Arrhythmias D 3
Arrhythmias D 3
Arrhythmias D 3
Reentrant
Atrial
SVTs (AVNRT,
fibrillation
AVRT)
Focal Atrial
Tachycardia
Atrial Flutter
Sinus Tachycardia
• SA node discharge rate > 100/min (100-180)
with normal P waves and QRS complexes
• often results from
– increased sympathetic tone
– decreased vagal tone
• appropriate physiologic response to exercise
• sympathetic stimulation in pathologic
conditions fever, hypoxemia,
hyperthyroidism, hypovolemia and anemia
Atrial Premature Beats
• originate from automaticity or reentry in an
atrial focus outside the SA node
• often exacerbated by sympathetic stimulation
• On ECG; APB appears as an earlier than
expected P wave with an abnormal shape
• the QRS complex that follows the P wave is
usually normal, resembling the QRS during
sinus rhythm
Atrial Premature Beat
• If the abnormal focus fires very soon after
previous beat, resulting in a blocked impulse that
does not conduct to the ventricles blocked APB
• If the ectopic focus fires just a bit later in diastole,
it may conduct through the AV node but
encounter portions of the His-Purkinje system
that are still refractory impulse is conducted
more slowly produce wider QRS complexes
APB with aberrant conduction
Atrial Flutter
• characterized by rapid, regular atrial activity at a
rate of 180 to 350/min
• many of these impulses are not conducted to
ventricles slower ventricular rate
• e.g; Atrial rate 300/min, 2:1 block V rate 150 /
min
• Vagal maneuvers decrease AV nodal conduction
increase the degree of block slow the ventricular
rate better visualization of underlying atrial
activity
Atrial Flutter
• In the common form; the circuit is the atrial
tissue along the tricuspid valve annulus
• Because the large part of atrium is
depolarized throughout the cycle, P waves
often have a sinusoidal or “sawtooth”
appearance
• usually associated with areas of atrial scarring
from disease, prior heart surgery, or ablation
procedures
Atrial Fibrillation
• chaotic rhythm with an atrial rate so fast
(350-600 discharges/min) that distinct P waves
are not discernible on the ECG
• only some of the depolarizations are conducted
to ventricles in a very irregular fashion
irregularly irregular rhythm
• average ventricular rate in untreated AF is
140-160 /min
• discrete P waves are not visible on ECG, the
baseline shows low amplitude undulations
punctuated by QRS complexes and T waves
Atrial Fibrillation Mechanism
• multiple wandering reentrant circuits within the
atria
• often initiated by rapid firing of foci in sleeves of
atrial muscle that extend into the pulmonary veins
• AF is often associated with RA or LA enlargement
• HF, HT, CAD and Pulmonary disease increase
atrial pressure promote AF
• Thyrotoxicosis and alcohol consumption
precipitate AF in some people
Atrial Fibrillation
• Potentially dangerous, because;
– rapid ventricular rates may compromise cardiac
output hypotension and pulmonary congestion
– absence of organized atrial contraction promotes
blood stasis in the atria increased risk of
thrombus formation (particularly in LA
appendage) cause stroke
Paroxysmal Supraventricular
Tachycardias
• PSVTs are manifested by
– sudden onset and termination
– atrial rates between 140-250/min
– narrow (normal) QRS complexes unless aberrant
conduction is present
• Mechanism; most often reentry involving the AV
node, atrium and ventricle
• Less common causes; Enhanced automaticity
and triggered activity in the atrium or AV node
AV Nodal Reentrant Tachycardia
• AVNRT is the most common form of PSVT in
adults
• The atrial extensions of AV node constitute
two (or more) potential pathways for
conduction through the AV node;
– slow
– fast conducting pathways
AVNRT
• ECG; a regular tachycardia with normal width
QRS complexes
• P waves may not be apparent; because
retrograde atrial depolarization typically
occurs simultaneously with ventricular
depolarization
• P is hidden in the QRS complex
Atrioventricular Reentrant Tachycardias
• AVRTs are similar to AVNRTs except that one limb
of the reentrant loop is constituted by an
accessory pathway (bypass tract)
• Accessory Pathway; an abnormal band of
myocytes that spans the AV groove and connects
atrial to ventricular tissue separately from the
normal conduction tissue
• Accessory pathways allow an impulse to conduct
– from atrium to ventricle antegrade conduction
– from ventricle to atrium retrograde conduction
– in both directions
AVRT
• Depending on the characteristic of the
pathway;
– The ventricular pre-excitation syndrome
– PSVT resulting from a concealed accessory
pathway
Ventricular Pre-excitation Syndrome
• Wolff-Parkinson-White (WPW) Syndrome
• atrial impulses can pass in an anterograde
direction to the ventricles through the both the
AV node and the accessory pathway
• Ventricles are stimulated earlier than by normal
conduction over the AV node
• ECG;
– PR interval is short (<0.12 sec)
– QRS has a slurred rather than a sharp upstroke delta
wave
– QRS complex is widened
WPW Syndrome
• Patients with WPW Syndrome are
predisposed to PSVTs because AP provides a
potential limb of a reentrant loop
• The most common PSVT in WPW patients is
Orthodromic AVRT (antegrad AV node,
retrograde AP)
• ECG; QRS width is normal, retrograde P waves
visible soon after each QRS complex
WPW Syndrome
• in < 10% of patients Antidromic AVRT
(anterograde AP, retrograde AV node)
• ECG; characterized by a wide QRS complex
• Third type of arrhythmia anterograde
conduction over AP when AF or A flutter is
present Ventricular rates ≈ 300 /min may
result VF and cardiac arrest
Concealed Accessory Pathways
• APs capable of only retrograde conduction
• During sinus rhythm, the ventricles are
depolarized normally through the AV node
alone and the ECG is normal
• result in orthodromic AVRT
Focal Atrial Tachycardia
• Focal AT results from either automaticity of
an atrial ectopic site or reentry
• ECG; a P wave before each QRS complex but P
wave morphology is different than sinus
rhythm depolarization of atrium from
different site
• Paroxysmal or persistent
Multifocal Atrial Tachycardia
• ECG shows an irregular rhythm with multiple
(at least three) P-wave morphologies
• caused by
– abnormal automaticity in several foci
– triggered activity
• most often in severe pulmonary disease and
hypoxemia
Ventricular Arrhythmias
• Common ventricular arrhythmias are;
– Ventricular Premature Beats (VPB)
– Ventricular Tachycardia (VT)
– Ventricular Fibrillation (VF)
• more dangerous than SVTs
• responsible for many of the sudden cardiac
deaths
Ventricular Premature Beats
• common, even in healthy and asymptomatic
people
• arises when an ectopic ventricular focus fires an
action potential
• On ECG; widened QRS complex and not related to
a preceding P wave
• occur in repeating patterns;
– every alternate beat is VPB bigeminy
– two normal beats precede every VPB trigeminy
– consecutive VPB; couplets or triplets
Ventricular Tachycardia
• is a series of three or more VPBs
• divided into 2 categories;
– Sustained VT; persists for > 30 secs
– Nonsustained VT; self terminating episodes
• VT is most commonly found in;
– Myocardial ischemia, infarction
– Heart failure
– Ventricular hypertrophy
– Primary electrical diseases
– Congenital cardiac abnormalities
VT ECG
• QRS complexes are wide (>0.12 sec)
• rate 100-200 /min
• Classification according to QRS morphology;
– Monomorphic every QRS complex is same and
rate is regular
– Polymorphic QRS complexes continually change
in shape and rate varies from beat to beat
VT
• Monomorphic VT usually indicates a
structural abnormality reentry circuit in
region of myocardial scar
• Polymorphic VT; multiple ectopic foci or a
continually changing reentry circuit is the
cause
VT
• Symptoms depend on the rate, duration of
the tachycardia and underlying heart disease
• Sustained VT can cause low cardiac output
resulting in loss of consciousness, pulmonary
edema or progress to cardiac arrest
Ventricular Fibrillation
• immediately life-threatening arrhythmia
• results in disordered, rapid stimulation of the
ventricles with no coordinated contractions
• occurs in patients with severe underlying
heart disease
• major cause of mortality in Acute MI
VF
• often initiated by an episode of VT, which
degenerates
• On ECG chaotic irregular appearance without
discrete QRS waveforms
• If untreated; VF rapidly leads to death