HTitle
1Why Rhythms Matter
2Four Patients
3Reading the Room
4Framework + SBAR
● Self-guided mode
quiz server
The Room
Thompson Health ICU · Nursing Education

The Rhythm Isn't
the Problem.

What your patients need you to know about cardiac output, compensatory failure, and the difference between recognizing a rhythm and understanding what it's doing.

Presenter mode · Live polling enabled

QR code
Join on your phone
quiz.danamitchell.icu

v2026.03.17c

Part 1 of 4

Why Rhythms Matter

It was never about the strip.
What is your patient's cardiac output right now?
Not the number — the trend. Is it where it was an hour ago? Is it adequate for this patient, with this physiology, today? The strip tells you how fast the heart is firing. It doesn't tell you how much it's delivering.

Cardiac Output = The Only Number Your Tissues Care About

CO = HR x SV · Normal 4-8 L/min at rest
CO = HR x SV
HR = how often the ventricle fires
SV = how much it ejects each time
CO = what your patient's organs actually receive

What low CO looks like at 0300

MAP trending down despite pressors. Lactate trending up. Urine output quietly disappearing. A patient who was talking and is now not quite right.

"CO of 5 L/min can be achieved many ways — and some of those ways are unsustainable."
Anchor

CO is oxygen delivery. When it drops, your patient's organs notice before the monitor does. Trust that.

Cardiac Output Simulator
CO = HR x SV — See what happens when the numbers change
❤️
72 bpm
72 x 70 mL = 5.0 L/min
HR
72
SV
70 mL
CO
5.0 L
Cor.
Perf.
100%
Heart Condition
Good compliance. Tolerates rate increases. CO holds up to ~HR 140.
Normal resting cardiac output. The heart fills completely, ejects efficiently, and meets tissue oxygen demand with room to spare.
Wherever You Practice

Tachycardia that won't break? Ask first: "Is this the cause or the compensator?" If CO is already low and the fast rate is maintaining it, slowing it drops them. This logic applies anywhere there's a monitor — step-down, PACU, ED, floor.

Why Faster Isn't Better

The heart feeds itself during diastole. Tachycardia starves the muscle.
0.67s
diastole @ HR 60
0.25s
diastole @ HR 120
~0
diastole @ HR 150+
"At HR 150, the heart is working harder on less fuel. The coronary arteries fill during diastole — and diastole has almost disappeared."
Anchor

Fast rate = less fill time = less output. AND the heart feeds itself during diastole. Tachycardia is never benign in a sick patient.

Wherever You Practice

Sustained HR > 130 that won't break — before you treat the rate, ask what it's compensating for. If you slow it without addressing the cause, you may precipitate the decompensation you were trying to prevent.

Why Filling Time Matters: Frank-Starling

Preload drives output — but only up to a point.

Frank-Starling — Plain Language

Stretch the muscle fiber, it contracts harder. That's preload working for you. But there's a ceiling. Overstretch it, and contractility falls. The heart can't outwork its own geometry — and at HR 150+, it's trying to.

"Less filling time = less stretch = less contraction force. The Frank-Starling curve is the reason rate matters — not just for beats per minute, but for what each beat actually delivers."
Anchor

Think of the heart like a rubber band. The more you stretch it (preload), the harder it snaps back — up to a point. Cut the time to stretch it and you cut the output. That's Frank-Starling in plain English.

Part 2 of 4

The Big
Destabilizers

AFib with RVR (rapid ventricular response) · Complete Heart Block (CHB) · Ventricular Tachycardia · Junctional Rhythms
Four rhythms. For each one — draw a straight line from the strip to the blood pressure to what your patient is telling you.
Your Anchor

Normal Sinus Rhythm

Everything else today is a departure from this picture. Keep it.
Normal Sinus Rhythm · HR 72 · Regular · QRS <0.12s
P wave
Atrial depolarization
= atrial kick
QRS complex
Ventricular contraction
= pulse you feel
T wave
Ventricular repolarization
= reset for next beat
PR interval
P before every QRS
= AV node conducting

What makes it normal

Regular rhythm. P before every QRS. Narrow QRS (<0.12s). Rate 60–100. One impulse, one pathway, coordinated.

"When something looks different from this — P missing, QRS wide, rate wrong — start your assessment there."
Regular + P for every QRS + narrow complex = normal. Anything that changes one of those three is where your thinking starts.
Cardiac Physiology
The Atrial Kick
The 30% nobody accounts for — until it's gone.
Healthy Heart
Passive
Fill
75–85%
Kick
15–25%
Lose kick →
SV ↓ 15–20%
Sick / Stiff Heart
Passive
Fill
60–65%
Kick
up to 40%
Lose kick →
SV ↓ 35–40%
30%
riding on
one contraction

Who loses the most when kick disappears

Hypertensive heart disease with LVH (left ventricular hypertrophy) and diastolic dysfunction. Diastolic heart failure (HFpEF). Post-MI remodeling. The elderly patient whose ventricle has been stiffening for decades.

"In a young heart: lose kick, compensate. In a sick heart: lose kick, lose perfusion."
Anchor

AFib doesn't just change the rhythm — it removes a mechanical contribution your patient may not be able to afford. The amber segment is what disappears.

Room 6, ICU — 2118
Ed Hennessey
71 · Retired dairy farmer, Naples NY · NSTEMI — cath at Rochester yesterday, transferred back to Thompson ICU
Ed came back from Strong Memorial after a successful cath — LAD stented, TIMI 3 flow. By 1900 he was sitting up, giving you a hard time about the food. His wife Martha has been at the bedside all day.

30 years of hypertension. T2DM. Hyperlipidemia. EF (ejection fraction) 50%, diastolic dysfunction grade II.

You walk in for your 2000 assessment. Martha meets your eyes before you even look at the monitor.
Heart Rate
138 — Irregular
Was 78 sinus at 1900
BP
98/62
Was 130/78
UO — last hr
15 mL
Was 55-60 all day
"He says his heart feels like it's fluttering. Martha says he's been 'not quite right' for the last hour."
When the family member meets your eyes like that — slow down. Look at everything.
What rhythm is this?
AFib with RVR — HR ~148, Irregular
No P waves · Irregularly irregular R-R intervals · Fibrillatory baseline · Narrow QRS
Team Decision · AFib with RVR
Ed Hennessey — Each role has a different question. Scan to get yours.
HR138irregular — new AFib
BP98/62down from 130/78
UO15 mLlast hour
Post-NSTEMI day 1, returned from cath lab. Grade II diastolic dysfunction. EF 50%. 30-year hypertensive, T2DM.
QR code
Scan to join as your role
0 players connected
quiz.danamitchell.icu

Rate vs Rhythm control

Rate control (metoprolol, diltiazem) slows ventricular response via AV node. Does NOT convert the rhythm. In HFrEF with EF <40%: avoid diltiazem — negative inotrope. Rate control first is generally safer unless AFib duration <48h and patient hemodynamically unstable.

AFib · HR 138 · Irregular

AFib with RVR — The Double Hit

Hit One — No Atrial Kick

Atrial chaos, no organized contraction. Normal ventricle loses 15-20% EDV. A stiff, hypertensive, diabetic ventricle — the kind you see at Thompson — can lose 30-40%. The atrial kick isn't a bonus. It's what's filling the ventricle.

Hit Two — Rate Kills Filling Time

At HR 138, diastole is 0.2 seconds. No time to fill. Stroke volume craters. Two mechanisms stack — a patient who was borderline compensated is now in cardiogenic territory.

The patient who "always does fine" with AFib — that was a different ventricle than the one in front of you now.
Expert depth: Post-MI AFib incidence is 10-20% in the first 48-72 hours, highest with inferior and posterior STEMI. New-onset AFib in the post-MI period independently increases 30-day mortality. Rate control first — rhythm control later if needed.
40%
EDV loss — stiff ventricle
before rate even matters
Room 6 — The Next 10 Minutes
2000 — You call.
"Mr. Hennessey is in new AFib at 138. BP has dropped from 130/78 to 98/62 over the last hour. UO is down to 15 mL. I'm concerned about hemodynamic compromise." (Trend, not snapshot.)
2104 — Orders.
Metoprolol 5mg IV push. 12-lead. BMP, troponin. BP q15 min.
2112 — After metoprolol.
HR 104. Still irregular. BP 108/70. Ed: "It feels less fluttery." Martha exhales.
Ed converted to sinus on his own by morning — new-onset AFib in post-MI patients often self-terminates within 24h with rate control and electrolyte repletion.

Why not cardiovert him?

Duration unknown — could have started hours ago. AFib >48h carries thromboembolic risk on cardioversion. Rate control first is the safer bridge.

What saved Ed

You trended the BP instead of treating each value in isolation. 130 to 112 to 104 to 98 over one hour is a pattern — and you called it before the 80s.

Post-MI AFib: 10-20% incidence. Common in the first 48-72 hours. Not a crisis by itself. A crisis when it's not caught early.
Three questions.
Every patient. Every rhythm.
01 — Rate problem?
02 — Rhythm problem?
03 — Perfusion problem?
We'll build these out at the end. For now — keep them in your pocket.
ICU Room 3 — 6 hours post-PCI
Russell Granger
68 · Retired, Gorham NY · Inferior STEMI, RCA stented 6 hours ago
Russell drove himself 35 minutes from Gorham because the heartburn radiating to his left shoulder "hadn't gotten better by lunch."

ED ECG: inferior STEMI. RCA 100% occluded — opened and stented. He arrived in the ICU post-PCI chatting about his garden. Two hours later, the monitor catches your eye.

You walk in. Russell is sitting up. "I don't feel right," he says. His voice is calm. His pressure is 74 systolic.
Heart Rate
38
Regular · Wide complex · P waves unrelated to QRS
BP
74/52
SpO2
91%
That calm is not reassurance. The ventricular escape is maintaining some output. Not much. But enough to be talking. Don't let the talking fool you.
What rhythm is this?
Complete Heart Block — HR ~35, Wide Escape
P waves march independently · Wide QRS escape at 35 BPM · No relationship between P waves and QRS · AV dissociation
Team Decision · Complete Heart Block
Russell Granger — Your role determines your question. Scan in.
HR38wide complex — regular — dissociation
BP74/52MAP 59
SpO291%
Inferior STEMI, RCA stented 6h ago. Patient conscious. TCP pads available. Wide-complex ventricular escape.
QR code
Scan to join as your role
0 players connected
quiz.danamitchell.icu
TCP is the answer

Wide complex escape = infra-hisian block. TCP is the only thing that will move this ventricular rate.

Complete Heart Block · HR 35 · Dissociation
CO = HR x SV = 35 x 65 mL =
2.3
L/min
Normal resting CO is 4-8 L/min. Cardiogenic shock is a CI below 2.2. This patient is in it.
5-6
L/min normal at rest
<2.2
L/min/m2 cardiogenic shock CI
2.3
L/min CHB at HR 35

P waves march through. QRS complexes ignore them.

Do NOT give atropine for wide-complex escape
The Atropine Trap: Atropine speeds up the sinus node — but the AV node is completely blocked. The atria fire faster. The ventricles don't follow. Wide-complex escape means the block is infra-hisian. Atropine cannot help here.

What's happening

The AV node is completely blocked. Atria fire at their own rate (60-100 BPM). Ventricles fire at theirs — escape at 20-40 BPM, originating below the His bundle. Wide QRS because depolarization spreads muscle-to-muscle, not through the fast conduction system.

Do Not Give Atropine for Wide-Complex Escape

Atropine accelerates the sinus node via vagal blockade. The sinus rate goes up. The ventricles do not follow. More P waves. Same ventricular rate. You made the dissociation worse.

TCP Is a Bridge — Not a Solution

Electrical capture does not equal mechanical capture — feel the pulse. TCP hurts — have fentanyl + midazolam ready BEFORE you press the button. Pads go on before the phone call.

Anchor

CHB = atria and ventricles completely disconnected. The fix is pacing — not atropine, not waiting. Pacing pads go on before the phone call.

RCA and AV Node

The RCA supplies the AV nodal artery in ~85% of patients. Inferior STEMI = risk for progressive AV block up to CHB. Lyme carditis — endemic in the Finger Lakes — also causes complete AV block.

CHB · HR 38 · Wide Escape

After TCP — What You're Managing

Electrical capture ≠ Mechanical capture

You'll see the pacing spike + wide QRS. That's electrical capture. Now feel for a pulse. If no pulse — you're pacing a heart that isn't responding. Increase output or reposition pads.

What to watch while pacing

BP trending up? Good. Mentation improving? Good. Urine returning? Good. Patient still obtunded despite capture? You may have mechanical failure — notify covering provider immediately.

Sedation matters

TCP is painful. Fentanyl + midazolam before and during. A patient who won't tolerate pacing will fight it — and lose capture. Comfort is part of clinical care, not a bonus.

Transfer decision

Russell needs a transvenous pacemaker. TCP is a bridge. While you're managing at the bedside, the covering provider is calling Strong. Your job: maintain capture, maintain hemodynamics, document the response.

ICU Room 2 — 0318
Donna Marchetti
64 · School bus driver, Victor NY · Ischemic cardiomyopathy, EF 28%
Ischemic cardiomyopathy. EF 28% on last echo. Anterior MI at 57. On amiodarone and carvedilol. Her cardiologist has been recommending an ICD for months. She keeps putting it off.

At 0318 the alarm fires. You walk in. Donna's eyes are open. Diaphoretic. "Something's wrong," she says. She's right.
Heart Rate
182
Wide complex — Regular — Monomorphic
BP
82/50
SpO2
88%
She has a pulse. That matters enormously. The algorithm for a pulsed wide-complex tachycardia is completely different from pulseless.
What rhythm is this?
Monomorphic VTach — HR ~182, Regular
Wide QRS · Regular R-R · No discernible P waves · Monomorphic (uniform) complexes
Team Decision · VTach with Pulse
Donna Marchetti — Every role has a job. What's yours?
HR182wide complex regular — VTach
BP82/50pulse confirmed
SpO288%
EF 28%. Chronic amiodarone. Awake and diaphoretic. BP 82/50 and falling. 18hr post-LAD stent.
QR
Scan to join as your role
0 players connected
quiz.danamitchell.icu
Sync vs Unsync

She has a pulse. Unsynchronized on a patient with a pulse risks T-wave delivery and VFib. The mode is not a technicality.

The pivot

Midazolam 2mg IV. Confirm sync mode. 100J. Sinus rhythm HR 74. BP 106/68 in 90 seconds.

Why VTach Hits Different

It's not just fast — the squeeze itself is broken

Three Problems at Once

1. Too fast to fill — you already know this from the CO simulator. HR 182 = diastolic filling time cut drastically.

2. Atrial kick is gone — AV dissociation means atria and ventricles aren't coordinated. Same loss as AFib, but at a much higher rate.

3. The contraction itself is inefficient — depolarization spreads cell-to-cell through muscle instead of the fast His-Purkinje highway. The ventricle wrings instead of squeezing.

VTach is a warning shot. The myocardium is irritable enough to sustain a re-entrant circuit. That circuit can fragment into VFib in one beat.
Anchor

Wide complex = VTach until proven otherwise. You will be right far more often than wrong, and the consequences of assuming SVT with aberrancy when it's VTach are much worse than the reverse.

At Thompson

No cath lab means recurrent VTach or VTach with acute MI triggers a transfer conversation to Strong. Your job: identify fast, treat aggressively, keep the patient alive for definitive care. The best transfers leave before the patient crashes.

Monomorphic VTach · HR 182 · Regular

First question.
Is there a pulse?

The rhythm determines what you see on the monitor. The pulse determines what you do about it. Same strip. Two completely different algorithms.

No Pulse

Pulseless VTach = cardiac arrest. CPR immediately. Defibrillate (unsynchronized). ACLS algorithm. Now.

Pulse Present

Stable: amiodarone 150mg IV over 10 min. Unstable (altered, BP tanking): sedation + synchronized cardioversion.

Monomorphic vs polymorphic matters. Torsades (polymorphic, pause-dependent, long QT): treat with Mg 2g IV. Do NOT give amiodarone — worsens QT.
Anchor

Wide and fast on the monitor — feel for a pulse. Pulse determines the algorithm. The strip tells you what you're seeing. Your hands tell you what to do.

Critical Concept — Know This Before You Press the Button
The Vulnerable Period

The T wave = ventricular repolarization. During this window, cells are vulnerable to chaotic re-excitation. A shock delivered on the T wave does not cardiovert your patient. It induces ventricular fibrillation.

SYNCHRONIZED

Shock timed to QRS peak

Machine waits for R wave. Use for VTach with pulse, AFib, SVT.

UNSYNCHRONIZED

Shock fires immediately

No R-wave sensing. Use for pulseless VTach and VFib.

The error: Unsynchronized on a patient in VTach with a pulse. Shock lands on the T wave. VTach becomes VFib. You made it worse.

Quick Reference

● AFib + pulse: Sync
● SVT + pulse: Sync
● VTach + pulse: Sync
● Pulseless VTach: Unsync
● VFib: Unsync

ICU Room 4 — POD 1, 0640
Joe Scarcella
73 · Retired bartender, Canandaigua NY · Admitted for urosepsis — day 2 ICU
Chronic AFib for 6 years — rate-controlled on digoxin 0.125mg daily and carvedilol. EF 40%. CKD stage 3, baseline creatinine 1.9. Admitted with urosepsis, improving on pip-tazo.

Night nurse reports in-and-out AFib all night, rate controlled 70s-80s. He got his digoxin 0.125mg at 0600 this morning. First hospital dose.
Heart Rate
88
Regular · Narrow · No P waves · Was AFib all night
BP
104/68
Was 118/74 at 0500
SpO2
97%
Joe says he feels fine. Mild nausea — "probably the antibiotics." He didn't finish breakfast.
The rhythm looks better on the monitor. Regular, narrow, not fast. This is the trap.
What rhythm is this?
Junctional Rhythm — HR ~50, Regular
Narrow QRS · Regular R-R · No visible P waves · Rate 40-60 BPM · Backup pacemaker
Team Decision · Junctional / Digoxin Toxicity
Joe Scarcella — The rhythm looks better. Is it? Scan to find out your role.
HR52regular — narrow — no P waves
BP104/68was 118/74 at 0500
SpO297%
Chronic AFib on digoxin 0.125mg daily. CKD3, baseline Cr 1.9. Admitted for urosepsis day 2. Got morning digoxin dose at 0600. Was in AFib all night, now junctional. Nauseated.
QR code
Scan to join as your role
0 players connected
quiz.danamitchell.icu
The trap

Regular narrow at 52 looks like an improvement over chaotic AFib. It's not. New rhythm + nausea + recent digoxin dose + AKI on CKD = digoxin toxicity until proven otherwise.

Context the rhythm

Hold digoxin. Stat digoxin level + BMP. The nurse who noticed the rhythm change against the medication timeline caught this.

Junctional · HR 48 · Narrow · No P waves

The backup pacemaker fired.
Your job is to find out why.

The AV node has taken over pacing. Rate 40-60 BPM. It's a safety mechanism. But something caused the sinus node to fail. That something needs a diagnosis.

What you see on ECG

Rate 40-60 BPM. Narrow QRS. No visible P waves, or retrograde P waves. Regular.

Common Causes

Beta blockers / CCBs. Digoxin toxicity. Inferior MI / ischemia. Vagal tone. Sick sinus syndrome. AKI with electrolyte shifts.

The junctional rhythm is the symptom. Find the cause — don't just treat the rate.

Accelerated Junctional (>60 BPM)

Rate 60-100. AV node firing faster than normal escape. Digoxin toxicity is the classic cause — especially with AKI reducing clearance.

Junctional Rhythm — The Double Hit to Cardiac Output

Slow rate + no atrial kick = thinner margin than you think

Why It's More Than “Just Slow”

AFib loses atrial kick but is usually fast. Junctional loses atrial kick AND is usually slow. Go back to CO = HR x SV. Both sides of the equation are taking a hit. A patient who “looks fine” has less reserve than you'd expect — a little volume loss or vasodilation and they can't compensate.

The Rate Tells a Story

Escape junctional (40-60): The SA node failed or the signal didn't get through. This is a rescue rhythm.

Accelerated junctional (60-100): The junction is firing faster than it should — something is irritating it. Think digoxin toxicity, post-op inflammation, inferior MI.

Same rhythm shape, very different “so what.”

Your Assessment Checklist

Is this new? Post-surgical junctional is common and usually transient. New junctional in a medical patient = the SA node is telling you something.

Check the med list: Digoxin (especially with renal changes), beta-blockers, CCBs, amiodarone. Anything started, increased, or combined recently?

Hemodynamic tolerance: MAP >65? Mental status baseline? Urine output dropping? Are pressors masking what would otherwise be hypotension? (Floor nurses: you may not titrate pressors — but recognizing when a patient needs them is the same skill)

Anchor

Stable junctional at 55 since surgery this morning = keep watching. New junctional at 42 with SBP 88 = call now. You're calling because CO can't keep up, not because of the rhythm name.

Resolution — Joe Scarcella
"Looking better on the monitor doesn't always mean getting better."

Labs — 0720

Digoxin level: 2.4 ng/mL
Potassium: 3.1 mEq/L
Creatinine: 2.7 (baseline 1.9 — AKI on CKD)
First hospital dose pushed into toxic range.

Management

Digoxin held. KCl 40 mEq IV over 4h. Magnesium 2g IV. By 1400: digoxin level 1.5, rhythm back to AFib, nausea resolved. Joe ate all of lunch.

What caught it

The nurse recognized that regular narrow without P waves in a patient who was in AFib is not a good sign — even when it looks better. Context the rhythm. What changed? What was just given?

Wherever You Practice

New regular narrow rhythm after a digoxin dose — especially with AKI or low potassium — is digoxin toxicity until proven otherwise. This happens on cardiac floors all the time. Context the rhythm change against what was just given to the patient.

The monitor is the last thing that tells you your patient is in trouble.
You already knew. You just didn't trust it yet.

The Compensation Arc — A Body Fighting to Survive

When CO starts to fall, the body doesn't quit. For 15-30 minutes, the BP looks fine.
1

Narrow Pulse Pressure EARLIEST

SBP - DBP < 25 mmHg. Stroke volume drops, body vasoconstricts to hold MAP. BP looks stable. The gap narrows.

"The blood pressure is lying. The pulse pressure is telling the truth."
2

A-line Waveform Change IF PRESENT

Rounded upstroke. Reduced amplitude. Pulsus alternans = call right now.

"The shape changes before the number does."
3

Urine Output Falls

Drop >30% sustained over 1-2h. Kidneys autoregulate to MAP ~65. UO drop is a perfusion message. (On a med-surg floor: MAP trending down + patient confused = call)

"When UO drops, ask why renal perfusion pressure is falling."
4

Hypotension LATE

By the time BP drops, every compensatory mechanism is exhausted. This is rescue.

"When the BP drops, the window has already closed."
5

Altered Mentation

Restlessness, confusion, unresponsive. Cerebral autoregulation holds to MAP ~50-60.

"Restlessness is not anxiety. It is a low-perfusion state until you prove it isn't."
Expert depth: Pulse pressure narrows before BP falls because of compensatory vasoconstriction — the body maintains MAP by increasing SVR. By the time systolic falls, compensation has already been maxed for minutes to hours.
Wherever You Practice

Signs 1 and 3 are catchable with a standard BP cuff and a foley. Narrow pulse pressure trending down + UO dropping — that's a call on any unit. You don't need an A-line to hear the whisper before the alarm.

BODY COMPENSATINGBODY FAILING

What the A-line Is Telling You

Not every patient has an A-line. When they do — learn to read the shape, not just the number.
The A-line makes the physiology visible in real time. But everything it shows you is happening whether or not the line is in. Knowing what to look for — with or without the line — is the skill.

Healthy

Systolic peak Dicrotic notch
  • Steep upstroke — strong LV contractility
  • Clear dicrotic notch — aortic valve closing cleanly
  • Consistent amplitude — stable stroke volume

Hemodynamic Compromise

Rounded upstroke No dicrotic notch
  • Rounded upstroke — contractility falling
  • Reduced amplitude — stroke volume dropping
  • Blunted/absent notch — afterload/compliance change

Pulsus Alternans CALL NOW

Large Small Large Small
  • Alternating large/small beats — LV can't maintain SV
  • Sign of severe LV dysfunction
  • Stop your assessment. Call. Now.
A-line: Respiratory Variation >13%

Waveform amplitude rises and falls with the ventilator cycle >13% = volume-responsive. Fully ventilated patients only — TV ≥8 mL/kg, no significant arrhythmia.

Without an A-line

Pulsus alternans: two consecutive cuff BPs 10+ mmHg apart — same finding as alternating waveform, same call.

Compromise pattern: pulse pressure narrowing (SBP−DBP <25), cool extremities, MAP trending, mental status shifting.

Volume responsiveness: passive leg raise — if MAP rises ≥10%, they're preload-responsive. No line needed.

You see the rhythm.
Now what?
The strip doesn't tell you what to do. Your thinking does.

Three Questions. Run Them in Order.

Not a checklist. A way of thinking.
01

Rate Problem?

Is HR causing the hemodynamic compromise?
Too Fast

Rate control — but know why it's fast first. Compensatory tachycardia is not a rate problem.

Too Slow

TCP pads on now. Atropine if vagally mediated. Wide complex escape at 38: pads first.

If rate is fine, go to 02
02

Rhythm Problem?

Is loss of organized rhythm causing the compromise?
Organization Lost

AFib with RVR + compromise: rate control vs cardioversion. VTach with pulse: synchronized cardioversion. CHB: TCP now.

Rhythm Organized

A patient can be in sinus and be dying. If rate and rhythm are adequate and the patient is decompensating — go to 03.

If organized and rate adequate, go to 03
03

Perfusion Problem?

Even with adequate rate and rhythm — is this patient perfusing?
The Pivot Question

Is the dysrhythmia causing the compromise — or is the compromise causing the dysrhythmia?

Perfusion Failing

Tamponade, tension pneumo, papillary muscle rupture — treat the cause, not the rhythm.

Question 03 + deteriorating = provider at the bedside, not on the phone
What Your Team Decided
Four patients. Four rhythms. Click any card to expand.
End of Shift
Four patients. Here's how your team's decisions landed.
Loading outcomes…
Most saves don't look like saves.
The nurse who checks the pulse pressure at 0215, notices it's narrowed, and calls before the blood pressure drops — that nurse changed the outcome. Nobody saw the save. The patient never knew how close it was. The chart will say "bedside echo, emergent pericardiocentesis" and not a word about what happened in the two hours before that.
You know. That's enough. Come back tomorrow and do it again.