Moderator: Prof G.P. Singh
Presented by: Dr Rajesh Raman
& Dr Ravi Prakash
Moderator: Prof G.P. Singh
Presented by: Dr Rajesh Raman
& Dr Ravi Prakash
reduced (more
positive) resting
potential bringing
it closer to the
threshold potential
originate during
phase 2 or 3 of the
action potential
originating from
phase 4
circulation of
an activation
wave around
an inexcitable
of impulses
Types of Cardiac Arrhythmias
Sinus arrhythmia (cyclic changes in heart rate during breathing)
Sinus tachycardia (the SA node emits impulses faster than normal)
Sick sinus syndrome (the SA node fires improperly)
Premature supraventricular contractions (a premature impulse initiation in the
atria causes the heart to beat prior to the time of the next normal heartbeat)
Supraventricular tachycardia (early impulse generation in the atria speed up the
heart rate)
Atrial flutter (rapid firing of signals in the atria cause atrial myocardial cells to contract
quickly, leading to a fast and steady heartbeat)
Atrial fibrillation (electrical impulses in the atria are fired in a fast and uncontrolled
manner, and arrive in the ventricles in an irregular fashion)
Wolff-parkinson-white syndrome (abnormal conduction paths between the atria
and ventricles cause electrical signals to arrive in the ventricles too early, and subsequently
reenter the atria)
Supraventricular arrhythmias Supraventricular arrhythmias
«Types of Cardiac Arrhythmias
Premature ventricular complexes (electrical signals
from the ventricles cause an early heartbeat, after which the
heart seems to pause before the next normal contraction of
the ventricles occurs);
Ventricular tachycardia (increased heart rate due to
ectopic signals from the ventricles);
Ventricular fibrillation (electrical impulses in the
ventricles are fired in a fast and uncontrolled manner, causing
the heart to quiver).
Ventricular arrhythmias Ventricular arrhythmias
Vaughan Williams'
Class Electrophysiology Examples
I. Na-Channel Blockers
q phase 0
qq conduction v
o repolarisation
mq phase 0
q conduction v
q repolarisation
tocainide, mexiletine
qqqq phase 0
qqqq conduction v
s repolarisation
ecainide, lorcainide
atenolol, esmolol
III. Prolong Repolarisation
¹u·u=!!v ¦v K · ·h=uu÷! ¦!··k)
oo repolarisation
bretylium, sotalol
IV. Calcium Entry

fast inflow of
Na+ ions
Outflow of k
Slow inflow of Ca
outflow of K
Fast outflow of K
fully repolarised state
channel blocker Na
channel blocker
ȕ-blockers ȕ-blockers
channel blockers K
channel blockers
channel blockers Ca
channel blockers
Antiarrhythmic Drug Actions
Most of anti arrhythmic drugs have actions which can be
attributed to more than one class
Drugs unclassified in the Vaughan Williams system Drugs unclassified in the Vaughan Williams system
Bind to sodium channels and inhibit or block sodium
Decrease in the rate of rise of phase 0 of the cardiac
membrane action potential and a slowing of the
conduction velocity
Suppress both normal purkinje fiber and his bundle
automaticity in addition to abnormal automaticity resulting
from myocardial damage
Bind more rapidly to open or inactivated sodium channels
than to channels that are fully repolarized
Greater degree of blockade in tissues that are frequently
ERP of fast-response fibers is prolonged
These can depress myocardium at high doses
Reduce rate of phase 4 depolarization in automatic cells
These have been divided into 3 classes on basis of
quantitative rates of drug binding to, and
dissociation from, sodium ion channels
‡ IB : interact rapidly with Na channel
‡ IC: interact slowly
‡ IA: intermediate
Include Quinidine, procainamide
and disopyramide
Intermediate kinetics of binding
and dissociation
Combined sodium and potassium channel blockade
Moderate phase 0 depression and conduction slowing,
prolonging of action potential duration by blocking
outward K+ current
Blockade is greater in cells with greater frequency of
Block Na channel conduction q QRS duration o
Block K channel action potential duration o QT interval o effective refractory periodo
Quinidine Quinidine
Prototype class IA drug.
Slows the rapid upstroke during phase 0 and
decreases the slope of phase 4 spontaneous
In circuit loops in purkinje fibres, quinidine
frequently converts one-way conduction block into
two-way block, thus abolishing the reentry circuit
Electrocardiographic Changes Electrocardiographic Changes
Quinidine prolongs the PR, the QRS, and the QT intervals
Hemodynamic Effects Hemodynamic Effects
In patients with compromised myocardial function, quinidine
may depress cardiac contractility sufficiently to result in a
decrease in cardiac output, a significant rise in left ventricular
end-diastolic pressure, and overt heart failure.
Can relax vascular smooth muscle directly as well as indirectly
Quinidine produces adrenergic receptor blockade and vagal
inhibition. Thus the intravenous use of quinidine is associated with
marked hypotension and sinus tachycardia
Clinical Uses Clinical Uses Clinical Uses Clinical Uses
(1)Abolition of premature complexes that have an atrial,
A-V junctional, or ventricular origin;
(2)Restoration of normal sinus rhythm in atrial flutter and
atrial fibrillation after controlling the ventricular rate with
(3)Maintenance of normal sinus rhythm after electrical
conversion of atrial arrhythmias;
(4)Prophylaxis against arrhythmias associated with
electrical countershock;
(5) Termination of ventricular tachycardia; and
(6) Suppression of repetitive tachycardia associated with
wolff- parkinson-white (WPW) syndrome.
Because of the high incidence of ventricular
proarrhythmia associated with its use and numerous
other equally efficacious agents, quinidine is now
used sparingly
Procainamide Procainamide
Derivative of the local anaesthetic procaine
Longer half-life, does not cause CNS toxicity at
therapeutic plasma concentrations, and is effective
Slows phase 0 & impulse conduction
Increased ERP, APD, QRS and QT interval
Procainamide is a particularly useful antiarrhythmic
drug, effective in the treatment of supraventricular,
ventricular, and digitalis-induced arrhythmias
Adverse effects
With chronic use, it causes a reversible lupus lupus
erythematosus erythematosus--like syndrome like syndrome
CNS side effects include depression, hallucination
and psychosis.
Gastrointestinal intolerance is less frequent than with
Toxic concentrations of procainamide may cause
asystole or induction of ventricular arrhythmias.
The intravenous route is rarely used because
hypotension occurs if the drug is too rapidly infused.
Terminate monomorphic VT monomorphic VT
Prevent recurrence of VF but is rarely used for
chronic therapy due to high incidence of lupus like
Negative inotropic effect that is greater than the weak
effect exerted by quinidine and procainamide, and unlike
the latter drugs, disopyramide causes peripheral
No effect on sinus rate
Less prolonged PR & QRS broadening
Used for treatment of ventricular arrhythmias as an
alternative to procainamide or quinidine.
line drug for prevention of recurance of VT/VF
Maintaince therapy after cardioversion of AF/AFl
Disopyramide shows effects of anticholinergic activity, for
example, dry mouth, urinary retention, blurred vision, and
Lidocaine, mexiletine, tocainide, phenytoin
Pure sodium channel blockers
Decrease the duration of action potential and ERP of
purkinje fibres
Minimal effect on the rate of depolarization
Minimal effect on conduction velocity in ventricular
Associate and dissociate rapidly within the timeframe
of the normal heartbeat with channel recovery time <
1 second
Binds to open channels during phase 0 of the action
potential (affecting the rate of rise very little, but
leaving many of the channels blocked by the time the
action potential reaches its peak)
Dissociation occurs in time for the next action potential
A premature beat, however, will be aborted because
the channels are still blocked
Bind selectively to refractory channels and thus block
preferentially when the cells are depolarised, for
example in ischaemia.
Lignocaine Lignocaine
Unlike quinidine or procainamide, most of its effects on the heart
are by direct action
† No important interactions with the ANS
Causes suppression of automaticity of ectopic foci but SA node is
not depressed
† Enhanced phase 4 depol. in partially depol. purkinje fibers and
delayed after depolarizations are antagonized
Almost no change in the APD of normal specialised atrial fibres
Substantially decreases APD in purkinje fibres and ventricular
The ERP is also shortened but not to the same degree as the APD,
@o's ERP:APD ratio
Lignocaine and Reentry
Can abolish ventricular reentry, either by,
† Establishing 2-way conduction blockade
Eg. Ischemia
† Improving conduction
Eg. Low [k]
Much less effective than quinidine or procainamide in
slowing the atrial rate in AF or flutter, or in
converting these to SR
† In keeping with minimal effects on atrial tissue
Lignocaine & ECG
In striking contrast to quinidine or procainamide,
lignocaine causes little or no change in the ECG
The Q-T interval may shorten, but the QRS does not
Usually no change in the refractory period of the AV
† This may be shortened in some patients, who show an
increased ventricular rate in AF
† In patients with bundle branch disease, lignocaine may cause
complete AV block within the H-P system
Lignocaine: Kinetics
Well absorbed after oral administration
Subject to extensive first pass metabolism
† pBioavailability ~ 33%
Almost completely absorbed after IM administration
Kinetics after IV administration follow a two compartment
† Distribution half-life t
~ 8 mins
† Elimination half-life t
~ 100 mins
Lignocaine: Interactions
Negative inotropic action may be potentiated by,
† Disturbances of acid-base, or electrolyte balance
† Hypoxia
† Other myocardial depressant drugs
† Pre-existing myocardial disease
Treating ventricular arrhythmias arising during
myocardial ischemia
Drug of choice for treatment of the electrical
manifestations of digitalis intoxication
Used prophylactically in MI to prevent VF
Adverse effects
One of the least toxic antiarrhythmic
Mainly due to its actions on the central nervous
system and include drowsiness, disorientation and
Analogue of lidocaine
Mechanism of action that is similar to lidocaine
It is orally active
Used to prevent or treat ventricular tachycardias
Tocainide can lead to pulmonary fibrosis.
Resembles lidocaine and tocainide
Orally active
Effects on cardiac electrophysiology are similar to
that of lidocaine
Used in the treatment of ventricular arrhythmias,
however, due to proarrhythmic side effects; it is
generally not used with less severe arrhythmias
Effective in post MI ventricular arrhythmias as
alternative to lidocaine resistant cases
Class IC
Associate and dissociate with sodium channels
much more slowly
Most potent sodium channel blockers
They reach a steady-state level of block that does not vary
appreciably during the cardiac cycle; they also show only a
marginal preference for refractory channels, so are not
specific for damaged myocardium.
Cause a rather general reduction in excitability and do not
discriminate particularly against occasional premature
Significantly prolong the refractory period within the AV
node and in accessory bypass tracts
Have minimal effects on the APD
Used to prevent supraventricular arrhythmias in patients who
have otherwise structurally normal hearts
High pro-arrhythmic potential
Propafenone Propafenone
Its major electrophysiological effect is to slow
conduction in fast-response tissues
Propafenone prolongs PR and QRS durations
Like other Na
channel blockers, it also can be used in
ventricular arrhythmias, but with only modest efficacy.
It has ȕ-blocking properties and can aggravate
congestive heart failure and
Chronic therapy with oral propafenone is used to
maintain sinus rhythm maintain sinus rhythm in patients with
supraventricular tachycardias supraventricular tachycardias, including atrial
Potent blocker of sodium and potassium channels
with slow unblocking kinetics
Used for patients with otherwise normal hearts who
have supraventricular arrhythmias.
Flecainide has a negative inotropic effect and can
aggravate congestive heart failure.
It is used orally to suppress and prevent the
recurrent of documented life-threatening ventricular
arrhythmias and supraventricular tachyarrhythmias
in patients not associated with CHF
Used orally to suppress and prevent recurrence of
documented life-threatening ventricular arrhythmias
ȕ ȕ- -adrenoceptor antagonists adrenoceptor antagonists
Class II Class II
drugs: drugs:
ȕ ȕ- -adrenoceptor antagonists adrenoceptor antagonists
Ventricular dysrhythmias following myocardial infarction are partly the
result of increased sympathetic activity, providing a rationale for using
ȕ-adrenoceptor antagonists in this setting
AV conduction depends critically on sympathetic activity; ȕ-
adrenoceptor antagonists increase the refractory period of the AV node
and can therefore prevent recurrent attacks of SVT
These decrease slope of phase 4 depolrization and automaticity in SA
node, Purkinje fibers & other ectopic foci, only when this has been
increased under adrenergic action
The ȕ-adrenoceptor antagonists are used to prevent paroxysmal attacks
of atrial fibrillation when these occur in the setting of sympathetic
Also frequently used to slow the ventricular rate in atrial flutter and
fibrillation by impairing conduction and increasing the refractoriness of
the AV node
The ȕ -blockers must be tapered off gradually for 1 week.
Propranolol Propranolol
Propranolol is a non-selective ȕ-antagonist
Effective in attenuating supraventricular cardiac
arrhythmias but are generally not effective against
ventricular arrhythmias (except those induced by
Propranolol reduces the incidence of sudden
arrhythmic death after myocardial infarction
Adverse effects include: Bronchoconstriction,
hypoglycemia, Na+ retention, Sexual impairment
Sinus Tachycardia
Atrial & nodal extrasystole evoked by
Control ventricular rate in AF/A Fl
Reduces digitalis induced tachyarrhythmias
Arrhythmias associated with Pheochromocytoma
and halothane anaesthesia
Short-acting ȕ blocker used primarily as an
antiarrhythmic drug for intraoperative and other acute
Preferentially blocks the ȕ
Esmolol·s electrophysiological actions are similar to
those of propranolol.
Esmolol decreases arterial pressure, heart rate,
ventricular contractility, and pulmonary vascular
Treatment of supraventricular tachyarrhythmias for
rapid control of ventricular rate and reduction of
myocardial oxygen consumption
Agents Prolonging Agents Prolonging Repolarisation Repolarisation
These drugs substantially prolong the cardiac action
potential usually by K
channel block
Action potential prolongation is least marked at fast rates
(where it is desirable) and most marked at slow rates
Action potential prolongation increases the refractory
period(tissue remains refractory even after full
repolarization) , accounting for powerful and varied
antidysrhythmic activity, for example by interrupting re-
entrant tachycardias and suppressing ectopic activity
Can cause torsade de pointes
Class III antiarrhythmic agent effective orally & IV in
the treatment of ventricular and atrial arrhythmias
Analogue of thyroid hormone
Prolongs APD and ERP, of atrial, nodal and
ventricular tissues
† Explains its broad spectrum of activity
Decreases automaticity in the SA node by reducing the
slow phase 4 depolarization
Inhibits myocardial Ca
channels and has ȕ blocking
The oERP of atrial fibres is responsible for its
effectiveness in SVTs
Decreases the conduction velocity and increases the
ERP of the AV node, both anterograde and
retrograde, making it particularly useful for reentry
o ERP of His Purkinje and myocardial fibres
Minimal effect on SA node
Oral absorption is incomplete and erratic,
bioavailability ~ 22-86%
Half life is long: t
~ 14-59 days
Drug accumulates in adipose and highly perfused
Pharmakokinetics after IV administration differ
Removal being relatively rapid, t
~ 20 hrs, due to
Amiodarone Toxicity
N & V - rarely constipation
abnormal LFT's
abnormal TFT's
† q's peripheral conversion T
† q's conversion in the pituitary po TSH levels
† both hyper & hypothyroidism may occur and the onset may be abrupt
cardiovascular effects : *usually minimal
† atypical VT - Torsade de pointes
† bradycardia
† rarely exacerbation of CCF
photosensitive skin rashes
corneal micro-deposits
pneumonitis & interstitial pulmonary fibrosis
Amiodarone - Drug Interactions
Digoxin - potential severe bradycardia
&-blockers - potential severe bradycardia
Ca-antagonists - potential severe bradycardia
Disopyramide - long QT syndrome
Quinidine - long QT syndrome & atypical VT
Mexiletine - long QT syndrome
Procainamide - serum levels significantly increased
Warfarin - inhibits metabolism
Sotalol Sotalol
It is a nonselective ȕ adrenergic receptor antagonist that also
prolongs cardiac action potentials by inhibiting K+ currents
Sotalol prolongs action potential duration throughout the
heart and QT interval on the ECG
It decreases automaticity, slows AV nodal conduction, and
prolongs AV refractoriness by blocking both K+ channels and
ȕ adrenergic receptors, but it exerts no effect on conduction
velocity in fast-response tissue
Sotalol is approved for use in patients with both ventricular
tachyarrhythmias and atrial fibrillation or flutter.
The most serious side effect is torsade de pointe, the QTc
interval must be watched carefully for excess prolongation
Orally active
Selectively blocks K+ current: pure class
Used to maintain and convert AF/Afl to sinus
Newer class III antiarrhythmic used to convert
AF/AFl to sinus rhythm
Ca Ca
2+ 2+
channel blockers channel blockers Ca Ca
2+ 2+
channel blockers channel blockers
Class Class IV IV
Selective blockade of the slow L-type cardiac
calcium channels
They are most potent in tissues in which the action
potential depends on calcium currents, such as the
SA and AV nodes
Within nodal tissue, calcium channel blockade
elevates the threshold potential, decreases the rate
of rise of phase 0 depolarization and conduction
velocity, and lengthens the refractory period of the
AV node
Clinical effects caused are:
† The heart rate slows;
† transmission of rapid atrial impulses through the AV node to the ventricles
decreases, thus slowing the ventricular rate in atrial fibrillation and atrial
flutter; and
† reentrant rhythms traveling through the AV node may terminate
Used in treatment of reentrant PSVT, to slow the ventricular rate
in patients with atrial fibrillation or flutter.
A derivative of papaverine and was first used as a
coronary vasodilator
Produces Ca
-channel blockade in cardiac and
smooth muscle membranes
Substantially slows the rate of impulse formation in
the SA node in vitro
However, this is offset in vivo due to reflex SNS activity
resulting from arteriolar vasodilation
Normally the rate slows ~ 10-15%
No significant effects on intra-atrial conduction
q Rate of phase 4 depolarisation in H-P fibres
† Can block delayed ADP's and triggered activity resulting
from digitalis toxicity
Most marked effect of verapamil is on the AV node
p q conduction velocity & o ERP
Results directly from ca
-channel blockade
† However is not seen at usual therapeutic concentrations of
other Ca
-channel blockers, eg. Nifedipine
† To prevent recurrence of paroxysmal supraventricular
tachycardia (SVT)
† To reduce the ventricular rate in patients with atrial
fibrillation, provided they do not have wolff-parkinson-
white or a related disorder.
Similar to verapamil but has relatively more smooth
muscle-relaxing effect and produces less
Diltiazem is effective in controlling the ventricular rate
in patients with atrial flutter or atrial fibrillation
Digoxin shortens the refractory period in atrial and
ventricular myocardial cells while prolonging the
effective refractory period and diminishing
conduction velocity in Purkinje fibers.
bind specifically to the Na
-ATP'ase, inhibit its
enzymatic activity
Digoxin enhances the inotropic state by increasing
the intracellular calcium concentration
Used to treat and prevent sinus and supraventricular
fibrillation, flutter, and tachycardia
Most of the purine agents have acute vasodilating
properties in most vascular beds
Adenosine is an important autocoid and endogenous
vasodilator in man
Decreases conduction velocity, prolongs the
refractory period, and decreases automaticity in the
AV node.
Adenosine has an extremely short duration of action
(about 15 seconds).
Adenosine - Actions
Termination of PSVT
† Demonstrated safely and effectively in older children and adults
Induced hypotension
Direct negative inotropic effect
Coronary blood flow increases
Pulmonary vascular resistance decreases but not to the same
extent as SVR
Decreased GFR in the kidney
Atropine shortens AV node ERP and increases
conduction velocity in bundle of his
When A-V block is due to vagal overactivity, eg.
Digitalis toxicity, it can be overcome by atropine
Adrenaline and isoprenaline can overcome partial
heart block by facilitating AV Conduction and
shortening ERP of conducting tissues
Antiarrhythmic Therapy
Patient-Specific Contraindications
Heart failure Disopyramide, flecainide
Sinus or AV node Digoxin, verapamil, dil-
dysfunction tiazem, ȕ adrenergic
receptor antagonists,
Wolff²Parkinson²White Digoxin, verapamil,
syndrome (risk of diltiazem
extremely rapid rate
if atrial fibrillation
Infranodal conduction Na+ channel blockers,
disease amiodarone
Aortic/subaortic stenosis Bretylium
History of myocardial Flecainide
Prolonged QT interval Quinidine, procainamide,
disopyramide, sotalol,
dofetilide, ibutilide,
Cardiac transplant Adenosine
Diarrhea Quinidine
Prostatism, glaucoma Disopyramide
Arthritis Chronic procainamide
Lung disease Amiodarone
Tremor Mexiletine, tocainide
Constipation Verapamil
Asthma, peripheral vas- ȕ Adrenergic blockers,
cular disease, propafenone
Sinus Bradycardia Sinus Bradycardia
Heart rates lower than 40 beats/min are poorly
tolerated, even in healthy patients, and should be
evaluated on the basis of their effect on cardiac
Treatment is recommended if hypotension,
ventricular arrhythmias, or signs of poor peripheral
perfusion are observed
When treatment is deemed necessary, the following
approach may be considered
atropine, 0.5 to 1.0 mg by intravenous bolus
repeated every 3 to 5 minutes, up to 0.04 mg/kg
ephedrine, 5 to 25 mg by intravenous bolus;
dopamine or dobutamine (if blood pressure is
adequate), 5 to 20 µg/kg/min by intravenous infusion;
epinephrine, 2 to 10 µg/min by intravenous infusion;
isoproterenol, 2 to 10 µg/min by intravenous infusion.
Temporary transcutaneous or transvenous pacing may
be necessary for severe, drug-refractory sinus
Sinus Tachycardia Sinus Tachycardia
Prolonged tachycardia in patients with underlying heart
disease can precipitate MI and congestive heart failure
(CHF) as a result of the increased myocardial work
required and decreased myocardial oxygen supply
because of decreased diastolic coronary perfusion time
The underlying disorder should be treated.
Hypovolemia and light anesthesia are the most common
causes. In patients with ischemic heart disease in whom
tachycardia develops, ȕ-adrenergic blockers should be
used judiciously to prevent myocardial ischemia
regardless of whether ST-segment changes are present.
Paroxysmal Supraventricular Tachycardia Paroxysmal Supraventricular Tachycardia
When a patient is anesthetized, PSVT can be precipitated by changes in
autonomic nervous system tone, by drug effects, or by intravascular volume
shifts and can produce severe hemodynamic deterioration
Vagal maneuvers
Adenosine, which is the drug of choice
Verapamil (2.5 to 10 mg given intravenously) terminates AV nodal reentry
successfully in about 90% of cases
Phenylephrine (100 µg by intravenous bolus) is administered if the patient
is hypotensive
Intravenous digitalization is performed with one of the short-acting digitalis
Synchronized cardioversion may be performed with incremental doses of
energy of 100, 200, 300, and 360 J,
Atrial Flutter Atrial Flutter
Atrial flutter does not always indicate severe heart
disease. It can be seen in patients with CAD, mitral
valve disease, pulmonary embolism, hyperthyroidism,
cardiac trauma, cancer of the heart, and myocarditis.
Initial treatment should consist of control of the
ventricular response rate with drugs that slow AV node
† ȕ-Blockers such as esmolol (1 mg/kg by intravenous bolus)
or propranolol.
† Calcium channel blockers such as verapamil (5 to 10 mg
given intravenously) or diltiazem
If the ventricular response is excessively rapid or hemodynamic
instability is present, or both, the following guidelines should be used:
† Synchronized DC cardioversion starting at a relatively high energy of
100 J and gradually increasing to 360 J is indicated.
† ibutilide (1 mg in 10 mL saline or 5% dextrose in water [D
W] infused
slowly intravenously over a 10-minute period) has been documented to
convert atrial flutter to sinus rhythm in most patients with relatively new-
onset atrial flutter.
This may be repeated once, and although it is highly
effective, life-threatening torsades de pointes may occur hours after
ibutilide administration, thus making 4- to 8-hour monitoring after treatment
highly desirable.
† Procainamide (5 to 10 mg/kg for the intravenous loading dose, infused no
faster than 0.5 mg/kg/min) may rarely be used in an attempt to restore
sinus rhythm after the ventricular response has been adequately
† Amiodarone (150-mg intravenous loading dose infused over a 10-minute
period, followed by 1 mg/min intravenously for 6 hours, a 0.5-mg/min
intravenous infusion for 18 hours, and then a reduced intravenous dose or
switching to an oral dose) has recently been shown to be effective.
Atrial Fibrillation
Atrial fibrillation is the most common
postoperative arrhythmia and has significant
Numerous studies support the efficacy of ȕ-
blockers in the prevention of postoperative atrial
fibrillation. Perioperative administration of
amiodarone, sotalol, nondihydropyridine
calcium channel blockers, and magnesium
sulfate has also been associated with a
reduction in the occurrence of atrial fibrillation
Acute atrial fibrillation: Treatment of acute atrial
fibrillation is very similar to that for atrial flutter.
Primary attention should be focused on controlling
the ventricular response, especially with the
administration of diltiazem or esmolol
Junctional Rhythms Junctional Rhythms
Junctional rhythms are common in patients under
anesthesia (about 20%), especially with halogenated
anesthetic agents. Junctional rhythms frequently
decrease blood pressure and cardiac output by about
15%, but they can decrease it up to 30% in patients
with heart disease
Usually, no treatment is required, and the rhythm reverts
spontaneously. If hypotension and poor perfusion are
associated with the rhythm, treatment is indicated.
Atropine, ephedrine, or isoproterenol can be used in
an effort to increase the activity of the SA node so that
it will take over as the pacemaker.
Ventricular Premature Beats
VPBs are common during anesthesia, where they
account for 15% of observed arrhythmias. They are
much more common in anesthetized patients with
preexisting cardiac disease.
VPBs result from ectopic pacemaker activity arising
below the AV junction
The new onset of VPBs must be considered a
potentially serious event because the arrhythmia
may progress to VT or VF d/t coronary artery
insufficiency, MI, digitalis toxicity with hypokalemia,
and hypoxemia
In most patients, VPBs (occurring as single, bigeminy, or
trigeminy but excluding nonsustained VT) do not need to
be treated, particularly if the patient does not have an
acute coronary syndrome, and treatment is generally
dictated by the presence of symptoms attributable to the
First step in treatment is to correct any underlying
abnormalities such as decreased serum potassium or low
arterial oxygen tension.
If the arrhythmia is of hemodynamic significance or if it is
believed to be a harbinger of worse arrhythmias,
lidocaine is the treatment of choice, with an initial bolus
dose of 1.5 mg/kg. Recurrent VPBs can be treated with
a lidocaine infusion at 1 to 4 mg/min; additional
therapy includes esmolol, propranolol, procainamide,
quinidine, disopyramide, atropine, verapamil, or
overdrive pacing.
Ventricular Tachycardia
The presence of three or more sequential VPBs
defines VT
Acute onset is life threatening and requires immediate
If the patient is hemodynamically stable, amiodarone
administered as one or more intravenous doses of
150 mg in 100 mL saline or D
W over a period of 10
minutes, followed by an intravenous infusion of
1 mg/min for 6 hours and 0.5 mg/min thereafter, is the
recommended current treatment (maximum intravenous
dose, 2.2 g/24 hr)
Lidocaine and procainamide have been used with
varying degrees of success to treat VT
Synchronized cardioversion is the indicated
nonpharmacologic intervention in any wide-complex
tachycardia, whether monomorphic VT or a wide-
complex SVT.
Polymorphic VT with a normal QT interval is
treated with amiodarone and cardioversion
Polymorphic VT with a prolonged QT interval is a
more serious rhythm disturbance, and the
recommended current treatment is an intravenous
infusion of 1 g of magnesium administered over a
2- to 3-minute period.
Ventricular Fibrillation
Ventricular fibrillation is an irregular rhythm that results
from a rapid discharge of impulses from one or more
ventricular foci or from multiple wandering reentrant circuits
in the ventricles
There is no effective cardiac output, and life must be
sustained by artificial means, such as external cardiac
Cardiopulmonary resuscitation must be initiated
immediately, and then defibrillation must be performed as defibrillation must be performed as
rapidly as possible rapidly as possible.
Asynchronous external defibrillation should be performed
with a DC defibrillator using incremental energies in the
range of 200 to 360 J.
Early administration of 1 g of magnesium sulfate
may facilitate defibrillation. In some instances,
epinephrine has been used to facilitate
defibrillation. Vasopressin has been added as a
drug for the treatment of ventricular fibrillation
Supportive pharmacologic therapy may include
lidocaine, amiodarone, bretylium, procainamide,
phenytoin, or esmolol.

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