When is atropine indicated in the treatment of bradycardia?
If the slowing of the rhythm is extremely pronounced, then drugs such as atropine, alupent, isadrine, isoproterenol are used. Ephedrine is sometimes more effective, which is especially shown to the patient who does not tolerate atropine and isadrin.
What is an alternative to atropine for bradycardia?
· If atropine is ineffective, two treatment pathways are available. The patient’s heart can be paced either intravenously or transcutaneously (TCP), or more emergency medicine can be given. The two pharmacologic choices are dopamine 2 to 20 mcg/kg/min and/or epinephrine 2 …
What is the first drug of choice for symptomatic bradycardia?
· Recently, vasopressin has been the focus of considerable research. Adrenaline is the best studied and most widely administered adrenergic agonist used in the treatment of cardiac arrest. Adrenaline stimulates α 1 and α 2 receptors almost equally, and β 1 and β 2 receptors in a ratio of approximately 1: 4. The American Heart Association and the European …
What is the role of atropine in the treatment of heart block?
a muscarinic acetylcholine receptor antagonist used to treat abnormally slow heart rhythms konwn as bradydysrhythmias it blocks the action of the vaugus nerve (which slows down the …
Which of the following is an alternative to atropine in treating bradycardia?
Dopamine: Second-line drug for symptomatic bradycardia when atropine is not effective. Dosage is 5-20 micrograms/kg/min infusion. Epinephrine: Can be used as an equal alternative to dopamine when atropine is not effective.
What is the treatment for symptomatic bradycardia?
The American Heart Association recommends atropine sulfate as the first line of treatment for symptomatic bradycardia, regardless of whether it is due to AVB or not. This is where the nuance of complete heart blocks comes in.
What is the second-line therapy for an unstable patient with symptomatic bradycardia?
Epinephrine and dopamine are second-line drugs for symptomatic bradycardia. They are both used as infusions in the bradycardia algorithm if atropine is ineffective.
What is the most common treatment for bradycardia?
Bradycardia treatment may include lifestyle changes, medication changes or an implanted device called a pacemaker. If an underlying health problem, such as thyroid disease or sleep apnea, is causing the slow heart rate, treatment of that condition might correct bradycardia.
What is the priority intervention for symptomatic bradycardia?
The initial interventions within the bradycardia algorithm for all infants and children with symptomatic bradycardia include the following: Identify and treat the underlying cause. Provide oxygen. Attach a cardiac monitor for rhythm identification.
When do you use atropine vs epinephrine?
Epinephrine provides a greater amount of hemodynamic support. Patients dying with bradycardia aren't truly dying from bradycardia itself, but rather from cardiogenic shock (low cardiac output). Atropine offers these patients an increased heart rate, nothing more.
What is the first-line drug for acute symptomatic bradycardia?
Atropine sulfate is the first-line drug for acute symptomatic bradycardia and an initial dose of 0.5 mg is recommended.
Which of the following should the ACLS provider do when treating bradycardia?
Symptomatic bradycardia, heart rate typically <50 beats per minute with presence of symptoms, is identified and treated directed at the underlying cause. Maintain a patent airway with assisted breathing as necessary. Administer supplemental oxygen if hypoxic.
Why is dopamine used for bradycardia?
Dopamine is a peripheral vasostimulant used to treat low blood pressure, low heart rate, and cardiac arrest. Low infusion rates (0.5 to 2 micrograms/kg per minute) act on the visceral vasculature to produce vasodilation, including the kidneys, resulting in increased urinary flow.
What is symptomatic bradycardia?
Based on Mrs. Brown's targeted history and physical assessment findings, you suspect symptomatic bradycardia, defined as a heart rate less than 60 with signs and symptoms of poor perfusion caused by the slow heart rate.
When does bradycardia require treatment ACLS?
Regardless of the patient's rhythm, if their heart rate is too slow and the patient has symptoms from that slow heart rate, the bradycardia should be treated to increase the heart rate and improve perfusion, following the steps of the bradycardia algorithm below.
Which medication increases the heart rate?
Certain medicines used to treat depression can raise your heart rate. They include serotonin and norepinephrine reuptake inhibitors (SNRIs) such as desvenlafaxine, duloxetine, and venlafaxine, and tricyclic antidepressants such as amitriptyline, clomipramine, desipramine, and others.
How to treat bradycardia?
A bradycardic rhythm is most often treated only when symptoms are present. If reversible causes aren’t immediately identified and/or if reversing the cause is taking too long, pharmacologic interventions are the first-line approach for bradycardia treatment. Atropine 0.5 mg intravenous (IV) is given up to a total of 3 mg. 1 Atropine sulfate acts by reversing the cholinergic-mediated decreases in the heart rate and AV node conduction. 1
When a patient is evaluated for symptomatic bradycardia, an in-depth history and physical is
When a patient is evaluated for symptomatic bradycardia, an in-depth history and physical is important, along with the identification of possible reversible causes. The following is a list of conditions associated with bradycardia and conduction disorders: 11
What pharmacologic choice is given for heart pacing?
The two pharmacologic choices are dopamine 2 to 20 mcg/kg/min and/or epinephrine 2 to 10 mcg/min. 1.
How much atropine is given?
Atropine 0.5 mg intravenous (IV) is given up to a total of 3 mg. 1 Atropine sulfate acts by reversing the cholinergic-mediated decreases in the heart rate and AV node conduction. 1. If atropine is ineffective, two treatment pathways are available.
What percentage of patients with sleep apnea have sinus bradycardia?
The prevalence of sinus bradycardia in patients with sleep apnea can be as high as 40%, with episodes of second- or third-degree AV block in up to 13% of patients. 8
What are the symptoms of bradycardia?
5. Common bradycardia symptoms include: syncope. presyncope. transient dizziness or lightheadedness. fatigue. dyspnea on exertion. heart failure symptoms.
What is bradycardia heart rate?
What is bradycardia? The National Institutes of Health defines bradycardia* as a heart rate <60 bpm in adults other than well-trained athletes. 9 The determination on whether or not treatment is necessary for bradycardic events is generally based on the presence of bradycardia symptoms. The clinical manifestations of bradycardia can vary widely from insidious symptoms to episodes of frank syncope. 5
How to treat wide QRS complex tachycardia?
Once the hemodynamically stable patient has been cardioverted and stabilized, it is important to evaluate the preconversion 12-lead ECG for the QRS configuration and signs of AV dissociation as described elsewhere in this manuscript. In patients with sustained (duration > 30 s), hemodynamically stable, monomorphic VT, amiodarone (150-300 mg in 5 min i.v., followed by an infusion of 1050 mg/ day) plays an important role in terminating the arrhythmia; this drug is discussed in detail later. An alternative treatment is the administration of procainamide (10 mg/kg i.v.) or ajmaline (50-100 mg i.v. over 5 min), both of which can provide high termination rates [Figure 5]. In patients with VT in the setting of acute myocardial ischemia, lidocaine (100-150 mg i.v.) was for long the treatment of choice but this therapy is now outdated and is not recommended in the newer guidelines. In addition, it has been well known for a long time that the efficacy of ajmaline is better than that of lidocaine and, besides, lidocaine is associated with a high risk of degeneration of monomorphic VT into ventricular fibrillation.[19] Therefore, lidocaine is no more indicated in patients with VT and should be avoided. When in doubt about the origin of a wide-QRS complex tachycardia, verapamil should not be used and, in these cases, ajmaline is an acceptable drug to terminate both SVT and VT. It has been reported that during emergency treatment of wide-QRS complex tachycardia of unknown origin there was a 44% incidence of severe hemodynamic deterioration when verapamil (5 mg i.v.) was administered during VT, necessitating immediate cardioversion.[20] Hypotension, with resulting ischemia, may render the arrhythmia impossible to cardiovert. Ajmaline (in English-speaking countries the preference is generally for procainamide) has advantages in the termination of both VT and SVT. Ajmaline prolongs the refractory period of the ventricles as well as that of any accessory pathway and the retrograde fast AV nodal pathway. Ajmaline may therefore terminate VT, CMT by an accessory pathway, and the common form of AVNRT [Figure 5].
What is the best treatment for tachycardia?
Adenosine, calcium channel blockers, or beta- blocking agents are the drugs of first choice. Adenosine was approved by the Food and Drug Administration in 1990 and is today the treatment of choice for acute therapy of SVT [Figure 5]. Adenosine is a naturally occurring substance. It binds to cardiac A1 receptors in the SA and AV nodes. Adenosine has negative chronotropic effects in the SA node, depresses conduction, and increases refractoriness in the AV node. Adenosine has a half- life of approximately 10 s. This short half-life is due to rapid metabolism, via deamination, and uptake into cells. The drug does not have clinically significant negative inotropic effects.[12] It is possible to give adenosine in pregnant patients without any risk to the mother or fetus.[14] Adenosine can cause flushing due to peripheral vasodilatation, and it can cause dyspnea due to stimulation of respiration. Some patients may also develop noncardiac chest pain. These symptoms usually resolve within 30-60 s because of adenosine's rapid metabolism. Adenosine is a very effective drug in SVT, with the ability to terminate the arrhythmia in > 90% of cases.[15] It is not effective in terminating atrial flutter or atrial fibrillation, but it does transiently slow the ventricular rate by producing high-grade AV block. In a randomized double-blind trial, adenosine (at a dose of 12 mg) terminated 91% of paroxysmal SVTs compared with 16% with placebo.[16,17] When adenosine (12 mg) was compared with verapamil (12.5 mg) in a randomized double-blind trial, both had very high rates of conversion of paroxysmal SVT to sinus rhythm (93% vs91%, P= ns).[16] Adenosine is initially administered as a rapid bolus of 6 mg over 1-2 s. If the SVT is not terminated within 3 min, a 12 mg bolus can be given in a similar fashion. We have demonstrated that SVT termination is possible in 81% of cases when 12 mg adenosine is administered, and it was possible to achieve an even better success rate of 94% with a dose of 18 mg.[18] Higher doses are not recommended as they can result in an increase in sympathetic tone and cause exacerbation of the arrhythmia.
What is the leading clinical sign of ventricular flutter?
In patients with ventricular flutter or ventricular fibrillation, syncope following cardiac arrest is the leading clinical sign.
Is a wide QRS complex tachycardia a VT?
Because a drug given for the treatment of SVT may be deleterious to a patient with ventricular tachycardia (VT), the differential diagnosis in broad-QRS tachycardia is critical. Wide-QRS complex tachycardias (QRS duration > 0.12 s) often pose a difficult diagnostic and therapeutic problem [Figure 1]. Errors are made because emergency care professionals wrongly consider VT unlikely if the patient is hemodynamically stable, and they are often unaware of the ECG findings that quickly and accurately distinguish VT in more than 90% of cases.[8] To make the right diagnosis, it is ideal to have a 12-lead ECG. Diagnostic clues for differentiation of VT from SVT are seen in leads V1 and V6; in addition, a QRS of 0.14 s or more favors a diagnosis of VT. There are several possible mechanisms and reasons of wide- QRS tachycardia [Table 2]. In intensive care and emergencies it is necessary to divide wide-QRS complex tachycardia into those with monomorphic or polymorphic morphologies as well as torsade de pointes tachycardia.[9]
What is narrow QRS complex?
The narrow-QRS complex indicates that AV conduction occurs through the AV node. ECG documentation of the tachycardia is extremely important so that the mechanism of the tachycardia can be diagnosed and the patient can be given the correct emergency treatment. Causes of narrow QRS tachycardia are sinus tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation, AV nodal reentry tachycardia (AVNRT), and orthodromic circus movement tachycardia (CMT) [Figure 2]. There are many cardiac and extracardiac reasons for supraventricular tachyarrhythmias [Table 2].
What is the QRS of a narrow QRS?
Narrow-QRS tachycardia is a cardiac rhythm with a rate faster than 100 beats per minute and a QRS duration of less than 0.12 s. The patient with narrow-QRS tachycardia usually seeks medical attention because of palpitations, light-headedness, shortness of breath, or anxiety. In many patients with narrow-QRS tachycardia, the heart rate is very high (180-240 beats per min) and therefore, after onset of the tachycardia, the patient will arrive very soon in an intensive care unit for diagnosis and treatment.
Is amiodarone an antiarrhythmic?
Amiodarone is currently regarded as the most effective antiarrhythmic drug available for the treatment of patients with both supraventricular and ventricular tachyarrhythmias. It is considered to be particularly useful in patients with life-threatening ventricular tachyarrhythmias [Figure 5]. The most relevant antiarrhythmic effect of amiodarone is due to its prolongation of cardiac repolarization. Amiodarone has been classified as a class-III drug after the Vaughan- Williams classification. However, its low rate of proarrhythmic complications (incidence approximately 1%) as compared to other class-III drugs is at least in part explained by its multiple actions on different ionic channels and ion currents. In patients with sustained (duration > 30 s), hemodynamically stable, monomorphic VT, amiodarone should be administered as bolus initially (150-300 mg in 5 min i.v.), followed by an infusion of 1050 mg/day. In addition, emergency treatment with amiodarone is also clearly indicated in patients with polymorphic VT.[21] Despite all considerations about the ‘ideal’ therapeutic strategy, in patients with polymorphic VT, evaluation of the underlying disease and the mechanism of the arrhythmia is the most important step. In some cases, acute myocardial ischemia is present (‘acute coronary syndrome’) and reperfusion therapy (Percutaneous coronary intervention, thrombolysis, and bypass grafting) will successfully terminate the arrhythmia. Of course, in these cases, reperfusion therapy is indicated and not antiarrhythmic drug treatment. Amiodarone is a highly efficacious antiarrhythmic agent for many cardiac arrhythmias, ranging from atrial fibrillation to malignant ventricular tachyarrhythmias [Figure 5]. In most published studies, intravenous amiodarone has been administered in patients with ventricular tachyarrhythmias only after failure of other antiarrhythmic drugs. In 1999, Kudenchuk studied 504 randomized patients with out-of-hospital cardiac arrest due to refractory ventricular arrhythmias (ARREST study) and reported that treatment with amiodarone (single 300 mg i.v. dose) resulted in a higher rate of survival to hospital admission (44%) compared to placebo (34%) (P= 0.03).[21] The role of amiodarone as an emergency drug has been reported recently by Taylor.[22] Today, amiodarone is the drug of choice for patients with VT and in patients with ventricular fibrillation, when DC countershock has failed. Another important indication for amiodarone therapy is in patients with a new atrial fibrillation: amiodarone has a conversion rate in atrial fibrillation of up to 80%.[23,24] Despite many publications on the safety and efficacy of intravenous amiodarone in the treatment of patients with recent-onset atrial fibrillation, there are an increasing number of reports highlighting occasional serious acute pulmonary toxicity in critically ill patients. Therefore, caution in the use of short- term administration of intravenous amiodarone in the critically ill patient with recent-onset atrial fibrillation is absolutely necessary and the duration of therapy should not exceed 24-48 h, except when absolutely necessary
What is the first line of medication for bradycardia?
Atropine . Atropine is the first line medication for the treatment of bradycardia. The administration of atropine typically causes an increase in heart rate. This increase in the heart rate occurs when atropine blocks the effects of the vagus nerve on the heart. When the vagus nerve is blocked, the SA node increases its rate ...
What is the primary objective of atropine?
When symptomatic bradycardia occurs, the primary objective is to identify and treat the cause of the problem. Medications are indicated if symptomatic bradycardia cannot be corrected by treating an underlying cause or if the cause cannot be determined. 2020 AHA Update The single-dose administration of atropine was increased from 0.5 mg to 1 mg.
How slow should a heart block be?
Since new-onset Mobitz II and complete heart block are commonly associated with myocardial infarction, it is recommended to maintain a slow HR (50-60) in order to increase the diastolic filling time. Any time you increase HR, the diastolic filling time is reduced and this reduces the coronary perfusion.
What is the second degree AV block type II?
With Mobitz-II, aka, second-degree AV block type II, the situation is similar. There is a partial block in the electrical impulses from the atria (SA) to the ventricles, and thus the effects of atropine would not significantly change the status of the ventricles. This block can also rapidly progress to 3rd-degree block.
How does atropine work?
First, let’s look at atropine and how it works. Atropine increases the firing of the sinoatrial node (atria) and conduction through the atrioventricular node (AV) of the heart by blocking the action of the vagus nerve.
Can ACLS be used for bradycardia?
Prior to the use of ACLS drugs in the treatment of symptomatic bradycardia, contributing factors of the bradycardia should be explored then ruled out or corrected.
What is the second line of drugs for bradycardia?
Epinephrine and Dopamine. Epinephrine and dopamine are second-line drugs for symptomatic bradycardia. They are both used as infusions in the bradycardia algorithm if atropine is ineffective. ACLS guidelines state that if bradycardia is unresponsive to atropine, an equally effective alternative to transcutaneous pacing is the use ...
What are the medications used in the Bradycardia algorithm?
There are 3 medications that are used in the Bradycardia ACLS Algorithm. They are atropine, dopamine (infusion), and epinephrine (infusion). More detailed ACLS pharmacology information is reviewed following this page.
What is the best drug for symptomatic bradycardia?
Atropine: The first drug of choice for symptomatic bradycardia. The dose in the bradycardia ACLS algorithm is 1 mg IV push and may repeat every 3-5 minutes up to a total dose of 3 mg. Dopamine: Second-line drug for symptomatic bradycardia when atropine is not effective. Dosage is 5-20 micrograms/kg/min infusion.
What is the dose of epinephrine?
Epinephrine: Can be used as an equal alternative to dopamine when atropine is not effective. Dosage is 2-10 micrograms/min.
What is the dopamine infusion rate?
Also, the dopamine infusion rate for chemical pacing was changed to 5-20 mcg/kg/min. The previous rate from the 2015 guidelines was 2-20 mcg/kg/min.
Is bradycardia physiologic or physiologic?
A: Bradycardia may be physiologic in the hypothermic patient. This type of bradycardia is an appropriate response to the decreased metabolic rate that normally occurs with hypothermia.
Is it safe to use TCP for bradycardia?
In the case of bradycardia caused by MI, it would be safer to transcuta neous pace (TCP) at a rate of 60 and move toward some type of cardiac intervention. You should use the 12 lead ECG to help determine MI. This will help determine if atropine may exacerbate the patient’s condition.
Does atropine cause bradycardia?
First, atropine may be used for any type of block but may negatively affect outcomes if the bradycardia is being caused by myocardial infarction. This negative effect may occur because atropine increases the heart rate and myocardial oxygen demand.
How to treat bradycardia?
Initial treatment of any patient with bradycardia should focus on support of airway and breathing (Box 2). Provide supplementary oxygen, place the patient on a monitor, evaluate blood pressure and oxyhemoglobin saturation, and establish intravenous (IV) access. Obtain an ECG to better define the rhythm. While initiating treatment, evaluate the clinical status of the patient and identify potential reversible causes.
What is the goal of bradycardia therapy?
The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable. Pacing or drugs, or both, may be used to control symptomatic bradycardia. Cardioversion or drugs, or both, may be used to control symptomatic tachycardia.
When to initiate transcutaneous pacing?
Be prepared to initiate transcutaneous pacing quickly in patients who do not respond to atropine (or second-line drugs if these do not delay definitive management). Pacing is also recommended for severely symptomatic patients, especially when the block is at or below the His-Purkinje level (ie, type II second-degree or third-degree AV block).
What is the bradycardia algorithm?
This bradycardia algorithm focuses on management of clinically significant brady cardia (ie, bradycardia that is inadequate for clinical condition).
What is irregular narrow complex tachycardia?
An irregular narrow-complex or wide-complex tachycardia is most likely atrial fibrillation with an uncontrolled ventricular response. Other diagnostic possibilities include MAT. We recommend a 12-lead ECG and expert consultation if the patient is stable.
Is synchronized cardioversion appropriate for monomorphic wide complex tachycardia?
Synchronized cardioversion is appropriate for treatment of monomorphic (regular) wide-complex tachycardia, particularly if the patient is symptomatic (eg, signs of altered level of consciousness). If the rhythm is identified as likely VT in a stable patient, IV antiarrhythmic drugs may be effective. If antiarrhythmics are administered, we recommend amiodarone (Class IIa). Give 150 mg IV over 10 minutes; repeat as needed to a maximum dose of 2.2 g IV per 24 hours. Alternative drugs for wide-complex regular tachycardias are procainamide and sotalol (see below).
What is the first step in the management of tachycardia?
The first step in the management of any tachycardia is to determine if the patient’s condition is stable or unstable (Box 3). An unstable patient with wide-complex tachycardia is presumed to have VT, and immediate cardioversion is performed (Box 4 and see above).
What is the TCP rate for atropine?
If atropine fails to alleviate symptomatic bradycardia, TCP should be initiated. TCP rate should use 60/min as a starting rate and adjust up or down based on the patient's clinical response. The dose for pacing should be set at 2mA (milliamperes) above the dose that produces observed capture.
What is the dose of dopamine for bradycardia?
Dopamine: Second-line drug for symptomatic bradycardia when atropine is not effective. Dosage is 2-20 micrograms/kg/min infusion. Epinephrine: Can be used as an equal alternative to dopamine when atropine is not effective. Dosage is 2-10 micrograms/min. decision point for ACLS intervention in the bradycardia algorithm.
What is the goal of therapy?
goal of therapy is to improve the patient's clinical status rather than target an exact heart rate.
Can you give atropine if you have bradycardia?
Yes- give atropine, if ineffective transcutaneous pacing and/or dopamine/epinephrine infusion. consider expert consultation or transvenous pacing if other efforts are ineffective. Transcutaneous Pacing (TCP) If atropine fails to alleviate symptomatic bradycardia, TCP should be initiated.
What is symptomatic bradycardia?
symptomatic bradycardia criteria. 1.) The heart rate is slow; 2.) The patient has symptoms, and 3.) The symptoms are due to the slow heart rate. Functional or relative bradycardia. when a patient may have a heart rate within normal sinus range, but the heart rate is insufficient for the patient's condition.
What is the definition of Bradycardia?
Bradycardia definition. any rhythm disorder with a heart rate less than 60 beats per minute. symptomatic bradycardia. a heart rate less than 60/min that elicits signs and symptoms, but the heart rate will usually be less than 50/min. symptomatic bradycardia criteria. 1.) The heart rate is slow; 2.)
Is TCP contraindicated for hypothermia?
TCP is contraindicated in the patient with hypothermia and is not a recommended treatment for asystole. Bradycardia and Atropine. 0.5 mg IV every 3-5 minutes as needed, and the maximum total dosage that can be given is 3 mg. Use cautiously in: MI and Hypoxia. AVOID IN: Mobitz type II/Second degree block type 2.
What is atropine used for?
Atropine is a prescription medicine used to treat the symptoms of low heart rate ( bradycardia ), reduce salivation and bronchial secretions before surgery or as an antidote for overdose of cholinergic drugs or mushroom poisoning. Atropine may be used alone or with other medications.
How to report atropine side effects?
These are not all the possible side effects of Atropine. For more information, ask your doctor or pharmacist. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088 .
Does atropine cause ventricular contractions?
Cardiovascular adverse reactions reported in the literature for atropine include, but are not limited to, sinus tachycardia, palpitations, premature ventricular contractions, atrial flutter, atrial fibrillation, ventricular flutter, ventricular fibrillation, cardiac syncope, asystole, and myocardial infarction [see ADVERSE REACTIONS ]. In patients with a recent myocardial infarction and/or severe coronary artery disease, there is a possibility that atropine-induced tachycardia may cause ischemia, extend or initiate myocardial infarcts, and stimulate ventricular ectopy and fibrillation. Atropine should be used with caution in patients with known cardiovascular disease or cardiac conduction problems.
Can barbiturates be used for convulsions?
Barbiturates are potentiated by the anticholinesterases; therefore, barbiturates should be used cautiously in the treatment of convulsions resulting from exposure to Atropine.
Can pralidoxime and atropine be used together?
When atropine and pralidoxime are used together, the signs of atropinization (flushing, mydriasis, tachycardia, dryness of the mouth and nose) may occur earlier than might be expected when atropine is used alone because pralidoxime may potentiate the effect of atropine.
Can you overdose on atropine?
Administering additional 2 mg Atropine autoinjectors by mistake in the absence of actual nerve agent or insecticide poisoning may cause an overdos e of atropine which could result in temporary incapacitation (inability to walk properly, see clearly or think clearly for several or more hours). Patients with cardiac disease may be at risk for serious adverse events, including death.
How long does it take for atropine to take effect?
Wait 10 to 15 minutes for Atropine to take effect. If, after 10 to 15 minutes , the patient does not develop any of the severe symptoms listed in Table 1, no additional Atropine injections are recommended. If possible, a person other than the patient should administer the second and third 2 mg Atropine autoinjectors.