Clinical Cardiac Emergencies

Disease-a-Month
Volume 59 Number 3 March 2013
Approach to clinical
cardiac emergencies
Rahul Wadke, MD
Currently working at Monteore Medical Center
Dept. of Internal Medicine, Division of Hospitalist
Bronx, New York
Stephen Boateng, DO
NorthShore University HealthSystem
Department of Medicine
Evanston Hospital
Evanston, IL
Timothy Sanborn, MD
Division of Cardiology
Department of Medicine
NorthShore University HealthSystem
Evanston Hospital
Evanston, IL
Scott Leikin, BA
Lincoln Memorial University Debusk College of Osteopathic Medicine
Harrogate, TN
Andrew Pierce, MD
University Inpatient Physicians
Methodist University Hospital
Memphis, TN
Michael Nelson, MD
Department of Emergency Medicine
John H Stroger Jr Hospital of Cook County
Toxikon Consortium
Chicago, IL
Disease-a-Month 59 (2013) 66
Contents lists available at SciVerse ScienceDirect
Disease-a-Month
journal homepage: www.elsevier.com/locate/
disamonth
Foreword
Approach to clinical cardiac emergencies
This issue of Disease-a-Month is devoted to an update of acute cardiac issues that are frequently
encountered by the Primary Care Physician: acute myocardial infarction, tachycardia and atrial
brillation. Each of these conditions has seen signicant diagnostic and therapeutic advances over
the past decades, which are highlighted in this issue. Also included in this issue is a review of Sudden
Cardiac Death in younger athletes.
The rst 3 sections written by Stephen Boateng, DO, Timothy Sanborn, MD, and Rahul Wadke, MD
from the Department of Medicine, NorthShore University HealthSystem in Evanston, Illinois were
adapted from Conns Current Therapy 2013 (edited by Edward T. Bope and Rick D. Kellerman) were
published in December 2012 by Elsevier (elsevierhealth.com). The Sudden Cardiac Death section
was written specically for this issue in Disease-a-Month and was authored by Scott Leikin, BA,
Andrew Pierce, MD and Michael Nelson, MD.
We believe that this issue and the upcoming textbook will be valuable resources for the Primary
Care Physician for years to come.
Jerrold B. Leikin, MD
Editor-in-Chief
0011-5029/$ - see front matter & 2013 Published by Mosby, Inc.

http://dx.doi.org/10.1016/j.disamonth.2012.12.001
Disease-a-Month
journal homepage: www.elsevier.com/locate/disamonth
Atrial brillation
Rahul Wadke, MD
Epidemiology
Atrial brillation (AF)
AF is the most common arrhythmia in clinical practice. Current prevalence of 12% of the
population is estimated to at least double in the next 50 years. It is a very costly public health
problem with $3600 spent annually per patient in the European Union. The prevalence of AF
increases with age, from o 0.5% at 4050 years, up to 810% in those older than 80 years. The
lifetime risk of developing AF in 40-year olds is 25%. Men are more often affected compared
to women, with exception of those over 75 years or older. The prevalence and incidence in nonCaucasian population is less well studied.
Pathophysiology
Atrial factors: Any kind of structural heart disease may trigger remodeling of both the atria
and ventricles. Structural remodeling facilitates initiation and perpetuation of AF. Atrial
refractoriness shortens within rst days of new onset AF. Even in patients with single episode
of AF, brosis and inammatory changes have been documented.
Electrophysiological mechanisms: Focal mechanisms of triggered activity and re-entry have
attracted much attention recently. Wavelet hypothesis suggests several independent wavelets
propagating AF rather than a single focus. Familial component should be investigated with
early onset AF.
AF reduces left atrial ow velocities and causes delayed emptying from atrial appendage and
are implicated in thrombus formation.
Causes/risk factors
Reversible causes of AF: AF can be related to temporary causes like alcohol use (holiday heart
syndrome), surgery, MI, pericarditis, pulmonary embolism, electrocution, hyperthyroidism, and
other metabolic syndromes. AF remains a common early postoperative complication of
cardiothoracic surgeries. Successful treatment of underlying medical problems often causes
termination of AF (Table 1).
0011-5029/$ - see front matter & 2013 Mosby, Inc. All rights reserved.
68
R. Wadke / Disease-a-Month 59 (2013) 6773
Table 1
Types of atrial brillation.
1 First diagnosed AF
2 Paroxysmal AF
3 Persistent AF
4 Long-standing
persistent AF
5 Permanent AF
6 Silent AF
First time diagnosis of AF irrespective of duration of arrhythmia, presence of symptoms,

or severity of symptoms
Usually self-terminating within 48 h. After 48 h likelihood of spontaneous conversion is
low and anticoagulation should be considered
AF episode lasting 47 days or requiring cardioversion (chemical or direct current)
Lasting 4 1 year
Presence of AF is accepted by patient and physician. Rhythm control usually not pursued
in patients with permanent AF
Patient presents with AF related complications (thromboembolic stroke,
cardiomyopathy) or incidental nding on ECG in an asymptomatic patient
Obesity is an important risk factor for development of AF. Studies suggest a possible
physiologic basis, increasing left atrial size correlates with increase in weight and regression
has been observed in left atrial size.
About 3045% cases of paroxysmal AF in young adults have no demonstrable underlying
heart disease.
Cardiovascular conditions associated with AF include mitral valve disease, heart failure,
coronary artery disease (CAD), hypertension associated with left ventricular hypertrophy.
Other associations include hypertrophic obstructive cardiomyopathy (HOCM), dilated
cardiomyopathy, atrial septal defect, restrictive cardiomyopathies, cardiac tumors, and
constrictive pericarditis. AF is commonly found in patients with obstructive sleep apnea (OSA).
Clinical manifestations
Patient may or may not have symptoms with AF. Commonly associated symptoms include
palpitations, shortness of breath, fatigue, decreasing exercise tolerance, or chest discomfort.
An irregular pulse should raise the suspicion for AF. Patients may present initially with TIA
or ischemic stroke. Most patients experience asymptomatic episodes of arrhythmias before
being diagnosed. Patients with mitral valve disease and heart failure often have higher
incidence of AF.
Intermittent episodes of AF may progress in duration and frequency and over time many
patients will develop sustained AF.
For a newly diagnosed patient of AF, reversible causes such as pulmonary embolism,
hyperthyroidism, pericarditis and MI should be investigated.
Diagnosis
An irregular pulse can raise the suspicion of AF, but ECG remains essential in diagnosing AF.
AF is dened with the following characteristics:
1. Arrhythmia absoluta: Absolutely irregular RR intervals.
2. No distinct P waves on ECG. Occasionally there might be regular atrial activity noted on
lead V1.
3. Atrial cycle length (interval between two atrial activations) is usually variable and o 200 ms
(4300 bpm).
There are multiple options available to capture AF rhythm depending on the frequency of
symptoms. 12-Lead ECG is recommended as rst step (Fig. 1). Noncontinuous ECG methods
69
Fig. 1. Atrial brillation 12-lead EKG.
include scheduled or symptoms activated ECGs, Holter (24 h to 7 days), and external loop
recorder. Implantable loop recorder can be used to monitor over a 2-year period.
Differential diagnosis
Arrhythmias that can mimic AF include atrial tachycardia, atrial utter with variable AV
block, frequent atrial ectopies, and antegrade atrioventricular nodal conduction. Any episode of
suspected AF should be recorded by a 12-lead ECG. An ECG recording will help in
differentiating AF from rare supraventricular arrhythmias with irregular RR intervals.
Occasionally use of atrioventricular nodal blocking using Valsalva maneuver, carotid massage,
or intravenous adenosine (Adenocard)z may be necessary to establish the diagnosis.
Treatment
Management of patients with AF is aimed at reducing symptoms by rate control or
correction of rhythm disturbances and prevention of thromboembolism. Rate control strategy
attempts control of ventricular rate without restoration or maintenance of sinus rhythm.
Rhythm control strategy attempts restoration and maintenance of sinus rhythm with attention
to rate control.
Regardless of strategy chosen, the need for anticoagulation depends upon stroke risk and
not on type of rhythm.
Risk stratication for stroke and thromboembolism (Tables 2 and 3)

The risk factor-based approach for patients with nonvalvular AF is CHA2DS2-VASc (see
Table 2). New risk stratication scheme builds on the original CHADS2 scheme by considering
z
Not FDA approved for this indication.
70
additional risk factors. Major risk factors are prior stroke or TIA or thromboembolism, and older
age (475 years). Clinically relevant nonmajor risk factors include heart failure, moderate to
severe systolic LV dysfunction (LVEF o40%), hypertension, diabetes, female sex, age 6574
years, and vascular disease (MI, peripheral artery disease, complex aortic plaque).
There is a clear relationship between the CHA2DS2-VASc score and stroke rate. In patients
with a CHA2DS2-VASc score of two or more, chronic anticoagulation therapy is recommended
unless contraindicated. When using warfarin, the goal INR is in the range of 2.03.0 (see
Table 3). An assessment of bleeding risk should be a part of the patient assessment before
starting anticoagulation. It is reasonable to use the HAS-BLED (hypertension, abnormal renal/
liver function, stroke, bleeding history or predisposition, labile INR, elderly more than 65-years
old, drugs or alcohol use) to assess the bleeding risk in atrial brillation patients. The fear of
falls is usually overstated. The patient may need to fall approximately 300 times per year for
the risk of intracranial hemorrhage to outweigh the benets of anticoagulation in the stroke
prevention.
Newer antithrombotic agent: Dabigatran (Pradaxa) was recently approved by FDA for
nonvalvular atrial brillation. Dabigatran is a prodrug that is rapidly converted to an active
direct thrombin inhibitor independent of cytochrome P-450.
Rate control
Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial found no
difference in mortality or stroke rate between the patients assigned to either rhythm control
over ventricular rate control strategies (Table 4).
The Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) trial
found rate control not to be inferior to rhythm control for prevention of death.
The RACE II study shows that lenient ventricular rate control less than 110 bpm is not
inferior to the strict rate control less than 80 bpm. Lenient rate control is generally more
convenient, requires fewer outpatient visits, and generally fewer medications.
None of the major trials demonstrated any signicant difference in the quality of life with
ventricular rate control compared to rhythm control. In older patients with persistent atrial
brillation along with hypertension or heart disease, rate control is a reasonable initial therapy.
Table 2
CHA2DS2-VASc score.
Risk factor
Score
Congestive heart failure/LV dysfunction

Hypertension
Age 4 75 years
Diabetes mellitus
Stroke/TIA/thromboembolism
Vascular disease (MI/PAD/Complex aortic plaque)
Age 6574 years
Female sex
Maximum score
1
1
2
1
2
1
1
1
9
Table 3
Approach to thromboprophylaxis.
CHA2DS2-VASc score
Recommended therapy
2 or more
1
0
Anticoagulation
Anticoagulation or aspirin 75325 mg daily
Aspirin 75325 mg daily or no antithrombotic therapy
71
Table 4
Medications for rate control.
Beta blockers
Metoprolol CR/XL (Toprol
XL) (see footnote z)
Bisoprolol (Zebeta) (see
footnote z)
Atenolol (Tenormin) (see
footnote z)
Esmolol (Brevibloc)
Propranolol (Inderal)
Carvedilol (Coreg) (see
footnote z)
Intravenous
administration
Oral maintenance
dose
Major side effects
2.55 mg IV bolus;
up to 3 doses
N/A
100200 mg daily
Bradycardia, hypotension, heart

blocks, asthma, heart failure
2.510 mg daily
N/A
25100 mg daily
50200 mg/kg/min IV N/A

13 IV
1040 mg TID
N/A
3.12525 mg BID
Nondihydropyridine calcium channel antagonists

Verapamil (Calan)
510 mg bolus
40 mg BID to
360 mg max daily
60 mg TID to
360 mg XL daily
Hypotension, heart blocks, heart

failure
Diltiazem (Cardizem)
0.250.35 mg/kg
Digitalis glycosides
Digoxin (Lanoxin)
0.51 mg
0.1250.5 mg daily
Digitalis toxicity, bradycardia, heart

blocks
Others
Amiodarone (Cordarone)
(see footnote z)
Dronedarone (Multaq)
5 mg/kg loading,
50 mg/h IV
N/A
100200 mg daily
Hypotension, heart blocks,

bradycardia
400 mg BID
Ventricle rates between 60 and 80 bpm at rest, and between 90 and 115 bpm during moderate
exercise are considered at goal for patients opting for rate control.
Negative chronotropic medications like beta blockers, amiodarone (Cordarone) (see
footnote z), digitalis glycosides, or nondihydropyridine calcium channel antagonist prolong
the refractory period of AV node thus effectively controlling the heart rate. Bradycardia and
heart blocks are some of the side effects of these medications.
Rhythm control
Rhythm control in certain studies resulted in better exercise tolerance than rate control but
did not show any improvement in the quality of life. In younger patients with paroxysmal atrial
brillation, ablation is considered a better approach. For patients remaining symptomatic
despite an adequately controlled ventricular rate, rhythm control is an appropriate next step.
Antiarrhythmic agents signicantly reduce the rate of recurrence of atrial brillation; the
likelihood of maintaining the sinus rhythm is approximately doubled with the use of
antiarrhythmic drugs. If one antiarrhythmic drug fails, it is acceptable to try another
antiarrhythmic drug. QT prolongation and drug-induced torsades de pointes are some of the
signicant side effects of these medications. Amiodarone (Cordarone) (see footnote z),
ecainide (Tambocor), propafenone (Rythmol), and sotalol (Betapace) are frequently used in
Western countries (Table 5).
Cardioversion
Cardioversion may be considered emergently or electively to restore the sinus rhythm in
patients with atrial brillation. Anticoagulation is considered mandatory before elective
72
Table 5
Medications for rhythm control.
Flecainide (Tambocor)
Flecainide XLa
Propafenone (Rythmol)
Propafenone SR
(Rythmol SR)
Sotalol (Betapace)
Amiodarone (Cordarone) (see
footnote z
Dronedarone (Multaq)
a
Intravenous
administration
Oral maintenance
dose
Major side effects
1.53.0 mg/kga
N/A
1.52.0 mg/kga
N/A
50150 mg BID
200 mg daily
150300 mg TID
225425 mg BID
Hypotension, atrial utter

with high ventricular rate
Hypotension, atrial utter
with high ventricular rate
N/A
80160 mg BID
5 mg/kg loading, 50 mg/ 100200 mg daily
h IV
N/A
400 mg BID
Bradycardia, hypotension
Hypotension, bradycardia,
QT prolongation, torsades de
pointes
Not available in the United States.
cardioversion for atrial brillation of more than 48 h or atrial brillation of unknown duration
because of the increased risk of thromboembolic following cardioversion. The current data
suggest that patient needs to be anticoagulated for at least a 3-week duration before
cardioversion. Immediate cardioversion should be performed in patients for hemodynamically
unstable and patient should be anticoagulated before cardioversion. Transesophageal echoguided cardioversion strategy can be applied as an alternative to precardioversion anticoagulation. Cardioversion can be performed with the help of drugs or electrical shocks. Drugs
like dofetilide (Tikosyn) or ecainide (Tambocor) are usually tried before a direct current
cardioversion. Pharmacologic cardioversion is usually most effective within seven days after
the onset of an episode of atrial brillation.
Ablation
Patients, who are symptomatic or with tachycardia-mediated cardiomyopathy related to the
rapid ventricular rate that cannot be controlled adequately with pharmacologic agents, are
most likely to benet from AV nodal ablation in conjunction with permanent pacemaker
implantation.
Postablation anticoagulation should be continued for a minimum of 3 months, and
thereafter depending upon the individuals stroke risk.
Prevention
Measures for primary prevention of AF have not been widely studied. Losartan (Cozaar) (see
footnote z) (LIFE trial) and candesartan (Atacand) (see footnote z) (CHARM trial) reduced
incidence of AF in hypertensive patients with LVH and symptomatic HF, respectively. These
results suggest a role for ACE inhibitor or ARB in primary prevention of AF associated with
hypertension, MI, HF, or diabetes. Statins may protect against AF, but this has been
inadequately explored. Dietary interventions, pharmacologic interventions, or pacing have
insufcient data in prevention of AF.
Special considerations
The elderly
The elderly patients usually have multiple medical problems including cardiovascular
comorbidities such as a higher incidence and prevalence rate of atrial brillation, higher
73
thromboembolic risk and bleeding risk. The prevalence of atrial brillation is as high as 18% in
those aged more than 85 years. The Screening for Atrial Fibrillation in the Elderly (SAFE) trial
found that ECG for irregular pulse is an effective screening tool. All patients aged more than 75
years with atrial brillation should be considered for anticoagulation. In elderly patients, sinus
rhythm is often difcult to maintain. For rate control, beta blockers and nondihydropyridine
calcium channel antagonists can be considered.
Postoperative atrial brillation

Atrial brillation is the most common complication after coronary artery bypass graft
(CABG)30%, valvular surgery40%, and combined CABG/valvular surgery50%. The peak
incidence of atrial brillation is during postoperative days 2 and 4. Beta blocker therapy is most
effective in prevention of postoperative atrial brillation. Prophylactic amiodarone (Cordarone)
(see footnote z) decreases the incidence of postoperative atrial brillation and signicantly
shortens the duration of hospital stay. Hypomagnesaemia is an independent risk factor for
postoperative atrial brillation. The use of statins is associated with lower risk of postoperative
atrial brillation. Majority of the postoperative hemodynamically stable patients will convert
spontaneously to sinus rhythm within 24 h of initial management which includes correction of
predisposing factors such as pain management, correcting electrolytes and metabolic
abnormalities, addressing hypoxia, addressing anemia, and hemodynamic optimization.
References
[1] Olshansky B, Rosenfeld LE, Warner AL, et al. The Atrial Fibrillation Follow-up Investigation of Rhythm Management
(AFFIRM) study: approaches to control rate in atrial brillation. J Am Coll Cardiol 2004;43:12011208.
[2] Wann LS, Curtis A, January CT, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with
atrial brillation (update on dabigatran): American College of Cardiology Foundation American Heart Association
Task Force on practice guidelines. J Am Coll Cardiol 2011;57:223242.
[3] Hagens VE, Crijins HJ, Veldhuisen DJ, et al. Rate control versus rhythm control for patients with persistent atrial
brillation with mild to moderate heart failure: results from the Rate Control versus Electrical cardioversion (RACE)
study. Am Heart J 2005;149(6):11061111.
[4] Van Gelder IC, Groenveld HF, et al. Lenient versus strict rate control in patients with atrial brillation. N Engl J Med
2010;362:13631373.
[5] Lip GYH, Nieuwlaat R, Pisters R, et al. Rening clinical risk stratication for predicting stroke and
thromboembolism in atrial brillation using a novel risk factor-based approach: the Euro Heart Survey on atrial
brillation. Chest 2010;137(2):263272.
[6] Camm AJ, Kirchhof P, Lip GYH, et al. Guidelines for the management of atrial brillation the task force for the
management of atrial brillation of the European Society of Cardiology (ESC). Eur Heart J 2010;31:23692429.
Disease-a-Month
Tachycardia
Stephen Boateng, DO
Epidemiology
Supraventricular tachycardias
Though rarely life threatening, supraventricular tachycardias are common, may be
persistent and often reoccur throughout ones lifetime. The etiology of supraventricular
tachycardias varies with age, sex, and comorbid conditions. Paroxysmal supraventricular
tachycardias (PSVT) are estimated to have a prevalence of 2.25 per 1000 and an incidence of 35
per 100,000 person years according to the Marsheld Epidemiologic Study Area (MESA)
conducted in Wisconsin. In this study, the mean age of onset of PSVT was 57 years, and age of
onset ranged from infancy to more than 90 years old. Females were shown to have a two-fold
risk compared with their male counterparts in the MESA study.
Ventricular tachycardias
Ventricular tachycardias have a prevalence of about 20 per 100,000 persons in the general
population and occur more frequently in men. An appreciable percentage (3.5%) of ventricular
tachycardias occur post myocardial infarction (post-MI), and the incidence of post-MI VT
increases with age.
Pathophysiology
All tachycardias are produced by one or more mechanisms which include disorders of
impulse initiation (automaticity) and abnormalities of impulse conduction (re-entrant). Tissues
exhibiting abnormal automaticity that underlie SVT can reside in the atria, the AV junction, or
vessels that communicate directly with the atria, such as the vena cava or pulmonary veins.
Normally, the sinus node contains the dominant pacemaking function and is made of cells with
faster rates of phase 4 diastolic depolarization (Fig. 1). Cells with abnormal automaticity
(enhanced diastolic phase 4 depolarization) may arise in other locations (ectopic foci) and if
their ring rate exceeds that of the sinus node, then the ectopic focus becomes the
predominant pacemaker of the heart.
Reentry is the most common mechanism by which SVT occurs. It is also the mechanism for
atrial utter, atrioventricular (AV) node reentry tachycardia (AVNRT), some atrial tachycardias,
S. Boateng / Disease-a-Month 59 (2013) 7482
75
Fig. 1. (A) Diagram of reentry. The impulse is initiated at P. I and II represent two distinct pathways. a represents
unidirectional block, b represents slow conduction, and c shows the propagation of the wavefront reentering the
circuit. (B) A cardiac action potential. The different phases of the action potential are 04. Phase 4 demonstrates
automaticity, which, when it reaches threshold, will initiate the next cardiac action potential. (C) A cardiac action
potential demonstrating early after depolarization (EAD) at the end of phase 2. (D) A cardiac action potential
demonstrating a delayed after depolarization (DAD) during phase 4.
AV reciprocating tachycardia (AVRT), some ventricular tachycardias (VTs), and ventricular

brillation (VF). Initiation and maintenance of a reentrant tachycardia requires a unidirectional
block in one limb of the circuit and slow conduction in the other. A unidirectional block may
result from acceleration of the heart rate, or a premature impulse that is blocked during the
refractory period of the pathway.
Q
As shown in Fig. 1A, a normal impulse arriving at
is propagated down both a and b.
Conduction through pathway a is initially faster and unimpeded whereas conduction through b
is slow. A normal sinus beat is produced. A second impulse attempts to go down a and b;
however, this time, nds arefractory, thus no conduction occurs (unidirectional block).
Pathway b, which is slow conducting and has a shorter refractory period, conducts the impulse.
This results in a premature supraventricular beat with a prolonged PR interval. The impulse
through b may continue in a retrograde pathway (c) to a, and if a is past its refractory period, a
circuit is created through which the impulse may continue to circle producing a persistent
reentrant tachycardia.
Patients with paroxysmal arrhythmias are often asymptomatic on presentation. When
symptoms are present, they may include palpitations, fatigue, lightheadedness, chest
discomfort, dyspnea, presyncope, and syncope. Syncope is observed in about 15% of patients
with SVT. Patients with ventricular arrhythmias more often present with presyncope, syncope,
or even cardiac arrest. A history of syncope should warrant immediate referral to an
electrophysiologist.
Diagnosis
History taking is useful for aiding in the diagnosis and denition of tachycardia. It is
important for the clinician to assess whether or not the palpitations are regular or irregular,
number of episodes, possible triggers, and nature of onset and termination (whether abrupt or
76
gradual). Recurrent episodes with abrupt onset and termination are designated paroxysmal.
Episodes with a gradual onset and termination are nonparoxysmal (e.g., sinus tachycardia).
Irregular palpitations are likely due to premature depolarizations suggesting atrial brillation
(AF) or multifocal atrial tachycardia (MAT). MAT is often encountered in patients with
pulmonary disease. Premature beats are often described by the patient as pauses, followed by a
sensation of a strong heart beat or irregularities in heart rhythm.
On physical examination, if irregular cannon A waves are observed in the jugular vein or
variation in the intensity of the S1 heart sound is heard , then a ventricular origin is strongly
suggested. Termination of the tachycardia with vagal maneuvers strongly suggests a reentrant
tachycardia involving AV nodal tissue such as AVNRT or AVRT.
A resting echocardiogram should be recorded. In the absence of symptoms, this may be of
low diagnostic yield. However, the presence of preexcitation (see Fig. 6) on the EKG suggests
AVRT and is enough to make a presumptive diagnosis. Baseline EKG with preexcitation in
combination with a history consistent with paroxysmal palpitations strongly suggests episodic
atrial brillation (AF) and is concerning. These patients are at a risk for sudden cardiac death
and require immediate electrophysiological evaluation. Patients without concerning symptoms
such as syncope or persistent regular tachycardia may be sent home with an event monitor
with follow-up at a later date. A 24-h Holter monitor can be used in patients who report daily
transient tachycardia. In patients with infrequent arrhythmias, a loop recorder is more useful.
An implantable loop recorder may be used in patients with rare episodes, associated with
hemodynamic instability.
Narrow QRS-complex tachycardia
Narrow QRS-complex (less than 120 ms) supraventricular tachycardias are differentiated
according to the their mechanism and include sinus tachyarrythmias, atrioventricular nodal
reciprocating tachycardia (AVNRT), focal and nonparoxysmal junctional tachycardias, atrioventricular reciprocating tachycardia (AVRT), focal atrial tachycardias and macro-re-entrant
atrial tachycardia (MAT).
Wide QRS-complex tachycardia
Wide QRS-complex tachycardias may be supraventricular or ventricular in origin. Examples
of wide QRS-complex supraventricular tachycardia include SVT with AV conduction via an
accessory pathway, such as in WolfParkinsonWhite (WPW), or any supraventricular
tachycardia with aberrant conduction or ventricular pacing.
Specic tachycardias
Supraventricular tachycardias
Sinus tachyarrrhythmias. Sinus tachycardia may result from physiologic stimulation of the sinus
node or sinus node reentry (sinus node reentry tachycardia). The latter results in paroxysmal,
nonsustained episodes of tachycardia. Normally sinus tachycardia occurs as an appropriate
response to physiologic stimulus such as exercise. Pathologic causes that may induce sinus
tachycardia include hyperthyroidism, pyrexia, hypovolemia, infections or anemia. Drugs that
may cause sinus tachycardia include atropine, aminophylline, catecholamines, and anticancer
treatments (such as doxorubicin [Adriamycin]). Stimulants such as caffeine, alcohol, and
nicotine; and recreational drugs such as cocaine, amphetamines, and ecstasy may all induce
sinus tachycardia. It may also result from an excessive stimulus such as hyperthyroidism.
Findings on ECG reveal a normal axis with upright p waves in I, II and aVF and a negative
77
p wave in aVR. In addition to eliminating the underlying offensive agent such as excessive
caffeine use or hyperthyroidism, beta blockers are very effective for terminating and
suppressing sinus tachycardia. Nondihyhdropyridine calcium-channel blockers, such as
diltiazem (Cardizem) or verapamil (Istopin) may also be used. Vagal maneuvers, adenosine
(Adenocard), beta blockers, and nondihydropyridine calcium-channel blockers are effective in
treating reentry sinus tachycardia. In rare cases where inappropriate sinus tachycardia is
refractory, catheter ablation may be performed.
Atriventricular nodal reciprocating tachycardia
This is the most common form of PSVT and it produces rates of tachycardia between 140
and 250 beats/min (Fig. 2). It is more prevalent in females. Patients typically report associated
palpitations, dizziness, and neck pulsations. The mechanism of AVNRT is a reentry circuit which
is now known to involve perinodal atrial tissue as well and is not always conned to the
compact AV node as previously believed. In AVNRT, reciprocation occurs between two distinct
pathways: the rst, fast pathway, which is located near the apex of Kochs triangle; the second
is a slow pathway which extends from the compact AV-node tissue and stretches along the
septal margin of the tricuspid annulus at the level of, or slightly superior to, the coronary sinus.
The fast pathway conducts rapidly with a slow recovery time and a longer refractory period,
and the second pathway conducts slowly with a short refractory period. AVNRT is initiated
when a premature impulse nds the fast pathway refractory, and is thus conducted
anterogradely through the slow pathway. The impulse continues past the AV node, down the
His-Purkinje system, activates the ventricles, and approaches the His bundle. Here, the impulse
Fig. 2. A 12-lead electrocardiogram depicting typical atrioventricular node reentry tachycardia. Note the absence of
obvious atrial activity or p wave.
Fig. 3. (A) Normal conduction system. AVN atrioventricular node; LA left atrium; LBB left bundle branch; LV
left ventricle; RA right atrium; RBB, right bundle branch; RV right ventricle; SN, sinus node. (B) Diagram of heart
depicting typical atrioventricular node reentry tachycardia (AVNRT) with antegrade conduction via the slow AVN and
retrograde conduction via the fast AVN. (C) Diagram of the heart depicting orthodromic atrioventricular reciprocating
tachycardia (o-AVRT) with antegrade conduction via the AVN and retrograde conduction via the accessory
pathway (AP).
78
Fig. 4. Electrocardiogram lead V1 recorded during administration of adenosine. Termination of atrioventricular node
reentry tachycardia occurs in the antegrade slow pathway. The arrow points to retrograde atrial activity at the terminal
portion of the QRS which is sometimes apparent during tachycardia.
Fig. 5. Electrocardiogram lead III recording of a QRS demonstrating ventricular preexcitation (arrow), also called
WolffParkinsonWhite pattern.
nds the fast pathway in recovery. The fast pathway then serves as a retrograde pathway for
conduction back to the atria (Fig. 3). This produces a p wave during or very close to the QRS
complex often with a pseudo-r0 in V1. Rarely, an atypical AVNRT may occur in which there is
anterograde conduction through the fast pathway and retrograde conduction through the slow
pathway producing a long R-P tachycardia. The p wave, negative in III and aVF, is inscribed
prior to the QRS. Sometimes, though infrequently, the circuit may be composed of slowly
conducting tissues in both limbs of the circuit, resulting in a p wave inscribed after the QRS (a
retrograde p wave) (Fig. 4).
Adenosine (Adenocard) 6 mg IV push is administered to terminate the rhythm, and if the
initial dose is unsuccessful, two more doses of 12 mg of adenosine may be administered.
Adenosine has a half-life of only 9 s, and terminates the circuit by causing transient block in
AVN conduction. Long-term therapy with a beta-blocker or calcium channel blocker can
prevent recurrence. If AVN is recurrent, radiofrequency ablation is the treatment of choice and
has a low risk of complication.
Atrioventricular reciprocating tachycardia (extra nodal accessory pathways)

An accessory pathway is a pathway outside the AV node which connects the myocardium of
the atrium and the ventricle. Accessory pathways may be located across the mitral or tricuspid
annulus and may be capable of anterograde or retrograde conduction or both. Accessory
pathways that conduct in a retrograde function are referred to as concealed because they do
not reveal preexcitation on ECG. Those capable of anterograde conduction are referred to as
manifest. A patient is diagnosed with WPW if they have both preexcitation on ECG and
tachyarrhythmias (Fig. 5). AVRT may be orthodromic or antidromic. Orthodromic AVRT occurs
79
Fig. 6. A 12-lead electrocardiogram depicting orthodromic atrioventricular reciprocating tachycardia. The arrow
highlights the atrial activity, which is occurring well after the QRS complex.
when there is anterograde conduction down the AV node and retrograde conduction up the
accessory pathway (Fig. 6). In antidromic AVRT the reverse occurs.
Atrial brillation is considered life-threatening in patients with WPW. This is because
rapid repetitive conduction can occur via the accessory pathway (which has a short
refractory period), resulting in a rapid ventricular rate which can degenerate into ventricular
brillation.
Administration of adenosine can precipitate atrial brillation in 1015% of patients of
patients with an extra nodal accessory pathway. Therefore, if it is unknown whether or not the
patient has an anterogradely conducting accessory pathway. It is good practice to have a
debrillator present at the bedside during administration of adenosine. For patients with
known WPW syndrome (or delta wave on baseline ECG), procainamide (Pronestyl)1 or ibutilide
(Corvert), drugs that slow conduction over the accessory pathway, can be adminitered instead
of adenosine.
Focal and nonparoxysmal junctional tachycardia
Focal junctional tachycardia. This generally rare phenomenon may occur by automaticity or
reentry mechanisms. By denition, focal junctional tachycardia originates from the AV node or
His bundle. On ECG, focal junctional tachycardia may be varied in its features. It often has a rate
of 110250 with narrow QRS complexes or a bundle branch block (BBB) conduction pattern. AV
dissociation often occurs. However, one-to-one retrograde conduction may also occur. Focal
junctional tachycardia often occurs in young adulthood and is precipitated by exercise or stress.
Patients may respond to beta blockers or Flecainide (Tambocor) (which may be administered IV
initially to terminate the tachycardia, followed by an oral dose), but drug therapy is not always
effective. Catheter ablation is most effective and can be curative, though there is a 510% risk of
AV block.
Nonparoxysmal junctional tachycardia
This is a benign arrythmia that his characterized by narrow QRS complexes at a rate of 70
120 bpm. It occurs via automaticity and may be indicative of some serious underlying
pathology such as digitalis toxicity, hypokalemia, hypoxia, or myocardial ischemia. It is treated
by correcting the underlying abnormality.
Focal atrial tachycardias
These are usually benign tachycardias unless persistent when they may cause tachycardiainduced cardiomyopathy. They usually manifest with rates between 100 and 250 bpm, rarely
1
80
Fig. 7. Electrocardiogram of leads II and III depicting typical atrial utter. Note the sawtooth atrial activity.
gettting up to 300 bpm. The mechanism is thought to be via automaticity, and the majority
originate along the crista terminalis from the SA node to the AV node. Recommended initial
therapy is with calcium channel blockers or beta-blockers. Flecainide (Tambocor) or
propafenone (Rythmol) may be added if these are unsuccessful. If refractory to drug therapy,
catheter ablation may be performed and has a success rate of up to 86% in one study, though
inadvertent, AV node blockage is of concern.
Multifocal atrial tachycardia

Multifocal atrial tachycardia (MAT) is exemplied by ECG ndings of an irregular
tachycardia with three or more different p-wave morphologies at different rates. It is
commonly associated with underlying pulmonary disease or electrolyte abnormalities. Calcium
channel blockers are a highly successful form of treatment. There is no role for DC
cardioversion, antiarrythmic drugs or ablation.
Macro-re-entrant atrial tachycardia (atrial utter)

Atrial utter (AFl), also known as macroreentrant atrial tachycardia, is characterized by an
organized atrial rhythm at a rate between 250 and 350 bpm and occurs via a reentry
mechanism (Fig. 7). Typical atrial utter, is sometimes called isthmus-dependent utter, so
named because it involves the cavotricuspid isthmus (CTI). Patients typically present with a 2:1
AV conduction block producing a ventricular rate of about 150 bpm. Patients may also present
with a variable AV block producing an irregular rhythm. Acute management focuses on
ventricular rate control using AVN blocking agents such as b-blockers or calcium channel
blockers. Rapid, atrial overdrive pacing can also terminate the arrhythmia. Direct current
cardioversion is also a very effective mode of therapy, for patients who present with
hemodynamic collapse. An energy level of 50 J is typically effective. In patients with atrial
utter for more than 48 h, anticoagulant therapy should be started, and an echocardiogram
obtained (to rule out the presence of a intracardiac clot), prior to cardioversion. Anticoagulation
is usually achieved with warfarin (Coumadin) with an INR goal of 23.
Cure of AFl can be achieved with radiofrequency ablation (RFA) in more than 98% of the
patients. The macroreentrant circuit in AFl uses the atrial tissue between the tricuspid valve
annulus and the inferior vena cava, and radiofrequency energy delivered across the
81
cavotricuspid isthmus prevents AFl from recurring. RFA is the treatment of choice for patients
with recurrent AFl.
Ventricular tachycardias
There are three broad categories of pathologies which contribute to the development of VT.
These are structural heart diseases, prolonged QT syndrome, and accelerated idioventricular
rhythm.
Structural heart disease
VT in patients with structural heart disease (SHD) is secondary to reentry and is a result of
brotic tissue or inltrative disease causing areas of slow conduction. Common causes of
structural heart disease include ischemia, congestive heart failure and inltrate heart disease
(e.g., sacoidosis, amyloidosis and Chagas disease). The mainstay of treatment is implantation of
an implantable cardioverter-debrillator (ICD) to prevent sudden death from VT or ventricular
brillation (VF). An ICD is indicated in CHF patients with an ejection fraction (EF) less than 35%
which is refractory to medical treatment. The administration of a class III anthiarrhytmic drug
or beta-blocker can also reduce episodes of VT.
Long QT syndrome
A long QT interval may be congenital or drug induced. Patient with a long QT interval are
prone to a specic form of polymorphic VT called torsades de pointes. This is characterized by
rapid, irregular QRS complexes, which follow a twisting pattern around the baseline of the ECG.
Torsades de pointes may degenerate into VF, causing signicant hemodynamic compromise
and death.
Congenital long QT syndrome (LQTS) occurs due to genetic defects in cardiac ion channels,
which enhance sodium or calcium inward currents or inhibit outward potassium currents
during the plateau phase of the action potential. This results in prolongation of the action
potential and causes the observed long QT. A common scenario for LQTS on board questions is a
young patient in whom sudden cardiac death is precipitated by exercising, especially
swimming. Common drugs that may cause a prolonged QT include class Ia, Ic, or III
anthiarrythmic agents, tricyclic antidepressants, phenothiazine and certain antivirals and
antifungals. Torsades de pointes is usually treated with unsynchronized direct-current
cardioversion and sometimes debrillation.
Accelerated idioventricular rhythm
This usually has a heart rate that ranges from 60 to 120 beats/min. It is characterized by
gradual onset and offset. It is typically self-limiting and brief in duration. It is often
encountered in the setting of cocaine intoxication, acute myocarditis, digoixin intoxication, and
postoperative cardiac surgery.
Suggested Reading
Carina Blomstrom-Lundqvist
et al., 2003. Carina Blomstrom-Lundqvist,
et al. ACC/AHA/ESC guidelines for the
management of patients with supraventricular arrhythmiasexecutive summary a report of the American college
of cardiology/American heart association task force on practice guidelines and the European society of cardiology
committee for practice guidelines (writing committee to develop guidelines for the management of patients with
supraventricular arrhythmias). Developed in Collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol
2003;42:14931531.
Orejarena et al., 1998. Orejarena LA, Vidaillet Jr H, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the
general population. J Am Coll Cardiol 1998;31:150157.
Cheung, 1981. Cheung DW. Pulmonary vein as an ectopic focus in digitalis-induced arrhythmia. Nature 1981;294:
582584.
Luchsinger and Steinberg, 1998. Luchsinger JA, Steinberg JS. Resolution of cardiomyopathy after ablation of atrial
utter. J Am Coll Cardiol 1998;32:205210.
Delacretaz, 2006. Delacretaz E. Supraventricular tachycardia. N Eng J Med 2006;354:10391051.
82
Epstein et al., 2008. Epstein AE, Dimarco JP, Ellenbogen KA, et al. American college of cardiology/American heart
association task force on practice; American Association for thoracic surgery; Society of thoracic surgeons: ACC/
AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary. Heart
Rhythm 2008;5(6):934955.
Haqqani et al., 2009. Haqqani HM, Morton JB, Kalman J. Using the 12-lead ECG to localize the orgin of atrial and
ventricular tachycardias. Part 2: Ventricular tachycardia. J Cardiovasc Electrophysiol 2009;20:825832.
Monteforte and Priori, 2009. Monteforte N, Priori S. The long QT syndrome and catecholaminergic polymorphic
ventricular tachycardia. Pacing Clin Electrophysiol 2009;32:S5257.
Pappone et al., 2003. Pappone C, Santinelli V, Manguso F, et al. A randomized study of prophylactic catheter ablation in
asymptomatic patients with the WolffParkinsonWhite syndrome. N Eng J Med 2003;349:18031811.
Teh et al., 2009. Teh AW, Kistler PM, Kalman JM. Using the 12-lead ECG to localize the orgin of ventricular and atrial
tachycardias. Part I: Focal atrial tachycardia. J Cardiovasc Electrophysiol 2009;20:706709.
Vereckei et al., 2007. Vereckei A, Duray G, Szenasi G, et al. Application of a new algorithm in the differential diagnosis of
a wide QRS complex tachycardia. Eur Heart J 2007;28:589600.
Zipes et al., 2006. Zipes DP, Camm AJ, Borggrefe M. European Heart Rhythm Association; Heart Rhythm Society,
American College of Cardiology; American Heart Association Task Force; European Society of Cardiology
Committee for Practice Guidelines, et al: ACC/AHA/ESC 2006 guidelines for management of patients with
ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of
Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice
Guidelines (writing committee to develop guidelines for management of patients with ventricular arrhythmias and
the prevention of sudden cardiac death). J Am Coll Cardiol 2006;48(5):e247e346.
Disease-a-Month
Acute myocardial infarction

Stephen Boateng, DO and Timothy Sanborn, MD
An acute myocardial infarct (AMI) is a subset of a spectrum of acute coronary syndrome

(ACS) which includes unstable angina (UA) and AMI with or without ST elevation (see Table 1).
The diagnosis of AMI is conrmed by a typical rise and fall in the level of biochemical markers
of myocardial necrosis with at least one of the following: ischemic symptoms, EKG changes (ST
elevation or depression, pathologic q waves, or imaging evidence of new myocardial injury).
Epidemiology
There is an estimated ve-million emergency department visits each year in the US for acute chest
pain. Annually, over 800,000 people experience an AMI, of which 27% die (mostly before reaching the
hospital). These statistics, though dismal, represent signicant improvement in mortality. There has
been a signicant decline in cardiovascular deaths since the 1970s due to advances in diagnosis and
management of AMI. In one estimate, the in-hospital mortality prior to the era of cardiovascular
intensive care units was greater than 30%. Today, with percutaneous coronary intervention (PCI) and
stenting, antithrombotic therapy, and routine use of adjunctive medical treatment, the in-hospital
mortality of ST-segment elevation MI (STEMI) has reached a low value of 67%.
Pathophysiology
An AMI occurs when there is a reduction in myocardial perfusion, which is sufcient to cause
cell necrosis. This is most commonly due to thrombus formation in a coronary artery. The
inciting event is rupture or ssuring of an atherosclerotic plaque, which exposes the blood to
thrombogenic lipids and leads to activation of platelet and clotting factors. The coronary plaques
that are most prone to rupture are those with a rich lipid core and thin brous cap. Other rare
causes of a myocardial infarct include coronary artery embolism from a valvular vegetation or
intracardiac thrombi, cocaine use, coronary artery dissection, hypotension, and anemia.
Risk factors
Risk factors for an MI fall into three general categories: non-modiable risk factors (age,
gender, and family history), modiable risk factors (smoking, alcohol intake, physical inactivity,
84
S. Boateng, T. Sanborn/ Disease-a-Month 59 (2013) 8396
Table 1
The spectrum of acute coronary syndromes.
Unstable angina
Anginal pain with at

least one of the following
features:
Of new onset and severe.

Occurs at rest or with
minimal exertion.
Pain is worsening in
Non-ST-segment
elevation myocardial
infarction (NSTEMI)
Characterized by clinical
features of unstable angin
a in addition to elevated
cardiac markers. Cardiac
markers are elevated as
a result of myocardial
necrosis.
ST-segment elevation
myocardial infarction
(STEMI)
Characterized by clinical
features of myocardial
infarction in addition to
ST-segment elevation on
a 12-lead EKG.
severity and length of

each episode (i.e.,
occurring in a crescendo
pattern).
poor diet, hypertension, diabetes, dyslipidemias, and metabolic syndrome), and emerging risk
factors (C-reactive protein (CRP), brinogen, coronary artery calcication (CAC), homocysteine,
lipoprotein(a), and small, dense (LDL)). The Framingham Heart Study developed a coronary risk
estimate using the major risk factors to estimate the 10-year cardiovascular risk of an individual.
Primary prevention
Primary prevention of an AMI is aimed at reducing the modiable risk factors. Goals include
lifestyle changes such as regular exercise, a healthy diet, smoking cessation, and a reduction in
alcohol intake. Medications aimed at controlling blood pressure and reducing cholesterol are
also recommended.
Patients with AMI usually present with chest pain due to involvement of a neural reex pathway
via the thoracic and cervical nerves. It is a deep and visceral pain which is usually described as a
heavy, squeezing, tightness, crushing, and sometimes stabbing or burning pain. It is typically
substernal in location and may radiate to the corresponding dermatomes (C7T4) that supply afferent
nerves to the same segments of the spinal cord as the heart. These include the epigastrum, shoulders,
arms, back (interscapular region), lower jaw, and neck. Radiation to both arms is a stronger predictor
of acute myocardial infarction. In about 20% of patients (diabetics, elderly, postoperative, or female),
chest pain may be absent. These patients may only have atypical symptoms corresponding to the
dermatomes C7T4 as described previously. Physical examination ndings are usually absent;
however, when present, they are of prognostic value (Table 2: Killip class and hospital mortality).
Diagnosis
The initial evaluation of a patient with a suspected AMI should include a focused clinical
history, physical examination, electrocardiography, cardiac markers, and a chest radiograph.
85
ECG
An ECG is especially useful for distinguishing between a non-ST-elevation myocardial
infarction (NSTEMI) and an ST-elevation myocardial infarction (STEMI). It should be performed
within 510 min of arrival into an emergency department. In addition, posterior leads (V7V9)
and leads V3R and V4R should be used in patients with suspected posterior and right ventricle
(RV) infarctions, respectively. ECG ndings predictive of adverse outcomes in patients with a
NSTEMI/Unstable Angina (UA) include ST-segment depression, new ST-segment deviation
(Z0.05 mV), and new deep T-wave inversions Z0.3 mV (other t-wave changes are sensitive for
ischemia, but not specic for an AMI).
Diagnosis of a STEMI is established by ECG ndings revealing greater than 1-mm J point
(junction of the ST segment and QRS complex) elevation in two or more contiguous limb leads
or precordial leads V4V6; or greater than 2 mm in two or more precordial leads V1V3.
Development of a new left bundle branch block should be considered as a STEMI equivalent
until proven otherwise. A signicant number of patients with an AMI go on to develop Q waves.
The diagnosis of an AMI may be difcult in the presence of a left bundle branch block (LBBB) or
a pacemaker. In the presence of a left bundle branch block, the Sgarbossa criteria may be
applied:

ST-segment elevation Z1 mm concordant with a predominantly positive QRS complex in at

least one lead (5 points).
ST depression Z1 mm in leads V1, V2, or V3 (3 points).
ST elevation Z5 mm discordant (in the opposite direction from) a predominantly negative
QRS complex (2 points).
If all three criteria are met, the specicity for acute myocardial infarction is 90%, though the
sensitivity is only 20%. The third criterion has been shown to add little diagnostic or prognostic
value. Greater than 5-mm elevation in discordant segments has been described in
uncomplicated LBBB, particularly in the presence of left ventricular hypertrophy.
Serum markers
Serum biomarkers of myocardial necrosis include cardiac specic troponins T and I, MB
isoforms of creatine (CK-MB), creatine kinase (CK), and myoglobin.
Troponins T and I are highly specic for myocardial injury and preferred for the diagnosis of
an AMI. They are rarely elevated in non-cardiac conditions and are only mildly elevated in
other cardiac conditions such as tachycardia, heart failure and inammatory conditions such as
myocarditis. They begin to rise 46 h after the onset of symptoms. Thus, they should be
measured on admission and again 69 h later. They peak at 1824 h after the onset of
symptoms and may remain elevated for 710 days after a STEMI. These have replaced other
biomarkers due to their higher sensitivity, specicity, and prognostic value.
Table 2
Killip class and hospital mortality.
Killip class
Clinical classication
Mortality (%)
I
II
III
IV
No heart failure
Mild heart failure, rales, S3, congestion on chest radiograph
Pulmonary edema
Cardiogenic shock
6
17
38
81
Data from Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two-year experience
with 250 patients. Am J Cardiol. 1967;20(4):457464.
86
Levels of CK-MB are less specic for myocardial infarction than troponins; however, they are
considerably more specic than CK. They serve as the next best alternative to cardiac troponins.
Cardiac surgery, myocarditis, and electrical cardioversion often result in elevated serum levels of
CK-MB isoenzyme. CK-MB levels increase within 48 h, peak at 24 h, and return to normal by 48
72 h. Levels of total CK are generally not very useful for predicting an acute MI since they are not
specic for an AMI. However, a ratio of CK-MB to CK activity Z2.5%, even in the presence of
skeletal muscle injury, is usually due to an AMI. Myoglobin also lacks cardiac specicity; it usually
returns to normal within 24 h of the onset of an AMI. Other non-specic but notable reactions
include leukocytosis (usually 12,00015,000), which may persist for 37 days, and elevated ESR
that rises slowly, peaks during the rst week, and sometimes remains elevated for 1 or 2 weeks.
Imaging
2-Dimensional echocardiography
Myocardial injury is diagnosed as wall motion abnormalities on echocardiography. An
echocardiogram, however, cannot distinguish between an acute STEMI from an old myocardial
scar or from acute severe ischemia, but ease and safety make it useful as a screening tool to aid
management decisions. It is particularly useful for detecting complications of a myocardial
infarction such as ventricular septal defects, acute mitral regurgitation, ventricular aneurysms,
pericardial effusions, a left ventricle (LV) thrombus, or valvular abnormalities.
There are several other causes of chest pain that can masquerade as a myocardial infarction.
Most notable include acute pericarditis, pulmonary embolism, acute aortic dissection,
costochondritis, and gastroesophageal reux disease.
Treatment
The goals of initial treatment of an MI are relief of pain, immediate identication of ST
changes via 12-lead EKG, initiation of reperfusion (if the patient is a candidate), and assessment
and treatment of hemodynamic abnormalities. Pain relief is best achieved with oxygen,
nitroglycerin, and morphine sulfate. Patients with ST-segment elevation or a new LBBB with
symptoms for 12 h or less are candidates for reperfusion therapy. Further treatment of an MI
may be separated into two pathways depending on whether or not the patient has a STEMI or a
NSTEMI (see Fig. 1).
STEMI
The diagnosis of a STEMI mandates immediate reperfusion; however, PCI is not promptly
available in many areas. The best choice of reperfusion therapy for particular clinical settings
remains controversial. For facilities that can offer PCI, however, current literature indicates that
this approach is superior to pharmacological reperfusion. The American College of Cardiology
and American Heart Association (ACC/AHA) recommends a door to needle time of 30 min and a
door-to-balloon time of 90 min. Most interventional cardiologists now aim for a median doorto-balloon time of less than 60 min.
Intravenous brinolytic therapy is widely available, but it is slightly less effective than
PCI in randomized trials and carries a risk of hemorrhagic stroke. Fibrinolytics should be
administered within 30 min of arrival at the emergency department. The greatest benet is
87
seen when this is performed within the rst 4 h of onset of pain resulting in an absolute 3%
reduction in mortality but is associated with 0.4% increase in stroke rate. The decision
regarding which therapy to employ should be made based on a written institution-specic
protocol, which considers symptom duration, availability of PCI locally, time to transfer to
a facility, and brinolytic contraindications (see Fig. 1). In general, patients presenting
within 2 h of symptoms onset derive signicant benet from brinolytics; if transfer time
to a PCI facility results in a door-to-balloon time of longer than 90 min, brinolytics are
preferred.
Primary percutaneous coronary intervention

Although brinolytic therapy is easy to administer and widely available, it provides early
reperfusion in only 80% of patients and is usually not administered in a signicant number of
patients due to perceived or actual contraindications in a signicant number of patients (see
Table 3). In contrast, primary PCI has only a few contraindications and leads to a higher
reperfusion rate (approximately 90%). Randomized trials performed in high-volume academic
centers comparing brinolytic therapy with PCI for acute MI demonstrated a 30% reduction in
mortality and reinfarction rates and a signicant reduction in cerebrovascular accidents with
PCI. Primary PCI should be performed within 6090 min of arrival to the hospital.
Adjunct therapy for a STEMI

Adjunct therapy has been shown to reduce mortality, facilitate and maintain coronary reperfusion,
limit the consequences of myocardial ischemia, and reduce the likelihood of recurrent events.
Relieving chest pain

Nitroglycerin
To relieve chest pain, 0.4 mg sublingual nitroglycerin tablets (Nitrostat) or aerosol sprays
(NitroMist) should be given every 5 min for up to three doses. Nitroglycerin should, however,
be avoided in patients who have taken a nitric oxide synthetase inhibitor or phosphodiesterase
inhibitors within the past 24 h to avoid hypotension. Nitroglycerin should also be avoided in
the following situations:

patients with hypotension (systolic blood pressure less than 90 mmHg or greater than or
equal to 30 mmHg below baseline)
severe bradycardia (less than 50 beats per min)
infarct in the distribution of the RCA.
Morphine
Morphine is the analgesic of choice in patients with STEMI. The patient may be administered
morphine, 24 mg IV push over 5 min every 515 min as needed for pain. In rare instances,
morphine can be a respiratory depressant, can reduce myocardial contractility, and is a potent
venous vasodilator. In hemodynamically unstable patients, the concomitant elevation of the
lower extremities (to facilitate venous return) or administration of atropine (0.51.5 mg) may
overcome hypotension and bradycardia secondary to morphine.
88
Fig. 1. Selection of reperfusion therapy. DTB, door-to-balloon time; PCI, percutaneous coronary intervention.
Antiplatelet therapy
Aspirin
Unless there is a history of allergic reactions, aspirin in a dose of 162325 mg should be
administered immediately on arrival to the emergency room and continued indenitely at a
dose of at least 75162 mg/day in all patients with a STEMI. In patient with severe nausea and
vomiting, an aspirin suppository of 300 mg may be administered. Patients with a true aspirin
allergy should be administered clopidogrel (Plavix) instead.
89
Table 3
Indications and contraindications for brinolytic therapy in acute myocardial infarction.
Indications
ST-segment elevation Z1 mV in Z2 contiguous limb leads or Z2 mV in contiguous precordial leads
New left bundle branch block
Posterior MI: ST-segment depression 42 mV in leads V1 and V2 with either imaging evidence of posterior LV
wall motion abnormality or ST-segment elevation of 1 mV in the posterior leads V7V9
Contraindications
Absolute
Active bleeding
Prior intracranial hemorrhage; other strokes or neurologic events within 1 year; intracranial neoplasm
Recent major surgery (o6 wk) or major trauma (o 2 wk)
Recent vascular puncture in a non-compressible site (o2 wk)
Suspected aortic dissection
Relative
Active peptic ulcer disease or recent gastrointestinal bleeding (o 4 wk)
Severe uncontrolled hypertension on presentation (BP 4180/110 mmHg) or chronic severe hypertension
Cardiopulmonary resuscitation 410 min
Prior non-hemorrhagic stroke
Pregnancy
Bleeding diathesis or INR 42
Abbreviations: BP, blood pressure; INR, international normalized ratio.
Thienopyridine
This group of antiplatelets blocks the ADP receptor on platelets, resulting in platelet
aggregation. Prime examples of these are clopidogrel (Plavix) and prasugrel (Efent). A loading
dose of 3006001 mg of clopidogrel or 60 mg of prasugrel is recommended by the ACC/AHA,
for administration at the time of PCI; after which a maintenance dose of 75 mg daily for
clopidogrel and 10 mg daily for prasugrel is initiated. It is now recommended that the duration
of thienopyridine therapy should be at least 12 months irrespective of whether the patient
received a bare-metal stent (BMS) or a drug-eluting stent (DES). Dual therapy with clopidogrel
and aspirin is associated with a lower mortality and morbidity than that seen with
aspirin alone.
Glycoprotein IIb/IIIa antagonists

This group of drugs inhibits the nal common pathway in platelet aggregation, by blocking
IIb/IIIa receptors that activate brinogen. They are the most potent antiplatelets available.
Currently available glycoprotein IIb/IIIa antagonists include the chimeric monoclonal antibody
abciximab (Reopro) and the synthetic peptide eptibatide (Integrilin). Studies investigating the
role of glycoprotein IIb/IIIa antagonists in STEMI have demonstrated a reduction in the
composite end point of death, MI, and target revascularization in patients treated with
PCI. Results appear to be better if the drug is initiated at least 6 h before PCI and continued
for 1824 h thereafter. GP IIb/IIIa inhibitors are not recommended for patients receiving
brinolytics. The adjunctive use of GP IIb/IIIa therapy in the setting of dual-antiplatelet
(aspirin and plavix) therapy with UFH or bivalirudin as the anticoagulant has been shown
to be benecial only at the time of primary PCI. It may also be used in patients with a large
thrombus burden or patients who did not receive adequate thienopyridine loading during
primary PCI.
1
Exceeds dosage recommended by the manufacturer.
90
Anticoagulant medications
Anticoagulant medications such as unfractionated heparin (UFH), low molecular weight
heparin (LMWH), or bivalirudin (Angiomax) have been shown to decrease reocclusion and
reinfarction following reperfusion therapy and are given routinely to Acute Coronary Syndrome
(ACS) patients unless contraindicated. UFH and LMWH are considered equal in patients with
STEMI who do not receive reperfusion therapy. In patients who undergo reperfusion by either
angioplasty or thrombolytics, UFH or bivalirudin is recommended.
Unfractionated heparin (UFH)
For patients undergoing primary PCI, 60100 units/kg of UFH, with a target-activated
clotting time (ACT) of 250350 s is recommended. Patients receiving a glycoprotein IIb/IIIa
inhibitor should be administered 5070 units/kg of UFG with a target ACT greater than 200 s.
The activated partial thromboplastin time (aPTT) should be checked at 46 h after initiation of
heparin and then every 68 h for a target of 1.52 times control. This makes unfractionated
heparin more complicated to use. Anticoagulation with UFH may be continued in patients postPCI, for 48 h, if there is a large anterior MI, known LV thrombus, and atrial brillation or if
symptoms persist. Otherwise, short-term anticoagulation may be discontinued immediately
following PCI. Long-term anticoagulation with warfarin (Coumadin) may be indicated in
patients with an intracardiac thrombus, atrial brillation, or ejection fraction (EF) less than 30%
following MI. The effects of heparin are short lived and can be reversed by either stopping
heparin or administration of protamine sulfate.
Low molecular weight heparin (LMWH)
Enoxaparin (Lovenox) is the prototypical low molecular weight heparin (LMWH) and has
been studied widely in STEMI and acute coronary syndromes. Compared to unfractionated
heparin, LMWH products have better bioavailability, are easier to administer by weight-based
regimens, and do not require aPTT monitoring. There is also a lower risk of heparin-induced
thrombocytopenia. Enoxaparin is typically administered as a 30-mg IV bolus followed by 1 mg/
kg SC every 12 h until hospital discharge. It should be used with caution in patient with renal
insufciency and its effects are not immediately reversible.
Alternative to heparin
For STEMI patients who have a history of heparin-induced thrombocytopenia (HIT) or
patients in who there is a high risk of bleeding, bivalirudin (Angiomax) may be used as an
alternative. An initial dose of 0.75 mg/kg IV followed by 1.75 mg/kg/h is recommended for the
duration of PCI; the infusion may be continued for up to 4 h postprocedure. An IV infusion of
0.2 mg/kg/h can then be initiated for up to 20 h if needed.
b-Adrenergic antagonist drugs

Early intravenous b-blocker therapy, metoprolol (Lopressor), 5 mg IV every 15 min for up to
3 doses is indicated in all patients except for those with contraindications. This should be
followed by oral metoprolol 50 mg every 6 h for 24 h, then 100 mg twice per day thereafter.
Contraindications to b-blocker administration include bradycardia, heart block, and hypotension. b-blockers reduce myocardial workload and oxygen demand by reducing contractility,
heart rate, and arterial pressure. When given within the rst few hours, b-adrenergic
antagonist drugs improve prognosis by reducing infarct size, incidence of ventricular
arrythmias, and mortality.
91
Angiotensin-converting enzyme inhibitors (ACE inhibitors) and angiotensin II receptor

blockers (ARBs)
ACE inhibitors reduce cardiac workload and decrease post-MI cardiac remodeling. ACE
inhibitors have been shown to reduce mortality in MI patients, especially those with anterior
infarction, pulmonary congestion, or ejection fraction less than 40%. ACE inhibitors should be
administered orally within 24 h of symptoms. [e.g., lisinopril (Prinivil) 5 mg daily]. In the ISIS-4
trial, an initial 6.25 mg dose of captopril (Capoten) was given and, if tolerated, was followed by
12.5 mg 2 h later, 25 mg 1012 h later, and then 50 mg twice per day. Contraindications
include hypotension, renal failure (creatinine 42.5), and bilateral renal artery stenosis.
Angiotensin II receptor blockers may be an effective alternative for patients who cannot
tolerate ACE inhibitors.
HMG CoA reductase inhibitors

HMG CoA (3-hydroxy-3-methyl-glutaryl coenzyme A) reductase inhibitors (statins) are
used for prevention of coronary artery disease and ACS, since LDL cholesterol plays a critical
role in the pathogenesis of atherosclerosis. There is an increasing evidence that they also have
short-term benets in the treatment of AMI. Treatment with statins in the acute setting can
promote plaque stabilization, reverse endothelial dysfunction, and decrease thrombogenecity.
A lipid prole should be assessed within 24 h of the AMI and, unless contraindicated,
statin therapy should be started as soon as possible. Goal LDL levels of 7080 mg/dL are
recommended.
Nitrates
Nitroglycerin dilates veins, arteries, and arterioles, reducing preload and afterload. It
reduces myocardial oxygen demand, increases perfusion of ischemic zones, and enhances
collateral blood ow. IV nitroglycerin should be administered to patient within the rst
2448 h for patients with heart failure, large anterior AMI, persistent chest discomfort, or
hypertension. Nitrates should be used with caution in patients with RV infarction or
dehydration (who are preload dependent) to avoid excessive hypotension. Blood pressures
should be monitored carefully and kept above 90 mmHg systolic. Nitroglycerin should be
avoided in patients who have taken nitric oxide synthetase inhibitors or phosphodiesterase
inhibitors within 24 h prior to presentation.
Calcium channel blockers

Calcium channel blockers have vasodilatory, antianginal, and antihypertensive actions.
Calcium channel blockers do not reduce mortality in patients with MI and are not
recommended for routine therapy or secondary prevention. In patients in whom betaadrenergic antagonists are contraindicated, verapamil (Isoptin)2 or diltiazem (Cardizem) (see
footnote 2) may be appropriate as an alternative.
Unstable angina and non-ST-elevation myocardial infarction

An unstable angina/NSTEMI occurs when there is an incompletely occluded coronary thrombus
or extensive collateral blood supply (or both) which results in a subendocardial infarct. The
2
92
presentation may be identical to that of a STEMI, except for the absence of acute ST-segment
elevation or Q waves. ST-segment depression and/or T-wave inversion may be present.
Initial therapy
Management differs from STEMI in that emergent reperfusion therapy is not indicated.
Exceptions to this are patients with persistent pain (despite initial medical treatment), or
hemodynamic deterioration. The focus of initial therapy is medical stabilization with oxygen to
keep saturations above 90%, morphine for pain control, aspirin to prevent clot propagation,
nitrates and b-blockers for anti-ischemic effects (if no contraindications: see Fig. 2), and fulldose acute coronary syndrome (ACS) anticoagulation. As part of the initial management of a
NSTEMI, it is important to risk stratify patients into two groupshigh or low risk. A useful tool
for risk stratication is the TIMI risk score calculator (Table 4). Patients with a score greater
than 3, markedly elevated cardiac markers, or persistent symptoms should be considered to be
at high risk. Risk stratication is essential in guiding the approach to further therapy (see
Fig. 2). Within the rst 2448 h of hospitalization, patients with unstable angina usually
undergo stress testing, then angiography if the stress test is positive for ischemia. Patient with
a NSTEMI undergo coronary angiography.
A non-interventional approach and a trial of medical management is used for those in whom
angiography demonstrates only a small area of myocardium at risk, lesion morphology not
amenable to PCI, anatomically insignicant disease (o50% coronary stenosis), or signicant
left main disease in patients who are candidates for CABG. Angiography or PCI should be
deferred in favor of medical management for patients with a high risk of procedure-related
morbidity or mortality.
Adjunct therapy
Anticoagulants
Anticoagulant medications such as low molecular weight heparin or unfractionated
heparin should be started in all high-risk patients. Because its effects can be easily
reversed, unfractionated heparin is favored over LMWH in patients who require urgent
catheterization. Also UFH is preferred in patient with CrCl less than 30 or weight greater
than 150 kg. Enoxaparin (Lovenox) has shown modest outcome benets over unfractionated heparin in patients with NSTEMI. Bivalirudin (Angiomax), a direct thrombin
inhibitor, may be used as an alternative to the heparins in patients with a high risk of
bleeding or with a history of heparin-induced thrombocytopenia (HIT). For patients with
NSTEMI, an initial dose of bivalirudin at 0.1 mg/kg IV followed by a drip of 0.25 mg/kg/h is
administered.
Antiplatelets
In addition to aspirin, clopidogrel (Plavix) is benecial in NSTEMI. However, the benet
must outweigh the bleeding risk if coronary bypass surgery is performed within 5 days of drug
administration. Generally, clopidogrel administration is avoided until establishment of
coronary anatomy and a decision is made regarding the need for a bypass. Clopidrogel is
given as a 300600 (see footnote 1) mg oral load, then 75 mg daily.
Several large studies have investigated the role of glycoprotein IIb/IIIa antagonists in
patients with unstable angina or NSTEMI with some controversial results. Studies using
tiroban (Aggrastat) and eptibatide (Integrilin) have demonstrated signicant risk reduction
in composite end points with the greatest benet in patients with diabetes, patients with
troponin elevation, and patients undergoing PCI.
93
Fig. 2. Denite or possible acute myocardial infarction (MI). CABG, coronary artery bypass graft; ECG, electrocardiogram; EF, ejection fraction; PCI, percutaneous coronary intervention; SL NTG, sublingual nitroglycerin.
b-Adrenergic antagonist drugs, HMG CoA reductase inhibitors and angiotensin-converting

enzyme inhibitors (ACE inhibitors), and angiotensin II receptor blockers (ARBs)
The use of b-blockers and statins is similar to that in STEMI. The role of ACE inhibitors is less
well dened, but may be selectively useful for the treatment of hypertension and in those with
LVEF less than 45%.
Elective catheterization
Meta-analyses of trials of early elective catheterization versus initial medical therapy
have shown lower rates of mortality and recurrent MI. Rates of rehospitalization are lower
for recurrent unstable angina after an early invasive approach. Benets of early elective
catheterization are predominantly in intermediate to higher risk patients, especially
those older than 65 years old and those who have resting ST depression or elevated
biomarkers.
94
Table 4
TIMI risk score for ST-elevation myocardial infarction.
Risk factor
Points
Risk score
30-Day mortality (%)
Age Z75 year

Age 6574 year
Diabetes or hypertension
Systolic BP o 100 mmHg
Heart rate 4100/min
Killip class IIIV
Anterior MI or LBBB
Weight o67 kg
Time to treatment 44 h
3
2
1
3
2
2
1
1
1
0
1
2
3
4
5
6
7
8
48
0.8
1.6
2.2
4.4
7.3
12.4
16.1
23.4
26.8
35.9
Data from Morrow DA, Antman EM, Charlesworth A, et al. TIMI risk score for ST-elevation myocardial infarction: A
convenient, bedside, clinical score for risk assessment at presentation: An intravenous nPA for treatment of infarcting
myocardium early II trial substudy. Circulation. 2000;102:20312037.
Abbreviations: BP, blood pressure; TIMI, thombolysis in myocardial infarction (trial).
Complications of acute myocardial infarction

Electrical dysfunction
Arrhythmias and conduction abnormalities occur in greater than 90% of MI patients. These
commonly cause death within the rst 3 days and include tachycardia, Mobitz type II block or
complete AV block, ventricular tachycardia, and ventricular brillation. Amiodarone (Cordarone)
is the drug of choice for treating symptomatic ventricular arrhythmias in the setting of an MI.
Lidocaine may also be used for 2448 h to treat ventricular tachycardia and following
resuscitation for ventricular brillation.
Sinus node disturbances may lead to sinus bradycardia or sinus tachycardia of which the
former is most common. Sinus bradycardia is treated if the heart rate is less than 50 beats per
min and if it is associated with hypotension. Then, 0.51 mg IV of atropine sulfate may be
administered every 35 min for up to 3 mg. A temporary transvenous pacemaker may also be
inserted. When encountered, sinus tachycardia may be treated with low doses of IV metoprolol
(Lopressor) 2.55 mg every 5 min for up to 3 doses. AV blocks may also occur and may include
Mobitz type I, Mobitz type II, or a complete heart block. Mobitz type II and complete heart
blocks require implantation of a temporary transvenous pacemaker. Mobitz type I does not
require treatment.
Atrial brillation (AF) and atrial utter may occur in about 10% of MI patients. For atrial
brillation, IV b-blockers such as metoprolol 5 mg 5 min for up to 3 doses may be initiated to
slow the ventricular rate. IV digoxin (Lanoxin), diltiazem (Cardizem), or verapamil (Isoptin)
may also be considered. If AF compromises circulatory status (e.g., causing LV failure,
hypotension, or chest pain), urgent synchronized electrical cardioversion with at least 100 J of
energy, followed by 200 J (if needed), should be performed. For AF that has been present for
greater than 48 h, electrical cardioversion should be performed only after the presence of an
intracardiac thrombus is ruled out with an echochardiogram. Electrical cardioversion with
50100 J of energy is the treatment of choice for an initial episode of atrial utter, as
pharmacologic rate control is more difcult to achieve.
Ventricular arrhythmias such as ventricular tachycardia (VT) and ventricular brillation (VF)
are not uncommon. Non-sustained VT (less than 30 s) does not require treatment in the short
term. Sustained VT causing hemodynamic compromise is treated with synchronized
cardioversion with 100200 J of energy. Sustained VT in a hemodynamically stable patient
may be treated with 150 mg of amiodarone (Cordarone) IV over 10 min (may repeat once
in 5 min) or Lidocaine which is given as 1.01.5 mg/kg IV every 35 min up to 3 mg/kg.
95
Cardiogenic shock
Cardiogenic shock occurs in approximately 7% of patients with MI and has a mortality rate
of approximately 8090% if untreated. When treated with early revascularization using PCI or
coronary artery bypass graft surgery (CABG), the 30-day mortality rate is close to 50%.
Cardiogenic shock is characterized by systemic hypotension (systolic BP persistently less than
90 mmHg or Mean Arterial Pressure (MAP) greater than 30 mmHg below baseline), reduced
cardiac index (less than 1.8), and elevated pulmonary artery wedge pressure (greater than
16 mmHg). Initial stabilization should be attempted with inotropes such as dobutatmine
(Dobutex), together with intraaortic balloon counterpulsation. Intraaortic balloon counterpulsation reduces cardiac afterload and improves coronary artery perfusion by increasing
systolic blood pressure. Early angiography and revascularization with either PCI or CABG have a
signicant effect in reducing mortality and should be considered in patients with
cardiogenic shock.
Structural disorders
Structural complications which may result from AMI include papillary muscle rupture,
ventricular aneurysms, interventricular septal rupture, and ventricular free wall rupture.
Papillary muscle rupture may be repaired surgically if it causes severe valvular regurgitation.
Interventricular septal rupture may be diagnosed with a balloon-tipped catheter revealing a
signicant drop in pO2 from the right ventricle. It can be repaired surgically, after a 6-week
wait period to allow healing of the ventricular muscle. Free wall rupture may also be repaired
surgically; however, it is almost always fatal.
Right ventricular infarction
RV infarction occurs in approximately 40% of patients with acute inferior MI; however,
hemodynamicaly signicant RV dysfunction is less common. Patients usually present with an
elevated jugular venous pressure without hemodynamic compromise. Some patients present
with hypotension, particularly after the administration of vasodilators such as nitrates. On
physical examination, patients might have an elevated jugular venous pressure, Kussmual sign
(ling of the jugular vein on inspiration), clear lungs, and a right-sided gallop on cardiac
auscultation. The diagnosis is strengthened by demonstrating the presence of at least 1 mm of
ST-segment elevation in leads V1, V3R, or V4R or RV dysfunction by echocardiography. The
treatment is supportive with intravenous uids and inotropic support with dopamine or
dobutamine if needed. These interventions may be tailored using guidance from hemodynamic
data obtained from a pulmonary artery catheter. Patients with RV infarction are more likely to
have complications with bradycardia or atrioventricular block that can require temporary atrial
or ventricular pacing. Most patients improve spontaneously after 4872 h. Patients with shock
might benet from early revascularization with PCI to the right coronary artery.
Implantable cardioverter-debrillator
ICD implantation reduces the occurrence of sudden cardiac death in certain high-risk
patients such as those with late (424 h after the onset of symptoms) sustained ventricular
tachycardia and ventricular brillation and in patients with EF persistently less than 3035%.
An ICD may also be benecial in patients with late non-sustained ventricular tachycardia who
have an EF of less than 40% and ventricular tachycardia induced during an electrophysiology
study. ICD therapy should be considered when the patient is judged to be at continuous high
risk for ventricular arrhythmia after revascularization for signicant spontaneous or inducible
ischemia.
96
Cardiac rehabilitation and secondary prevention

Cardiac rehabilitation should be initiated before discharge from the hospital, with the goals
of improving quality of life, facilitating return to normal activities, encouraging regular
exercise, and promoting secondary prevention. Secondary prevention is aimed at smoking
cessation and at an aggressive dietary and pharmacologic treatment of hyperlipidemia,
hypertension, and diabetes mellitus. Blood pressure goal should be less than 140/90 mmHg
or less than 130/80 mmHg in patients with diabetes or chronic kidney disease. Lipid
management should involve statin use and dietary restrictions. There should be a reduction
in intake of saturated fats (to less than 7% of total calories), trans fatty acids, and cholesterol
(to less than 200 mg/day). Goal LDL cholesterol should be substantially less than 100 mg. If
triglcerides are greater than or equal to 200 mg/dL, non-HDL-C should be less than 130 mg/dL.
Physical activity should be emphasized with a goal of 30 min, at a minimum of 5 days per week.
Patients with diabetes should have a hemoglobin A1c goal of less than 7%. An annual inuenza
vaccine is also recommended in all patients with cardiovascular disease. Patients with
cardiovascular disease are candidates for pneumococcal vaccination. Finally, weight management is essential and a goal BMI should be 18.524.9 kg/m2. Men should have a waist
circumference of less than 40 inches and women less than 35 inches.
Suggested Reading
Fuster V, Alexander RW, ORourke RA, et al. Hursts The Heart. 12th ed, McGraw-Hill Professional Publishing; 2009.
Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redeneda consensus document of the Joint
European Society of Cardiology/American College of Cardiology Committee for the redenition of myocardial
infarction. J Am Coll Cardiol 2000;36:959969.
Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable
angina/non-ST-elevation myocardial infarction. I Am Coll Cardiol 2007;50:e1e157.
Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation
myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients With Acute
Myocardial Infarction). J Am Coll Cardiol 2004;44(3):E1E211.
Antman E, Hand M, Armstrong P, et al. 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of
Patients With ST-Elevation Myocardial Infarction. J Am Coll Cardiol 2008;51:210247.
Wright S, Anderson J, Adams C, et al. ACCF/AHA Focused Update of the Guidelines for the Management of Patients With
Unstable Angina/NonST-Elevation Myocardial Infarction (Updating the 2007 Guideline). A report of the American
College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation
2011;123:20222060.
Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: a method for
prognostication and therapeutic decision making. J Am Med Assoc 2000;284:835842.
Cannon CP, Hand MH, Bahr R, et al. Critical pathways for management of patients with acute coronary syndromes: an
assessment by the National Heart Attack Alert Program. Am Heart J 2002;143:777789.
Krumholz HM, Anderson JL, Brooks NH, et al. ACC/AHA clinical performance measures for adults with ST-elevation and
nonST-elevation myocardial infarction: a report of the ACC/AHA task force on performance measures (STElevation and Non-ST-Elevation Myocardial Infarction Performance Measures Writing Committee). J Am Coll Cardiol
2006;47:236265.
Mehta SR, Cannon CP, Fox KA, et al. Routine vs selective invasive strategies in patients with acute coronary syndromes:
a collaborative meta-analysis of randomized trials. J Am Med Assoc 2005;293:29082917.
Smith Jr SC, Allen J, Blair SN, et al. AHA/ACC guidelines for secondary prevention for patients with coronary and other
atherosclerotic vascular disease: 2006 update endorsed by the National Heart, Lung, and Blood Institute. J Am Coll
Cardiol 2006;47:21302139.
Smith Jr SC, Feldman TE, Hirshfeld JW Jr, et al. ACC/AHA/SCA1 2005 guideline update for percutaneous coronary
intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary
Intervention). Circulation 2006;113(7):e166e286.
Weaver WD, Cerqueira M, Hallstrom AP, et al. Prehospital-initiated vs hospital-initiated thrombolytic therapy. The
Myocardial Infarction Triage and Intervention Trial. J Am Med Assoc 1993;270:12111216.
Disease-a-Month
Sudden cardiac death in young athletes

Scott M. Leikin, BA, Andrew Pierce, MD and Michael Nelson, MD
Sudden Cardiac Death (SCD) is dened as an unexpected death within one hour of the onset
of symptoms that cannot be attributed to any type of trauma. This vague denition makes the
pre-participation screening the most important time to identify an at risk patient before they
take to the athletic elds. A study done by Maron et al investigating SCD proled the deaths of
young athletes who passed away from 1985 through 1995 demonstrates a few demographics
that paint a picture of the prole of people at risk for SCD. The study ages ranged between 12
40 years old with a mean of 17 years. Additionally 90% of these were male and 44% were of
African descent. Based on these stats, the last barrier to preventing SCD is the pre-athletic
physical to help identify at risk patients. The strong linkage of SCD to athletes is due to
underlying cardiovascular pathology added with extra stress placed on the heart during times
of exercise. In the United States, roughly 100150 SCD occur annually in the competitive
athlete.
When dealing with the sudden collapse of any individual, including athletes, evaluate for the
presence of respirations and pulse rst. Standard Advanced Cardiac Life Support (ACLS) protocol
algorithms should be employed. The most feared complication that leads to death in these cases
is a fatal ventricular dysrhythmia. Even when the rst responder follows proper protocols, a
successful resuscitation and full neurological recovery rarely occur. Additionally, studies by
Drezner et al in 2005 and 2011 in NCAA athletes fail to demonstrate the effectiveness of
standard use of cardiopulmonary resuscitation (CPR) and automated external debrillator (AED)
in the sudden collapse of an athlete. Due to the poor outcomes of resuscitative efforts, detecting
those at risk for SCD is paramount. The best methods for screening athletes are debatable.
Additionally there are physical, psychological and social implications if a predisposing condition
is discovered. Furthermore, no evidence exists that athletic restriction improves outcomes. The
athletes screening exam, however, attempts to detect those at risk for SCD and should focus on a
few common cardiac conditions. The hope is that preventing a high-risk patient from
participating in strenuous exercise will reduce mortality.
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) can be an elusive diagnosis due to controversy in
diagnostic screening and management. The most devastating consequence of HCM is SCD,
especially in young individuals, and unfortunately SCD may be the initial manifestation. HCM is
the most common cause of sudden cardiovascular death in competitive athletes. Due to this risk,
98
S.M. Leikin et al. / Disease-a-Month 59 (2013) 97101
an early diagnosis is crucial before physical exertion at an athletic level. HCM results in left
ventricular hypertrophy that can be asymmetric (involving only the apical wall vs. anterior
septum, etc.) or concentric. This hypertrophy, however, does not always result in outow tract
obstruction as prior names for HCM may suggest (Hypertrophic Obstructive Cardiomyopathy,
Idiopathic Hypertrophic Sub-aortic Stenosis). Actually only 25% of patients with HCM have left
ventricular (LV) outow tract obstruction and it is more commonly seen in elderly patients. The
pathophysiology behind HCM is complex and not fully understood with dynamic outow
obstruction having a suggested association without denitive evidence. Highest risk of SCD from
HCM is associated with history of prior cardiac arrest, sustained ventricular tachycardia, sudden
death in close relatives, syncope especially with exertion, dysrhythmias, hypotension with
exercise, and left ventricular hypertrophy (LVH) with maximal wall thickness greater than 30 mm.
The diagnosis of HCM is multifaceted but begins with a substantial family history. Noticing a
trend of recent early deaths in family members can help peak a clinicians suspicion to explore
a diagnosis of HCM. HCM exhibits an autosomal dominant genetic inheritance pattern and can
occur from a mutation in any one of 10 different genes with b-myosin, cardiac troponin T, and
myosin binding protein C being the most prevalent. A physical examination is not reliable in
making or excluding the diagnosis of HCM because most patients will not have the outow
obstruction and examination may be unremarkable. Physical examination, however, may
demonstrate a systolic murmur that decreases in intensity when the patient is in the supine
position and increases with standing and Valsalva maneuver.
An electrocardiogram (ECG) is typically abnormal in 75%95% of patients with HCM. A wide
variety of morphologic ECG patterns exist and no pattern is sensitive or specic for HCM. ECGs
however with an LVH pattern should raise suspicion in the right clinical setting. Obtaining a
2-dimensional echocardiography will further aide in diagnosis. Mild HCM can be dened as
1315 mm left ventricular wall thickness with massive HCM as anything greater than 30 mm.
Patients may harbor the genetic defect but have not developed phenotypic expression
depending on age as LV remodeling occurs during adolescence and hypertrophy may develop at
any point during that time
Reduction of strenuous activity and restriction from participation in competitive athletics
remain mainstays of treatment. Historically, prevention measures relied on treatment with
beta-adrenergic blockers, verapamil, and anti-arrhythmic agents, but little evidence exists
that prophylaxis reduces SCD risk. These medications may be appropriate in persistent
dysrhythmias associated with HCM such as atrial brillation or in patients with congestive
symptoms. In high-risk patients with HCM, implantable cardiac debrillators (ICD) may help
abort fatal ventricular dysrhythmias. Surgical options are available, including myotomymyectomy, alcohol septal ablation, and heart transplant, but are generally reserved for patients
with severe obstructive HCM and drug refractory symptoms (i.e. approximately o 5% of HCM
patients).
Commotio cordis
Commotio Cordis is a fatal dysrhythmia caused by blunt force to the chest during the
ventricular repolarization phase resulting in SCD. The transfer of kinetic energy from the
hockey puck or baseball to the myocardium is thought to lead to the dysrhythmia. Luckily, a
multitude of different events need to occur at an exact time intervals making this cause of SCD
extremely rare. Commotio cordis primarily affects male athletes in adolescence. Approximately
10 to 20 cases occur annually with a mean age of 15 and very few victims over the age of 20.
The most common sports involving commotio cordis events include baseball, lacrosse, soccer,
hockey, and softball but can occur from any direct trauma to the chest. It does not appear that
air lled projectiles (i.e. soccer balls) exhibit a lower risk that solid core projectiles (i.e.
baseballs) do. In swine models, impacts at 40 mph were most likely to induce ventricular
brillation. At velocities greater than 50 mph, the incidence of ventricular brillation decreased
but cardiac rupture increased. The initial rhythm is generally ventricular brillation and early
99
debrillation may result in successful resuscitation. Individuals susceptible may include those
with prolonged QT intervals or with drugs that affect cardiac repolarization. Initially thought to
be a uniformly fatal disease, more recent reports have demonstrated up to 35% successful
resuscitation in patients with commotio cordis. Therapeutic hypothermia may improve
outcome following successful resuscitation. Prevention includes avoidance of direct trauma to
the chest, improved protective equipment, and potentially more pliable safety balls in the
appropriate sport (i.e. baseball), which did reduce the risk of ventricular brillation in swine
models.
Dysrhythmias
Re-entrant ventricular tachycardia represents a nal common pathway for several of the
distinct dysrhythmia subtypes involving sudden cardiac death in the athlete. For instance, in
the case of hypertrophic cardiomyopathy, the resultant hypertrophied myocardium is prone to
microvascular ischemia, especially when placed under extreme workloads. This microvascular
ischemia can therefore lead to subsequent scarring and brotic myocardial remodeling. This
remodeled myocardium provides a fertile substrate for the development of re-entrant
ventricular tachy-dysrhythmias.
Arrhythmogenic Right Ventricular Cardiomyopathy, albeit much less common than HCM,
represents another etiology of SCD in athletes again via the development of fatal ventricular
tachycardia. Although incompletely understood, the underlying pathology is thought to involve
atypical desmosomal development, thereby leading to subsequent replacement of normal
myocardial cells with brous tissue. Once again, this remodeled substrate is prone to
developing re-entrant ventricular dysrhythmias.
Finally, any of the various inherited ion channelopathies may also cause SCD in athletes. These
include such entities as the Long QT Syndromes (LQTs), Brugada Syndrome, and catecholaminergic polymorphic ventricular tachycardia (CPVT). There are at least 10 different subtypes of the
LQTs, and they can be either acquired or congenital. For the scope of this discussion, two
congenital forms include the Romano-Ward LQT syndrome, consisting of a prolonged QT on ECG
without sensorineural hearing loss, and the Lange-Nielson variant, which includes the presence
of sensorineural hearing loss. Regarding the Brugada pattern on ECG, this consists of a pseudoRight Bundle Branch Block, as well persistent, downsloping ST segment seen in precordial
leadsV1-V3. The majority of Brugada patients are of Asian descent, with prevalence reported
from as low as 0.012% in North America, to as high as 0.6% in Japan. Inherited sodium channel
gene mutations lead to prolonged inactivation of the myocardium after depolarization and a
shortened cardiac myocyte action potential. Lastly, CVPT usually occurs in patients with no other
structural heart disease or associated syndromes. The development of ventricular tachydysrhythmias usually occurs during periods of emotional stress or extreme physical exertion.
Resting ECGs are usually normal if the patient is in sinus rhythm at the time of the ECG. The
condition is usually diagnosed by the presence of polymorphic ventricular tachycardia on ECG,
accompanied by a continuously-varying QRS morphology.
Fortunately, 7590% of the screening ECGs of patients with underlying HCM, ion
channelopathies, ARVD, and WPW will be abnormal. However, there are still many patients
that will not have an abnormality on ECG. A family history of un-explained premature cardiac
death will be present in up to 30% of these patients. Furthermore, Rausch et al suggest that as
many as 1 in 4 patients succumbing to sudden cardiac death had previously reported syncope
episodes. These facts only further illustrate the great importance of obtaining a thorough, yet
focused, patient and family history at the pre-participation screening examination.
In the event that dysrhythmias are found during the pre-participation screening of a
competitive athlete, then consider specic anti-arrhythmic therapy. Beta-adrenergic blockers
and similar nodal blocking agents comprise the majority of anti-dysrhythmia treatment.
However, some dysrhythmias may require myocardial conduction mapping and/or ablation
therapy (i.e. WPW or HCM with intermittent unstable tachycardia via an accessory pathway).
100
Because of the complexity and scarcity of these conditions, general consensus would support
deferring both the choice of anti-dysrhythmic treatment and the timing of initiation of that
agent to a cardiologist. Furthermore, this deferral ensures adequate and highly skilled
management and titration of therapy. No general recommendations currently exist for
initiation of anti-dysrhythmic therapy that would then uniformly justify participation of the
athlete in subsequent competitive athletics. This decision must be made on a case-by-case,
individualized basis.
Anomalous coronary artery origin

This entity represents another cause of sudden cardiac death in athletes. Most commonly,
this involves an anomalous origin of the left main coronary artery from the right coronary
sinus of Valsalva. The mechanism is thought to involve insufcient coronary artery blood
ow during periods of intense physical exertion. This decrease in adequate perfusion could
result either from the particular geometry of the ostial origin of the coronary artery, or simply
from extrinsic compression upon the artery from the surrounding great vessels. Very
commonly, these patients have no preceding symptoms, and normal baseline ECGs.
Screening recommendations
Current guidelines recommend children considering participation in competitive athletics
obtain a careful history and physical examination by a Primary Care Physician or Sports
Medicine Physician. Trying to determine whether the young athlete is at risk for the above
conditions is the objective of the pre-athletic physical and history. Pre-participation screening
consists of a focused personal history, a family history, and a physical exam. The key features to
note are a family history with a premature sudden death or heart disease in a surviving relative
that has genetic linkage. If the athlete presents with a murmur, systemic hypertension,
excessive fatigue, exertional chest pain, syncope with exertion, or shortness of breath with
exertion, then the clinician should have a higher index of suspicion of disease processes that
may place the athlete at risk. The physical assessment should be directed toward possible
pathologic etiologies of a cardiac condition. Careful assessment of the pulses, cardiac
auscultation (sitting and standing) and measuring of brachial artery blood pressure should
be a part of any exam. Femoral pulses should be evaluated in order to exclude coarctation of the
aorta. Screen for other conditions like Marfans syndrome verify the family history/patients
history with the athletes guardian. Younger patients may not be aware of a sudden
young death in their family and if it was related to a cardiac event or genetic. Although
screening electrocardiograms have been utilized for young athletes in Europe, currently an
electrocardiogram or echocardiogram is not recommended as an initial screening tool in the
United States as this places a large burden on the health care system for a relatively infrequent
disease. Additionally, such screening may not be accessibly in children from low-income
families. Patients with suspicious ndings on initial screening exam should be referred for
further evaluation and testing and may include evaluation by a cardiologist. Access to
automatic external debrillators at athletic venues combined with immediate cardiopulmonary resuscitation may improve outcomes, although this has not been validated.
Suggested Reading
Koester MC. A review of sudden cardiac death in young athletes and strategies for participation cardiovascular
screening. Journal of Athletic Training 2001;32(2):197204.
Ferreira M, Santos-Silva RP, de Abreu LC, Valenti VE, Crispim V, Imaizumi C, et al. Sudden cardiac death athletes: A
systemic review. Sports medicine, arthroscophy, rehabillitation, therapy and technology 2010;2(19). Retrieved from
http://www.smarttjournal.com/content/2/1/19. Accessed on January 11, 2013.
101
Maron BJ. JAMA. Hyptertrophic cardiomyopathy 2002;287:13081320.

Corrado D, Basso C, Pavei A, Michieli P, Schiavon M, Thiene G. Trends in sudden cardiovascular death in young
competitive athletes after implementation of a preparticipation screening program. Journal of American Medical
Association 2006;296(1593):1601.
Carlson DW, Pearson RD, Haggarty PF. Commotic cordis, therapeutic hypothermia and evacuation from a United States
military base in Iraq. J Emerg Med 2012;08:014.
Corrado C, Basso C, Schiavon M. Pre-participation screening of young competitive athletes for prevention of sudden
cardiac death. Journal of American College of Cardiology 2008;52:24.
Maron BJ, Thompson PD, Ackerman MJ, Balady G, Berger S, Cohen D, et al. Recommendations and Considerations
Related to Preparticipation Screening for Cardovascular Abnormalities in Competitive Athletes. Circulation
2007;115:16436155.
Maron BJ, Mckenna WJ, Danielson GK, Kappenberger LJ, Kuhn HJ, Seidman CF, et al. American College of Cardiology/
European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy 2003;42:
16871713.
Rausch C. Sudden Cardiac Death in Young Athletes, A Brief Review. 2011 Practice Update. Childrens Hospital of
Colorado.
Maron BJ, Douglas PS, Graham TP, Nishimura RA, Thompson PD. Task Force 1: Pre-participation screening and diagnosis
of cardiovascular disease in athletes. JACC 2005;45(8):13221326.
Chiang CE, Roden DM. The Long QT Syndrome:Genetic Basis and Implications. J Am Coll Cardiology 2000;36:112.
Brugada P, Brugada J. Right Bundle Branch Block, Persistent ST Segment Elevation and Sudden Cardiac Death, a Distinct
Clinical and Electrocardiographic Syndrome. J Am Coll Cardiology 1992;201:1391.
Priori SG, Napolitano C, Memmi M, Colombi B, Drago F, Gasparini M, et al. Clinical and Molecular Characterization of
Patients with Congenital Polymorphic Ventricular Tachycardia. Circ 2002;106:69.
Drezner JA, Rogers KJ. Sudden cardiac arrest in intercollegiate athletes: detailed analysis and outcomes of resuscitation
in nine cases. Heart Rhythm 2006;3(7):755759.
Maron BJ, Ahluwalia A, Hass TS, Semsarian C, Link MS, Estes NA. Global epidemiology and demographics of commotion
cordis. Heart Rhythm 2011;8(12):19691971.
Drezner JA, Rogers KJ, Zimmer RR, Sennet BJ. Use of Automated External Debrillators at NCAA Division I Universities.
Medicine and Science in Sports & Exercise 2005;37(9):14871492.
Drezner JA, Rogers KJ, Horneff JG. Automated external debrillator use at NCAA Division II and III universities. British
Journal of Sports Medicine 2011;45:11741178.
Seto CK, Pendleton ME. Preparation Cardiovascular Screening in Young Adults: Current Guidelines and Dilemmas.
Current Sports Medicine Reports 2009;8(2):5964.
Link MS, Estes 3rd NA. Sudden Cardiac Death in the Athlete: Bridging the Gaps Between Evidence, Policy, and Practice.
Circulation 2012;125(20):25112516.
Palacio LE, Link MS. Commotio Cordis. Sports Health 2009;1(2):174179.

Clinical Cardiac Emergencies

Cargado por

Información del documento

Derechos de autor

Formatos disponibles

Compartir este documento

Compartir o incrustar documentos

Opciones para compartir

¿Le pareció útil este documento?

¿Este contenido es inapropiado?

Copyright:

Formatos disponibles

Clinical Cardiac Emergencies

Cargado por

Copyright:

Formatos disponibles

Disease-a-Month

Volume 59 Number 3 March 2013

Contents lists available at SciVerse ScienceDirect

Approach to clinical cardiac emergencies

0011-5029/$ - see front matter & 2013 Published by Mosby, Inc.

Disease-a-Month 59 (2013) 6773

Contents lists available at SciVerse ScienceDirect

R. Wadke / Disease-a-Month 59 (2013) 6773

First time diagnosis of AF irrespective of duration of arrhythmia, presence of symptoms,

R. Wadke / Disease-a-Month 59 (2013) 6773

Fig. 1. Atrial brillation 12-lead EKG.

Risk stratication for stroke and thromboembolism (Tables 2 and 3)

Not FDA approved for this indication.

R. Wadke / Disease-a-Month 59 (2013) 6773

Congestive heart failure/LV dysfunction

R. Wadke / Disease-a-Month 59 (2013) 6773

Major side effects

Bradycardia, hypotension, heart

50200 mg/kg/min IV N/A

Nondihydropyridine calcium channel antagonists

Hypotension, heart blocks, heart

Digitalis toxicity, bradycardia, heart

Hypotension, heart blocks,

R. Wadke / Disease-a-Month 59 (2013) 6773

Major side effects

Hypotension, atrial utter

Not available in the United States.

R. Wadke / Disease-a-Month 59 (2013) 6773

Postoperative atrial brillation

Disease-a-Month 59 (2013) 7482

Contents lists available at SciVerse ScienceDirect

S. Boateng / Disease-a-Month 59 (2013) 7482

AV reciprocating tachycardia (AVRT), some ventricular tachycardias (VTs), and ventricular

S. Boateng / Disease-a-Month 59 (2013) 7482

S. Boateng / Disease-a-Month 59 (2013) 7482

S. Boateng / Disease-a-Month 59 (2013) 7482

Atrioventricular reciprocating tachycardia (extra nodal accessory pathways)

S. Boateng / Disease-a-Month 59 (2013) 7482

Not FDA approved for this indication.

S. Boateng / Disease-a-Month 59 (2013) 7482

Multifocal atrial tachycardia

Macro-re-entrant atrial tachycardia (atrial utter)

S. Boateng / Disease-a-Month 59 (2013) 7482

S. Boateng / Disease-a-Month 59 (2013) 7482

Disease-a-Month 59 (2013) 8396

Contents lists available at SciVerse ScienceDirect

Acute myocardial infarction

An acute myocardial infarct (AMI) is a subset of a spectrum of acute coronary syndrome

S. Boateng, T. Sanborn/ Disease-a-Month 59 (2013) 8396

Anginal pain with at

 Of new onset and severe.

severity and length of

S. Boateng, T. Sanborn/ Disease-a-Month 59 (2013) 8396

ST-segment elevation Z1 mm concordant with a predominantly positive QRS complex in at

S. Boateng, T. Sanborn/ Disease-a-Month 59 (2013) 8396

S. Boateng, T. Sanborn/ Disease-a-Month 59 (2013) 8396

Primary percutaneous coronary intervention

Adjunct therapy for a STEMI

Relieving chest pain

S. Boateng, T. Sanborn/ Disease-a-Month 59 (2013) 8396

S. Boateng, T. Sanborn/ Disease-a-Month 59 (2013) 8396

Glycoprotein IIb/IIIa antagonists

Exceeds dosage recommended by the manufacturer.

S. Boateng, T. Sanborn/ Disease-a-Month 59 (2013) 8396

Of new onset and severe.