Arrhythmias Flashcards
Tachyarrhythmias
> 100bpm
Supraventricular Tachyarrhythmias
o Sinus Tachycardia o Focal Atrial Tachycardia o Multifocal Atrial Tachycardia o AVRT o AVNRT o Atrial Flutter o Atrial Fibrillation
Ventricular Tachyarrhythmias
o Ventricular Tachycardia
§ Monomorphic
§ Polymorphic
§ Normal QT
§ Prolonged QT- Torsades de Pointes
o Ventricular FibrillationBradyarrhythmia
<60 bpm
Sinus Bradycardia
• First Degree Heart Block
• Second Degree Heart Block
• Mobitz I (Wenckebach)
• Mobitz II
• Third Degree Heart BlockSick Sinus Syndrome
SA node Dysfunction caused Sinus Bradycardia
Concomitant Compensatory Supraventricular Tachycardia
o Atrial Fibrillation, Atrial Flutter, SVT
• Tachycardia-Bradycardia Syndrome
• Usually require combination therapy
o Beta-blocker or calcium channel
blocker for SVT
o Permanent Pacemaker for
Bradycardia
How does increased SNS activity manifest as in Tachyarrhythmia
o Pain o Exercise o Hypovolemia o Hypoxia o Pulmonary Embolism o Sympathomimetics
what are the effects of increased metabolic activity during Tachyarrhythmia
Fever
Hyperthyroidism
What are the effects of Decreased Automaticity? Increased vagal tone (PSNS) (Bradyarrhythmia)
Increased vagal tone (PSNS)
Sleeping
Athletes
Inferior wall MI (Right Cor. Artery occlusion)
What are the effects of Decreased Automaticity? Slow AV conduction
beta blockers
Ca blockers
digoxin
What are the effects of Decreased Automaticity? Dec Metabolism
hypothermia
Hypothyroidism (myxedema coma)
What are the effects of Decreased Automaticity? Electrolytes
Hyperkalemia
What are the effects of Decreased Automaticity? inc. Intracranial pressure- causes herniation
Cushing’s Triad
Dec. HR, HTN, Irregular RR
SNS tone in Increased Automaticity (Sinus Tachycardia)
Hypovolemia
Hypoxia- Low RBCs, Lung disease, Pul. Emb
Drugs that can increase automaticity?
Sympathomimetics
Psychological factors that increase automaticity
Pain/Anxiety
Increased metabolic activity that causes an increase in Automaticity
Fever
Hyperthyroid
What causes Delayed After Depolarization
o Infarction o Inflammation (myocarditis) o Stretched myocardium (Cardiomyopathy, Mitral Regurgitation) o Hypoxia o Catecholamine excess (Increased SNS)
What causes Early After Depolarization
Hypokalemia, calcemia, magnesemia
Drugs that cause EAD
A- anti-arrhytmics-Type 1a,1c 3 B- Antibiotics- Macrolides- micins C- Antipsychotics- haloperidol D- Antidepressants- TCA and SSRi E- Anti-emetics- Ondansetron
EAD’s EGCs
usually causes Torsade’s- Polymorphic VT (long QT)
DAD’s ECG
Multifocal AT, Focal Atrial
Tachycardia, VTach (normal QT)
Re-entrant Circuit Tachyarrhythmias
AVNRT/AVRT, AFlut/Afib, Vtach and VFib
AVRT (Atrioventricular re-entrant Tachycardia)
Due to accessory pathway- bidirectional between atria and ventricles § Bundle of Kent • WPW syndrome § Bundle of James • LGL (Long-Ganong-Levine) syndrome
Orthodromic AVRT- Down AV node, up Bundle of KEnt
§ More common type § Conduction moves through AV node-ventricles-accessory pathway-atria-AV node § Narrow Complex WPW § Not as dangerous Normal conduction pathway
Antidromic AVRT Down BK, to Ventricle- Depol. Bundle branches and His- Up AV node and Atria and come back to BK
§ Less Common § Conduction moves down accessory pathwayàventriclesàAV nodeàAtriaàaccessory pathway § Wide Complex WPW § Very dangerous
Atrial Flutter
Reentrant circuit near Cavo-tricuspid isthmus
Atrial Fibrillation
Multiple micro-reentrant circuits in atria due to:
§ Structural Cardiac Disorders: CHF, VHD’s, MI, HT
V-Tach
Large reentrant circuit in ventricles due to MI, Ischemia
V-Fib
Multiple micro-reentrant circuits in ventricles due to MI ischemia
AVNRT
o Due to fibrosis or Myocardial
scar in AV nodes = develop
two pathways
Alpha pathway
§ Slow Conduction
§ Fast Refractory period
Beta Pathway
§ Fast Conduction
§ Slow Refractory Period
What is the commonest form of AVNRT
Movement down the slow
and up the fast pathway is
most common
Conduction Block of AV node cause of Bradycardia
• Inferior wall MI (RCA) • Inflammation o Myocarditis • Infiltrative diseases o Amyloidosis o Sarcoidosis • Idiopathic fibrosis of conduction system • Hyperkalemia
infections that can cause Bradyarrhytmia
Lyme’s disease
MEdications responsible for BRadyarrhytmia
o Beta Blockers
o Calcium Channel Blockers
Narrow QRS, Regular Rhythm- Sinus Tach
o Sinus P wave upright in lead II and
Inverted in aVR
o Atrial Rate is usually between 100-
150bpm
Narrow QRS, Regular Rhythm- Focal Atrial Tachycardia
o Most common example is inverted p
wave in lead II, III, aVF
o Atrial Rate is usually between 150-
250bpm
Narrow QRS, Regular Rhythm- Atrial Flutter Tachy
o Saw tooth waves in II, III, aVF and V1 o 2:1 or 3:1 is common; constantly without variation o Atrial Rate is usually between 250- 350bpm
Narrow QRS, Regular Rhythm-Orthodromic AVRT
o Retrograde p wave or hidden in QRS
o Best seen in II, III, aVF
o Atrial Rate is usually between 150-250bpm
Narrow QRS, Regular Rhythm- AVNRT
o Retrograde p wave or distorted terminal QRS
o Best seen in II, III, aVF
o Atrial Rate is usually between 150-250bpm
Narrow QRS, Irregular Rhythm- Atrial Fibrillation
o Fibrillation waves in V1
o Irregularly Irregular Rhythm
o Atrial Rate is usually > 350bpm
Narrow QRS, Irregular Rhythm- Multifocal Atrial Tachycardia
o 3 different p wave morphologies
o Hx of lung Disease, CHF
o Atrial Rate is usually is between 150-250bpm
Narrow QRS, Irregular Rhythm- Atrial Flutter with variable block
o Saw tooth waves in II, III, aVF and V1
o But may have 2:1, 3:1 occurring variably
o Atrial Rate is usually between 250-350bpm
Wide QRS, Regular Rhythm- VT
o Most Common Wide Complex Tachycardia o >35 years old o Hx of heart disease (MI, CAD, HTN) o Wider QRS for VT as compared to SVT with aberrancy o Av dissociation with VT o ERAD with VT
Wide QRS, Regular Rhythm- SVT with aberrancy
o Previous ECG with BBB
o Previous ECG showing SVT
amendable to adenosine
o Usually, younger patients
Wide QRS, Regular Rhythm- Antidromic AVRT
o Very rare
o Very difficult to differentiate from
VT
Wide QRS, Irregular Rhythm-
Ventricular Fibrillation
Wide QRS, Irregular Rhythm-
Polymorphic VT
o Normal QT
o Prolonged QT
§ Torsades de pointes
Wide QRS, Irregular Rhythm- Atrial Fibrillation with WPW
o Very fast rates (atrial and ventricular rates >300bpm)
o Varying QRS morphology and amplitude
o Difficult to differentiate from PMVT
Wide QRS, Irregular Rhythm- Atrial Fibrillation with aberrancy
o Most common cause in this category
o Difficult to Differentiate from PMVT
o Relatively Consistent QRS morphology
o Slower rate than AF with WPW
Sinus Tachycardia
o Treat Underlying Cause § Fluids for hypovolemia § Tylenol for fever § Oxygen for hypoxia § TPA or heparin for P.E. § D/C sympathomimetics § Beta-blockers and Antithyroid meds for Hyperthyroidism
Focal Atrial Tachycardia, Atrial Flutter, Orthodromic AVRT
reatment in order: o Vagal Maneuver o Adenosine o Beta Blocker or Calcium Channel Blocker o Cardiovert if Unstable o RFA long term
Atrial Fibrillation, Atrial Flutter with variable block, Multifocal Atrial Tachycardia
Treatment in order:
o Beta Blocker or Calcium Channel Blocker- Flecainide (Class 1C)
o Cardiovert if Unstable
o RFA long term
o Anticoagulants for AF based on CHAD-VASC score > 2
Ventricular Tachycardia (VT)
SVT with aberrancy, Antidromic AVRT (unknown wide complex tachycardia)
equence of treatment
§ Adenosine if unknown WCT (cautiously!!!)-If no
response-Amiodarone (Alternativity, Lidocaine) or procainamide(Class 1A)-prepare for cardioversion
§ Look for MI or ischemia for VT once stable
• Cath lab if needed
Long term Treatment § Radiofrequency Ablation § AICD if malignant VT or underlying diseases like: Brugada syndrome, ARVC or HF with low EF Mexiletine (Class 1B)+Amiodarone
Ventricular Fibrillation
o CPR, Epinephrine/Amiodarone, Defibrillate
o Look for MI or ischemia for VF once stable
§ Cath lab if needed
o AICD long term for VF or underlying diseases that predispose to VF like:
Brugada syndrome, ARVC or HF with low EF
Polymorphic VT (Normal QT)
Amiodarone or Lidocaineà prepare for defibrillation (harder to synchronize
cardiovert b/c of irregular QRS waves)
Polymorphic VT (Prolonged QT)
o Magnesium Sulfate and potassium repletion
o Overdrive pacing or Isoproterenol
§ This attempts to increase HR to shorten the QT
o D/C triggering Meds listed above
Atrial Fibrillation with WPW
o Procainamide, Amiodarone Disopyramidde
o Avoid AV blockersàthis can lead to VF
Atrial Fibrillation with aberrancy
o Beta Blocker
o Calcium channel blocker
Bradyarrhythmia Treatment
1. Atropine
o Decreases vagal tone to heart
2. Epinephrine
o Increases sympathetic tone to heart
3. Pacing
o Transcutaneous
o Transvenous
4. Permanent pacemaker long term if
neededMedications for BA
o CCBàcalcium
o Beta BlockersàGlucagon
o DigoxinàDigibind
Inferior Wall MI
Cath lab
Hyperkalemia
o Calcium gluconate
§ Stabilize cardiac membranes
o D50 with insulin
§ Insulin pushes potassium into cells
o HCO3-
§ Hyperkalemia can cause acidosis
o Albuterol
§ Albuterol pushes potassium into cells
o Lasix or kayexalate
§ Urinate out potassium with Lasix
§ Defecate out potassium with
kayexalate
o Dialysis if severe hyperkalemiaLyme disease
Ceftriaxone
Hypothyroidism
Levothyroxine
Hypothermia
Therapeutic Rewarming
Class I Antiarrhythmic Drugs
Class I antiarrhythmic drugs act by blocking voltage-sensitive Na+
channels. They bind more rapidly to open or inactivated Na+
channels than to channels that are fully repolarized. Therefore, these drugs show a greater degree of the blockade in tissues that are frequently depolarizing. This property is called use dependence (or state dependence),
and it enables these drugs to block cells that are discharging at an abnormally high frequency, without interfering
with the normal beating of the heart.
The use of Na+
channel blockers has declined due to
proarrhythmic effects, particularly in patients with
reduced left ventricular function and atherosclerotic heart disease.
Class IA antiarrhythmic drugs
Quinidine, procainamide, and
Disopyramide
Because of their concomitant class III activity, they can precipitate arrhythmias that can progress to ventricular fibrillation.
Mechanism of action of Class 1A
Quinidine binds to open and inactivated Na+ channels and prevents Na+
influx, thus slowing the rapid upstroke
during phase 0
It decreases the slope of phase 4 spontaneous depolarization, inhibits K+
channels, and blocks Ca2+ channels. Because of these actions, it slows conduction velocity and increases refractoriness.
Quinidine
also has
mild α-adrenergic blocking and anticholinergic actions
procainamide and disopyramide have
actions similar to those of quinidine, there is
less anticholinergic activity with procainamide and more with
disopyramide. Neither procainamide nor disopyramide has α-blocking activity. Disopyramide produces a greater
negative inotropic effect, and unlike the other drugs, it causes peripheral vasoconstriction.
Quinidine sulfate or gluconate
rapidly and well absorbed after oral administration
Metabolism of Class 1 A
e hepatic cytochrome P450 3A4 (CYP3A4) isoenzyme, forming active metabolites
N-acetylprocainamide (NAPA)
A portion of procainamide is acetylated in the liver which has the properties and adverse effects of a class III drug
NAPA is eliminated via the
kidney; therefore, dosages of procainamide should be
adjusted in patients with renal dysfunction
Disopyramide
well absorbed after oral administration and is metabolized in the liver by CYP3A4 to a less active metabolite and several inactive metabolites. About half of the drug is excreted unchanged by the kidneys
Adverse effects of Class 1A
Due to enhanced proarrhythmic effects and ability to worsen heart failure symptoms
Class 1A contraindicated in
atherosclerotic heart disease or systolic heart failure
Large doses of quinidine
induce the symptoms of cinchonism (for example, blurred vision, tinnitus, headache, disorientation, and psychosis)
Why are Drug interactions are common with quinidine
since it is an inhibitor of both CYP2D6 and P-glycoprotein
Intravenous
administration of procainamide may cause
hypotension
Class1A drug that has the most anticholinergic effect
Disopyramide; dry mouth, urinary retention, blurred vision, and constipation
Class IB antiarrhythmic drugs
Lidocaine and mexiletine
Class 1B MO
In addition to Na+ channel blockade, lidocaine and mexiletine shorten phase 3 repolarization and decrease the duration of the action potential
Neither drug contributes to negative inotropy
. Lidocaine may also be used in combination with amiodarone for
VT storm
Why is Lidocaine given IV?
Lidocaine is given intravenously because of extensive first-pass transformation by the liver. The drug is dealkylated
to two active metabolites, primarily by CYP1A2 with a minor role by CYP3A4. Lidocaine should be monitored
closely when given in combination with drugs affecting these CYP isoenzymes.
How is Mexletine metabolized
well-absorbed after
oral administration. It is metabolized in the liver primarily by CYP2D6 to inactive metabolites and excreted mainly
via the biliary route.
therapeutic Index of Lidocaine
wide-safe
CNS effects of Lidocaine
include nystagmus (early
indicator of toxicity), drowsiness, slurred speech, paresthesia, agitation, confusion, and convulsions, which often
limit the duration of continuous infusions
Mexiletine
narrow therapeutic index and caution should be used
when administering the drug with inhibitors of CYP2D6. Nausea, vomiting, and dyspepsia are the most common
adverse effects.
Class IC antiarrhythmic drugs
Flecainide and propafenone
These drugs slowly dissociate from resting Na+
channels and show prominent effects even at normal heart rates
Class 1C drugs are contraindicated in
Due to their negative inotropic and proarrhythmic effects, use of these agents is avoided in patients with structural heart disease (left ventricular hypertrophy, heart failure, atherosclerotic heart disease)
MO of Class 1C drugs
Flecainide [FLEK-a-nide] suppresses phase 0 upstroke in Purkinje and myocardial fibers (Figure 19.7). This causes
marked slowing of conduction in all cardiac tissue, with a minor effect on the duration of the action potential and
refractoriness.
Automaticity is reduced by an increase in the threshold potential, rather than a decrease in slope of
phase 4 depolarization. Flecainide also blocks K+
channels, leading to increased duration of the action potential.
Propafenone [proe-PAF-e-none], like flecainide, slows conduction in all cardiac tissues but does not block K+
channels. It possesses weak β-blocking property
Flecainide uses (Class 1C)
maintenance of sinus rhythm in atrial flutter or fibrillation in patients without structural
heart disease and in treating refractory ventricular arrhythmias.
propafenone (class 1C)
estricted mostly to atrial
arrhythmias: rhythm control of atrial fibrillation or flutter and paroxysmal supraventricular tachycardia prophylaxis
in patients with AV reentrant tachycardias
Flecainide is well absorbed after oral administration and is metabolized by
CYP2D6 to multiple metabolites. The
parent drug and metabolites are mostly eliminated renally
Propafenone is metabolized to
active metabolites
primarily via CYP2D6, and also by CYP1A2 and CYP3A4. The metabolites are excreted in the urine and the feces.
Adverse effects of Class 1C
Flecainide: generally well tolerated, with blurred vision, dizziness, and nausea occurring most frequently
Propafenone has a similar side effect profile, but may cause bronchospasm and should be avoided in patients with
asthma. Propafenone is also an inhibitor of P-glycoprotein. Both drugs should be used with caution with potent
inhibitors of CYP2D6
Class II Antiarrhythmic Drugs
Class II agents are β-adrenergic antagonists, or β-blockers
These drugs diminish phase 4 depolarization and, thus,
depress automaticity, prolong AV conduction, and decrease heart rate and contractility
Class II agents are useful in
treating tachyarrhythmias caused by increased sympathetic activity
They are also used for atrial flutter and
fibrillation and for AV nodal reentrant tachycardia
Most widely used B-blocker of Cardiac arrhythmias
Metoprolol
Why is metoprolol better than Propanolol
Compared to nonselective β-blockers, such as propranolol [pro-PRAN-oh-lol], it reduces the risk of bronchospasm.
It is extensively metabolized by CYP2D6 and has CNS penetration (less than propranolol, but more than atenolol
[a-TEN-oh-lol]). Esmolol [ES-moe-lol] is a very short and fast-acting β-blocker used for intravenous administration
in acute arrhythmias that occur during surgery or emergency situations
Esmolol
rapidly metabolized by esterases
in red blood cells. As such, there are no pharmacokinetic drug interactions. Common adverse effects with β-blockers
include bradycardia, hypotension, and fatigue
Class III Antiarrhythmic Drugs
Class III agents block K+ channels and, thus, diminish the outward K+ current during repolarization of cardiac cells.
These agents prolong the duration of the action potential without altering phase 0 of depolarization or the resting
membrane potential
Instead, they prolong the effective refractory period, increasing refractoriness. All class III drugs have the potential to induce arrhythmias
Amiodarone
Amiodarone [a-MEE-oh-da-rone] contains iodine and is related structurally to thyroxine. It has complex effects, showing class I, II, III, and IV actions, as well as α-blocking activity. Its dominant effect is prolongation of the action potential duration and the refractory period by blocking K+ channels.
Therapeutic uses of Amiodarone
effective in the treatment of severe refractory supraventricular and ventricular tachyarrhythmias.
Amiodarone has been a mainstay of therapy for the rhythm management of atrial fibrillation or flutter. Despite its
adverse effect profile, amiodarone is thought to be the least proarrhythmic of class I and III antiarrhythmic
drugs.
Pharmacokinetics of Amiodarone
Amiodarone is incompletely absorbed after oral administration. The drug is unusual in having a prolonged half-life
of several weeks, and it distributes extensively in tissues. Full clinical effects may not be achieved until months after
initiation of treatment unless loading doses are employed
Toxicity of amiodarone
Amiodarone shows a variety of toxic effects, including pulmonary fibrosis, neuropathy, hepatotoxicity, corneal
deposits, optic neuritis, blue-gray skin discoloration, and hypo- or hyperthyroidism. However, use of low doses and
close monitoring reduce toxicity, while retaining clinical efficacy.
Why should Amiodarone be used cautiously with other drugs
Amiodarone is subject to numerous drug
interactions, since it is metabolized by CYP3A4 and serves as an inhibitor of CYP1A2, CYP2C9, CYP2D6, and Pglycoprotein
Dronedarone
Dronedarone [droe-NE-da-rone] is a benzofuran amiodarone derivative, which is less lipophilic and has a shorter
half-life than amiodarone.
Why is Dronedarone better than Amiodarone?
It does not have the iodine moieties that are responsible for thyroid dysfunction
associated with amiodarone.
Drugs that have class 1,2,3,4 actions
amiodarone
Dronedarone
When is Dronedarone contraindicated?
symptomatic heart failure or permanent atrial fibrillation due to an increased risk of death. Currently,
dronedarone is used to maintain sinus rhythm in atrial fibrillation or flutter, but it is less effective than amiodarone.
Sotalol
class III antiarrhythmic agent, also has nonselective β-blocker activity. The levorotatory isomer (L-sotalol) has β-blocking activity and D-sotalol has class III antiarrhythmic action.
Sotalol blocks
rapid outward K+ current, known as the delayed rectifier current. This blockade prolongs both repolarization and duration of the action potential, thus lengthening the effective refractory period
Sotalol is used
for
maintenance of sinus rhythm in patients with atrial fibrillation, atrial flutter, or refractory paroxysmal
supraventricular tachycardia and in the treatment of ventricular arrhythmias. Since sotalol has β-blocking properties,
it is commonly used for these indications in patients with left ventricular hypertrophy or atherosclerotic heart
disease
Side-effects of Sotalol
This drug can cause the typical adverse effects associated with β-blockers but has a low rate of adverse
effects when compared to other antiarrhythmic agents. The dosing interval should be extended in patients with renal
disease, since the drug is renally eliminated. To reduce the risk of proarrhythmic effects, sotalol should be initiated
in the hospital to monitor QT interval.
Dofetilide
Dofetilide [doe-FET-i-lide] is a pure K+
channel blocker. It can be used as a first-line antiarrhythmic agent in
patients with persistent atrial fibrillation and heart failure or in those with coronary artery disease. Because of the
risk of proarrhythmia, dofetilide initiation is limited to the inpatient setting. The half-life of this oral drug is 10
hours. The drug is mainly excreted unchanged in the urine. Drugs that inhibit active tubular secretion are
contraindicated with dofetilide.
Ibutilide
Ibutilide [eye-BUE-til-ide] is a K+
channel blocker that also activates the inward Na+
current (mixed class III and IA
actions). Ibutilide is the drug of choice for chemical conversion of atrial flutter, but electrical cardioversion has
supplanted its use. It undergoes extensive first-pass metabolism and is not used orally. Initiation is also limited to the
inpatient setting due to the risk of arrhythmia.
Class IV Antiarrhythmic Drug
nondihydropyridine Ca2+ channel blockers verapamil [ver-AP-a-mil] and diltiazem [dil-TYEa-zem]. Although voltage-sensitive Ca2+ channels occur in many different tissues, the major effect of Ca2+ channel
blockers is on vascular smooth muscle and the heart.
Verapmil vs Dilitezam
Both drugs show greater action on the heart than on vascular
smooth muscle, but more so with verapamil
In the heart
verapamil and diltiazem bind only to open depolarized
voltage-sensitive channels, thus decreasing the inward current carried by Ca2+. These drugs are use-dependent in that they prevent repolarization until the drug dissociates from the channel, resulting in a decreased rate of phase 4
spontaneous depolarization
Class 4 arrhythmic drugs are used for
These agents are more effective against atrial than against ventricular arrhythmias.
They are useful in treating reentrant supraventricular tachycardia and in reducing the ventricular rate in atrial flutter and fibrillation.
Common adverse effects include of Class 4`
radycardia, hypotension, and peripheral edema. Both drugs are
metabolized in the liver by CYP3A4. Dosage adjustments may be needed in patients with hepatic dysfunction. Both
agents are subject to many drug interactions as they are CYP3A4 inhibitors, as well as substrates and inhibitors of Pglycoprotein
Digoxin
Digoxin [di-JOX-in] inhibits the Na+
/K+ -ATPase pump, ultimately shortening the refractory period in atrial and
ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in
the AV node.
Digoxin is used in
ventricular response rate in atrial fibrillation and flutter; however,
sympathetic stimulation easily overcomes the inhibitory effects of digoxin
Digoxin toxicity
ectopic ventricular beats that may result in VT and fibrillation. [Note: Serum trough concentrations of 1.0 to 2.0
ng/mL are desirable for atrial fibrillation or flutter, whereas lower concentrations of 0.5 to 0.8 ng/mL are targeted for
systolic heart failure.]
Adenosine
Adenosine [ah-DEN-oh-seen] is a naturally occurring nucleoside, but at high doses, the drug decreases conduction
velocity, prolongs the refractory period, and decreases automaticity in the AV node.
Intravenous adenosine
is the drug of choice for converting acute supraventricular tachycardias. It has low toxicity but causes flushing, chest pain,
and hypotension. Adenosine has an extremely short duration of action (approximately 10 to 15 seconds) due to rapid uptake by erythrocytes and endothelial cells.
Magnesium sulfate
Magnesium is necessary for the transport of Na+, Ca2+, and K+ across cell membranes. It slows the rate of SA node
impulse formation and prolongs conduction time along with the myocardial tissue
Intravenous magnesium sulfate
salt used to treat arrhythmias, as oral magnesium is not effective in the setting of arrhythmia. Most notably,
magnesium is the drug of choice for treating the potentially fatal arrhythmia torsades de pointes and digoxin-induced
arrhythmias.
Ranolazine
Ranolazine [ra-NOE-la-zeen] is an antianginal drug with antiarrhythmic properties similar to amiodarone. However,
its main effect is to shorten repolarization and decrease the action potential duration similar to mexiletine.
Ranolazine Uses
refractory atrial and ventricular arrhythmias, often in combination with other antiarrhythmic drugs. It is well
tolerated with dizziness and constipation as the most common adverse effect
Ranolazine is metabolized by
Ranolazine is extensively
metabolized in the liver by CYP3A and CYP2D6 isoenzymes and is mainly excreted by the kidney. Concomitant
use with strong CYP3A inducers or inhibitors is contraindicated.
Procainamide, disopyramide, quinidine (Class 1A)
↑ or ↓a- PR interval
↑↑- QRS
↑↑- QT
Lidocaine, mexiletine (1B)
no effects on PR, QRS and QT
Flecainide (1C)
↑ (slight) - PR
↑↑- QRS
No eff. on QT
Amiodarone 3, 1A, 2, 4
↑- PR
↑↑- QRS
↑↑↑↑- QT
Ibutilide, dofetilide 3
No effect pn PR and QRS
↑↑↑- QT interval
Sotalol 3, 2
↑↑- PR
↑↑↑- QT
No eff on QRS
Verapamil 4
↑↑- PR interval
no eff on QRS and QT
Adenosine
↑↑↑- PR
No eff QRS and QT
