TTM: where are we now?
Presentation by Lars W. Andersen
- 26 RCTs from 2002 to 2019 + TTM2 ongoing and HYPERION trial to be released soon
- Following 2 RCTs in 2002 (Bernard et al + HACA) the use of TTM T32-34C became widespread
- Improves neurologically intact survival but the mechanism is uncertain
- T36C became widely used after TTM trial (Nielsen et al, 2013) found no difference T33C vs. T36C
- Controversies/uncertainties regarding patient selection, target temperature, timing of initiation, duration, and method
Coronary angiography: to whom and when?
Presentation by Kjetil Sunde
- Ischemic heart disease is the most common cause of OHCA
- STEMI: immediate coronary angiography
- Without STEMI: ER “pit-stop” for a fast diagnostic workup (history, TTE/TEE, CT scan, lab tests)
- PRO: diagnosis, early PCI reduces infarct size, heamodynamic stabilization, improves LVEF, TTM during PCI
- CON: overlook other causes, heparin, delayed TTM, lot of multidisciplinary resources, infrastructure, logistics needed
Presentation by Markus Skrifvars
- Anoxic brain injury impairs brain perfusion autoregulation
- Targeting MAP > 70 mmHg
- Lower HR = better neuro outcomes
- Focus on CO and lactate
- “Physiologic”: MAP>70mmHg, bradycardic, moderate vasopressors, urinary output >0.5 ml/kg, lactate < 2 mmol/l after 12h, low/normal CI, normal SvO2, complete/adequate reperfusion
- “Phatologic”: MAP<60mmHg, high vasopressors, urinary output <0.5 ml/kg, lactate>3-4mmol/l after 12h, recurrent CA, tachycardia/rapid AF, low CI/SvO2, consider IABP/ECMO.
We need to monitor what and how?
Presentation by Claudio Sandroni
- rapidly detect ABCD abnormalities and trigger adequate responses
- A+B: mantain normoxia/normocarbia
- C: be aware of post-resuscitation myocardial dysfunction and sepsis-like syndrome,
- monitor: ECG, arterial line, lactate using ABG, CO, fluid responsiveness
- D: EEG for prognostication/seizure detection, benefit of aggressive antiepilectic treatment??
- monitor: body T, motor response, brainstem reflexes, pupillometry, seizures, rSO2??
Patient outcome related to multi-organ failure
Presentation by Sharon Einav
- Organ dysfunction is common after cardiac arrest and associated with worse outcome
- Full spectrum of multiple organ failure (heart, kidney, liver, brain) must be considered to reduce morbidity, increase survival and optimize the use of healthcare resources
- End-of-life care must be considered: withholding/withdrawing all invasive and supportive care as a collegial process between team and family
Is there a place for Vitamin C?
Presentation by Angelique Spoelstra-de Man
- Vitamin C is the primary antioxidant
- Ischemia and reperfusion injury causes damage to the hearth and brain increasing mortality
- After CA plasma levels of Vitamin C are low reducing protection against oxidative stress (massive consumption?)
- In preclinical studies vitamin C decreased myocardial damage, improved survival/neuro outcome
- Vitamin C in Post-cardiac Arrest (VITaCCA) RCT will determine if early high doses of vitamin C improve organ function after cardiac arrest. ClinicalTrials.gov Identifier: NCT03509662
Infographic on the topic by Tommaso Scquizzato @tscquizzato