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16. Alboni P, Botto GL, Baldi N,
et al. Outpatient treatment of
recent-onset atrial fibrillation
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approach. N Engl J Med. 2004;
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17. Reiffel JA. Atrial fibrillation:
what have recent trials taught
us regarding pharmacologic
management of rate and
rhythm control? PACE. 2011;
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18. Gage BF, Waterman AD,
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285(22):2864–2870.
19. Lip GY, Niewlaat R, Pisters R,
et al. Refining clinical risk
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stroke and thromboembolism
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novel risk factor-based
approach: the euro heart survey
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oral anticoagulant drugs in
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21. Connolly SJ, et al. Dabigatran
versus warfarin in patients with
atrial fibrillation. New England
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22. Pollack CV Jr, Reilly PA,
Eikelboom J, et al.
Idarucizumab for dabigatran
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A prospective, randomized trial
of an emergency department
observation unit for acute
onset atrial fibrillation. Ann
Emerg Med. 2008 Oct; 52
(4):322–328.
24. Vinson DR, Hoehn T, Graber
DJ, et al. Managing emergency
department patients with
recent – onset atrial fibrillation.
J Emerg Med. 2012; 42
(2):139–148.
25. Koenig BO, Ross MA, Jackson
RE. An emergency department
observation unit protocol for
acute-onset atrial fibrillation is
feasible.
Ann Emerg Med. 2002;
39:374–381.
26. Ross MA, Comptom S,
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Atrial Fibrillation
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Section IVA
Chapter
25
Clinical – Cardiac
Syncope
T. Andrew Windsor, MD, RDMS, FAAEM
Amal Mattu, MD, FACEP, FAAEM
Introduction
Syncope is a common presenting complaint in the
emergency department (ED) representing 1–3%
of annual E D visits and up to 6% of hospital
admissions yearly.
1,2
It is defined as a transient
loss of consciousness and postural tone with
spontaneous full recovery and is a result of cerebral hypoperfusion. The differential diagnosis for
syncope is broad, encompassing many possible
etiologies from benign, self-limited events to lifethreatening disease. This wide spectrum frequently prompts inpatient admissions with a
mean cost of $5,400 per admission and approximately $2 billion annually.
3,4,5
Inpatient syncope
evaluations are often low-yield, and serious cardiac or neurologic etiologies are only found in less
than 20%.
6
Several clinical decision rules and novel
protocols have been developed to help providers
determine the short-term risk of death after
syncope, including Osservatorio Epidemiologicosulla Sincopenel Lazio (OESIL); Table 25.1),
7
Syncope Evaluation in the Emergency Department
Study (SEEDS),
8
San Francisco Syncope Rule
(SFSR; Table 25.2),
9
Short Term Prognosis of
Syncope (STePs),
10
Evaluation of Guidelines in
Syncope Study (EGSYS),
11
and Risk stratification
of Syncope in the Emergency Department (ROSE;
Table 25.3).
12
Unfortunately there is no clear
consensus on a standardized evaluation or risk
profile, and the majority of these rules have not
been reliably validated. As well, there is a lack of
convincing evidence showing which patients
benefit from short-term observation to prevent
future adverse events.
The concept of syncope units (dedicated observation units [OUs]) that are equipped with the
capability for common applicable diagnostic tests
and ready access to specialist consultation and
follow-up) has been introduced and lauded by
some.
8,11
Early studies have showed that the
patients who were managed in these units had
significantly lower inpatient hospitalization rate
and shorter length of stay (LOS) without negatively affecting the adverse outcomes or recurrence
rates. Furthermore, there was an associated cost
savings of approximately 20%.
11
In the SEEDS
paper, there was small but significantly higher
diagnostic yield in the syncope unit group when
compared to standard care.
8
Table 25.17The OESIL Score:
1 point awarded for each; score 2 indicates
increased risk of cardiac death:
Age > 65 years
History of CV disease
Syncope without prodromes
Abnormal ECG
Table 25.29San Francisco Syncope Rule:
A patient is high risk for serious outcome if they
have any of the following:
C - History of congestive heart failure
H - Hematocrit < 30%
E - Abnormal ECG
S - Shortness of breath
S - Systolic blood pressure < 90 mmHg
Table 25.312ROSE Rule:
Admit if any of the following are present:
B - Brain natriuretic peptide (BNP) levels of
300 pg per mL or greater
- Bradycardia of 50 beats per minute or less
R - Rectal examination with positive fecal
occult blood test (physician discretion)
A - Anemia (hemoglobin of 9 g per dL or less)
C - Chest pain with syncope
E - ECG with Q waves
S - Oxygen Saturation of 94% or less on
room air
028
20:44:04
Pathophysiology
Syncope is classified as cardiac, neurally mediated
(reflex), orthostatic, or neurologic. [13 Table 25.4
provides examples of each type. Neurally mediated is the most common type and is mostly seen
in older adolescents and young adults.
14
The most
worrisome etiologies are cardiovascular (such as
acute coronary syndrome [ACS], arrhythmias, and
structural or functional disease) and neurologic
(preceding stroke or due to severe basilar insufficiency). Orthostatic syncope is most commonly
encountered in the setting of volume depletion or
a drug effect, but it is important to note that
persons with underlying cardiac disease can have
features similar to orthostatic intolerance.
Discussion
A primary motivator for inpatient admission
should be a high concern for a risk of dysrhythmia or sudden death, and that further observation
may establish a diagnosis, detect a future event, or
allow intervention in a potentially life-threatening
circumstance. The reality is that a large proportion of people admitted with a diagnosis of syncope are discharged without a specific etiology for
their symptom. Exactly which patients benefit
from brief hospitalization is not well defined in
the literature. Furthermore, hospitalization has
not been shown to reduce long-term adverse
events.
10
The major benefits of OUs are that they
have been shown to provide high-quality and
cost-effective care for many conditions, and may
be appropriate for those patients who are neither
high-risk nor very low-risk but need further
evaluation.
Initial risk stratification can help a clinician
decide which patients are at higher risk for
adverse events and therefore require early workup
with hospital or OU admission. Unfortunately the
clinical decision rules developed for this purpose
do not uniformly address length of prognosis.
Some of these rules have not always performed
as well as initially presented in attempts at external validation, but it is notable that there is vast
heterogeneity amongst the structure of study
design, endpoints and application of the individual rule criteria. The SFSR used an endpoint of
7 days and has evaluated the short-term risk of
patients discharged from the ED with a reported
96% sensitivity and 62% specificity.
9,15
In a review
by Serrano et al. the SFSR and OESIL have
been determined to be sufficiently developed for
clinical practice.
16
In another study,17the SFSR
Table 25.4
13
Classification Type Example
Cardiovascular Arrhythmia AV block (2nd degree type II or 3rd degree, bradyarrhythmias, Brugada
syndrome, pre-excitation QRS complex (WPW), supraventricular or
ventricular tachyarrhythmias
Functional ACS, CHF
Obstructive Cardiac myxoma, hypertrophic cardiomyopathy
Structural Aortic dissection, aortic stenosis, pulmonary embolus, pulmonary stenosis
Neurally
Mediated
Carotid
hypersensitivity
Carotid massage, head rotation or shaving
Situational Cough, defecation, urination, visualization of blood
Vasovagal Stress, fear response
Neurologic Cerebrovascular Severe basilar artery insufficiency, subclavian steal
Psychiatric Psychogenic Anxiety, somatization disorders, “spells”
Orthostatic Autonomic
insufficiency
Connective tissue diseases, diabetes mellitus, spinal cord injury
Drug effect Alcohol, anti-hypertensives, drugs of abuse, vaso- or venodilators
Volume/Blood
Deficit
Hypovolemia Dehydration, hemorrhage
Syncope
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20:44:04
and OESIL were compared with clinical judgment
and not found to be statistically different for
predicting adverse events at 10 days. It is notable,
however, that following each clinical rule, no discharged patient would have died, but two patients
in the clinical judgment arm died. The relatively
novel ROSE rule has an 87% sensitivity and a 98%
negative predictive value for 1-month serious outcome in patients with syncope presenting to the
ED.
12
It has been shown to perform poorly with
an inadequate sensitivity for predicting adverse
outcomes at 1 year, however.
18
Evidence suggests that younger patients with
an initial normal evaluation, symptoms consi stent
with vasovagal or orthostatic syncope, no history
of heart disease, and no family history of sudden
death are at low risk of an adverse event and may
be safely followed as outpatients without further
immediate intervention or treatment.
4,19
Patient Criteria
Patient Selection – Inclusion
It is appropriate to admit an adult patient to an
OU who presents to the ED after suffering an
unexplained syncopal event for further evaluation
and possible diagnostic testing with the goal of
establishing a definitive cause. It may also be
appropriate to admit a patient to an OU for
whom a history of syncope is unclear but cannot
be ruled out based on history and physical
exam alone.
Patient Selection – Exclusion
Patients who are inappropriate to admit to an OU
include (1) those with a clearly identified cause of
syncope during the initial ED evaluation and who
do not need further treatment and (2) patients
with any condition that would require hospital
admission independently from the syncopal
event, including sustained bradycardia, type II
second-degree or complete heart block, sustained
supraventricular tachycardia (SVT) or ventricular
tachycardia (VT), pre-excited QRS complex,
Brugada syndrome, confirmed acute coronary
syndrome (ACS), evidence of heart failure, stroke,
subarachnoid hemorrhage, shock, coma, symptomatic anemia, major trauma, or cardiac arrest.
Patients with known non-syncope syndromes,
including light-headedness, dizziness, vertigo,
seizure, mechanical falls, metabolic syndrome,
intoxication, etc.
8,10
may not need OU admission
for syncope, but may be appropriate candidates
for the OU for other reasons including patients in
whom the above diagnoses are unclear and/or
need further evaluation. (See on Vertigo and
Dizziness Chapter 37, Geriatrics Chapter 55,
Seizures Chapter 36, etc.)
Management
Patients appropriately admitted to an OU will
likely benefit from continued monitoring and
further diagnostic testing. All patients should
have orthostatic vital signs and standard 12-lead
electrocardiography
4,19
, and will likely already
have had these performed during the initial ED
evaluation. A chest radiograph is appropriate for
patients with an abnormal physical examination,
chest pain, shortness of breath, or concern for
pneumonia. Laboratory testing should only be
ordered as clinically indicated by the history and
physical examination and not as a routine broad
laboratory panel. Only 2–3% of patients evaluated
for syncope will have abnormal laboratory
results.
20
A reasonable initial laboratory evaluation might include a fingerstick blood glucose
measurement, a pregnancy test for women of
childbearing age, a CBC if SFSR or ROSE are
intended to be used for risk stratification, and a
BNP measurement if the ROSE tool is utilized.
BNP seems to rise from baseline to a peak
between 18 hours and 1 week after an acute syncopal episode in many patients. The reasons for
this are not clear.
21
The American Heart Association (AHA)/
American College of Cardiology Foundation
(ACCF) and the American College of Emergency
Physicians (ACEP) guidelines regarding the
evaluation of syncope offer an algorithmic
approach. If the initial evaluation (history, physical examination, electrocardiogram (ECG),
appropriate labs) is nondiagnostic, echocardiography and ischemic evaluation are recommended.
Those whose syncope remains unexplained at this
point may require tilt-table testing, electrophysiologic studies, or continuous electrocardiographic
monitoring.
4, 19
A study evaluating 341 consecutive patients referred to a syncope unit showed
that history and physical were more reliable in
establishing a diagnosis (14%) than results from
ECG (10%), Holter monitor (5%), electrophysiology (5%), or echocardiography (1%).
22
T. Andrew Windsor and Amal Mattu
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20:44:04
Echocardiography
Echocardiography is a rapid, noninvasive modality
that enables the provider to ascertain functional
and structural information about the heart and
some of the surrounding structures. It can be diagnostic in aortic stenosis or dissection, pericardial
effusions/tamponade, hypertrophic cardiomyopathy, obstructive cardiac lesions, and wall motion
abnormalities suggestive of ischemic disease . It has
been shown to be more useful for those with an
abnormal cardiac history or abnormal ECG.
23
In
an observation setting, those with a normal cardiac
history and normal ECG are unlikely to have an
abnormal structural echocardiogram.
2
Graded Exercise Testing
Options for exercise testing include treadmill or
bicycle testing while performing an ECG or echocardiogram. Treadmill testing is the traditional
form of exercise stress testing, but can be difficult
for the elderly, obese, or those with orthopedic
problems. Bicycle testing may be better tolerated
by some while still allowing for full physical exertion. If the ECG is abnormal at baseline, or the
test would be difficult to interpret alone, echocardiography allows dynamic assessment of cardiac
function. Myocardial perfusion scanning exists as
another option for patients unsuitable for physical exercise test. Stress testing has been shown to
be more useful at confirming coronary artery
disease (CAD) than excluding it.
24
(See Stress
Testing Chapter 26.)
Electrocardiographic Monitoring
The purpose of continuous electrocardiographic
monitoring or telemetry is to capture any potential
arrhythmia events if clinically suspected. Despite
being commonplace in ED and OUs, prolonged
continuous telemetry monitoring is not routinely
recommended by the AHA/ACCF and ACEP guidelines.
4,19
Those who have a high pre-test probability
for arrhythmias or syncope recurrence, or those
with ECG abnormalities should be monitored. The
criteria for an abnormal ECG vary greatly among
guidelines, however a generally applicable definition
would be any non-sinus rhythm, or an ECG with
any new changes compared to a previous ECG. In
addition to evaluating the ECG for changes indicative of ischemia, the ECG should be closely inspected
for dysrhythmias and AV blocks, prolonged QT,
pre-excitation, ventricular hypertrophy, Brugada
Syndrome, and arrhythmogenic foci. The diagnostic
yield of ECG monitoring during short-stay admissions to detect dysrhythmias may be as high as 16%
and increases with length of surveillance.
25
Tilt-Table Testing
Indications for tilt-table testing include suspicion
for neurally mediated syncope. However, the 2006
AHA/ACCF scientific statement does not recommend its routine use in the evaluation of syncope.
The sensitivity ranges from 26% to 80%, and the
specificity is approximately 90%. If the pre-test
probability is high in an otherwise healthy patient,
a negative test does not effectively exclude the
diagnosis.
19
Electrophysiology
Routine electrophysiologic evalu ation is not recommended, but indications for electrophysiology
include patients with structural heart disease,
CAD with syncope, CAD with an ej ection fraction
< 35%, and possibly non-ischemic dilated
cardiomyopathy.
19
Computed Tomography
There is no compelling evidence to suggest that a
Computed Tomography (CT) scan of the head is
routinely indicated in a patient with simple history of syncope and an otherwise normal neurologic examination.
4
Outcome
The primary outcome in an observation setting is
to rule out immediately life-threatening etiologies,
such as ACS, arrhythmias or neurologic causes
if clinically appropriate. A possible secondary outcome is establishing an etiology for the patient’s
syncope. Patients who develop abnormal vital
signs, ECG abnormalities, additional symptoms,
or other high-risk features should have immediate
specialist referral or admission. If clinical suspicion for arrhythmia is high, but observation
monitoring has not revealed any further episodes,
the patient may be referred for outpatient monitoring with a 48-hour Holter monitor, 30-day
monitor, or implantable loop recorder. Any
patient discharged from an OU should have close
follow-up either with a primary care provider or a
specialist within 24–48 hours.
Syncope
028
20:44:04
Conclusion
The use of OUs in the evaluation of syncope is
increasing, and a definitive, validated management plan for the observation setting has not yet
been established. There are a number of clinical
decision tools at the disposal of the treating physician to aid in determining which patients may be
at higher risk for adverse events and warrant
admission. These rules help the clinician with risk
stratification, but they have not been well validated and are varied in short-term reliability.
Common findings amongst these studies that
portend poor outcomes include 1) older age, 2)
ECG abnormalities, 3) history of cardiac disease,
and 4) lack of typical prodrome and/or additional
symptoms before syncope. Several national specialty organizations have offered their recommendations for appropriate workup of patients
presenting with syncope, and some are moving
towards a standardized evaluation. Further
research is needed to develop and validate this
standardized application. A multidisciplinary
approach to the patient with syncope aids in
management, and dedicated syncope units with
treating physicians and ready access to cardiologists, electrophysiologists, and diagnostic testing
may decrease admission length and improve
diagnostic yield.
References
1. Soteriades ES, Evans JC, Larson
MG, et al. Incidence and
prognosis of syncope. N Engl
J Med. 2002 Sep 19;347(12):
878–885.
2. Anderson KL, Limkakeng A,
Damuth E, et al. Cardiac
evaluation for structural
abnormalities may not be
required in patients presenting
with syncope and a normal
ECG result in an observation
unit setting. Ann Emerg Med.
2012 May 24. (Epub ahead of
print)
3. Sun BC, Emond JA, Camargo
CA, Jr. Direct medical costs of
syncope-related
hospitalizations in the United
States. Am J Cardiol. 2005; 95
(5): 668–671.
4. Huff JS, Decker WW, Quinn
JV, et al. American College of
Emergency Physicians. Clinical
policy: critical issues in the
evaluation and management of
adult patients presenting to the
emergency department with
syncope. Ann Emerg Med.
2007; 49(4): 431–444.
5. Alshekhlee A, Shen WK,
Mackall J, et al. Incidence and
mortality rates of syncope in
the United States. Am J Med.
2009 Feb; 122(2): 181–188.
6. Kapoor W.N., Hanusa B.H. Is
syncope a risk factor for poor
outcomes? Comparison of
patients with and without
syncope. Am J Med. 1996 Jun;
100(6): 646–655.
7. Colivicchi F, Ammirati F,
Melina D, et al. Development
and prospective validation of a
risk stratification system for
patients with syncope in the
emergency department: the
OESIL risk score. Eur Heart J.
2003; 24: 811–819.
8. Shen WK, Decker WW, Smars
PA, et al. Syncope Evaluation
in the Emergency Departments
(SEEDS): a multidisciplinary
approach to syncope
management. Circulation.
2004; 110: 3636–3645.
9. Quinn JV, Stiell IG,
McDermott DA, et al.
Derivation of the San Francisco
Syncope Rule to predict
patients with short-term
serious outcomes. Ann Emerg
Med. 2004; 43: 224–232.
10. Costantino G, Perego F,
Dipaola F, et al. on behalf of
the STePS Investigators. Shortand long-term prognosis of
syncope, risk factors, and role
of hospital admission results
from the STePS (Short-Term
Prognosis of Syncope) study.
J Am Coll Cardiol 2008; 51:
276–283.
11. Del Rosso A, Ungar AR, Maggi
R, et al. Clinical predictors of
cardiac syncope at initial
evaluation in patients referred
urgently to a general hospital:
the EGSYS score. Heart 2008;
94: 1620–1626.
12. Reed MJ, Newby DE, Coull AJ,
et al. The ROSE (risk
stratification of syncope in the
emergency department) study.
J Am Coll Cardiol. 2010; 55(8):
713–721.
13. Gauer RL. Evaluation of
syncope. Am Fam Physician.
2011 Sep 15;84(6): 640–650.
14. Linzer M, Yang EH, Estes NA
III, et al. Diagnosing syncope.
Part 1: Value of history,
physical examination, and
electrocardiography. Clinical
Efficacy Assessment Project of
the American College of
Physicians. Ann Intern Med.
1997; 126(12): 989–996.
15. Quinn J, McDermott D, Stiell I,
et al. Prospective validation of
the San Francisco Syncope Rule
to predict patients with serious
outcomes. Ann Emerg Med.
2006 May; 47(5): 448–454.
16. Serrano LA, Hess EP, Bellolio
MF, et al. Accuracy and quality
of clinical decision rules for
syncope in the emergency
department: a systematic
review and meta-analysis. Ann
Emerg Med. 2010 Oct; 56(
4):
362–373.e1.
17. Dipaola FCG, Perego F, Borella
M, et al. San Francisco Syncope
T. Andrew Windsor and Amal Mattu
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Rule, Osservatorio
Epidemiologicosulla
Sincopenel Lazio risk score,
and clinical judgment in the
assessment of short-term
outcome of syncope. Am
J Emerg Med. 2010; 28:
432–439.
18. Reed MJ, Henderson SS,
Newby DE, et al. One-year
prognosis after syncope and the
failure of the ROSE decision
instrument to predict one-year
adverse events. Ann Emerg
Med. 2011 Sep; 58(3): 250–256.
19. Strickberger SA, Benson DW,
Biaggioni I, et al. AHA/ACCF
scientific statement on the
evaluation of syncope: from the
American Heart Association
Councils on Clinical
Cardiology, Cardiovascular
Nursing, Cardiovascular
Disease in the Young, and
Stroke, and the Quality of Care
and Outcomes Research
Interdisciplinary Working
Group; and the American
College of Cardiology
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Society. J Am Coll Cardiol.
2006; 47(2): 473–484.
20. Sarasin FP, Louis-Simonet M,
Carballo D, et al. Prospective
evaluation of patients with
syncope: a population-based
study. Am J Med. 2001; 111(3):
177–184.
21. Reed MJ, Gibson L. The effect
of syncope on brain natriuretic
peptide. Emerg Med J. 2011
Dec; 28(12): 1066–1067.
22. Alboni P, Brignole M, Menozzi
C, et al. Diagnostic value of
history in patients with
syncope with or without heart
disease. J Am Coll Cardiol.
2001; 37(7): 1921–1928.
23. Sarasin FP, Junod AF, Carballo
D, et al. Role of
echocardiography in the
evaluation of syncope: a
prospective study. Heart. 2002;
88
(4): 363–367.
24. Banerjee A, Newman DR, Van
den Bruel A, et al. Diagnostic
accuracy of exercise stress
testing for coronary artery
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meta-analysis of prospective
studies. Int J Clin Pract. 2012
May; 66(5): 477–492.
25. Croci F, Brignole M, Alboni P,
et al. The application of a
standardized strategy of
evaluation in patients with
syncope referred to three
syncope units. Europace.
2002;4(4): 351–355.
Syncope
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20:44:04
Subpart IVA
Chapter
26
Clinical – Cardiac
Stress Testing
Kami M. Hu, MD
Amal Mattu, MD, FACEP, FAAEM
Introduction
Chest pain is one of the leading chief complaints
in the emergency department (ED), accounting
for approximately 5.2% of all visits in 2012.
1
Unfortunately only 30% of these patients are discharged with a definitive diagnosis,
2
and studies
have reported a miss rate of approximately 2–5%
for acute coronary syndrome (ACS) in patients
discharged home from the ED.
3,4
A missed acute
myocardial infarction (MI) carries a 30-day mortality rate of up to 39%,
3
and diagnostic errors in
chest pain complaints and acute MI are responsible for the majority of malpractice lawsuits, the
highest percentage of settled cases, and the highest
payouts.
5
These facts account for why, despite a
less than 20% incidence of ACS in ED patients
with chest pain,
3,4
approximately half are admitted for further assessment, resulting in an estimated annual cost of over $13 billion.
6
Observation units (OUs) and “chest pain units”
(CPUs) have been proven to lower these costs
without worsening outcomes,
7,8
and chest pain
patients are increasingly admitted to OUs for
further monitoring, serial cardiac biomarkers,
and frequently, cardiac stress tests. The immediate purpose of these actions is to determine
whether obstructive coronary artery disease
(CAD), leading to ACS, is the cause of the
patient’s chest pain. Which type of stress test the
patient undergoes is influenced by institutional
protocol, but it is important for health care providers to know about these tests and how to select
them based on a patient’s personal history and
best interests.
Discussion
Pretest Probability
While knowledge regarding the variety of
available tests is important, a discussion of
test selection without a discussion on pretest
probability is inappropriate. Statistically, the
posttest probability of a diagnosisisdependent
on the pretest probability and the diagnostic
accuracy of the test in question. The reliability
of a stress test result, therefore, depends on the
patient’s inherent likelihood of CAD, a nd this
probability should help determine the chosen
modality.
The pretest probability of CAD can be esti-
mated based on the patient’s age, sex, chest
pain characteristics, and is classically categorized
as very low, low, int ermediate, or high risk
(Table 26.1).
9
OUs are primarily utilized for
patients at low or intermediate risk – patients
who cannot be discharged home but do not
clearly warrant inpatient care. The 2014 ACC/
AHA guideline for the management of non-STelevation ACS offers a Class IIa recommendation
for non-inv asive testing for patients with “possible ACS” and negative initial work-up either
prior to or within 72 hours of ED discharge.
9,10
Of note, very-low risk patients should not
undergo stress testing, and high-risk patients
should be referred for functional imaging or invasive coronary angiography.
11
Pharmacologic Stress Agents
The primary pharmacologic stress agents
include coronary vasodilators (adenosine, dipyridamole/persantine, regadenoson/lexiscan) and
a synthetic catecholamine (dobutamine). They
should be utilized in patients who cannot exercise maximally in order to a chieve appropriate
stress on the heart, but the agent chosen should
depend on the individual patient. In nuclear
stress tests, for example, vasodilators should
be utilized in patients with bundle branch
blocks or ventricular pacemakers in order
to overcome false-positive perfusion defects
that occur in these patients during exercise.
Dobutamine, however, is the agent of choice
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20:44:19
in patients with active bronchospastic disease
(COPD, asthma), and in patients who cannot
tolerate medications that will interfere with the
vasodilator agents (xanthine derivatives, such as
theophylline). Further information regarding
the various stress agents is listed in Table 26.2.
Types of Stress Tests
Stress tests evaluate a patient’ s cardiac response
to increased work and myocardial oxygen
demand. The “ stress” is provided by either exercise or pharmacologic mimics, and depending on
the modality, these tests provide information
about the patient’s coronary integrity either by
anatomic or functional assessment (or both, in
some cas es).
Stress Electrocardiogram (treadmill stress
test, exercise tolerance test/ETT) – This test
assesses for ECG changes such as ST-segment
depression or elevations, elicited by patient exercise via bicycle or, most commonly, treadmill.
The most standard proto col used is the Bruce
protocol, in which patients are subjected to
gradually increasing treadmill speed and incline.
Patient heart rate and blood pressure are monitored before, during, and after the test, and the
reactivity and stability of these parameters and
patient’s exercise c apacity provide prognostic
information, even if no ischemic ECG changes
are noted. The Duke Treadmill Score (DTS),
determined by exercise capacity, ST changes,
and anginal severity, is also used for risk stratification and has proven predictive value.
A higher risk by DTS is proportional to risk of
CAD and mortality; a low risk DTS is associated
with a 0.25% annual mortality risk, while there
isa5%annualmortalitywithahighrisk
DTS.
12
ETT has the lowest overall sensitivity
and specificity for detecting cardiac ischemia,
68% and 77%, respectively,
10
but has a high
negative predictive value in low to intermediate
risk patients
13
and remains the initial test of
choice in patients with a normal baseline ECG
who are able to exercise and are not on digoxin,
in whom the accuracy approaches that of stress
imaging.
14
Nuclear Stress Test – Nuclear scanning, a
form of myocardial perfusion imaging (MPI),
involves the intravenous injection of radioactive
isotopes such as thallium-201, technetium-99m
sestamibi, or technetium-99 tetrofosmin in
conjunction with gamma imaging, such as with
single positron emission computed tomography
(SPECT) or cardiac positron emission tomography (PET), to capture and measure the blood
flow to the heart during stress and at rest.
SPECT is the more commonly used imaging
technique, with an averag e sensitivity of 88%
and specificity of 7 4%,
15
and in addition to
assessing for coronary artery stenosis, it provides information on left ventricle size and
measurements of prior infarcts, if present. The
Table 26.1 Pretest Probability of Coronary Artery Disease by Age, Gender, and Symptoms
Age (y) Gender Character of Chest Pain/Likelihood of Angina Pectoris
Typical/Probable Atypical/Possible Nonanginal Asymptomatic
30–39 Male Intermediate Intermediate Low Very low
Female Intermediate Very Low Very Low Very low
40–49 Male High Intermediate Intermediate Low
Female Intermediate Low Very Low Very low
50–59 Male High Intermediate Intermediate Low
Female Intermediate Intermediate Low Very low
60–69 Male High Intermediate Intermediate Low
Female High Intermediate Intermediate Low
Pretest probability of CAD: High > 90%, Intermediate 10–90%, Low < 10%, Very Low < 5%
Adapted from the 2002 ACC/AHA Updates for Exercise Testing.9
Stress Testing
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Table 26.2 Pharmacologic Stress Agents*
Drug Side Effects Contraindications Additional Notes
Coronary Vasodilators
Adenosine Chest pain
Flushing
Headache
Nausea
Dizziness
Dyspnea
Active bronchospasm or reactive
airway disease
2nd–3rd degree AV heart block
without pace maker
Sinus node disease (aka sick sinus
syndrome or symptomatic
bradycardia) without pace maker
Hypersensitivity to adenosine
Relative:
Hypotension (sbp
< 90 mmHg)
Ineffective in patients
who have taken
xanthine derivatives
(theophylline,
aminophylline, caffeine)
or dipyridamole in the
past 24 hours
For serious side effects,
discontinuation of
medication is effective
due to extremely short
half life
Dipyridamole
(Persantine)
Chest pain
Hypotension
Flushing
Headache
Nausea
Dizziness
Dyspnea
Active bronchospasm or reactive
airway disease
2nd–3rd degree AV block
without pacer
Hypersensitivity to dipyridamole
Relative:
Heart failure/severe left
ventricular dysfunction
Atrial tachycardias with rapid
ventricular response
Hypotension (sbp
< 90 mmHg)
Ineffective in patients
who have taken
xanthine derivatives
(theophylline,
aminophylline, caffeine)
in the past 24 hours
Administration of
aminophylline
counteracts effects
Regadenoson
(Lexiscan)
Chest pain
Tachycardia
Arrhythmia
Headache
Flushing
Nausea
Dizziness
Dyspnea
2nd–3rd degree AV block or
sinus node dysfunction
without pacer
Relative:
Active bronchospasm or reactive
airway disease
Hypotension (sbp
< 90 mmHg)
May be ineffective in
patients who have taken
xanthine derivatives
(theophylline,
aminophylline, caffeine)
in the past 24 hours
Administration of
aminophylline
counteracts effects
Synthetic Catecholamines
Dobutamine Tachyarrhythmia
Hypertension
Chest pain
Headache
Tremor
Palpitations
Chills
Significant aortic stenosis or
obstructive cardiomyopathy
Hypersensitivity to dobutamine
Relative:
Uncontrolled hypertension
Atrial tachyarrhythmias with
rapid ventricular response
Hypovolemia
Agent of choice in
bronchospastic patients
Administration of
esmolol counteracts
effects
* Information collected from Lexicomp and Micromedex databases, June 2012.
AV = atrioventricular
Sbp = systolic blood pressure
Kami M. Hu and Amal Mattu
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