Transcript Sinus Rhythms - Beaumont Emergency Medicine

Cardiac Arrhythmias
A Guide For Medical Students
William Beaumont Hospital
Department of Emergency Medicine
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 Bradycardia
 What is it?
 What causes it?
 When do you treat it?
 How do you treat it?
Sinus Bradycardia
 Characteristics:
 Sinus rhythm
 Normal intervals
 Rate less than 60 bpm
 Etiology:
 Normal variant
 Beta blocker overdose
 Digoxin overdose
 Hypothermia
 Hypothyroidism
 Brady-tachy syndrome
 SA node ischemia
Sinus Bradycardia
 Treatment:
 Requires treatment only if there is evidence of hypoperfusion
 Two treatment options:
 Pacing: transvenous or transcutaneous
 Atropine 0.5 mg IVP
Sinus Tachycardia
 Characteristics:
 Sinus rhythm
 Faster than 100 bpm
 Etiology:
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Usually a physiologic response to a stressor
Volume depletion / low stroke volume
Hypoxia
Systemic pathology: fever, anemia, hyperthyroidism
Drugs
 Treatment:
 Treat the underlying cause
Atrial Arrhythmias
Premature Atrial Contraction (PAC)
Multifocal Atrial Tachycardia (MAT)
Atrial Fibrillation (A-fib)
Atrial flutter (A-flutter)
Supraventricular Tachycardia (SVT)
Pre-excitation Syndromes (WPW)
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 hypomagnesemia
 Treatment:
 Treat the underlying disorder – usually hypoxia
 Unlike the other atrial tachyarrhythmias, cardioversion is of no
value in MAT
MAT Rule of Threes
3 different p waves, 3 different pr intervals and 3 different r to r
intervals
Atrial Fibrillation: Causes
 Cardiovascular – CAD, HTN, CHF, myopathy, myo-, endo-
and pericarditis, infiltrative disease, valvular, congenital
 Metabolic – thyroid, electrolytes
 Pulmonary – pulmonary HTN, PE
 Toxic – cocaine, ETOH (holiday heart), beta agonists
 Sepsis
 Idiopathic
Atrial Fibrillation: EKGs
 Regularity – irregularly irregular
 Rate – atrial rate usually > 350
 Controlled – ventricular rate < 100
 RVR – ventricular rate > 100
 P wave – none discernable, may be flutter waves
 QRS
 Less that 0.12 seconds
 If > 0.12 sec must rule out VT (which is usually more regular)
Atrial Fibrillation with RVR
 Ventricular rate > than 100-120 bpm
 Patients usually symptomatic requiring rapid treatment
 Unstable – cardioversion
 Stable – control rate with calcium channel blockers, beta blockers or digitalis
Atrial Fibrillation Treatment
 Recognize the underlying cause
 A rate under 120 in an asymptomatic patient generally requires
no emergent treatment
 Unstable 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 duration
 Unstable – Cardiovert, synchronized if possible, with 50-100 J
 May also cardiovert electively in symptomatic, stable patients
 Pharmacologic cardioversion
 Procainamide
 Amiodarone
 Ibutilide
Atrial Fibrillation Treatment
 Longer duration predisposes the patient to atrial clot
formation and failure of conversion
 Greater than 48 hours duration
 Rate control with diltiazem, beta blockers or digitalis
 Do not attempt cardioversion unless emergently indicated
 Anticoagulation 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 Flutter
 Unstable – immediate synchronized cardioversion
 Stable
 Vagal manuevers – if no carotid bruits
 Adenosine – 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 tachycardia
 Usually regular, narrow complex tachycardia without p waves
 Treatment
 Adenosine
 Beta blockers
 Calcium channel blockers
 Digoxin
SVT – HR around 150s
Is it SVT, a-fib, a-flutter, sinus tach?
Wolf-Parkinson-White Syndrome
 Pre-excitation Syndrome
 AV re-entrant tachycardia (accessory pathway)
 Short PR interval, delta waves
 Treatment:
 Treat like SVT if the QRS is narrow
 If the QRS is wide or if afib is present, use amiodarone or
procainamide
 Slow the atrial rate and increase conduction through the AV node
 Avoid ABCD – adenosine, beta blockers, calcium channel blockers, digoxin
if wide QRS
Narrow complex WPW
Wide complex WPW
Atrioventricular Blocks
•First Degree
•Second Degree - Type I
•Second Degree - Type II
•Third Degree
Second Degree AV Blocks
 Group to group beating
 Second degree blocks are partial blocks
 Two 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 QRS
 May be associated with inferior MI
 Treatment:
 Generally requires no treatment
 Atropine, temporary pacing if symptomatic
Second Degree, Mobitz Type II
 Conduction fails suddenly, no change in the PR interval
 This is NOT a benign rhythm
 Often progresses to a complete heart block
 Associated with anteroseptal MI
 May have wide QRS
Second Degree, Type II: Treatment
 No pharmacologic treatment
 Atropine has no effect on the His-Purkinje system and may
worsen the conduction ratio
 Emergency treatment – transcutaneous or transvenous
pacing
Third Degree Block
 Complete block – there is total AV Dissociation
 None of the atrial impulses are conducted through to the
ventricles
 P and QRS are independent, P-P and R-R intervals constant
 An 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
Ventricular Arrhythmias
•Premature Ventricular Contraction (PVC)
•Ventricular tachycardia (VT)
•Ventricular fibrillation (V-fib)
PVCs: Causes
 Generally benign
 May be a consequence of a pathology, especially if
multifocal
 More 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-tach
 Morphologically consistent QRS complexes
 Most common form of V-tach
 Seen primarily with cardiac ischemia
 Also seen in cardiomyopathy, valvular disease, electrolyte
imbalance, myocarditis
Polymorphic V-tach
 QRS complexes vary in structure and amplitude
 Predominantly caused by CAD
 Associated with more severe disease
Torsades de Pointes
 A specific form of polymorphic v-tach
 Associated with prolonged QT
 May be due to drugs (tricyclics), electrolyte imbalance
(hypo K, Mg or Ca), or subarachnoid hemorrhage
V-Tach: Treatment
 Unstable:
 Immediate unsynchronized cardioversion
 100J, 200J, 300J, 360 J
 Stable:
 Amiodorone 150 mg IVP or lidocaine 1 mg/kg
 Prepare for elective synchronized cardioversion
 Torsades de Pointes: magnesium sulfate 1-2g IV
Ventricular Fibrillation
 An irregularly irregular rhythm with no p waves or definite QRS
complexes
Treatment of V Fib
 Defibrillate
 Adult: 360/360/360 joules
 Children: 2 J/kg
 Epinephrine 1 mg IVP q 3-5 min (0.01 mg/kg)
 Amiodarone
 Lidocaine
 Magnesium
Other EKG Abnormalities
•Osborne Waves
•Brugada Syndrome
Osborne Waves
 Not a true arrhythmia, but an EKG abnormality suggestive of
underlying pathology
 Seen primarily in hypothermia, < 35.6 degrees
 May also be seen in other conditions, such as hypercalcemia or brain
injury
 Also 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-V3
No signs of ischemia
Short 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:
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Documented V-fib
Polymorphic VT
Family history of sudden cardiac death at <45 yo
Inducibility of VT with electrical stimulation
Coved-type ECGs in family members
syncope
nocturnal agonal respiration.
Brugada Syndrome
The End
Any Questions?