Precision pathophysiology in high-performance CPR in out-of-hospital cardiac arrest

The temptation for nihilism around advanced interventions in out-of-hospital cardiac arrest (OOHCA) can be strong, given the large number of negative randomized control trials that frequent literature. While specific ‘enhanced interventions’ seem to have minimal impact, the attendance of prehospital critical care teams is associated with improved outcomes.1 These teams need to think beyond algorithms and evolve more precise models of care.

Essex & Herts Air Ambulance (EHAAT) operate a physician-paramedic team in the UK. In addition to trauma activations, EHAAT attend approximately 500 medical cardiac arrests annually. Beyond standard advanced life support (ALS), the team offer enhanced diagnostics with ultrasound, blood gas analysis, pupillometry, invasive lines, and additional drug therapies. Precision pathophysiology and delivery of high-performance cardiopulmonary resuscitation (HP-CPR) are core strategic priorities for the organization. To progress this physiologically guided approach, EHAAT are evaluating the role of the CorplusCPR and Chest Compression Synchronized Ventilation (CCSV) via the MEDUMAT Standard2 ventilator. CCSV is a specialized ventilatory mode for resuscitation where a short mechanical breath is applied in synchrony with each chest compression. A complex OOHCA is outlined to provide physiological insights into the potential impact of these devices.

Case description

In a recent case, a 54-year-old man suffered a witnessed OOHCA with immediate lay rescuer CPR. Asystole was initially observed by the ambulance service and standard ALS was initiated including ongoing CPR, iGEL insertion, and 3mg total of epinephrine. Return of spontaneous circulation (ROSC) was achieved after 28min of low-flow but transitioned back into pulseless electrical activity (PEA) quickly. EHAAT arrived and undertook an ultrasound-enhanced primary survey showing the area of maximal compression (AMC) to be over the left ventricular outflow tract, right heart dilatation, and an extreme low cardiac output state (ELCOS) PEA subphenotype.

Concurrent activity included intubation/ ventilation and CorpulsCPR placement with AMC adjustment, while the physician placed femoral central venous and arterial catheters. With a central infusion of epinephrine at 100µg/min, a gradual increase in the ‘diastolic’ or Tissue plasminogen activator and sodium bicarbonate were administered given the likelihood of pulmonary embolism and the later metabolic phase of cardiac arrest.

CCSV was initiated with opening tidal volumes below 100mL and attenuated inspiratory flows, chest compression depth was reduced to 4cm and volumes increased to 200mL. With this, the morphology of the intra-arrest waveform changed with a lower initial recoil pressure (rBP), increased ‘systolic’ compression pressure (cBP) and increase in ‘diastolic’/ DcBP (Fig 2). This could suggest improved recoil/venous entrainment and coronary perfusion pressure.

Intra-arrest blood gas showed pH 6.7, partial pressure of oxygen (PaO2 ) 24kPa, partial pressure of arterial carbon dioxide (PaCO2 ) 17kPa, base excess (BE) -18, and pupillometry showed diameters of 5.9/5.6mm and a neurological pupil index (NPi) of 0.5/0.6. After a total low-flow time of 70min, a stable ROSC was confirmed with invasive pressures and good common femoral artery velocity on a pulsed-wave Doppler (Fig 3). This was sustained into hospital with ongoing inopressors titration and appropriate neuroprotective measures.

Conclusion

This case hopefully offers interesting physiological insights into the real-time impact of HP-CPR incorporating CCSV in a super refractory OOHCA. Further research is needed to confirm these initial findings.

References

1. Boulton AJ, Edwards R, Gadie A, et al. Prehospital critical care beyond advanced life support for out-of-hospital cardiac arrest: A systematic review. Resusc Plus. 2024;21:100803.

Figure legend

• Fig 1. Pulsed-wave-Doppler of femoral artery after return of spontaneous circulation.