The bradycardia and tachycardia algorithms sit at the heart of every ACLS advanced cardiovascular life support response. Cardiac arrest gets the headlines, but most ACLS scenarios you actually run in the ED, ICU, or rapid response team involve a patient who is still alive yet decompensating from a rhythm disturbance. Knowing when to give atropine versus when to pace, when to push adenosine versus when to shock — those are the decisions that separate a recovered patient from a code blue.
Both algorithms share the same opening move. Assess airway, breathing, and circulation. Put the patient on a monitor. Get a 12-lead ECG. Secure IV or IO access. Apply oxygen if hypoxic with a target SpO2 above 94%. Then ask the only question that matters: is the patient stable or unstable? That answer drives everything that follows on the rhythm algorithms.
An unstable rhythm is defined the same way for both ends of the spectrum. Look for hypotension with systolic BP under 90 mmHg, acutely altered mental status, signs of shock such as cool clammy mottled skin and poor capillary refill, ischemic chest discomfort with new ST changes, or acute heart failure with pulmonary edema and JVD. Any one of these in the presence of an abnormal rate means the rhythm is the problem, not just a symptom. Treat the rhythm fast, then treat the cause.
Stable patients get monitoring, expert consultation, and pharmacologic therapy delivered in a controlled order. Unstable patients get electricity or potent IV drugs immediately — the algorithms do not let you stall. Most students and even seasoned providers get caught freezing on whether the patient is unstable enough to act. The 2020 AHA guidance is clear: if you can name a single sign of instability, treat as unstable. Hesitation is the most common reason megacode candidates fail their scenarios.
This guide walks you through every decision branch the American Heart Association built into the 2020 guidelines (still current for the 2026 testing cycle), the drug doses you need committed to memory, and the rhythm strips you will see on the written exam and in the resus bay. The doses, energies, and decision rules below are the exact numbers that appear on the AHA written test and the megacode scoring rubric. If you are still building foundation knowledge, our acls algorithm overview maps how this fits with cardiac arrest, post-arrest care, and the systematic approach.
Unstable signs (any one triggers immediate intervention):
Stable patient = time to think. Get a 12-lead, identify the rhythm, treat reversible causes, consult cardiology. Unstable patient = act now. Bradycardia → atropine or pace. Tachycardia → synchronized cardioversion.
HR <50 bpm with symptoms. Assess for instability. If stable, identify and treat the underlying cause (hypoxia, electrolytes, drug effect from beta-blockers, calcium channel blockers, or digoxin toxicity). If unstable: Atropine 1 mg IV bolus, repeat every 3-5 min, max 3 mg. If atropine fails or is ineffective, start transcutaneous pacing or a chronotropic infusion (dopamine 5-20 mcg/kg/min or epinephrine 2-10 mcg/min). Call for expert consult and prepare for transvenous pacing in refractory cases or high-grade AV block.
HR >150 bpm, patient maintaining perfusion. Get 12-lead ECG. Narrow QRS (<0.12s): Try vagal maneuvers (Valsalva, modified Valsalva, carotid massage). Then adenosine 6 mg rapid IV push followed by 20 mL flush, then 12 mg if no conversion, repeat 12 mg once. Consider beta-blocker or calcium channel blocker for rate control if not converted. Wide QRS (>0.12s): Assume VT until proven otherwise. Amiodarone 150 mg IV over 10 min (may repeat), or procainamide 20-50 mg/min, or sotalol 100 mg IV over 5 min.
HR >150 bpm with hypotension, AMS, shock, ischemia, or HF. Move straight to synchronized cardioversion. Sedate if conscious (etomidate 0.1-0.3 mg/kg or ketamine 1-2 mg/kg). Energy depends on rhythm: narrow regular 50-100 J, narrow irregular (a-fib) 120-200 J biphasic, wide regular VT 100 J, wide irregular polymorphic VT — defibrillate at maximum (do NOT sync). Reassess after each shock. If pulseless, switch to the cardiac arrest algorithm immediately.
Bradycardias: sinus brady, junctional escape, Mobitz Type I (Wenckebach), Mobitz Type II (concerning — usually paces), third-degree complete AV block (always serious). Tachycardias: sinus tach (treat cause — fever, pain, sepsis, dehydration, hypoxia), SVT/PSVT (vagal + adenosine), atrial fibrillation with RVR (rate control vs cardioversion), atrial flutter (often 2:1 conduction at 150 bpm), monomorphic VT, polymorphic VT, torsades de pointes (magnesium sulfate 1-2 g IV plus defibrillation if unstable).
HR <50 bpm AND symptomatic. Look for hypotension, AMS, shock, chest pain, ischemic ECG changes, acute HF, or syncope. Place on monitor, 12-lead ECG, pulse oximetry, IV access, oxygen if hypoxic (SpO2 <90%).
If stable, monitor and observe. Identify and treat underlying causes: hypoxia, electrolyte disturbance (K+, Mg++, Ca++), drug effect (beta-blockers, calcium channel blockers, digoxin toxicity), increased vagal tone, hypothermia, hypothyroidism, ischemia.
If unstable: atropine 1 mg IV push, repeat every 3-5 minutes, maximum total dose 3 mg. Atropine is less effective in high-grade AV block (Mobitz II, complete heart block) and post-cardiac transplant — do not delay pacing in those rhythms.
If atropine fails or is contraindicated: transcutaneous pacing (apply pads, start at 60-80 mA, increase 5-10 mA until electrical capture, confirm mechanical capture by pulse), OR dopamine infusion 5-20 mcg/kg/min, OR epinephrine infusion 2-10 mcg/min.
Call cardiology for transvenous pacing in refractory or persistent symptomatic AV block. Treat reversible causes simultaneously. Reassess pulse, BP, and mental status after every intervention.
Symptomatic bradycardia means a heart rate below 50 beats per minute that is producing clinical signs. A heart rate of 45 in a marathon runner at rest is normal physiology and needs nothing more than reassurance. A heart rate of 45 in a 78-year-old who just collapsed with hypotension and confusion is a code-level emergency. The algorithm exists to help you separate the two scenarios and act on the second one without hesitation.
Identify the rhythm on the monitor and on the 12-lead. Common bradyarrhythmias you will see include sinus bradycardia, sinus arrest with junctional escape, first-degree AV block, Mobitz Type I (Wenckebach) which is usually benign, Mobitz Type II second-degree block which is concerning, and third-degree complete AV block which is the highest-risk scenario. Each rhythm has a different probability of responding to atropine, and the algorithm assumes you can identify them quickly from a strip.
Atropine 1 mg IV is the first-line pharmacological treatment for symptomatic bradycardia. It works by blocking the vagal tone that slows the SA and AV nodes. Push it fast and follow with a 10 to 20 mL saline flush. You can repeat every 3 to 5 minutes up to a total of 3 mg. The 2020 AHA guideline change increased the initial dose from 0.5 mg to 1 mg — make sure the version you trained on matches the current standard. Our aha acls reference covers every guideline update from the most recent cycle.
Atropine is largely ineffective in two situations: high-grade AV block (Mobitz Type II second-degree or third-degree complete heart block) and the post-cardiac transplant patient (denervated heart). Do not waste time pushing repeat doses while the patient deteriorates. Move directly to transcutaneous pacing or a chronotropic infusion. This is one of the most-tested distinctions on the written exam and one of the most common real-world errors at the bedside.
Apply the pacing pads in either anterior-posterior or anterior-lateral position. Set the rate at 60 to 80 bpm. Start the milliamps low and titrate up by 5 to 10 mA at a time until you see electrical capture on the monitor (a pacer spike followed by a wide QRS complex). Then confirm mechanical capture by palpating a femoral or radial pulse that matches the pacer rate. Mechanical capture is the only proof the heart is actually responding.
Pacing is painful for awake patients — give sedation with midazolam 1-2 mg IV or analgesia with fentanyl 25-50 mcg IV once the patient is stabilizing. Continue pacing until a transvenous pacer is placed or the underlying cause is reversed. If you are still preparing for certification, our acls classes near me guide explains how AHA-approved courses run the pacing megacode skills station.
If pacing is not immediately available or fails to capture, start dopamine 5 to 20 mcg/kg/min titrated to BP and HR, or epinephrine 2 to 10 mcg/min titrated similarly. Both are positive chronotropes and inotropes. Epinephrine adds vasoconstriction at higher doses, which is useful when hypotension is the dominant feature. Dopamine is easier to start peripherally for short-term use, though central access is preferred for prolonged infusions.
While you are working through atropine, pacing, and pressors, send a basic metabolic panel, magnesium, troponin, and a venous blood gas. The H's and T's still apply: hypoxia, hydrogen ion acidosis, hyperkalemia or hypokalemia, hypothermia, and the toxins category which covers most drug-induced bradycardias. Calcium chloride 1 g IV slow push reverses hyperkalemic conduction effects. Glucagon 3-10 mg IV is the antidote for beta-blocker overdose. High-dose insulin (1 unit/kg bolus then 0.5-1 unit/kg/hr) plus calcium and a glucose infusion treats calcium channel blocker overdose. Digoxin-immune Fab reverses dig toxicity.
Severely hypothermic patients (core temp below 30°C) often present with bradycardia or asystole and will not respond to atropine, pacing, or chemical chronotropes until rewarmed. Avoid aggressive interventions in stable hypothermic bradycardia. Focus on active core rewarming, gentle handling, and supportive care. Cardiac drugs may accumulate in the cold patient and cause toxicity once rewarming starts and metabolism resumes. Knowing this distinction is a high-yield boards item.
Look at three things on every strip before you make a treatment decision. First, the P-wave to QRS relationship — is every P followed by a QRS, are some Ps dropped, or is there complete dissociation between Ps and QRSs? Second, the PR interval — is it normal (under 200 ms), prolonged but constant (first-degree block), progressively lengthening before a dropped beat (Mobitz I), or normal until a sudden dropped beat with no warning (Mobitz II)? Third, the QRS width — narrow suggests junctional or higher origin, wide suggests ventricular escape and a much sicker conduction system.
If you can answer those three questions in 10 seconds, you can pick the right algorithm branch. A patient with sinus bradycardia at 42 bpm and a normal PR will likely respond to atropine. A patient with complete heart block, P-waves at 80 and ventricular escape at 30, will not respond to atropine and needs the pads on right now. Memorize the strip patterns by the time you walk into your acls certification exam.
Three scenarios trip up most candidates. First, asymptomatic bradycardia — a sleeping athlete at 38 bpm needs no intervention. Do not pace, do not push atropine. Second, bradycardia from inferior MI — the bradycardia itself is often vagally mediated and responds well to atropine, but the underlying MI is the real problem and gets reperfusion priority. Third, hypothermic bradycardia — covered above, rewarm before drugs. The exam loves these because they punish reflex protocol-following without thinking.
First-line for symptomatic bradycardia. Blocks vagal tone at SA/AV nodes. Ineffective in high-grade AV block.
Stops conduction at AV node. First-line for stable narrow-complex SVT after vagal maneuvers fail.
Class III antiarrhythmic. Drug of choice for stable wide-complex tachycardia and VT.
Chronotrope and inotrope. Used as infusion when atropine fails in bradycardia or while preparing pacing.
Chronotrope, inotrope, and vasopressor. Alternative to dopamine for refractory bradycardia.
Specific treatment for torsades de pointes (polymorphic VT with prolonged QT).
The tachycardia algorithm handles any heart rate above 100 bpm but the decision tree only activates at rates greater than 150 with symptoms or a sustained tachydysrhythmia. Below that range, sinus tachycardia is almost always physiological — the heart speeding up to compensate for fever, pain, sepsis, dehydration, hypovolemia, hypoxia, anxiety, or hyperthyroidism. Treat the cause, not the rate. Pushing a beta-blocker into a septic patient with HR 130 is a textbook way to crash the BP and earn a rapid response.
Once you confirm a pathological tachycardia, the first split is QRS width. A narrow QRS (under 120 ms) tells you the rhythm originates above the ventricles — sinus tach, SVT, PSVT, atrial fibrillation, atrial flutter, or multifocal atrial tachycardia. A wide QRS (over 120 ms) means the rhythm is ventricular (VT) or supraventricular with aberrancy. Until proven otherwise, treat wide-complex tachycardia as VT. The clinical cost of being wrong about SVT-with-aberrancy is small. The cost of treating real VT as SVT is fatal.
Start with vagal maneuvers. The modified Valsalva — a semi-recumbent strain followed by passive leg raise — converts SVT in roughly 43% of patients in published trials, far better than the standard Valsalva (around 17%). Carotid sinus massage is an alternative in younger patients without bruits or cerebrovascular disease. Auscultate for bruits first and never massage both carotids simultaneously.
If vagal maneuvers fail, push adenosine 6 mg fast IV, then 12 mg if no conversion, then 12 mg one more time. Use the two-syringe technique with a 20 mL flush into the most proximal port. After three failed doses, switch strategies — diltiazem 15-20 mg IV (rate control for a-fib), metoprolol 5 mg IV, or expert consultation. Reviewing the rate-control algorithms is part of every acls course skills station.
Get a 12-lead. Look for AV dissociation, fusion or capture beats, very wide QRS (>160 ms), and concordance across the precordial leads — all favor VT over SVT with aberrancy. The Brugada and Vereckei criteria help formalize this differentiation if you have time and a clean strip.
For stable monomorphic VT, amiodarone 150 mg IV over 10 minutes is first-line. Alternatives include procainamide 20-50 mg/min until arrhythmia suppression, hypotension, QRS widens by more than 50%, or maximum 17 mg/kg; and sotalol 100 mg IV over 5 minutes. Avoid sotalol and procainamide in patients with prolonged QT or heart failure with reduced ejection fraction. For polymorphic VT with normal QT, treat ischemia and revascularize urgently. For polymorphic VT with long QT (torsades), give magnesium 1-2 g IV. Recertifying providers will recognize these patterns from acls renewal testing.
Synchronized cardioversion. Sedate if the patient is awake — etomidate 0.1-0.3 mg/kg or ketamine 1-2 mg/kg are reasonable choices that preserve hemodynamics. Confirm sync mode is engaged on the defibrillator (you should see markers on each R wave). Energy selection: narrow regular SVT 50-100 J, narrow irregular a-fib 120-200 J biphasic, wide regular VT 100 J, polymorphic VT — defibrillate at maximum energy unsynchronized because the irregular morphology prevents reliable sync.
After each shock, reassess pulse, rhythm, mental status, and BP. Re-press SYNC before each subsequent shock because most defibrillators reset to unsynchronized mode automatically after a discharge. If the patient becomes pulseless at any point, you are now in the cardiac arrest algorithm — start CPR, deliver unsynchronized shock at max energy, and follow the VF/pulseless VT pathway covered in our acls and pals comparison guide.
A-fib with rapid ventricular response is the most common irregular narrow-complex tachycardia you will see. If the patient is stable, rate control with diltiazem 0.25 mg/kg IV (then 5-15 mg/hr infusion) or metoprolol 2.5-5 mg IV every 5 minutes is reasonable. If onset is clearly under 48 hours and the patient is stable, cardioversion (electrical or chemical) is an option. If onset is unclear or over 48 hours, anticoagulate first or get a TEE — cardioverting a clot-loaded left atrium is how strokes happen.
If the same patient becomes unstable, synchronized cardioversion overrides the anticoagulation discussion. Start at 120-200 J biphasic and escalate. The risk of an embolic stroke is real but smaller than the risk of imminent cardiovascular collapse. Document the decision clearly and start anticoagulation as soon as the patient is stable post-cardioversion.
If at any point in the tachycardia algorithm your patient loses pulse, immediately transition. Pulseless VT and ventricular fibrillation are both treated identically: start high-quality CPR, deliver unsynchronized shock at maximum biphasic energy (200 J on most modern defibrillators, 360 J monophasic), epinephrine 1 mg IV every 3-5 minutes, and amiodarone 300 mg IV bolus after the second shock (then 150 mg after the fifth). The transition from tachycardia algorithm to arrest algorithm is often the difference between a save and a death. Practice this handoff on every megacode you run.
Once the rhythm converts to sinus, the work is not done. Get a 12-lead ECG immediately to look for ischemia, post-cardioversion ST changes, and any new conduction abnormalities. Send troponin, electrolytes, magnesium, and a TSH if a-fib was the rhythm. Start or continue anticoagulation per CHADS-VASc score for any patient with paroxysmal or persistent a-fib. Consider electrophysiology consultation for recurrent or refractory rhythms. Document the rhythm strip before and after, energy delivered, drugs given, and the patient response so the receiving team has a complete picture.
The algorithm walk-through is essential but rote memorization fades fast under stress. Run timed scenarios with a partner where one of you reads out a vital-sign change and a rhythm strip every minute and the other has to call the next step. Use the megacode skill stations in your acls training course as the rehearsal benchmark — if you can name the drug, dose, and energy without looking, you are ready for both the exam and the resus bay.