Arrhythmias In The ICU

Frederik Meijer Heart & Vascular Institute
Arrhythmias in the ICU:
A Practical Approach
Nagib Chalfoun, MD, FHRS
Chair, Education
Cardiac Electrophysiology
Spectrum Health Cardiovascular Services/Medical Group
Program Director, Cardiology Fellowship
GRMEP/Michigan State College of Human Medicine
Assistant Professor of Medicine
Michigan State College of Human Medicine

Outline:
 Atrial fibrillation/Atrial flutter
 Wide Complex Tachycardia
 Bradycardia
 SVT

Atrial Fibrillation/Atrial Flutter:
Rate or rhythm control?
■ Options for rate control
■ Options for rhythm control
■ Anticoagulation: understanding the CHADS VASc score

ACC Guidelines1 Definition
Paroxysmal AF: If the arrhythmia terminates spontaneously,
and lasts less than 7 d, usually less than 24 hours.
Persistent: More than 7 days
■ termination with pharmacological therapy or DC cardioversion does
not change the designation – although often used that way.
Permanent AF: often arbitrary but refers to AF where
cardioversion has failed or deemed inappropriate/not
attempted.
Recurrent AF: 2 or more episodes.
“Lone AF”: young individuals (under 60 y of age) without
clinical or echocardiographic evidence of cardiopulmonary
disease.
1. Fuster et al. JACC Vol. 48, No. 4, 2006

e) thr
Afib:

Afib or Flutter?
6

Afib or Flutter?
7

First Question: Stable or Unstable?
If Unstable: the answer is the easiest of the management
strategies
**********DC CARDIOVERSION************
Signs of Unstable Patient:
• Hypotension
• CHF/respiratory compromise
If Stable: More complicated...
8

Unstable Afib: Think outside the box
• Afib alone rarely causes hypotension unless other underlying
issues are present or 1:1 Atrial flutter
• Think of the following:
• Severe LV dysfunction
• Pulmonary Embolism
• Severe valvular disease: AS/MS/Acute MR OR AI
• Hypovolemia
• Sepsis
9

After Cardioversion:
• Consider Loading with amiodarone to avoid Afib recurrence
if patient was hemodynamically unstable or has recurrent
Afib complicating management.
• Bolus IV amiodarone over 30 minutes causes less hypotension then
over 10 minutes
• Amiodarone should be used as temporary measure ideally
and If no contraindications such as :
• Pulmonary fibrosis
• Liver failure from amiodarone in past
• Hyperthyroidism from amiodarone
10

Rhythm or Rate Control: The Big Question
Randomized clinical trials to date have shown no significant difference
with respect to mortality, major bleeding, and thromboembolic events,
at least on an intention-to-treat analysis.
 1) Hohnloser et al. Rhythm or rate control in atrial fibrillation—Pharmacological Intervention in Atrial
Fibrillation (PIAF): a randomized trial. Lancet 2000; 356: 1789–94.
 2) Van Gelder IC, et al; Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation
Study Group. A comparison of rate control and rhythm control in patients with recurrent persistent
atrial fibrillation. N Engl J Med 2002; 347:1834–40.
 3) The AFFIRM Investigators. A comparison of rate control and rhythm control in patients with atrial
fibrillation. N Engl J Med 2002; 347: 1825–33.
 4) Carlsson J, et al; STAF Investigators. Randomized trial of rate-control versus rhythm-control in
persistent atrial fibrillation: the Strategies of Treatment of Atrial Fibrillation (STAF) study. J Am Coll
Cardiol 2003; 41: 1690–96.
 5) Opolski G, et al; Investigators of the Polish How to Treat Chronic Atrial Fibrillation Study. Rate
control vs rhythm control in patients with nonvalvular persistent atrial fibrillation. The results of the
Polish How to Treat Chronic Atrial Fibrillation (HOT CAFÉ) study. Chest 2004; 126: 476–86.
In Stable Patients:

So how do we decide?
Remember limitations of the major randomized trials:
■ older patients (60-70 yo)
■ relatively short period of follow up time
■ analyzed on intention to treat in general.
Consider patients in the real world on individual basis:
■ Symptoms: many patients may not realize their degree of symptoms from AF
until they are cardioverted to SR. If symptomatic then rhythm control is the
strategy.
■ Age: the older the more favor towards rate control
■ Consider Long term outcome of AF: if young patient “especially those with
paroxysmal lone AF, rhythm control may be a better initial approach” per
guidelines document.
■ Long-term AF can cause significant atrial remodeling which would make restoration
to SR in future more difficult if needed due to symptoms.
■ CHF: patients with poor LV function may not tolerate AF as well due to loss of
atrial kick.
■ Also need to prevent tachycardia induced cardiomyopathy.

Options for Rate Control
 Goal HR:
 Vary with patient age but usually target ventricular rates
between 60 and 80 beats per minute at rest and between
90 and 115 beats per minute during moderate exercise.1
■ if mitral stenosis closer to 60 bpm
 “Lenient” strategy OK HR <110 bpm as long as
no significant LV dysfunction and symptoms
controlled.

Lip G, Tse HF, The Lancet 370:04–18.

ACC Guidelines, Fuster et al. JACC Vol. 48, No. 4, 2006

Clinical Pearls: Acute Setting
Hemodynamically Unstable:
■ DC cardioversion
Hemodynamically Stable:
■ IV Beta blockers or calcium channel blockers
■ Do not use verapamil in patient with LV dysfunction due to its potent
negative inotropic effect -- drug of choice for patients with HCM and normal
LV function
■ Prefer Beta blockers as first line, especially if hyperadrenergic state is
the etiology of AF (i.e. post-operative, thyrotoxicosis, infection)
■ In AFFIRM, beta blockers were the most effective drug class for rate
control, achieving the specified heart rate endpoints in 70% of patients
compared with 54% with use of calcium channel blockers
■ Avoid in bronchospastic disorders
■ Careful in patients with LV dysfunction in acute setting although in the
chronic setting they are the drugs of choice due to mortality benefits of BB
in CHF.

■ Use Digoxin IV or amiodarone if borderline BP or CHF
■ Watch for patients with renal failure and hypo/hyperkalemia when
using digoxin
■ Digoxin can take several hours to have effect and usually ineffective
in hyperadrenergic states
■ Can also consider esmolol due to short acting properties.
■ Do not use amiodarone in thyrotoxicosis due to iodine load.
■ Of note if patients on pressors and develop AFIB switch agent to
vasopressin or Neo (unless inotropes needed for CHF – Milrinone a
little less tachycardia then Dobutamine/dopamine<epinephrine

■ Wolf-Parkinson White: do not use AV nodal blocking
agents as they can paradoxically enhance conduction
down the AP and cause VF.
■ Treatment focuses on cardioversion (pharmacologic or DC
cardioversion and ablation of AP)
■ Procainamide is drug of choice for cardioverting patients in this
setting pharmacologically.
18

Within the first 24 h, up to 50% of patients with new onset of atrial
fibrillation convert back to sinus rhythm.1
If the patient does not convert spontaneously, pharmacological or
electrical cardioversion should be attempted if the rhythm control
strategy has been chosen.
Generally, in patients with non-valvular atrial fibrillation lasting less than
48 h, cardioversion can be safely done if sure of onset of AF.
■ WOULD STILL GIVE NOAC/ANTICOAG 2 hours before cardioversion if CHADSVASC=>2
If unsure about timing of AF, then can anti-coagulate for 3 weeks then
cardiovert and anticoagulate for an additional 4 more weeks; or
perform a TEE guided cardioversion and anticoagulate for at least 4
more weeks.
Options for Rhythm Control
1. Naccarelli GV, et al. Am J Cardiol 2003; 91: 15–26D.

Antiarrhythmics
Patients after electrical or pharmacological cardioversion may
need to be placed on chronic antirrhythmics or PRN “pill in
the pocket”.
■ Decision is often multifactorial and patient specific, and is
typically made in conjunction with cardiology consultation

Class 1C: Fleicainide and Propafenone
■ Generally well tolerated
■ Make sure patients stay on AV nodal blocking agents as
these 1C drugs can increase conduction in AV node and
therefore increase HR during AF.
■ If patients develop CAD or LV dysfunction, find alternative
drugs if possible.
Sotalol:
■ monitor QTc at return visits as well as creatinine.
■ In-hospital initiation for 72 hour observation for most
patients – unless have an ICD
■ AVOID ALL QT PROLONGING DRUGS

Dofetilide:
■ Approved in patients with LV dysfunction
■ Monitor Qtc (<440 msec; <500 msec if bundle branch block)
and creatinine.
■ In-hospital initiation for 72 hour observation.
Avoid electrolyte disturbances (K and Mag) in all patients on
antiarrhythmics due to pro-arrhythmias.
AVOID ALL QT PROLONGING DRUGS

So in summary…If you get called for Afib:
1) stable or unstable
2) First goal is to achieve rate control and assess CHADS
VASc score
3) For rate control if BP OK, then give 10-20 mg of IV diltiazem
and repeat in ten minutes if still fast and start either oral
toprol 25 BID or diltiazem CD 120 CD
■ Especially if infection, CAD/MI or LV dysfunction use Beta
blockers instead.
■ Watch for wheezing and avoid BB

Can repeat Diltiazem 10 mg bolus every 1-2 hours PRN. If
having to repeat often can start IV diltiazem drip as oral
agents are kicking in.
If severe decompensated CHF, use IV amio or cardiovert.
IF BP soft , can use IV digoxin as it does not affect BP but
watch in renal failure.
■ if patients on pressors and develop AFIB switch agent to
vasopressin or Neo (unless inotropes needed for CHF)

Rhythm Control
First decide when Afib started: if <48 hours can pursue rhythm
control without TEE
■ Start heparin/lovenox/NOAC to avoid need for TEE if cannot
cardiovert within 48hours.
In setting of Post op/Sepsis: consider using Amio transiently for
1-2 months
For others, decide on symptomatic or not before pursuing rate
or rhythm control.

Rate control overnight and place NPO for possible TEE/Cardioversion.
If someone cannot be on anticoagulation, rhythm control within <48
important so start amio earlier on (even for short term). If you
cardiovert (chemical or DC) beyond 48 hours then would need long-
term anticoagulation for AT LEAST 1 month REGARDLESS OF
CHADSVASC

Anticoagulation in ICU:
• Anticoagulation in ICU challenging as patients may have
contraindications.
• Use the CHADS-VASC score to determine who needs to be
anticoagulated.
• CHADSVASC >=1 need to be considered for
anticoagulation, or if they have Mitral stenosis or
hypertrophic cardiomyopathy regardless of
CHADSVASC.
• Cannot use NOACs for mechanical valves
• Antidote for Pradaxa but not other NOACs (coming this
summer!)

CHA2DS2-VASc Score
 C: Congestive Heart Failure (EF< 40%) 1 Point
 H: HTN 1 Point
 A2: Age > 75 2 Points
 D: Diabetes 1 Point
 S2: Stroke 2 Points
 V: Vascular (PVD/CAD) 1 Point
 A: Age 65-74 1 Point
 Sc: Female Sex 1 Point

Wide Complex Tachycardia

Outline
Differential Diagnosis of a Wide Complex Tachycardia (WCT)
SVT vs. VT
Treatment
Examples

Differential
Is it Fast?
Is it Regular?
Is it truly Wide?

Differential Cont’d
Narrow Wide
Sinus Tachycardia Ventricular Tachycardia
Regular Atrial Flutter Antidromic Tachycardia (WPW)
SVT Abberrancy
Other (Junctional Tach, etc.)
Atrial Fibrillation Polymorphic VT / VF/ Torsades
Irregular Atrial Flutter with Variable AV Block AF with Bypass Tract (WPW)
Sinus Tachycardia with PAC's Aberrancy
Multifocal Atrial Tachycardia

Common Causes of WCT
If the patient has structural heart disease
■VT, VT, VT, VT… until proven otherwise
If the patient has a normal heart
■ SVT with aberrancy > idiopathic VT
■ WPW

SVT with Aberrancy
• Conduction to the ventricles via the His-Purkinje system with
one of the following:
– RBBB
– LBBB
– IVCD
• These can be either
– Pre-existing BBB
– Rate/SVT associated

LBBB

LBBB Example

RBBB

RBBB with LAFB Example

Ventricular Tachycardia
A focal or reentrant arrhythmia arising within the ventricles
They are wide complex because they almost always involve
myocyte-to-myocyte conduction as opposed to utilization of
the existing conduction system
--exceptions are Fascicular VTs.

Other causes of wide QRS:
Don’t forget that electrolyte abnormalities and/or drug effects
can cause QRS widening
■ Drug Effects:
■ Class IC antiarrhythmics (flecainide and propafenone)
cause use-dependent QRS widening
■ Tricyclic Anti-depressants
■ Hyperkalemia
■ Causes QRS widening

Approach to WCT
• 1) Clinical assessment of the patient (i.e. h/o MI, currently
hypotensive, etc.)
• 2) Classic RBBB or LBBB strongly points towards SVT with
aberrancy
• 3) Features Suggestive of VT
– AV dissociation
– Fusion/Capture Beats
– QRS morphology that doesn’t meet BBB criteria

Features Suggestive of VT
• QRS Morphology NOT consistent with classic BBB
– Not exact match of BBB
– Positive or negative concordance
• Rare (<5% prevalence), highly specific (near 100%)
• Other morphological criteria
– Many, several of which are incorporated into Brugada criteria
• VA dissociation
– ~50% prevalence, highly specific
• Capture and Fusion Complexes
– Rare (<7% prevalence), highly specific

VA Dissociation

Fusion Beat

Capture & Fusion Beats

Management:
Remember, if a patient is in a WCT and is hemodynamically
unstable… electricity is the answer. DC CARDIOVERSION
-then look at ECG, if QTC OK can use amiodarone if recurs. If
QTc long then use lidocaine if recurs.
If you have a stable patient, take your time to make a diagnosis

Stable and irregular:
-think Afib with aberrancy or Afib with WPW
-others include Polymorphic VT/torsades
-if not sure , cardioversion.
-if Afib with WPW – Procainamide (or cardioversion)
-if torsades rarely stable: avoid amiodarone as most torsades
are due to long Qtc. Use lidocaine instead.
• Consider Isuprel or Temporary Pacing to increase HR
and shorten Qt
-

• if polymorphic VT : rarely stable; Amiodarone versus
cardioversion
• NEVER GIVE ADENOSINE OR AV Nodal agents in that
situation unless you are comfortable that it is Afib with
aberrancy

Stable and Regular
- VT until proven otherwise in structurally abnormal Heart
- In young otherwise healthy think SVT/ with aberrance or
WPW/ART, or Fascicular VT
- START with adenosine unless you know it is scar related VT
- If does not work : try amiodarone most often , (or
procainamide). Lidocaine second choice if cannot be on
amiodarone . DC cardioversion if does not work.
- If narrow and has RBBB almost typical morphology can try
verapamil for fascicular VT.

Secondary Management of WCT
• Correct electrolytes
• Discontinuation of precipitating medications
• Beta blockade
• Heart failure optimization
• ICD programming
• Laboratory analysis – BNP, cardiac enzymes etc
• Heart catheterization especially if polymorphic!!
• Isuprel / pacing if bradycardia with long Qtc

Structural Heart Disease No Structural Heart Disease
CAD
NICM
HCM
ARVD
Sarcoid
Myocarditis
MVP
Congenital / acquired LQTS
SQTS
CPVT
Brugada Syndrome
WPW
Bradycardia & short-coupled PVC
induced
Digoxin toxicity
Coronary spasm
Commotio Cordis
Idiopathic
Polymorphic VT/VF

Monomorphic VT
• Usually from scar related ischemic Cardiomyopathy
ro structurally abnormal hearts (congenital)
• Can be from infiltrative diseases (sarcoid)
• Hypertrophic cardiomyopathy
• Idiopathic (RVOT VT)

Polymorphic VT/VF in the
absence of long QT is most often
ischemic and LHC is needed

Brugada Pattern

Acute Treatment : Polymorphic VT/VF due to channelopathy
LQTS – beta blockade if not bradycardic, lidocaine, Temp pacing
Mexilitine/Flecainide (type 3)
CPVT – Flecainide, BB, autonomic inhibition
Brugada Syndrome – Isuprel, Quinidine

HRS Expert Consensus on Ventricular Arrhythmias; JACC 2014
Management of VT/VF Storm > 3 episodes in 24 hours

Examples

28 yo male.

Treatment:?

Treatment: ??

40 yo in with pneumonia and
normal heart: Treatment?

Bradycardia
• Differential:
• Sinus Bradycardia
• Sinus Pauses
• Mobitz 1 or 2
• Complete heart block
• Artifact

Management:
• Stable or Unstable?
• If stable even in complete heart block DO NOT
TRANSCUATENOUSLY PACE as you may loose underlying
escape and then become unstable.
• Rule out common causes of bradycardia:
• Drugs: AV nodal agents, antiarrhyhmics,Ticagrelor
(brilinta), lithium.
• Hyperkalemia
• Profound sepsis
• Intracranial Process (herniation)
• Vagal mechanism (trach patients)

Indications for permanent pacing in stable
patients (EP consult):
• Mobitz 2
• Complete heart block
• Symptomatic sinus pauses >3 seconds or sinus bradycardia
that is symptomatic (no real indication for bradycardia or
complete heart block during sleep since can be vagal
mediated)

Unstable Bradycardia:
• Causes typically:
• Long recurrent Pauses causing syncope or recurrent
torsades.
• Complete heart block usually <30 (?40) bpm to be
unstable
• Mobitz 2/paroxysmal AV block
•

2015 AHA Guidelines for ACLS
Treatment of Bradycardia

Treatment:

SVT: Differential
AVNRT
ORT
AT
JT
Other: Afib and Flutter

HRS Guideline Statement for SVT; JACC 2016
Treatment of SVT

SVT:
• Rarely hemodynamically significant unless patient already critically ill
• AV nodal agents first
• If on pressors and has incessant SVT can use amiodarone TRANSIENTLY
with EPS consult for plans of potential ablation in future
• Consider Flecainide if no CAD and normal heart and no significant renal or
liver failure.

a) Sinus tachycardia
b) Atrial tachycardia
c) Atrial flutter
d) Re-entrant SVT
e) Other

SVT, likely AVNRT

Carotid Massage

c) Atrial flutter

Thank You!

Arrhythmias In The ICU

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