A Guide For Medical Students William Beaumont Hospital Department of Emergency Medicine Cardiac Arrhythmias.

A Guide For Medical Students

William Beaumont HospitalDepartment of Emergency Medicine

Cardiac Arrhythmias

Evaluating Arrhythmias Rate – Is it fast or slow?

If slow, is there group to group beating?Rhythm – Is it regular, irregular or irregularly

irregular?P waves – Are they present?QRS – Is it narrow or wide?

Sinus BradycardiaWhat is it?What causes it?When do you treat it? How do you treat it?

Sinus BradycardiaCharacteristics:

Sinus rhythmNormal intervalsRate less than 60 bpm

Etiology: Normal variantBeta blocker overdoseDigoxin overdoseHypothermiaHypothyroidismBrady-tachy syndromeSA node ischemia

Sinus BradycardiaTreatment:

Requires treatment only if there is evidence of hypoperfusion

Two treatment options:Pacing: transvenous or transcutaneousAtropine 0.5 mg IVP

Sinus TachycardiaCharacteristics:

Sinus rhythmFaster than 100 bpm

Etiology:Usually a physiologic response to a stressorVolume depletion / low stroke volumeHypoxiaSystemic pathology: fever, anemia,

hyperthyroidismDrugs

Treatment:Treat the underlying cause

Premature Atrial Contraction (PAC)Multifocal Atrial Tachycardia (MAT)Atrial Fibrillation (A-fib)Atrial flutter (A-flutter)Supraventricular Tachycardia (SVT)Pre-excitation Syndromes (WPW)

Atrial Arrhythmias

Multifocal Atrial Tachycardia

Three distinct p waves in a narrow complex tachycardia

Causes:Almost always associated with pulmonary

disease (hypoxia) Less often due to hypokalemia or

hypomagnesemiaTreatment:

Treat the underlying disorder – usually hypoxiaUnlike the other atrial tachyarrhythmias,

cardioversion is of no value in MAT

MAT Rule of Threes3 different p waves, 3 different pr intervals

and 3 different r to r intervals

Atrial Fibrillation: CausesCardiovascular – CAD, HTN, CHF,

myopathy, myo-, endo- and pericarditis, infiltrative disease, valvular, congenital

Metabolic – thyroid, electrolytesPulmonary – pulmonary HTN, PE Toxic – cocaine, ETOH (holiday heart), beta

agonistsSepsis Idiopathic

Atrial Fibrillation: EKGsRegularity – irregularly irregularRate – atrial rate usually > 350

Controlled – ventricular rate < 100RVR – ventricular rate > 100

P wave – none discernable, may be flutter wavesQRS

Less that 0.12 seconds If > 0.12 sec must rule out VT (which is usually

more regular)

Atrial Fibrillation with RVRVentricular rate > than 100-120 bpmPatients usually symptomatic requiring rapid treatment

Unstable – cardioversionStable – control rate with calcium channel blockers, beta

blockers or digitalis

Atrial Fibrillation TreatmentRecognize the underlying causeA rate under 120 in an asymptomatic patient

generally requires no emergent treatmentUnstable patients with acute rapid a-fib

should receive synchronized cardioversion with 50-100 J

Treatment otherwise depends on the duration

Atrial Fibrillation Treatment

Less than 48 hours durationUnstable – Cardiovert, synchronized if

possible, with 50-100 JMay also cardiovert electively in symptomatic,

stable patients Pharmacologic cardioversion

ProcainamideAmiodaroneIbutilide

Atrial Fibrillation Treatment

Longer duration predisposes the patient to atrial clot formation and failure of conversion

Greater than 48 hours durationRate control with diltiazem, beta blockers or

digitalisDo not attempt cardioversion unless emergently

indicatedAnticoagulation and arrangement for echo

Atrial Flutter

Patients usually with cardiac or pulmonary disease

Conduction through the AV node may be at a 2,3, 4, or 5:1 rate

If you see a ventricular rate close to 150, consider atrial flutter

Frequently is a transient rhythm which may degenerate into atrial fibrillation or convert to sinus

Treatment of Atrial FlutterUnstable – immediate synchronized

cardioversionStable

Vagal manuevers – if no carotid bruitsAdenosine – will not terminate the atrial

tachycardia, but may allow flutter waves to become more apparent

Dig, beta blockers or calcium channel blockers for AV nodal blockade to slow the ventricular rate

Supraventricular Tachycardia (SVT)

AV nodal reentrant tachycardiaUsually regular, narrow complex tachycardia

without p wavesTreatment

AdenosineBeta blockersCalcium channel blockersDigoxin

SVT – HR around 150s

Is it SVT, a-fib, a-flutter, sinus tach?

Wolf-Parkinson-White Syndrome

Pre-excitation SyndromeAV re-entrant tachycardia (accessory

pathway)Short PR interval, delta wavesTreatment:

Treat like SVT if the QRS is narrowIf the QRS is wide or if afib is present, use

amiodarone or procainamide Slow the atrial rate and increase conduction through

the AV nodeAvoid ABCD – adenosine, beta blockers, calcium

channel blockers, digoxin if wide QRS

Narrow complex WPW

Wide complex WPW

•First Degree•Second Degree - Type I•Second Degree - Type II•Third Degree

Atrioventricular Blocks

Second Degree AV Blocks

Group to group beating Second degree blocks are partial

blocksTwo types

Type I, Mobitz I or Wenckebach – transient

Type II, Mobitz II or Classic – often degenerates into 3rd degree heart block

Second Degree: Mobitz Type I

Decremental conduction: grouped beats with progressively longer PR intervals until an impulse is not conducted (a p without a QRS)

Usually narrow QRSMay be associated with inferior MITreatment:

Generally requires no treatmentAtropine, temporary pacing if symptomatic

Second Degree, Mobitz Type II

Conduction fails suddenly, no change in the PR interval

This is NOT a benign rhythmOften progresses to a complete heart block Associated with anteroseptal MIMay have wide QRS

Second Degree, Type II: Treatment

No pharmacologic treatmentAtropine has no effect on the His-Purkinje system and may

worsen the conduction ratioEmergency treatment – transcutaneous or transvenous

pacing

Third Degree BlockComplete block – there is total AV

DissociationNone of the atrial impulses are conducted

through to the ventricles P and QRS are independent, P-P and R-R intervals

constantAn escape rhythm will drive the ventricles

If the escape rhythm originates in the AV junction, the ventricular rate will be in the range of 40-60 with a narrow QRS

If the escape rhythm originates in the ventricles, the ventricular rate will be in the range of 20-40 with a wide QRS

Third Degree Block: Treatment

Although patients may be asymptomatic, transcutaneous or transvenous pacing is warranted

Autonomic drugs such as atropine will have no effect on ventricular rate

Type I anti-arrhythmics should be avoided as they may suppress the escape rhythm

•Premature Ventricular Contraction (PVC)•Ventricular tachycardia (VT)•Ventricular fibrillation (V-fib)

Ventricular Arrhythmias

PVCs: Causes

Generally benignMay be a consequence of a pathology,

especially if multifocalMore concerning causes including

hypoxia, ischemia, MI, toxins/drugs, acidosis or alkalosis, hypokalemia

Ventricular Tachycardia

Results from a dysrhythmia originating at or below the bundle of His

Has a wide QRS complex (>0.12 second)May be monomorphic or polymorphic

Monomorphic V-tachMorphologically consistent QRS complexesMost common form of V-tachSeen primarily with cardiac ischemia Also seen in cardiomyopathy, valvular

disease, electrolyte imbalance, myocarditis

Polymorphic V-tachQRS complexes vary in structure and

amplitudePredominantly caused by CADAssociated with more severe disease

Torsades de PointesA specific form of polymorphic v-tachAssociated with prolonged QTMay be due to drugs (tricyclics), electrolyte

imbalance (hypo K, Mg or Ca), or subarachnoid hemorrhage

V-Tach: Treatment

Unstable:Immediate unsynchronized cardioversion100J, 200J, 300J, 360 J

Stable:Amiodorone 150 mg IVP or lidocaine 1 mg/kgPrepare for elective synchronized

cardioversionTorsades de Pointes: magnesium sulfate 1-2g

IV

Ventricular FibrillationAn irregularly irregular rhythm with no p

waves or definite QRS complexes

Treatment of V FibDefibrillate

Adult: 360/360/360 joulesChildren: 2 J/kg

Epinephrine 1 mg IVP q 3-5 min (0.01 mg/kg)

AmiodaroneLidocaineMagnesium

•Osborne Waves•Brugada Syndrome

Other EKG Abnormalities

Osborne WavesNot a true arrhythmia, but an EKG

abnormality suggestive of underlying pathologySeen primarily in hypothermia, < 35.6 degreesMay also be seen in other conditions, such as

hypercalcemia or brain injuryAlso called J-waves, Camel backs, hathooks

Osborne Waves – Hypothermia

Osborne Waves – Hypercalcemia

Brugada Syndrome Genetic disease – autosomal dominant Mutation in the gene that controls the Na channel Prevalence for Asians Characteristic ECG:

ST segment elevation V1-V3No signs of ischemiaShort QT interval

Most common cause of sudden death in young males with no underlying cardiac disease Cause of death – polymorphic V-tach or V-fib Treatment:

AICD to abort lethal arhythmias

Brugada Syndrome: Diagnostic Criteria

Type I is the only ECG criterion that is diagnostic of Brugada (see figure).

Definitive diagnosis – Type 1 ST-segment is observed in greater than one right precordial lead (V1 to V3) PLUS one of the following: Documented V-fibPolymorphic VT Family history of sudden cardiac death at <45 yoInducibility of VT with electrical stimulationCoved-type ECGs in family members syncope nocturnal agonal respiration.

Brugada Syndrome

Any Questions?

The End