST-segment elevation myocardial infarction (NSTEMI).
NSTEMI and Unstable Angina are usually caused by an imbalance between
myocardial oxygen supply and demand, which may be due to one or more of the
following causes:
Non-occlusive thrombus developing on a pre-existing plaque (the most frequent
cause). Arterial inflammation or infection can predispose to plaque rupture.
Dynamic obstruction – spasm of an epicardial artery or intramural
vasoconstriction.
Progressive coronary narrowing without spasm or thrombus. May be due to
progressive atherosclerosis or restenosis after a PCI.
Secondary UA (‘demand ischaemia’). Patients with chronic atherosclerotic
narrowing are subjected to increased myocardial oxygen demand (fever,
tachycardia) or reduced oxygen delivery (hypotension, anaemia).
Development of thrombus upon eroded plaque results from:
1. platelet adherence and activation, and
2. coagulation pathway activation.
Platelets aggregate to form”white thrombus”, however this thrombus is seldom totally
occluding. Activation of coagulation pathways by exposed lipid and fibrin, as well as by
the now-activate platelets, leads ultimately to thrombin activation and the laying-down
of fibrin clot. Red cells are enmeshed in this so-called ”red thrombus” complex, which
surrounds the white thrombus.
These processes have immediate relevance to treatment:
Antiplatelet agents prevent platelet adherence, which limits and even reverses the
development of “white thrombus” these agents may target the adenosine
diphoshate (ADP) receptor (e.g. clopiogrel, prasugrel, ticagrelor) or may inhibit
cyclo-oygenase and synthesis of thromboxane A2 (e.g. aspirin), but it fails to block
platelet activation by thrombin, ADP and collagen
Fibrinolytic agents lyse “red thrombus” but are not active against “white thrombus”
Antithrombin agents (eg heparins) may limit thrombin activation. Current
thrombolytic agents lyse fibrin and red cell thrombus, but paradoxically may
increase surface thrombin activation
Totally occluding thrombus causes myocardial necrosis and is often accompanied
by ST-segment elevation (STE) on the ECG
If thrombus is largely white thrombus, with minimal or non-occlusive may cause
USA or MI, especially if spasm or distal embolisation of thrombus occurs non-
occlusive plaque it is indicative of unstable plaque and is strongly associated with
reinfarction and death in following months.
3. 2. Pathophysiology of the complications and sequelae of
Myocardial Infarction
Ischaemic necrosis results in cellular disruption, loss of function, thinning and
softening of the affected myocardium with an increase in ventricular compliance. As
fibrosis takes place compliance is decreased. With time, there is often expansion of
the infarcted segment and compensatory hypertrophy of unaffected myocardial cells is
also known as ventricular remodelling.
After an AMI, mechanical problems that result from dysfunction or disruption of critical
myocardial structures may occur portending a significantly worse outcome.
After an AMI, mechanical problems that result from dysfunction or disruption of critical
myocardial structures may occur portending a significantly worse outcome.
Cardiogenic shock usually results from extensive loss of left ventricle contractile
function.
Severe ischemia or infarction can lead to papillary muscle dysfunction or rupture,
resulting in mitral valve regurgitation of varying severity.
Ventricular septal defects may occur with extensive anterior and inferior wall
infarction.
Acute free wall rupture is a catastrophic event presenting with severe
hypotension.
Right ventricle infarction may lead to decreased compliance and decreased
systolic function thus causing venous congestion and low cardiac output.
In the long term, the left ventricle will undergo a transformation of its size and
shape through a process known as negative remodelling, this adversely affects
left ventricular function and can eventually lead to chronic heart failure.
Additionally, a wide diversity of potentially life-threatening cardiac dysrhythmias may
result from electrical instability due to ischemia, conduction disturbances, and
excessive sympathetic stimulation that occurs during the course of AMI.
Infarct size determines:
left ventricular systolic and/or diastolic function impairment
stroke volume decrease
ventricular filling pressure rise leads to pulmonary congestion and hypotension
that may impair coronary perfusion pressures and exacerbate the myocardial
ischaemia
 
3. 3. Understanding normal coronary artery anatomy
The main arteries of the heart are the:
Left main coronary artery which divides soon after its origin into:
Left anterior descending coronary artery (LAD)
Circumflex coronary artery (LCX)
Right coronary artery (RCA)
 Note
 
Remember, anatomy of the coronary vessels is highly variable between people
A detailed understanding of coronary anatomy is not necessary, but will significantly
improve the understanding of patients experiencing infarction. It is vital if you are
involved in the care of postoperative CABG (Coronary artery bypass grafting) patients.
 Think
Review the anatomy of the coronary vessels in any textbook and try to relate
anatomy, ECG changes, angiographic findings and clinical presentation when
reviewing any patient. See also table ‘Localisation of infarct using
electrocardiogram’.
Think about the Acute Coronary Syndrome in relation to the gender and the aging
process and in special situations (e.g. cocaine abuse and in pregnant women).
3. 4. Cardiogenic Shock
3. 4. 1. Etiology
Acute MI dysfunction due to acute occlusion of one or more coronary arteries with
subsequent LV due to ischaemic myocardium or necrosis is the most common clinical
entity leading to cardiogenic shock. As many as 81% of patients presenting with CS
had an underlying acute coronary syndrome (ACS), although up to 30% of the CS can
present in patients with a smaller infarction and previously chronic HF.
Cardiogenic shock complicates about 7–10% of STEMI and about 2–3% of NSTEMI.
While sometimes present at admission, shock most often does not arise until some
hours later. The median time after STEMI for the occurrence of shock is in the range of
5–6 hours. Shock complicating UA or NSTEMI seems to occur at a later time period,
with a median of 76 and 94 hours, respectively.
 Note
A high index of suspicion and rapid echocardiography are required for diagnosis
of CS.
In general, a loss of > 40% of functional myocardium is required to cause CS.
However, mechanical complications, such as acquired ventricular septal defect (VSD),
free wall rupture (FWR), and papillary muscle rupture or dysfunction, with subse-quent
ischaemic mitral regurgitation (MR), also contribute to CS after AMI 20. The causes of
CS have been described with an incidence of 78.5% for LV failure, 3.9% for VSD,
6.9% for ischaemic MR, 2.8% for right ventricular (RV) failure, and 1.4% for cardiac
tamponade.
In general, the underlying pathophysiology is a profound depression of myocardial
contractility, resulting in a vicious and potentially deleterious spiral of reduced cardiac
output, low blood pressure, further coronary ischaemia, and subsequent reduction in
contractility and cardiac output. This cycle may lead to death, if not interrupted by
adequate treatment. This classic paradigm also includes compensatory, although
pathological, systemic vasoconstriction that occurs in response to a depression of
cardiac function and ineffective stroke volume.
Although ineffective stroke volume is the inciting event, inadequate circulatory
compensation may also contribute to shock.
Extremity and vital organ hypoperfusion is the hallmark of CS. Compensatory
mechanisms by vasoconstriction lead to an intermittent improvement in the coronary
and peripheral perfusion, at the cost of an increased afterload. However,
vasoconstriction can be counterbalanced by systemic inflammation, leading to
subsequent pathologic vasodilatation that occurs frequently with increasing shock
duration.
Endothelial and inducible nitric oxide (NO) synthase may play a major role in the
production of high NO levels, along with peroxynitrite, which has a negative inotropic
effect and is cardiotoxic. Other inflammatory mediators such as interleukins and tumor
necrosis factor can also contribute to systemic vasodilation and have been associated
with mortality in CS.
In addition, bleeding and transfusions of stored blood products may also contribute to
inflammation induced by alterations in erythrocyte NO biology.
 Note
Cardiogenic shock may complicate myocardial infarction - remember the vicious
cycle of cardiogenic shock
Challenge
Review the following diagram (Figure 2) and article relating to the pathogenesis of
cardiogenic shock. Work through the diagram to understand the inexorably
progressive nature of cardiogenic shock. Try and relate it to the clinical findings and
investigation abnormalities that one might find.
https://collaboration.esicm.org/203. 4. 2. Downward spiral of Cardiogenic Shock
 
Figure 2: Downward spiral of Cardiogenic Shock.
Esicm Academy 2019
In Chapter References
(van Diepen et al. 2017; Van Herck et al. 2015; Kolte et al. 2014; Thiele et al. 2010;
van Diepen 2018; Crossman 2004; Reynolds and Hochman. 2008; Vahdatpour, Collins
and Goldberg 2019) 
 References
van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, Kilic
A, Menon V, Ohman EM, Sweitzer NK, Thiele H, Washam JB, Cohen MG;
American Heart Association Council on Clinical Cardiology; Council on
Cardiovascular and Stroke Nursing; Council on Qu, Contemporary
Management of Cardiogenic Shock: A Scientific Statement From the
American Heart Association., 2017, PMID:28923988
Van Herck JL, Claeys MJ, De Paep R, Van Herck PL, Vrints CJ, Jorens PG,
Management of cardiogenic shock complicating acute myocardial
infarction., 2015, PMID:25624526
Kolte D, Khera S, Aronow WS, Mujib M, Palaniswamy C, Sule S, Jain D,
Gotsis W, Ahmed A, Frishman WH, Fonarow GC., Trends in incidence,
management, and outcomes of cardiogenic shock complicating ST-
elevation myocardial infarction in the United States., 2014, PMID:24419737
Thiele H, Allam B, Chatellier G, Schuler G, Lafont A., Shock in acute
myocardial infarction: the Cape Horn for trials?, 2010, PMID:20610640
van Diepen S, Norepinephrine as a First-Line Inopressor in Cardiogenic
Shock: Oversimplification or Best Practice?, 2018, PMID:29976292
Crossman DC, The pathophysiology of myocardial ischaemia., 2004,
PMID:15084567
Reynolds HR, Hochman JS., Cardiogenic shock: current concepts and
improving outcomes., 2008, PMID:18250279
Vahdatpour C, Collins D, Goldberg S, Cardiogenic Shock., 2019,
PMID:30947630
https://collaboration.esicm.org/dl1550?display
https://www.ncbi.nlm.nih.gov/pubmed/28923988
https://www.ncbi.nlm.nih.gov/pubmed/25624526
https://www.ncbi.nlm.nih.gov/pubmed/24419737
https://www.ncbi.nlm.nih.gov/pubmed/20610640
https://www.ncbi.nlm.nih.gov/pubmed/29976292
https://www.ncbi.nlm.nih.gov/pubmed/15084567
https://www.ncbi.nlm.nih.gov/pubmed/18250279
https://www.ncbi.nlm.nih.gov/pubmed/30947630
4. Recognition, Immediate Measures and Risk
Stratification of the Patient with Acute
Myocardial Ischaemia
Diagnosis of ACS is particularly challenging, due to numerous cardiac and noncardiac
potentially life-threatening causes and comorbidities that can mimic it. Every patient
with chest pain should rapidly have a comprehensive evaluation including assessment
of symptoms at presentation, clinical history and examination of the cardiovascular
system, standard 12-lead ECG, and evaluation of serum markers of myocardial injury.
When AMI is diagnosed, risk stratification based on the data obtained during the initial
workup is a next step to predict the risk of adverse events and guide optimal treatment
(Figure 3)
Figure 3: Guide optimal treatment. Esicm
Academy 2019.
 Note
 
ECG is important for the recognition of acute ischaemia. In patients with
suspected ACS it should be acquired and interpreted promptly (i.e. target within
10 min). A very low threshold should be used to determine whether an ECG is
necessary, since presentations may be atypical.
ACS is often associated with dynamic changes in ECG waveform and serial ECG
acquisition can provide critical information, particularly if the ECG at initial presentation
is not diagnostic.
4. 1. Clinical features of ischaemic chest pain
The diagnosis of suspected myocardial ischaemia is usually made on the basis of
clinical history and ECG. It is important to realize the the clinical presentation can often
be atypical or silent in the intensive care setting.
In text References 
(Carroll, Mount and Atkinson 2016; Booker et al. 2003; Guest et al. 1995; Ko et al.
2013) 
Initial patient assessment is directed to accurately characterize the patient’s discomfort
and identify its location, duration, aggravating, and relieving factors.
https://collaboration.esicm.org/dl1538?display
Patients with myocardial ischaemia can present with:
Chest pain or pressure
Syncope
Palpitations
Dyspnoea
Sudden death.
Abdominal pain
Typically the pain of myocardial infarction is:
Severe
Constant
Retrosternal
Spreading across the chest. May radiate to the throat and jaw, down the ulnar
aspect of both arms or to the interscapular area.
Duration > 20 minutes.
Sweating, nausea, pallor, dyspnoea and anxiety often present.
 Note
 
Focus your history. A high index of suspicion is necessary in the ICU
 Note
Prodromal symptoms of myocardial ischaemia occur in 20–60% of patients in
the days preceding the infarct.
Assessment of clinical symptoms alone is insufficient for risk stratification and severity
of pain does not usually correlate with the extent of infarction
The pain of unstable angina may be similar, although it’s often milder. Features
indicating myocardial ischaemia may include:
Waxing and waning.
Often reproducible upon minimal exertion or with emotion
Often associated with autonomic symptoms.
The pain may sometimes be atypical in terms of location or perception. It may be: 
• Epigastric 
• Confined to jaw, arms, wrists or interscapular region 
• Perceived as burning or as a “pressure” 
• Sharp or stabbing in nature (uncommon) 
• Reproduced by chest pressure (uncommon) in some patients.
Pain may not be the pre-eminent symptom and in many patients nauseas and
vomiting, collapse, dyspnoea and diaphoresis may be more troublesome symptoms.
 Note
Skill is required to elicit warning symptoms in some patients, especially women
and the elderly.
In some patients, myocardial infarction may occur without any symptoms (silent
presentation) and are less likely to receive definitive treatment. For example patients
with diabetes mellitus can have only minimal or no symptoms.
In text References 
(Chiariello and Indolfi. 1996) 
Failure in the differential diagnosis of myocardial infarction may have life-threatening
consequences:
Aortic dissection
Pulmonary embolism.
Pericarditis
 Note
 
History taking and physical examination are crucial but... do not delay specific
treatment.
A targeted review for other significant patient’s medical history should aim at
identifying problems including usual medical treatment, cardiovascular risk factors,
previous cardiovascular disease, other conditions affecting the oxygen supply–demand
ratio or acting as ischemia precipitants and those relevant to thrombolysis,
anticoagulation and angiography.
It will help you appreciate the importance of obtaining a time efficient but accurate
history if you prepare your own checklist with the items prioritised. In the next ten
patients with chest pain you see and determine how relevant and useful your list
proves to be. Especially develop skills in determining features of acute coronary
syndromes.
 Note
Recognition of the variable symptoms of acute coronary syndrome is crucial.
However, symptoms alone are not sufficiently specific to allow accurate risk
stratification and treatment selection for patients with ACS. Special test are
required.
 Note
Develop skills to get a good history of acute and chronic cardiac disease
In text References 
(Boon. 2019) 
 References
Carroll I, Mount T, Atkinson D, Myocardial infarction in intensive care units:
A systematic review of diagnosis and treatment., 2016, PMID:28979516
Booker KJ, Holm K, Drew BJ, Lanuza DM, Hicks FD, Carrigan T, Wright M,
Moran J., Frequency and outcomes of transient myocardial ischemia in
critically ill adults admitted for noncardiac conditions., 2003,
PMID:14619356
Guest TM, Ramanathan AV, Tuteur PG, Schechtman KB, Ladenson JH,
Jaffe AS., Myocardial injury in critically ill patients. A frequently
unrecognized complication., 1995, PMID:7783306
Ko Y, Park C, Kim W, Jeong B, Suh G, Lim S, Kwon J, Jeon K, Coronary
artery disease in patients clinically diagnosed with myocardial infarction in
the medical intensive care unit, 2013,
https://www.sciencedirect.com/science/article/abs/pii/S0883944113000063
Chiariello M, Indolfi C., Silent myocardialischemia in patients with diabetes
mellitus., 1996, PMID:8925575
Boon N., Cardiovascular and physical examination., 2019,
ISBN:9780198784906
4. 2. Triage and early risk stratification
The clinical presentation of myocardial ischaemia is most often acute chest discomfort.
It is essential that initial assessment and management are rapid but methodical
according to the institutional protocols for triaging and managing patients who present
with symptoms suggestive of myocardial ischaemia.
Initial examination should include assessment of hemodynamic and respiratory status
and a screening neurologic evaluation.
Heart rate, arterial blood pressure, auscultation of the lung and peripheral pulses
palpation are essential parts of physical examination.
Patients with severe infarction and extensive myocardial injury often show signs of
autonomic activation (pallor, sweating, agitation) as well as heart failure symptoms and
even cardiogenic shock may be apparent and are associated with particular poor
outcome.
Right ventricular infarction results in hypotension and marked elevation of the jugular
venous pressure.
Early risk stratification of acute and persistent chest pain suggestive of myocardial
ischaemia is based on simple criteria:
History, clinical symptoms and signs
ECG
https://www.ncbi.nlm.nih.gov/pubmed/28979516
https://www.ncbi.nlm.nih.gov/pubmed/14619356
https://www.ncbi.nlm.nih.gov/pubmed/7783306
https://www.sciencedirect.com/science/article/abs/pii/S0883944113000063
https://www.ncbi.nlm.nih.gov/pubmed/8925575
Biochemical markers (serial)
 Note
 
Other investigations (e.g. echocardiography) are required in certain situations.
Early triage thus allows some patients to be diagnosed as having:
STEMI
NSTEMI
Non-coronary chest pain (including potential life-threatening conditions such as
aortic dissection, pulmonary embolism, and oesophageal rupture) or
Stable angina suitable for outpatient management
See Risk scoring systems for further details
 Note
Identify patients with non-cardiac chest pain and with stable angina.
4. 3. Immediate management of ACS
If acute coronary syndrome (ACS) is the leading suspected differential diagnosis,
immediate and rapid clinical evaluation of a patient complaining of chest pain, includes
non-invasive blood pressure measurement, pulse oximetry and continuous ECG
monitoring.
Delay in initiating therapy is associated with worsening outcome. Immediate treatment
and management is critical and include:
12-lead ECG within 10 minutes after first medical contact (Table 3). The ECG
should be repeated at 15 to 30-minute intervals if the initial study is not diagnostic
but the patient remains symptomatic and high clinical suspicion for ACS persists.
ECG, arterial pressure and SpO2 continuous monitoring.
Oxygen should be administered via facemask or nasal cannula when blood
oxygen saturation is < 90% or if the patient is in respiratory distress.
Venous access (reserve right arm for radial access during the ICP). Blood is
drawn for cardiac biomarkers (high sensitive cardiac troponin if available),
biochemical and haematological work-up including indices of coagulation and
renal function,
Intravenous nitrates must be considered (intravenous are more effective than
sublingual nitrates), their dose should be titrated upwards until symptoms are
relieved. Beyond symptom control, there is no indication for nitrate treatment.
https://collaboration.esicm.org/AMI+Terminology%2C+Pathophysiology+and+Recognition%3A+Recognition+of+AMI%3A+Risk+Scoring+Systems?page_ref_id=3188
Sublingual nitroglycerin should be administered at a dose of 0.4mg every five
minutes for a total of three doses, after which an assessment of blood pressure
and pain relief should guide the need for a more effective intravenous nitroglycerin
(intravenous are more effective than sublingual nitrates). Doses should be titrated
upwards until symptoms are relieved. Once the symptoms are controlled nitrates
are removed. Side effects include hypotensive reactions and a hypotensive
bradycardic response (Bezold-Jarisch Reflex). All patients should be questioned
about the use of phosphodiesterase-5 inhibitors. Nitrates are contraindicated if
these drugs have been used in the previous 24-48 hours because of the
propensity to cause potentially severe hypotension. Extreme care should also be
taken before giving nitrates in the setting of an inferior myocardial infarction with
possible involvement of the right ventricle. In these setting nitrates can cause
severe hypotension.
Analgesia if nitroglycerin and lessening of anxiety are not sufficient. Consider
intravenous morphine (2-4 mg). Repeat doses with increments of 2 to 8 mg, at 5
to 15 minute intervals may be given for pain relief.
Aspirin 160 - 325 mg should be chewed and swallowed on arrival, followed by a
daily oral dose of ≤100 mg. In the ISIS-2 study this reduced mortality by 23%
compared with placebo.
A platelet P2Y12 receptor blocker (Clopidogrel, Tcagrelor or Prasugrel) is
indicated in patients with AMI (STEMI and NSTEMI) depending on the estimated
risk and therapeutic strategy chosen.
Beta-adrenergic blockers should be used in patients without evidence of heart
failure or hypotension/cardiogenic shock in the first 24 hours. According to the
COMMIT/CCS2 trial, the largest placebo-controlled trial ever performed with beta
blockers in acute MI, it seems reasonable to defer intravenous beta blockers in
patients who are hemodynamically compromised in whom mortality may actually
be increased by such therapy. Once the patient is stable, an oral beta-blocker can
be started with gradual up titration to the maintenance doses.
Pulmonary oedema, if present, is treated with upright posture, intravenous
furosemide, intravenous nitroglycerin and CPAP or non-invansive ventilation.
 Note
 
Decisions can usually be made with readily available clinical data
In patients with ST-segment elevation or evidence of new (or presumed new) left or
right bundle branch block (LBBB o RBBB) a decision about how to reopen the
occluded coronary artery should be made expeditiously.
In text References 
(No authors 1988; Valgimigli et al. 2018; Mateos et al. 2015) 
 Note
Decisions can usually be made with readily available clinical data
In patients with ST-segment elevation or non-interpretable ST-segments on the ECG
such as those with evidence of new (or presumed new) left bundle branch block
(LBBB) or ventricular pacing, a decision about how to reopen the occluded coronary
artery should be made expeditiously, preferably through a primary PCI strategy.
 Note
Rapidly evolving area of medicine
Reperfusion therapy is indicated in all patients with symptoms of ischaemia of ≤ 12 h
duration and persistent ST-segment elevation. A primary PCI strategy is recommended
over fibrinolysis within indicated timeframes.
If timely primary PCI cannot be performed after STEMI diagnosis, fibrinolytic therapy is
recommended within 12 h of symptom onset in patients without contraindications
(Table 3)
In the absence of ST-segment elevation, a primary PCI strategy is indicated in patients
with suspected ongoing ischaemic symptoms suggestive of MI and at least one of the
following criteria present:
Haemodynamic instability or cardiogenic shock
Recurrent or ongoing chest pain refractory to medical treatment
Life-threatening arrhythmias or cardiac arrest
Mechanical complications of MI
Acute heart failure
Recurrent dynamic ST-segment or T- wave changes, particularly with intermittent
ST-segment elevation.
In patients with time from symptom onset >12 h, a primary PCI strategy is indicated in
the presence of ongoing symptoms suggestive of ischaemia, haemodynamic
instability, or life-threatening arrhythmias.
Table 3: Summary of important time targets in acute STEMI. From Ibanez et al., 2018
Intervals
Time
targets
Maximum time from FMC to ECG and diagnosis ≤10 min
Maximum expected delay from STEMI diagnosis to primary PCI (wire
crossing) to choose primary PCI strategy over fibrinolysis (if this targettime cannot be met, consider fibrinolysis)
≤120 min
Maximum time from STEMI diagnosis to wire crossing in patients
presenting at a primary PCI hospitals
≤ 60 min
Maximum time from STEMI diagnosis to wire crossing in transferred
patients
≤ 90 min
Maximum time from STEMI diagnosis to bolus or infusion start of
fibrinolysis in patients unable to meet primary PCI target times
≤10 min
Time delay from start of fibrinolysis to evaluation of its efficacy (success
or failure)
60 – 90
min
Time delay from start of fibrinolysis to angiography (if fibrinolysis is
successful)
2 – 24 h
Abbreviations:
ECG= electrocardiogram
FMC= first medical contact
PCI = percutaneous coronary intervention
STEMI = ST-segment elevation myocardial infarction.
 Note
 
Risk profiling in acute myocardial infarction
High risk can be defined by clinical features (presentation in congestive heart failure),
haemodynamic criteria (SBP <100 mmHg, HR >100 bpm), size of infarction (anterior
ST elevation >2 mm in two or more contiguous leads), RV involvement, or LV
dysfunction (EF <35%).
In text References
(Ibanez et al. 2018; Andersen et al. 2003; Keeley, Boura and Grines. 2003; O'Gara et
al. 2013) 
 References
No authors listed, Randomised trial of intravenous streptokinase, oral
aspirin, both, or neither among 17,187 cases of suspected acute myocardial
infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival)
Collaborative Group., 1988, PMID:2899772
Valgimigli M, Bueno H, Byrne RA, Collet JP, Costa F, Jeppsson A, Jüni P,
Kastrati A, Kolh P, Mauri L, Montalescot G, Neumann FJ, Petricevic M, Roffi
M, Steg PG, Windecker S, Zamorano JL, Levine GN; ESC Scientific
Document Group; ESC Committee for Practice, 2017 ESC focused update
on dual antiplatelet therapy in coronary artery disease developed in
collaboration with EACTS: The Task Force for dual antiplatelet therapy in
coronary artery disease of the European Society of Cardiology (ESC) and
of the European , 2018, PMID:28886622
Mateos A, García-Lunar I, García-Ruiz JM, Pizarro G, Fernández-Jiménez
R, Huertas P, García-Álvarez A, Fernández-Friera L, Bravo J, Flores-Arias
J, Barreiro MV, Chayán-Zas L, Corral E, Fuster V, Sánchez-Brunete V,
Ibáñez B, METOCARD-CNIC Investigators., Efficacy and safety of out-of-
https://www.ncbi.nlm.nih.gov/pubmed/2899772
https://www.ncbi.nlm.nih.gov/pubmed/28886622
https://www.ncbi.nlm.nih.gov/pubmed/25129820
hospital intravenous metoprolol administration in anterior ST-segment
elevation acute myocardial infarction: insights from the METOCARD-CNIC
trial., 2015, PMID:25129820
Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H,
Caforio ALP, Crea F, Goudevenos JA, Halvorsen S, Hindricks G, Kastrati A,
Lenzen MJ, Prescott E, Roffi M, Valgimigli M, Varenhorst C, Vranckx P,
Widimský P; ESC Scientific Document Gr, 2017 ESC Guidelines for the
management of acute myocardial infarction in patients presenting with ST-
segment elevation: The Task Force for the management of acute
myocardial infarction in patients presenting with ST-segment elevation of
the European Socie, 2018, PMID:28886621
Andersen HR, Nielsen TT, Rasmussen K, Thuesen L, Kelbaek H, Thayssen
P, Abildgaard U, Pedersen F, Madsen JK, Grande P, Villadsen AB, Krusell
LR, Haghfelt T, Lomholt P, Husted SE, Vigholt E, Kjaergard HK, Mortensen
LS; DANAMI-2 Investigators., A comparison of coronary angioplasty with
fibrinolytic therapy in acute myocardial infarction., 2003, PMID:12930925
Keeley EC, Boura JA, Grines CL., Primary angioplasty versus intravenous
thrombolytic therapy for acute myocardial infarction: a quantitative review of
23 randomised trials., 2003, PMID:12517460
O'Gara PT, Kushner FG, Ascheim DD, Casey DE Jr, Chung MK, de Lemos
JA, Ettinger SM, Fang JC, Fesmire FM, Franklin BA, Granger CB, Krumholz
HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N, Radford MJ,
Tamis-Holland JE, Tommaso CL, Tracy CM, Woo YJ,, 2013 ACCF/AHA
guideline for the management of ST-elevation myocardial infarction: a
report of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines., 2013, PMID:23247304
4. 4. On going physical examination
A more detailed physical examination is undertaken but should not delay immediate
treatment. It is often insensitive and non-specific but is aimed at:
Diagnosing specific complications.
Excluding alternative diagnoses, both cardiovascular (e.g. pericarditis, aortic
dissection) as well as non-cardiac (pulmonary embolism, pleuro-pneumonia,
gastric ulcer, pancreatitis, cholecystitis).
Distended jugular veins signal right ventricular diastolic pressure elevation, and the
appearance of pulmonary crackles (in the abscense of pulmonary disease) indicate left
ventricular filling pressures. See the ESICM module on heart failure for further
information.
https://www.ncbi.nlm.nih.gov/pubmed/25129820
https://www.ncbi.nlm.nih.gov/pubmed/28886621
https://www.ncbi.nlm.nih.gov/pubmed/12930925
https://www.ncbi.nlm.nih.gov/pubmed/12517460
https://www.ncbi.nlm.nih.gov/pubmed/23247304
https://collaboration.esicm.org/Left+sided+Heart+Failure
A systolic bulge occasionally can be palpated on the precordium in the area of the
apex of the heart, representing contact of an ischaemic dyskinetic segment of the left
ventricle with the chest wall. Auscultation of the precordium during an ischaemic
episode may reveal the presence of a fourth heart sound (indicative of a non-compliant
left ventricle).
 Note
Patients should be examined to exclude shock and left ventricular failure
Left ventricular failure is associated with higher mortality and is suggested by the
presence of pulmonary crackles, tachypnoea, tachycardia, and a S3 gallop. A third
heart sound (S3) usually indicates a large infarction with extensive muscle damage.
A systolic murmur of mitral regurgitation may be present and result from a papillary
muscle dysfunction or left ventricle dilatation. A pansystolic murmur may also be due
to an acute ventricular septal defect due to septal rupture.
Physical examination is also important to exclude alternative diagnoses and to suggest
further investigations. A friction rub may indicate the presence of pericarditis. Unequal
arm pressures should raise the suspicion of aortic dissection. Cardiac tamponade may
present with a low cardiac output state and elevated neck vein pulsations, which move
paradoxically during respiratory cycle. Hypoxaemia, hypotension and a clear lung
examination should raise the suspicion of pulmonary embolism.
 Note
Patients should have targeted examination to exclude other relevant medical
(especially respiratory and neurological) problems
 Note
Cardiogenic shock presents as hypotension, oliguria and features of low cardiac
output and is associated with a particularly poor outcome.
Cardiogenic shock may occasionally be present with evidence of hypoperfusion but
without hypotension. Cardiogenic shock may not develop until hours after the onset of
symptoms and regular examination is therefore required. For full consideration of
diagnosis and management of cardiogenic shock, refer to the “Management of
Complications” section (Part 2).
In text References 
(Goldberg et al. 2009; Jeger et al. 2007) 

What are the clinical features of right ventricular infarction and
why is it important to make this diagnosis?
COMPLETE TASK THEN CLICK TO REVEAL THE ANSWER
 With right ventricular infarction, there may be marked elevation of
the jugular venous pressure (JVP), usually with clear lungs and low or
normal wedge pressure. Recognition of RV infarction is important
because decreasing filling pressures in this setting may precipitate
hypotension and, conversely, hypotension may respond to judicious
fluid administration.
In text References
(Pöss et al. 2017; Albulushi et al. 2018) 
 References
Goldberg RJ, Spencer FA, Gore JM, Lessard D, Yarzebski J., Thirty-year
trends (1975 to 2005) in the magnitude of, management of, and hospital
death rates associated with cardiogenicshock in patients with acute
myocardial infarction: a population-based perspective., 2009,
PMID:19237658
Jeger RV, Lowe AM, Buller CE, Pfisterer ME, Dzavik V, Webb JG, Hochman
JS, Jorde UP; SHOCK Investigators., Hemodynamic parameters are
prognostically important in cardiogenic shock but similar following early
revascularization or initial medical stabilization: a report from the SHOCK
Trial., 2007, PMID:17951622
Pöss J, Köster J, Fuernau G, Eitel I, de Waha S, Ouarrak T, Lassus J,
Harjola VP, Zeymer U, Thiele H, Desch S, Risk Stratification for Patients in
Cardiogenic Shock After Acute Myocardial Infarction., 2017,
PMID:28408020
Albulushi A, Giannopoulos A, Kafkas N, Dragasis S, Pavlides G, Chatzizisis
YS, Acute right ventricular myocardial infarction., 2018, PMID:29902098
4. 5. Investigations
4. 5. 1. Electrocardiography
The ECG 12 standard leads is considered the initial single most important test for
diagnosing and guiding the emergency treatment of MI, and should be acquired and
interpreted promptly (i.e. target within 10 min) after first medical contact.
https://www.ncbi.nlm.nih.gov/pubmed/19237658
https://www.ncbi.nlm.nih.gov/pubmed/17951622
https://www.ncbi.nlm.nih.gov/pubmed/28408020
https://www.ncbi.nlm.nih.gov/pubmed/29902098
Pre-hospital ECGs reduce the time to diagnosis and treatment, and can facilitate a
strategy for immediate reperfusion therapy. When coupled with communication of
STEMI diagnosis and preferential transport to a PCI-capable hospital, has been shown
to result in rapid reperfusion times and excellent clinical outcomes.
Initial ECGs may reveal significant ST-segment elevation (STEACS) or that lack
significant ST-segment elevation (NSTEACS). In addition serial ECGs may give
information about localization, size and guide possible therapies.
Acute myocardial ischaemia is often associated with dynamic changes in ECG
waveform and serial ECG acquisition can provide critical information,
Acute and complete occlusion of a coronary artery usually leads to serial EGC
changes in leads subtending the area of ischaemia, where the number of leads
involved broadly reflects the extent of myocardium involved, the height of initial ST
segment changes is correlated with the degree of ischaemia and acute resolution of
STEACS correlates well with reperfusion acute and early changes where STEACS is
present identifies patients in whom reperfusion therapy may interrupt, prevent or
minimise myocardial necrosis.
You can review the use of the electrocardiogram and ECG interpretation in the
following references.
In text References 
(Zimetbaum and Josephson. 2003) 
4. 5. 1. 1. ECG changes of AMI
ECG changes of AMI often evolve in a characteristic pattern. Acute and complete
occlusion of a coronary artery usually leads to serial ECG changes in leads subtending
the area of ischaemia. All clinicians should recognise these changes and their
variations (Figure 4)
Hyperacute (0-20 minutes) tall, peaking T-waves and progressive upward coving and
elevation of ST-segments. Increased hyperacute T wave amplitude, with prominent
symmetrical T waves in at least two contiguous or more anatomically leads, is an early
sign that may precede the elevation of the ST-segment.
Acute (minutes to hours) persisting STE, gradual loss of R-wave in the infarcted area
ST-segments begin to fall and there is progressive inversion of T-waves
Early (hours to days) loss of R-wave and development of pathological Q-waves in
area of ischaemia. Return of ST-segments to baseline. Persistence of T-wave
inversion
Indeterminate (days to weeks) pathological waves with persisting T-wave inversion.
ST-segments normalise (unless there is aneurysm)
Old (weeks to months) persisting deep waves with normalised ST-segments and T-
waves.
Figure 4: ECG changes of AMI. Esicm Academy
2019.
Changes above are 'stereotyped'. ECG changes in clinical practice are highly variable
in their occurrence and combinations. Patients may progress more rapidly through
these stages. Successful revascularisation may interrupt these changes and prevent
or minimise myocardial necrosis.
 Note
If the ECG is equivocal or does not show evidence to support the clinical
suspicion of MI, ECGs should be repeated and, when possible compared with
previous recordings.
 Note
It is vital that clinicians identify acute changes and ST-segment elevation so that
early reperfusion strategies can be initiated.
4. 5. 1. 2. Pattern of ECG changes
The pattern of ECG changes may give a guide to the area and extent of infarction. The
number of leads involved broadly reflects the extent of myocardial injury.
Acute myocardial ischaemia is often associated with dynamic changes in ECG
waveform and serial ECG acquisition can provide critical information, particularly if the
ECG at initial presentation is non-diagnostic. If this is the case, the 12 lead ECG with
fixed electrodes should be repeated (eg, at 15- to 30-minute intervals during the first
hour), especially if symptoms recur.
Continuous computer-assisted with 12-lead ECG monitoring (if available) to detect
dynamic ECG changes may be a reasonable alternative in patients whose initial ECG
is nondiagnostic or with persistent or recurrent symptoms and who are at risk of ACS.
Serial or continuous ECG recordings may be helpful in determining reperfusion or re-
occlusion status. Reperfusion is usually associated with a large and prompt reduction
in ST-segment elevation.
A normal ECG may also be associated with left circumflex or right coronary artery
occlusions, which can be electrically silent or be associated with ST segment
depressions in the anterior leads (in which case posterior electrocardiographic leads
V7 to V9 and right-sided leads (V3R to V4R) may be helpful (Table 4)
 Note
https://collaboration.esicm.org/dl1539?display
https://collaboration.esicm.org/V7%20to%20V9
Some patients with an acute coronary occlusion may have an initial ECG
without ST-segment elevation, and be denied for urgent reperfusion therapy,
resulting in a larger infarction and worse outcomes.
Table 4: ECG monitoring recommendations for the initial diagnosis
12-lead ECG recording and interpretation is indicated as soon as
possible at the point of First Medical Contact, with a maximum
target delay of 10 min.
ECG monitoring with defibrillator capacity is indicated as soon as
possible in all patients with suspected STEMI
The use of additional posterior chest wall leads (V7–V9) in
patients with high suspicion of posterior MI (circumflex occlusion)
and anterior ST segment depression should be considered.
The use of additional right precordial leads (V3R and V4R) in
patients with inferior MI should be considered to identify
concomitant RV infarction.

Review this ECG from the Arrhythmia module. What changes are
present and what is their relevance? (Figure 5)
Figure 5:
COMPLETE TASK THEN CLICK TO REVEAL THE ANSWER
 
The first ECG displays inferior infarction of recent onset. There is no
evidence of posterior extension. The Arrhythmia module states this case
illustrates an acute inferior wall myocardial infarction with an ST score
(the total amount, in millimetres, of ST elevation in the inferior leads II,
III, aVF) of more than 7 mm, indicating an extensive myocardial
infarction. The additional recording of lead V4R would have been of help
in identifying the presence of right ventricular myocardial infarction. If
this were a clinical concern, echocardiography would be useful
diagnostically and would also likely assist in ongoing management.
Right ventricular involvement, as diagnosed by V4R, does suggest
https://collaboration.esicm.org/dl1540?display
proximal or RCA (Right coronary artery) occlusion but the real reason to
record V4R is not so much to determine where the RCA is occluded but
rather to get a sense of whether there is RV infarction, with its distinctive
physiology.
Review of all leads may thus suggest the coronary territory involved, the presence of
right ventricular myocardial infarction and risk of developingAV nodal block. The latter
was already present in this patient – indicating the proximal location of the obstruction
in the right coronary artery, leading to a large inferior wall infarction with right
ventricular involvement. When high-degree AV nodal block occurs in acute myocardial
infarction, the in-hospital mortality rate is two and one-half times that of inferior
myocardial infarction without high-degree AV block. This patient should be referred for
primary percutaneous coronary intervention.

Review this ECG from the Arrhythmia module. What changes are
present and what is their relevance? (Figure 6)
Figure 6:
COMPLETE TASK THEN CLICK TO REVEAL THE ANSWER
 
The second ECG displays LBBB complicating anterior myocardial
infarction. New or presumed new LBBB is an indication for reperfusion
therapy. Lack of a previous ECG should not be a reason to withhold
such therapy when the clinical setting suggests myocardial infarction.
Where there is uncertainty, echocardiography may confirm a regional wall motion
abnormality. Angiography can also be diagnostic and may allow for definitive
revascularisation (which may be superior to thrombolysis in this setting). The
https://collaboration.esicm.org/dl1541?display
Arrhythmia module states this case illustrates an acute anterior myocardial infarction
complicated by a left bundle branch block. The development of bundle branch block
during the acute phase of myocardial infarction indicates extensive anterior wall
infarction, because such conduction problems indicate an occlusion proximally in the
LAD coronary artery. When anterior myocardial infarction is complicated by bundle
branch block, early death occurs because of pump failure and ventricular tachycardia
or fibrillation. The finding of a bundle branch block as a complication of anterior wall
infarction calls for aggressive treatment. This patient should be referred for primary
percutaneous coronary intervention (PCI). Development of second or third degree
heart block in association with bundle branch block during anterior MI necessitates
temporary pacing.
In text References 
(Sgarbossa, Birnbaum and Parrillo. 2001; Smith et al. 2012) 
Electrocardiographic manifestations suggestive of acute myocardial ischaemia include
(in the absence of left ventricular hypertrophy and bundle branch block):
ST-elevation: New ST-elevation at the J-point in two or more anatomically
contiguous leads with the cut-point ≥ 1 mm (1 mm = 0.1 mV) in all leads other
than leads V2–V3 where the following cut-points apply: ≥ 2mm in men > 40 years;
≥ 2.5 mm in men ≤ 40 years, or ≥ 1.5 mm in women regardless of age.
ST-depression ad T wave changes: New horizontal or down sloping ST-
depression ≥ 0.5 mm in two or more anatomically contiguous leads and/or T
inversion ≥ 1 mm in two or more anatomically contiguous leads with prominent R
wave or R/S ratio ≥ 1.
Patients with ACS but without significant ST-segment elevation probably have
active, non-occluding thrombus. ECGs in these patients may be normal or display
ST-segment depression, T-wave inversion or normalisation of previous inverted
waves.
Patients who present with ischaemic chest pain and a non-diagnostic initial ECG
supplemental leads, as well as serial ECG recordings, should be deployed with a
very low threshold. Recording of V7, V8 and V9 leads is strongly recommended in
patients with high clinical suspicion of acute circumflex occlusion (e.g. initial ECG
non-diagnostic or ST-segment depression in leads V1–V3 may be suggestive of
inferobasal myocardial ischaemia (previously termed posterior infarction))
Patients with inferior and suspected right ventricular infarction, leads aVR or V1
may exhibit ST-segment elevation ≥ 1 mm. The early recording of right precordial
leads V3R and V4R should be performed
The presence of ST depression ≥ 1 mm in eight or more surface leads
(inferolateral ST depression), coupled with ST-segment elevation in aVR and/or
V1, suggests multivessel ischemia or left main coronary artery obstruction,
particularly if the patient presents with haemodynamic compromise.
 Note
Remember, anatomy of the coronary vessels is highly variable between people
Patients with clinical suspicion of ongoing myocardial ischaemia and left bundle
branch block (LBBB) should be managed in a way similar to STEMI patients,
regardless of whether the LBBB is previously known (Table 5)
Patients with new right bundle branch block (RBBB) have a poor prognosis. Therefore,
a primary PCI strategy (emergent coronary angiography and PCI if indicated) should
be considered when persistent ischaemic symptoms occur in the presence of RBBB.
In text References 
(Wang et al. 2018) 
Other ECG signs associated with acute myocardial ischaemia include cardiac
arrhythmias, intraventricular bundle branch blocks, atrioventricular conduction delays
and loss of precordial R wave amplitude (Table 5).
Table 5: Atypical ECG signs that should prompt PCI strategy in
patients with ongoing symptoms consistent with myocardial ischemia
Bundle branch block 
Criteria used to improve the diagnostic accuracy of STEMI in LBB
Concordant ST-segment elevation ≥ 1 mm in leads with a
positive complex
Concordant ST-segment depression ≥ 1 mm inV1-V3
Discordant ST-segment elevation ≥ 5 mm in leads with a
negative QRS complex
The presence of RBBB may confound the diagnosis of STEM
Ventricular pacing rhythm 
During RV pacing, the ECG also show LBBB and the above rules
also apply for the diagnosis of myocardial infarction during pacing;
however, they are less specific
Isolated posterior myocardial infarction 
Isolated ST depression ≥ 0.5 mm in leads V1-V3 and ST-segment
elevation (≥ 0.5 mm) in posterior chest Wall leads V7-V9
Ischaemia due to left main coronary artery occlusion or
multivessel disease 
ST depression ≥ 1 mm in eight or more surface leads, coupled
with ST-segment elevation in aVR and/or V1, suggest left main or
left main equivalent-coronary obstruction, or severe three vessel
ischemia
4. 5. 1. 3. Localisation of infarct using electrocardiogram
It is usual to use the ECG in initial clinical assessments to localise the area of
myocardial ischaemia. The pattern of lead involvement may assist with localisation of
the MI (Table 6). There is a reasonable correlation between the site of infarction as
defined by the ECG, the occluded coronary artery, and the infarcted region of
myocardium according to coronary anatomy.
Table 6: Infarct localisation and ECG
Area of
infarction
ECG
leads
Infarct-related artery
Inferior II, III, AVF
RCA (right coronary artery) or
posterolateral branch of Cx
Anterior V2, V3, V4 LAD or diagonal branch of LAD
Lateral
I, aVL, V5,
V6
Cx
True
posterior
Tall R wave
in V1
Posterolateral branch of Cx or
Posterior Descending Branch of
RCA
Septal V1-V3 LAD or diagoinal branch of LAD
Anterolateral
I, aVL, V2-
V6
Proximal LAD
Inferolateral
II, III, aVF, I,
aVL, V5, V6
Proximal Cx or large RCA in right
dominant system
Right
ventricular
V3R, V4R RCA
Abbreviations:
RCA= Right Coronary Artery
LAD= Left Anterior Descending Coronary Artery
Cx= Circumflex Coronary Artery
LV= Lateral Ventricular Artery
In text References 
(Zimetbaum and Josephson. 2003; Sanaani et al. 2017) 
You will find examples of ECGs on the following websites.
ECG Wave-Maven
ECG Library
ECG Learning Center
Life in the Fast Lane
https://ecg.bidmc.harvard.edu/maven/mavenmain.asp
https://ecglibrary.com/ecghome.php
https://ecg.utah.edu/
https://lifeinthefastlane.com/
 Note
Clinicians should be aware of conditions in which the ECG may mimic
ischaemia so that inappropriate therapy is not given.
 Note
ECGs should always be interpreted in clinical context
The ECG by itself is often insufficient to diagnose acute myocardial ischaemia or
infarction, since ST deviation may be observed in other conditions, such as:
Pericarditis
Left ventricular hypertrophy
Left ventricular aneurysm (persisting ST-segment elevation following older
infarction)
Brugada Syndrome (ST-segment elevation in V1-V3