Evaluation and Management of Acute Unstable Bradycardia

July 14, 2021 via Shahriar Lahouti



Severe progressive sinus bradycardia is a common pathway of impending death from any terminal disease state. In this post the principles of management of unstable patients with bradycardia is discussed.

Clinical significance of bradycardia

Bradycardia is defined as a heart rate of less than 50 bpm 1 in adults (non-well-conditioned athletes). Generally severe bradycardia is more worrisome than tachycardia for the following reasons:

1.Cardiac output is dependent on heart rate and stroke volume. In mild-moderate tachycardia the effect of the increased heart rate predominates and cardiac output is increased. However in severe tachycardia, the cardiac output drops since the diastolic filling time is reduced (causing reduced stroke volume). Bradycardia can directly pull down cardiac output and cause hemodynamic instability 2. Theoretically slowing down the heart rate may cause a minimal increase in diastolic filling, thereby increasing the stroke volume.  However, this compensatory factor is weak and extremely limited.

2.Progressive bradycardia is often a harbinger of death☠️

3.Torsade de pointes is a pause-dependent arrhythmia, which is more likely to occur at slower heart rates. Moreover, bradycardia itself may prolong the QT interval. Leaving patients in a severely bradycardic state may increase their risk of torsade.


Medications 3

  • Beta-blockers, calcium channel blockers
  • Digoxin
  • Antiarrhythmics
  • Central alpha-2 agonist (e.g. clonidine, dexmedetomidine)
  • Cholinergic agents
    • Direct receptor agonist: Bethanechol
    • Indirect-acting (working at synapses, i.e. acetylcholine esterase inhibitors)
      • Edrophonium, neostigmine, pyridostigmine, rivastigmine, donepzil.
      • Insecticide (organophosphate, carbamate)
  • Opioid intoxication
  • Sedative­-hypnotics: Barbiturates, Benzodiazepines.   


  • Hyperkalemia: An increased likelihood of short-term adverse events was found for hyperkalemic patients whose ECG demonstrated QRS prolongation, bradycardia (HR<50), and/or junctional rhythm 4.
  • BRASH Syndrome(Bradycardia, Renal failure, AV node blockade, Shock and Hyperkalemia)
  • Severe hypoxia / hypercapnia / acidemia
  • Hypermagnesemia
  • Hypothyroidism 
  • Hypoglycemia
  • Hypothermia

Myocardial infarction

  • Inferior MI: nodal ischemia and vagal response (self-limiting or responds to atropine)
  • Anterior MI: infranodal ischemia (often requires pacing)

Neurocardiogenic or reflex-mediated

  • Increased ICP (cushing reflex) 
  • Intra-abdominal hemorrhage
  • Neurogenic shock
  • Vagal response e.g. after urinary catheter insertion for urinary retention 5


  • Lyme disease, syphilis
  • Aortic valve endocarditis with ring abscess (conduction block)

Clinical manifestation

Ranges from asymptomatic to shock, including impending cardiac arrest (figure 2).

The first step in the approach to management of bradycardia is to recognize whether the patient’s hemodynamic status is stable or not.

By enlarge hemodynamic instability is defined as a myriad of hypotension and signs and symptoms of poor organ perfusion including altered mental status (AMS), ischemic chest pain and dyspnea from acute heart failure. However hemodynamic instability  is not all-or-none rather it  has a spectrum.

  • Occult bradycardic shock: In some patients with adequate physiologic reserve, compensatory vasoconstrictor response may maintain blood pressure and mental status despite the low cardiac output and poor organ perfusion (remember that BP is not equal to cardiac output). They require monitoring and urgent therapy, but they are not actively dying!
  • Overt bradycardic shock: represent severe hemodynamic derangement with low BP and organ malfunction. These patients have worsening symptoms and deteriorating vital signs (e.g. HR< 30bpm or progressively worsening bradycardia) with imminent threat of cardiac arrest. Hence emergent resuscitation is warranted for these patients, the term bradycardic peri-arrest  is a better term used for such a condition (aka impending cardiac arrest). 

General approach to bradycardia in ED

Fundamental concepts

The principles of management of bradycardia involves the following essential concepts:

  • Always consider the major life threatening causes of bradycardia and evaluate the patient throughout the resuscitation to identify and correct the primary problem (e.g. hyperkalemia, drug intoxication, myocardial infarction and neurologic catastrophe).
  • Remember that sinus bradycardia is a common pathway of impending death from any terminal disease state such as massive pulmonary embolism, septic shock etc.
  • In patients with bradycardic peri-arrest with deteriorating vital signs focus your efforts on immediate resuscitation rather than reading the rhythm on EKG!

The general approach to bradycardia is shown in the following figure (figure 3)

Step 1: Evaluate hemodynamic status (see above). In unstable bradycardic patients promptly start resuscitation

Step 2: Determine if the bradycardia is causing symptoms (an older patient with underlying cardiac disease with chest pain and syncope), or if symptoms are the cause for bradycardia (e.g. vasovagal bradycardia).

Step 3: Read the rhythm. Correct identification of the location of the problem (SA node vs. AV node vs. His Purkinje) guides management of bradycardia (whether urgent pacing is required or not). The simplified approach to Identify the location of problem involves:

  • QRS width?
    • Narrow QRS indicates proximal (SA/AV node disease) site of the problem.
    • Wide QRS indicates either proximal or distal (His Bundle disease) site of the disease. In this situation, assess rhythm prior to bradycardia:
      • If sinus bradycardia → more likely to be proximal.
      • If sinus tachycardia →more likely to be distal disease.

Proximal problems (sinus and AV nodal dysfunction) rarely lead to life-threatening complications and are treated with watchful waiting, atropine or sympathetic medications such as epinephrine and dopamine. However, distal His-Purkinje block is much more serious, and tend not to respond to atropine and sympathetic stimulation. These patients almost always need pacing and a definitive pacemaker.

👉Assess for potential life-threatening causes of bradycardia in parallel with above 3 steps.



  • Obtaining a detailed history will assist in discovering the underlying etiology of the patient’s bradycardia as:
    • Renal impairment or failure suggestive for hyperkalemia
    • History of ischemic chest pain may suggest myocardial infarction
    • Recent head trauma, headache, altered mentation may suggest elevated ICP e.g. ICH, SAH.
    • Blunt trauma, abdominal pain, distention, pregnancy (ectopic): Intra Abdominal hemorrhage
    • Medication review
      • Recent change in home medication including dose titration  
      • Renally cleared meds plus acute kidney injury
      • Even eye drops with sympatholytic properties may be enough to cause bradycardia in elderly patients 6
      • Some medications can unexpectedly cause bradycardia (e.g. donepezil, tizanidine) 7 .

Physical exam

  • Hemodynamic stability: should be assessed first and adequacy of perfusion confirmed. 
    • Overt bradycardic shock: Low MAP; altered mental status in addition to other signs and symptoms of poor organ perfusion.
    • Occult bradycardic shock: MAP and mental status intact, but cool extremities & poor urine output. 
  • Neuro/toxicologic exam
    • Evidence of elevated intracranial pressure (e.g. stupor, widened optic nerve sheath)?
      • 👉Patients with bradycardia can be drowsy or confused solely on the basis of decreased cardiac output. However when mental status is disproportionately depressed for a given heart rate (e.g. GCS 8 in patient with HR 45 bpm), one should consider neurologic causes of bradycardia like increased ICP and drug overdose.
    • Pinpoint pupils may suggest toxic ingestion (e.g. clonidine or cholinergic agent)

Bedside US: Cardiopulmonary and abdominal exam

  • Volume status?
  • Evidence of myocardial infarction (e.g. inferior wall motion abnormality)?
  • Evidence of pulmonary congestion (e.g. B-lines throughout the lung fields)?
  • Evidence of intra-abdominal free fluid?

ECG: Focus on the following

  • Signs of hyperkalemia (e.g. peaked T-waves, prolonged PR interval)
  • Signs of ischemia
  • Rhythm diagnosis (e.g. sinus bradycardia vs. heart block)
  • Deep symmetric TWI in anterior leads may suggest neurologic insults e.g. SAH

Labs and imaging

  • Fingerstick glucose 
  • Chemistries including Ca & Mg
  • Troponin, if MI suggested by history/EKG
  • Digoxin level, for patients taking digoxin
  • Consider checking TSH
  • Infectious titers (rapid plasma reagin for syphilis or Lyme)
  • Complete blood count with cultures if an infection is suspected
  • Coagulation panel
  • Head CT scan to rule out increased intracranial pressure (ICP), if suspected to intracranial pathology (e.g. hemorrhage, mass etc.)
  • CT of the abdomen if there is concern for intra-abdominal hemorrhage.


Bradycardic peri-arrest may be defined as severe or progressive bradycardia with marked shock and concern for immediate cardiac arrest and therefore a maximally aggressive strategy should be chosen in order to prevent further deterioration into cardiac arrest (below algorithm). This involve employment of two arms of treatment simultaneously; the medical (table 1) and electrical arms.

For patients with mild signs of organ malperfusion (e.g. normal blood pressure but poor urine output), then a more gradual and stepwise approach may be most appropriate. For example, simply starting an epinephrine infusion will often improve heart rate and perfusion. 




  • Atropine has a vagolytic effect and essentially fires up the SA node; therefore it is effective only if the distal conduction system is conducting normally. Appropriately dosed atropine is usually effective for proximal AV block, sinus bradycardia and junctional rhythms but is not useful (nor harmful) in distal AV block (idioventricular rhythms and second-degree type II and third-degree AV block).
  • Caveats:
    • At low doses, atropine may cause paradoxical bradycardia 8
    • It is ineffective in heart transplant patients due to lack of vagal innervation. Studies have shown that atropine may precipitate paradoxical asystole 9 in denervated hearts and therefore it is contraindicated to use in heart transplant patients. 
    • It has been shown that only ~ 28% of patients with bradycardia respond to atropine 10. Therefore it is prudent not to delay other therapies while waiting for atropine to work
  • Strategy when atropine is used:
    • Atropine is traditionally the first line of treatment, however for most unstable patients (Peri-Arrest bradycardia) epinephrine is more effective and preferable.
    • If atropine is the most immediately available drug, then it is administered, however do not expect that it will fix everything. For very unstable bradycardia, give atropine while simultaneously preparing epinephrine and transcutaneous pacing, with the full expectation that the atropine will often fail.
  • Atropine dosing: 1 mg IV every 3 minutes, max 3mg. 
    • In the latest 2020 AHA update the recommended single dose administration of atropine was increased from 0.5 mg to 1 mg based on data suggesting that at low doses, atropine may cause paradoxical bradycardia. At low doses, atropine decreases heart rate by blocking M1 acetylcholine receptors in the parasympathetic ganglion controlling the SA node. At higher doses, atropine increases heart rate by blocking M2 acetylcholine receptors on the myocardium itself. 
  • Cholinergic poisoning may require higher doses using a doubling approach: 1mg, then 2mg, 4mg, 8mg etc 11.


  • Unlike atropine, epinephrine stimulates the entire myocardium. This provides epinephrine with a broader spectrum of efficacy for various mechanisms of bradycardia.
  • Mechanism of hemodynamic stabilization:
    • Vasoconstriction via alpha-­1 receptor
    • Increased Inotropy (contractility) and chronotropy (heart rate) via beta-­1 receptor
    • At low dose (<8-10 mcg/kg/min), the predominant effect is an inotrope and chronotrope with a minimal vasoconstrictive effect while at higher doses (>10mcg/kg/min) the vasoconstrictive effect (alpha-agonist effects) predominates.
  • It is safe to use a proximal peripheral line initially with frequent limb checks12
  • Preparation and use of epinephrine drip is shown in figure 5 below. 
  • Dosing:
    • Boluses for peri-arrest patient
      • Boluses will stabilize the patient for a few minutes, but this is only a temporary bridge to an epinephrine infusion.
      • Bolus doses ~ 20-50 mcg epinephrine.
    • Epinephrine infusion
      • The usual dose is 2-10 mcg/min (but there is no upper limit in a crashing patient).
      • Dosing strategy depends on how unstable the patient is. For more unstable patients, start high and down-titrate as the patient responds. For patients who are fairly stable, start low and gradually up-titrate.



  • Consider IV calcium chloride or calcium gluconate; If atropine, epinephrine and pacing are ineffective, and the cause of bradycardia is unclear.
  • Calcium-responsive bradycardias:
    • Hyperkalemia
    • Hypocalcemia
    • Hypermagnesemia
    • Calcium-channel blocker overdose
    • Beta-blocker (may be effective)
  • Dosing:
    • Bradycardia of unknown etiology: try calcium chloride 1g or calcium gluconate 3g. 13
    • Known or suspected hyperkalemia: calcium chloride 1g or calcium gluconate 3g. If ineffective and the patient is unstable, may repeat the dose once or twice if needed. 14

Other medications


  • It is a pure beta-agonist.
  • Some patients who don’t respond to epinephrine will respond to isoproterenol.
  • Dosing: 20 to 60 microgram IV bolus, then 5mcg/min IV infusion.


  • Traditionally used in symptomatic bradycardia.  
  • Mechanism: It has a variety of receptors at different dose ranges. It is often difficult to figure out what dopamine is doing to the patient. For example, low-dose dopamine can actually cause hypotension (due to a predominant effect of vasodilation), which can make it difficult to wean off the dopamine.
  • Disadvantages of dopamine compared to epinephrine:
    • Dopamine can cause skin necrosis with prolonged infusion.
    • Dopamine has a variety of different effects at different doses in different patients. This makes it difficult to titrate in any rational fashion (up-titration may cause dopamine to function via a different mechanism entirely).
    • At high doses (>10-20mcg/kg/min) may act predominantly as a vasoconstrictor (which may be an undesirable effect) and is also associated with tachydysrhythmias.
    • Dopamine may directly stimulate diuresis via action on dopamine-receptors, thereby falsely suggesting that renal perfusion is adequate 15.
  • Strategy: If dopamine is the most readily available agent, then use it. When you have time, consider switching over to an epinephrine infusion.
  • Dosing: 5 mcg/kg/minute; may increase by 5 mcg/kg/minute every 2 minutes until desired effect; maximum dose 20 mcg/kg/minute.

High insulinemic euglycemia (HIE)

  • Mechanism: several studies have demonstrated that insulin administered in higher doses has strong positive inotropic properties16.
  • Indications: The most convincing evidence is in CCB toxicity, but HIE appears to work in BB toxicity as well (It works best in patients with myocardial dysfunction e.g. bradycardia, and especially reduced ejection fraction. It is unlikely to help in patients with predominantly vasodilatory shock (e.g. echocardiography showing a normal or increased ejection fraction).
  • Insulin: Start with 1 unit/kg IV bolus, followed by a 1 unit/kg/hour infusion. If the response is unsatisfactory, insulin may be up-titrated every 10-15 minutes within a range of 1-10 units/kg/hour 17 .
  • Dextrose: Administer 1-2 ampules of D50W (50-100 mL) when starting HIE, unless the glucose is already >250 mg/dL.The ideal way to provide dextrose is a continuous infusion of D50W via central line, beginning at a rate of ~1 mL/kg/hour (e.g., ~75 mL/hour D50W).
  • Follow the glucose q15-30 min until stable, then space out to every hour. Target a moderately elevated glucose level (~125-250 mg/dL).
  • Frequently check all electrolytes including magnesium and phosphate. 
    • Serum potassium: Replete to a target potassium of >3mM.
    • Insulin may promote hypomagnesemia and hypophosphatemia, requiring active repletion.


  • Background
    • It may be useful in patients with bradycardia and cardiac pump failure (especially those with beta-blocker rather than CCB intoxication) 18.
    • It is unlikely to be helpful in patients with predominantly vasodilatory shock and CCB intoxication.
    • Glucagon often induces vomiting so be cautious in patients with risk of aspiration.
    • Glucagon should be reserved as a last resort and should not be given routinely.
  • Glucagon test dose: Start with a loading dose of 5 mg IV over 5 minutes (may repeat if ineffective).
  • Glucagon infusion: If the test dose causes hemodynamic improvement, this may be followed with a continuous infusion at a rate between 1-10 mg/hour, set equal to the dose of glucagon that caused clinical improvement (e.g., if 5 mg worked, set the infusion equal to 5 mg/hour).
    • Glucagon has a half-life of about 15 minutes, so a continuous infusion is needed.
    • Glucagon infusions may exhaust the hospital’s glucagon supply, so this may not be a sustainable long-term strategy.  However, a glucagon infusion could be useful as a bridge for a few hours, until the high-dose insulin infusion starts to work.

Digoxin-specific antibody fragments (DSFab)

  • Digoxin toxicity can cause almost any bradyarrhythmia from junctional bradycardia to complete heart block19.
  • DSFab is indicated (best treatment) for hemodynamically significant bradyarrhythmias 20. Each vial contains 40mg of antibody fragments, which neutralize 0.5 mg of digoxin.
  • Formula for calculating the number of vials required 21:
    • Chronic poisoning:  Number of vials is estimated as (digoxin level in ng/ml)x(wt in kg)/100.  However, lower doses may be considered initially, for patients with chronic digoxin toxicity who are clinically stable (e.g., initiate therapy with three vials and follow clinically to determine whether additional treatment is warranted).
    • Acute ingestion of known dose:  Number of vials is estimated as (mg of digoxin ingested)x(1.6)
    • Empiric administration if levels are unknown:
      • Acute toxicity: give 5 vials (if hemodynamically stable) or 10 vials (if unstable), reevaluate clinically in 30 minutes.
      • Chronic toxicity:  start with 3-6 vials, reevaluate clinically.
  • 👉Atropine is a good temporizing measure (since patients with digoxin toxicity have excess vagal tone).
  • 👉Avoid pacing or beta-agonists if possible, as these may provoke ventricular tachycardia 22.

Lipid emulsion therapy (intralipid)

  • Background
    • It is the first line of treatment in patients suspected of local anesthetic systemic toxicity (LAST) 23. Suspect in any bradycardic patient on lidocaine infusion or recently treated with nerve block.
    • Intralipid may also be considered for the following intoxications:
      • Lipophilic BB e.g. propranolol, carvedilol, penbutolol 
      • CCB
      • TCAs
  • Dosing: Newer guidelines recommend a revised dosing scheme with a reduced maintenance infusion, which could optimize the risk/benefit balance.  These recommend the following dosing scheme for 20% lipid emulsion (e.g. Intralipid) 24:
    • Start with a bolus of 1.5 mL/kg over 2-3 minutes (e.g. 100 mL). Repeat bolus may be considered if there is no response to the first bolus.
    • Give an additional 0.75 mL/kg over three minutes (e.g. 50 mL).
    • Start a maintenance infusion rate of 0.025 mL/kg/min.
    • If there is an initial response to the bolus followed by re-emergence of instability during the maintenance infusion, consider re-bolusing and/or increasing the infusion rate.  There is no known maximal dose, but it may be best to limit the dose to ~10 mL/kg/day tota

Transcutaneous pacing

In bradycardic peri-arrest, pacing should be started in parallel with medication (figure above). Transcutaneous pacing is a temporary measure until more definitive stabilization is possible (e.g. transvenous pacing).

Pad configuration

There are 2 placement configurations recommended for optimal capture in transcutaneous pacing. One option is to center a pad over the apex of the heart and place the other pad on the right upper chest. Alternatively, a pad may be placed over the V3 lead position while the other is placed between the left scapula and the thoracic spine.

Setting the output on pacer

Principles: An initial pacing rate should be set at least as high as the intrinsic heart rate of the patient (although a standard rate of 80 beats/min can be selected) with the current set to minimal output. Initially, pacer spikes may be visualized without resultant cardiac depolarization. The current can be increased 5 to 10 mA at a time until a clear QRS complex and T wave is demonstrated following each pacer spike. Check the patient’s pulse at this point to confirm that the electrical “capture” has resulted in a mechanical response. This level is defined as the pacing threshold, and it will be found between 40 and 80 mA for most healthy patients. Final current output should be set to 5 to 10 mA above the threshold level to ensure continued capture.

  • Patients with obesity and COPD typically require ~40-80 mA more than other patients to capture.
  • Be aware of pseudo-pacing: It is when the pacemaker isn’t capturing the myocardium, but the monitor displays a heart rate equal to the transcutaneous pacemaker. This provides a false sense of security, because the monitor looks great. Always confirm real capture that results in a ventricular beat with femoral pulse checks (ideally using POCUS) and pulse oximetry wave. Do not rely solely on the monitor/ECG. Do not use a carotid pulse check for the assessment of circulation as TCP can create muscular movements that may feel like a carotid pulse. Assess circulation using the femoral pulse (with POCUS ideally).


Transcutaneous pacing can be quite uncomfortable for patients who are awake, as it requires the discharge of electrical impulses through the skin and chest wall muscles. Therefore, procedural sedation should be considered in order to reduce this discomfort. Consider ketamine as your first line analgesic for the patient undergoing transcutaneous pacing as it is least likely to cause hypotension, may help increase the heart rate and it helps maintains respirations

Transcutaneous pacing In crashing patient: start at a maximal current (e.g. 100mA) and titrate downward to 5-20mA above the minimum energy required for capture; if not capturing, increase to max 130mA and if still not capturing, move the pads to improve the vector through the heart and try again.

Pacing in non-crashing patient: start low and titrate up.

  • If the patient is doing ok, then you probably wouldn’t really want to do transcutaneous pacing at all.  However, it may be useful to determine if the patient responds to transcutaneous pacing.  Proving that transcutaneous pacing will capture the heart may help you decide whether placing a transvenous pacemaker is necessary in a borderline patient.

Transvenous pacing

Transvenous is much more effective than transcutaneous pacing with success rates of >95%. Transvenous pacing is indicated as following:

  • Unstable bradycardia which doesn’t respond to other medication and/or interventions.
  • High-degree AV blocks that leave the patient at ongoing risk of deterioration (e.g. Mobitz II, third-degree heart block with wide-complex escape rhythm).

Video transvenous pacing procedure


  • Do not rely solely on blood pressure to identify unstable patients. Keep in mind that BP is not equal to cardiac output. Some patients vasoconstrict and maintain normal blood pressure, despite organ malperfusion.
  • For very unstable patients, start both medical and electrical arms of treatment until something works!
  • Evaluate your patients throughout the resuscitation process for life-threatening common causes of bradycardia.
  • Remember that bradycardia can be caused by myocardial infarction and various intoxications; so fixing the heart rate may not be enough to fix the patient. Reverse any other underlying cause of bradycardia.
  • Don’t be fooled by transcutaneous pacemaker pseudocapture. The fact that the chest is twitching and the monitor shows a normal heart rate means nothing; it’s still possible that the myocardium isn’t being captured.
  • Pacing is unlikely to be successful in B-blocker, Ca-blocker and digoxin poisonings.

Going further

Post Peer Reviewed By: Mojtaba Chardoli. MD.


Expand to view the reference list

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Shahriar Lahouti

Founder, Chief Editor
I am Shahriar Lahouti and RECAP EM is my primary FOAMed project. The philosophy of RECAP EM is to promote critical thinking and enlightening the mindsets with most rational, current evidence towards a safer practice.

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