Tachyarrhythmias in the ICU

ACNP/PA Critical Care Boot CampVanderbilt University Medical Center

September 21, 2015

Ariel KappaRN, MSN, ACNP-BC

• “Acute Arrhythmias are the gremlins of the ICU because they pop up unexpectedly, create some havoc, and are often gone in a flash…”

-Paul Marino

(The ICU Book, 2007)

Objectives

• Review

– EKG characteristics

– Initial Considerations

– Pharmacology

• Interactive Case Studies

Blocks? Infarction?

Morphology of QRS

Regularity? Appreciable P waves?

Stable or Unstable (Shock ?)

Tachycardia

Regular

Narrow

Sinus Tachycardia,

Atrial Tachycardia,

AVNRT/AVRT, Atrial flutter

Wide

Monomorphic VT,

SVT with aberrancy/blo

ck/pacing-mediated

Irregular

Narrow

Atrial fibrillation,

MAT

Wide

Polymorphic VT/VF/

Torsades, Irregular SVT

with aberrancy/blo

ck

Initial considerations

• Stable?

– Hypotension, AMS, signs of shock, CP

– 12-lead EKG

• Pharmacological management

• Non-Pharmacological management

– Synchronized cardioversion (50-200 J)

• Oxygen, airway, monitor, sedation

Pharmacology

Class Common Examples Mechanism Clinical Use

Ia QuinidineProcainamide

Na+ Channel blocker; Fast (effects QRS)

Pre-excited afib, Stable monomorphic VT

Ib Lidocaine, Mexilitine, Phenytoin

Na+ Channel blocker; No effect on conduction; may prolong APD

VT

Ic Fleicanide, Propafenone

Na+ Channel blocker; (no effect on QRS)

SVT, PVCs, WPW

II Metoprolol, Esmolol, Propranalol

Block beta-adrenergic receptors Afib rate control, Narrow Stable SVT

III Amiodarone*, Sotalol*, Ibitulide

K+ channel blocker SVT (Regular and Irregular)

IV Verapamil, Diltiazem Non-dihydropyridine Calciumchannel blocker, vasodilate, negative inotrope

Rate control SVT*Avoid in CHF/VT Pre-exited Afib

Misc. Digoxin, AdenosineMagnesium

Dig- parasympathetic AV, + InotropeAdenosine- AVMag- effect Na/K transport

Dig- SVT, Afib in HF,Adenosine- SVT, stable WCTMg- Polymorphic VT/Torsades

Case 1

• 73 yo female with history of HTN, Aortic Stenosis, DMII, COPD

• POD 1 s/p AVRt with EF of 60% c/o SOB.

• Vitals: HR: 162, SBP: 131/71, RR: 26

Case 1

• What does this EKG show?

• 1. Atrial tachycardia

• 2. AV nodal reentrant tachycardia

• 3. Atrial fibrillation

• 4. Atrial flutter

What is the best next step?

• 1. Prepare for synchronized cardioversion of atrial fibrillation.

• 2. Initiate IV amiodarone bolus and infusion.

• 3. Assess timing, electrolytes and consider IV diltiazem bolus and infusion.

• 4. Administer 5mg IV metoprolol.

Rate vs. Rhythm control

• AFFIRM TRIAL

• True or False:

• Rhythm control is more important than rate control

• 1. True

• 2. False

• RACE II

• True or False:

• HR less than 110 is non-inferior to HR less than 80 in morbidity/mortality outcomes

• 1. True

• 2. False

(AFFIRM, NEJM, 2002), (VanGelder et al., NEJM, 2010)

Atrial Fibrillation

EKG Characteristics: Irregularly Irregular.

Etiology: Numerous waves of depolarization spreading throughout the atria, leading to an absence of coordinated atrial contraction.

Treatment: Class II, Class IV, Class III, Digoxin: HF (inotropic support). Unstable: Low voltage DCCV

AFFIRM trial (NEJM, 2000): Rate control not rhythm control

Race II Trial: (NEJM, 2010): Lenient rate control

Case 2

• 68 yo male with COPD exacerbation admitted to MICU.

• HR: 151, SBP: 121/73, RR: 28

Case 2

• What does this EKG show?

• 1. Atrial tachycardia

• 2. Sinus tachycardia

• 3. Atrial fibrillation

• 4. Atrial flutter

Atrial Flutter

EKG Characteristics: ‘Sawtooth’ pattern: atrial rate ~300, ventricular rate 75-150 bpm (unless irregular). Usually with 2:1/4:1block at AV node. Rhythm constant amplitude, morphology, duration. **May be variable and irregular

Etiology: Reentrant circuit in the wall of the atrium

Treatment: Class III (Ibutilide, sotalol, amiodarone): prolong refractory period (not slowing conduction) *Small risk for torsades. Ventricular rate control can be difficult, AV nodal blockers prevent 1:1 conduction. Unmasking of flutter waves with adenosine.

*Nonpharmacological : Rapid pacing or low voltage DC cardioversion is effective.

(Blomstrom-Lundqvist, et al., 2003)

Case 3

• 24 yo female admitted to Trauma ICU with pelvic fracture s/p MVC complaining of palpitations.

• Vitals: HR: 148, SBP 118/58, RR: 22

Case 3

• What does this EKG show?

• 1. Sinus Tachycardia

• 2. AV nodal reentrant tachycardia

• 3. Atrial fibrillation

• 4. Atrial flutter

AV Nodal Reentrant Tachycardia (AVNRT)

• EKG characteristics: Rate 140-280, P wave undetected (activation atria/ventricle simultaneously),

• Etiology: Triggered by PACs, “Micro” Reentry at AV node (atrial stretch, inflammation, irritability- catecholamines)

• Treatment: Vagal maneuvers, Adenosine 6-12 mg IV push,

Ca++ channel blockers, Digoxin, Beta blockers

(Blomstrom-Lundqvist, et al., 2003)

Multifocal Atrial Tachycardia (MAT)

• EKG characteristics: at least 3 P wave morphologies, variable intervals P-P, R-R, P-R, look for isoelectric baseline

• Etiology: No single dominant pacemaker, multiple atrial foci fire independently. COPD/CHF

• Treatment: Treat underlying cause (electrolyte derangement, hypoxemia). Rate control- Class IV- CCBs, Class II- Beta-blockers

ST • PACs

Atrioventricular Reentrant Tachycardia (AVRT)

• Etiology: Macrorentry through normal conduction system with accessory AV pathway; Delayed activation of atria = visible P wave

• Treatment: Similar to treatment of AVNRT, AV nodal blockers, eventual ablation

Sinus Tachycardia Atrial Tachycardia

EKG characteristics:

Constant PR interval

Varies with stimulation/respiration

Normal Rate 220 bpm –age (yrs)

Etiology: Physiologic

Treatment: Fix underlying

physiologic insult

(Fever, anxiety, thyrotoxicosis,

exogenous catecholamines,

anticholinergic, LV dysfunction- MI

etc.

EKG characteristics:

Atrial rate 150-250

Distinct P wave morphology

Etiology: CHF, HTN,

electrolyte abnormalities

Treatment: Adenosine, Class

II, Class III, *Dig toxicity?

Case 4

• 38 yo male with PMH: Appendectomy

• Presented to ED with SBO s/t incarcerated groin hernia now POD 3 s/p SBO repair.

• Vitals: HR 148, SBP 100/58, RR: 20

• BMP:

148 19 41

2.1 21 1.6

Case 4

What is your next course of action?

• 1. Correct hypokalemia and prepare amiodarone for administration.

• 2. Grab the crash cart and prepare for emergent cardioversion.

• 3. Correct hypokalemia and prepare lidocaine for bolus/infusion.

• 4. Grab the crash cart and ask the nurse to give sotalol.

Monomorphic VT

EKG characteristics: 3 consecutive beats >100 bpm, QRS >120ms

Brugada criteria: Precordial leads- No RS complex or RS >100ms, AV dissociation, QRS morphology- Fusion beats

Etiology: CAD, CM, Ischemia

Treatment: Correct aggravating conditions (hypokalemia, ischemia)

Class I: Wide QRS presumed VT if unclear ( LOE: C). *DCCV unstable ( LOE: C). Class II: Procainamide- careful in LV dysfunction, CHF, hypotension-prolong QT. Class III- Sotalol, Amiodarone (benefit IV to PO). Class IIb- IV lidocaine initial treatment associated with MI (LOE: C).

(Zipes et al., 2006)

Wide Complex SVT

•EKG characteristics: Regular, Wide complex, Fails Brugada’s Criteria (from previous slide)

•Etiology: BBB/IVCD, Pre-excitation, Presence of PPM/ICD

•Treatment: WPW- Procainamide (*Avoid AV nodal blockers)

•Vagal maneuvers, Adenosine, Class III, Cardioversion

Delta wave

WPW Pacemaker-Mediated

Which of these below is not a treatment option?

• 1. DC Cardioversion

• 2. Metoprolol

• 3. Amiodarone

• 4. Procainamide

Case 5

• Lets go back to the 38 yo. male with VT

• Unfortunately you look up at the monitor and see this…

Case 5

1. Give magnesium

2. Defibrillate

3. Stop all QT prolonging

medications

4. All of the above.

What do you do next?

Irregular, Wide Complex

• Polymorphic VT– Etiology: Ischemia, Catecholamines

– Treatment: Defibrillation

• Ventricular fibrillation, Torsades de pointes– Etiology- QT prolongation, Class I, III- prolong refractory period

General Tips

• Narrow complex tachyarrhythmias can be diagnosed or possibly terminated in most cases with IV adenosine.

• If the origin of arrhythmia is unclear on a symptomatic patient, it is generally consider safe to treat as ventricular in origin.

References• The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators . A comparison of

rate control and rhythm control in patients with atrial fibrillation. New England Journal of Medicine. 2002, 347, 1825-1833.

• Carina Blomstrom-Lundqvist, Melvin M. Scheinman, Etienne M. Aliot, Joseph S. Alpert, Hugh Calkins, A. John Camm…Hans-Joachim Trappe. CC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias−−Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation, 2003, 108:1871-1909. doi: 10.1161/01.CIR.0000091380.04100.84.

• Delle Karth G, Geppert A, Neunteufl T , et al. Amiodarone versus diltiazem for rate control in critically ill patients with atrial tachyarrhythmias. Critical Care Medicine. 2001, 29, 1149-1153.

• Douglas P. Zipes, A. John Camm, Martin Borggrefe, Alfred E. Buxton, Bernard Chaitman, Martin Fromer…Cynthia Tracy. CC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart

Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society. Circulation, 2006, 114, e385-e484. doi: 10.1161/CIRCULATIONAHA.106.178233.

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