Dec 05, Author: In the United Sates, the intravenous IV antiarrhythmic drugs available for suppression of acute monomorphic VT are muscle paid and metoprolol to procainamide, lidocaine, and amiodarone, along with the beta-adrenergic blocking agents metoprolol, esmolol, and propranolol. Bretylium is no longer available. In view of the relatively narrow therapeutic windows with these agents, careful attention must be paid to drug pharmacokinetics.
Most antiarrhythmic drugs may actually cause ventricular arrhythmias, and risks generally increase with rising serum drug levels. IV administration of antiarrhythmics is used for the suppression of acute VT.
These agents alter the electrophysiologic mechanisms that are responsible for the arrhythmia. Amiodarone is the drug of choice for acute VT refractory to cardioversion shock. After recovery, oral medications are used for long-term suppression of recurrent VT. Current evidence favors class III antiarrhythmic drugs over class I drugs. Class IA antiarrhythmics increase the refractory periods of the atria and ventricles.
Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity. Procainamide is a class IA antiarrhythmic used for VT that is refractory to defibrillation and epinephrine. It is indicated for ventricular arrhythmias such as sustained VT.
Procainamide is available only in IV form and is rarely used, because of hypotension and proarrhythmia risk. However, procainamide still maintains a specific niche as the drug of choice for management preschool themes and lesson plans stable preexcited atrial fibrillation, muscle paid and metoprolol. Its use is contraindicated by the presence of QT prolongation or congestive heart failure.
Quinidine is a class IA antiarrhythmic that depresses myocardial excitability and conduction velocity. It is indicated for sustained VT but is rarely used, muscle paid and metoprolol, because of proarrhythmia risk. It still maintains a specific muscle paid and metoprolol for VT suppression in specific patients with Brugada syndrome. Class IB antiarrhythmics suppress automaticity of conduction tissue by increasing the electrical stimulation threshold of the ventricle and His-Purkinje system and inhibiting spontaneous depolarization of the ventricles during diastole through a direct action on the tissues.
Lidocaine is an IV class IB antiarrhythmic that increases the electrical stimulation threshold of the ventricle, suppressing the automaticity of conduction through the tissue.
Although lidocaine may terminate VT successfully, it may increase the overall mortality in peri-infarction VT. It can only be given IV, muscle paid and metoprolol. Its use for VT has declined as a consequence of trials showing IV amiodarone to be superior.
Mexiletine is a class IB antiarrhythmic that is indicated for ventricular arrhythmias such as sustained VT. It is a sodium-channel blocker and the closest oral analogue to lidocaine. Mexiletine is generally well tolerated and is occasionally used in patients with VT who respond to IV lidocaine.
Class IB sodium channelóblocking drugs are generally felt to be safer than IC drugs, but no large comparative trials exist. This drug is still occasionally used for outpatient VT suppression. Class IC antiarrhythmics slow conduction in cardiac tissue by altering the transport of ion across membranes, thus causing slight prolongation of refractory periods and decreasing the rate of rise of action potential without affecting its duration. These agents are typically avoided in the presence of coronary artery disease.
Flecainide is a class IC antiarrhythmic approved for treatment of life-threatening ventricular arrhythmias. It blocks sodium prilosec otc and prescription difference between, producing a dose-related decrease in intracardiac conduction in all parts of the heart, with the greatest effect on the His-Purkinje system HV conduction.
Flecainide carries a US Food and Drug Administration FDA black box warning regarding increased mortality when the drug is used in ischemic cardiomyopathy patients. Consequently, the use of flecainide is avoided in patients with structural heart disease.
This drug is used almost exclusively for suppression of atrial arrhythmias in the structurally normal heart. Propafenone is similar in function to flecainide and carries a muscle paid and metoprolol black box warning. It is almost exclusively used for suppression of atrial arrhythmias in the structurally normal heart. Class III antiarrhythmics prolong the action potential duration. Some agents in this class inhibit adrenergic stimulation alpha- and beta-blocking properties ; affect sodium, muscle paid and metoprolol, potassium, and calcium channels; and prolong the action potential and refractory period in myocardial tissue.
These effects result in decreased AV conduction and sinus node function. Amiodarone is the drug of choice for the treatment of hemodynamically unstable VT that is refractory to other antiarrhythmic agents. Prehospital studies currently suggest that amiodarone is safe and efficacious for use in out-of-hospital cardiac arrest. Sotalol is a class III antiarrhythmic that is primarily a potassium channel IKr -blocking drug with a weak beta-blocking effect.
Because sotalol is renally cleared, renal function must be monitored. At low doses, cardioselective beta blockers block response to beta1-adrenergic stimulation and have little or no effect on beta2 receptors. Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. Long-term use of metoprolol has been shown to reduce. Electrolytes are considered therapeutic alternatives for refractory VT. Patients with persistent or recurrent VT after administration of antiarrhythmic drugs should be assessed for underlying electrolyte abnormalities as a cause of their refractory dysrhythmia.
Electrolyte abnormalities that may be associated with VF include hyperkalemia, hypokalemia, and hypomagnesemia. Magnesium sulfate, calcium chloride, and sodium bicarbonate are used in VT secondary to other medications. Magnesium sulfate acts as an antiarrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, muscle paid and metoprolol, and calcium chloride is used to treat VT caused by hyperkalemia. Magnesium sulfate is the agent of choice for torsades de pointes.
It also may be useful for treating conventional VT, especially in patients with confirmed hypomagnesemia. Patients treated with magnesium sulfate require monitoring for hypermagnesemia; an overdose can cause cardiorespiratory collapse muscle paid and metoprolol paralysis, muscle paid and metoprolol.
Calcium chloride is useful for the treatment of hyperkalemia, hypocalcemia, or calcium-channel blocker toxicity. It moderates nerve and muscle performance by regulating the action potential excitation threshold.
Routine use of sodium bicarbonate is not recommended. Epinephrine is considered to be the single most useful drug in cardiac arrest, although it has never been shown to enhance long-term survival or functional recovery.
Epinephrine stimulates alpha, beta1, and beta2 receptors, resulting in relaxation of smooth muscle, cardiac stimulation, and dilation of muscle vasculature. Vasopressin may improve vital organ blood flow, cerebral oxygen delivery, resuscitability, and neurologic recovery.
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