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Bradycardia Algorithm

 

Bradycardia Algorithm Review

(includes 2010 AHA Guideline Update)

The major ECG rhythms classified as bradycardia include:
Sinus Bradycardia
First-degree AV block
Second-degree AV block
Type I —Wenckenbach/Mobitz I
Type II —Mobitz II
Third-degree AV block complete block

(See the ECG Interpretation section for images and more detailed information on rhythms)

Bradycardia vs. Symptomatic Bradycardia

Bradycardia is defined as any rhythm disorder with a heart rate less than 60 beats per minute. (Typically it will be <50/min) This could also be called asymptomatic bradycardia. Bradycardia can be a normal non-emergent rhythm. For instance, well trained athletes may have a normal heart rate that is less than 60 bpm.

Symptomatic bradycardia however is defined as 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 exists when the following 3 criteria are present: 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 occurs when a patient may have a heart rate within normal sinus range, but the heart rate is insufficient for the patients condition. An example would be a patient with an heart rate of 80 bpm when they are experiencing septic shock.

Bradycardia Pharmacology

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 can be found here.

2010 AHA Update: For symptomatic bradycardia or unstable bradycardia IV infusion chronotropic agents (dopamine & epinephrine) is now recommended as an equally effective alternative to external pacing when atropine is ineffective.

Atropine: The first drug of choice for symptomatic bradycardia. Dose in the Bradycardia ACLS algorithm is 0.5mg IV push and may repeat up to a total dose of 3mg.

Dopamine: Second-line drug for symptomatic bradycardia when atropine is not effective. Dosage is 2-10 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.

Bradycardia Algorithm

The decision point for ACLS intervention in the bradycardia algorithm is determination of adequate perfusion. For the patient with adequate perfusion, you should observe and monitor. If the patient has poor perfusion, preparation for transcutaneous pacing should be initiated, and an assessment of contributing causes (H’s and T’s) should be carried out.

Click below to view the bradycardia algorithm diagram. When done click again to close the diagram. Bradycardia Algorithm Diagram» or Members Download the Hi-Resolution PDF Here

Transcutaneous pacing (TCP)

Preparation for TCP should be taking place as atropine is being given. If atropine fails to alleviate symptomatic bradycardia, TCP should be initiated. Ideally the patient should receive sedation prior to pacing, but if the patient is deteriorating rapidly, it may be necessary to start TCP prior to sedation.

For the patient with symptomatic bradycardia with signs of poor perfusion, transcutaneous pacing is the treatment of choice.

Do not delay TCP for the patient with symptomatic bradycardia with signs of poor perfusion. 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.

TCP is contraindicated for the patient with hypothermia and is not a recommended treatment for asystole.

A carotid pulse should not be used for assessment of circulation as TCP can create muscular movements that may feel like a carotid pulse. Assess circulation using the femoral pulse.

Identification of contributing factors for symptomatic bradycardia should be considered throughout the ACLS protocal since reversing of the cause will likely return the patient to a state of adequate perfusion.

  190 Responses to “Bradycardia Algorithm”

  1. Is Atropine used for treatment of relative bradycardia?

    • Yes, atropine could be used to treat relative bradycardia. In these situations, you would want to ensure that significantly increasing the heart rate will not worsen the patient’s condition. For instance, in the case of MI, significantly increase the heart rate with atropine could worsen the ischemia to the heart.
      You would treat relative bradycardia just as you would treat any bradycardia. Use the bradycardia algorithm and consider the H and T’s for bradycardia.

      Kind regards,
      Jeff

  2. I read the NEJM publication about outcomes of some cohort using dopamine vs NA, showing an elevation of mortality rate using dopamine in cardiogenic and septic shock. Now, in many ICU and emergency units we don’t give dopamine to our patients with a synthomatic bradycardia with complete AV block. My question is about dopamine vs another vasoactive drug, if I don’t have transcutaneous pacemaker.

    Thank you in advance,
    Manuel.

    • I don’t know if there is an exact answer for dopamine vs. norepinephrine but my preference would be norepinephrine. The clinical trials seem to lean toward norepinephrine.
      Here are a couple of articles regarding this issue:
      Norepinephrine vs. Dopamine

      Norepinephrine vs. Dopamine #2

      Kind regards,
      Jeff

    • In the past the good old standby drug used as a “Pacemaker” was Isuprel, a pure beta agonist ,which seems to have fallen into disfavor. Comments?

      A suggestion inre ACLS Cardiac Arrest Algorithm.Why not raise the patient’s legs, or at least utilise the Trendelenberg position to provide added central volume by “auto-transfusion”. The degree of extra volume provided could easily be adjusted by what would be such simple and non-invasive manouvers . As many will have observed, when patients are “crashing” during even very cautious induction for CABG surgery, with low LVEF, raising adults’ legs can provide 1.0 to1.2 L auto- transfusion with laudable results.I used the latter example to illustrate the point,and am aware that it is not strictly analogous.Feedback please.

  3. Please clarify: in the above algorithm, for Dopamine it’s written as “Dosage is 2-10 micrograms/kg/min infusion.” For Epinephrine, it’s written as “Dosage is 2-10 micrograms/min.” Is Dopamine weight driven and epi is not? Or is this a typo?

    Thanks!!

  4. Hey, I’ve got a scenario that I am hoping you could give me some feedback on. 58 y/o female with every text book S/S of ACS, Short of vomiting, syncope, or AMS. Pt has PMHx of AMI and also said her that in the past her BP has bottomed out during cardiac events. Over the past couple weeks, Pt has been popping Nitro like tictacs. She took x3 rounds of NTG with in the last hour or two before she called 911. The last round of NTG was 15 mins ago before.

    Her BP is now 80/40. Her ecg revealed sinus Brady with a HR ranging btwn 50-60 BPM. ST elevation at 1mm to just barely 2 mm ST across inferior leads and reciprocal changes suggestive of a RCA occlusion. We gave ASA, started a NS fluid bolus, and 2 lpm of O2 to maintain SaO2 at 99%, and activated the cath lab (largely based off Pt presentation). Approx 15 min emergency transport to the hospital.

    I was on the fence about giving Atropine, to boost cardiac output in hopes of helping out her BP, but ultimately elected not to. My reasoning was that the cause of hypotension was reduced preload due to an right-sided/ inferior AMI and NTG overload. I was worried that Atropine would caue increased Cardic O2 consumption and create an increased work load on the heart. I didn’t want to throw more drugs on the mess already created, and possibly cause more harm than good. I imagined a worse case scenario of creating a second or third degree heart block, since this type of AMI is notorious for causing Infarction damage to the AV node,

    Was I out of line wth my thinking? And I was wondering where to draw the line between the Brady Cardic and ACS algorithms, or if they should be conducted simaltaneously? My thoughts at the time was that I would start TCP if her heart rate dropped into the 40’s, but it never dropped below 50 bpm. Thanks in advance for your feedback.

    • I think that you made the right choice to hold the Atropine. You are correct in that atropine could have pushed the workload up and worsened an infarction. The BP was borderline and I would have been satisfied with this BP at 80/40. You made the right decision to use TCP if the HR dropped below 40. I think that your decisions were well thought out and correct given the situation. You can use both the ACS algorithm and Bradycardia algorithm at the same time. Just make your decisions with saving as much of the myocardium as possible.
      Kind regards,
      Jeff

    • Could atropine be given as IV infusion in bradycardia?? and if possible what is the conc and max rate of infusion

      • The half-life of atropine is 2 hours. Therefore, it would not be necessary to give it as an infusion. Something with a half-life of this length should be given as needed by IV bolus. There would be better medication to use in this type of situation. You would use dopamine or epinephrine. These 2 medications have been found to be very effective in the treatment of symptomatic bradycardia.

        Kind regards,
        Jeff

      • Atropine as a potent anticholinergic agent has been employed as a continuous infusion in the treatment of tetanus and organophosphate poisoning. Kind regards, Jeff

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