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EMERGENTQuick Reference

Code Blue & Rapid Response

Your pocket card for running or assisting in a code. ACLS algorithms, drug doses, H's & T's, post-ROSC care with temperature control, and the rapid response assessment framework. Launch Code Clock for real-time code documentation.

⏱️ Code Clock App

Real-time code documentation -track interventions, drug times, rhythm checks, and generate a code summary.

🚀 Launch Code Clock →

⚡ Cardiac Arrest -ACLS

Shockable Rhythms: VFib / Pulseless VTach

CPR

High-quality CPR immediately. Rate 100–120/min, depth 2–2.4 inches, full chest recoil. Minimize interruptions (< 10 sec for rhythm checks). Rotate compressors q2 min.

Shock

Defibrillate as soon as possible. Biphasic: 200J first shock, escalate if needed. Resume CPR immediately after shock × 2 min before rhythm check.

Epinephrine

Epinephrine 1 mg IV q3–5 min (give after 2nd shock if VFib/pVT). Do NOT delay shocks for epi.

Antiarrhythmic

Amiodarone 300 mg IV bolus (after 3rd shock if refractory VFib/pVT). 2nd dose: 150 mg. Alternative: lidocaine 1–1.5 mg/kg then 0.5–0.75 mg/kg.

H's & T's

Find and treat the cause. See below.

Non-Shockable: PEA / Asystole

CPR + Epinephrine 1 mg IV q3–5 min. No shock. No antiarrhythmic.
Focus on finding and treating the cause -PEA/asystole rarely responds to CPR alone without correcting the underlying etiology.
Asystole: confirm in ≥ 2 leads (rule out fine VFib). No atropine (removed from algorithm). No defibrillation.

H's and T's -Reversible Causes

PEA and asystole will NOT respond to CPR alone -you MUST find and fix the underlying cause. Run through H's and T's every 2-minute cycle.

Cause	Clues (History & Exam)	Intervention
H's
Hypovolemia	Trauma, GI bleed (hematemesis, melena), ruptured AAA, ruptured ectopic. Flat neck veins, pale, bloody NG aspirate.	Aggressive IVF boluses. Activate massive transfusion protocol. Blood products 1:1:1. Surgical consult if hemorrhagic.
Hypoxia	Pre-arrest desaturation, cyanosis, COPD/asthma history, mucus plug, aspiration event, known difficult airway.	Confirm ETT placement (ETCO₂). Auscultate both lungs. If no breath sounds unilateral → mainstem intubation or PTX. Suction. Increase FiO₂ to 100%.
Hydrogen ion (acidosis)	Known DKA, renal failure, severe sepsis, toxic ingestion (methanol, ethylene glycol, ASA). Pre-arrest ABG with pH < 7.1.	Sodium bicarbonate 1 mEq/kg IV push. Ventilate aggressively (blow off CO₂). Treat underlying cause (insulin for DKA, dialysis for renal failure, fomepizole for toxic alcohols).
Hyper/Hypokalemia	Renal failure (hyperK), dialysis patient who missed session, recent K⁺ lab, ECG changes (peaked T waves, wide QRS). HypoK: diuretic use, GI losses, prolonged QT.	HyperK: Calcium chloride 1–2g IV push (stabilize membrane) → insulin 10 units + D50 → bicarb → albuterol. HypoK: KCl 40 mEq IV + MgSO₄ 2g IV.
Hypothermia	Found down outdoors, drowning, exposure, elderly. Core temp < 30°C (86°F). "Not dead until warm and dead."	Active rewarming: warm IVF (40°C (104°F)), warm humidified O₂, forced-air warming blankets. If < 30°C (86°F): defib may not work until rewarmed → limit to 1 shock attempt, hold meds until temp > 30°C (86°F). Continue CPR. Consider ECMO rewarming if available. This row is accidental hypothermia as the CAUSE of the arrest. After ROSC the logic is different: see post-ROSC temperature control.
Hypoglycemia	Diabetic on insulin/sulfonylureas, altered mental status pre-arrest, missed meals, liver failure, adrenal crisis.	D50 (dextrose 50%) 1 amp (25g) IV push. Recheck in 15 min. If no IV access: glucagon 1 mg IM.
T's
Tension pneumothorax	Absent breath sounds unilaterally, JVD, tracheal deviation (late sign), recent central line or thoracentesis, trauma, patient on positive pressure ventilation.	Needle decompression: 14–16G needle, 2nd intercostal space midclavicular line (or 5th ICS anterior axillary). Do NOT wait for CXR. Follow with chest tube (28–32 Fr).
Tamponade (cardiac)	Beck's triad: JVD + hypotension + muffled heart sounds. Recent cardiac surgery, pericardial effusion on prior imaging, dialysis patient (uremic pericarditis), trauma, malignancy, post-MI (free wall rupture).	Pericardiocentesis: subxiphoid approach, US-guided. Remove even 20–30 mL → dramatic improvement. In post-surgical: emergent sternotomy (re-open).
Toxins	Pill bottles at scene, history of depression/suicidal ideation, drug paraphernalia. Wide QRS (TCAs, Na-channel blockers). Opioid presentation (pinpoint pupils). Bradycardia (beta-blocker, CCB, digoxin). Seizure history (local anesthetic toxicity).	Specific antidotes: Naloxone (opioid), sodium bicarb (TCA -QRS > 100), intralipid 20% (local anesthetic toxicity, lipophilic drug OD), glucagon (beta-blocker), calcium + high-dose insulin (CCB), DigiFab (digoxin). See Toxicology.
Thrombosis -coronary (MI)	Pre-arrest chest pain, STEMI on last ECG, known CAD, cardiac risk factors. PEA with organized narrow-complex rhythm on monitor.	Consider emergent PCI (cath lab activation during CPR -some centers do this). If no PCI available: fibrinolytics (tPA 50 mg IV during CPR) -consider if high suspicion and no other cause found. Continue CPR for 60–90 min after lytics.
Thrombosis -pulmonary (Category E PE)	Pre-arrest dyspnea + pleuritic pain + tachycardia, recent surgery/immobilization/cancer, known DVT, RV strain on prior echo, dilated RV on bedside echo during CPR.	Systemic thrombolytics: tPA 50 mg IV bolus (can give during CPR). Continue CPR for 60–90 min after lytics to allow time to work. If available: consider surgical embolectomy or catheter-directed therapy. Bedside echo during CPR showing RV dilation supports PE diagnosis.

💊 Code Drug Doses

Drug	Dose	Indication
Epinephrine (Adrenalin)	1 mg IV q3–5 min	All cardiac arrest rhythms. First-line vasopressor.
Amiodarone (Cordarone)	300 mg IV push (1st dose), 150 mg (2nd dose)	Refractory VFib/pVT after 3+ shocks.
Lidocaine	1–1.5 mg/kg IV, then 0.5–0.75 mg/kg	Alternative to amiodarone for VFib/pVT.
Atropine	1 mg IV q3–5 min (max 3 mg)	Symptomatic bradycardia (NOT for asystole or PEA).
Adenosine (Adenocard)	6 mg rapid IV push → if no effect → 12 mg (two doses only)	Stable SVT. Must use rapid push + flush at proximal IV site.
Calcium chloride	1–2 g IV (10–20 mL of 10%)	Hyperkalemia with ECG changes, calcium channel blocker OD, hypocalcemia.
Calcium gluconate	3 g IV (30 mL of 10%)	Same indications. 3× less elemental calcium than CaCl₂. Safer peripherally.
Sodium bicarbonate	1 mEq/kg IV	Severe metabolic acidosis, TCA overdose, hyperkalemia (adjunct).
Magnesium	2 g IV over 15 min	Torsades de pointes. Also hypomagnesemia-related arrhythmias.
Vasopressin (Pitressin)	40 units IV × 1	Can replace first or second epi dose in cardiac arrest (AHA 2020 removed specific recommendation but still acceptable).

🌡️ Post-ROSC Care & Temperature Control

What changed in the 2025 AHA post-cardiac arrest guideline. CHANGED Temperature control now runs for at least 36 hours (2020 said at least 24 hours at target). UNCHANGED from the 2023 focused update: any constant target from 32 to 37.5°C (89.6 to 99.5°F) is acceptable (2020 capped it at 36°C (96.8°F)), so normothermia with active fever prevention is a full-fledged option, not a fallback. CHANGED Oxygen target widened to SpO₂ 90-98% (2020: 92-98%). UNCHANGED MAP at least 65, PaCO₂ 35-45, and no neuroprognostication before 72 hours.

The First 10 Minutes After You Get a Pulse

Airway / O₂

100% oxygen until the SpO₂ reads reliably, then titrate down to SpO₂ 90-98% (PaO₂ 60-105). Both ends hurt: hypoxemia extends the ischemic injury, and hyperoxemia generates reactive oxygen species in tissue that is reperfusing. Do not hyperventilate: keep PaCO₂ 35-45, because hypocapnia constricts cerebral vessels in a brain that is already ischemic. Pulse oximetry can overread in darker skin, so confirm with a gas if the number and the patient disagree.

Pressure

MAP at least 65. Cerebral autoregulation can be impaired after arrest, so brain perfusion may follow the MAP passively and hypotension becomes secondary brain injury. No vasopressor has proven better than another; norepinephrine is the usual first choice. Expect post-arrest myocardial stunning on the echo, which is usually reversible over 48-72 hours.

12-lead ECG

ST elevation goes to the cath lab now, coma or not (Class 1): the coronary lesion is the treatable cause, and neurologic status cannot be judged this early. No ST elevation: emergency angiography is NOT routine (Class 3, no benefit) unless there is cardiogenic shock, recurrent ventricular arrhythmia or ongoing ischemia.

Find the cause

Re-run the H's and T's, because an uncorrected cause re-arrests the patient. Glucose, potassium, gas and lactate; bedside echo; CT (head, chest, or as the story directs) is reasonable to find the cause and the complications of CPR such as rib fractures, pneumothorax and liver laceration.

The fork

Does the patient follow verbal commands? Yes: no temperature device is needed; treat any fever and continue supportive care. No: start temperature control (next table), and order an EEG, since 10 to 35% of these patients seize and some seizures are visible only on EEG. Do not give prophylactic antiseizure drugs (Class 3, no benefit); treat seizures that are seen or recorded.

Temperature Control: Who, What Target, How Long

It is "temperature control" now, not "therapeutic hypothermia", and the point is that fever is the enemy. Cooling to 33°C (91.4°F) has not beaten normothermia with active fever prevention in the modern trials, but every arm of every one of those trials actively controlled temperature with a device. What has never been shown safe is doing nothing: post-arrest fever is consistently associated with worse neurologic outcome. Why fever hurts this brain in particular: every 1°C (1.8°F) rise pushes cerebral metabolic demand up by roughly 6 to 10%, in a brain whose blood flow is already impaired, so oxygen supply falls short of demand. Heat also amplifies the injury cascade that reperfusion started: more glutamate release and calcium influx (excitotoxicity), more free radicals, a leakier blood-brain barrier with more edema, and a lower seizure threshold. The post-arrest inflammatory response makes fever common in the first 2 to 3 days, which is exactly when the injured neurons are most vulnerable. Do not confuse this with the Hypothermia row in the H's and T's, which is accidental hypothermia as a cause of arrest and is treated by rewarming.

Decision	What to do (2025 AHA)	Why
Who	Every adult who does not follow verbal commands after ROSC, whatever the rhythm and wherever the arrest happened (Class 1). That includes the in-hospital PEA arrest on the ward, not only the out-of-hospital VF arrest.	The brain injury is from ischemia and reperfusion, which does not depend on rhythm or location. Excluding non-shockable or in-hospital arrests is a habit left over from the 2002 trials, which enrolled only witnessed shockable arrests.
Target	Pick one constant temperature between 32 and 37.5°C (89.6 to 99.5°F) and hold it (Class 1). Two common protocols: normothermia 36 to 37.5°C (96.8 to 99.5°F) with a feedback device, or hypothermia 32 to 34°C (89.6 to 93.2°F) followed by normothermia. Use a core probe (esophageal or bladder), not an axillary or tympanic reading.	TTM2, 2021 found no difference between 33°C (91.4°F) and normothermia, and hypothermia caused more arrhythmia with hemodynamic compromise. The pooled trials do not exclude a benefit at lower temperatures and none showed harm, which is why the whole range stays acceptable. Whether sicker patients do better colder is unknown (Class 2b).
How long	At least 36 hours of total temperature control (Class 2a). The clock covers the whole period of active management: the hypothermic phase, if one is used, plus the normothermic fever-prevention phase after it. Many units still run the 72 hours used in the TTM trials, which the guideline permits: 36 hours is the floor.	BOX, 2023 compared 36 with 72 hours of device-based control and found no difference in death or severe disability (32.3% vs 33.6%), which is where the 36-hour floor comes from. Fever after the first 24 hours is still associated with poor outcome, so stopping the device is not the end of fever prevention.
How	A device with temperature feedback, surface pads or an intravascular catheter; both are acceptable, and the same machines serve both strategies (see the comparison below). Ice packs and fans overshoot and drift. Rapid cold IV saline before hospital arrival is not recommended (Class 3, no benefit).	Prehospital cold-fluid loading showed no outcome benefit and a signal of harm (re-arrest and pulmonary edema). In hospital, cold saline is still used by some protocols to speed induction (the TTM2 hypothermia arm allowed it), but it is a volume load into a heart that is usually stunned, and it cannot hold a target: the feedback device does that.
Shivering	Treat it early and in steps: scheduled acetaminophen, skin counter-warming, buspirone and magnesium first; then sedation (Propofol (Diprivan) 5-50 mcg/kg/min) and Meperidine (Demerol) 25-50 mg IV PRN; neuromuscular blockade last, ideally with EEG monitoring in place.	Shivering generates heat and raises oxygen consumption, so it fights the device and defeats the target. Paralysis hides seizures, which is why EEG should be running before it is used.
Rewarming	No faster than 0.5°C per hour (0.9°F per hour) (Class 2b), whether coming out of a hypothermic target or treating a patient who arrived spontaneously cold after ROSC. Trials used 0.25 to 0.5°C per hour (0.45 to 0.9°F per hour).	Fast rewarming causes vasodilation with hypotension, a potassium shift back out of cells, and rebound hyperthermia. Spontaneous hypothermia after ROSC usually marks a more severe brain injury, so do not rewarm it aggressively.
Expect at low targets	Bradycardia (leave it alone if the MAP is adequate), cold diuresis with hypokalemia and hypomagnesemia, insulin resistance, mild coagulopathy, and slowed clearance of sedatives and opioids.	Replace potassium cautiously while cold, because it shifts back out of cells on rewarming and overcorrection produces hyperkalemia at exactly the wrong time. Slowed drug clearance is one reason the prognostication clock starts late.
Prognosis	No neuroprognostication until at least 72 hours after return to normothermia AND off sedation (Class 2a), and never on a single finding: exam, EEG, SSEP, imaging and biomarkers together (Class 1).	Sedatives, cold and the early post-injury period all suppress the exam and mimic a devastating injury. Withdrawing care on an early exam becomes a self-fulfilling prophecy.

What You Actually Use: Inducing Hypothermia vs Preventing Fever

The machines are the same; the set point and the workload are what differ. Both strategies are active, device-based temperature control. The common mistake is to treat fever prevention as the passive option.

	Inducing hypothermia (32 to 34°C / 89.6 to 93.2°F)	Preventing fever (36 to 37.5°C / 96.8 to 99.5°F)
Device	Required from the start. Surface: adhesive hydrogel pads or water-circulating wraps with a feedback console. Intravascular: a femoral or central cooling catheter that circulates cold saline inside balloons (closed loop, nothing is infused). Intravascular tends to hold the target more tightly; surface is faster to set up and needs no line.	The same devices, set higher. Pads or catheter set to 36 to 37.5°C, either from the start or the moment the temperature crosses the trigger (37.8°C / 100°F in TTM2). In TTM2, 2021, 46% of the normothermia arm still needed a device, so have one at the bedside: about half of patients need more than antipyretics.
Getting to target	Induce as fast as practical: device on maximum, ice packs to groin, axillae and neck as a bridge, and in some protocols cold (4°C / 39°F) crystalloid as an adjunct if the heart and lungs can take the volume. Sedate and control shivering first, because a shivering patient will not cool.	Nothing to induce. Many patients arrive mildly cool (around 35 to 36°C / 95 to 96.8°F) after an arrest. Do not actively warm a mildly cool patient; let them drift up slowly (no faster than 0.5°C / 0.9°F per hour) and cap them at the target.
Drugs	Antipyretics do not produce hypothermia. The drugs here are for shivering and sedation: scheduled acetaminophen, buspirone, magnesium, then Propofol (Diprivan) or Dexmedetomidine (Precedex), Meperidine (Demerol), and neuromuscular blockade for refractory shivering.	Scheduled acetaminophen as the base layer, plus the device. Exposure, fans and cool room air are adjuncts only. Look for and treat an infectious source (aspiration pneumonia is common after CPR), but do not wait for cultures before controlling the temperature: in this brain the fever itself is the injury.
Workload and side effects	Deeper sedation, more shivering, bradycardia, cold diuresis with potassium and magnesium shifts, insulin resistance, mild coagulopathy, slowed drug clearance, and more arrhythmia with hemodynamic compromise in TTM2. Needs a controlled rewarming phase.	Lighter sedation, little shivering, fewer electrolyte shifts, no rewarming phase, and an earlier clean neurologic exam. This is why most US units now default here.
Monitoring	Continuous core temperature wired to the device: esophageal probe is the most responsive; a bladder probe reads falsely when urine output is low; an intravascular catheter carries its own sensor. Skin, axillary and tympanic readings lag and mislead. Check potassium, magnesium and glucose every 4 to 6 hours while at a hypothermic target and through rewarming. EEG for anyone not following commands, and before any paralytic.
The clock	Typical: about 24 hours at target, rewarm at 0.25 to 0.5°C (0.45 to 0.9°F) per hour, then keep the device on for fever prevention. The whole sequence counts toward the 36-hour minimum; the TTM trials ran 72.	Device on for at least 36 hours total. BOX, 2023 ran 36°C for 24 hours, then 37°C, and found 36 hours no worse than 72. After the device comes off, keep treating any fever.

Full protocol, ventilator and hemodynamic targets, and the neuroprognostication workup: Post-Cardiac Arrest Management. Accidental hypothermia as the cause of an arrest: Hypothermia and Drowning.

🏥 Rapid Response Assessment

When You Get the Call -ABCDE

A -Airway

Speaking? Stridor? Secretions? Can they protect their airway? If not → jaw thrust, suction, consider intubation. Call anesthesia early if airway is threatened.

B -Breathing

RR, SpO₂, work of breathing, auscultate. Wheezing → bronchodilator. Crackles → fluid overload vs pneumonia. Absent breath sounds → PTX? Stridor → upper airway obstruction → call ENT/anesthesia. Apply O₂ while assessing.

C -Circulation

HR, BP, rhythm, mental status, cap refill, urine output. If hypotensive → IVF bolus (unless cardiogenic). If no pulse → call code, start CPR. Get 12-lead ECG. Access: 2 large-bore IVs.

D -Disability

GCS, pupils, glucose (stat fingerstick -ALWAYS check). New focal deficit → stroke alert. Seizure → benzos (lorazepam 4 mg IV). AMS → consider naloxone 0.4 mg IV (opioid reversal).

E -Exposure/Environment

Expose the patient -look for rashes (anaphylaxis, meningococcemia), surgical sites, lines, drains, skin findings. Check temperature. Review meds + recent changes. What changed?

Common Rapid Response Triggers

Trigger	First Steps	Think
Acute desaturation	O₂, check SpO₂ probe, auscultate, CXR, ABG	PE, mucus plug, PTX, flash pulm edema, pneumonia, aspiration
Acute hypotension	Passive leg raise (NOT Trendelenburg -no evidence), IVF bolus, HR check, 12-lead ECG	Sepsis, hemorrhage, PE, cardiogenic, anaphylaxis, adrenal crisis
Tachycardia	12-lead ECG, BP, fluid status, pain assessment	SVT, Afib/RVR, PE, sepsis, hypovolemia, pain, anxiety, withdrawal
Acute AMS	Glucose, O₂, vitals, pupils, review meds	Hypoglycemia, opioids, stroke, seizure (postictal), sepsis, hypercarbia
Acute chest pain	12-lead ECG within 10 min, troponin, vitals, O₂	ACS, PE, dissection, PTX, pericarditis

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