| Sinus |
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Sinus tachycardia
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A normal sinus rhythm at a rate of 95 or
greater. |
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An accelerated sinus rate that is a physiologic
response to a stressor. |
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It is characterized by a regular rhythm
and heart rate faster than 100 beats per minute |
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Underlying physiological stresses such as
exercise, fever, hypoxia, hypovolemia, anxiety, pain, hyperthyroidism,
can induce sinus tachycardia |
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Inappropriate Sinus tachycardia |
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An accelerated baseline sinus
rate (defined as a 24 hour average heart rate > 95) in the absence
of a physiological stressor. |
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an exaggerated response of
the sinus node |
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It is characterized by a
regular rhythm and heart rate faster than 100 beats per minute |
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Hypersensitivity of the sinus
node to autonomic input or an abnormality within the sinus node, its
autonomic input, or both, often seen in young women without structural
heart disease but also in diabetes and autonomic dysfunction. Also
in elderly females it is associated with hypertension and psychiatric
disorders. |
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SA Node Reentrant Tachycardia
(SANRT) |
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Due to a reentry circuit, either in or near
the sinus node with abrupt onset and offset. |
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P waves are similar or identical to sinus
P waves (i.e. high right atrium to low right atrium activation sequence),
so resembles sinus tachycardia; but starts and ends abruptly. |
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Heart rate usually is 100-150 bpm, and
ECG usually demonstrates a normal sinus P wave morphology |
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Often there is underlying structural heart
disease |
| Atrial |
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Atrial Ectopic Tachycardia |
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Caused by a rapid regular impulse formation
in the atria outside of the sinus node area. |
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Atrial tachycardia usually creates a P wave
that is at least slightly different from sinus rhythm dependent on
the site of origin of the tachycardia. There are 3 or more consecutive
impulses at a rate >100 and usually < 250 |
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Unifocal atrial tachycardia |
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Possible digoxin toxicity |
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Single P wave morphology |
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Multifocal atrial tachycardia
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Fairly uncommon and is typically observed
in elderly patients with pulmonary disease. |
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Composed of 3 or more P wave morphologies.
Heart rate is greater than 100 bpm, and ECG findings typically include
an irregular rhythm |
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Atrial Fibrillation |
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Arrhythmia arising from chaotic atrial
depolarization |
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The atria contract irregularly and very rapidly
producing variable R-R intervals. |
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An irregular rhythm with fibrillatory atrial
activity. No regular P waves are identifiable and the baseline is
undulating. The ventricular response may be slow (<60), normal
(60-100), or rapid (>100). The ventricular rate may be 170 bpm
or higher |
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AF is an extremely common rhythm associated
with rheumatic heart disease, hypertension, ischemic heart disease,
pericarditis, thyrotoxicosis, alcohol intoxication, mitral valve prolapse,
and digitalis toxicity |
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Ashemans phenomenon |
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"Conduction is delayed or aberrant when the stimulus
falls during the relative or absolute refractory period...which lengthens
with slower heart rate. When aberrant ventricular conduction of a
beat ending a short cycle is preceded by a longer cycle during atrial
fibrillation it is called Ashman's Phenomenon.. Such aberration is
generally of right bundle branch block configuration and may have
left anterior or left posterior divisional block. " (Am Heart
J 1947;34:366; Circulation 1969;39:345).
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Atrial Flutter |
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Atrial flutter is a tachyarrhythmia arising
above the AV node with an atrial rate of 250-350 bpm |
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Atrial flutter is due to a large reentrant
circuit confined to the right atrium in over 85% of cases |
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Negative sawtooth flutter waves in leads
II, III, and AVF. AV conduction most commonly is 2:1, which yields
a ventricular rate of approximately 150 bpm |
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Commonly is observed in patients with ischemic heart
disease, myocardial infarction, cardiomyopathy, myocarditis, pulmonary
embolus, toxic ingestion (eg, alcohol), or chest trauma |
| Atrioventricular tachycardias |
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Junctional tachycardia
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Any rapid heart action arising from the
region of the AV junction-- a regular narrow complex tachycardia |
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Near simultaneous activation of the atrium
and ventricle occurs. Therefore, the P-wave or atrial activation may
be hidden within the QRS complex and may not be noticeable on the
surface ECG. Retrograde P-wave conduction may be notable as a negative
P wave in leads I and II and positive in aVL |
| Atrioventricular Reentrant Tachycardia |
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AVRT is the result of 2 or more conducting
pathways: the AV node and 1 or more bypass tracts.Sustained reentry
occurs over a circuit comprising the AV node, His Bundle, ventricle,
accessory pathway and atrium. |
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Two main categories: |
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1.orthodromic reciprocating tachycardia (ORT),where the circuit
is anterograde via the AV node and His bundle and retrograde via
an accessory pathway. Retrograde P waves are seen on the following
ST segment and the QRS configuration is as in normal sinus rhythm.
2. antidromic reciprocating tachycardia (ART), where the circuit
is anterograde via the accessory pathway and retrograde via the
His Purkinje system and AV node. The QRS is deformed by delta waves
e.g. rapid atrial fibrillation via an accessory pathway and may
resemble VT. When impulses travel down the accessory pathway in
an anterograde manner, ventricular preexcitation results. This produces
a short PR interval and a delta wave as seen in Wolff-Parkinson-White
(WPW) syndrome
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Atrioventricular reentrant tachycardia (AVRT)
is the second most common form of PSVT, more frequent in males than
females (2:1) |
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Atrioventricular Nodal Reentrant Tachycardia |
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AVRT is the result of 2 or more conducting
pathways: the AV node and 1 or more bypass tracts.Sustained reentry
occurs over a circuit comprising the AV node, His Bundle, ventricle,
accessory pathway and atrium. |
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Heart rate is 120-250 bpm and typically is quite regular
There are at least two types:
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1. The common form (90%) is called 'slow-fast' with an anterograde
slow pathway and a fast retrograde pathway. The retrograde P wave
is obscured in the corresponding QRS or occurs at the end of the
QRS complex in V1 producing a pseudo r' or a pseudo S II and S III
may also occur
2. The uncommon form or 'fast-slow' has the direction reversed
with a fast anterograde and a slow retrograde pathway. This results
in a retrograde P wave beyond the T wave producing an inverted P
in leads II, III and aVF
Onset of AVNRT is triggered by a premature atrial impulse. A premature
atrial impulse may reach the AV node when the fast pathway (beta)
is still refractory from the previous impulse but the slow pathway
(alpha) may be able to conduct. The premature impulse then conducts
through the slow pathway (alpha) anterogradely; the (beta) pathway
continues to recover because of its longer refractory period. After
the impulse conducts anterogradely through the slow (alpha) pathway,
it may find the fast (beta) pathway recovered; the impulse then
conducts retrogradely via the fast (beta) pathway. If the slow pathway
(alpha) has repolarized by the time the impulse completes the retrograde
conduction, the impulse then can reenter the slow (alpha) pathway
and initiate AVNRT
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The most frequent mechanism of SVT, usually
a regular narrow QRS tachycardia . May occur in healthy, young individuals,
and it most commonly occurs in women. Most patients do not have structural
heart disease. |
| Ventricular |
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| Accelerated Idioventricular Rhythm |
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A rapid ventricular rhythm, but an independent
sinus rhythm or atrial rhythm may coexist. |
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Ventricular tachycardia |
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Electrocardiography is the criterion standard
for diagnosis of VT. Tthe challenge is to discriminate between VT
and aberrantly conducted SVT.
Specific findings for VT include:
1. absence of RS complexes in the precordial ECG leads (V1-V6),
2. RS duration greater than 100 milliseconds in any precordial lead,
3. and ventriculoatrial dissociation. |
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Torsade du pointes |
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Patients have paroxysms of 5-20 beats,
with a heart rate faster than 200 bpm; sustained episodes occasionally
can be seen.
Progressive change in polarity of QRS about the isoelectric line occurs.
Complete 180° twist of QRS complexes in 10-12 beats is present.
Usually, a prolonged QT interval and pathological U waves are present,
reflecting abnormal ventricular repolarization. The most consistent
indicator of QT prolongation is a QT of 0.60 s or longer or a QTc
(corrected for heart rate) of 0.45 s or longer.
A short-long-short sequence between the R-R interval occurs before
the trigger response. |
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Ventricular fibrillation |
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Chaotic, random, asynchronous electrical activity of
the ventricles resulting in rapid, irregular bizarre QRS complexes.
Wavy chaotic ventricular dopolartization resulting in fibrilatory
waves. |
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Brugada Syndrome |
It is a rare condition in the western world
that appears to be considerably more common amongst young men in South
East Asia. It is also known as "Sudden Unexpected Death Syndrome"
(SUDS). ECG changes described as follows: "right bundle branch
block with J point elevation and concave ST elevation". Brugada
Syndrome of RBBB, ST segment elevation and sudden death.
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