ACLS Algorithms in Brief

In depth

The one-page summary above is what the PDF prints. These sections go further.

High-quality CPR: perfusion physiology and feedback

Compressions move blood two ways: they squeeze the heart between sternum and spine (the cardiac pump) and raise intrathoracic pressure so blood leaves the chest (the thoracic pump). Done well, they deliver roughly a quarter to a third of normal cardiac output. The myocardium is perfused almost entirely during the release phase, driven by coronary perfusion pressure (CPP): aortic diastolic pressure minus right atrial diastolic pressure.

Paradis 1990 (JAMA) measured CPP in 100 arrests: ROSC occurred only when the maximal CPP reached 15 mm Hg or more, and those with ROSC reached a mean maximum of 25.6 mm Hg against 8.4. CPP builds over uninterrupted compressions and falls as soon as they stop, so every pause costs more than its own length. Epinephrine raises CPP; leaning, slow rates and overventilation lower it.

Rescuers misjudge fatigue: on manikins, correct compressions fell from 93% in minute 1 to 39% by minute 3, yet rescuers felt tired only at about 4 minutes (Hightower 1995), hence 2-minute swaps and real-time feedback. EtCO₂ below 10 mm Hg means compressions need fixing and 20 or more is the goal (AHA 2025 supportive text), provided ventilation is steady. With an arterial line, diastolic (relaxation) pressure is the closest bedside proxy for CPP: the AHA 2010 algorithm said to improve CPR below 20 mm Hg, pediatric data link 25–30 mm Hg or more with survival (Berg 2018), and AHA 2025 sets no adult number.

Defibrillation: physics, pads and refractory VF

A shock ends VF by depolarizing a critical mass of myocardium at once so an organized pacemaker can take over. Current, not the energy setting, does this, and it falls as transthoracic impedance rises with poor pad contact, air under the pad, chest hair and lung inflation. Biphasic waveforms end VF at lower energy than monophasic ones and compensate for impedance. In BIPHASIC (Stiell 2007, 221 OHCA), escalating 200–300–360 J ended VF more often than a fixed 150 J when several shocks were needed (82.5% vs 71.2%).

In Chan 2008 (in-hospital VF and pulseless VT), defibrillation was delayed beyond 2 minutes in 30% of patients, and survival to discharge fell from 39.3% to 22.2%. Shock monitored VF at once, compress until the defibrillator arrives, and resume compressions immediately after every shock without a pulse check, because the post-shock rhythm is usually slow or stunned.

• Anterolateral: right pad below the right clavicle; left pad at the apex in the midaxillary line (V6), beside or under the breast, not on it.
• Anteroposterior: front pad over the left precordium, back pad left of the spine below the scapula (the DOSE-VF vector-change position).
• Pacemaker or ICD: pads at least 8 cm from the generator; free-flowing oxygen 1 m from the chest (ERC 2021).

Refractory VF persists after three standard shocks. DOSE-VF (Cheskes 2022, 405 OHCA in Canada) randomized these patients to standard shocks, vector change (pads moved to anteroposterior) or double sequential defibrillation (DSED: a second defibrillator on anteroposterior pads fired right after the first). Survival to discharge was 13.3%, 21.7% and 30.4%, and only DSED improved good neurologic outcome (RR 2.21). The trial stopped early for COVID-19 and was unblinded; AHA 2025 rates both techniques 2b, usefulness not established.

Airway and ventilation during arrest

In witnessed VF the blood stays oxygenated for the first minutes, so compressions and shocks come first; in asphyxial arrests (drowning, overdose, airway obstruction, many in-hospital arrests) oxygen and ventilation are part of the treatment. Every positive-pressure breath impedes venous return. Aufderheide 2004 recorded professional rescuers ventilating at 30 breaths/min; in pigs, 30/min versus 12/min lowered CPP (16.9 vs 23.4 mm Hg) and survival (1 of 7 vs 6 of 7). Hence 30:2 without an advanced airway and, with one, a breath every 6 seconds over about 1 second, just enough for visible chest rise.

The best airway is the one the team can place quickly without stopping compressions. AHA 2020 allows bag-mask or an advanced airway in any setting, favoring a supraglottic airway out of hospital where intubation success is low. In hospital, Andersen 2017 (108,079 GWTG-R arrests) linked intubation in any given minute of the first 15 with lower survival (16.3% vs 19.4%); the data are observational but argue against pausing CPR for the tube. Confirm any advanced airway with waveform capnography and recheck it after every move.

Drugs in arrest: what the trials show

No drug given during cardiac arrest has consistently improved survival with good neurologic function. Epinephrine's α₁ effect raises aortic diastolic pressure and CPP; its β effects raise myocardial oxygen demand and promote arrhythmias. PARAMEDIC2 (Perkins 2018, 8,014 UK OHCA) compared 1 mg epinephrine with placebo: 30-day survival 3.2% vs 2.4% (OR 1.39), favorable neurologic survival 2.2% vs 1.9% (not significant), and severe neurologic impairment in 31.0% vs 17.8% of survivors.

In nonshockable in-hospital arrest, survival fell stepwise with each 3-minute delay to the first dose (Donnino 2014, 25,095 patients; adjusted OR 0.63 when given after more than 9 minutes versus 1–3), so epinephrine is given as soon as access allows. In shockable in-hospital arrest, epinephrine within 2 minutes of the first shock was associated with lower survival (Andersen 2016, OR 0.70), consistent with giving it after the second shock.

ALPS (Kudenchuk 2016, 3,026 shock-refractory VF OHCA) found survival to discharge of 24.4% with amiodarone, 23.7% with lidocaine and 21.0% with placebo. Neither drug was significantly better overall, but both beat placebo in bystander-witnessed arrests. AHA treats the two as alternatives.

Reversible causes: bedside clues and ultrasound

In PEA, QRS width narrows the search (Littmann 2014, a teaching approach, not AHA guidance). A narrow complex suggests a mechanical problem that ultrasound can show: tamponade, tension pneumothorax, hypovolemia or massive PE. A wide, slow complex suggests hyperkalemia, a sodium channel blocker or a failing ischemic ventricle, and points toward calcium and bicarbonate. Pseudo-PEA (cardiac motion, no palpable pulse) does better than a still heart (Gaspari 2016).

Ultrasound lengthens pauses: pulse checks with it took 21 versus 13 seconds in Huis in 't Veld 2017 and 17 versus 11 seconds in Clattenburg 2018. Record a clip during the pause and review it during compressions; the leader should not be the scanner. In REASON (Gaspari 2016, 793 patients), cardiac activity predicted survival, yet 0.6% without it survived to discharge, so a still heart alone does not justify stopping. A dilated right ventricle appeared in 57% of intra-arrest TEE studies (Teran 2019), so in a prolonged arrest it does not prove PE.

Special circumstances and ECPR

From about 20 weeks the uterus compresses the vena cava and aorta; manual displacement keeps the patient supine for good compressions. Drugs and energies do not change, delivery is prepared from the first minute, and a magnesium infusion is stopped, with calcium for suspected toxicity.

Below 30 °C, AHA 2025 suggests one shock, then holding further shocks and IV drugs until the core is above 30 °C (2b); ERC allows up to three shocks and doubles the epinephrine interval between 30 and 35 °C. AHA 2020 had allowed standard drugs and shocks during rewarming. Both favor extracorporeal rewarming, and case series report good neurologic survival after hours of CPR.

ECPR restores flow with venoarterial ECMO during refractory arrest. ARREST (Yannopoulos 2020, 30 refractory VF OHCA, one center) stopped early with survival to discharge of 43% versus 7%. Prague OHCA (Belohlavek 2022, 256 patients) narrowly missed its endpoint (180-day good neurologic survival 31.5% vs 22.0%, P=0.09), and INCEPTION (Suverein 2023, 134 patients at 10 Dutch centers, half of which cannulated two or fewer) found 20% vs 16%. AHA calls ECPR reasonable in selected patients within a trained, equipped system (2a, 2023), and AHA 2025 Part 4 adds regional programs and experienced cannulators.

• Favor ECPR: bystander CPR, shockable rhythm, intermittent ROSC or signs of life, short low-flow time; against: age cutoffs, high lactate, low pH, low EtCO₂ (AHA 2025 Part 4).
• During cannulation, keep compressions going (a mechanical device frees the groin), have heparin and blood ready, and keep an exact low-flow clock; ELSO 2021 aims for flow within 60 minutes.
• Mechanical CPR did not beat manual CPR in LINC or PARAMEDIC; use it for transport, the cath lab and ECPR.

Post-arrest care: targets, temperature and prognosis

Post-cardiac arrest syndrome combines brain injury, myocardial dysfunction, a sepsis-like ischemia-reperfusion response and the cause of the arrest. Stunning usually improves within about 24 hours (Laurent 2002); brain injury causes most deaths after OHCA admission.

HACA 2002 (275 VF survivors, 32–34 °C for 24 h) raised favorable outcome from 39% to 55%; TTM 2013 (939 patients) found 33 °C no better than 36 °C; HYPERION 2019 (581 nonshockable arrests) favored 33 °C (good outcome 10.2% vs 5.7%); TTM2 2021 (1,850 patients) found 33 °C no better than normothermia with fever prevention, and 33 °C caused more unstable arrhythmias (24% vs 17%). Hence the wide AHA range; the constant is preventing fever. Prehospital cold saline added rearrest (26% vs 21%) without benefit (Kim 2014).

• Temperature: feedback-controlled surface or intravascular device, bladder or esophageal probe, rewarming no faster than 0.5 °C/h.
• Shivering: score it (Bedside Shivering Assessment Scale) and step up from acetaminophen, buspirone, magnesium and skin counterwarming to sedation and opioid, paralysis last.
• Expect at 33 °C: sinus bradycardia, cold diuresis, falling potassium, rising glucose; potassium climbs again on rewarming.
• Evaluate for organ donation everyone who progresses to death by neurologic criteria or planned withdrawal (AHA 2025 Part 4, class 1).

Prognostication is multimodal and delayed: AHA 2020 counted the 72-hour minimum from normothermia, ERC-ESICM 2021 from ROSC, and both wait for sedation to clear. ERC-ESICM 2021 calls a poor outcome likely when a patient with a motor score of 3 or less at 72 hours or later has two or more of: absent pupillary and corneal reflexes, bilaterally absent N20 SSEP waves, a highly malignant EEG after 24 hours, NSE above 60 µg/L at 48 or 72 hours, status myoclonus within 72 hours, or diffuse anoxic injury on CT or MRI.

In-hospital arrest: systems, teams and debriefing

Nearly 300,000 in-hospital arrests occur in the US each year, and about 19% of adults survive to discharge (AHA 2025 Parts 3 and 4). Most are preceded by visible decline: in Schein 1990, 84% of ward patients who arrested had documented deterioration within 8 hours, usually in breathing or mental status. AHA 2025 rates early warning scores, rapid response teams and safety huddles 2a; the nurse's escalation is the intervention.

AHA 2025 Part 4 recommends code teams of ALS-trained members (class 1) and designated or dedicated teams with defined roles and simulation training (2a), the pit crew model. Roles: leader, two or more compressors rotating every 2 minutes, airway, defibrillator, access and drugs, recorder, and a CPR coach who reads the feedback so the leader can think about causes. Closed-loop communication (order, read back, report done), a leader who summarizes each cycle aloud, and members who speak up hold the team together.

AHA 2025 Part 3 makes family presence the recommended approach in most situations; in Jabre 2013, relatives not offered the chance to watch had more PTSD symptoms (adjusted OR 1.7), with no effect on the resuscitation. No fixed duration ends an attempt: hospitals whose median attempt in nonsurvivors was 25 rather than 16 minutes had more survival to discharge (adjusted RR 1.12; Goldberger 2012, 64,339 arrests).

AHA 2025 Part 4 rates performance-focused debriefing 2a, ideally with objective data: compression rate, depth and fraction, defibrillator and EtCO₂ tracings, and the code record. A trained facilitator leads, and a hot debrief right after the event and a cold one a day to weeks later surface different problems. In Edelson 2008, weekly data-driven debriefing plus real-time feedback raised ROSC from 44.6% to 59.4%, though not survival to discharge.

What changed in 2025

Exam pearls

• CPP is aortic minus right atrial diastolic pressure; no patient reached ROSC below 15 mm Hg (Paradis 1990).
• Compression fraction at least 60%; pre-shock pause under 10 seconds; charge during compressions.
• Overventilation lowers CPP: with an advanced airway, 1 breath every 6 seconds and nonstop compressions.
• EtCO₂ under 10 mm Hg means improve CPR; a sudden rise of more than 10 suggests ROSC.
• Epinephrine: after the second shock in VF, as soon as possible in PEA or asystole; it improves survival, not proven neurologic recovery (PARAMEDIC2).
• Amiodarone and lidocaine are alternatives after the third shock; neither raised overall survival to discharge in ALPS.
• Narrow-complex PEA suggests a mechanical cause (tamponade, pneumothorax, PE, hypovolemia); wide suggests hyperkalemia, toxins or ischemia.
• Pregnancy: manual left uterine displacement, and delivery within 5 minutes if there is no ROSC.
• After ROSC: SpO₂ 90–98%, PaCO₂ 35–45, MAP 65 or more, 32–37.5 °C for at least 36 h, emergent angiography for STEMI.
• Prognosis: no earlier than 72 hours, two or more concordant findings, never one test.