Management of Acute

C o ro n a r y S y n d ro m e
Joel Atwood, MD

KEYWORDS
 Acute coronary syndrome  Myocardial infarction
 ST segment elevation myocardial infarction
 Non-ST segment elevation myocardial infarction  Unstable angina

KEY POINTS
 The underlying cause of cardiac ischemia directs management.
 Early identification and revascularization of patients with ST-Segment elevation myocar-
dial infarction improve outcomes.
 All patients with suspected or confirmed acute coronary syndrome (ACS) should immedi-
ately receive aspirin.
 Emergency providers should identify and treat early complications of ACS.

DEFINITIONS

An acute coronary syndrome (ACS) is caused by coronary plaque rupture/erosion and

thrombus formation leading to obstruction of blood flow and distal myocardial
ischemia.1,2 The degree of coronary artery obstruction and cardiac ischemia highlight
the pathophysiological differences between the clinical entities of ST-Segment eleva-
tion myocardial infarction (STEMI), Non-ST-Segment elevation myocardial infarction
(NSTEMI), and unstable angina (UA). In STEMI, the coronary artery is completely or
nearly occluded resulting in evidence of transmural ischemia on electrocardiogram
(ECG) (ST-segment elevation), symptoms of angina, and myocardial cell death on
troponin assays. In NSTEMI, the coronary artery is at least partially occluded resulting
in subendocardial ischemia, symptoms of angina, and myocardial cell death; however,
there are no ST-segment elevations on ECG. In UA, the coronary artery thrombus re-
sults in symptoms or ECG changes typical of myocardial ischemia; however, there is
no measurable myocardial cell death (Fig. 1).
Although ACS is the primary concern for most providers when encountering a pa-
tient with compatible symptoms, alternative pathologies leading to myocardial injury
are common. Causes are numerous and result in any circumstance where myocardial

Department of Emergency Medicine, 1300 South George Street, York, PA 17402, USA
E-mail address: jatwood@wellspan.org

Emerg Med Clin N Am 40 (2022) 693–706

https://doi.org/10.1016/j.emc.2022.06.008 emed.theclinics.com
0733-8627/22/ª 2022 Elsevier Inc. All rights reserved.
694 Atwood

Clinical Presenta on
Concerning for Cardiac
Angina

Non-ACS Cause
Apparent at Any Time ACS Probable
During Evalua on

Further Treatment
Directed at Underlying ST Segment Eleva ons No ST Segment
Cause on ECG Eleva ons on ECG

Rise and Fall of

Presumed Diagnosis of Troponin with one Nega ve or Flat
STEMI value greater than 99th Troponin Values
percen le URL

Ini ate Immediate

NSTEMI Unstable Angina
Reperfusion Strategy

Ini ate/Con nue

Treatments for ACS

Fig. 1. Conceptualization of ACS. ACS, acute coronary syndrome; ECG, electrocardiogram;

NSTEMI, non-ST segment myocardial infarction; STEMI, ST-segment elevation myocardial
infarction; URL, upper reference limit.

oxygen demands exceed supply. Common examples include coronary vasospasm,

sepsis, and anemia (Fig. 2). After a provider identifies evidence of myocardial ischemia
by history, ECG, or laboratories, a rapid evaluation to determine the underlying cause
is imperative. Treatment of non-ACS causes of myocardial ischemia is directed at cor-
recting the underlying abnormality that created the oxygen imbalance. Typical ACS
strategies are unlikely to be helpful and more likely to result in iatrogenic harm in these
circumstances. In this article, we focus on the treatment of acute myocardial ischemia
caused by ACS.

INITIAL APPROACH TO ACUTE CORONARY SYNDROME MANAGEMENT

After the emergency clinician diagnoses ACS, simultaneous efforts to improve and
prevent worsening of oxygen mismatch are initiated. The time course of strategies
is dictated by the type of ACS encountered (STEMI vs. NSTEMI vs. UA) as well as
patient-specific factors, including comorbidities, medications, bleeding risk, and dura-
tion of symptoms. In addition to supportive care, the approach to treatment is directed
at optimizing myocardial ischemia through three different mechanisms:
 Management of Acute Coronary Syndrome 695

Fig. 2. Pathophysiology of type 2 myocardial infarction. (This article was published in Jour-
nal of the American College of Cardiology, 70(13), Januzzi JL, Sandoval Y, The Many Faces of
Type 2 Myocardial Infarction, 1569–1572, Copyright Elsevier 2017.)

 Improving myocardial oxygen imbalance

 Decreasing coronary artery thrombus propagation
 Coronary artery reperfusion through revascularization

OPTIMIZING OXYGEN DELIVERY

It has been previously taught that all patients suffering from ACS should be started on
supplemental oxygen to improve oxygen delivery to the ischemic myocardium. How-
ever, standard use of oxygen is potentially detrimental because hyperoxia can cause
coronary vasoconstriction and increased oxidative stress. Randomized trials have not
shown the benefits of routine oxygen supplementation and potential harm.3 Currently,
oxygen is only recommended when levels drop below 90% or in cases of respiratory
distress.4
Anemia is common in patients with ACS with up to 10% of patients requiring a blood
transfusion during hospitalization.5 Although transfusion will increase oxygen carry
696 Atwood

capacity and myocardial oxygen supply, side effects include increased thrombogen-
esis and volume overload. For these reasons, there is continued debate regarding the
appropriate transfusion threshold. Routine transfusion beginning at a hemoglobin level
of 8 g/dL is reasonable.6

DECREASING MYOCARDIAL DEMAND

Ischemic pain and anxiety should be treated to alleviate symptoms as well as

decrease myocardial oxygen demand generated from sympathetic nervous system
activation and increased work of breathing. Nitroglycerin improves coronary perfusion
and decreases cardiac preload and afterload, relieving ischemic discomfort. Nitro-
glycerin should be avoided in patients with concerns for right ventricular ischemia,
ongoing hypotension, recent phosphodiesterase use, or known aortic stenosis. In suit-
able patients who have improved with sublingual nitroglycerin treatment, a low dose
infusion titrated to pain or systolic blood pressure is indicated.
Liberal use of morphine for patients with ischemic discomfort was previously
encouraged; however, studies suggest morphine and other opiates, such as fentanyl
impact early P2Y12 antiplatelet agent metabolism which has been associated with
early treatment failures.7,8 For this reason, morphine and other opiates should be
used judiciously in refractory pain. Treatment with low-dose benzodiazepines is
reasonable in appropriate patients.4
Hypertension is common in patients presenting with ACS and results in increased
myocardial oxygen demand. Early and aggressive use of IV beta-blockers to reduce
hypertension, cardiac contractility, and heart rate results in lower rates of recurrent
myocardial infarction and ventricular fibrillation (VF) but higher rates of early cardio-
genic shock.9 Risk factors for beta-blocker-induced cardiogenic shock include
advanced age (>70), tachycardia, systolic blood pressures less than 120, or evidence
of heart failure on presentation. IV beta-blockers are commonly avoided because of
concerns of iatrogenic harm; however, it is appropriate to treat select ACS patients
with refractory pain and hypertension with IV metoprolol.10

SUPPORTIVE CARE

All patients with ACS should have reliable IV access and continuous telemetry and
pulse oximetry monitoring to detect abnormalities so that providers can intervene at
the first sign of decompensation. Electrolyte derangements are associated with ar-
rhythmias, thus it is recommended to routinely administer potassium and magnesium
to goal levels of 4.0 mEq/L and 2.0 mEq/L, respectively.

ST SEGMENT ELEVATION MYOCARDIAL INFARCTION

Initial Identification
Early identification and evaluation for STEMI are of pivotal importance as rapid treat-
ment improves outcomes.11 An ECG should be obtained within 10 minutes of first
medical contact.10 A presumptive diagnosis of STEMI requires a history consistent
with cardiac angina and a compatible ECG (Box 1). The diagnosis of STEMI is finalized
when the left heart catheterization reveals evidence of an acutely occluded artery. In
patients treated with a noninvasive revascularization approach, the diagnosis is
confirmed by new ischemic Q waves, evidence of ischemia on imaging, or a typical
rise and fall of troponin levels.12
 Management of Acute Coronary Syndrome 697

Box 1
Definition of ST segment elevation on ECG

New ST-segment elevation at the J-point in two contiguous leads

ST-segment elevation is defined as 1.0 mm in all leads other than V2–V3, V3R–V4R, and V7–V9
ST-segment elevation definitions in leads V2-V3 vary by patient age/sex
2.5 mm in men less than 40 years of age
2 mm in men  40 years of age
1.5 mm in women regardless of age
ST-Segment elevation definitions in leads V3R and V4R vary by patient age/sex
0.5 mm in men  30 years of age and all women
1.0 mm in men less than 30 years of age
ST-Segment elevation is defined as  0.5 mm in leads V7–V9

Abbreviation: ECG, electrocardiogram.

Data from Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial
Infarction (2018). J Am Coll Cardiol. 2018;72(18):2231-2264. https://doi.org/10.1016/j.jacc.
2018.08.1038 and Wagner GS, MacFarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations
for the standardization and interpretation of the electrocardiogram: Part VI: Acute ischemia/
infarction: A scientific statement from the American Heart Association Electrocardiography
and Arrhythmias Committee, Council on Clinical Cardiology; The American College of Cardiol-
ogy Foundation; And the Heart Rhythm Society. Circulation. 2009;119(10):262-270. https://doi.
org/10.1161/CIRCULATIONAHA.108.191098.

Approach to Revascularization
Once a patient with STEMI is identified, the efforts to restore coronary artery perfusion
via percutaneous coronary intervention (PCI) or fibrinolytic therapy should be initiated
immediately. Primary PCI is the proven superior treatment in patients with STEMI
because it is associated with lower rates of recurrent myocardial infarction, stroke,
and death.13 PCI is a highly technical, resource-intensive procedure, which is not
available in all settings. When PCI cannot be accomplished within 120 minutes of first
medical contact, fibrinolytic therapy should be administered in appropriate patients.10
Preparing Patient for Percutaneous Coronary Intervention
The primary responsibility of the emergency provider is to ensure the patient is stable
to tolerate PCI and administration of appropriate medications. The rapid evaluation in-
cludes an assessment of the patient’s airway, respiratory status (including the ability to
comfortably lay supine), hemodynamics, and ability to cooperate and follow com-
mands. There should be a low threshold to initiate aggressive supportive care mea-
sures, such as noninvasive positive pressure ventilation or endotracheal intubation
to decrease the risk of untimely decompensation during left heart catheterization.
Early Medications for Patients Undergoing Percutaneous Coronary Intervention
Antithrombotic medications are administered to prevent thrombus propagation as well
as iatrogenic complications during PCI. All patients presenting with suspected STEMI
should receive aspirin. This low-risk intervention saves one life for every 42 patients
treated.14 Ideally, enteric-coated aspirin is avoided and the tablet should be chewed
or crushed rather than swallowed. Rectal aspirin should be administered to patients
who are unable to take it orally.
An additional antiplatelet P2Y12 inhibitor is recommended for all patients treated for
STEMI with PCI. These medications, which include clopidogrel, ticagrelor, prasugrel,
698 Atwood

and cangrelor, are proven to further decrease the risk of thrombotic complications. In
most cases of STEMI, ticagrelor or prasugrel is recommended with head-to-head trials
showing a slight advantage of prasugrel in carefully selected patients.15 P2Y12 inhib-
itor use must be balanced with an individual patient bleeding risk. Patients at higher
risk of hemorrhage should receive clopidogrel.16 Whereas there are theoretic benefits
to early P2Y12 inhibitor use and many protocols recommend these agents be given
routinely in the emergency department, administration before angiogram has never
been shown to be superior to the administration at the time of PCI. Accordingly, it is
not unreasonable to defer the drug selection and administration by the interventional
cardiologist.10 In cases where there is high suspicion for proximal left anterior
descending artery occlusion or left main coronary artery occlusion on ECG, the deci-
sion to start a second antiplatelet agent should be made at the time of angiogram, as
these patients are at high risk for requiring coronary artery bypass grafting (CABG)
procedures and PGY12 use before CABG significantly increases the risk of hemorrhag-
ic complications.
Anticoagulation is recommended in all patients with STEMI undergoing a PCI revas-
cularization strategy. The two most commonly used agents are unfractionated heparin
and bivalirudin. Fondaparinux is associated with increased periprocedural thrombotic
complications and is not recommended.17 Low molecular weight heparin has not been
studied extensively in the modern era of STEMI PCI management. Results from ran-
domized trials between unfractionated heparin and bivalirudin reveal subtle differ-
ences between bleeding risk and thrombotic complications that are influenced by
the site of arterial puncture, patient risk of bleeding, and other antithrombotic agent
selection.16 Both agents are reasonable choices and clinicians should follow institu-
tional protocols or cardiology recommendations.
GP IIb/IIIa receptor antagonists work to inhibit the glycoprotein activation site and
thus prevent platelet activation. Before the routine use of P2Y12 inhibitors, there
was evidence that routine early use of these agents decreased mortality.18 However,
in the P2Y12 inhibitor era, additional GP IIb/IIIa receptor antagonists have not shown to
have a meaningful difference with the two most widely available agents (tirofiban and
eptifibatide) and are not routinely recommended before angiography.10

Fibrinolytic Reperfusion Strategy

In nonprimary PCI centers, even with close transport times, up to one-third of patients
are unable to achieve guideline-directed PCI within 120 minutes of first medical con-
tact.19 Unexpected events within a primary center also can result in an inability to
perform PCI, thus all emergency providers should be prepared to pursue a fibrinolytic
strategy. Fibrin-specific agents (alteplase, reteplase, and tenecteplase) are the
preferred agents for treating STEMI.20 Teneceteplase may have a lower bleeding
risk when compared with other agents.21 The less expensive, but less efficacious,
nonfibrin-specific agent streptokinase is still used in many parts of the world.
The risk profile of fibrinolytic therapy differs from PCI; so, a rapid evaluation should
be performed that weighs the benefits of fibrinolysis against the potential risks of hem-
orrhage. Patients who present immediately after symptom onset, are less than 65 year
old, have a low bleeding risk profile, and are hemodynamically stable will benefit the
most. Reperfusion through fibrinolytic therapy should be performed within 30 minutes
of arrival.10 Given an estimated risk of intracranial bleeding of 1% with systemic fibri-
nolytic therapy, a careful evaluation for contraindications should be performed rapi-
dly22(Box 2). The patient should understand the risks and benefits of therapy and
agree to treatment.
 Management of Acute Coronary Syndrome 699

Box 2
Contraindications and precautions to fibrinolytic therapy

Contraindications
Active internal bleeding
Recent (within 3 months) intracranial or intraspinal surgery or serious head trauma
Intracranial conditions that may increase the risk of bleeding (neoplasm, AV malformation,
aneurysm, prior intracranial hemorrhage)
Bleeding diathesis
Current severe uncontrolled hypertension (SBP >180 and/or DBP >110)
Warning and Precautions
Recent major surgery or procedure
Known prior cerebrovascular disease
Recent gastrointestinal or genitourinary bleeding
Significant hepatic dysfunction or renal dysfunction
Pregnancy
Recent trauma
Major surgery or puncture of noncompressible vessels

Abbreviations: AV, arteriovnenous; DBP, diastolic blood pressure; SBP, systolic blood pressure.

Data from Alteplase. Package insert. Genentech Pharmaceuticals. 2018.

Adjunctive Medications During Fibrinolysis

All patients should receive aspirin. Clopidogrel is the only P2Y12 inhibitor studied in pa-
tients receiving fibrinolytic therapy and is recommended as it improves outcomes.
Alternative P2Y12 inhibitors and GIIb/IIIa receptor antagonists are not recommended
given their documented increased risk of hemorrhage in other STEMI populations.20
Anticoagulation with unfractionated or low molecular weight heparin is generally
recommended.23

Post-Fibrinolytic Care
In the immediate post-fibrinolysis period successful treatment is indicated by
decreased chest pain, stable hemodynamics, and improvement in ST elevations at
60 to 90 minutes.23 Accelerated idioventricular reperfusion arrhythmias are common
and do not cause clinical instability or require treatment. After fibrinolytic therapy is
initiated, immediate transfer to a PCI center is recommended as treatment failures
should receive urgent rescue PCI and most patients with treatment success also
benefit from PCI within 24 hours.24,25

Delayed Presentation
Delayed presentation of STEMI is common. All patients with STEMI presenting in
shock should undergo immediate revascularization regardless of the duration of
symptoms.10 Outside of this subset of patients there is no strong consensus on the
utility of emergency revascularization. Early trials of revascularization with fibrinolysis
in patients presenting greater than 12 hours after symptom onset failed to show a
benefit. Emergency PCI in patients presenting within 12 to 48 hours of symptom onset
has demonstrated prognostic benefits but there are no robust well-powered random-
ized trials to definitively guide emergency treatment.26 Currently, guidelines recom-
mend emergency PCI in patients presenting within 12 to 24 hours of pain that have
clinical signs of ongoing ischemia. Carefully selected STEMI patients with 12 to
24 hours of symptoms and large areas of myocardium at risk may also be reasonable
700 Atwood

candidates for fibrinolytic therapy.10 Management of asymptomatic patients or pre-

sentations of STEMI with less than 3 days of symptoms is even less well defined
because a completed myocardial infarction would not benefit from emergency reper-
fusion. Routine revascularization of STEMI patients with greater than 3 days of symp-
toms is not beneficial.27 After discussion with a cardiologist, select patients with
delayed presentations of STEMI may be hospitalized for medical management, further
provocative testing, or delayed PCI rather than emergently revascularized.

NON-ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

Overall acute management of patients presenting with NSTEMI and UA differs from
STEMI in that emergency revascularization is rarely required. Initial antithrombotic ap-
proaches initiated in the ED also vary.
Antiplatelet and Antithrombotic Agents
All patients with NSTEMI and UA should be given aspirin as soon as possible. In
contrast to patients with STEMI, routine upfront use of P2Y12 agents is discouraged
in patients receiving invasive revascularization strategies because trials have shown
an increased risk of hemorrhage without any benefit.28 A second agent can be admin-
istered after coronary angiography clarifies the anatomy and before PCI.4 In some set-
tings, dual antiplatelet therapy at the time of diagnosis may be reasonable, such as
when a noninvasive strategy or delayed invasive strategy for the treatment of ACS
is pursued. Prasugrel or ticagrelor are preferred over clopidogrel.4 Similarly, GPIIb/
IIIa receptor antagonists are not recommended routinely at the time of diagnosis in
the emergency department.
Anticoagulation with unfractionated heparin, low molecular weight heparin, bivalir-
udin, or fondaparinux therapy is routinely recommended for all patients diagnosed
with NSTEMI. There is no one anticoagulant that has a clear advantage when
compared with others in every common patient scenario and the selection of the
appropriate agent is complex. Factors that influence agent decision include bleeding
risk, interaction with other therapies, plans for invasive versus medical management,
time to an angiogram, and procedural technique. Agent selection is generally guided
by institutional protocols or cardiology consultation.
Indications for Emergency Revascularization
Trials have failed to show an immediate benefit of emergency revascularization with
PCI or fibrinolytic therapy in patients with NSTEMI. When an invasive revascularization
strategy is pursued it is reasonable to perform PCI within 24 to 72 hours of presenta-
tion depending on patient factors.29 However, very high-risk NSTEMI patients were
excluded from previous trials and have a poor prognosis. They should be treated anal-
ogously to STEMI patients with emergency PCI4 (Box 3).

MANAGEMENT OF ACUTE COMPLICATION OF ACUTE CORONARY SYNDROME

Electrical Complications
Ventricular arrhythmia in ACS carries a greater mortality risk and occurs in up to 5% of
patients.30 Immediate management includes cardioversion/defibrillation in unstable
patients. Emergency revascularization, preferably via PCI is indicated to correct the
underlying ischemia triggering the arrhythmia. Antiarrhythmic use in early ACS is
largely driven by expert consensus. Beta-blockers should be initiated in otherwise
stable patients to decrease sympathetic tone and decrease reoccurrence. Potassium
and magnesium should be repleted to goal levels of 4.0 to 5.0 mEq/L and 2.0 mEq/L.31
 Management of Acute Coronary Syndrome 701

Box 3
Indications for emergency PCI in NSTEMI

Hemodynamic instability/cardiogenic shock

Recurrent/refractory chest pain despite treatment
Life-threatening arrhythmia
Mechanical complications of MI
Acute heart failure clearly caused by ACS
ST-Segment depression greater than 1 mm in six leads plus ST-segment elevation in AVr and/or
V1 clearly caused by ACS

Abbreviations: ACS, acute coronary syndrome; MI, myocardial infarction.

Data from Collet JP, Thiele H, Barbato E, et al. 2020 ESC Guidelines for the management of
acute coronary syndromes in patients presenting without persistent ST-segment elevation.
Eur Heart J. 2021;42(14):1289-1367. https://doi.org/10.1093/eurheartj/ehaa575.

Recurrent ventricular tachycardia/VF in ACS should be treated similarly to other pa-

tients with electrical storms, including the use of antiarrhythmic therapy (most
commonly amiodarone).31
Bradycardia in early ACS is common and results from increased vagal tone or
ischemia to the cardiac conduction system. In the absence of hemodynamic insta-
bility, no treatment is needed and most cases will resolve over time with treatment
of ACS. When hemodynamically significant, initial medical treatment with atropine is
indicated. Frequently high-grade heart blocks will not respond to atropine, and in
these cases, transcutaneous or transvenous pacing is indicated while arranging emer-
gency revascularization. Sympathomimetic agents to increase heart rate are some-
times necessary but generally avoided because they may exacerbate coronary
malperfusion and increase cardiac oxygen demand.

Cardiogenic Shock and Acute Heart Failure

Acute heart failure and cardiogenic shock not caused by dysrhythmias in the immedi-
ate ACS period have a differential diagnosis that includes severe left ventricular heart
dysfunction, acute mitral valve insufficiency, ventricular/septal wall rupture, and acute
right heart failure. Rapid evaluation with bedside echocardiography is beneficial when
the underlying diagnosis is not clear. An emergency cardiology consultation should be
obtained because most patients will require emergency revascularization or cardiac
surgery.

Left Ventricular Failure

A cardiogenic shock from left ventricular pump failure has a mortality rate of 50%.32
Most patients with ACS that develop cardiogenic shock will have a STEMI but shock
can occur in NSTEMI patients as well. Revascularization with PCI is recommended as
soon as possible, even for patients with delayed presentations greater than 12 hours.10
An initial attempt to improve hemodynamics with a 250 cc bolus of isotonic fluid is
reasonable in patients without pulmonary edema or respiratory distress. Practitioners
should rapidly escalate to vasopressor therapy if there is continued hemodynamic
instability and evidence of malperfusion.
Vasopressor selection is variable and there is no high-quality data to recommend
one agent over another. Norepinephrine is generally recommended as a first-line
702 Atwood

agent as dopamine has been associated with worse outcomes in cardiogenic shock.33
It is prudent to use the lowest dose possible to achieve hemodynamic stability and
minimize iatrogenic coronary vasoconstriction. In cases of continued malperfusion
with stable blood pressures, a trial of dobutamine can be considered. Diuretics and
afterload reducers are rarely used in the emergency department for ACS-induced
cardiogenic shock and are generally considered in more stable patients when addi-
tional data clarify the hemodynamic state. Intra-aortic balloon pumps, left ventricular
assist devices, and extracorporeal membrane oxygenation do not have a strong evi-
dence base but are frequently used in refractory cases of a cardiogenic shock given
the high mortality rate and limited treatment options.
Acute mitral valve insufficiency should be suspected in cardiogenic shock or acute
pulmonary edema, particularly in the presence of a new systolic heart murmur. Rapid
dilation of mitral annulus due to left ventricular dilation, ischemia to the valve leaflet, or
papillary muscle/chordae tendineae rupture are the main causes and are readily iden-
tified on cardiac ultrasound. When there is evidence of papillary muscle/chordae ten-
dineae rupture, emergency cardiac surgery consultation is recommended for repair. In
other cases, emergency revascularization is indicated and potentially curative. Acute
afterload reducing agents are recommended in hemodynamically stable patients
awaiting definitive care.
Myocardial wall rupture is generally seen with delayed presentations of ACS
because prolonged periods of ischemia result in large areas of infarcted myocardium.
Depending on the location of the rupture, a pericardial effusion (left ventricular free
wall) or left to right shunt (intraventricular septum) can result. These events are often
rapidly fatal and emergency cardiac surgery consultation is recommended. If hemody-
namics permits, a rapid decrease in afterload is recommended to maximize blood flow
through the aorta in addition to supportive care.
Acute right-sided heart failure is suspected in ACS when the patient presents with
hypotension, distended neck veins, and evidence of a right-sided infarct on ECG.
Initial stabilization while arranging emergency revascularization includes a rapid infu-
sion of intravenous fluids to support right ventricular preload.10

UNIQUE CIRCUMSTANCES IN ACUTE CORONARY SYNDROME MANAGEMENT

Geriatric Patients
ACS is more common in geriatric patients and their presentations can be subtle, lead-
ing to delays in diagnosis and treatment. It is well documented that geriatric patients
are also at higher risk of short- and long-term outcomes from ACS and its treatment
side effects, including hemorrhage, heart failure, and death.34 Overall management
of ACS in the elderly is similar to younger patients. A provider should have a height-
ened level of awareness of comorbidities, which may impact the selection and dosing
of medications as well as the downstream therapeutic approach. Age is cited as one of
the leading reasons a more conservative approach to care is pursued; however, age
alone should not be the sole determination in this decision. Invasive strategies have
been shown to improve outcomes for patients in their 80s and 90s.35

Cardiac Arrest
It is well established that patients with STEMI who are resuscitated from cardiac arrest
should have emergency PCI once stabilized.36 When there is no evidence of STEMI on
ECG after cardiac arrest, the indications for emergency PCI are not clear. Many pa-
tients with cardiac arrest will have coronary artery disease; however, less than 25%
of these patients actually have a new culprit lesion that explains their presentation.
 Management of Acute Coronary Syndrome 703

Routine emergency PCI in the post-arrest period has not been shown to improve out-
comes in randomized trials.37 In practice, the available patient history (eg, preceding
chest pain), known comorbidities, initial heart rhythm, evidence of ongoing ischemia,
and early prognostication are all considered when deciding on an emergency PCI
strategy.38
Cocaine
Cocaine use can lead to acute coronary ischemia through multiple mechanisms
including coronary vasoconstriction and increased myocardial oxygen demand from
sympathetic stimulation as well as inciting acute plaque rupture or spontaneous
thrombogenesis.39 Risk of ACS is highest in the immediate post-ingestion period.40
Once a diagnosis of ACS is established management is similar to ACS in other situa-
tions with the following exceptions. Liberal use of nitroglycerin is encouraged to relieve
coronary constriction and high doses of benzodiazepines should be administered if
there is evidence of a sympathomimetic toxidrome (eg, agitation, tachycardia, hyper-
tension). Although there is no robust evidence, most practitioners avoid beta-blockers
due to concerns about triggering unopposed alpha stimulation leading to coronary
vasoconstriction.

SUMMARY

Patients are diagnosed with ACS routinely on every shift. The range or presentation
includes the subtle symptoms in the well-appearing patients to the overtly critically
ill in the patient with ischemia-induced shock. Cornerstones of management include
aggressive supportive care, early optimization of myocardial mismatch, prevention
of thrombus propagation, and improving early perfusion with PCI or fibrinolytic agents
in select patients.

CLINICS CARE POINTS

 All patients with chest pain should have an electrocardiogram (ECG) within 10 minutes to
evaluate for ST-Segment elevation myocardial infarction (STEMI).
 All patients with suspected acute coronary syndrome (ACS) should receive aspirin as soon as
possible.
 All patients with ongoing or recurrent chest pain concerning for ACS should have serial ECGs
to evaluate for evolution of myocardial infarction and STEMI.
 Patients with STEMI should have revascularization (fibrinolytics vs. percutaneous coronary
intervention) as soon as possible.
 Follow institutional guidelines regarding additional antiplatelet agents and anticoagulation
because recommendations vary according to typical downstream management patterns.
 Avoid routine use of oxygen and morphine in patients with ACS.

DISCLOSURE

The author has nothing to disclose.

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