ANTIARRHYTHMIC DRUGS

Moderator: Prof G.P. SinghPresented by: Dr Rajesh Raman

& Dr Ravi Prakash

Mechanism of arrhythmias

reduced (morepositive) resting membrane potential bringing it closer to the threshold potential

Ischemia and electrolyte imbalances

2 0 depolarization originate duringphase 2 or 3 of the action potential

originating from phase 4

circulation of an activation wave around an inexcitable obstacle

Abnormal generation 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

…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

Vaughan Williams'

Class Electrophysiology Examples I. Na-Channel Blockers Ia. phase 0

conduction v repolarisation APD

quinidine disopyramide procainamide

Ib. phase 0 conduction v repolarisation APD

lignocaine phenytoin tocainide, mexiletine

Ic. phase 0 conduction v repolarisation APD

flecanide ecainide, lorcainide

II. blockers propranolol atenolol, esmolol

III. Prolong Repolarisation (usually by K+ channel block)

repolarisation amiodarone bretylium, sotalol

IV. Calcium Entry Blockers

verapamil diltiazem

fast inflow ofNa+ ions

Outflow of k+ ions

Slow inflow of Ca++ outflow of K+

Fast outflow of K+

fully repolarised state

Na+ channel blockerβ-blockers

K+ 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

SODIUM CHANNEL BLOCKERSCLASS I

Bind to sodium channels and inhibit or block sodium conductance

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 depolarizing

ERP of fast-response fibers is prolonged These can depress myocardium at high doses

Reduce rate of phase 4 depolarization in automatic cells

Classification

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

Class IA agents

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 depolrization

Block Na channel conduction QRS duration Block K channel action potential duration QT interval effective refractory period

IA

Quinidine

Prototype class IA drug. Slows the rapid upstroke during phase 0

and decreases the slope of phase 4 spontaneous depolarization.

In circuit loops in purkinje fibres, quinidine frequently converts one-way conduction block into two-way block, thus abolishing the reentry circuit

Electrocardiographic Changes

Quinidine prolongs the PR, the QRS, and the QT intervals

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 indirectlyQuinidine produces adrenergic receptor blockade and vagal inhibition. Thus the intravenous use of quinidine is associated with marked hypotension and sinus tachycardia

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 digitalis;

(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

Derivative of the local anaesthetic procaine Longer half-life, does not cause CNS toxicity

at therapeutic plasma concentrations, and is effective orally

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 erythematosus-like syndrome

CNS side effects include depression, hallucination and psychosis.

Gastrointestinal intolerance is less frequent than with quinidine.

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.

USES

Terminate monomorphic VT Prevent recurrence of VF but is rarely

used for chronic therapy due to high incidence of lupus like syndrome

Disopyramide

Negative inotropic effect that is greater than the weak effect exerted by quinidine and procainamide, and unlike the latter drugs, disopyramide causes peripheral vasoconstriction.

No effect on sinus rate Less prolonged PR & QRS broadening Used for treatment of ventricular arrhythmias as

an alternative to procainamide or quinidine. 2nd 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 constipation.

CLASS IB

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 myocardium Ib

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

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 muscle The ERP is also shortened but not to the same degree

as the APD, ­\'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]o

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 widen

Usually no change in the refractory period of the AV node 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

®­­Bioavailability ~ 33% Almost completely absorbed after IM

administration Kinetics after IV administration follow a two

compartment model Distribution half-life t½a ~ 8 mins

Elimination half-life t½b ~ 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

Uses

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 convulsions

Tocainide.

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.

Mexiletine.

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 beats

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

Ic

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 β-blocking properties and can aggravate congestive heart failure and

Chronic therapy with oral propafenone is used to maintain sinus rhythm in patients with supraventricular tachycardias, including atrial fibrillation

FLECAINIDE

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

Encainide

Used orally to suppress and prevent recurrence of documented life-threatening ventricular arrhythmias

β-adrenoceptor antagonists Class II drugs:

β-adrenoceptor antagonists

Ventricular dysrhythmias following myocardial infarction are partly the result of increased sympathetic activity, providing a rationale for using β-adrenoceptor antagonists in this setting

AV conduction depends critically on sympathetic activity; β-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 β-adrenoceptor antagonists are used to prevent paroxysmal attacks of atrial fibrillation when these occur in the setting of sympathetic activation.

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 β -blockers must be tapered off gradually for 1 week.

Propranolol

Propranolol is a non-selective β-antagonist Effective in attenuating supraventricular

cardiac arrhythmias but are generally not effective against ventricular arrhythmias (except those induced by exercise)

Propranolol reduces the incidence of sudden arrhythmic death after myocardial infarction

Adverse effects include: Bronchoconstriction, hypoglycemia, Na+ retention, Sexual impairment

Uses

Sinus Tachycardia Atrial & nodal extrasystole evoked by

exercise/emotion PSVT Control ventricular rate in AF/A Fl Reduces digitalis induced tachyarrhythmias Arrhythmias associated with

Pheochromocytoma and halothane anaesthesia

Esmolol

Short-acting β blocker used primarily as an antiarrhythmic drug for intraoperative and other acute arrhythmias

Preferentially blocks the β1 receptors Esmolol’s electrophysiological actions are similar

to those of propranolol. Esmolol decreases arterial pressure, heart rate,

ventricular contractility, and pulmonary vascular resistance.

Treatment of supraventricular tachyarrhythmias for rapid control of ventricular rate and reduction of myocardial oxygen consumption

CLASS III Agents Prolonging

Repolarisation

CLASS III

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

AMIODARONE

Amiodarone

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 β blocking properties

….Amiodarone

The ERP 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 phenomena

ERP of His Purkinje and myocardial fibres

Minimal effect on SA node

…..Amiodarone

Oral absorption is incomplete and erratic, bioavailability ~ 22-86%

Half life is long: t½b ~ 14-59 days Drug accumulates in adipose and highly

perfused tissues Pharmakokinetics after IV administration

differ markedly Removal being relatively rapid, t½ ~ 20

hrs, due to redistribution

Amiodarone Toxicity

N & V - rarely constipation abnormal LFT's abnormal TFT's

¯'s peripheral conversion T4 ® T3

¯'s conversion in the pituitary ® ­ 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 B-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

It is a nonselective β 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 β 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

Dofetilide

Orally active Selectively blocks K+ current: pure class

antiarrhythmic Used to maintain and convert AF/Afl to

sinus Rhythm

Ibutilide

Newer class III antiarrhythmic used to convert AF/AFl to sinus rhythm

Ca2+ channel blockersClass 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.

Verapamil

Verapamil

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%

Verapamil

No significant effects on intra-atrial conduction

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 conduction velocity & ERP

Results directly from ca++-channel blockade However is not seen at usual therapeutic

concentrations of other Ca++-channel blockers, eg. Nifedipine

Uses:

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.

Diltiazem

Similar to verapamil but has relatively more smooth muscle-relaxing effect and produces less bradycardia.

Diltiazem is effective in controlling the ventricular rate in patients with atrial flutter or atrial fibrillation

OTHER ANTIARRHYTHMICS

CARDIAC GLYCOSIDES: Digoxin

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+/K+-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

Adenosine

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

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

Sympathomimetics

Adrenaline and isoprenaline can overcome partial heart block by facilitating AV Conduction and shortening ERP of conducting tissues

SUMMARY: ANTIARRHYTHMIC DRUGS

Antiarrhythmic Therapy

Patient-Specific Contraindications

CONDITION EXCLUDE/USE WITH CAUTION

Cardiac Heart failure Disopyramide, flecainide Sinus or AV node Digoxin, verapamil, dil-dysfunction tiazem, β adrenergic

receptor antagonists, amiodarone

Wolff–Parkinson–White Digoxin, verapamil, syndrome (risk of diltiazem extremely rapid rate if atrial fibrillation develops) Infranodal conduction Na+ channel blockers, disease amiodarone Aortic/subaortic stenosis Bretylium History of myocardial Flecainide infarction Prolonged QT interval Quinidine, procainamide,

disopyramide, sotalol, dofetilide, ibutilide, amiodarone

Cardiac transplant Adenosine

CONDITION EXCLUDE/USE WITH CAUTION

Noncardiac Diarrhea Quinidine Prostatism, glaucoma Disopyramide Arthritis Chronic procainamide Lung disease Amiodarone Tremor Mexiletine, tocainide

Constipation Verapamil Asthma, peripheral vas- β Adrenergic blockers, cular disease, propafenone hypoglycemia

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 output

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 bradycardia

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, β-adrenergic blockers should be used judiciously to prevent myocardial ischemia regardless of whether ST-segment changes are present.

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 Amiodarone Esmolol Phenylephrine (100 µg by intravenous bolus) is administered if

the patient is hypotensive Intravenous digitalization is performed with one of the short-

acting digitalis preparations Synchronized cardioversion may be performed with incremental

doses of energy of 100, 200, 300, and 360 J,

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 conduction: β-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 [D5W] 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.[42] 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 controlled.[43]   

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 consequences

Numerous studies support the efficacy of β-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 intravenously

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 VPBs

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 treatment.

If the patient is hemodynamically stable, amiodarone administered as one or more intravenous doses of 150 mg in 100 mL saline or D5W 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 massage

Cardiopulmonary resuscitation must be initiated immediately, and then defibrillation must be performed as 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.

Thank you