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148 J. A. Salotto
Dose: 0.25 mg IV over 3 minutes, followed by 0.25 mg every six hours
to a total dose of 10 mcg/kg lean body weight. It will begin to act within
30 minutes. Follow with 0.125–0.25 mg/ day.
• Rhythm control re-synchronizes the atrium and the ventricle back to normal
sinus rhythm. It may be accomplished through pharmacological or electrical
means, via direct current cardioversion.
The physician can use one of the following in a single oral dose to convert
back to sinus rhythm:
Flecanide 300 mg PO
Propafenone 600 mg PO
These agents may increase risk of ventricular tachycardias and si-
Ö
nus bradycardia. They are contraindicated in coronary artery disease.
Ibutilide is a safe and effective agent for rhythm control. It may be used for
unstable hemodynamics. Side effects include nausea.
Ibutilide 1 mg over 10 minutes, then maintain with 1–4 mg/minute.
Amiodarone is a good choice for those patients in atrial fi brillation with
heart failure or structural heart disease (see above for dose).
Direct current (DC) cardioversion can be used for ongoing stable atrial
fi brillation after 48 hours, atrial fi brillation refractory to medical therapy,
early atrial fi brillation in patients who cannot tolerate decreased coronary
or ventricular fi lling, or unstable hemodynamics. It is not indicated for
asymptomatic arrhythmias.
120–200 joule biphasic or 200 joule monophasic shock should be per-
formed in synchrony with the QRS complex after sedation has been
given.
If AF has been present over 48 hours, exclude intracardiac thrombus
with TEE before cardioversion.
The success rate of DC cardioversion for atrial fi brillation in postop-
erative patients has been shown to be as low as 35% (see below).
Agents used for maintenance of sinus rhythm after rhythm conversion:
Amiodarone: load with 150 mg/minute for 10 minutes, then 1 mg/
minute for 6 hours. Follow with an IV infusion at 0.5–1mg/minute.
Sotalol 80 mg PO twice daily, monitor QT interval.
Dysrhythmias 149
Begin anticoagulation with intravenous heparin in the absence of contrain-
dications after 12–24 hours.
Can use lepirudin as an alternative to heparin in patients with heparin-
induced thrombocytopenia.
• Atrial flutter
Atrial fl utter is a reentrant arrhythmia in which an alternate circuit rotates
around the tricuspid valve annulus. It is characterized by a regular sawtooth pattern of P waves on EKG in leads II, III, avF. The usual rate of
atrial fl utter is 240–320 beats per minute.
A rate of exactly 150 beats per minute should cause the clinician to
suspect atrial fl utter with 2:1 AV block.
Ventricular rate control can be attempted with diltiazem, verapamil, or
beta-blockade. Digoxin is a good choice in congestive heart failure (see
above for dosage information).
Ibutilide, dofetilide, and sotalol are the pharmacological agents typically
used to terminate atrial fl utter. These drugs are proarrhythmic in that they
may prolong the QT interval and lead to torsades de pointes (see below).
Ibutilide: 1 mg over 10 minutes, then maintain with 1–4 mg/minute.
Dofetilide: 500 mcg orally every 12 hours; must adjust dose with im-
paired creatinine clearance.
Sotalol: 80 mg orally every 12 hours.
Patients are frequently treated with DC cardioversion starting with a 50
joule biphasic shock with sedation. Often a 100 joule shock is effective.
Recurrent atrial fl utter is often treated with catheter ablation.
• Supraventricular tachycardia (SVT)
Common subtypes include atrioventricular nodal reentrant tachycardia,
atrioventricular reciprocating tachycardia, and focal atrial tachycardia.
SVT frequently has a sudden onset and termination, and is not necessarily
associated with any underlying cardiac disease.
Most types of SVT have narrow QRS complexes <120 milliseconds.
A wide QRS complex can be seen if SVT is present in conjunction
with a bundle-branch block, an accessory pathway, or a ventricular
tachycardia.
150 J. A. Salotto
The P wave may be buried within the QRS complex if both atrium and
ventricle are simultaneously activated.
Vagal maneuvers including carotid massage and the Valsalva maneuver
are effective fi rst-line therapy for SVT in hemodynamically stable patients. These maneuvers stimulate baroreceptors which trigger an increase
in vagal nerve activity, and this slows impulse conduction through the AV
node. To perform carotid massage, apply pressure to one carotid artery at
the level of the cricoid in a circular motion for 10 seconds, and follow with
the other side as needed. Carotid massage should not be performed in the
presence of known carotid plaque or a bruit on auscultation.
If vagal maneuvers fail, intravenous adenosine or verapamil is safe and
effective to terminate SVT.
Adenosine is an AV nodal blocking agent with a half life of about 10
seconds. It is the fi rst-line drug for converting narrow complex SVT
and can also be useful in diagnosis and treatment of wide-complex
SVT. Administration of adenosine should be done under cardiac monitoring with defi brillation pads in place, as transient asystole or ventricular fi brillation may result.
Adenosine 6 mg IV push, repeat with 12 mg IV after 1–2 minutes
Ö
as needed.
Common side effects include facial fl ushing, chest pain and hypo-
Ö
tension.
Contraindications include: atrial fi brillation, those with a heart
Ö
transplant, obstructive lung disease, wide QRS complex tachycardias (unless certain it is SVT with aberrancy) and Wolff-ParkinsonWhite syndrome.
Verapamil (5 mg IV every 3–5 minutes, up to 15 mg) and diltiazem
(0.25 mg/kg IV bolus) are calcium channel blockers used in patients
with recurrent SVT after adenosine. CCBs may result in vasodilation
or bradycardia; use with caution in patients with low cardiac output.
Do not use in Wolff-Parkinson-White syndrome or wide complex
tachycardia.
Esmolol (500 mcg/kg IV loading dose over 1 minute, followed by
50–200 mcg/kg/min drip), a beta-blocker, is useful to terminate SVT.
Avoid use in patients with renal disease, bradycardia, and asthma.
Dysrhythmias 151
SVT refractory to the agents listed may be treated with antiarrhythmics.
These agents prolong the QT interval and may increase the risk of torsades
de pointes (see below).
Procainamide 15 mg/kg IV over 60 minutes follow with 1–4 mg/ min-
ute IV drip.
Ibutilide 1 mg over 10 minutes, then maintain with 1–4 mg/minute.
Recurrent, symptomatic SVT should be treated with prophylactic beta-
blockade or calcium channel blockade.
If hemodynamically unstable, perform R-wave synchronous DC conver-
sion with 100–200 joules.
• Ventricular tachyarrhythmias
Premature ventricular contractions (PVCs)
On EKG, PVC is noted as an aberrant wide QRS complex which may
occur in a pattern of bigeminy, where every sinus beat is followed by a
PVC, or trigeminy, where two sinus beats are followed by one PVC.
Often asymptomatic and incidental on telemetry, these PVCs increase
with age and with the presence of structural cardiac abnormalities.
Three or more consecutive PVCs are termed ventricular tachycardia (VT).
In the absence of heart disease, PVCs are benign and require no treat-
ment. In those with underlying heart disease, PVC runs of greater than
10 beats may indicate an increased risk of adverse events.
Nonsustained ventricular tachycardia (NSVT)
NSVT is the occurrence of three or more PVCs which terminate spon-
taneously in less than 30 seconds.
In a patient with prior myocardial infarction and depressed ejection
fraction, NSVT should trigger further workup and evaluation for an
implantable defi brillator.
Sustained ventricular tachycardia (VT) and ventricular fi brillation (VF)
VT and VF are accelerated heart rhythms in which an impulse origi-
nates below the bundle of His at a rate >100 beats per minute. In most
cases, hemodynamic instability results which can lead to inadequate
cardiac output, poor end organ perfusion, hypotension, and cardiac arrest if untreated.
152 J. A. Salotto
Hemodynamic stability depends on the rate, underlying heart disease
and function, ability to compensate, and the presence of retrograde
conduction.
In sustained VT, the wide (>120 millisecond) QRS complex may be
monomorphic or polymorphic.
Monomorphic VT demonstrates a uniform morphology of the QRS
Ö
complex. It is usually secondary to an underlying cardiac structural
abnormality such as scarring of the myocardium after an infarction.
Polymorphic VT demonstrates a changing shape of the QRS com-
Ö
plex and suggests underlying ischemia or infl ammation of the
heart.
One example of polymorphic VT is torsades de pointes.
Ö
— Torsades de pointes is VT associated with a long QT and
twisting of the peaks of the QRS complexes around an isoelectric line on EKG.
— Drugs which can lengthen the QT interval and lead to tor-
sades include dofetilide, ibutilide, procainamide, quinidine,
sotalol, amiodarone, clarithromycin, erythromycin, haloperidol, and methadone.
Any form of polymorphic VT should prompt an ECHO to evaluate car-
Ö
diac size and function. If a new wall motion abnormality or depressed
systolic function is identifi ed, the patient should be further evaluated
for ischemic heart disease. If right ventricular dilation is identifi ed, this
could be the structural abnormality underlying arrhythmia.
“VT storm” is the term for more than two episodes of VT in one day.
It is often secondary to underlying ischemia.
Ventricular fi brillation is caused by discharge from an ectopic ven-
tricular pacemaker other than the sinus node, and is usually more than
300 beats per minute. It is an irregular rhythm with variable QRS complex durations, morphologies and amplitudes. Ventricular fi brillation
indicates an electrically unstable heart.
Treatment of ventricular tachycardias
Monomorphic VT
Ö
— Use direct current (DC) synchronized cardioversion with 100
joules if hemodynamically unstable. This is rapidly effective,
Dysrhythmias 153
but requires sedation. Defi brillation does not prevent recurrence.
— A procainamide infusion is fi rst-line treatment in stable
monomorphic VT. Dose: 20–50 mg/minute until arrhythmia
is suppressed with a maximum dose of 17 mg/kg; follow with
a maintenance infusion of 1–4 mg/kg.
— An amiodarone infusion can be utilized for unstable, refrac-
tory, or recurrent monomorphic VT. Use a loading dose of
150 mg/minute for 10 minutes, then 1 mg/minute for 6 hours.
Follow with an IV infusion at 0.5–1mg/minute.
— If VT is suspected to be from underlying ischemia, use lido-
caine 1–3 mg/kg IV at 20–50 mcg/minute, follow with an IV
infusion of 1–4 mg/minute.
— If cardiac function is poor, lidocaine or amiodarone is accept-
able.
Torsades de Pointes
Ö
— Stop any drugs which prolong the QT interval.
— Treat with IV magnesium sulfate 25–50 mg/kg up to 2 g.
— Use temporary pacing if torsades is refractory or secondary to
heart block.
Polymorphic VT or VF
Ö
— In unstable VT/VF, perform synchronous defi brillation at 360
joules if using a monophasic shock, and 200 joules if a biphasic shock.
— Infusions of lidocaine, procainamide, or amiodarone can be
used in stable VT/VF. Amiodarone is especially useful in patients with a low ejection fraction. See recommended doses
under the treatment of monomorphic VT.
— Correct underlying acidosis and electrolyte abnormalities.
— Use IV beta-blockers for recurrent polymorphic VT, espe-
cially if ischemia is the suspected etiology.
VT Storm
Ö
— Use IV Beta-blockade if polymorphic VT, and defi brillation
for unstable hemodynamics.
— Perform urgent revascularization if ischemia is present.
154 J. A. Salotto
Calcium channel blockers should not be used to terminate wide-complex
tachycardias.
Consider ischemia as an underlying mechanism and treat accordingly.
CABG is recommended in patients resuscitated from sudden cardiac
death or for sustained ventricular tachycardia believed to be caused by
signifi cant coronary artery disease.
Evaluate for an internal cardiac defi brillator (ICD)
An ICD should be considered for patients with an ejection fraction
<35%, with a history of non-sustained ventricular tachycardia, and for
those with inducible VT on electrophysiological testing.
An ICD is recommended for patients after cardiac arrest from VT/VF,
for those with structural heart disease and spontaneous sustained VT,
for those with VT leading to hemodynamic compromise, and for those
with VT and depressed systolic function.
Practical Algorithm(s)/Diagrams
Management of New-onset Narrow Complex Tachycardia (QRS <120 msec)
Perform 12-lead EKG
Atrial
Flutter
Regular rhythm
Saw-tooth pattern
P waves at 300 bpm
Rate 100-150 bmp
Rate Control:
- Calcium Channel
Blockers
- Beta-Blockers
- Digoxin: heart
failure
Fig. 1. Management of new-onset narrow complex tachycardia.
Supraventricular
Tachycardia
Regular rhythm
P wave often buried in
QRS complex
Rate 140-220 bpm
Rhythm Control:
- Ibutilide
- Dofetilide
- Sotalol
Ye s
Hemodynamically
Stable?
Atrial
Fibrillation
Vagal maneuvers
Adenosine
Calcium Channel Blockers
Beta-Blockers
No
Electrical Cardioversion
Irregularly irregular
Absence of P waves
Rate 100-160 bpm
Early: <24 hours After 24-48 hours
Rate Control:
- Beta-Blockers
- Calcium Channel Blockers
- Amiodarone
If heart failure:
- Digoxin, Amiodarone
Procainamide
Ibutilide
Consider
cardioversion
Amiodarone
Ibutilide
Structural Heart
Disease?
Ye s N o
ECHO
Sedation
Electrical
Pharmacological
Amiodarone
Ibutilide
Flecainide
Propafenone
Dysrhythmias 155
Review of Current Literature with References
• A prospective database was used to study patients undergoing major non-
cardiac thoracic surgery at a single institution from 1998 to 2002. They
studied 2,588 patient records to identify risk factors associated with the onset
of atrial fibrillation after thoracic surgery. The rate of atrial fibrillation was
12.3%. They found statistically significant risk factors to include male
sex, age over 50 (with incremental increase in risk each decade above 50), a
history of congestive heart failure, a history of arrhythmias, intraoperative
transfusions, and increasing risk with increasing amounts of lung resected
(lobectomy, relative risk 3.89; pneumonectomy relative risk 8.91). The development of atrial fibrillation significantly increased mortality rates (from 2.0%
to 7.5%), length of stay, and cost of stay (J Thorac Cardiovasc Surg 2004;
127: 779–786).
• Siu et al. performed an open-label, randomized control trial of 150 patients
with symptomatic, new-onset atrial fibrillation in order to compare the effectiveness of diltiazem, digoxin, and amiodarone for rate control and symptom
improvement. Time to rate control, percentage rate controlled, and symptom
improvement was best achieved with diltiazem. There was no difference
noted in rhythm conversion. Excluded patients with hypotension, congestive
heart failure, recent myocardial infarction, or unstable angina, and they used
lower doses of digoxin and amiodarone than the maximal recommended
doses [Crit Care Med 2009; 75(11): 1653–1654].
• One non-blinded, randomized trial looked at the rate of conversion to sinus
rhythm in 64 non-cardiac surgery ICU patients with supraventricular tachycardias at 2 and 12 hours after treatment. A majority of patients were in atrial
fibrillation. All patients were initially given adenosine, and those who
remained in SVT were then randomized to receive IV diltiazem or IV esmolol
for rate control. None of the patients converted to sinus rhythm with adenosine. In the patients getting esmolol, 59% of patients converted in 2 hours,
after 12 hours 85% had converted. In those randomized to diltiazem, 33%
converted by 2 hours, and 62% had converted at 12 hours. Although there was
no significant difference in rates of conversion at 12 hours, the time to conversion was significantly shorter with esmolol (Anesthesiology 1998; 89:
1052–1059).
• A prospective study was performed to examine the primary success rate of
direct-current cardioversion in postoperative ICU patients with new-onset
supraventricular tachycardias. Of 37 patients, 31 presented in atrial fibrillation. Sinus rhythm restored in 35% after 1 shock, with 100% converted after
156 J. A. Salotto
4 shocks. At 48 hours, only 13.5% remained in sinus rhythm. They speculate
that different pathophysiologic mechanisms may exist in surgical patients,
making them less responsive to direct current cardioversion (Crit Care Med
2003; 31: 401–405).
• One retrospective review examined rates of ventricular tachycardia and
fibrillation (VT/VF) in 9211 patients with acute coronary syndromes. They
found risk factors for VT/VF to include prior heart failure, an ejection fraction
<30%, and triple vessel coronary artery disease. In this high-risk patient
population, VT/VF was as likely to occur after 48 hours of infarction as
within the first 48 hours, and median time to arrhythmia was 5 days. They
recommend telemetry monitoring to continue beyond 48 hours after infarct
(Circulation 2012; 126: 41–49).
• A multicenter, retrospective, observational study examined 197 patients with
wide QRS complex tachycardias. Of those patients, a response to adenosine
was noted in 90% with supraventricular tachycardia and 2% in patients with
ventricular tachycardia. They noted no adverse events in either of the patient
groups. A response to adenosine increased the odds of SVT by 36 times, and
a nonresponse increased the odds of ventricular tachycardia by 9 times. They
conclude that adenosine can be safely used in patients with a wide-complex
tachycardia as both a diagnostic measure and as a treatment (Crit Care Med
2009; 37: 2512–2518).
Chapter 5-(vii)
Acute Coronary Syndromes
Jennifer A. Salotto, MD*
* Fellow, Trauma and Acute Care Surgery, Denver Health Medical Center
Take Home Points
• The term ‘acute coronary syndrome’ includes three clinical entities: unstable
angina, non-ST-segment elevation myocardial ischemia (NSTEMI), and
ST-segment elevation myocardial ischemia (STEMI).
• The three diagnoses included under ACS often share a common etiology:
coronary plaque disruption with subsequent thrombosis. If a thrombus causes
significant obstruction to coronary blood flow, myocardial ischemia can
result.
• Coronary atherosclerosis is the predominant feature underlying acute coro-
nary events.
• The majority of postoperative deaths after surgery are traced to cardiovascular
etiologies.
• Myocardial infarction (MI) in the postoperative period may be asympto-
matic and clinically dissimilar to myocardial infarction in the non-operative
population.
Contact information: Denver Health Medical Center, University of Colorado Health
Sciences Center, 777 Bannock Street, MC 0206, Denver, CO 80204; Tel.: 857-928-4766,
email: Jennifer.salotto@ucdenver.edu
157