Should I give Atropine?

Good posts start with good questions. Have an ER question? Send it here.

KEY

🔍- Deep Dive

📌- Clinical Application

🔸 - Weak Evidence

🔹 - Strong Evidence

📑 - Evidence summaries

✅ - Recommended treatment

⚠️ - Critical Information

When I started writing this post, I wondered if it was redundant. After all, the AHA has a beautiful algorithm, and ACLS drills it into our heads repeatedly. We do know what to do.

But the more I read, and the more I thought about real patients, the more I realised something else. Maybe the algorithm was also narrowing our focus.

Bradycardia isn’t a single problem. And atropine isn’t the decision. It is just one possible response.

👉

Jump to what matters ⏬

What is Bradycardia?

Bradycardia has traditionally been defined as a heart rate less than 60/min.

More recent guidelines (AHA 2018) recognise that clinically significant bradycardia is usually less than 50/min.

Why do we care?

Cardiac output = heart rate × stroke volume

Stroke volume cannot compensate indefinitely for a falling heart rate
In severe bradycardia, cardiac output must be low. This is simple physiology
A normal blood pressure does not exclude shock here

If a patient is “bradying down” in front of you, don’t wait for hypotension. Act early

Progressive bradycardia is often a pre-terminal rhythm
Some patients may appear deceptively stable due to a strong sympathetic response

One more reason to fear bradycardia: torsade de pointes

Torsade de pointes is a pause-dependent arrhythmia
Bradycardia prolongs the QT interval and increases the risk of malignant ventricular arrhythmias
Leaving patients profoundly bradycardic is not benign

Firstly: Is this actually a rhythm problem?

Not all bradycardia is primary “electrical disease”.

Bradycardia may be:

Physiologic (sleep, athletes)

A response to metabolic, toxicologic, or ischemic stress

Before treating the rhythm, identify the cause.

⚠️

Start by ruling out the dangerous and reversible causes:

Hyperkalemia

Cardiac ischemia

Toxicologic causes

Raised intracranial pressure (Cushing reflex)

This is how I remember the causes of bradycardia:

The BRADI mnemonic

B – BRASH / Hyperkalemia

R – Reduced vitals (hypoxia, hypoglycemia, hypothermia with or without hypothyroidism)

A – Acute coronary occlusion

D – Drugs (beta-blockers, calcium channel blockers, digoxin)

I – Intracranial pathology / Infection

Treat the cause whenever possible.

Bradycardia often improves when physiology improves.

Reversible causes to address early

Cardiac ischemia:

The primary goal is urgent reperfusion. Transfer to the cath lab as soon as possible.

Bradycardia medications or transcutaneous pacing should be used only as a bridge while definitive management is arranged

If vasoactive support is needed, use minimal doses of dopamine or epinephrine, as both can worsen myocardial ischemia

⚠️

Inferior MI: Nodal ischemia with increased vagal tone, typically producing narrow-complex, transient bradycardia that often responds to atropine.

Anterior MI: Infranodal conduction system ischemia, more commonly producing wide-complex bradycardia that usually requires pacing.

Hypothermia:

Rewarming is the first-line treatment and often corrects the bradycardia without the need for medications or pacing.

Myxedema coma:

Treat with thyroxine. Bradycardia typically improves as the underlying endocrine abnormality is corrected.

Toxicological causes:

Beta-blocker or calcium channel blocker toxicity:

Consider high-dose insulin therapy, with or without lipid emulsion
Consider glucagon when appropriate
Pacing is often ineffective

📌

A practical clue:

Calcium channel blocker toxicity tends to cause hyperglycemia

Beta-blocker toxicity tends to be normoglycemic or hypoglycemic

Propranolol toxicity: Consider sodium bicarbonate due to sodium-channel blockade

Digoxin toxicity: Can produce almost any bradyarrhythmia, from junctional rhythms to complete heart block. Consider digoxin-specific antibody fragments (DigiFab)

Special populations

Post-cardiac transplant /Spinal cord injury

Aminophylline:

6 mg/kg IV in 100–200 mL over 20–30 minutes

Theophylline:

300 mg IV, then oral 5–10 mg/kg/day

Typical total daily dose ~450 mg
Target serum levels 10–20 mcg/mL

Inferior MI with high-grade AV block

Aminophylline: 250 mg IV bolus

⚠️

Atropine should be avoided in transplant patients due to the risk of high-grade AV block or asystole.

Calcium

If the cause is unclear or hyperkalemia or toxicity is suspected, calcium is reasonable.

Calcium-responsive bradycardias include:

Hyperkalemia

Hypocalcemia

Hypermagnesemia

Calcium channel blocker overdose

Dose:

Calcium chloride 1 g IV

OR calcium gluconate 3 g IV

Calcium is relatively safe and reasonable when the etiology of bradycardia is unclear.

What Next: Is this a rhythm atropine actually works on?

Before giving atropine, ask two questions:

Is the patient symptomatic?

Is this a rhythm atropine can fix?

Is the patient symptomatic?

Symptoms suggesting unstable bradycardia (CHAAS):

Chest pain

Hypotension

Acute heart failure

Altered mental status

Signs of shock, including syncope

Even without overt instability, some rhythms are high risk:

Mobitz II AV block

Complete heart block with wide QRS

Ventricular pauses greater than 3 seconds

Recent asystole

These patients require treatment in the emergency department.
In the absence of instability or high-risk rhythms, close monitoring and cardiology referral are appropriate.

Is this a rhythm atropine can fix?

Atropine blocks vagal tone at the AV node. It only works if the distal conduction system is intact.

Atropine is likely to respond to:

Sinus bradycardia

Vagal-mediated bradycardia

Proximal AV block

⚠️

Atropine is likely to fail in

Mobitz II

Complete heart block

Wide-complex bradycardia

Post-cardiac transplant patients

Proceed early to pacing or vasoactive support.

Only about 25–30% of patients have a meaningful response to atropine.

Failure is common and expected.

Atropine dosing and why the dose matters

For symptomatic bradycardia, give atropine 1 mg IV or IO.

Repeat every 3–5 minutes to a maximum total dose of 3 mg.

🔍

Why did we move from 0.5 mg to 1 mg?

Low doses can paradoxically worsen bradycardia:

Below 0.5 mg, M1 receptor blockade may transiently slow the heart

At higher doses, M2 blockade predominates and heart rate increases

This is why current practice starts at 1 mg IV.

When atropine should be avoided

Atropine is ineffective or potentially harmful in:

Cardiac transplant patients

Mobitz II or third-degree AV block with wide QRS

Narrow-angle glaucoma

Bladder outlet obstruction without catheterisation

Ileus or obstructive GI disease

Significant tachycardia or hypertension

Fever or heat exposure

Atropine didn’t work: Now what?

Atropine commonly fails in sick bradycardias.

Options include:

Chronotropic or vasoactive agents - such as epinephrine or dopamine

Transcutaneous pacing

It is often difficult to predict which patients will respond best to medical therapy versus electrical pacing.

In peri-arrest states, stepwise pharmacology is often impractical. A single agent that supports both heart rate and blood pressure is usually preferred. Epinephrine often fulfills this role.

Prepare epinephrine and pacing simultaneously.

📑

A randomized feasibility study comparing dopamine versus transcutaneous pacing in patients who failed atropine showed no difference in survival to discharge.

Why epinephrine works better than atropine.

Epinephrine:

Increases heart rate

Increases myocardial contractility

Improves preload and afterload

Acts above and below the AV node

In unstable bradycardia, epinephrine provides meaningful hemodynamic support.

✅

Do not wait for atropine to “kick in.” If the first dose of atropine is ineffective, prepare epinephrine and pacing simultaneously.

Chronotropic or vasoactive agents

Epinephrine

Dose: 2–10 mcg/min IV infusion

(or 0.1–0.5 mcg/kg/min, titrated to effect)

Provides combined chronotropy, inotropy, and vasoconstriction

Often preferred in peri-arrest or shock states, where global hemodynamic support is required

Dopamine

Dose: Start at 5 mcg/kg/min IV

Titrate by 5 mcg/kg/min every 2 minutes (usual range 5–20 mcg/kg/min)

Doses above 20 mcg/kg/min increase the risk of vasoconstriction and arrhythmias

Less predictable than epinephrine, particularly in severe conduction disease

Isoproterenol

Dose:

IV bolus 20–60 mcg, followed by 10–20 mcg boluses as needed
OR infusion 1–20 mcg/min, titrated to heart rate

Useful in selected settings, but requires close monitoring for ischemia

Transcutaneous pacing

Transcutaneous pacing is often the fastest way to increase heart rate in unstable bradycardia.

It is a temporary measure, used to stabilize the patient while preparing for more definitive management, such as transvenous pacing or correction of the underlying cause.

Think of TCP as buying time, not fixing the problem.

✅

In patients with severe bradycardia and shock, pacing may be initiated while vascular access is being established.

Use it for:

High-grade AV block

Peri-arrest bradycardia

Drug-refractory instability

Pad placement

Effective pacing depends heavily on pad position.

Optimal pad placement continues to be an area of ongoing research

Air is a poor conductor, so directing current through lung tissue is less effective

Anterior–posterior placement is generally preferred and more likely to achieve capture

📑

A prospective study of 20 patients undergoing elective cardioversion in an electrophysiology laboratory found that anterior–posterior pacing was more likely to achieve capture than the anterolateral position

Energy settings

Adjust energy based on patient stability:

Crashing or unconscious peri-arrest patient:

Start at a high current to achieve rapid capture. If needed, increase immediately to maximum output (typically 140–200 mA), then titrate down once the patient is stabilized.