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158 J. A. Salotto
• A careful history and physical, risk stratification, electrocardiography,
echocardiography, and cardiac biomarkers are fundamental to the diagnosis
of ACS.
• Patients with suspected ACS should be managed promptly with antiplatelet
agents, anti-anginal medications, and anti-coagulants in the absence of
contraindications.
• In UA/NSTEMI, the goal of therapy is to prevent further thrombosis and to
allow innate fibrinolysis to dissolve thrombus and reduce the degree of
stenosis. Revascularization therapies are employed in high-risk patients to
increase blood flow and prevent recurrent ischemia.
• STEMI represents a complete coronary vessel occlusion. Treatment modali-
ties focus on pharmacological thrombolysis or catheter-based reperfusions.
Urgent/emergent coronary artery bypass is indicated in certain populations.
• Important sequelae of acute myocardial infarctions include: heart failure,
cardiogenic shock, right ventricular infarct, new-onset mitral regurgitation,
cardiac rupture, ventricular aneurysm, pericardial effusion, pericarditis, and
arrhythmia. The surgical intensivist must be aware of the diagnosis and
treatment of these potential complications.
Background
• Cardiac physiology
The cardiac cycle consists of systole (contraction of cardiac muscle) and
diastole (relaxation of cardiac muscle). The coronary arteries fi ll during
diastole.
Cardiac output is the product of stroke volume and heart rate.
Heart rate is infl uenced by sympathetic and parasympathetic input to the
sinoatrial node, drugs, hormones, age, gender, and physical condition.
Ö Sympathetic neurotransmitters (epinephrine and norepineprhine)
increase heart rate, electrical conduction velocity, and contractility.
Ö The parasympathetic neurotransmitter acetylcholine slows the
heart rate, reduces electrical conduction velocity, and decreases
contractility.
The determinants of stroke volume include preload, afterload, and
contractility.
Ö Preload is mainly determined by the pressure and volume of blood
within the left ventricle at the end of diastole [See the Starling
Curve, Chapter 5-(iv)].
Acute Coronary Syndromes 159
Ö Afterload is the pressure that the left ventricle must work against
to push blood forward into circulation. Key determinants include
systemic blood pressure, aortic stenosis, and peripheral vascular
resistance.
Ö Contractility is the ability of the heart to squeeze. Contractility
depends on the degree of stretch of cardiac myocytes at the end of
diastole.
Ö Factors which influence contractility include heart rate, sympa-
thetic or parasympathetic stimulation, and cardiac glycosides such
as digitalis.
Cardiac oxygen supply and demand
Cardiac oxygen consumption is directly related to the amount of ten-
sion generated by the ventricles. Factors infl uencing this include heart
rate, cardiac contractility, size of the heart, and afterload.
Ö During tachycardia, diastole is shortened and coronary blood flow
is decreased. Contraction of the ventricle narrows the coronary
arteries and this also impedes flow.
Ö Wall stress is proportional to ventricular pressure and volume, and
inversely proportional to wall thickness.
The coronary circulation can increase blood fl ow to the heart up to fi ve
times during exercise. Factors which infl uence coronary vasodilation
include neural input, adenosine, and nitric oxide.
Coronary oxygen extraction at rest is nearly maximal. In times of
maximal demand, increasing oxygen supply depends on increasing
coronary blood fl ow.
• Pathophysiology of myocardial infarction
In the majority of patients, obstruction of coronary blood fl ow is caused by
the rupture of an unstable atherosclerotic plaque, leading to local thrombus formation. This may lead to partial (NSTEMI) or complete (STEMI)
occlusion of the coronary artery. Plaques may rupture multiple times
before causing a clinically signifi cant stenosis.
In surgical patients, perioperative MIs may also be caused from an increase in
oxygen demand with a fi xed supply secondary to baseline coronary stenosis.
Rare causes of acute myocardial infarction include coronary artery dissec-
tion, coronary arteritis, coronary emboli, and coronary spasm.
After cardiac ischemia, cell death begins within 30 minutes and is complete
in 3–6 hours.
160 J. A. Salotto
There is a key window of time in which restoration of blood fl ow will
reverse ischemic changes and restore cardiac function.
Severity of myocardial ischemia depends on the location of fl ow
obstruction, metabolic activity of the threatened myocardium, and degree
of preexisting collateralization.
In surgical patients, contributors to post-operative myocardial infarction
may include:
Baseline atherosclerosis.
An imbalance of myocardial oxygen supply and demand.
Ö Increased demand: tachycardia, hypertension
Ö Decreased supply: blood loss, hypothermia, hypoxia
Physical and emotional stress.
The hypercoagulable state of surgery as well as platelet hyper-
reactivity.
A heightened infl ammatory state.
Most post-operative myocardial infarctions will occur within four days of
surgery and are ST-segment depression in nature.
Main Body
Defining the acute coronary syndromes
• Unstable angina
Unstable angina is a syndrome of myocardial ischemia without bio-
chemical evidence of cell death (no troponin elevation). It is caused by
an atherosclerotic plaque with exposed mural thrombus. Forward fl ow
through the vessel is maintained, preventing infarction.
Clinical features of unstable angina include pain at rest, usually lasting
>20 minutes and located in the chest, shoulder, back, jaw or arm, or newonset severe angina.
In unstable angina, episodes are unpredictable and worsen over time.
• Non-ST-segment elevation myocardial infarction (NSTEMI)
In the case of NSTEMI, a ruptured atherosclerotic coronary plaque leads
to thrombosis. When this thrombus causes partial occlusion of a cardiac
vessel, insuffi cient blood supply will lead to cardiac ischemia and cell death.
The clinical picture is that of chest pain, biochemical evidence of myocar-
dial necrosis, and ST-segment depressions on electrocardiogram.
Acute Coronary Syndromes 161
• ST-segment elevation myocardial infarction (STEMI)
A STEMI results when the rupture of an atherosclerotic plaque with throm-
bus formation leads to complete occlusion of a major coronary artery.
The clinical picture includes cardiac chest pain, serologic evidence of
myonecrosis, and ST-segment elevations on electrocardiogram.
The loss of coronary blood fl ow leads to myocardial ischemia and necrosis
unless urgent revascularization is undertaken.
New left bundle branch block (LBBB) is considered a STEMI equivalent.
• Defining acute myocardial infarction
Myocardial infarction is cardiac cellular injury caused by prolonged, inad-
equate oxygen supply of any etiology.
The following is the American College of Cardiology and the European
Society of Cardiology’s consensus defi nition of myocardial infarction
from 2012:
Detection of a rise and/or fall of cardiac biomarker values, preferably
cardiac troponin, with at least one value above the 99th percentile
upper limit and one of the following:
Ischemic symptoms, new or presumed new ST-segment T-wave
Ö
changes or new left bundle branch block, development of pathological Q waves on EKG, imaging evidence of new loss of
viable myocardium or new regional wall motion abnormality, or
intracoronary thrombus by angiography or autopsy.
In the setting of recent coronary artery bypass, MI is defi ned by both:
Elevation of cardiac biomarkers in setting of a normal baseline troponin.
Evidence of new pathological q waves or LBBB, angiographic evi-
dence of graft or coronary artery occlusion, or imaging evidence of new
loss of viable myocardium or new regional wall motion abnormalities.
Evaluation of a patient with a suspected acute coronary syndrome
• History:
Anginal pain is often localized to the substernal, epigastric, and inter-
scapular regions.
It is not positional or not reproducible with palpation and may be
described as dull, a pressure sensation, or chest heaviness. Pain may
radiate to the neck, lower jaw, left arm, or left shoulder.
162 J. A. Salotto
Pain usually lasts >20 minutes with an acute myocardial infarction.
Most perioperative MIs occur within 48 hours of surgery.
Anginal equivalents include: dyspnea, fatigue, nausea, vomiting, and dia-
phoresis.
• Physical Exam:
Evaluate vital signs and hemodynamic stability.
Physical fi ndings include diaphoresis, vomiting, syncope, new-onset
bibasilar rales, or a new murmur.
Atypical presentations are seen especially in diabetics, women, or those
on post-operative pain medications.
High-risk patients are commonly asymptomatic.
• Differential:
Chest pain: MI, pulmonary embolus, pneumothorax, pneumonia, dissec-
tion, pericarditis.
Epigastric pain: MI, cholecystitis, gastro-esophageal refl ux, peptic ulcer.
• Assess Cardiac Risk Factors
Use to quickly identify patients at high risk for cardiovascular events.
Cardiac risk factors Include:
Previous history of CAD, peripheral vascular disease, CABG, or
stroke.
Hypertension, smoking or smoke exposure, diabetes, hyperlipidemia.
Abdominal aortic surgery, vascular surgery, surgery lasting over three
hours, or emergency surgery put a patient at higher risk for adverse coronary events.
One evidence-based risk assessment model is the TIMI Risk Score (www.
timi.org).
Identifi es patients with ACS who are at risk for death, myocardial
infarction or recurrent ischemia within 14 days of hospitalization.
Variables (1 point each):
Age ≥65
Ö
≥3 risk factors (hypertension, DM, family history, lipids, smoking)
Ö
Known CAD (stenosis ≥50%)
Ö
Aspirin use in past 7 days
Ö
Severe angina (≥2 episodes within 24 hours)
Ö
Acute Coronary Syndromes 163
ST-segment deviation ≥0.5 mm
Ö
Elevated cardiac biomarkers
Ö
Risk of death or ischemic event through 14 days:
Low 0–2 points (<8.3% event rate)
Ö
Intermediate 3–4 points (<19.3% event rate)
Ö
High 5–7d (41% event rate)
Ö
— Indicates role for early invasive therapy.
Early diagnostic measures
• Electrocardiogram (EKG)
Perform within 10 minutes of initial evaluation for ACS. An EKG may be
non-diagnostic in early ACS, so consider serial EKGs every 30 minutes.
Compare with prior EKGs on record.
Ventricular tachycardia, ventricular fi brillation, or total AV block may be
the fi rst sign of myocardial infarction.
What to look for on an EKG:
Classic fi ndings in UA:
EKG changes that correlate with symptoms.
Ö
Transient ST-segment elevations or depressions and T-wave inver-
Ö
sions.
Classic EKG fi ndings in NSTEMI:
ST-segment depressions in more than 2 contiguous leads, more
Ö
than 1 mm below the baseline; persist over 20 minutes.
Classic EKG fi ndings in STEMI:
ST-segment elevation in more than 2 contiguous leads, >2 mm in
Ö
men or >1.5 mm in women; persist over 20 minutes.
New Q-waves.
Ö
New left bundle branch block.
Ö
— Never physiologic.
— QRS complex >0.12 seconds.
• Coronary biomarkers
The detection of cardiac biomarkers in the bloodstream is a common
method used to detect myocardial infarction, as they are released from
164 J. A. Salotto
cells upon cell death. Cardiac biomarkers include Troponin I, T, and
creatine kinase MB fraction (CKMB).
Cardiac troponin (T or I) is the preferred coronary biomarker due to high
sensitivity and specifi city.
CKMB has limited specifi city — it is also released from skeletal mus-
cle and is often elevated after surgery.
Elevated biomarkers alone are insuffi cient to diagnose acute myocardial
infarction. They are sensitive and specifi c to myocardial injury, but nonspecifi c to the cause of the injury.
Non-ACS sources of elevated troponins include:
Cardiac contusion, myocarditis, rhabdomyolysis, tachyarrythmias
Ö
and bradyarrhythmias, acute stroke, pulmonary embolism, pulmonary hypertension, sepsis, shock, and congestive heart failure.
Drug toxicity may elevate troponins, responsible agents include:
Ö
adriamycin, 5-fl ourouracil, and herceptin.
Blood samples to test for Troponins should be drawn at the fi rst assess-
ment for ACS and repeated 3–6 hours later.
Do not wait for results to begin treatment if clinical suspicion is high.
It may take 6–12 hours after cell death for a troponin assay to be abnormal.
Relying on a single troponin value should be avoided: diagnostic
accuracy is improved with serial measurements.
Patients with cardiac or renal failure may have chronic elevations of
cardiac troponins. It is necessary to document the trend.
Troponin levels remain elevated for 5–14 days after infarction. For this
reason, they are not useful to detect recurrent ischemia after a myocardial
infarction.
• Chest X-Ray (CXR)
A CXR should be obtained early in the work-up of chest pain to rule out
alternative sources of pain including pneumothorax and pneumonia.
Cardiac imaging
• Echocardiogram (ECHO)
A sonogram of the heart, which employs 2-dimensional, 3-dimensional,
and Doppler ultrasound to capture images of the heart. Low in cost and
imparts no radiation.
Evaluates size, shape, function, and structure of the heart.
Acute Coronary Syndromes 165
ECHO may be performed trans-thoracic (TTE) or trans-esophageal (TEE).
TTE: non-invasive, accurate, quick.
TEE: invasive, requires sedation; used if TTE not sensitive enough.
ECHO is highly sensitive for myocardial ischemia in the setting of a non-
diagnostic EKG.
In MI, ECHO will show a new wall motion abnormality or reduced
myocardial contractility.
The absence of wall motion abnormalities excludes major myo-
cardial ischemia.
Helpful to rule out pericardial effusion, aortic dissection, or pulmo-
nary embolus.
• Coronary angiography
Coronary angiography is the radiographic visualization of the coronary
vessels after injection of radiopaque contrast.
Coronary angiography allows for intervention (balloon angioplasty, stent-
ing), determines extent and location of coronary stenoses, and provides
hemodynamic measurements of cardiac pressures and function. It is
expensive and invasive.
When is coronary angiography recommended?
In patients with cardiogenic shock, STEMI or suspected STEMI,
high-risk patients with UA/NSTEMI, or suspected ACS with new
wall motion abnormality or perfusion defect on a stress imaging
study.
In patients with a prior CABG, angiography is recommended for
intermediate- or high-risk fi ndings on noninvasive studies and/or
worsening symptoms.
Recommended for patients resuscitated after cardiac arrest and for
those with ventricular fi brillation/sustained ventricular tachycardia of
unknown etiology.
Treatment of acute coronary syndrome
• Early interventions:
Oxygen if oxygen saturations <90%, heart failure or dyspnea.
There is no data to support the use of oxygen to improve outcomes
in ACS.
Use caution in COPD and in patients with carbon dioxide retention.
166 J. A. Salotto
Telemetry monitoring for arrhythmias.
Evaluate need for blood transfusion.
The ideal transfusion trigger for patients with ACS is currently under
debate [Chapter 9-(i)].
Red blood cell transfusion for hemoglobin <8 g/dL may be benefi cial
in patients with ACS.
There is no evidence that transfusing for a hemoglobin >8 g/dL
improves outcomes or mortality, but there is evidence to suggest that
it may be harmful. RBC transfusion promotes platelet activation and
adhesion and increases blood viscosity. This promotes the thrombotic
etiology of ACS. Transfusion also activates infl ammatory cascades
and increases infection potential.
Consider placing a pulmonary artery catheter for patients with shock and
questionable right ventricular failure or pulmonary hypertension.
• Pharmacological therapy
Anti-ischemic therapy
These medications decrease myocardial oxygen demand and/or in-
crease myocardial oxygen supply.
Agents include nitroglycerin, morphine, beta-blockers, and calcium
channel blockers.
Nitroglycerin
Ö
— Reduces myocardial oxygen demand by decreasing left ven-
tricular preload and afterload through systemic vasodilation.
It also dilates coronary arteries, increasing coronary blood
fl ow.
— Dose: Nitroglycerin 0.4 mg sublingual tablets, up to three dos-
es, each fi ve minutes apart until pain subsides.
— A nitroglycerin drip may be indicated for persistent or recur-
rent chest pain or uncontrolled hypertension.
9 Start nitroglycerin drip at 5–10 mcg/min, titrate by 10 mcg/
min every 5 minutes until symptom relief or systolic blood
pressure <100 mmHg.
— Avoid in suspected right ventricular infarct, hypotension, or
recent 5′-phosphodiesterase inhibitor use.
Acute Coronary Syndromes 167
Morphine
Ö
— Pain relief and anxiolysis leads to decreased sympathetic
activation, heart rate, and coronary oxygen demand. Also causes
systemic vasodilation which reduces ventricular preload.
— Use for pain refractory to nitroglycerin.
— Dose: Morphine 4–8 mg IV bolus, with additional 2 mg at 5–15
minute intervals until pain is controlled.
9 May result in a decrease in blood pressure, and must moni-
tor respiratory rate.
NSAIDs (except aspirin) should be avoided or discontinued in
Ö
cases of suspected ACS or in post-CABG patients, as they have
been shown to increase the risk of death and re-infarction.
Beta-blockers: metoprolol.
Ö
— Inhibit beta-1 adrenergic receptors in the myocardium, which
decreases heart rate, blood pressure, and cardiac contractility,
and therefore cardiac oxygen demand.
— Beta-blockers have been demonstrated to reduce the risk of
recurrent myocardial infarction in patients with ACS.
— Oral beta-blocker therapy should be initiated within 24 hours
of the onset of ACS.
9 Dose: Metoprolol, 25 mg PO twice daily, titrate to heart
rate of 50–60 beats per minute.
9 Use IV beta-blockers for hypertension or arrhythmias.
9 Contraindications: hypotension, bradycardia, heart block,
decompensated heart failure, asthma, cocaine-induced myocardial infarction.
Calcium Channel Blockers
Ö
— Inhibit contraction of the myocardium and vascular smooth
muscle, leads to coronary vasodilation and decreased after-
load.
— Recommended for refractory angina after nitrates and beta-
blockers, or for contraindications to beta-blockade.
— Recommended agents: diltiazem or verapamil. These agents
also decrease heart rate.
— Avoid in heart failure or pulmonary edema.