Keywan Bayegan

Emergency preservation and resuscitation improve survival after 15 minutes of normovolemic cardiac arrest in pigs

Objective: Outcome after prolonged normovolemic cardiac arrest is poor, and new resuscitation strategies have to be found. We hypothesized that the induction of deep hypothermia for emergency preservation and resuscitation (EPR) during prolonged cardiac arrest, before the start of reperfusion, will mitigate the deleterious cascades leading to neuronal death and will thus improve outcome. Design: Prospective experimental study. Setting: University research laboratory. Subjects: Thirteen pigs, Large White breed (27–37 kg). Interventions: After 15 mins of ventricular fibrillation, pigs were subjected to 1) EPR (n = 6), 20 mins of hypothermic stasis induced with a cold saline aortic flush; or 2) 20 mins of conventional resuscitation (n = 7). Then cardiopulmonary bypass was initiated in both groups, followed by defibrillation. Controlled ventilation and mild hypothermia were continued for 20 hrs; survival was for 9 days. For neurologic evaluation, neurologic deficit score (100% = brain dead, 0–10% = normal), overall performance category (1 = normal, 5 = dead or brain dead), and brain histologic damage score were used. Measurements and Main Results: In the EPR group, brain temperature decreased from 38.5°C ± 0.2°C to 16.7°C ± 2.5°C within 235 ± 27 secs. Five animals achieved restoration of spontaneous circulation and survived to 9 days: two pigs with overall performance category 2 and three pigs with overall performance category 3. Their neurologic deficit score was 45% (interquartile range 35, 50) and histologic damage score was 142 (interquartile range 109, 159). In the control group, four pigs achieved restoration of spontaneous circulation: one survived to 9 days with overall performance category 3, neurologic deficit score 45%, and histologic damage score 226 (restoration of spontaneous circulation, p = .6; survival, p = .03; overall performance category, p = .02). Conclusions: EPR is feasible in an experimental pig model and improves survival after prolonged cardiac arrest in pigs. Further experimental studies are needed before this concept can be brought into clinical practice.

Cold aortic flush and chest compressions enable good neurologic outcome after 15 mins of ventricular fibrillation in cardiac arrest in pigs.

Objective:The induction of deep cerebral hypothermia via ice-cold saline aortic flush during prolonged ventricular fibrillation cardiac arrest, followed by hypothermic stasis and delayed resuscitation (emergency preservation and resuscitation), improved neurologic outcome after cardiac arrest in pigs, as compared to conventional resuscitation. We hypothesized that emergency preservation and resuscitation with chest compressions would further improve outcome in the same model. Design:Prospective experimental study. Setting:University research laboratory. Subjects:Twenty-four female, large, white breed pigs (27–37 kg). Interventions:Fifteen minutes of ventricular fibrillation cardiac arrest were followed by 20 mins of resuscitation with chest compressions (control, n = 8), deep cerebral hypothermia via 200 mL/kg 4°C saline aortic flush and hypothermic stasis (emergency preservation and resuscitation, n = 8), and emergency preservation and resuscitation combined with chest compressions (emergency preservation and resuscitation plus chest compressions, n = 8). At 35 mins after cardiac arrest, cardiopulmonary bypass was initiated, followed by defibrillation. Mild hypothermia was continued for 20 hrs. Pigs were evaluated after 9 days using a neurologic deficit (neurologic deficit score: 100% = brain dead; 0%–10% = normal) and an overall performance category score (overall performance category score: 1 = normal; 2 = slightly handicapped; 3 = severely handicapped; 4 = comatose; 5 = dead/brain dead). Measurements and Main Results:Brain temperature decreased from 38.5°C to 15.3°C ± 3.3°C in the emergency preservation and resuscitation group, and to 11.3°C ± 1.2°C in the emergency preservation and resuscitation plus chest compressions group. In the control group, restoration of spontaneous circulation was achieved in four out of eight pigs, and one survived to 9 days. In the emergency preservation and resuscitation group, restoration of spontaneous circulation was achieved in seven out of eight pigs and five survived; in the emergency preservation and resuscitation plus chest compressions group, all had restoration of spontaneous circulation and seven survived (restoration of spontaneous circulation, p = .08). Neurologic outcome for (median and interquartile range) the control group included overall performance category score of 3, neurologic deficit score of 45%; for the emergency preservation and resuscitation group, overall performance category score was 3 (2–5) and neurologic deficit score was 45% (36; 50) and in the emergency preservation and resuscitation plus chest compressions group, overall performance category score was 2 (1–3) and neurologic deficit score was 13% (5; 21) (overall performance category score, p = .04; neurologic deficit score emergency preservation and resuscitation vs. emergency preservation and resuscitation plus chest compressions, p = .003). Conclusions:Emergency preservation and resuscitation by deep cerebral hypothermia combined with chest compressions during prolonged cardiac arrest in pigs are feasible and improve neurologic outcome.

Rapid induction of cerebral hypothermia by aortic flush during normovolemic cardiac arrest in pigs

Objective:Induction of deep cerebral hypothermia before reperfusion might improve neurologic outcome after cardiac arrest. We hypothesized that an aortic flush with cold saline during cardiac arrest is able to induce deep cerebral hypothermia and that the cooling efficiency can be enhanced by a) increasing the arteriovenous pressure gradient during the flush with vasopressin; b) improving the cerebral microcirculation during the flush with the thrombolytic agent alteplase; and c) increasing the arteriovenous pressure gradient further with venting the right heart by draining blood during the flush. Design:Prospective randomized experimental study. Setting:University research laboratory. Subjects:Twenty-four pigs Large White breed (31–42 kg). Interventions:After 10 mins of ventricular fibrillation, pigs received an aortic flush (100 mL/kg, 4°C, flow rate 35 mL/kg/min) into the descending aorta via a balloon catheter. The animals were subjected randomly to either an aortic flush with saline, saline plus vasopressin 1.2 IU/kg, saline plus alteplase 1 mg/kg, saline plus a combination of vasopressin 1.2 IU/kg and alteplase 1 mg/kg, or saline plus vasopressin 1.2 IU/kg and venting the right heart. Arterial and venous pressures and brain temperatures were recorded for an observation time of 10 mins after flush. Measurements and Main Results:A sufficient arteriovenous pressure gradient and deep cerebral hypothermia were only achieved with a flush containing vasopressin (brain temperature 16.1 ± 1.3°C in the vasopressin group vs. 35.4 ± 1.5°C in the saline group, p < .001); combining vasopressin with alteplase, or venting the right heart, did not further enhance the cooling effi-ciency of the flush. Conclusions:A cold saline aortic flush with vasopressin rapidly decreases brain temperature during prolonged normovolemic cardiac arrest in pigs. Whether deep cerebral hypothermia induced before reperfusion can improve neurologic outcome after cardiac arrest needs further investigation in large animal outcome studies.

Intra-aortic balloon counterpulsation in the emergency department: a 7-year review and analysis of predictors of survival

BACKGROUND Intra-aortic balloon pump (IABP) counterpulsation in cardiogenic shock (CS) is suggested as bridging therapy to definite emergency revascularization, heart transplantation and acute valvular repair. Data concerning the use of IABP counterpulsation in an emergency department (ED) are rare. PATIENTS AND METHODS We reviewed retrospectively the charts of patients who had been treated by IABP counterpulsation in the ED of a tertiary care university hospital during a 7-year period. We analyzed indications for IABP treatment, complications of IABP use and studied various predictors for 30-day survival. RESULTS Overall 88 (68 male) patients, median age 60 years (IQR 53-69 years) were treated with IABP counterpulsation. CS was caused by acute coronary syndrome (ACS), acute cardiomyopathy decompensation of (CMP) and aortic stenosis (AS) in 77 (87%), ten (12%) and one (1%) patients, respectively. Complications attributed to the insertion or maintenance of IABP were observed in nine (10%) patients. Thirty four patients (38%; 24 male) survived. Compared to non-survivors, these patients were younger (56 vs. 63 years; P<0.023) and had significant lower serum lactate levels before IABP insertion (3 vs. 5.5 mmol/l; P<0.002). Logistic regression analysis identified age (P<0.04) and serum lactate serum level before IABP (P<0.01) as independent predictors for survival. In the 77 patients with ACS PTCA tended to be associated with a higher rate of survival (P<0.09). CONCLUSION Initiation of IABP counterpulsation in patients with CS in an ED appears safe. Low levels of serum lactate and younger age were independent predictors of survival. In patients with ACS PTCA may contribute to improved outcome.