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Part III
Cardiovascular Critical Care
Chapter 10
Acute Coronary Syndrome (ACS)
NicholasBarker, DustyLisi, andAdeleRobbins
Cardiovascular disease (CVD) is the leading cause of death globally, representing
32% of all deaths [1]. Eighty percent of all CVD deaths globally are related to myocardial infarction (MI) and stroke [1]. In the United States, over 40% of CVD deaths
are attributed to myocardial infarction [2]. Acute coronary syndrome (ACS) encompasses a number of conditions associated with acute myocardial ischemia caused by
an acute reduction in coronary blood ow and is one of the most common.
It is important to note that myocardial infarction can occur from a number of different causes. The type of myocardial infarction is classied based on a number of
characteristics, such as pathophysiology, clinical presentation, and electrocardiographic (ECG) changes.
10.1 Type 1–5 Myocardial Infarctions
Myocardial infarctions (MIs) are categorized into ve distinct types based on the
underlying etiology [3]. This has helped triage patients who have signicant elevations in cardiac troponin, a sensitive and specic biomarker for cardiac damage.
Type 1 and 2 MIs account for the majority of MI cases.
N. Barker (*)
Cardiovascular Intensive Care Unit, Emory Saint Joseph’s Hospital, Atlanta, GA, USA
e-mail: nicholas.barker@emoryhealthcare.org
D. Lisi
Heart Failure, Emory Saint Joseph’s Hospital, Atlanta, GA, USA
A. Robbins
Advanced Heart Failure and Transplant, Piedmont Hospital, Atlanta, GA, USA
Switzerland AG 2025
Y. Alzaidi, M. A. Gebily (eds.), The Pharmacist’s Expanded Role in Critical
Care Medicine, https://doi.org/10.1007/978-3-031-77335-8_10
269© The Author(s), under exclusive license to Springer Nature
270
N. Barker et al.
Type 1 MI occurs when atherosclerotic plaque is dislocated, typically rupture or
erosion, resulting in thrombus formation in one or more coronary arteries. Plaque
rupture is a result of plaque integrity disruption allowing more contact with the
platelet-rich interior of the plaque. In response, multiple pro-thrombotic substances
are released and promote platelet activation/aggregation and thrombus formation,
leading to coronary artery occlusion (partial or complete). Type 1 MI is further classied based on 12-lead ECG interpretation into ST-segment elevation myocardial
infarction (STEMI) and NSTE-ACS. NSTE-ACS is classied as either non-STsegment elevation myocardial infarction (NSTEMI) or unstable angina (UA) [4, 5].
Type 1 MI will be the primary focus of this chapter. Duration of ischemia and damaged tissue location correlate with the degree of damage and potential complications, which will be discussed later in this chapter.
Type 2 MI occurs when there is an oxygen supply/demand mismatch instead of
coronary artery occlusion. A number of conditions such as hypertension, hypoxia,
anemia, and tachyarrhythmias may precipitate type 2 MI.Atrial brillation (AF) is
the most common cause of type 2 MI, and tachyarrhythmias are responsible for as
much as 47% of occurrences [6].
Type 3 MI references sudden cardiac death with a high suspicion for myocardial
ischemia believed to be a result of new thrombus. Death occurs prior to appropriate
testing that includes dening diagnoses such as cardiac biomarkers.
Type 4 MI is associated with percutaneous coronary intervention (PCI). This is
further divided into two subcategories. Type 4a is diagnosed based on the elevation
of cardiac biomarkers following PCI. Type 4b signies stent thrombosis, a potential
risk after stent placement.
Type 5 MI occurs when there is an elevation of cardiac biomarkers following
coronary bypass grafting (CABG). This may be related to graft thrombosis.
10.2 Acute Coronary Syndrome (Type 1 MI)
Type 1 MI is classied as either STEMI or NSTE-ACS (NSTEMI or UA). This is
determined by the presence of elevated troponin and evidence on a 12-lead
ECG.Understanding the various types of MI is important for appropriate diagnosis,
treatment, and future management.
STEMI accounts for up to 40% of all myocardial infarctions [7]. STEMI occurs
when resulting thrombus from plaque rupture completely blocks one or more coronary arteries, resulting in ischemia and signicant damage to cardiac tissue. This is
evidenced by ST-segment elevation on a 12-lead ECG and elevated troponin. Due to
the severity of complication and high risk for mortality, it is considered a medical
emergency. NSTE-ACS is another frequent type 1 MI. This is a result of partial
blockage of a coronary artery, which is evident by the lack of ST-segment elevation
on a 12-lead ECG.
10 Acute Coronary Syndrome (ACS)
271
10.3 Clinical Presentation/Evaluation
Patients may present in a varying degree of symptoms. While the most common
symptom is chest discomfort, up to 60% of all MIs are asymptomatic or unrecognized. Approximately one-third of patients will present with symptoms other than
chest pain/discomfort [8]. This is more common in women, elderly adults, and
patients with diabetes. Chest pain can be persistent or increasing and radiate to other
locations such as the jaw, neck, and arms. The less common/more atypical symptoms include diaphoresis, syncope, unexplained fatigue, indigestion, and nausea/
vomiting. More extreme symptoms include acute decompensated heart failure, cardiogenic shock, and cardiac arrest.
Most evaluation and treatment strategies use rst medical contact (FMC) as the
guiding point in time. This is the time at which trained medical personnel who can
interpret an ECG assess a patient. FMC should include an initial evaluation of vital
signs, personal history, physical examination, troponin level collection, and
ECG. 12-Lead ECG recording and interpretation should be completed as soon as
possible, with a target of less than 10min from FMC [4].
STEMI is diagnosed based on 12-lead ECG ndings. STEMI is diagnosed when
two contagious leads have ST elevation of ≥2.5mm in men <40years, ≥2mm in
men ≥40years, or ≥1.5 mm in women regardless of age in leads V2–V3 and/or
≥1 mm in the other leads (in the absence of left ventricular hypertrophy or left
bundle branch block) [4]. In patients who present with a left bundle branch block or
a ventricular paced rhythm, Sgarbossa Criteria may be used to assist in diagnosis,
which has a high specicity but low sensitivity [10]. Location of ST elevation on
ECG has a high predictive value for the location of coronary artery occlusion and
guides reperfusion strategies. Objective ndings of NSTEMI/UA may include ST
depression, T-wave inversion, or no ECG changes [4].
Figure 10.1 illustrates ST elevation in the anterior and lateral leads. Lateral leads
consist of I, aVL, V5, and V6 [9]. These typically correlate with blockage of the
circumex artery. The anterior leads consist of V3 and V4, which correlate with the
left anterior descending (LAD) artery. Figure10.2 provides an example of an inferior STEMI. Inferior leads consist of II, III, and aVF and are characteristic of right
coronary artery occlusion. ST elevation found in septal leads (V1, V2) also correlates with LAD occlusion. Figure 10.3 is an example of a recent or evolving
STEMI.This is evident by the negative deection of the Q wave.
Serial troponin levels should be collected at FMC and at 3–6h as the initial troponin may not be positive [4]. Cardiac troponins are detectable within 6h of insult
and may remain elevated for approximately 10days [11].
Early therapies can be initiated to manage ischemia and treat pain. The common
acronym associated with these therapies is “MONA.” Morphine (M) is the most
common analgesic utilized in the management of chest pain, in part due to potential
vasodilatory effects. Morphine has a IIb recommendation by ACC/AHA guidelines
due to at least one trial nding an association between morphine administration and