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by signs and symptoms of inadequate end- organ perfusion:
altered mental status, hypotension, chest pain, hypoxia, or
shortness of breath (a sign of pulmonary edema). Under
general anesthesia, however, subjective symptoms are impossible to elicit and the clinician is relegated to assessment of
cardiopulmonary stability via oxygenation, ETCO2, pulse,
and blood pressure. Stable patients can be dealt with in a less
emergent and more systematic manner, although vigilance
for emerging clinical instability is warranted at all times.
At its most extreme, clinical instability is characterized by pulselessness, the absence of discernable forward
cardiac ow. Attention should be given to rapid search
for a pulse (for 10 seconds or less), early CPR with an
emphasis on eective chest compressions, and (in the
Figure 7.1 American Heart Association (AHA) Adult Cardiac Arrest Algorithm— 2015 update. The owchart summarizes the performance of advanced
cardiovascular life support, including assessment and treatment. Notable changes from 2010 include the removal of vasopressin from the algorithm
and a preference for amiodarone over lidocaine for refractory shockable rhythms. SOURCE: Adapted from “Part 7: Adult Advanced Cardiovascular Life Support.”
by M.S. Link, 2015, Circulation, 132(18 suppl 2), S444– S464. Copyright by American Heart Association, Inc. Reprinted with permission.
36 PART II. CARDIAC CRISES
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37
event of a shockable rhythm) rapid shock delivery5
(Figure 7.1). In the presence of an arterial waveform,
care must be taken to avoid the academic exercise of distinguishing an extremely low pulse pressure from true
understanding of each is needed in order to be able to
make a rapid assessment and begin immediate treatment,
as delays in treatment are strongly associated with poor
outcomes.
pulselessness. Such a distinction is unlikely to yield much
clinical benet, and only serves to delay the appropriate
treatment. If the forward cardiac output is deemed to be
negligible, using adjunct monitors such as ETCO2 and
pulse oximeter, treatment for a pulseless rhythm should
commence immediately.
PULSELESS ELECTRICAL ACTIVITY/ ASYSTOLE
Pulseless electrical activity (PEA) is recognized as the
presence of a perfusing rhythm on EKG (not ventricular
brillation or ventricular tachycardia), without the pres-
ence of a discernable pulse. Asystole exists when there is
QRS MORPHOLOGY (NARROW VS. WIDE)
Rhythms are grouped based on the QRS width. Narrow
complex rhythms have QRS durations <120 ms and represent depolarization originating above ventricular myocar-
no ventricular electrical activity,6 and is treated in a similar
manner to PEA; hence, these two rhythms are addressed
simultaneously.
Pulseless electrical activity is diagnosed in the unre-
sponsive patient in the following manner:
dium. Wide complex rhythms (QRS duration >120 ms)
usually are caused by rhythms originating from the ventricle itself, although in the presence of underlying disease of
the ventricular conduction system, rhythms may originate
above the ventricle yet still display prolonged ventricular
conduction. A baseline EKG is helpful to discern the presence of underlying conduction abnormalities.
RHYTHM (REGULAR VS. IRREGULAR)
Arrhythmias can be further subclassied into regular versus irregular. Irregular rhythms require special attention
due to their diculty to treat and, in the case of irregular wide- complex rhythms, the potential for development
of unstable arrhythmias. Atrial brillation comprises the
majority of irregular rhythms encountered in the perioperative period.
Regardless of classication scheme, routine management of all perioperative arrhythmias should include attention to adequate oxygenation and ventilation, appropriate
IV access, adequate depth of anesthesia, appropriate acidbase and electrolyte status, normothermia, and a review of
known cardiac history and/ or pathology. If time allows, 12lead electrocardiography is oen helpful in identifying the
nature of the rhythm.
Figure 7.2 presents a useful organization scheme for
assessing rhythm disturbances. e following sections
address the management of specic scenarios.
CLINICAL SCENARIOS— TACHYARRYTHMIAS
e following sections discuss pulseless cardiac arrest
as well as pulsatile tachyarrhythmias. A thorough
• Loss of pulse for 10 seconds (carotid, femoral, radial), or
inability to identify pulse within 10 seconds
• Loss of arterial line tracing (unresponsive to ushing of
the line and removal of kinks)
• Loss of end- tidal CO
2
• Loss of plethysmography
Common sense should prevail: the loss of an arterial pressure waveform is unlikely to be signicant if pulse oximetry and ETCO2 waveforms are unchanged. at said, if
there is reasonable doubt about the presence of a pulse
aer 10 seconds of searching, PEA should be assumed
and cardiopulmonary resuscitation should be initiated
immediately.
6
e cornerstone of successful treatment of PEA is early
recognition of pulselessness and rapid initiation of cardiopulmonary resuscitation with an emphasis on high- quality
chest compression with minimal interruptions, per AHA
protocol (Figure 7.1). ere is a 7% to 10% decrement in
survival for each minute that CPR is not provided during
an arrest.
7
Ecacy of chest compressions should be assessed using
available monitors: end- tidal CO2 or arterial catheter.
Adequate chest compressions and an increased likelihood
of return of spontaneous circulation (ROSC) are associated
with4:
• ETCO2 >20 mmHg
• diastolic pressure >30 mmHg as measured by an arterial
catheter
CARDIAC DYSRHYTHMIAS 37
38
Usually AFib + aberrant conduction
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Pulse?
Stable?
Fast/Slow?
QRS Morphology?
Regular rhythm?
BRADY
Observe
Pacing
Regular
Adenosine
β1 Blocker
Calcium Antagonist
(Amiodarone)
Narrow QRS
STABLE
TACHY
Irregular
Usually AFib
β1 Blocker
Calcium Antagonist
Digoxin
Amiodarone
PULSE?
± Confirm with ETCO2
or arterial line
YES
Wide QRS
Regular
Adenosine
Amiodarone
Procainamide
Sotalol
Intralipid (Local
anesthetic toxicity)
UNSTABLE
BRADY
Atropine
β1 Agonist
NO
Pacing
CPR ± Defib
(see FIG 1)
TACHY
Synchronized
Irregular
Amiodarone
DCCV
Procainamide
NO Adenosine
NO β1 Blocker
NO Calcium Antagonist
NO Digoxin
Shock
Figure 7.2 Flowchar t summarizing the assessment and treatment of perioperative dysrhythmias. SOURCE: Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult
Advanced Cardiovascular Life Support. Circulation. 2015;132(18 suppl 2):S444- S464. doi:10.1161/ CIR.0000000000000261.
Interruptions in CPR must only occur for pulse and
rhythm checks, which will occur every 2 minutes. Pharmacotherapy in the form of 1 mg epinephrine IV bolus should
be administered soon aer the initiation of CPR— to be
repeated every 3 to 5 minutes (every other cycle of CPR).
As of 2015, bolus vasopressin is no longer advised for
treatment of cardiac arrest8 (Figure 7.1). Airway patency
and adequacy of ventilation and oxygenation must also be
attended to. However, it is important that hyperventilation and associated auto- PEEP is avoided, hence, a respiratory rate of 8 to 10 breaths per minute should be targeted.9
If high end- expiratory pressure does develop, it can be
reduced quickly by separating the patient from the breathing circuit; this will relieve positive airway pressure via passive exhalation.
10
Of note, routine use of atropine during PEA or
asystole is unlikely to have a therapeutic benefit and
atropine should not be given for this rhythm.6 Sodium
bicarbonate can paradoxically induce intracellular acidosis and should not be routinely administered during
PEA arrest.6 On the other hand, bicarbonate can be beneficial in tricyclic antidepressant overdose, or when the
laboratory tests identify metabolic acidosis (pH < 7.25)4
or hyperkalemia.
There may be confusion on the part of the clinician in distinguishing very fine ventricular fibrillation
from asystole. However, neither shocks nor pacing are
indicated for asystolic arrest. It does not improve outcome and may increase mortality due to delayed chest
compressions.
7
Finally, in order to achieve and/ or maintain return
of spontaneous circulation (ROSC), it is important to
address the root cause of cardiovascular collapse; otherwise, a patient who has achieved ROSC may quickly
devolve into a pulseless rhythm again. PEA is not a homogenous entity and correspondingly the causes of PEA and
38 PART II. CARDIAC CRISES
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39
TABLE 7.1 H’S AND T’S— MNEMONIC DIFFERENTIAL
DIAGNOSIS OF NONSHOCKABLE CARDIAC ARREST
Hypoxia
Hypovolemia
Hyper- / Hypokalemia
Hydrogen ions (acidemia)
Hypothermia
Hypoglycemia
Malignant Hyperthermia
Hypervagal (visceral or oculocardiac stimulus)
Toxins (anaphylaxis/ anesthesia, including local anesthetic systemic
toxicity)
Tension pneumothorax
Thrombosis/ Embolus, pulmonary (VTE, gas, fat, amniotic uid)
Thrombosis— coronary
Tamponade
Trauma (hemorrhagic shock, CV injury)
qT prolongation
Pulmonary hyperTension
CV = cardiovascular. VTE = venous thromboembolism.
SOURCE: Adapted from Moitra VK, Gabrielli A, MacCioli GA, O’Connor MF. Anesthesia
advanced circulatory life support. Can J Anesth. 2012. doi:10.1007/ s12630- 012- 9699- 3.
asystole are quite varied. A helpful mnemonic of “H’s
and T’s” can be used to ensure that a relatively thorough
assessment for various causes is implemented (Table 7.1).
Additional causes of PEA can be found in Table 7.2.
TABLE 7.2 ADDITIONAL ANESTHETIC- RELATED CAUSES
OF NON- SHOCKABLE CARDIAC ARREST
Pulseless electrical activity/ a systole is often preceded
by a period of clinical instability prior to full cardiac
deterioration. The cardiac rhythm during this antecedent period can have diagnostic utility that points to the
cause of hemodynamic collapse (Table7.3). As always,
situational awareness is important. Attention should be
paid to the most proximal events, and patient- specific
as well as procedure- specific risk factors should be considered in order to discern a cause. Anaphylaxis should
be a primary concern in the otherwise stable patient
who has just received IV medications or blood products. In the post- cardiac- surgery patient, tamponade
should be the diagnosis of exclusion and may require
the cutting of sternal wires in the ICU. For PEA after
central venous cannulation, tension pneumothorax
should be immediately considered. In surgery or trauma
of the abdomen or lower extremities, blood loss and
pulmonary embolism should be the primary concerns.
It is often helpful to consult with procedural colleagues
to understand procedural maneuvers or complications
that may help explain the clinical picture.
TABLE 7.3 PRE- ARREST RHYTHMS AND MOST COMMON
CAUSES OF SUBSEQUENT PEA OR ASYSTOLIC ARREST
Pre- Arrest Rhythm Causes of PEA/ Asystole
Bradycardia VasovagalHypoxia
Tension pneumothorax
Auto- PEEP
Hypovolemia
RV dysfunction
Long QT syndrome
Narrow complex tachycardia Tension pneumothoraxAuto PEEP
Hypovolemia
Tamponade
RV dysfunction
Anaphylaxis
Hypoglycemia
Neuraxial block with high level sympathectomy
Electroconvulsive therapy
Local anesthetic systemic toxicity
Tube displacement
Tube obstruction
Equipment failure (eg. O2 gas supply failure)
Auto- PEEP (COPD or acute bronchospasm)
Increased intra- abdominal pressure (laparoscopic surgery, manual
compression of IVC)
Pacemaker failure
Transfusion reaction
CARDIAC DYSRHYTHMIAS 39
Ventricular tachycardia /
Ventricular brillation
RBBB Pulmonary artery hypertension
Q waves Coronary syndrome/ LV dysfunction
Wide QRS complex Hyperkalemia
J or Osborne waves Hypothermia
ST depression/ elevation Coronary syndrome/ LV arrest
Peaked T waves VasovagalHyperkalemia
Flattened T waves Hypokalemia
U waves Hypokalemia
SOURCE: Adapted from Gabrielli A, O’Connor MF, Maccioli GA. Anesthesia advanced
circulatory life support. Comm Crit Care Med. 2008.
Coronary syndrome/ LV dysfunction
40
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As CPR is underway, further diagnostic test-
ing such as serum electrolytes, arterial blood gas, and
TABLE 7.4 ROOT CAUSES OF PEA/ ASYSTOLE
AND ASSOCIATED THERAPIES
blood hemoglobin concentration can be initiated. In
the operating room (OR) setting, transesophageal
echocardiography (TEE) should be relatively easily
obtained and can readily distinguish11 hypovolemia
(both ventricles empty but contractile) from pulmonary embolism (empty left ventricle [LV], dilated and
hypocontractile right ventricle [RV]), and tamponade
(pericardial fluid with systolic RA collapse or diastolic
RV collapse). Outside of the immediate intraoperative
setting an electrocardiogram, chest radiograph, and/ or
transthoracic echocardiogram (TTE) may additionally
be of value. Portable chest radiography can detect the
widened mediastinum characteristic of tamponade and
Hypoxia supplemental O2, advanced airway
Airway obstruction suctioning, beroptic bronchoscopy,
and consider exchange of the airway
Severe volume loss or sepsis empirical IV/ IO crystalloid
Severe blood loss blood transfusion
Presumed pulmonary embolus consider empirical brinolytic therapy
Clinically suspected tension
pneumothorax
Hyperkalemia calcium, Na bicarbonate, insulin/
Hypoglycemia 50% dextrose
needle decompression, chest tube
glucose, albuterol
pneumothorax. In the hands of an experienced echocardiographer, TTE may be able to distinguish hypovolemia, pulmonary embolism, and tamponade similar
to TEE. In addition, TTE can detect the presence of
pneumothorax.12 Rapid diagnostic information allows
Toxin reversal/ antidote for offending agent
SOURCE: Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiovascular life
support: 2010 American Heart Association Guidelines for Cardiopulmonar y Resuscitation
and Emergency Cardiovascular Care. Circulation. 2010;122(SUPPL. 3).
doi:10.1161/ CIRCULATIONAHA.110.970988.
selection of patients for urgent transfer to the cath
lab or radiology department for imaging and therapy,
including pulmonary angiography for embolism, pericardiocentesis for tamponade, and pleural drainage for
tension pneumothorax. In the event of tension pneumothorax, needle thoracostomy for decompression
may be required to maintain ROSC. To perform needle
thoracostomy, a large bore needle (14G or 16G) should
be advanced perpendicular to the skin, superior to the
third rib (second intercostal space) in the midclavicular
line. Attaching the needle to a three- way stopcock and
50- mL syringe partially filled with saline will allow confirmation of pneumothorax. Withdraw on the plunger
as the needle is advanced and a rush of bubbles will con-
WIDE COMPLEX TACHYCARDIA
Wide complex (QRS >120 ms) tachycardias (WCTs) are
primarily of ventricular origin— usually ventricular brillation (VF) or ventricular tachycardia (VT). However, in the
presence of aberrant ventricular conduction or conduction
through an accessory AV pathway (Wol- Parkinson- White
[WPW] syndrome), supraventricular tachycardias (SVT)
will also demonstrate a widened QRS complex. Table 7.5
summarizes the WCTs and their identifying characteristics.
Treatments for sustained WCTs depend on the presence or absence of a pulse, clinical stability, and whether the
rhythm is regular or irregular.
firm access to the air- filled pleural space.13 Therapies
for commonly reversible causes of PEA are detailed
in Table 7.4.
Following ROSC, efforts should focus on continuing the process of obtaining necessary central
venous access and invasive monitoring (if not already
obtained), as well as identifying and controlling the
root cause of cardiovascular collapse. Final surgical and
anesthetic plans should be addressed and, if needed,
transfer to the ICU must be coordinated. Even after
reversal of the root causes of arrest, many post- cardiacarrest patients will require continued infusions of
vasoactive medications to maintain ROSC— proactive
provision of this support should be routine, as it can
avoid return to PEA.
4
Pulseless Wide Complex Tachycardias
As rhythm identication is proceeding, simultaneous assessment must be made regarding presence of a pulse via palpation of carotid, femoral, or radial arteries, observation of the
arterial pressure waveform, and observing for loss of endtidal CO2 or plethysmography. e assessment should take
no more than 10 seconds. A pulseless rhythm (cardiac arrest)
necessitates immediate debrillation and initiation of CPR.
Polymorphic VT is usually associated with pulselessness,
while VF is synonymous with cardiac arrest. In the absence
of data to the contrary (pulsatile arterial waveform or robust
ETCO2), identication of these rhythms on EKG should
immediately signal that the patient is in cardiac arrest. In the
40 PART II. CARDIAC CRISES
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41
TABLE 7.5 IDENTIFICATION AND CHARACTERISTICS OF WIDE COMPLEX TACHYCARDIAS
Rhythm Pulse vs. Pulseless Regular vs. Irregular Identication
Ventricular Fibrillation (VF) Pulseless Irregular Fine ventricular activity without organized QRS complexes
Polymorphic Ventricular
Tachycardia (pVT)
Monomorphic Ventricular
Tachycardia (mVT)
Nonsustained VT Pulse Regular > 3 wide QRS complexes (>120 ms), at a rate > 100 bpm lasting less
SVT with aberrancy Usually with pulse Regular or Irregular Wide QRS complex (>120 ms) with a single QRS morphology. May be
absence of a pulse, immediate delivery of high- energy shock
is indicated. Wide complex tachycardias without a pulse are
the only “shockable” cardiac arrest rhythms, and early debrillation is the most important factor in successful treatment.6
Use biphasic energy starting at 120– 200 J. Debrillation is
delivered in an unsynchronized manner. Place debrillator
electrodes anterior- le lateral (although anteroposterior,
anterior- right- infrascapular, and anterior- le infrascapular
are reasonable placements as well7) (Figure 7.3). It is important for providers to be familiar with debrillator equipment
function prior to an emergency situation.
As the debrillator is being prepared, initiate eective
Usually pulseless,
occasionally with pulses
Usually with pulses,
occasionally pulseless
Irregular Wide QRS complex (>120 ms) rhythm with various QRS morphologies
Polymorphic VT associated with a prolonged QT interval is also known
as Torsades de Pointes (TdP)
Regular Regular wide complex (QRS > 120 ms) rhythm, for >30 seconds with
identical QRS morphologies
Represents 80% of WCT (ref)
than 30 seconds
difcult to distinguish from VT
immediately following debrillation, if ROSC has not
been achieved. As of 2015, bolus vasopressin is no longer
advised for treatment of cardiac arrest.8 If the patient has
not achieved ROSC at the pulse check following administration of epinephrine, debrillation should be applied as
before, followed immediately by administration of amiodarone. e rst dose of amiodarone is a 300- mg IV bolus.
A second dose of amiodarone (150 mg) is given aer 3– 5
minutes if VF/ VT persists. In essence, if the rhythm remains
shockable, each pulse and rhythm check (performed every
2 minutes) is followed by debrillation and then medica-
tion. See Figure 7.1.
chest compressions while minimizing interruptions (for
debrillation and pulse/ rhythm checks only). Use end- tidal
CO2 or arterial catheters, if available, to gauge the ecacy
of chest compressions. Target ETCO2 >20 mmHg and
diastolic blood pressure >30 mmHg.4 Ventilate the patient
with an advanced airway at 8 to 10 breaths/ minute.
Chest compressions must continue for 2 minutes at a
time. Every 2 minutes, a brief pause in chest compression
should be used to assess the rhythm and the presence of
pulses. If a shockable rhythm is still present, chest compressions must immediately restart and the debrillator
is charged. Subsequent debrillation attempts should be
performed at the same or greater energy levels (up to 200 J
of biphasic energy). Once the debrillator is fully charged,
only then should chest compressions be held. With all
hands o the patient, discharge the debrillator and immediately resume chest compression without checking for
a pulse— the pulse will be reassessed aer completion of
another 2- minute round of chest compressions.
Drug therapy should be given at this time and involves
a 1- mg IV bolus of epinephrine repeated every 3– 5 minutes
Figure 7.3 The most typical placement of debrillator pads— anterior and
left lateral. Other acceptable positions are anterior/ posterior, anterior/
right- infrascapular, and anterior/ left infrascapular. SOURCE: Adapted from
“Part 4: The Automated External Debrillator: Key Link in the Chain of Survival.” 2000,
CIRCULATION, 102(Supplement 1), I– 60– I– 76. Copyright by American Heart Association.
Reprinted with permission.
CARDIAC DYSRHYTHMIAS 41
42
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In the case of pulseless polymorphic VT (torsades de
pointes), magnesium sulfate at a dose of 1 to 2 g diluted in
10 mL D5W should also be given as an IV bolus6 in addition to the therapies above. Furthermore, if torsades de
pointes is suspected to be due to a prolonged QT interval,
isoproterenol and overdrive pacing may also have a role.
6
While performing this algorithm, a search should continue to identify and correct immediately reversible causes,
which are oen related to electrolyte imbalances and/ or
acute myocardial ischemia.
15
If the WCT is undierentiated, a debrillator should
be available prior to administering adenosine.6 If SVT with
aberrancy is identied with the administration of adenosine, the rhythm should be treated per the “Stable Narrow
Complex Tachycardia” section. If a ventricular rhythm
is identied, however, verapamil should be avoided, as
it may precipitate profound hypotension in ventricular
arrhythmias.
18
If SVT with aberrancy is not high on the dierential, treatment may proceed with the assumption that the
rhythm is of ventricular origin. For stable regular WCT
Unstable Wide Complex Tachycardia with a Pulse
If, on the other hand, initial assessment reveals that a
pulse is present, but the patient is clinically unstable, then
the rst step is synchronized DCCV. Compressions can
be withheld. IV sedation may be given to the conscious
patient if readily available, but should not delay therapy.
See Figure 7.3 for proper electrode placement. Administer
biphasic synchronized cardioversion starting at 100 J
and increase energy in a stepwise fashion for subsequent
shocks if the rst is unsuccessful9 (up to a maximum of
200 J). Measures should also be taken to treat identied
causes of the unstable rhythm. Acute myocardial ischemia
is commonly associated with WCT
15,16
and following
appropriate treatment of the arrhythmia, denitive diagnosis and treatment of ischemic myocardium is in order.
(usually monomorphic VT), the treatment of choice is
amiodarone, 150- mg IV bolus over 10 minutes followed by
an infusion. A repeat bolus of 150 mg can be given. Dosing
details are outlined in Table 7.6. Procainamide and sotalol
are also options for treatment, but should not be given to
patients with QT prolongation or reduced le ventricular ejection fraction. Fat emulsion (Intralipid) should be
considered therapeutically if ventricular tachycardia is suspected to be due to local anesthetic toxicity. e starting
dose is a 1.5 mL/ kg (lean body mass) bolus of 20% fat emulsion followed by an infusion of 0.25– 0.5 mL/ kg/ min.
19
It should be noted that nonsustained VT (duration less
than 30 seconds) with a pulse, while similar in morphology
to VT, does not carry the same risks. Likewise, isolated premature ventricular contractions (PVCs) occur frequently
(at a rate of about 15%) in the perioperative period20 but are
not denitively associated with worse outcomes. However,
Stable Regular Wide Complex Tachycardia
Clinically stable patients do not require emergency treatment and should be further evaluated as outlined in the
following sections, although appropriate treatment should
not be delayed unnecessarily as even stable WCTs have
the potential to develop into malignant rhythms.17 If the
patient is stable, there is a pulse, and SVT with aberrant
ventricular conduction is known or suspected, administration of adenosine can aid in the identication of the rhythm
prior to denitive treatment. Ventricular rhythms (VT
and VF) do not respond to adenosine. On the other hand,
SVT with aberrancy typically responds with a conversion
to sinus rhythm or slowing of the ventricular rate, allowing
the risk is not zero. ese rhythms are frequently due to
catecholamine excess associated with anesthesia and direct
cardiac manipulation associated with surgery,21 rather than
myocardial ischemia. Due to the lack of evidence that pharmacologic treatment changes outcome, treatment should
focus on measures that reduce myocardial ischemia and
catecholamine stimulation— correct hypoxia, hypercarbia,
acidosis, and electrolyte abnormalities.22 In the absence of
hemodynamic instability or longer runs of VT, treatment
with medications is not warranted.
23,24
If pharmacologic
treatment is desired for instability or in high- risk patients
(reduced LVEF or history of malignant arrhythmias), beta
blockers, lidocaine (100 mg IV bolus), or procainamide are
reasonable choices.
14,21
identication of the underlying atrial activity.
Adenosine MUST NOT be administered to patients with known
or suspected accessory pathways (WPW), or patients with
irregular WCTs.
It may induce fatal ventricular arrhythmias.
42 PART II. CARDIAC CRISES
Stable Irregular Wide Complex
Tachycardia— Treatment
If a WCT is irregular or polymorphic, adenosine is con-
traindicated, as it may precipitate VF.
If a stable irregular monomorphic WCT is encoun-
tered, it should be assumed to be atrial brillation with
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43
TABLE 7.6 PHARMACOLOGIC TREATMENT OF TACHYARRHYTHMIAS
Medication Indications Contraindications Dosing
Adenosine Stable SVT
Stable regular WCT
Diltiazem Stable SVT resistant to adenosine
Atrial brillation/ utter
Verapamil Stable SVT resistant to adenosine
Atrial brillation/ utter
Esmolol Stable SVT resistant to adenosine
Atrial brillation/ utter
Metoprolol Stable SVT resistant to adenosine
Atrial brillation/ utter
Amiodarone Stable irregular SVT (atrial brillation)
Stable regular SVT
Control of ventricular rate in
preexcited atrial arrhythmias
Digoxin Rate control of SVT Ventricular brillation 8 to 12 mcg/ kg loading dose;
Procainamide Hemodynamically stable
monomorphic VT
Preexcited atrial brillation
Irregular WCT
Asthma
Avoid in patients with heart
failure
Contraindicated in patients
with heart failure
Hypersensitivity to beta
blockers
Bradycardia
Hypersensitivity to beta
blockers
Bradycardia
Long- term use:
Pulmonary toxicity
Liver toxicity
2nd- degree or 3rd- degree
heart block
torsades de pointes
SLE
6- mg rapid IV bolus;
may repeat as 12- mg bolus in 2 minutes
IV bolus 0.25 mg/ kg (15 to 20 mg) over 2 minutes;
repeat bolus 0.35 mg/ kg (20 mg to 25 mg) in 15 minutes
if needed;
maintenance infusion of 5 to 15 mg/ hour
IV bolus 2.5 to 5 mg over 2 minutes;
Repeat bolus 5 to 10 mg every 15 minutes if needed
(maximum dose 30 mg)
IV bolus 0.5 mg/ kg over 1 minute;
maintenance infusion of 50 to 300 mcg/ kg/ min
repeat bolus 0.5 mg/ kg over 1 minute if needed
IV bolus 5 mg over 1 to 2 minutes;
repeat 5- mg dose every 5 minutes as needed (maximum
dose of 15 mg)
IV bolus 150 mg over 10 minutes
repeat bolus once if necessary
maintenance infusion of 1 mg/ min infusion for 6 hours,
then 0.5 mg/ min
Total dose over 24 hours ≤ 2.2 grams.
give half of loading dose over 5 minutes
give other half as 25% fractions at 4- to 8- hour intervals
20 to 50 mg/ min or 100 mg IV every 5 minutes until
arrhythmia is controlled, QRS prolonged by 50% of original
width, hypotension occurs, or total cumulative dose of
17 mg/ kg
Sotalol Hemodynamically stable
monomorphic VT
Atrial brillation
SOURCE: Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonar y Resuscitation and
Emergency Cardiovascular Care. Circulation. 2010;122(SUPPL. 3). doi:10.1161/ CIRCULATIONAHA.110.970988.
ventricular preexcitation. is rhythm is particularly insidious due to the high likelihood of inducing malignant ventricular arrhythmias with the use of nodal blocking agents.
Do not administer adenosine, calcium channel blocker,
digoxin, or beta blockers. Attempt electrical cardioversion
if the patient is unstable and seek the assistance of a cardiologist if time permits. Amiodarone or procainamide may
be attempted as pharmacologic treatment
Polymorphic VT is also an irregular WCT, but it
should not be confused with stable irregular monomorphic
WCTs discussed above. Polymorphic VT is characterized
by its variation in the amplitude and morphology of QRS
complexes as compared to the uniform QRS morphology
seen in irregular monomorphic VT. Furthermore, polymorphic VT is most oen pulseless and should always be
treated as VF.
QT prolongation 75 mg IV over 5 hours. However, in clinical studies
1.5mg/ kg infused over 5 minutes
e most common cause of WCT is ventricular tachy-
15,26
cardia,
and monomorphic ventricular tachycardia is
typically due to old myocardial ischemia and related scar.16
Electrolyte imbalances (hypokalemia, hyperkalemia, hypomagnesemia), and medication toxicity (digoxin, local anesthetic, dobutamine, class IA and class III antiarrhythmics)
27
6,25
(Table 7.6).
are other frequent causes.
In the perioperative period, patients with myocardial irritability and remodeling (due to ischemic cardiac
disease) possess a myocardial substrate prone to ventricular arrhythmias. When combined with high catecholamine levels and electrolyte disturbances that commonly
accompany major procedures, the risk of ventricular
tachyarrhythmias in these patients is further increased.27
Attempts should be made to avoid factors that precipitate
myocardial ischemia: hypoxia, hypotension, and anemia.
CARDIAC DYSRHYTHMIAS 43
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Furthermore, patients with a preexisting history of coronary artery disease and congestive heart failure will require
additional vigilance.
Both VF and polymorphic VT are known complications of acute myocardial ischemia,28 hence assessment
and treatment for acute MI should be a high priority, in
addition to a thorough assessment using the mnemonic
of H’s and T’s (Table 7.1) in the setting of cardiac arrest.
Consideration should also be given to the occurrence of
an “R- on- T” phenomenon caused by a premature beat.
Stable monomorphic VT, on the other hand, is oen more
consistent with a reentrant rhythm that occurs around old
myocardial scar.
16
Special mention should be made of prolonged QT
intervals— which represent prolonged ventricular repolarization. A long QT interval increases the risk that subsequent ventricular depolarization will occur during a period
of repolarization. Such events can precipitate VF or polymorphic VT.29 Prolonged QT segments can be a feature
of rare congenital channelopathies (congenital long QT or
Brugada syndromes) but, more commonly, QT prolongation
is drug induced. Preoperative antiarrhythmics and a number
of drugs that are commonly administered in the operating
room (antibiotics, antiemetics, oxytocin) are oen to blame.
A list of such medications is displayed in Box 7.1.52 It is vital
to avoid polypharmacy with QT- prolonging medications in
patients known to be at risk. 12- lead EKG monitoring of
QT intervals is essential in patients with known QT prolongation and a recent or chronic history of dysrhythmia.
Furthermore, IV lidocaine (1.5 mg/ kg bolus) administered
prior to endotracheal intubation, has been shown to reduce
the QT prolongation that can occur with this stimulus in
otherwise healthy patients.
30
Following resolution of wide complex tachyarrhythmias, the immediate goals are to maintain oxygenation, a
stable perfusing rhythm, and adequate perfusion pressure.
is necessitates appropriate airway management, and may
require initiation, repeat bolus, or an infusion of antiar-
BOX 7.1 MEDICATIONS KNOWN TO CAUSE PROLONGATION
OF THE QT INTERVAL
Antiarrhythmics
Dofetilide, Ibutilide, Procainamide, Quinidine, Sotalol,
Amiodarone, Flecainide
Antiemetic
Chlorpromazine, Droperidol, Ondansetron, Granisetron,
Dolasetron
Antimicrobials
Clarithromycin, Erythromycin, Trimethoprim-
Sulfamethoxasole, Azithromycin, Levooxacin, Moxioxacin,
Ketoconazole, Fluconazole, Voriconazole
Antipsychotics
Haloperidol, Ziprasidone, Quetiapine, Risperidone
Bronchodilators
Albuterol
Cardiovascular
Nicardipine (Dopamine, Isoproterenol, Dobutamine,
Epinephrine, Norepinephrine, Phenylephrine, Ephedrine)
Endocrine
Oxytocin
Gastrointestinal
Octreotide
Muscle relaxants
Tizanidine
Narcotics
Methadone (Sefentanil)
Neuromuscular blockers
(Succinylcholine)
Volatile anesthetics
(Sevourane)
SOURCE: Adapted from Barnes BJ, Hollands JM. Drug- induced arrhythmias. Crit Care
Med. 2010;38(6 Suppl):S188– S197. doi:10.1097/ CCM.0b013e3181de112a;
Fazio G, Vernuccio F, Grutta G, Re G Lo. Drugs to be avoided in patients with long
QT syndrome: Focus on the anaesthesiological management. World J Cardiol.
2013;5(4):87– 93. doi:10.4330/ wjc.v5.i4.87.
rhythmic medications. Vasopressor infusions may also be
needed to maintain adequate blood pressure.
Electrolyte imbalances (especially magnesium and
potassium) should be corrected. Steps, such as laboratory
analysis and a 12- lead EKG, must then be taken to denitively assess for the presence of myocardial ischemia, delta
waves, or prolonged QT interval. erapy should be sought
for treatable ischemic causes. ought must also be given to
the need for central venous access, invasive blood pressure
monitoring, TTE, electrophysiological assessment and the
need for ICU admission.
Narrow Complex Tachycardia
Narrow complex tachycardias (QRS complex <120 ms)
originate in, or proximal to, the AV node and the HisPurkinje system. ey are thus referred to as supraventricular tachycardias (SVTs).
Intraoperative and perioperative tachycardia are common,
and the etiologies are numerous. e estimated incidence of
intraoperative SVT is 40.5%, however only 2% of these are
estimated to be severe enough to require signicant therapy.
1
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45
TABLE 7.7 SUPRAVENTRICULAR TACHYCARDIAS AND DEFINING CHARACTERISTICS, LISTED IN ORDER OF FREQUENCY
Rhythm Regular vs. Irregular Pathophysiology Identication
Sinus tachycardia Regular adrenergic stimulation or loss of vagal
stimulation leading to accelerated conduction
through the usual conduction pathways
AV nodal reentrant
tachycardia (AVNRT)
Atrioventricular
reciprocating
tachycardia (AVRT)
Atrial tachycardia Regular Accelerated ectopic atrial pacemaker Appear similar to sinus tachycardia, but P wave
Junctional
tachycardia
Atrial brillation Irregular Disorganized electrical activity of the atrium,
Atrial utter Irregular or Regular
Multifocal atrial
tachycardia (MAT)
SOURCE: Adapted from Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonar y
Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(SUPPL. 3). doi:10.1161/ CIRCULATIONAHA.110.970988.
Regular Reentrant circuit within the AV node P wave usually buried within QRS complex
Regular Accessory pathway connecting atrium and
ventricle. Orthodromic conducts down AV
node with return through the accessory
pathway. Antidromic conduction proceeds
down the accessory pathway with return
through the AV node.
Regular Rare rhythm with accelerated area of
depolarization originating just below the AV
node.
often originating from the pulmonary veins,
with rapid conduction through the AV node
Reentrant focus within the atrium Sawtooth pattern of atrial activity at 300 bpm. QRS
(if there is variable
AV nodal conduction)
Irregular Rare condition with various ectopic atrial foci
that rapidly depolarize in a spontaneous and
unpredictable manner
Usually <140, unless young healthy patient.
1:1 P to QRS association.
Normal P wave axis (up in II and biphasic in V1)
P wave is inverted due to excitation from the
ventricle and is usually after the QRS complex.
Orthodromic conduction features a narrow QRS
complex. Antidromic conduction (less common)
produces a wide QRS complex
axis is abnormal
P wave is inverted due to excitation from the
ventricle and is usually after the QRS complex.
Irregular QRS rhythm, brillation and/ or absence
of P waves
rate usually occurs 150 bpm.
Irregular rhythm. P waves with at least three
distinct morphologies
e various narrow complex tachycardias and their
dening characteristics can be seen in Table 7.7. Each SVT
diers from others in terms of refractoriness, recurrence,
and response to pharmacologic therapy. However, the
pharmacological treatment of narrow complex tachycardia
focuses primarily on AV nodal blockade and hence is surprisingly homogeneous across the various SVTs despite the
fact that the arrhythmogenic foci derive from anatomically
dierent locations. For this reason, it is not always necessary to identify the exact rhythm to achieve successful treatment. In fact, exact rhythm identication can be elusive due
to the rapidity of the rhythms and the associated fusion of
P, QRS, and T waves.
cardioversion, while stable patients should be treated
without cardioversion.
At rates >150 bpm, SVT can oen cause hemodynamic compromise.6 If at any point in treatment a patient
becomes unstable (acute altered mental status, shortness of
breath, new- onset chest pain, hypotension, loss of ETCO2
and SaO2 waveform, or signs of shock), electrical cardioversion must be immediately attempted.
Synchronized direct current cardioversion (DCCV) is
the treatment of choice for all unstable SVTs, regardless of
the regularity of the rhythm. If readily available, IV sedation can be administered to the conscious patient, but this
should not delay therapy. Debrillator electrodes should
be placed as depicted in Figure 7.3. e anterior- le lateral
Unstable Supraventricular Tachycardia Treatment
e treatment of SVT with a pulse is distinguished based
on clinical stability, and whether the rhythm is regular
or irregular. e approach to narrow complex tachyarrhythmias begins with an assessment of the patient’s
stability. Unstable patients require rapid synchronized
electrode position is most commonly chosen.
Equipment should be synchronized to avoid delivering energy during the myocardial refractory period. With
unstable atrial brillation, initiate cardioversion with
biphasic energy at 120 to 200 J. All other SVTs should be
initiated at 50 to 100 J. If initial cardioversion attempts
are unsuccessful, energy must be increased in a stepwise
CARDIAC DYSRHYTHMIAS 45
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