What it is:Sudden loss of effective cardiac mechanical activity, confirmed by no pulse, no responsiveness, and no normal breathing. There's no cardiac output, so there's no perfusion anywhere, brain included.
The core problem:Every minute without effective circulation is a minute of hypoxic injury stacking up, mostly to the brain. CPR is a stopgap that buys maybe 25% of normal cardiac output. It isn't a fix, it's a bridge to a fix (defibrillation, or reversing whatever caused the arrest).
What you do about it:Compress hard and fast, minimize interruptions, shock a shockable rhythm immediately, and give epinephrine on a clock. Everything else is secondary to those basics.
Cardiac arrest management is a rhythm-driven fork in the road, not a single protocol. Once you know whether the rhythm is shockable (VF/PVT)or nonshockable (PEA/asystole), almost every subsequent decision, defibrillate or don't, which drugs, what you're hunting for, follows automatically. Learn the fork, not a flat list of steps.
Two classification questions matter, and they answer different things.
| Axis | Answers | Categories |
|---|---|---|
| Cause | Was oxygenation adequate at the moment of arrest? | Primary:blood was fully oxygenated when the arrest hit (usually an arrhythmic event on top of structural heart disease) · Secondary:respiratory failure caused progressive hypoxemia and hypotension that led to the arrest |
| Rhythm | Is there organized electrical activity a shock can fix? | Shockable:VF, pulseless VT (PVT) · Nonshockable:PEA, asystole |
Rhythm, not cause, decides whether you defibrillate.Historically VF/PVT were the dominant presenting rhythms; current data show nonshockable rhythms (asystole, PEA) are now more common. That matters clinically because survival to hospital discharge is meaningfully higher after a shockable rhythm than a nonshockable one, defibrillation is a far more effective intervention than anything in a syringe.
In adults, coronary artery disease is the single most common substrate, and it drives roughly 75% of sudden cardiac deaths. In children, the story is different: arrest is usually the end result of respiratory failure, asphyxiation, or progressive shock rather than a primary arrhythmia, which is why pediatric resuscitation leans more heavily on airway and breathing than adult ACLS does.
Other non-cardiac triggers include drowning, choking, asphyxia, electrocution, trauma, poisoning, severe asthma, pneumonia, drug overdose, and sudden infant death syndrome. Every one of these can produce either the primary or secondary pattern described above.
Most adult cardiac arrests are electrical events layered on top of ischemic or structurally diseased myocardium. That's the mechanistic reason VF and PVT used to dominate the numbers, diseased ventricle plus an ischemic trigger equals chaotic, disorganized depolarization. The shift toward more nonshockable presentations reflects sicker baseline patients and different arrest circumstances, but the underlying myocardial substrate is often the same.
VF is electrical anarchy, disorganized depolarization with zero coordinated contraction and zero cardiac output. A shock doesn't "restart" the heart, it depolarizes the whole myocardium simultaneously so the native pacemaker can take back control of an organized rhythm. That's why defibrillation works for VF/PVT and does nothing for asystole (no electrical activity to reset) or PEA (electrical activity is already organized, the problem is somewhere else, like the Hs and Ts).
Arrest is sometimes preceded by a prodrome: anxiety, shortness of breath, crushing chest pain, nausea, vomiting, diaphoresis. But by the time you're called, the picture is the arrest itself.
| Finding | What you see |
|---|---|
| Respiratory | Apnea, or only agonal gasping (this counts as "not breathing," don't let gasping fool you into withholding CPR) |
| Circulatory | No detectable pulse, hypotension, cold and clammy extremities, cyanosis |
| Neurologic | Loss of consciousness, syncope, unresponsiveness |
Agonal gasps look like breathing to a bystander and are a classic reason CPR gets delayed. "No breathing or no normalbreathing" is the trigger to start CPR, not "completely silent and motionless."
Diagnosis is clinical and immediate: unresponsive, apneic or gasping, no pulse. You don't wait for confirmatory testing before starting CPR, speed is the entire game here.
Once compressions are underway, the ECG is what actually determines drug therapy, because the four arrest rhythms split into two completely different treatment pathways.
| Rhythm | What the ECG shows | Category |
|---|---|---|
| VF | Chaotic, disorganized waveform. No coordinated ventricular contraction, no cardiac output. | Shockable |
| PVT | Organized-looking wide-complex tachycardia, but no palpable pulse | Shockable |
| PEA | Some organized electrical rhythm present on the monitor, but no detectable pulse | Nonshockable |
| Asystole | Flat line, no electrical activity at all | Nonshockable |
The AHA frames resuscitation as a chain of survival. The links differ slightly depending on where the arrest happens, but "high-quality CPR" and "rapid defibrillation" are non-negotiable in both settings.
| Setting | Chain of survival |
|---|---|
| Out-of-hospital | (1) Early recognition + activate emergency response → (2) high-quality CPR → (3) rapid defibrillation → (4) ACLS → (5) post-arrest care → (6) recovery |
| In-hospital | (1) Early recognition and prevention → (2) activate emergency response → (3) high-quality CPR → (4) prompt defibrillation → (5) post-arrest care → (6) recovery |
Basic life support runs on the mnemonic CAB (circulation, airway, breathing), a deliberate reversal of the old "ABC" because starting compressions immediately, before fumbling with an airway, is what actually keeps blood moving to the brain.
| Step | What to do |
|---|---|
| 1 | Check responsiveness. If unresponsive with no breathing or only gasping, activate the emergency response team and get an AED. |
| 2 | Check for a pulse. If not definitely felt within 10 seconds, start compressions. |
| 3 | Compress at 100-120/min, depth at least 2 in (5 cm)in adults (about one-third of chest diameter in kids: ~1.5 in/4 cm infants, ~2 in/5 cm children). |
| 4 | Open the airway, give 2 rescue breaths, then resume compressions. Cycle is 30 compressions: 2 breaths. |
| 5 | Continue until the AED is ready or ACLS providers take over. |
| 6 | AED available → check rhythm. Shockable → one shock, then immediately resume CPR for 2 minutes before the next rhythm check. Not shockable → resume CPR immediately for 2 minutes and repeat the cycle until ACLS arrives or the patient starts moving. |
10 secondsto confirm a pulse before starting compressions. 100-120/mincompression rate (not "as fast as possible," too fast reduces filling time). At least 2 indepth in adults. 30:2compression-to-breath ratio. 2-minutecycles between rhythm checks. Once an advanced airway is placed, ventilation becomes 1 breath every 6 secondswith continuous, uninterrupted compressions running simultaneously, no more 30:2 pause once the airway is secured.
Once ACLS providers take over, the pulseless arrest algorithm forks on rhythm. Everything downstream, shock or no shock, which drug, is a consequence of that one branch point.
1.Persistent VF/PVT on rhythm check → one shock→ resume CPR immediately.
2.During that 2-minute cycle, give epinephrine 1 mg IV/IO.
3.Recheck rhythm. Still VF/PVT → another shock → resume CPR, continue epinephrine every 3-5 minutes.
4.Still refractory after defibrillation and epinephrine → consider amiodarone or lidocaine.
5.Throughout, actively hunt for and treat a reversible cause.
6.ROSC at any point → move to postresuscitation care. Rhythm converts to PEA/asystole → switch to that pathway.
1.No shock, ever, for these rhythms.
2.CPR plus epinephrine 1 mg IV/IO as soon as possible, then every 3-5 minutes.
3.The entire game here is finding and reversing the underlying cause, this pathway lives or dies on the reversible-causes workup.
There's no disorganized rhythm to reset, PEA already has organized electrical activity and asystole has none at all. Shocking either one does nothing therapeutic and the resulting parasympathetic discharge can actually reducethe chance of ROSC.
| Drug | Dose | Role |
|---|---|---|
| Vasopressor | ||
| Epinephrine | 1 mg IV/IO every 3-5 min | First-line for all four arrest rhythms; higher doses studied but not recommended |
| Vasopressin | (historical, not routinely added) | No outcome advantage over epinephrine alone or over the combination |
| Antiarrhythmics (VF/PVT refractory to defib + epi only) | ||
| Amiodarone | 300 mg IV/IO ×1, then 150 mg IV/IO ×1 | Preferred antiarrhythmic option |
| Lidocaine | 1-1.5 mg/kg IV/IO, then 0.5-0.75 mg/kg q5-10min, max total 3 mg/kg | Alternative to amiodarone |
| Situational | ||
| Magnesium sulfate | 1-2 g in 10 mL D5W, IV/IO push over 15 min | Only for VF/PVT associated with torsades de pointes; not for routine use |
| Sodium bicarbonate | Not routinely dosed; reserve for specific indications | Hyperkalemia, TCA overdose, salicylate toxicity |
| Tenecteplase (fibrinolytic) | Not routine | May be considered only if PE is the suspected cause of arrest |
Epinephrine 1 mg IV/IO every 3-5 minutesis the single drug given in every arrest rhythm, shockable or not. If you remember nothing else, remember that one.
Epinephrine is a combined α- and β-receptor agonist. The α-mediated vasoconstriction is the part that actually matters during arrest: it raises aortic diastolic pressure, which is what drives coronary and cerebral perfusion pressure during CPR. The β effects (increased rate and contractility) matter more once there's a perfusing rhythm to speed up.
Practical point:dose is fixed at 1 mg IV/IO regardless of the rhythm on the monitor, repeated every 3-5 minutes for as long as resuscitation continues. Higher doses have been studied and don't improve outcomes, so there's no "pushing more epi" escalation strategy.
Vasopressin is a potent nonadrenergicvasoconstrictor, it raises BP and systemic vascular resistance through V1 receptors rather than catecholamine pathways. On paper that's an appealing alternative in a low-perfusion, acidotic environment where catecholamine receptors may be less responsive. In practice, outcomes with vasopressin were not superiorto standard-dose epinephrine alone, and adding it to epinephrine didn't beat epinephrine alone either. That's why the current pulseless-arrest algorithm centers on epinephrine as the sole vasopressor rather than routinely pairing the two.
Both drugs exist to prevent recurrenceof VF/PVT after defibrillation and epinephrine haven't converted the rhythm, not to convert it themselves. Neither has been shown to improve survival to hospital discharge in trials, the justification for using them is stabilizing a rhythm that's already proven refractory, not a mortality benefit.
Amiodarone 300 mg IV/IO, followed by a second dose of 150 mgif VF/PVT persists, is generally reached for first given the stronger overall antiarrhythmic evidence base.
Lidocaineis the alternative: 1-1.5 mg/kginitial bolus, then 0.5-0.75 mg/kgevery 5-10 minutes if VF/PVT persists, capped at a total of 3 mg/kg. Watch the max, it's easy to keep re-dosing through a prolonged code and blow past it.
Severe hypomagnesemia is associated with VF/PVT, which makes magnesium tempting to give broadly. It isn't. Routine magnesium in cardiac arrest has notimproved outcomes. The exception is arrest from torsades de pointes, where two trials showed improved ROSC. Limit magnesium to that specific scenario.Dose is 1-2 g diluted in 10 mL of D5W, IV/IO push over 15 minutes, notably slower than the push-dose drugs above it.
Most adult arrests trace back to either MI or pulmonary embolism, so giving a clot-busting drug during CPR is a logical idea that's been tested. A randomized trial of tenecteplase vs placeboduring CPR showed no improvement in ROSC or survival to discharge, and more intracranial hemorrhagein the thrombolytic arm. That's a clean net-harm signal for routine use. The one scenario where it may still be reasonable is arrest with a strongly suspected PEas the cause, where treating the underlying clot could plausibly be the only thing that reverses the arrest.
Arrest produces both metabolic acidosis (chest compressions generate only about 25% of normal cardiac output, so tissue perfusion and oxygen delivery are already inadequate) and respiratory acidosis (poor ventilation means CO₂ isn't being cleared). Acidosis itself is bad news: it reduces myocardial contractility and lowers the fibrillation threshold, making the heart more electrically unstable.
Despite that mechanistic rationale, routine bicarbonate has not been shown to improve ROSC or survival, and it carries potential downsides. Reserve it for specific situations where you know acidosis or a specific toxin is the driver: hyperkalemia, tricyclic antidepressant overdose, salicylate toxicity.In those cases you're treating the specific poison or electrolyte problem, not blindly buffering pH.
PEA and asystole don't respond to a shock, and antiarrhythmics have no role. Survival depends entirely on finding and fixing the underlying cause while CPR and epinephrine buy time. The classic list has 12 reversible causes, conventionally grouped into 6 Hs and 6 Ts.
| 6 H's | 6 T's |
|---|---|
| Hypovolemia | Toxins / drug overdose |
| Hypoxia | Cardiac Tamponade |
| Hydrogen ion (acidosis) | Tension pneumothorax |
| Hyper-/hypokalemia | Thrombosis, coronary |
| Hypothermia | Thrombosis, pulmonary |
| Hypoglycemia | Trauma |
Don't just memorize it, run it as a checklist mid-code. Blood glucose and a potassium value are fast. Ultrasound at the bedside can catch tamponade or a collapsed lung. History from bystanders or the chart (recent surgery, immobility, known cancer) points toward thrombosis. PEA and asystole are treated identically: CPR, airway control, IV access, and this workup running in parallel.
ROSC is not the finish line. Patients who regain a pulse can develop post-cardiac arrest syndrome: hypoxic brain injury, myocardial dysfunction, a systemic ischemia-reperfusion response, plus whatever originally caused the arrest is often still active. The goal of this phase is preventing a second, slower death from that syndrome.
Cooling suppresses the chemical cascade that follows reperfusion and can blunt cerebral injury. Trial data on hard neurologic and survival outcomes have been mixed, but guidelines still recommend it.
| Parameter | Target |
|---|---|
| Temperature range | 32-36°C |
| Duration | At least 24 hours |
| After the TTM period | Actively prevent fever |
Coagulopathy, dysrhythmias, bradycardia, diuresis (cold diuresis can drop volume and electrolytes fast), electrolyte disorders, infection risk, and altered drug distribution/clearance (cooling slows metabolism, so drug levels can run higher than expected). This isn't a "set it and forget it" intervention, it needs active monitoring the whole time it's running.
| Parameter | When | Watching for |
|---|---|---|
| Rhythm / pulse checks | Every 2-minute CPR cycle | Shockable vs nonshockable rhythm, whether the algorithm branch needs to change |
| ETCO₂ | Continuously in intubated patients during CPR | CPR quality and likelihood of ROSC; persistently <10 mm Hgsuggests ROSC is unlikely |
| Arterial diastolic pressure | If an arterial line is in place | Surrogate for coronary perfusion pressure; goal >25 mm Hg |
| Central venous O₂ saturation | If available | <30% indicates poor CPR quality |
| Oxygen saturation (post-ROSC) | Continuously after ROSC | Maintain 92-98%acutely, >94%in the postresuscitative phase; avoid both hypoxia and hyperoxia |
| Blood pressure | Continuously post-ROSC | Avoid hypotension, MAP <65 mm Hg or SBP <90 mm Hg; support toward MAP >80 in the immediate post-arrest window |
| Core temperature | Throughout TTM and after | Staying within 32-36°C during TTM, then strict fever avoidance |
| Glucose | Regularly post-ROSC | Maintain normoglycemia |
| EEG | Post-ROSC | Seizures are common after arrest and can be subclinical |
| Full systems review | Throughout hospitalization | Post-cardiac arrest syndrome can hit nearly any organ system |
Palpating a pulse to judge how well compressions are perfusing the patient has not been shown to be useful, and pausing compressions to feel for one wastes precious perfusion time. ETCO₂ and, if available, invasive hemodynamics are the actual quality signals during the code itself.
The patient obviously can't be counseled during the arrest. The conversations that matter happen with family in the moment, and with the survivor (or their caregivers) once they're stable enough to process what happened.