Targeted Temperature Management (TTM)

Targeted Temperature Management after Cardiac Arrest: 2026 Evidence & Trials

Current standard of care, organized by treatment area, with the trials behind each recommendation.

Reviewed by the DosePilot Medical Team · Last reviewed: Jun 2026 · Independent — no industry funding
How to read this page. Each treatment area opens with the current approach, then the trials behind it (design, key results, limitations), and a short practical note (In practice). All targets and figures are taken from the cited primary sources (DOI + PMID). In practice notes are general practical guidance, not a substitute for clinical judgment.
How we verify evidence & editorial policy
Written and maintained by the DosePilot Medical Team. Recommendations are based on randomized controlled trials and current society guidelines (GRADE). Every citation is verified directly against PubMed (PMID) and the publisher DOI — no memory-based or AI-generated references. Each topic is peer-reviewed by the clinical team before publication and re-reviewed at least every 12 months or when major new evidence appears.

Funding & conflicts of interest. Produced independently; no industry funding was received for this content and contributors report no relevant financial conflicts of interest.
On this page
  1. Evidence timeline
  2. Definition & who needs TTM
  3. Target temperature
  4. Active fever prevention
  5. Duration of temperature control
  6. Non-shockable rhythm & severe injury
  7. Timing & method of cooling
  8. Controlled rewarming
  9. Shivering management
  10. Neuroprognostication
  11. Where it’s heading
  12. Bottom line
  13. FAQ
  14. Related DosePilot tools
  15. Guidelines & evidence basis
At a glance — current standard of care
AreaCurrent approachKey trial(s)
Who needs TTMComatose adults after ROSC; shockable & non-shockable, IHCA & OHCAHACA; Bernard
Target temperature32–37.5°C individualized; 33°C no longer mandatedTTM1; TTM2; CAPITAL CHILL
Fever preventionActively maintain ≤37.5°C; ILCOR ≥72 hTTM2 (normothermia arm)
DurationAt least 36 h of active controlTTH48; ICECAP (ongoing)
Non-shockable rhythmConsider 33°C — improved favorable neuro outcomeHYPERION
AreaCurrent approachKey trial(s)
Timing / methodAvoid routine pre-hospital cold-fluid bolus; feedback devicesRINSE; Kim 2014
RewarmingSlow, controlled (~0.25–0.5°C/h); avoid rebound fever—
ShiveringBSAS; counter-warming first, then sedation/analgesia—
NeuroprognosticationDelay ≥72 h off sedation; multimodalERC–ESICM algorithm

1Evidence timeline (2002–2026)

2002HACA & Bernard — mild hypothermia (32–34°C) improves neuro outcome after VF arrest
2005ILCOR/AHA endorse therapeutic hypothermia (32–34°C) for comatose OHCA survivors
2013TTM1 (Nielsen) — 33°C vs 36°C: no difference; first signal that deeper cooling adds nothing
2014Kim — pre-hospital cold saline: faster cooling, no outcome benefit, more re-arrest
2016RINSE — intra-arrest cold saline reduces ROSC in shockable rhythm
2017TTH48 — 48 h vs 24 h of TTM: no significant difference
2019HYPERION (Lascarrou) — 33°C improves favorable neuro outcome in non-shockable rhythm
2021TTM2 (Dankiewicz) — 33°C vs active normothermia: no difference, more arrhythmia at 33°C; CAPITAL CHILL — 31°C vs 34°C: no benefit of deeper cooling
2022ERC–ESICM temperature-control guideline — shift from “therapeutic hypothermia” to “≤37.5°C / fever prevention”
2025AHA 2025 Part 11 — target 32–37.5°C (COR 1), ≥36 h (COR 2a); ESICM 2025 — active fever prevention ≤37.5°C
2025–26ICECAP / P-ICECAP — adaptive-duration RCTs ongoing; no new mortality-changing TTM result

2Definition & who needs TTM

Current approach (2026)
Consensus indication
Provide active targeted temperature management (TTM) to comatose / unresponsive adults after return of spontaneous circulation (ROSC) — those not following verbal commands. It applies to both shockable and non-shockable initial rhythms and to both out-of-hospital (OHCA) and in-hospital (IHCA) arrest. The modern goal is controlled normothermia / active fever prevention within a 32–37.5°C window, not mandatory deep hypothermia. TTM is one element of post–cardiac-arrest care alongside coronary reperfusion, hemodynamic and ventilation targets, seizure control, and delayed neuroprognostication.
  • Patient selection is by level of consciousness after ROSC (comatose / not obeying commands), not by initial rhythm or arrest location.
Evidence — old → new
2002
HACA & Bernard (the foundation). Two RCTs in comatose survivors of VF / shockable OHCA. HACA (n=275): hypothermia 32–34°C for 24 h improved favorable neurological outcome (55% vs 39%; RR 1.40, 95% CI 1.08–1.81) and 6-month mortality (41% vs 55%). Bernard (n=77): good outcome 49% vs 26% (P=0.046). Established cooling as standard for shockable OHCA.
2021
TTM2 (modern reframe). Largest trial to date (n=1,900) extended TTM questions to all-rhythm OHCA and tested 33°C vs active normothermia — confirming the indication is broad but the depth is not. (Full results below under Target temperature.)

What changed. The indication widened (any comatose post-ROSC patient, any rhythm, IHCA or OHCA) while the intervention narrowed (from mandatory 32–34°C hypothermia to individualized control with fever prevention).

Significance. Almost every comatose post-arrest patient should receive deliberate temperature control; the debate is now about target and duration, not whether.

In practice

If the patient does not follow commands after ROSC, start active temperature management regardless of rhythm or arrest location — and fold it into the wider post-arrest bundle (PCI as indicated, lung-protective ventilation, MAP and oxygenation targets, EEG for seizures).

Sources (2)
  • Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8):549–556. DOI 10.1056/NEJMoa012689. PMID 11856793.
  • Bernard SA, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346(8):557–563. DOI 10.1056/NEJMoa003289. PMID 11856794.

3Target temperature

Current approach (2026)
Guideline: COR 1 — control 32–37.5°C (AHA 2025)RCT: no deep-cooling benefit
Select an individualized constant target between 32°C and 37.5°C and hold it with active feedback control (AHA 2025 Part 11, COR 1). A mandatory 33°C is no longer required. A pragmatic choice of 37.5°C or 36°C is reasonable for most patients — higher targets cause less shivering and are easier to manage. Across large RCTs, lower / deeper targets confer no additional benefit, and 33°C is associated with more arrhythmia. Whatever target is chosen, avoid fever.
Evidence — old → new
2002
HACA / Bernard (deep-cooling era). Hypothermia 32–34°C beat uncontrolled normothermia in shockable OHCA (see above) — but the comparator was no temperature control, leaving open whether the benefit was hypothermia or simply avoiding fever.
2013
TTM1 (Nielsen) — first neutral signal. RCT, 950 patients, OHCA of presumed cardiac cause; 33°C vs 36°C for 36 h (both actively controlled). No difference in mortality (50% vs 48%; HR 1.06, 95% CI 0.89–1.28) or 6-month neurological outcome. Suggested the prior benefit was from controlled normothermia, not deep cooling.
2021
CAPITAL CHILL — deeper is not better. Double-blind RCT, 389 randomized (367 in the primary analysis), comatose OHCA; 31°C vs 34°C. No difference in the composite of death or poor neurological outcome at 180 days (48.4% vs 45.4%; RR 1.07, 95% CI 0.86–1.33). Deeper hypothermia added nothing.
2021
TTM2 (Dankiewicz) — the decisive trial. RCT, 1,900 patients, all-rhythm OHCA; 33°C hypothermia vs targeted normothermia (active treatment of fever ≥37.8°C). No difference in 6-month death (50% vs 48%; RR 1.04, 95% CI 0.94–1.14) or poor functional outcome (55% each). Arrhythmia with hemodynamic compromise more frequent at 33°C (24% vs 17%). No benefit in any subgroup (age, initial rhythm, time to ROSC).
TrialTarget comparisonKey result
TTM1 (2013)33°C vs 36°CNo difference (mortality 50% vs 48%)
CAPITAL CHILL (2021)31°C vs 34°CNo benefit of deeper target
TTM2 (2021)33°C vs active normothermiaNo difference; more arrhythmia at 33°C

What changed. From “cool every comatose survivor to 32–34°C” (2002–2015) to “control temperature anywhere in 32–37.5°C and prevent fever” (2021–2026). The 33°C target lost its mandatory status.

Significance. Over 3,200 randomized patients (TTM1, CAPITAL CHILL, TTM2) show no advantage to deeper cooling, with a real arrhythmia cost at 33°C — so a higher, easier-to-manage target is preferred unless a specific rationale favors hypothermia.

In practice

Pick one target (commonly 37.5°C or 36°C), set the feedback device, and defend it — the priority is tight control and no fever, not a low number. Reserve 33°C for selected cases (e.g., presumed severe brain injury) rather than as a default.

Sources (3)
  • Nielsen N, et al (TTM1). Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013;369(23):2197–2206. DOI 10.1056/NEJMoa1310519. PMID 24237006.
  • Le May M, et al (CAPITAL CHILL). Moderate vs mild therapeutic hypothermia on neurologic outcome after OHCA. JAMA. 2021;326(15):1494–1503. DOI 10.1001/jama.2021.15703. PMID 34665203.
  • Dankiewicz J, et al (TTM2). Hypothermia versus normothermia after out-of-hospital cardiac arrest. N Engl J Med. 2021;384(24):2283–2294. DOI 10.1056/NEJMoa2100591. PMID 34133859.

4Active fever prevention / normothermia

Current approach (2026)
Guideline: active fever prevention (AHA/ESICM/ILCOR)No direct RCT vs no control
Whatever the chosen target, actively prevent fever — keep core temperature ≤37.5°C for the temperature-control period. ILCOR and ESICM recommend active fever prevention for at least 72 hours after arrest (treating temperature ≳37.7°C). Use feedback-controlled cooling rather than antipyretics alone. Post-arrest fever is common and associated with worse neurological outcome.
Evidence
2021
TTM2 normothermia arm (the practical benchmark). The 1,900-patient trial’s comparator was targeted normothermia with active fever treatment (devices engaged at ≥37.8°C), and it matched 33°C — establishing that disciplined fever prevention, not deep cooling, is the active ingredient.

Important caveat. No RCT has compared active fever prevention with no temperature control (true “do nothing”) in the modern era. The benefit of fever prevention is inferred from the hypothermia trials and observational cohorts, not proven against an untreated arm.

What changed. The field reframed the goal from “induce hypothermia” to “guarantee normothermia and abolish fever” — a lower-risk, easier-to-deliver target.

In practice

Treat fever prevention as the non-negotiable core of TTM: use a feedback device set to ≤37.5°C, monitor core temperature continuously, and maintain control for ≥72 h. Recognize this rests on extrapolation, so keep the rest of the post-arrest bundle optimized too.

Sources (2)
  • Dankiewicz J, et al (TTM2). N Engl J Med. 2021;384(24):2283–2294. DOI 10.1056/NEJMoa2100591. PMID 34133859.
  • Sandroni C, Nolan JP, Cariou A, et al. ERC–ESICM guidelines on temperature control after cardiac arrest in adults. Intensive Care Med. 2022;48(3):261–269. DOI 10.1007/s00134-022-06620-5. PMID 35089409.

5Duration of temperature control

Current approach (2026)
Guideline: ≥36 h (AHA 2025, COR 2a)RCT: 48 h ≈ 24 h
Maintain active temperature control for at least 36 hours (AHA 2025 Part 11, COR 2a), then continue active fever prevention to complete a total of ~72 h. The optimal duration is unresolved — adaptive-duration trials (ICECAP / P-ICECAP) are ongoing. 36 h is a safe lower bound, not a proven optimum.
Evidence — old → new
2017
TTH48 (Kirkegaard) — longer is not clearly better. RCT, 355 patients, comatose OHCA; 48 h vs 24 h at 33°C. Favorable 6-month neurological outcome 69% vs 64% (difference 4.9%, 95% CI −5 to +14.8; P=0.33) — no significant difference, though the point estimate (and more adverse events with 48 h) leaves the question open. Underpowered for a small benefit.
ongoing
ICECAP / P-ICECAP (the duration trial). Adaptive RCTs randomizing comatose post-arrest adults (and children) to a range of durations (roughly 12–96 h) of temperature control to identify the response curve. The key study clinicians are awaiting to answer “how long?”

What changed. Guidelines moved from a fixed “24 h” (the 2002 trials) toward “at least 36 h,” acknowledging both TTH48’s null and uncertainty about the true optimum.

Significance. Until ICECAP reports, ≥36 h of control followed by fever prevention is the defensible default; do not shorten control to 24 h on the strength of the older trials alone.

In practice

Hold the target for ≥36 h, then keep preventing fever out to ~72 h from arrest. Avoid early rewarming, and don’t extend deliberately to 48 h expecting benefit — the evidence does not support it.

Sources (1)
  • Kirkegaard H, et al (TTH48). Targeted temperature management for 48 vs 24 hours and neurologic outcome after OHCA. JAMA. 2017;318(4):341–350. DOI 10.1001/jama.2017.8978. PMID 28742911.

6Special populations — non-shockable rhythm & severe brain injury

Current approach (2026)
RCT: benefit in non-shockable (HYPERION)Severe injury: COR 2b either way
In comatose survivors of non-shockable (asystole / PEA) arrest, 33°C is a reasonable option — the one modern RCT in this group (HYPERION) showed improved favorable neurological outcome versus targeted normothermia. For patients judged to have severe anoxic brain injury, both hypothermia and normothermia are acceptable (COR 2b), with the choice individualized; the supporting observational data are confounded by clinician selection.
Evidence — old → new
2019
HYPERION (Lascarrou) — the non-shockable exception. RCT, 584 randomized (581 analyzed), comatose survivors of non-shockable IHCA or OHCA; 33°C for 24 h vs targeted normothermia (37°C). Favorable 90-day neurological outcome (CPC 1–2) 10.2% vs 5.7% (difference 4.5%, 95% CI 0.1–8.9; P=0.04); 90-day mortality similar (81.3% vs 83.2%). Fragile result (small absolute difference, wide CI) but the best available randomized signal in this group.
2021
TTM2 subgroup (context). In the all-rhythm TTM2, the non-shockable subgroup showed no interaction favoring 33°C — so HYPERION’s signal is not strongly corroborated, and equipoise remains.

What changed. Non-shockable arrest, historically thought not to benefit from cooling, gained a positive (if fragile) RCT — making 33°C a defensible option there even as deeper cooling fell out of favor for shockable arrest.

Significance. Rhythm-specific nuance: a higher target suffices for most, but 33°C is reasonable in non-shockable arrest and may be chosen in presumed severe brain injury, where evidence is weakest and selection bias is real.

In practice

For non-shockable arrest, 33°C is a legitimate choice (HYPERION); for presumed severe anoxic injury, individualize between hypothermia and strict normothermia and document the rationale. Either way, fever prevention remains mandatory.

Sources (2)
  • Lascarrou JB, et al (HYPERION). Targeted temperature management for cardiac arrest with nonshockable rhythm. N Engl J Med. 2019;381(24):2327–2337. DOI 10.1056/NEJMoa1906661. PMID 31577396.
  • Dankiewicz J, et al (TTM2 — subgroup context). N Engl J Med. 2021;384(24):2283–2294. DOI 10.1056/NEJMoa2100591. PMID 34133859.

7Timing & method of cooling

Current approach (2026)
RCT: harm — routine pre-hospital cold fluidsDevice: surface ≈ endovascular
Do not routinely induce hypothermia with a large pre-hospital cold-saline bolus — it does not improve outcome and increases re-arrest and pulmonary edema. Begin temperature control after ROSC, in hospital, using a feedback-controlled device (surface pads or endovascular catheter — outcomes are comparable). Monitor core temperature continuously with a bladder or oesophageal probe (avoid less reliable peripheral sites).
Evidence — old → new
2014
Kim — pre-hospital cold saline (no benefit, some harm). RCT, 1,359 patients; up to 2 L of 4°C saline by paramedics after ROSC vs standard care. Reached target faster but no improvement in survival to discharge or neurological outcome, with more re-arrest and early pulmonary edema.
2016
RINSE — intra-arrest cold saline (harm signal). RCT, 1,198 patients; cold saline during CPR vs standard. No survival benefit, and in patients with an initial shockable rhythm reduced ROSC (41.2% vs 50.6%, P=0.03). Confirmed pre-/intra-arrest fluid cooling is not a useful induction route.

What changed. Early enthusiasm for “cool fast, cool in the field” was abandoned — speed of induction does not drive outcome, and cold-fluid loading is harmful. Modern practice cools in hospital with feedback devices.

Significance. The route and timing of induction matter for safety: avoid the cold-fluid bolus, and let device-based control (not raw cooling speed) deliver tight temperature management.

In practice

Skip pre-hospital cold-fluid induction. In the ICU/ED, apply a feedback surface or endovascular device, place a bladder or oesophageal core probe, and aim for stable control rather than the fastest possible drop.

Sources (2)
  • Kim F, et al. Effect of prehospital induction of mild hypothermia on survival and neurological status among adults with cardiac arrest. JAMA. 2014;311(1):45–52. DOI 10.1001/jama.2013.282173. PMID 24240712.
  • Bernard SA, et al (RINSE). Induction of therapeutic hypothermia during out-of-hospital cardiac arrest using a rapid infusion of cold saline. Circulation. 2016;134(11):797–805. DOI 10.1161/CIRCULATIONAHA.116.021989. PMID 27562972.

8Controlled rewarming

Current approach (2026)
Consensus practice
After the temperature-control period, rewarm slowly and under control — about 0.25–0.5°C per hour — using the feedback device, then continue active fever prevention. The main hazards are rebound hyperthermia (which must be avoided), hyperkalemia (potassium shifts back out of cells), and vasodilatory hypotension. Continue sedation until normothermia is re-established.
Evidence
obs.
Rewarming-rate cohorts. Observational data link rapid or uncontrolled rewarming and post-rewarming fever with worse neurological outcome, supporting a slow, device-controlled rate and strict fever prevention afterward. No RCT defines the optimal rate.

Why it matters. Physiologic reversals concentrate at rewarming: potassium re-enters the serum (hyperkalemia risk), vascular tone falls (hypotension), and any overshoot into fever undoes the benefit of the whole intervention.

In practice

Let the device rewarm at ~0.25–0.5°C/h, recheck potassium and hemodynamics during the climb, keep sedation running until normothermic, and then hold ≤37.5°C — the rewarming phase is where rebound fever and electrolyte swings bite.

Sources (1)
  • Sandroni C, Nolan JP, Cariou A, et al. ERC–ESICM guidelines on temperature control after cardiac arrest in adults. Intensive Care Med. 2022;48(3):261–269. DOI 10.1007/s00134-022-06620-5. PMID 35089409.

9Shivering management

Current approach (2026)
Consensus stepwise protocol
Assess shivering with the Bedside Shivering Assessment Scale (BSAS) and treat it stepwise, because shivering generates heat, raises metabolic demand, and defeats temperature control. Start with surface counter-warming (forced-air warming to the skin, gloves/socks), then add analgesia and sedation (propofol, dexmedetomidine, opioids such as fentanyl/remifentanil), with magnesium, buspirone, and paracetamol as adjuncts. Prefer short-acting agents so neuroprognostication is not delayed. Neuromuscular blockade is a last resort (it masks seizures — pair with EEG).
Evidence
—
BSAS & the anti-shivering ladder. Validated bedside scale (0 = none to 3 = severe) plus a stepwise pharmacologic protocol developed in neurocritical care; counter-warming raises the shivering threshold and reduces sedative requirement. Evidence base is largely physiologic and observational rather than outcome RCTs.

Why it matters. Uncontrolled shivering raises core temperature and oxygen consumption and can make a target unattainable; counter-warming first spares sedation and shortens the time to neurological assessment.

In practice

Score shivering with BSAS, apply surface counter-warming early, then escalate sedation/analgesia using short-acting agents; reserve paralysis for refractory shivering and run EEG when paralyzing, since it hides seizures.

Sources (1)
  • Badjatia N, et al. Metabolic impact of shivering during therapeutic temperature modulation: the Bedside Shivering Assessment Scale. Stroke. 2008;39(12):3242–3247. DOI 10.1161/STROKEAHA.108.523654. PMID 18927450.

10Neuroprognostication

Current approach (2026)
Guideline: multimodal, delayed (ERC–ESICM)
Delay neuroprognostication until at least 72 hours after return to normothermia and off sedation, and never rely on a single finding. Use a multimodal approach: clinical examination (pupillary/corneal reflexes, motor response, myoclonus), EEG, somatosensory evoked potentials (SSEP, N20), biomarkers (neuron-specific enolase, NSE), and neuroimaging (CT / MRI). Account for residual sedation and the confounding effect of temperature control on the exam.
Evidence — old → new
2025
ERC–ESICM prognostication algorithm. Recommends starting formal prognostication ≥72 h after ROSC in a comatose patient off confounders, using ≥2 concordant predictors (e.g., absent pupillary + corneal reflexes, bilaterally absent N20 SSEP, highly malignant EEG, markedly elevated NSE, diffuse anoxic injury on imaging) before predicting poor outcome — explicitly to avoid self-fulfilling prophecy and premature withdrawal.

What changed. TTM lengthened the window in which sedation and hypothermia cloud the neurological exam, pushing prognostication later and firmly toward multimodal, multi-predictor criteria.

Significance. Early single-test prognostication risks a self-fulfilling prophecy; the standard is to wait, remove confounders, and require concordant signals.

In practice

Resist early prognostic calls — wait ≥72 h after normothermia and off sedation, then combine exam, EEG, SSEP, NSE, and imaging, requiring at least two concordant adverse predictors before discussing withdrawal.

Sources (1)
  • Nolan JP, Sandroni C, et al. European Resuscitation Council and ESICM Guidelines 2025: Post-resuscitation care. Intensive Care Med. 2025. DOI 10.1007/s00134-025-08117-3. PMID 41123621.

11Where it’s heading (2026)

Optimal duration. ICECAP / P-ICECAP use adaptive randomization across a range of durations to map the dose–response of temperature control — the central open question after the depth question was settled.

Who (if anyone) benefits from hypothermia. No subgroup has yet been shown to gain from 33°C over normothermia (outside the fragile non-shockable signal); biomarker- and injury-severity–guided selection is the frontier.

Fever prevention vs true control. A trial of active fever prevention against no temperature control would test the one comparison the modern paradigm rests on but has never made directly.

12Bottom line — the current TTM bundle

  1. Treat every comatose post-ROSC patient with active temperature control — any rhythm, IHCA or OHCA.
  2. Target an individualized 32–37.5°C (COR 1); 37.5°C or 36°C is reasonable — 33°C is no longer mandatory.
  3. Prevent fever (≤37.5°C) as the non-negotiable core; maintain ≥72 h.
  4. Hold the target ≥36 h (COR 2a); optimal duration awaits ICECAP.
  5. Non-shockable rhythm: 33°C is a reasonable option (HYPERION).
  6. Avoid pre-hospital cold-fluid induction; cool in hospital with a feedback device and core probe.
  7. Rewarm slowly (~0.25–0.5°C/h); avoid rebound fever; watch potassium and BP.
  8. Control shivering with BSAS-guided counter-warming first, then short-acting sedation/analgesia.
  9. Delay neuroprognostication ≥72 h off sedation; use multimodal, concordant predictors.

13FAQ

Is 33°C still the target temperature after cardiac arrest?
No — 33°C is no longer mandatory. Current guidance (AHA 2025 Part 11) is to choose an individualized constant target anywhere from 32 to 37.5°C and prevent fever. TTM1, CAPITAL CHILL, and TTM2 found no benefit from deeper cooling, and TTM2 showed more arrhythmia at 33°C. A target of 37.5°C or 36°C is reasonable for most patients.
Who should receive targeted temperature management?
Any comatose / unresponsive adult who does not follow commands after return of spontaneous circulation (ROSC) — regardless of initial rhythm (shockable or non-shockable) and whether the arrest was out-of-hospital or in-hospital.
How long should temperature be controlled?
At least 36 hours of active control (AHA 2025, COR 2a), followed by active fever prevention out to about 72 hours. TTH48 found no significant difference between 48 and 24 hours; the optimal duration is being tested in ICECAP / P-ICECAP.
Does temperature management help after a non-shockable rhythm?
Yes — in HYPERION, 33°C improved favorable 90-day neurological outcome versus normothermia in comatose survivors of non-shockable arrest (10.2% vs 5.7%). The effect is small and fragile, but 33°C is a reasonable option in this group.
Should hypothermia be induced with cold IV fluids before hospital?
No. Pre-hospital cold-saline boluses (Kim 2014) and intra-arrest cold saline (RINSE) cooled faster but did not improve outcomes and caused more re-arrest and pulmonary edema. Cool in hospital with a feedback-controlled device instead.
How should the patient be rewarmed?
Slowly and under device control, about 0.25–0.5°C per hour, then continue fever prevention. Watch for rebound hyperthermia, hyperkalemia, and vasodilatory hypotension, and keep sedation running until normothermia is re-established.
How is shivering managed during TTM?
Score it with the Bedside Shivering Assessment Scale and treat stepwise: surface counter-warming first, then analgesia/sedation (propofol, dexmedetomidine, opioids), with magnesium, buspirone, and paracetamol as adjuncts. Prefer short-acting agents; reserve neuromuscular blockade (with EEG) for refractory cases.
When can neuroprognostication be performed after cardiac arrest?
Not before 72 hours after return to normothermia and off sedation, and never on a single test. Use a multimodal approach — clinical exam, EEG, SSEP (N20), NSE, and imaging — requiring concordant adverse predictors to avoid a self-fulfilling prophecy.

15Guidelines & evidence basis

Badges summarize each recommendation’s basis: Guideline: strong Guideline: conditional RCT benefit RCT neutral RCT harm. Guideline strengths use the GRADE / ACC-AHA classes of recommendation and are quoted from the documents below.

Guidelines referenced (3)
  • Hirsch KG, et al (American Heart Association). Part 11: Post–Cardiac Arrest Care: 2025 AHA Guidelines for CPR and Emergency Cardiovascular Care. Circulation. 2025. DOI 10.1161/CIR.0000000000001375. PMID 41122894. — target temperature 32–37.5°C (COR 1) in comatose patients; ≥36 h of active control (COR 2a); induced hypothermia no longer a default; hypothermia or normothermia both reasonable (COR 2b) in presumed severe brain injury.
  • Sandroni C, Nolan JP, Cariou A, et al. ERC–ESICM guidelines on temperature control after cardiac arrest in adults. Intensive Care Med. 2022;48(3):261–269. DOI 10.1007/s00134-022-06620-5. PMID 35089409. — actively prevent fever (≤37.5°C) for at least 72 h; no recommendation for routine therapeutic hypothermia; basis for the 2025 ESICM position.
  • Nolan JP, Sandroni C, et al. European Resuscitation Council and ESICM Guidelines 2025: Post-resuscitation care. Intensive Care Med. 2025. DOI 10.1007/s00134-025-08117-3. PMID 41123621. — comprehensive post-ROSC bundle including temperature control, core-temperature monitoring, and the delayed multimodal neuroprognostication algorithm; ILCOR-aligned active fever prevention.

Disclaimer. This page is an educational summary of published evidence for clinicians and is not a substitute for individual clinical judgment or institutional protocols. Targets and thresholds are taken from the cited trials; verify against current labeling, local guidelines, and patient-specific factors before applying. “In practice” notes are general practical guidance. Recommendation strengths are quoted from the cited guidelines (GRADE / ACC-AHA); reviewed by the DosePilot Medical Team (Jun 2026). All citations verified via PubMed/Europe PMC on 2026-06-22.