CHAPTER 123: TACHYARRYTHMIAS
Reflex sinus
Tachyarrhythmias may appear in the presence
or absence of structural heart disease; they are
more serious in the former. Conditions that
provoke arrhythmias include (1) myocardial
ischemia, (2) heart failure, (3) hypoxemia, (4)
hypercapnia, (5) hypotension, (6) electrolyte
disturbances (e.g., hypokalemia and/or
hypomagnesemia), (7) drug toxicity (digoxin,
pharmacologic agents that prolong the QT
interval), (8) caffeine consumption, (9) ethanol
consumption.
Diagnosis
Examine ECG for evidence of ischemic changes
(Chap. ll l), prolonged or shortened QT interval,
characteristics of Wolff-Parkinson-White (WPW)
syndrome (see below), or ST elevation in leads
V1-V, typical of Brugada syndrome. See Table
123-1 for diagnosis of tachyarrhythmias; always
identify atrial activity and relationship between
P waves and QRS complexes. To aid the
diagnosis:
SUPRAVENTRICULAR ARRYTHMIAS
Sinus tachycardia originates from SA node and
is not a primary arrythmia . The ECG shows a
normal P wave preceding each QRS complex ,an
upright p wave in lead II and downward p
wave in avL can be a physiologic response to
volume depletion, fever, pain, anxiety, shock,
hypoxia, or in patients on vasopressor or
inotropic support ,CHF, hyperthyroidism .
Human’s maximum heart rate (MHR) is age-
dependent and roughly limited to 220 − age in
years (e.g., in a 70-year-old man, MHR = 220 −
70 = 150).
Treatment of sinus tachycardia is directed at the
underlying cause, which includes treating
infections and fever, volume repletion,
anxiolytics, and pain control. Rate controlling
agents are generally not indicated unless the
rapid HR causes symptoms of low CO, such as
in severe anxiety and pain.
tachycardia may be important to maintain
adequate CO. Direct treatment of the
tachycardia without treatment of the underlying
cause may be deleterious .if symptomatic beta
blocker can be used .
Paroxysmal supraventricular tachycardias (PSVT)
are characterized by sudden onset and
termination (hence, the name). The most
common PSVT in adults is atrioventricular nodal
re-entrant tachycardia (AVNRT). It is caused by a
re-entrant electrical loop within the AV node.
The rate generally varies from 120 to 250 beats
per minute and is associated with a narrow QRS
complex in the absence of aberrancy or an
underlying bundle branch block. The atria and
ventricles typically depolarize at virtually the
same time, and thus the P waves are frequently
not visible, obscured by the QRS complexes. If
visible, they generally present as narrow
inverted P waves at the end of the QRS complex,
commonly described as a “pseudo R” in V1
and/or “a pseudo S” in lead II. AV nodal re-
entrant tachycardia is not associated with any
specific diseases, can occur at any age, and is
more common in women.
TREATMENT : vagal maneouvres (Valsalva,
carotid massage, face immersion in cold water
[diving reflex]) if unsuccessful
adenosine ,verapamil ,adenosine given as a 6 mg
IV bolus (t1/2 approximately 10 seconds). A
second 12-mg dose can be given after 1 to 2
minutes if the first was ineffective, and a third
dose of 12 or 18 mg can be given if needed, beta
blocker ,cardioversion (100-200 J ) . to prevent
reccurence beta
blocker,verapamil ,diltiazem ,digoxin,group 1 c
agent or cathetar ablation
PREEXCITATION SYNDROME (WPW)
Conduction occurs through an accessory
pathway between atria and ventricles. Baseline
ECG typically shows a short PR interval and
slurred upstroke of the QRS ("delta" wave).
Associated tachyarrhythmias are of two types:
• Narrow QRS "orthodromic" tachycardia
(antegrade conduction through AV
node),inverted p waves after qrs,delta wave
uncommon . Treat cautiously with IV adenosine
or beta blocker, verapamil, or diltiazem.
• Wide QRS complex "antidromic" tachycardia
(retrograde conduction through accessory
pathway); delta wave common ,p wave absent if
visible it is before qrs complex…wide complex
tachycardia may also be associated with AF with
a very rapid (>250/min) ventricular rate, which
can degenerate into VF. If hemodynamically
compromised, immediate cardioversion is
indicated; otherwise, treat with IV procainamide
or ibutilide , not digoxin, beta blocker, or
verapamil. Consider catheter ablation of
accessory pathway for long-term prevention.
ORTHODROMIC RE – ENTRANT
TACHYCARDIA :Accessory pathways may
conduct antegrade (forming the delta wave) or
retrograde. Concealed accessory AV pathways
only conduct retrograde, and are invisible in
sinus rhythm. Either of these pathways may
mediate an orthodromic re-entrant tachycardia in
which the electrical impulse propagates
antegrade through the AV node and retrograde
(from ventricle to atrium) through the accessory
pathway. The result is a narrow QRS complex
tachycardia, typically with inverted retrograde P
waves between the QRS and T wave (although
the QRS may be wide because of aberrancy, e.g.,
bundle branch block or fascicular block).
Ectopic atrial tachycardia occurs when there is
automaticity at a single focus outside the
sinoatrial (SA) node. A P wave precedes each
QRS as in sinus tachycardia, but the P wave axis
is altered with different contour from sinus P
wave . When increased automaticity occurs at
three or more different atrial sites, which may
include the SA node, it is termed multifocal
atrial tachycardia, with the alternating foci
causing at least three P wave morphologies
with varying PR intervals on ECG. Both can be
seen in cases of digitalis toxicity (which causes
increased automaticity), severe
cardiopulmonary disease, hypokalemia,
hyperadrenergic states, and as a side effect of
theophylline. Treatment: if digitalis toxic hold
digoxin correct k + .in absence use AV nodal
blocking agents and removal of inciting agents/
factors can attempt conversion with
procainamide or amiodarone .
ATRIAL PREMATURE BEATS :abnormal p
waves with irregular rhythm , qrs width
normal . ETIOLOGY : anxiety, CHF, hypoxia,
caffeine ,electrolyte abnormalities ,treatment :
treat cause ,if symptomatic beta blocker
Atrial fibrillation is a chaotic rhythm within the
atria of 350–600 beats per minute without an
appreciable P wave on ECG. All atrial beats are
not conducted because of the refractory period
in the atrioventricular (AV) node, and
conduction is variably timed, resulting in an
irregular ventricular rate. If the ventricular rate
is greater than 100 beats per minute, a rapid
ventricular response is said to be present. The
associated rapid HR and the lack of atrial
contribution to pumping blood can compromise
CO, requiring immediate treatment. Loss of
organized atrial contraction creates stasis of the
blood pool within the atria, which may facilitate
intracardiac thrombus formation and
thromboembolism.
Atrial fibrillation is seen in patients with chronic
cardiopulmonary disease( mitral valve disease ,
hypertension ,post cardiac surgery ,obstructive
lung disease,cardiomyopathy ) . It can also be
the presenting finding of the elderly with
conduction disturbances, thyrotoxicosis,
infection, pulmonary embolization, acute
alcohol intoxication, pericarditis, and stress, and
is common postoperatively. It is a rare
presentation of acute myocardial infarction.
 degrade to atrial fibrillation. Treatment
of atrial fibrillation and atrial flutter is
outlined in Algorithm 20.6.
Precipitating factors listed here should
be sought and treated. Preoperative
beta-blockers can reduce the incidence
of postoperative atrial
fibrillation/flutter. Thromboembolic
risk management typically involves
anticoagulation with IV heparin
overlapping with Coumadin until the
international normalized ratio (INR) is
>2. Patients with contraindications to
anticoagulation should be treated with
aspirin if possible. .Evaluate potential
underlying cause (e.g., thyrotoxicosis,
mitral stenosis, excessive ethanol
consumption, pulmonary embolism).

Typical atrial flutter is caused by a re-entrant

rhythm localized to the right atrium, which
generates impulses at a rate of approximately
300 beats per minute. The ventricular rate is
frequently 150 beats per minute (half the atrial
rate) due to 2:1 block within the AV node. In 3:1
block, every third beat is conducted, and the
ventricular rate is approximately 100 beats per
minute. A large portion of the atria is
depolarized at once, causing a classic
“sawtooth” appearance on the baseline of the
ECG, with fairly narrow, negative flutter waves
in the inferior leads (II, III, aVF). The ventricular
rate may be regular, but can be irregular if
conduction is variable (i.e., 2:1 alternating with
3:1). It is seen in patients with underlying heart
disease and is also commonly seen in patients
after open heart surgery. If left untreated, it may
Pts with rheumatic mitral valve disease or
CHA 2DS 2-VASc score ;OF2 (1 point each for
CHF, hypertension, diabetes, vascular disease,
age 65-75, female gender; 2 points each for age
75, history of stroke or TIA) should receive
anticoagulation with either warfarin (INR 2.0-
3.0) or, for AF not associated with valvular
disease, newer oral anticoagulants that do not
require prothrombin time monitoring-e.g.,
dabigatran 150 mg bid for creatinine clearance
(CrCI) >30 mUmin (75 mg bid for CrCI 1 5-30
m Umin), rivaroxaban. 20 mg daily with the
evening meal (1 5 mg daily for CrCI 1 5-50
mUmin; avoid if CrCI < 1 5), or apixaban 5 mg
bid (2.5 mg bid for 2 of the following: age ;?80,
weight :560 kg, serum creatinine ;? 1 .5
md/dl).

Can also consider anticoagulation

forCHA,D52-VA5c score of 1 . Prescribe
aspirin, up to 325 mg/d, for CHA,D52-VA5c
of 0-1 or if contraindication to systemic
anticoagulation exists.
Control ventricular rate (60-80 beats/min at
rest, < 1 00 beats/min with mild exercise) with
beta blocker, calcium channel blocker
(verapamil, diltiazem), or
digoxin.
Consider cardioversion (1 00-200 J) after >3
weeks therapeutic anticoagulation, or acutely
if no evidence of left atrial thrombus by
transesophageal echo, especially if symptomatic Tachyarrhythmias with wide QRS complex
despite rate control. Initiation of class IC, Ill, or beats may represent ventricular tachycardia or
IA agents prior to electrical cardioversion supraventricular tachycardia with aberrant
facilitates maintenance of sinus rhythm after conduction. Factors favoring ventricular
successful procedure. Class IC (Table 1 23-2) tachycardia include (l) AV dissociation,capture
drugs are preferred in pts without structural beats, fusion beats (2) QRS width >0.14 seconds
heart disease, and class Ill drugs are with RBBB > 0.16 sec With LBBB configuration
recommended in presence of left ventricular (3) QRS axis : left axis deviation with RBBB
dysfunction or coronary artery disease. morphology . Extreme left axis (northwest axis )
Anticoagulation should be continued for a deviation with LBBB morphology (4)
minimum of 3 weeks after successful concordance of QRS with monophasic R or S
cardioversion. Catheter-based ablation waves in Vl-V6 (5)Morphologic Pattern of QRS
(pulmonary vein isolation) can be considered for Complex
recurrent symptomatic AF refractory to
pharmacologic measures RBBB: V1- mono or biphasic , V6 - RS (with left
axis deviation ) or QS

LBBB : V1,V2 – BROAD R wave >0.04 sec, onset

of qrs to nadir of S wave >_ 0.07 sec, notched
downslope of S wave .. v6 –Q wave
Ventricular premature beats : wide QRS bizzare
appearance ,full compensatory pause between
normal beats . Risk factors :
CAD,MI,CHD,HYPOXIA ,HYPOKALEMIA ,
digitalis toxicity , prolonged QT interval
( congenital or acquired drugs – quinidine.other
antiarrythmics ,tricyclics ,phenothiazines ) .
treatment: treat cause , usually not required if
symptomatic beta blocker

Ventricular tachycardia : The two main

tachyarrhythmias arising from the ventricles are
VF and VT. VT may bem monomorphic, if the
QRS morphology is fixed, or polymorphic, if the
QRS complex is variable. Polymorphic VT is
more like VF than monomorphic VT in that it
results in chaotic ventricular activation, often
with hemodynamic instability, possibly leading
to cardiac arrest and sudden death. Also like VF,
it is more likely to occur in the setting of acute
ischemia, infarct, or acute heart failure.
Monomorphic VT results from re-entrant
electrical impulses within the ventriclesor from a
focal ventricular site with frequent spontaneous
action potentials that propagate to the
remainder of the ventricles. VT is characterized
on ECG by a wide QRS complex (>0.12 seconds),
and a rate usually between 100 and 200 beats per
minute (although it may be higher) capture
beats , fusion beats , AV DISSOCIATION. VT
that lasts <30 seconds is termed nonsustained VT
(NSVT), and sustained VT (just termed VT ) if it
lasts >30 seconds. The most common setting for
monomorphic VT is in healed myocardial
infarction. It occurs less commonly in acute
ischemia and infarct. Importantly, monomorphic
VT may occur in the absence of structural heart
disease. The “idiopathic VTs” do not have a
poor prognosis and may not cause
hemodynamic instability, emphasizing the need
to assess and treat the patient’s condition, and
not solely the ECG .treatment . if unstable
defibrillation > 200 J otherwise: acute:
amiodarone . Lidocaine, procainamide . chronic:
ICD

Ventricular fibrillation : erratic electrical

activity . treatment : electrical defibrillation
An important specific type of polymorphicVTis
torsades de pointes, which is polymorphic VT
associated with prolongation of the QT interval
(in sinus rhythm) from numerous causes,
including (a) drugs (especially tricyclic
antidepressants, antipsychotics, certain
antiarrhythmics, macrolides, and
fluoroquinolone; see (b) electrolyte
abnormalities (hypokalemia, hypomagnesemia,
and hypocalcemia); and (c) congenital long QT
syndromes. Torsades de pointes appears on
ECG as a characteristic pattern of oscillating
amplitude of the QRS, or “twisting,” around the
baseline. Torsades de pointes is generally
symptomatic but may be nonsustained. If
prolonged, hemodynamic instability, syncope,
and/sudden death may result. Treatment :
magnesium 2 gm IV if unstable cardioversion or
else amiodarone, procainamide .

Wide complex tachycardias (except clear sinus

tachycardia with aberrancy) should initially be
assumed to be VT, and the urgency of treatment
should depend on assessment of the patient and
the hemodynamic situation. Distinguishing VT
from SVT
with a wide QRS is therefore of secondary
importance. Mistaken diagnosis of “SVT with
aberrancy” can result in mistreatment. The
differential diagnosis of wide complex
tachycardia is threefold: (a) VT, (b) SVT with
aberrancy (typical bundle branch or fascicular
blocks or atypical aberrancy), and (c) pre-excited
supraventricular rhythm (including atrial
fibrillation) in which case the ECG in sinus
rhythm will typically
feature a delta wave. IF the diagnosis of the
wide complex rhythm is uncertain, it should be
assumed to be VT, and treatment should
proceed according to the patient’s condition.

Accelarated intervntriculr rhythm is a

ventricular rhythm consisting of 3 or more
consecutive monomorphic beats with gradual
onset and gradual termination ,rate usually 40-
120 . etiology : MI most commonly after
thrombolysis ,myocarditis , post cardiac arrest ,
electrolyte abnormalities . TREATMENT : treat
the cause usually self limited ,benign .