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Amiodarone is an antiarrhythmic medication that often finds use in preventing and treating several cardiac arrhythmias. These arrhythmias include ventricular tachycardia, ventricular fibrillation, and wide complex tachycardia. Apart from these, amiodarone also finds uses in atrial fibrillation and paroxysmal supraventricular tachycardia.
The medication can be given via several routes, including intravenous, intraosseous, and oral routes. The medicine belongs to class III of antiarrhythmic medications. It works by increasing the span of time before a heart cell contracts. The drug was first used in 1962 for treating chest pain due to cardiac complications.
Overall, amiodarone finds use in treating serious medical issues involving irregular heartbeat, which can prove fatal. Some examples include persistent ventricular fibrillation and tachycardia. In addition, the medication is an efficient tool for restoring normal heart rhythm and maintaining a steady heartbeat.
Here are the most important overall uses of amiodarone:
Amiodarone finds use in treating ventricular tachycardia, but not in all instances. Only patients suffering from hemodynamically stable ventricular tachycardia should be administered amiodarone. Those suffering from hemodynamically unstable ventricular tachycardia must not be given amiodarone initially. Cardioversion is a better option for the latter case. For the former case, the patient's situation, such as underlying heart function or ventricular tachycardia type, rarely matters. Polymorphic ventricular tachycardia and amiodarone are contraindicated, as antiarrhythmic drugs can worsen this condition.
Amiodarone must only be used when cardioversion and first-line medications like epinephrine fail to achieve the objective of VT/VF conversion. Before administering the drug, the Advanced Cardiac Life Support (ACLS) algorithm must be consulted for gaining knowledge of specific steps.
Here is a brief summary of these steps:
Patients who have undergone open-heart surgery are prone to developing atrial fibrillation. The risk for this development is significantly high in the early days post-surgery. In some trials, intravenous administration of amiodarone resulted in decreased atrial fibrillation. More research is needed when it comes to the accurate determination of amiodarone's effects on atrial fibrillation. However, it has shown the potential to be a favorable agent for hemodynamically unstable patients. UK's National Institute for Health and Clinical Excellence (NICE) recommends this role for amiodarone.
It is pertinent to mention here that this drug is also an excellent choice for the safe and effective treatment of persistent AF over years. However, there are a few side effects to consider when administering this drug, including:
Amiodarone has been administered in shock-refractory cases. However, the outcome of this treatment is classified as poor. The medication fails to create a massive difference in the chances of a patient surviving a cardiac arrest. In the event of ventricular fibrillation and ventricular tachycardia (which results in cardiac arrest), defibrillation and CPR is the preferred treatment to prevent the recurrence of arrhythmias and improve survival rates in patients.
If spontaneous circulation is returned, proceed to post-cardiac arrest management.
An iodine-containing compound that has reasonable structural similarity with thyroxine, amiodarone affects the thyroid gland to produce its effects. One of the key factors behind this drug's effects is its high iodine content. Amiodarone's bioavailability doesn't have an exact number. However, it is generally very poor.
It is pertinent to mention that Amiodarone's bioavailability increases when this drug is taken with food. Lipid solubility is excellent, so it is stored in fat and muscles in higher concentrations than other tissues. Apart from these regions, the drug is also stored in the liver, lungs, and skin. In addition, it can cross the placenta and attain measurable levels in breast milk.
Once amiodarone is broken down, many metabolites are produced. The key metabolite is desethylamiodarone (DAE), which has an antiarrhythmic profile. Certain foods and juices, such as grapefruit juice, inhibit this drug's metabolism. This leads to an elevation in the overall amiodarone levels, however more research is needed to determine the long-term impact of this elevation.
Amiodarone is a class III antiarrhythmic medication. Its mechanism of action is no different compared to the other antiarrhythmic drugs that belong to this class.
Primarily, it works by blocking the potassium rectifier currents. These potassium rectifier currents are responsible for heart repolarization. This repolarization event occurs in the third phase of the cardiac action potential. Once these potassium channels are blocked, it leads to an increase in the action potential duration. Not only that, but it also increases the refractory period in cardiac myocytes. Eventually, this translates into diminished myocyte excitability, which hinders reentry mechanisms and tachyarrhythmias perpetuation.
So far, we have discussed how amiodarone is similar in action to its fellow class III agents. However, amiodarone also functions differently by blocking the beta-adrenergic receptors (such as the beta-1 receptor) and sodium and calcium channels. It is worth mentioning that the electrophysiological manifestations of this drug aren't limited to the described actions only. A diminished sinoatrial node automaticity is AV node conduction, which also forms a crucial part of this context.
Just because these additional manifestations happen doesn't mean that they are beneficial. Instead, sometimes they can lead to unwanted side effects that are felt after amiodarone administration. These side effects include bradycardia, hypotension and TdP, i.e., Torsades de pointes. Oral amiodarone therapy can produce clinical effects in six weeks. But this time frame can vary from patient to patient. Once the amiodarone therapy is discontinued, it can take at least 4-12 weeks before pharmacological effects diminish or cease entirely within the patient's body.
Before using any medication, doing a precautionary analysis check is always good. Before administering amiodarone, primarily via the oral route, a few background checks must be made.
First, check for any allergies the patient may have had in the past, either to amiodarone or any other medication. If it is possible that the patient has had a severe reaction to amiodarone in the past, do not administer the drug.
If amiodarone is to be administered to an elderly patient, a few other additional boxes must be ticked. Elderly patients are more prone to health issues of hepatic, renal, and cardiac natures. If a patient is suffering from any disease or disorder, then the amiodarone dosage must be adjusted. For breastfeeding women, the benefits of amiodarone must be weighed against the cons (including passing on effects to the nursing infant) before deciding in favor of the drug.
How much of this drug should be administered? As mentioned earlier in the steps of administration, 300 mg IV is the preferred choice. For VF or pulseless VT, the first recommended dose is 300 mg IV/IO push and the second recommended dose is 150mg IV/IO push. However, the most critical factor in this context is the patient's medical condition. The dose also varies with respect to the patient's age and their response to previous amiodarone treatment. As a provider, you may want to start the medication at a higher dose and gradually decrease as the patient’s condition improves.
For life threatening arrhythmias, the maximum cumulative dose over 24 hours is 2.2g IV.
For a slow infusion, deliver 360 mg IV over 6 hours (or 1 mg per minute). The maintenance infusion is 540 mg IV over 18 hours (0 .5 mg/min).The administrator must ensure that rapid and slow infusions do not exceed 2.2g in a 24 hour period. The recommended dose can produce effects for up to 40 days.
Patients who are undergoing long-term oral amiodarone therapy don't feel the anti-arrhythmic effects of this medication immediately. Instead, it takes around two to three weeks before such effects are noted. However, if a regimen of higher dosage is given at the beginning of therapy, this period can be reduced significantly. In addition, amiodarone doses below 300 milligrams per day are not associated with an increased incidence of pulmonary adverse effects. Hence, physicians usually try to maintain a long-term dosage of 200 milligrams per day (or in some cases, even less).
Drug interactions are among the most important checks to make before administering amiodarone. In many cases, a doctor might want to change the dose based on possible drug interactions. Some of the medicines best not taken with amiodarone include Saquinavir, Pimozide, Terfenadine, Thioridazine, Tipranavir, Vernakalant, and Ritonavir. The complete list is an extensive one.
Amiodarone can inhibit the hepatic and renal metabolism of several drugs. The inhibition occurs via Cytochrome P450 pathways, the most important of which are CYP 2C9, CYP 2D6, and CYP 3A4. From a clinical point of view, interactions with warfarin and digoxin are of primary importance. Amiodarone diminishes warfarin clearance by a significant factor, which leads to an increased prothrombin time. It takes around seven weeks post-amiodarone administration before these effects peak. As for digoxin, the levels double after coadministration with amiodarone.
Because the use of amiodarone is often associated with several adverse effects, most physicians opt for the lowest possible dosage. Here are some of the most significant effects to monitor for:
Pulmonary toxicity is one of the most serious potential adverse effects of amiodarone therapy. It can result from either direct drug-induced phospholipids or an immune-mediated hypersensitivity reaction. Subacute cough and progressive dyspnea are hallmark features of the clinical presentation of pulmonary toxicity. Findings on chest radiographs, such as patchy interstitial infiltrate, confirm this suspicion of pulmonary toxicity. Although it is rare, adult respiratory distress syndrome is also one of the critical presentations of this condition. In terms of percentages, the frequency of this toxicity ranges between 2-17%. The primary treatment for this condition includes amiodarone withdrawal, corticosteroids, and supportive care. More often than not, it is possible to treat the condition entirely.
It is a common complication that often necessitates an intervention. 10% of the patients undergoing amiodarone therapy report thyroid abnormalities. Hypothyroidism and hyperthyroidism are the two possible results; the ratio of the former to the latter ranges from 2:1 to 4:1. Patients suffering from hypothyroidism can continue with the amiodarone therapy, provided that there is a strong clinical need. However, patients suffering from hyperthyroidism need to discontinue therapy and receive treatment. This treatment includes the withdrawal of amiodarone, addition of antithyroid medicines, and surgical thyroidectomy in some cases.
An increased level of transaminase manifests in liver toxicity. This kind of toxicity is common in patients undergoing long-term amiodarone therapy. Liver toxicity is rarely symptomatic; an increased level of liver enzymes often indicates it. Once it comes to a doctor's attention that the liver enzymes are at least three times higher than their normal concentration, therapy should be discontinued. Of course, this does not apply to a situation where medication withdrawal can lead to life-threatening conditions such as fatal arrhythmia.
A high dosage of amiodarone can lead to multiple side effects of a gastrointestinal nature. These include constipation, anorexia, and nausea. However, once the dosage is reduced or adjusted to a suitable level, a significant decrease in the GI adverse effects may be observed.
One of the common ocular observations in patients undergoing amiodarone therapy is the presence of corneal microdeposits. These deposits are clearly visible on slit-lamp examination. However, this is not worrisome in most cases because these deposits rarely demand discontinuation of amiodarone. That is because their impact on the vision is negligible. A small number of patients have been reported to suffer from optic neuropathy and optic neuritis. However, the sample size of past evaluations has not been large enough to draw conclusions on a general scale. Nevertheless, it is best to refer any amiodarone user for an ophthalmologic examination if they feel any abnormal changes in their visual activity.
Photosensitivity is one of the most common dermatologic adverse effects of amiodarone therapy. It is highly advisable for all patients to use sunblock during and after being treated with Amiodarone. Patients whose skin is repeatedly exposed to the sun may experience bluish skin discoloration. Once therapy is discontinued, this bluish discoloration diminishes and fades away in a few months.
Ataxia, tremor, and paresthesia are key highlights of amiodarone-therapy-induced neurologic toxicity. Dose plays a significant role in these conditions; a reduced dose improves the condition by a significant factor.
Up to three per cent of the patients undergoing amiodarone therapy report bradycardia and heart blockages. In patients with bradycardia or a heart block, IV amiodarone is not the best option if they don't have a pacemaker. Administering the drug through a central venous line is a better option.
The baseline assessment of a patient treated with this drug involves an overview of the patient's complete history and physical examination.
Special attention is paid to congestive heart failure and arrhythmia symptoms. Chest radiographs, thyroid studies, prothrombin time, pulmonary function tests, and liver transaminase level tests are key features of this baseline assessment.
Post-administration, there is still a chance for several complications. Factors that need to be assessed in this context are the drug's efficacy, appropriate dosage level, signs and symptoms of any complications, the possibility of drug interactions, and future planning based on the patient's present condition. ACLS guidelines recommend close monitoring of stable patients for expert opinion and aggressive treatment of patients with evidence of decompensation.
1. What is amiodarone used to treat?
Amiodarone is used to treat certain life-threatening cardiac problems classified as ventricular arrhythmias. It is a go-to medication in those situations when other medicines fail to stabilize the patient’s condition.
2. What is the long-term use of amiodarone?
Amiodarone is often used as a long-term treatment of persistent atrial fibrillation (AF) in addition to its uses within the ACLS algorithm.
3. What are the long-term side effects of amiodarone?
Some of the possible long-term side effects of amiodarone include bradycardia, hypothyroidism, hyperthyroidism, pulmonary toxicity, and ocular deposits. The list of adverse effects is quite extensive, and opting for this drug is a decision that must be made under advisement of a healthcare professional.
4. Is it better to administer amiodarone or perform ablation for AF?
While amiodarone is an effective option for treating persistent atrial fibrillation, one cannot ignore the multiple adverse effects associated with this medicine. It is rarely the first choice for many patients and doctors for persistent AF.
5. Amongst procainamide, lidocaine, and amiodarone, which antiarrhythmic is the best choice?
While lidocaine is a better option for cardiac arrest and procainamide has its advantages when perfusing VT, there is no universal answer. Multiple factors dictate the ideal drug choice for a patient, such as:
6. What should a doctor know before administering amiodarone to a patient?
It is extremely important for the doctor to be informed about any history of lung, liver, heart, or thyroid disease that a patient might have had in the past. Blood tests are performed to ensure that the patient’s liver and thyroid can sustain the adverse effects of amiodarone therapy. A breathing test can be performed to test the patient’s pulmonary function. Information about any medicines currently in use by the patient must be shared with the doctor as well. This helps in avoiding complications with respect to possible drug interactions.
Amiodarone is an essential drug to understand for the effective execution of advanced cardiovascular life support. It is also an effective agent for treating conditions like persistent ventricular fibrillation.
As an antiarrhythmic drug, it is most effective at normalizing the heart rhythm and maintaining a steady heartbeat by blocking the electric signals responsible for any irregular heartbeat. However, despite its effectiveness as an antiarrhythmic drug, its list of adverse effects makes it a difficult choice for doctors to treat issues revolving around irregular heartbeat.
The Advanced Cardiovascular Life Support (ACLS) guidelines recommend amiodarone to initially treat hemodynamically stable wide-complex tachycardia. However, amiodarone must only be used when cardioversion and first-line medications like epinephrine fail to achieve the objective of VT/VF conversion. Furthermore, it is imperative to understand the drug's mechanism of action and note key drug interactions.
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