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Transcript
PROPERTIES
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Arrhythmias - Part 1
Karima Sajadi, MD
Sarah A. Stahmer MD
Cooper University Hospital
Objectives
• Understand the basic mechanisms that give rise to
arrhythmias
• Review the basic types of tachy-arrhythmias and their
treatment
• Review the presentation of wide complex tachycardias
and their treatment
• Review the basic types of brady-arrhythmias and their
treatment
Slide 3
Mechanisms
• Enhanced automaticity – spontaneous depolarization of
the myocytes that are normally not arrhythmogenic
• Triggered activity – depolarizations that are triggered by
the preceding beat and occur during or after
repolarization
• Reentry – existence of slow and fast conducting
pathways that allow antero- and retrograde conduction
Slide 4
Tachydysrhythmias
Tachydysrhythmias
Regular
Irregular
Narrow complex
Wide complex
Narrow complex
Wide complex
Sinus Tachycardia
Atrial Tachycardia
Atrial Flutter
AVNRT/AVRT
Ventricular tachycardia
Pacer-mediated
tachycardia
SVT with pre-existing BBB
SVT with rate-dependent BBB
MAT
Atrial Fibrillation
Atrial Flutter with
variable block
Torsade des Pointes
Ventricular fibrillation
Slide 5
Regular Narrow-Complex
Tachyarrhythmias
1. Sinus tachycardia
2. Atrial tachycardia
3. 3. Atrial flutter
4. 4. Paroxysmal supraventricular tachycardia
– A. AVNRT (AV nodal reentry tachycardia)
– B. AVRT or ORT (Orthodromic reciprocating
tachycardia)
Slide 6
Sinus Tachycardia
• Physiologic response rather than a pathologic rhythm
• Maximal rate = 220 bpm – age (years)
Slide 7
Sinus Tachycardia
• Causes:
– Fever, anxiety, hypovolemia, thyrotoxicosis
– Peripheral vasodilatation
– Exogenous catecholamines (cocaine, amphetamine,
dopamine)
– Anticholinergics (TCAs, Benadryl)
– LV dysfunction (CHF, myocardial ischemia)
– RV dysfunction (PE, RV infarct)
Slide 8
Sinus Tachycardia
• ECG Recognition:
– Discrete P waves before every QRS, constant PR
interval
– Rate should vary in response to respirations, vagal
stimulation, pain, stress
– An isolated sinus tachycardia is a potentially life
threatening rhythm until the underlying cause is
identified and treated!
Slide 9
Sinus Tachycardia
Slide 10
Atrial Tachycardia
• A single ectopic atrial pacemaker
• Causes:
– Enhanced automaticity
– Reentry – patients with a history of cardiac surgery
– Triggered activity – think digoxin toxicity
• ECG recognition:
– Atrial rate 150-250 bpm – slower than atrial flutter, with which it
can be confused
– Ectopic P wave morphology distinct from baseline sinus node P
wave
Slide 11
Atrial Tachycardia
Slide 12
Atrial Flutter
• Mechanism: regular microreentry circuit that rotates
counterclockwise around right atrium
• Inherently unstable and converts to NSR or atrial
fibrillation
• Causes: ischemic heart disease, congestive CM, PE,
myocarditis, hyperthyroidism, etc
Slide 13
Atrial Flutter
• ECG recognition:
– atrial rate 250-230, ventricular rate 75-150 bpm
– if variable ventricular response then it is irregular
– sawtooth wave pattern in inferior leads.
• Treatment:
– depends on time of onset (> or < than 48 hrs)
– preserved or impaired heart function
– presence of WPW syndrome
Slide 14
Atrial Flutter: 1:1
Slide 15
Atrial Flutter 2:1
Slide 16
AVNRT
• Mechanism:
– reentry at AV node or perinodal tissue.
– triggered by premature atrial conduction (PAC)
– PAC conduction is blocked down the fast pathway
(with a long refractory period)
– conducted anterograde through the slow pathway
(with a short refractory period)
– reenters via recovered fast pathway
Slide 17
AVNRT
• ECG recognition:
– Narrow complex regular tachycardia at 140-280 bpm
– P wave not seen due to simultaneous atria/ventricular activation
• Causes:
– Atrial stretch (ACS, CHF)
– irritability (exogenous catecholamines)
– inflammation (pericarditis)
• Treatment:
– Vagal maneuvers, adenosine
– beta-blockers, diltiazem, digoxin
Slide 18
AVNRT
Slide 19
Atypical AVNRT
Slide 20
AVRT or ORT
• Less common than AVNRT, difficult to distinguish from AVNRT on
EKG
• Mechanism:
– macroreentry through normal conducting system and an
accessory AV pathway
– impulse conducts anterograde down the AVN
– reenters via an accessory pathway, resulting in narrow-complex
tachycardia
– P wave visible due to delayed activation of the atria
• ECG recognition:
– P wave follows QRS
Slide 21
ORT
• Causes: same as AVNRT
• Treatment:
– AV-nodal blocking agents are usually effective due to
antegrade activation of the ventricles via the AVN
– Ablation treatment has a 95% success rate
Slide 22
AVRT or ORT
Slide 23
ORT
Slide 24
ORT after Adenosine
Slide 25
Irregular Narrow-Complex
Tachyarrhythmias
1. Multifocal Atrial Tachycardia (MAT)
2. Atrial fibrillation
3. Atrial flutter with variable block
Slide 26
MAT
• Mechanism:
– absent single dominant pacemaker
– multiple atrial foci fire independently
• ECG recognition:
– at least 3 different P wave morphologies
– variable P-R, P-P, R-R intervals
– isoelectric baseline present to distinguish from atrial
fibrillation
Slide 27
MAT
• Causes:
–
–
–
–
COPD, hypoxia
Pulmonary Hypertension
CHF
Theophylline toxicity
– Electrolyte abnormalities (low K/Mg)
• Treatment:
– treat underlying cause
– Magnesium, Verapamil may be beneficial
Slide 28
MAT
Slide 29
Atrial Fibrillation
Slide 30
Atrial Fibrillation
• Mechanism:
– due to multiple reentrant wavelets between left and
right atria
• ECG recognition:
– irregularly irregular rhythm
– disorganized atrial activity
– no clear P waves between QRS complexes
Slide 31
Atrial Fibrillation
• Causes:
– Ischemic heart disease, HTN
– pericarditis
– “holiday heart”
– thyrotoxicosis, etc
• Treatment:
– Rate control
– Cardioversion (chemical or electrical)
– Anticoagulation
Slide 32
Atrial Flutter with Variable Block
• Mechanism:
– Atrial rate up to 300 bpm
– not all depolarizations conduct through the AV node
– especially in patients on medications that block AV
node
• ECG recognition:
– irregular narrow QRS complexes
– the ratio of atrial flutter waves to QRS complexes
varies (2:1, 3:1, etc)
Slide 33
Atrial Flutter with Variable Block
Slide 34
Conclusion
• This concludes part 1 of the arrhythmia presentation.
• Continue to Arrhythmias Part 2 for the next installment of
this lecture.
• Cases studies and references for this section are found
at the end of Arrhythmias Part 3.