Management of Arrhythmias in The Cardiovascular Intensive Care Unit

Management of Arrhythmias
in t he C a rd i o vas c u l ar
In t en si ve C are U n it
Brent Klinkhammer, MD, PharmDa,b,
Taya V. Glotzer, MD, FHRS, FACCa,b,*
KEYWORDS
Atrial fibrillation ICU Ventricular tachycardia Bradycardia Arrhythmia
KEY POINTS
Arrhythmias are common in the cardiovascular intensive care unit and are challenging to
manage given patient complexity and completing clinical interests.
Strategies such as identifying high-risk patient characteristics, choosing optimal medica-
tions, and effective hemodynamic/electrolyte management can reduce the risk of
arrhythmias.
Making the correct arrhythmia diagnosis is done by combining knowledge of the patient’s
clinical problems with the review of electrocardiogram tracings.
If there is hemodynamic instability, all tachyarrhythmias should undergo cardioversion.
If there is hemodynamic instability, all bradyarrhythmias should be treated with internal or
external pacing.
INTRODUCTION
Tachyarrhythmias and bradyarrhythmias are frequently encountered in the cardiovas-

cular intensive care unit (CVICU) and range from benign to life-threatening. Arrhyth-
mias can be challenging to manage due to the patient’s critical condition, the need
for treatment of the primary illness, and preexisting comorbidities. In this article, the
authors outline a pragmatic approach to the assessment and management of arrhyth-
mias seen in the CVICU.
GENERAL CONSIDERATIONS
All patients admitted to the CVICU are at an elevated risk of arrhythmia compared
with other inpatients. Risk factors include structural heart disease, ischemic heart
a
Division of Cardiac Electrophysiology, Hackensack University Medical Center, Hackensack, NJ
07601, USA; b Hackensack Meridian School of Medicine, Hackensack, NJ 07601, USA
* Corresponding author. Hackensack Meridian School of Medicine, Hackensack University Med-
ical Center, 20 Prospect Avenue, Suite 615, Hackensack, NJ 07601, USA
E-mail address: taya.glotzer@hmhn.org
Crit Care Clin 40 (2024) 89–103

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90 Klinkhammer & Glotzer
disease, obesity, obstructive sleep apnea, and substance abuse.1–3 A comprehensive

approach to all patients is imperative to assess the patient-specific factors which may
prompt arrhythmia prevention measures, provide insight into the etiology of arrhyth-
mias if they occur, and guide arrhythmia management strategies.
Every patient should have a thorough review of their medical records to ascertain
the presence of left or right ventricular dysfunction, coronary artery disease (CAD),
prior myocardial infarction (MI), thyroid disorders, arrhythmia syndromes, or history
of therapies for arrhythmia such as antiarrhythmic therapy, cardioversion, or prior
ablation. A thorough review of the patient’s medications is important, as it is common-
place for patients to receive one or more QTc-prolonging medications (antiemetics,
antibiotics, antipsychotics, and others). Other factors that increase the risk of QTc
prolongation include advanced age, female sex, heart failure (HF), acute coronary syn-
drome (ACS), and electrolyte abnormalities.4 Patients who have rhythm disturbances
and have a permanent pacemaker (PPM) or implantable cardioverter-defibrillator (ICD)
should have their device interrogated to ensure normal device function, review saved
arrhythmia events (may suggest an etiology of the patient’s presenting illness), and
ascertain any prior device-delivered therapies.
A high-quality 12-lead electrocardiogram (EKG) should be obtained in all patients
and compared with prior tracings; particular attention should be paid to evidence of
prior infarction, QRS and QT intervals, and EKG patterns suggestive of arrhythmia syn-
dromes such as Brugada, arrhythmogenic right ventricular dysplasia, or Wolff–Parkin-
son–White (WPW).5,6
Continuous cardiac telemetry is indicated in all CVICU patients. A common problem
with cardiac telemetry is frequent alarms for non-clinically significant arrhythmias and
provider “alarm fatigue.”7 Nuisance alarms can be avoided with proper and secure
lead placement. Studies have shown that suboptimal telemetry, leading to erroneous
interpretation, can result in unnecessary and potentially harmful interventions.8
Management of electrolytes is another opportunity to reduce the proarrhythmic
milieu of CVICU patients. Electrolyte abnormalities, such as hypokalemia and hypo-
magnesemia, are proarrhythmic; hypokalemia is frequently observed in patients
with documented ventricular tachycardia (VT) or ventricular fibrillation (VF).9 Previous
studies have shown that the lowest risk of ventricular arrhythmias in patients with ACS
and acute HF is when potassium is maintained more than 4.5 mmol/L.10
Sympathomimetic agents can be proarrhythmic and they should be used judi-
ciously.11 Inotropic therapy may exacerbate arrhythmias, including VT, and therefore,
the use of short-term mechanical circulatory support to reduce the need for inotropes
may be beneficial in selected cases.12
Atrial Fibrillation
The most common arrhythmia encountered in the CVICU is atrial fibrillation (AF) rep-
resenting approximately 19% of all arrhythmias (5–10% is “new onset” AF). AF is an
independent predictor of mortality in critically ill patients.13–16 Atrial contraction con-
tributes 25% of ventricular end-diastolic volume in the normal heart; therefore, the
loss of atrial contractility in the setting of critical illnesses (ACS, acute HF, shock, post-
operative vasoplegia) is more likely to be of hemodynamic significance.17 AF can be
the primary reason for impaired hemodynamics, or AF can be secondary to other med-
ical conditions; both need to be addressed during treatment. Factors that trigger AF,
such as hypervolemia, sympathetic excess (including medications), inflammation,
hypoxia, and anemia should be corrected if possible.18 Urgent synchronized direct
current cardioversion (DCCV) is indicated when there is hemodynamic compromise,
active ischemia/angina, CHF, or refractory symptoms.17
reservados.
Arrhythmias in the ICU 91
In the hemodynamically stable patient, rate control should be planned first.

Restoring sinus rhythm can be attempted several days or weeks later, once the critical
condition has improved. Stroke risk should be evaluated by calculating a CHA₂DS₂-
VASc score and if the score is 2 in men or 3 in women, stroke prophylaxis with
therapeutic anticoagulation should be initiated if not otherwise contraindicated.19
Rate control
Given the common comorbidities of CVICU patients including a high prevalence of
CAD and systolic HF, beta blockers are the first drugs of choice, because they opti-
mize the management of both conditions. Beta-blockade is also associated with lower
mortality for a wide range of critically ill patients.20 Short-acting, cardioselective, intra-
venous (IV) beta blockers such as metoprolol or esmolol are first line given their min-
imal proarrhythmic effects and ease of titration. Nondihydropyridine calcium channel
blockers (CCBs) such as diltiazem are commonly used outside of the CVICU (class I
indication for rate control in the current guidelines) but are often contraindicated in
CVICU patients, given the high prevalence of systolic dysfunction.17 However, in
selected stable CAD and postoperative patients with normal systolic function, CCBs
are an attractive option for IV rate control.21
Current guidelines give a class IIa recommendation for the use of IV amiodarone for
rate control in critically ill patients.17 Amiodarone has properties of all four Vaughan-
Williams classification of anti-arrhythmic drugs and may be effective in cases refrac-
tory to first-line rate control medications.22,23 The onset of action of amiodarone is
delayed when compared with beta blockers or CCB, making it less useful when rapid
rate control is imperative such as in acute ischemia.24,25 Amiodarone has minimal con-
traindications, can be used in a wide range of cardiac patients, and is less proarrhyth-
mic than other anti-arrhythmic drugs. Although there is a theoretical risk of torsades de
pointes (TdP) from amiodarone, it is rarely seen in clinical practice.26 When a patient
has been in AF for an unknown duration and has not been anticoagulated, there is
at times hesitancy to use amiodarone given the potential risk of stroke with possible
pharmacologic cardioversion.
Digoxin is another option that, like amiodarone, has few absolute contraindica-
tions in a broad range of cardiac patients. Digoxin has a role as adjunctive therapy
to beta blockers for rate control, especially in patients with HF or low blood pres-
sure. In the AFFIRM trial, the combination of beta blocker and digoxin was the most
effective two-drug combination for rate control.27 When used alone, digoxin has
consistently shown to be less effective than beta blockers for acute rate control,
and there are questionable associations of digoxin and increased mortality in
CHF patients.28,29
AF in the CVICU, in the post-cardiac surgery, and in the post-noncardiac surgery
setting is recurrent greater than 50% of the time, therefore dismissing AF as “pro-
voked” or “situational” should be avoided.30,31 A recent study using implantable
loop recorders found that in 70% of patients with AF after cardiac surgery, the AF
reoccurs after discharge.31 Therefore, continued stroke prevention therapy with anti-
coagulation should be considered.
Atrial Flutter
Atrial flutter is the second most common atrial arrhythmia seen in CVICU patients.
Atrial flutter often presents with very rapid ventricular rates, when 2:1 atrioventricular
(AV) conduction is present (Fig. 1). Ventricular rate control can be difficult to achieve
during atrial flutter, and high doses of rate control medications are often needed,
which increase the risk of hypotension. If hypotension occurs, atrial flutter can be
reservados.
Narrow Complex Tachycardia
Yes
Hemodynamic Instability, Angina, or Developing HF? Immediate DCCV
No
Regular or Irregular Rhythm?
Regular Rhythm Irregular Rhythm
Supraventricular Tachycardia Atrial Fluer Atrial Fibrillaon
Vagal Maneuvers or Rate Control and Rate Control and

Adenosine Ancoagulaon Ancoagulaon
(Classically diﬃcult to (Consider inial rhythm
Unsuccessful Successful rate control) control in select cases)
Consider Beta-blocker, Consider Fails Fails

CCB, or DCCV Beta-blocker or
CCB to Suppress DCCV DCCV
Further Episodes
If Cardioversion Consider Anarrhythmic (usually

amiodarone) for Rhythm Control
Fig. 1. Simplified approach to the initial management of narrow complex tachycardia.
managed with DCCV; atrial flutter is exquisitely sensitive to DCCV with as little as 50 J
of synchronized energy required.32
Atrial flutter is associated with a comparable stroke risk to AF; therefore, a similar
assessment for anticoagulation should be performed.33 Cardiac electrophysiology
(EP) consultation for definitive management with catheter ablation should be consid-
ered for all patients with atrial flutter. Studies have suggested improved survival in pa-
tients who undergo ablation for new-onset atrial flutter during their index
hospitalization; this seems to be especially true in the setting of systolic HF.34,35
Atrial Fibrillation Post-Cardiac Surgery
AF following cardiac surgery is observed in 20% to 40% of patients and is associated
with worse outcomes.36 The most robust evidence for preventing AF after cardiac sur-
gery is with preoperative initiation of oral amiodarone. One study demonstrated a 53%
relative risk reduction in AF incidence, shorter length of stay, and lower health care
costs with oral amiodarone started at least 7 days before elective surgery.37 Postop-
erative initiation of beta blockers or amiodarone is also effective at preventing AF;
however, the benefits of shortening the length of stay are less clear than with preop-
erative initiation.38,39
Another strategy to suppress post-cardiac surgery AF is overdrive atrial pacing;
however, there is conflicting evidence of the true benefits of this prophylactic treat-
ment.38–40 Epicardial injection of botulinum toxin has been evaluated for prevention
of post-cardiac surgery AF, but this strategy does not seem to significantly impact
AF occurrence.41 Finally, the postoperative initiation of colchicine is effective at sup-
pressing short-term (<30 days) post-cardiac surgery AF, shortening the length of stay,
reservados.
and suppressing longer term postpericardiotomy syndrome, but side effects limit its
use in all patients.42,43
There is limited evidence to guide the management of anticoagulation for AF post-
cardiac surgery, but patient-specific factors including CHA₂DS₂-VASc score and
bleeding risk should be evaluated, and anticoagulation started if permissible.
Supraventricular Tachycardia
Atrial-dependent arrhythmias
Atrial premature complexes (APCs) are commonly seen in the critically ill and can be a
precursor to the onset of AF.44 If hemodynamics and clinical circumstances allow,
frequent APCs can be suppressed with beta blockers or CCB, although their efficacy
to prevent AF had not been proven.44
Atrial tachycardia (AT) is occasionally seen in the CVICU, especially in intubated pa-
tients or those with underlying pulmonary disease. Focal AT can result from enhanced
automaticity, triggered activity, or reentrant mechanisms and may or may not respond
to adenosine (the latter mechanism being the most likely to respond).45,46 Unifocal AT
and multifocal AT can be rapid and difficult to treat as beta blockers are often contra-
indicated in patients with significant pulmonary disease. Most AT will not respond to
cardioversion because they are driven by automaticity and will recur. Medical options
for treatment include CCBs and amiodarone.46
Atrioventricular node-dependent arrhythmias
AV nodal reentrant tachycardia (AVNRT) is a reentry supraventricular tachycardia
(SVT) using two electrical pathways in the AV node and is the most common SVT in
adults (>50%).45,46 EKG often shows a short R-P interval that is usually less than
70 milliseconds. Sometimes, the P wave is not seen at all, and the arrhythmia may
look like rapid junctional tachycardia. Standard treatment starts with vagal maneuvers
(which may not be possible in CVICU patients) and administration of adenosine.46 (see
Fig. 1). Any SVT that causes hemodynamic instability should be treated with synchro-
nized DCCV. Medications for the prevention of AVNRT include beta blockers and
CCB.46
Preexcitation syndromes and accessory pathways
Syndromes of early activation of ventricular (WPW and Lown–Ganong–Levine) are
infrequently encountered in both clinical practice and the CVICU, but it is important
to understand their implications. The most clinically important of these is WPW, which
can cause reentry SVT and is associated with an increased risk of AF (10–30%).47
Orthodromic AV reciprocating tachycardia (AVRT) (narrow complex; antegrade con-
duction down AV node and retrograde conduction up the accessory pathway [AP]) or
antidromic AVRT (usually wide complex; antegrade conduction down the AP and retro-
grade conduction via the AV node) can be treated with adenosine which will transiently
block conduction in the AV node, an obligatory component of these arrhythmias.46
The most feared complication of WPW is anterograde conduction of atrial impulses
during AF down a rapidly conducting AP leading to a very rapid ventricular response
which can degenerate into VF.17 AV nodal blocking agents, especially CCBs and
digoxin, are contraindicated for AF with ventricular preexcitation because they can
direct the atrial impulses preferentially down the AP, making the risk of VF
higher.17,48,49 In stable patients, IV procainamide or ibutilide can be used to slow con-
duction over the AP and potentially terminate AF.17 In an unstable patient in AF with
preexcitation, DCCV is recommended.17 Finally, EP consultation is reasonable to
establish follow-up care for any patient with SVT, as potentially curative ablation pro-
cedures can be considered.50
reservados.
Wide Complex Tachycardia

Wide complex tachycardias (WCTs) are often intimidating for physicians because it is
frequently difficult to distinguish VT from SVT with aberrancy (Fig. 2). Regardless of the
etiology, cardioversion/defibrillation is indicated in the setting of hemodynamic insta-
bility. In a stable patient, steps to determine the mechanism of the arrhythmia and
guide treatment include evaluation of the baseline and current EKG, assessing the pa-
tient’s clinical history, and reviewing telemetry from prior sustained or non-sustained
arrhythmia episodes. Multiple approaches have been described to diagnose WCT
based on EKG characteristics; AV dissociation is the most specific EKG parameter
to confirm VT (Fig. 3).51–53 The most common cause of WCT in CVICU is VT, as a his-
tory of prior MI, CAD, or HF suggests VT with a very high probability.54
In a stable patient with an uncertain arrhythmia etiology, the administration of aden-
osine can be considered and may terminate the WCT if SVT with aberrancy is present.
The use of lidocaine or amiodarone is also reasonable, recognizing that an apparently
stable patient may decompensate rapidly either owing to the duration of the rhythm or
the hemodynamic effects of drugs.46,55,56 In contrast to regular WCT which is usually
VT, irregular WCT is rarely VT; diagnoses to consider for irregular WCT are AF with
aberrant conduction or AF with ventricular preexcitation.
Ventricular Arrhythmias
Ventricular premature complexes
Ventricular premature complexes (VPCs) are common and have multiple causes
including electrolyte abnormalities, hyperadrenergic state, sympathomimetics,
ischemia, and acute HF.55,57 Treatment of the underlying illness is crucial and beta
blockers can be used adjunctively if clinical circumstances allow.55 It should be noted
that prophylactic attempts to suppress VPCs or non-sustained ventricular tachycardia
in the post-MI period with class Ic or class III antiarrhythmics are harmful.58
Monomorphic ventricular tachycardia
Monomorphic VT is usually due to a reentrant mechanism around a scar from a prior
infarction, or less commonly can be due to nonischemic or infiltrative cardiomyopathies.55
Wide Complex Tachycardia
Yes
Hemodynamic Instability, Angina, or Developing HF ? Immediate DCCV
No
VT versus SVT with Aberrancy?

(High likelihood of VT with history of prior MI, CAD, or HF;
therefore treat as VT if diagnosis remains uncertain)
SVT with Aberrancy Monomorphic or Polymorphic VT
Irregular Rhythm Regular rhythm Monomorphic VT Polymorphic VT
Revasculariza on
Yes Lidocaine
AF Without Preexcita on AF with Preexcita on Likely AVNRT, Atrial IV Amiodarone Acute Coronary Syndrome??
Beta-blocker
Flu er, AVRT, or AT IV Lidocaine Amiodarone
DCCV No
Rate control Consider Early DCCV Likely Torsades de Pointes

DCCV Procainamide Adenosine
Ibu lide Rate control Amiodarone
(Avoid beta-blocker, DCCV Beta-blocker
CCB, digoxin, Magnesium
adenosine, and Overdrive Pacing
amiodarone) Isoproterenol
Stop Oﬀending Agent(s)
Fig. 2. Simplified approach to the initial management of wide complex tachycardia.

reservados.
AV Dissocia on
Precordial Concordance
Presence of an Ini al R-wave in Lead aVR
Presence of Fusion Complexes
QRS Width >140 milliseconds with a RBBB

Morphology or >160 milliseconds with a
LBBB Morphology
Notching on the Ini al Downstroke of a

Predominantly Nega ve QRS Complex in
Lead aVR
“Rabbit Ear” Complex (RR') with R Wave

Wider than R’
Fig. 3. Selected EKG criteria that distinguish ventricular tachycardia from other wide com-
plex tachycardias.
Once VT is terminated, a comprehensive evaluation to determine the etiology of VT, and

consideration of strategies to prevent VT recurrence should be undertaken. Predispos-
ing conditions such as myocardial ischemia, low cardiac output, electrolyte abnormal-
ities, medication side effects, and comorbid conditions should be addressed. Medical
therapies to prevent recurrent VT are beta blockers, amiodarone, or sotalol, the latter of
which is contraindicated in systolic HF.55 Lidocaine is an attractive option for ACS-
related VT; however, it is less effective as monotherapy for scar-based VT.55,59 In a pa-
tient with recurrent VT poorly responsive to medication, mechanical circulatory support
to unload the ventricle can be used. There is also growing evidence to support prompt
VT ablation for refractory monomorphic VT.60–62 VT ablation is particularly attractive in
patients who have mechanical circulatory support devices already in place as this may
help facilitate a successful VT ablation.63
Polymorphic ventricular tachycardia/torsades de pointes

Polymorphic VT (PMVT) has different and more life-threatening etiologies than mono-
morphic VT.55 Myocardial ischemia is the most common cause of PMVT, but other
causes include electrolyte disturbances, HF, bradycardia, long QT (acquired or
congenital), Brugada syndrome, and catecholaminergic PMVT.55 PMVT in the setting
of long QT duration is known as TdP and first-line treatment is directed at managing
the etiology of the QT prolongation.
Treatment of PMVT will vary depending on the etiology. First-line treatment of PMVT
with hemodynamic stability is a rapid bolus infusion of IV magnesium.55 Lidocaine is
the drug of choice for ischemic PMVT as studies have shown that the altered electrical
properties of ischemic myocardium enhance lidocaine binding making it particularly
effective in this setting.64 Revascularization should be performed as soon as possible.
Beta blockers should be used in the absence of cardiogenic shock or bradycardia.65
Pacing, external or internal, can be implemented for bradycardia-induced TdP, and
reservados.
pacing can be used for long QT (acquired or congenital) TdP.66 If pacing is not imme-
diately available, isoproterenol can be used if hemodynamics allow.67,68 Electrolyte
replacement is indicated in all cases.
Electrical storm/ventricular fibrillation
Electrical storm is defined as 3 episodes of sustained VT, VF, or appropriate shocks
from an ICD within 24 hours.55 Causes include ischemia, acute HF/shock, or hyperac-
tivation of a scar-related or automatic VT.55
Amiodarone is the first-line antiarrhythmic for electrical storm given its electrophys-
iological properties and relative lack of contradictions.69 Adjunctive use of other anti-
arrhythmics including beta blockers, lidocaine, and procainamide can be considered if
amiodarone fails and hemodynamics permit.69 A recent study showed that the nonse-
lective beta blocker propranolol was more efficacious than metoprolol in combination
with amiodarone in suppressing VT/VF storm.70 Intubation and sedation can also be
effective to treat VT storm.71,72 Finally, neuraxial blockade to reduce sympathetic
outflow via stellate ganglion blockade may be considered in refractory cases.73–75
ACCELERATED IDIOVENTRICULAR RHYTHM
Accelerated idioventricular rhythm (AIVR) is an ectopic ventricular rhythm usually at a

rate of 40 to 100 BPM. It is due to automaticity and can occur any time there has been
myocardial injury; commonly post-MI or post-cardiac surgery.76,77 AIVR occurs in
nearly half of all patients with ST-elevation MI.76,77 AIVR is a benign, self-limited
rhythm and resolves with revascularization or as the myocardial injury heals. Manage-
ment is observation in most cases, but it can be treated with beta blockers if suppres-
sion is warranted.
BRADYARRHYTHMIA
Bradyarrhythmias are caused by dysfunction of the sinus node or AV conduction

(Fig. 4). Bradycardia can develop from acute insults (ACS, electrolyte derangements,
or post-cardiac intervention) or exacerbation of a chronic process (infiltrative disease,
conduction system fibrosis).78,79 Bradycardia can also be secondary to medications,
sleep apnea, hypothermia, high vagal tone, or increased intracranial pressure.78,80,81
Bradycardias can be transient, commonly due to vagal nerve activation such as during
suctioning or turning, and should be recognized as a secondary event that does not
require primary treatment.
Sinus Node Dysfunction

Sinus node dysfunction will often resolve with clinical observation on telemetry, drug
washout, and/or correction of underlying etiologies (ischemia, acidosis, and hypox-
ia).78 IV dopamine can be used transiently to support sinus node function if needed.78
When sinus node dysfunction does not resolve and causes symptoms or hemody-
namic instability; pacing is indicated. Sinus bradycardia can be seen following cardio-
version of persistent AF secondary to suppression and remodeling of the sinus
node.82,83 This cause of bradycardia often resolves over hours to days and may not
require long-term pacing.82
Atrioventricular Block
Second-degree AV block is benign when it occurs in the AV node but often requires
pacing if the block is infra-nodal. EP study is indicated if the level of block is not clear.
AV block due to acute ischemia can occur in the CVICU, and knowledge of the
reservados.
Bradyarrhythmia
Yes
Acute Ischemia?
a? Revasculariza on and Ini a on of Pacing
Re
No
Type of Bradycardia
Sinus Node Second Degree AV Complete Heart

Dysfunc on Block Block
Symptoms or Asymptoma c Wide Complex Narrow Complex Rhythm/Escape Wide Complex

Hemodynamic Rhythm Escape
Instability
Close Asymptoma c Symptoms or

Observa on Close Hemodynamic Urgent Pacing
Dopamine Observa on Instability
with Plan for
Fails PPM Close
Observa on
Ini a on of Dopamine
Pacing
Fails
Ini a on of
Pacing
Fig. 4. Simplified approach to the initial management of bradyarrhythmias.
patient’s coronary anatomy is critical in determining management. Ischemia of the

right coronary artery which supplies the AV node can cause second or third-degree
AV block, which can be transient.84,85 AV nodal block is usually responsive to atro-
pine.78 AV block due to left anterior descending artery (LAD) ischemia is usually
infra-nodal and will either fail to respond or worsen with atropine.78 AV block caused
by LAD ischemia rarely resolves with revascularization and pacing is often indicated.86
Complete heart block (CHB) is the most life-threatening type of bradyarrhythmia.
Patients with CHB should be evaluated for potentially reversible causes such as acute
ischemia or Lyme disease. Routine blood chemistry, thyroid function, and Lyme serol-
ogies are indicated in all patients.78 If reversible causes are not found, permanent pac-
ing for CHB is indicated. Asymptomatic CHB with a narrow junctional escape can be
observed on telemetry until permanent pacing can be arranged, whereas CHB with a
wide QRS escape should be referred urgently for temporary or permanent pacing.78
External pacing can be used temporarily while awaiting internal pacing if a patient is
hemodynamically unstable.78 Ventricular capture can be difficult to confirm during
external pacing because telemetry tracings are markedly distorted by the large pacing
artifact; monitoring the pulse or the pulse oximetry tracing is a good way to confirm
ventricular capture.
Transient or permanent AV block following cardiac surgery is frequently seen; there-
fore, the placement of temporary epicardial pacing wires at the time of surgery has a
class I recommendation for most procedures.78,87 Older age, multivalve operations,
and preexisting conduction system disease are risk factors for postoperative bradyar-
rhythmias.88,89 AV block following transcatheter aortic valve replacement (TAVR) is
also common, with a 10% to 15% requirement for PPM.90 Pre-op assessment of
reservados.
the risk of conduction system injury following TAVR can be done by examining pre-op
EKG parameters; the highest risk features are first-degree AV block and right bundle
branch block.90
SUMMARY
Cardiac arrhythmias are common in the CVICU and can be the primary reason for
admission to the CVICU or a secondary consequence of the critical condition. Suc-
cessful management of arrhythmias requires a systematic approach, ability to inter-
pret EKG tracings, and sound clinical decision-making. Much of our understanding
of arrhythmias in this population has been gained from non-CVICU populations, and
more research is needed to fully elucidate the optimal strategies for arrhythmia man-
agement in the critical care setting.
FUNDING
None.
DISCLOSURES
No authors report conflicts of interest to declare.
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Management of Arrhythmias in The Cardiovascular Intensive Care Unit

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Management of Arrhythmias in The Cardiovascular Intensive Care Unit

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Management of Arrhythmias

Tachyarrhythmias and bradyarrhythmias are frequently encountered in the cardiovas-

Crit Care Clin 40 (2024) 89–103

disease, obesity, obstructive sleep apnea, and substance abuse.1–3 A comprehensive

In the hemodynamically stable patient, rate control should be planned first.

Narrow Complex Tachycardia

Regular or Irregular Rhythm?

Regular Rhythm Irregular Rhythm

Supraventricular Tachycardia Atrial Fluer Atrial Fibrillaon

Vagal Maneuvers or Rate Control and Rate Control and

Consider Beta-blocker, Consider Fails Fails

If Cardioversion Consider Anarrhythmic (usually

Fig. 1. Simplified approach to the initial management of narrow complex tachycardia.

Wide Complex Tachycardia

Wide Complex Tachycardia

VT versus SVT with Aberrancy?

SVT with Aberrancy Monomorphic or Polymorphic VT

Irregular Rhythm Regular rhythm Monomorphic VT Polymorphic VT

Rate control Consider Early DCCV Likely Torsades de Pointes

Fig. 2. Simplified approach to the initial management of wide complex tachycardia.

Presence of an Ini al R-wave in Lead aVR

Presence of Fusion Complexes

QRS Width >140 milliseconds with a RBBB

Notching on the Ini al Downstroke of a

“Rabbit Ear” Complex (RR') with R Wave

Once VT is terminated, a comprehensive evaluation to determine the etiology of VT, and

Polymorphic ventricular tachycardia/torsades de pointes

ACCELERATED IDIOVENTRICULAR RHYTHM

Accelerated idioventricular rhythm (AIVR) is an ectopic ventricular rhythm usually at a

Bradyarrhythmias are caused by dysfunction of the sinus node or AV conduction

Sinus Node Dysfunction

Sinus Node Second Degree AV Complete Heart

Symptoms or Asymptoma c Wide Complex Narrow Complex Rhythm/Escape Wide Complex

Close Asymptoma c Symptoms or

Fig. 4. Simplified approach to the initial management of bradyarrhythmias.

patient’s coronary anatomy is critical in determining management. Ischemia of the

No authors report conflicts of interest to declare.

13. Artucio H, Pereira M. Cardiac arrhythmias in critically ill patients: epidemiologic

70. Chatzidou S, Kontogiannis C. Propranolol versus metoprolol for treatment of elec-

Descargado para Anonymous User (n/a) en Technological University of Pereira de

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