This work investigates the potential of photoplethysmography (PPG) to detect a spontaneous pulse from the finger, nose or ear in order to support pulse checks during cardiopulmonary resuscitation (CPR). In a prospective single-center cross-sectional study, PPG signals were acquired from cardiac arrest victims who underwent CPR. The PPG signals were analyzed and compared to arterial blood pressure (ABP) signals as a reference during three distinct phases of CPR: compression pauses, on-going compressions and at very low arterial blood pressure. Data analysis was based on a qualitative subjective visual description of similarities of the frequency content of PPG and ABP waveform. In 9 patients PPG waveforms corresponded to ABP waveforms during normal blood pressures. During ABP in the clinically challenging range of 60 to 90 mmHg and during chest compressions and pauses, PPG continued to resemble ABP, as both signals showed similar frequency components as a result of chest compressions as well as cardiac activity. Altogether 1199 s of PPG data in compression pauses were expected to show a spontaneous pulse, of which 732 s (61%) of data were artifact-free and showed the spontaneous pulse as visible in the ABP. PPG signals at all investigated sites can indicate pulse presence at the moment the heart resumes beating as verified via the ABP signal. Therefore, PPG may provide decision support during CPR, especially related to preventing and shortening interruptions for unnecessary pulse checks. This could have impact on CPR outcome and should further be investigated.

Zusammenfassung: Für ausgewählte Patienten, in denen die konventionelle kardiopulmonale Reanimation (cCPR) erfolglos bleibt, sprechen die europäischen Leitlinien zur Reanimation 2021 erstmals eine Empfehlung zur extrakorporalen Reanimation (eCPR) als mögliche Rettungstherapie aus. Die eCPR wird im therapierefraktären Kreislaufstillstand etabliert, um Diagnostik und Therapie reversibler Ursachen, wie Herzinfarkt, Lungenembolie, akzidentielle Hypothermie, Intoxikationen mit herzwirksamen Substanzen und akute Hypoxie, zu ermöglichen. Selektionskriterien für eCPR umfassen prognostische Reanimationsfaktoren, wie beobachteter Kreislaufstillstand, Start von Reanimationsmaßnahmen in < 5 min, schockbarer Erstrhythmus, Zeichen effektiver cCPR wie Lebenszeichen während der Reanimation, anhaltendes Kammerflimmern, intermittierende Phasen von Spontankreislauf oder anhaltendes endtidales CO₂ > 10 mm Hg, Patientenalter und Gesundheitszustand. Die Zeitspanne vom Kreislaufstillstand bis zur eCPR ist eine der wichtigsten Determinanten für neurologisch gutes Überleben und sollte < 60 min liegen. Für die Einhaltung dieser Zielvorgabe muss eine entschlossene „Load-and-Go“-Strategie mit frühzeitiger Patientenselektion und raschem Transport unter mechanischer cCPR in ein eCPR-Zentrum verfolgt werden, oder es wird versucht, die eCPR präklinisch zum Einsatz zu bringen. Zwei randomisierte kontrollierte eCPR-Studien demonstrierten Überlebensraten von 43 % bzw. 31,5 % bei Patienten mit anhaltendem Kammerflimmern bzw. kardialem Kreislaufstillstand. Ob diese Ergebnisse außerhalb einzelner hochspezialisierter Zentren anwendbar sind, ist wie die Frage nach der besten präklinischen und innerklinischen Strategie Gegenstand zukünftiger Studien.

Evaluating beneficial effects of potential protective therapies following cardiac arrest in rodent models could be enhanced by exploring behavior and cognitive functions. The Morris Water Maze is a well-known cognitive paradigm to test spatial learning and memory. Behavioral testing with the Morris Water Maze in Sprague–Dawley rats (300 ± 25 g) resuscitated after 8 min of ventricular fibrillation cardiac arrest was carried out 5 and 12 weeks after cardiac arrest (CA) and compared to results of naïve rats (Control). At 5 weeks, within each group latency time to reach the hidden platform (reflecting spatial learning) decreased equally from day 1 to 4 (CA: 105.6 ± 8.2 vs. 8.9 ± 1.2 s, p < 0.001; Control: 75.5 ± 13.2 vs. 17.1 ± 4.5, p < 0.001) with no differences between groups (p = 0.138). In the probe trial 24 h after the last trial, time spent in the target sector (reflecting memory recall) within each group was significantly longer (CA: 25 ± 1.3; Control: 24.7 ± 2.5 s) than in each of the three other sectors (CA: 7.7 ± 0.7, 14.3 ± 2.5, 8.4 ± 0.8 and Control: 7.8 ± 1.2, 11.7 ± 1.5, 10.3 ± 1.6 s) but with no significantly differences between groups. Seven days later (reflecting memory retention), control group animals remained significantly longer in the target sector compared to every other sector, whereas the cardiac arrest group animals did not. Even 12 weeks after cardiac arrest, the single p values showed that the control animals displayed a trend to perform better than the resuscitated animals. Memory recall was impaired early after 8 min of ventricular fibrillation cardiac arrest and might be a more valuable tool for cognitive testing than learning recall after global ischemia due to cardiac arrest.

Cardiac arrest (CA) survivors often develop long-term neurological deficits, but its long-term impact on vulnerable brain regions and neurological outcomes remains unclear. In a previous CA model with conventional cardiopulmonary resuscitation, we found reduced heme oxygenase (HO) activity in the hippocampus and cortex 14 days post-CA, suggesting its potential as a functional outcome marker. Here, we used a rat model with 6 or 8 min of CA followed by extracorporeal cardiopulmonary resuscitation. While in the 6 min-CA group, 67% survived to day 14, increased mortality within 4 days resulted in only 33% survival in the 8 min group post-ROSC. All animals displayed neurological impairment assessed by daily neurologic deficit scoring (NDS). While deficits declined within the first 3–4 days in the 6 min-CA animals, the 8 min-CA group showed significantly worse neurological outcomes until day 14. Two weeks post-CA, neuroinflammatory and neurodegenerative markers (HO-1, TNF-R1, Iba1, and GFAP) were elevated in the hippocampus, while HO and 2-oxoglutarate dehydrogenase complex activities were reduced in all rats, indicating a decrease in anti-oxidative capacity and mitochondrial capacity for metabolizing glutamate. NDS at day 4–5 strongly correlated with the delayed CA-mediated enzymatic dysfunction determined in the hippocampus. This finding highlights this time point for identifying at-risk individuals and suggests a prolonged therapeutic intervention lasting at least until 4 days post-CA.