cardiac arrhythmias in the sicu n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Cardiac Arrhythmias in the SICU PowerPoint Presentation
Download Presentation
Cardiac Arrhythmias in the SICU

Loading in 2 Seconds...

play fullscreen
1 / 47

Cardiac Arrhythmias in the SICU - PowerPoint PPT Presentation


  • 161 Views
  • Uploaded on

Cardiac Arrhythmias in the SICU. Charles Hobson, MD MHA Surgical Critical Care NFSG VA Medical Center. Objectives. Review the etiology and recognition of common arrhythmias seen in the SICU. Review management of cardiac arrhythmias, with a focus on the relevant recent literature.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Cardiac Arrhythmias in the SICU' - ignacia-price


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
cardiac arrhythmias in the sicu
Cardiac Arrhythmias in the SICU

Charles Hobson, MD MHA

Surgical Critical Care

NFSG VA Medical Center

objectives
Objectives
  • Review the etiology and recognition of common arrhythmias seen in the SICU.
  • Review management of cardiac arrhythmias, with a focus on the relevant recent literature.
normal sinus rhythm
Normal Sinus Rhythm

www.uptodate.com

Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.

EKG Characteristics: Regular narrow-complex rhythm

Rate 60-100 bpm

Each QRS complex is proceeded by a P wave

P wave is upright in lead II & downgoing in lead aVR

mechanisms of arrhythmias
Mechanisms of Arrhythmias

Automaticity or

Ectopic Foci

Reentry / Conduction Block

decreased automaticity
Decreased Automaticity

www.uptodate.com

Sinus Bradycardia

increased abnormal automaticity
Increased/Abnormal Automaticity

Sinus tachycardia

Ectopic atrial tachycardia

www.uptodate.com

Junctional tachycardia

slide8

Ectopic Foci and Beats

QRS is slightly different but still narrow,

indicating that conduction through the

ventricle is relatively normal

Atrial Escape Beats

normal ("sinus") beats

sinus node doesn't fire leading to a period of asystole (sick sinus syndrome)

p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria.

slide9

Ectopic Foci and Beats

Paroxysmal Supraventricular Tachycardia (PSVT)

  • A single ectopic focus fires near the AV node, which then conducts normally to the ventricles (usually initiated by a PAC)
  • The rhythm is always REGULAR
  • Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter
  • May be terminated by carotid massage
  • Treatment: carotid massage, adenosine, Ca++ channel blockers, ablation
    • Adenosine preferred in hypotension, previous IV B-blocker

Note REGULAR rhythm in the tachycardia

Rhythm usually begins with PAC

slide10

Ectopic Foci and Beats

Multifocal Atrial Tachycardia (MAT)

  • Multiple ectopic foci fire in the atria, all of which are conducted normally to the ventricles
  • The rhythm is always IRREGULAR
  • P-waves of different morphologies (shapes) may be seen
  • Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF
        • Treatment:
          • Ca++ channel blockers, beta blockers, but antiarrhythmic drugs are often ineffective
          • potassium, magnesium (McCord et al, Chest 1998),

Note IRREGULAR rhythm in the tachycardia

slide11

Ectopic Foci and Beats

Junctional Escape Beats

QRS is slightly different but still narrow,

indicating that conduction through the

ventricle is relatively normal

there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction.

slide12

Ectopic Foci and Beats

Ventricular

Escape Beats

“PVCs”

QRS is wide and much different looking than the normal beats. This indicates that the beat originated somewhere in the ventricles.

  • no p wave, indicating that the beat did not originate anywhere in the atria
  • a "retrograde” p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles
slide13

PVC's are Dangerous When:

  • They are frequent (> 30% of complexes) or are increasing in frequency
  • The come close to or on top of a preceding T-wave (R on T)
  • Three or more PVC's in a row (run of V-tach)
  • Any PVC in the setting of an acute MI
  • PVC's come from different foci ("multifocal" or "multiformed")
  • These may result in ventricular tachycardia or fibrillation.

“R on T phenomenon”

time

Unconverted V-tach to V-fib

sinus beats

V-tach

slide14

Causes of Ectopic Foci and Beats

  • hypoxic myocardium - chronic pulmonary disease, pulmonary embolus
  • ischemic myocardium - acute MI, expanding MI, angina
  • sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism
  • drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia, imbalances of calcium and magnesium
  • bradycardia- a slow HR predisposes one to arrhythmias
  • enlargement of the atria or ventricles producing stretch in pacemaker cells
slide15

The Reentry Mechanism of Ectopic Beats & Rhythms

Electrical Impulse

Cardiac Conduction Tissue

Fast Conduction Path

Slow Recovery

Slow Conduction Path

Fast Recovery

  • Tissues with these type of circuits may exist:
    • in the SA node, AV node, or any type of heart tissue
    • in a “macroscopic” structure such as an accessory pathway in WPW
slide16

The Reentry Mechanism of Ectopic Beats & Rhythms

Premature Beat Impulse

Cardiac Conduction Tissue

Repolarizing Tissue (long refractory period)

Fast Conduction Path

Slow Recovery

Slow Conduction Path

Fast Recovery

  • 1. An arrhythmia is triggered by a premature beat
  • 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only
slide17

The Reentry Mechanism of Ectopic Beats & Rhythms

Cardiac Conduction Tissue

Fast Conduction Path

Slow Recovery

Slow Conduction Path

Fast Recovery

  • 3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrograde (backwards) up the fast pathway
slide18

The Reentry Mechanism of Ectopic Beats & Rhythms

Cardiac Conduction Tissue

Fast Conduction Path

Slow Recovery

Slow Conduction Path

Fast Recovery

  • 4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit
reentrant rhythms
Reentrant Rhythms
  • AV nodal reentrant tachycardia (AVNRT)
    • Supraventricular tachycardia
  • AV reentrant tachycardia (AVRT)
    • Wolf – Parkinson – White syndrome
  • Atrial flutter
  • Ventricular tachycardia
  • Atrial fibrillation
  • Ventricular fibrillation
slide20

Reentry Circuits as Ectopic Foci and Arrhythmia Generators

  • Atrio-Ventricular Nodal Re-entry
  • supraventricular tachycardia
  • Ventricular Re-entry
  • ventricular tachycardia
  • ventricular fibrillation
  • Atrial Re-entry
  • atrial tachycardia
  • atrial fibrillation
  • atrial flutter
  • Atrio-Ventricular Re-entry
  • Wolf Parkinson White
  • supraventricular tachycardia
av nodal reentrant tachycardia
AV Nodal Reentrant Tachycardia

Rate 100-270

Normal QRS

Aberrancy possible

  • Acute Rx:
    • Vagal maneuvers
    • Adenosine 6-12 mg IV push – beware of pro-arrhythmia
    • Ca++ channel blockers
atrial flutter
Atrial Flutter

www.uptodate.com

Atrial flutter is caused by a reentrant circuit in the wall of the atrium

EKG Characteristics: Typical: “sawtooth” flutter waves at a rate of ~ 300 bpm

Flutter waves have constant amplitude, duration, and morphology through the cardiac cycle

There is usually either a 2:1 or 4:1 block at the AV node, resulting in ventricular rates of either 150 or 75 bpm

dx and rx of flutter
Dx and Rx of Flutter

Unmasking of flutter waves with adenosine.

  • Acute Rx:
    • ventricular rate control can be difficult
    • AV nodal blockers prevent 1:1 conduction
    • Ibutilide 1-2mg rapid IV infusion – have paddles ready
    • Rapid pacing or low voltage DC cardioversion is effective
    • Anticoagulation as per atrial fibrillation
ventricular tachycardia
Ventricular Tachycardia

Rate 100-20

Wide QRS

Monomorphic vs

Polymorphic

  • Beware:
    • Accelerated idioventricular rhythm. Rate below 150, stable hemodynamics, benign prognosis.
    • SVT with aberrancy. Look at the 12 lead – not just a rhythm strip
    • Monomorphic vs. Polymorphic (long QT, bradycardia, ischemia)
  • Rx:
    • Unstable – DC cardioversion
    • Stable monomorphic – Procainamide, Amiodarone
    • Stable polymorphic - treat underlying etiology
atrial fibrillation
Atrial Fibrillation

www.uptodate.com

  • Atrial fibrillation is caused by numerous waves of depolarization spreading throughout the atria, leading to an absence of coordinated atrial contraction.
  • Classified as:
      • Recurrent: when AF occurs on 2 or more occasions
      • Paroxysmal: episodes that generally last </= 7 days (most last <24h)
      • Persistent: AF that last >/=7 days
      • Permanent: paroxysmal or persistent AF with failure to cardiovert or not attempted
dx and rx of atrial fibrillation
Dx and Rx of Atrial Fibrillation

Absent P waves

Irregularly irregular ventricular response

  • Acute Rx:
    • rate control not rhythm control – AFFIRM trial (NEJM 2002):
      • B-blockers, Ca++ channel blockers, digoxin, amiodarone
    • Ibutilide 1-2mg rapid IV infusion – have paddles ready
    • Oral propafenone or flecainide – beware pro-arrhythmia
    • Low voltage DC cardioversion
    • Anticoagulation as per atrial fibrillation
  • On the horizon: vernakalant, an atrial-selective Na and K channel blocker for conversion of short-duration atrial fibrillation
ventricular fibrillation
Ventricular Fibrillation

www.uptodate.com

Ventricular fibrillation is caused by numerous waves of depolarization spreading throughout the ventricles simultaneously, leading to disorganized ventricular contraction and immediate loss of cardiac function.

EKG Characteristics: Absent P waves

Disorganized electrical activity

Deflections continuously change in shape, magnitude and direction

rhythms produced by conduction block
Rhythms Produced by Conduction Block
  • AV Block (relatively common)
    • 1st degree AV block
    • Type 1 2nd degree AV block
    • Type 2 2nd degree AV block
    • 3rd degree AV block
  • SA Block (relatively rare)
1 st degree av block
1st Degree AV Block

The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

EKG Characteristics: Prolongation of the PR interval, which is constant

All P waves are conducted

Usually benign

2 nd degree av block
2nd Degree AV Block

Mobitz 1

(Wenckebach)

EKG Characteristics: Progressive prolongation of the PR interval until a P wave is not conducted.

As the PR interval prolongs, the RR interval actually shortens

Usually benign unless associated with underlying pathology, i.e. MI

2 nd degree av block1
2nd Degree AV Block

Mobitz 2

  • EKG Characteristics: Constant PR interval with intermittent failure to conduct
  • Rhythm is dangerous as the block is lower in the conduction system
  • May cause syncope or may deteriorate into complete heart block
  • Causes: anterioseptal MI, fibrotic disease of the conduction system
  • Treatment: may require pacemaker in the case of fibrotic conduction system
3 rd degree complete av block
3rd Degree (Complete) AV Block
  • EKG Characteristics: No relationship between P waves and QRS complexes
  • Constant PP intervals and RR intervals
  • May be caused by inferior MI and it’s presence worsens the prognosis
  • May cause syncopal symptoms, angina, or CFH
  • Treatment: usually requires pacemaker
slide33

Right Bundle Branch Block (RBBB)

  • Depolarization spreads from the left ventricle to the right ventricle.
  • This creates a second R-wave (R’) in V1, and a slurred S-wave in V5 - V6.
  • The T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.
slide34

Left Bundle Branch Block (LBBB)

  • Depolarization enters the right side of the right ventricle first and simultaneously depolarizes the septum from right to left.
  • This creates a QS or rS complex in lead V1 and a monophasic or notched R wave in lead V6.
  • The T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.
slide37

Class 1A agents: Procainamide, quinidine

  • Uses
      • Wide spectrum, but side effects limit usage
      • Quinidine : maintain sinus rhythms in atrial fibrillation and flutter and to prevent recurrent tachycardia and fibrillation     
      • Procainamide: acute treatment of supraventricular and ventricular arrhythmias (no longer in production)
  • Side effects
  • Hypotension, reduced cardiac output
  • Proarrhythmia (generation of a new arrhythmia) eg. Torsades de Points (QT interval)
  •               Dizziness, confusion, insomnia, seizure (high dose)
  •               Gastrointestinal effects (common)
  •               Lupus-like syndrome (esp. procainamide)
slide38

Class 1B agents: Lidocaine, phenytoin

Uses

acute : Ventricular tachycardia and fibrillation (esp. during ischemia)

Not used in atrial arrhythmias or AV junctional arrhythmias

Side effects

                Less proarrhythmic than Class 1A (less QT effect)

              CNS effects: dizziness, drowsiness

slide39

Class 1C agents: Flecainide, propafenone

Uses

Wide spectrum

Used for supraventricular arrhythmias (fibrillation and flutter)

              Premature ventricular contractions (caused problems)

Wolff-Parkenson-White syndrome

Side effects

Proarrhythmia and sudden death especially with chronic use (CAST study)

Increase ventricular response to supraventricular arrhythmias

CNS and gastrointestinal effects like other local anesthetics

slide40

Class II agents: Propranolol, esmolol

Uses

treating sinus and catecholamine dependent tachy arrhythmias

converting reentrant arrhythmias in AV

protecting the ventricles from high atrial rates (slow AV conduction)

Side effects

       bronchospasm

             hypotension

  beware in partial AV block or ventricular failure

slide41

Class III agents: Amiodarone, sotalol, ibutilide

Amiodarone

Uses

Very wide spectrum: effective for most arrhythmias

Side effects: many serious that increase with time

Pulmonary fibrosis

Hepatic injury

Increase LDL cholesterol

Thyroid disease

Photosensitivity

May need to reduce the dose of digoxin and class 1 antiarrhythmics

slide42

Class III agents: Amiodarone, sotalol, ibutilide

Sotalol

Uses

  Wide spectrum: supraventricular and ventricular tachycardia

Side effects

   Proarrhythmia, fatigue, insomnia

slide43

Class III agents: Amiodarone, sotalol, ibutilide

Ibutilide

Uses

conversion of atrial fibrillation and flutter with rapid IV infusion

Side effects

Torsades de pointes

slide44

Class IV agents: Verapamil and diltiazem

Uses

control ventricular rate during supraventricular tachycardia

convert supraventricular tachycardia (re-entry around AV)

Side effects

Caution when partial AV block is present. Can get asystole if β blocker is on board

Caution when hypotension, decreased CO or sick sinus Some gastrointestinal problems

slide45

Additional agents

Adenosine

Administration

rapid i.v. bolus, very short T1/2 (seconds)

Cardiac effects

Slows AV conduction

Uses

convert re-entrant supraventricular arrhythmias

hypotension during surgery, diagnosis of CAD

Magnesium

treatment for tachycardia resulting from long QT

slide46

Additional agents

Digoxin (cardiac glycosides)

Mechanism

enhances vagal activity, inhibits Na/K ATPase

 refractory period, slows AV conduction

Uses

treatment of atrial fibrillation and flutter

Atropine

Mechanism

selective muscarinic antagonist

Cardiac effects

blocks vagal activity to speed AV conduction and increase HR

Uses

treat vagal bradycardia

slide47

Selected References:

  • ACC/AHA/ESC Practice Guidelines:
    • Supraventricular Arrhythmias – JACC 2003;42:1993-531.
    • Atrial Fibrillation – JACC 2006;48:854-906
    • Ventricular Arrhythmias – JACC 2006;48:1064-1108
  • Thanks, and questions?