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