Core Hyperthermia Before Cardiac Surgery

Date
September 25, 2025
URL
https://x.com/WithAScalpel/status/1971184283655241816
Categories
Intensive CareCPB

Core Hyperthermia Before Cardiac Surgery

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“Core hyperthermia” before cardiopulmonary bypass (CPB) is not synonymous with infectious fever. In many congenital/paediatric cardiac patients, the primary driver is impaired heat dissipation or maldistributed perfusion rather than a hypothalamic set-point change. Heat production is ordinary, but cutaneous flow is restricted, so heat cannot be convectively and radiatively off-loaded; instead, it remains trapped in the heart–lung axis. The perioperative literature is rich on how to manage temperature around CPB (warming, monitoring, and rewarming rates) but provides limited mechanistic data specifically explaining pre-CPB hyperthermia from maldistribution alone [1–3].

Pathophysiologic buckets

1) Pulmonary over-circulation

Excess pulmonary blood flow warms intrathoracic blood and lung parenchyma while skin perfusion remains constrained, attenuating convective heat loss. Typical contexts include large left-to-right shunts (VSD/AVSD), prominent aortopulmonary collaterals, low PVR states (high FiO₂, low PaCO₂), and diastolic runoff lesions. Bedside, patients show a warm core–cool periphery pattern with a widened core–skin gradient.

2) Systemic–pulmonary collateral flow (SPCs)

SPCs deliver systemic arterial blood to the lungs outside the regulated RV-PA circuit, adding central heat without proportionate cutaneous perfusion. The mechanism and clinical signature mirror over-circulation—central heat retention with inefficient dissipation.

3) Heart failure with elevated SVR

Low forward flow with reflex vasoconstriction (↑SVR) preserves coronary/cerebral beds at the expense of the skin. Reduced skin blood flow sharply limits heat egress, so the measured core temperature rises despite normal or even reduced whole-body metabolic heat production. This physiology aligns with classic low-cardiac-output (LCO) states seen perioperatively; clinicians should expect cool, mottled extremities, narrow pulse pressure, and rising lactate, with the temperature pattern reflecting distribution more than pyrexia [6].

4) “True fever” and other mimics

Confirm measurement fidelity and keep hypermetabolic conditions in the differential. Probe artefact (malposition; esophageal probe influenced by ventilator gases; bladder probe above pooled urine; rectal probe abutting stool) can mislead. Less common—but critical—true hypermetabolic entities include malignant hyperthermia, sepsis, thyrotoxicosis, and transfusion reactions.

Why SVR matters

Across mechanisms 1–3, SVR is typically high. Cutaneous vasoconstriction diverts flow away from the skin, blocking heat egress; hence antipyretics underperform because the problem is distribution, not set-point. In LCO/LV failure phenotypes, this manifests as central warmth with peripheral coolness despite noninfectious aetiology [6].

Evidence landscape (what we know—and don’t)

  • Maintaining normothermia: Combined convective + conductive warming safely maintained normothermia before and after CPB in paediatric cohorts, underscoring the value of proactive thermal management rather than reactive treatment [1].
  • Rewarming strategy: Slower, controlled rewarming during CPB was associated with improved inotropy and less “afterdrop,” linking rewarming kinetics to haemodynamic stability [2].
  • Monitoring standards: Multi-society CPB temperature-management guidelines recommend specific monitoring sites and explicit limits to avoid hyperthermia during cooling/rewarming phases [3].
  • Limits of the gradient: Postoperative data show core–peripheral temperature gradient (CPTG) and skin temperature perform poorly as single predictors of major adverse events; older physiologic work likewise found CPTG does not reliably track cardiac output or SVR in children [4,5].

    • Collectively, the literature supports how to manage temperature but remains insufficient on the pre-CPB mechanistic link between maldistributed flow and measured hyperthermia—so clinicians must integrate perfusion distribution metrics, not temperature alone, when deciding how to initiate CPB [1–5].

Evaluation at the bedside

  • Confirm the number. Re-measure at a second core site (esophageal, bladder, PA catheter, or correctly sealed tympanic) to eliminate artefact.
  • Interrogate distribution. Track NIRS (cerebral vs somatic), venous oximetry, capillary refill, distal pulses, and lactate to infer whether heat is being centrally “trapped.” CPTG can be viewed, but it should not be used in isolation given limited predictive value [4,5].
  • Identify over-circulation drivers. Review ventilator settings (high FiO₂/low PaCO₂ → low PVR), anaemia, SPC burden, and diastolic runoff.
  • Screen for true fever. Culture selectively, review drugs/anaesthetics, and consider targeted tests (e.g., CK/CO₂ gap for malignant hyperthermia risk).

Implications for CPB initiation

  1. Titrate afterload down as you go on bypass.

    2. When SVR is high, “pushing” pump flow into a constricted vasculature risks malperfusion and persistent heat trapping. Use judicious afterload reduction (volatile anaesthetic, vasodilator) to open cutaneous/splanchnic beds, achieve temperature equilibration, and distribute flow more evenly. These principles align with guideline cautions to avoid hyperthermia and to control temperature gradients during cooling/rewarming [3].

  2. Monitor distribution—not just absolute flow.

    3. Follow regional oximetry (cerebral/somatic NIRS), mixed venous saturation, and lactate as CPB begins. If the core–skin gradient remains wide or NIRS suggests maldistribution, reassess SVR, ventilator-driven PVR, and collateral flow; adjust vasodilation, FiO₂/PaCO₂, and pump flow accordingly [3].

Practical management checklist (pre-CPB)

  • Verify temperature accurately (repeat with a second core method; correct probe issues).
  • Open the periphery (treat pain/shivering; begin gentle SVR reduction while maintaining MAP appropriate for coronary/cerebral beds).
  • Blunt over-circulation (normalize PaCO₂; avoid unnecessary high FiO₂ if safe; correct anaemia; consider systemic pressure targets to limit SPC flow).
  • Choose effective warming tools if hypothermia coexists or afterdrop is expected (forced-air/conductive warming are effective and guideline-concordant) [1,7].
  • Rule out hypermetabolic states early (e.g., dantrolene for malignant hyperthermia; source control/antibiotics for sepsis).
  • Align the team for CPB (explicit afterload targets, gradient-aware cooling/rewarming, and distribution-focused monitoring) [3].
  • Contextualize temperature strategy within broader practice: while some programs champion warm/normothermic perfusion, contemporary RCT data suggest normothermic CPB is as safe as hypothermic CPB in low-risk cohorts, with organ-protection nuances that do not obviate the need for distribution-aware management [8,9].

In pre-CPB cardiac patients, elevated core temperature often reflects where blood is going, not what the hypothalamus wants. Think distribution first—over-circulation, SPCs, and high-SVR heart failure—verify measurements, and enter bypass with afterload thoughtfully reduced and perfusion distribution actively surveilled [1–6].

References

[1] Eich C, Zink W, Schwarz SKW, Radke O, Bräuer A. A combination of convective and conductive warming ensures pre- and post-bypass normothermia in paediatric cardiac anaesthesia. Applied Cardiopulmonary Pathophysiology. 2009;13:3–10. ResearchGate

[2] Saleh M, Abdel Barr TMF. The Impact of Slow Rewarming on Inotropy, Tissue Metabolism, and “After Drop” of Body Temperature in Pediatric Patients. J Extra Corpor Technol. 2005;37(2):173–180. Ject+1

[3] Engelman R, Baker RA, Likosky DS, Grigore A, Dickinson TA, Shore-Lesserson L, Hammon JW; The Society of Thoracic Surgeons; The Society of Cardiovascular Anesthesiologists; The American Society of ExtraCorporeal Technology. Clinical Practice Guidelines for Cardiopulmonary Bypass—Temperature Management During Cardiopulmonary Bypass. Ann Thorac Surg. 2015;100(2):748–757. PubMed

[4] Kimura S, Butt W. Core-Peripheral Temperature Gradient and Skin Temperature as Predictors of Major Adverse Events Among Postoperative Pediatric Cardiac Patients. J Cardiothorac Vasc Anesth. 2022;36(3):690–698. PubMed

[5] Butt W, Shann F. Core-peripheral temperature gradient does not predict cardiac output or systemic vascular resistance in children. Anaesth Intensive Care. 1991;19(1):84–87. PubMed

[6] Shekerdemian L. Perioperative manipulation of the circulation in children with congenital heart disease. Heart. 2009;95(15):1286–1296. PubMed

[7] Guvakov DV, Cheung AT, Weiss SJ, et al. Effectiveness of forced-air warming after pediatric cardiac surgery employing hypothermic circulatory arrest without cardiopulmonary bypass. J Clin Anesth. 2000;12(7):519–524. PubMed

[8] Durandy Y. Warm pediatric cardiac surgery: European experience. Ann Thorac Surg. 2010;90(3):802–807. PubMed

[9] Caputo M, Rogers CA, Pagel C, et al. Normothermic versus hypothermic cardiopulmonary bypass in low-risk paediatric heart surgery: a randomised controlled trial. Heart. 2019;105(7):455–464. PubMed