Longer Arrest Times Research Articles

Moderate hypothermia circulatory arrest as a brain-protective strategy for type A aortic dissection.

Brain-protective strategies for acute type A aortic dissection (TAAD) remain controversial. Moderate hypothermia circulatory arrest (MHCA) without cerebral perfusion is not commonly used. However, we aimed to assess its safety and efficacy in 358 patients who underwent hemiarch replacement with MHCA for acute type A aortic dissection at our institution from August 2012 to August 2022. Clinical outcomes were compared according to circulatory arrest time [≤15 min (S group, n = 52) vs ≥16 min (L group, n = 306)]. The primary outcome was postoperative stroke. The S group had more older patients (72.5 vs 68.8 years; P = 0.04), a greater incidence of carotid artery malperfusion (21% vs 11%; P = 0.043) and a lower body mass index (21.7 vs 23.6 kg/m2; P < 0.01) and hemodynamic instability (3.8% vs 16%; P = 0.02) than the L group. The incidence of postoperative stroke (7.7% vs 12%; P = 0.33) and the rate of 30-day mortality (5.8% vs 6.5%; P = 0.83) did not significantly differ between groups. After adjusting for all potential confounding factors pre- and intraoperatively, there was no significant difference in postoperative outcomes between groups. MHCA alone for TAAD had comparable postoperative outcomes with circulatory arrest times under and over 15 min. However, longer arrest times were associated with a higher risk of stroke.

Early Thalamic Injury After Resuscitation From Severe Asphyxial Cardiac Arrest in Developing Rats.

Children who survive cardiac arrest often develop debilitating sensorimotor and cognitive deficits. In animal models of cardiac arrest, delayed neuronal death in the hippocampal CA1 region has served as a fruitful paradigm for investigating mechanisms of injury and neuroprotection. Cardiac arrest in humans, however, is more prolonged than in most experimental models. Consequently, neurologic deficits in cardiac arrest survivors arise from injury not solely to CA1 but to multiple vulnerable brain structures. Here, we develop a rat model of prolonged pediatric asphyxial cardiac arrest and resuscitation, which better approximates arrest characteristics and injury severity in children. Using this model, we characterize features of microglial activation and neuronal degeneration in the thalamus 24 h after resuscitation from 11 and 12 min long cardiac arrest. In addition, we test the effect of mild hypothermia to 34°C for 8 h after 12.5 min of arrest. Microglial activation and neuronal degeneration are most prominent in the thalamic Reticular Nucleus (nRT). The severity of injury increases with increasing arrest duration, leading to frank loss of nRT neurons at longer arrest times. Hypothermia does not prevent nRT injury. Interestingly, injury occurs selectively in intermediate and posterior nRT segments while sparing the anterior segment. Since all nRT segments consist exclusively of GABA-ergic neurons, we asked if GABA-ergic neurons in general are more susceptible to hypoxic-ischemic injury. Surprisingly, cortical GABA-ergic neurons, like their counterparts in the anterior nRT segment, do not degenerate in this model. Hence, we propose that GABA-ergic identity alone is not sufficient to explain selective vulnerability of intermediate and posterior nRT neurons to hypoxic-ischemic injury after cardiac arrest and resuscitation. Our current findings align the animal model of pediatric cardiac arrest with human data and suggest novel mechanisms of selective vulnerability to hypoxic-ischemic injury among thalamic GABA-ergic neurons.

P5608Acute respiratory failure after type A aortic dissection repair: data from the International Registry of Aortic Dissection (IRAD)

Abstract Background Acute Respiratory Failure (ARF) has been noted in up to 20% of patients undergoing cardiac surgery and is associated with increased mortality. Cardiopulmonary bypass (CPB) is often followed by pulmonary dysfunction, although literature on the subject in the setting of Type A acute aortic dissection (TAAAD) is limited. Methods This study identified the incidence of ARF after TAAAD, associated risk factors, and the impact of ARF on early and late outcomes. All data have been derived from the International Registry of Acute Aortic Dissection (IRAD). Results Postoperative ARF (defined as ventilator support for ≥3 days, tracheostomy, and/or pneumonia) occurred in 434 (24.6%) of 1764 surgically managed TAAAD patients (mean age 60.1±14.2 years) from November 2001 until November 2017. Peripheral vessel procedures (6.4% v 2.8%, p=0.002), cerebral perfusion (89.2% v 82.3%, p&lt;0.001), use of hypothermic circulatory arrest (93% v 87.7%), longer arrest time (median 39 (Q1-Q3 27–128 minutes) v 31 (Q1-Q3 22.0–52.9 minutes)), and lower extremity ischemia (18.8% v 6.7%, p&lt;0.001) were more common in ARF patients. On multivariable logistic regression analysis, age ≥70 years (OR 1.019, 95% CI 1.005–1.034, p=0.008), current smoking (OR 1.744, 95% CI 1.184–2.570, p=0.005), peripheral vessel procedures (OR 2.457, 95% CI 1.132–5.334, p=0.023), presenting hypotension/shock (OR 2.036, 95% CI 1.336–3.102, p=0.001), lower extremity ischemia at surgery (OR 2.77, 95% CI 1.574–4.875, p&lt;0.001), concomitant coronary artery bypass graft (CABG) (OR 2.982, 95% CI 1.597–5.568, p=0.001), pre-operative acute renal failure (OR 2.532, 95% CI 1.350–4.749, p=0.004), and prolonged circulatory arrest time in minutes (OR 1.005, 95% CI 1.003–1.007, p&lt;0.001) were independently associated with ARF development. Patients with aortic valve replacement (AVR) were less likely to develop ARF (OR 0.497, 95% CI 0.308–0.802, p=0.004). Post-operative complications were more common in ARF patients. In-hospital mortality was higher in the ARF cohort (16.4% v 4.7%, p&lt;0.001). Multivariable logistic regression identified ARF (OR 2.686, 95% CI 1.647–4.381, p&lt;0.001) as well as pre-operative hypotension (OR 1.89, 95% CI 1.130–3.159, p=0.015), lower extremity ischemia (OR 2.77, 95% CI 1.545–4.998, p=0.001), pre-operative myocardial infarction (OR 3.141, 95% CI 1.058–9.33, p=0.039), and CABG (OR 1.988, 95% CI 1.011–3.909, p-value 0.047) as independent predictors of death. Conclusions Post-operative ARF is common after TAAAD repair; in-hospital complications and death are higher in this cohort. Acknowledgement/Funding W.L. Gore &amp; Associates, Inc.; Medtronic; Varbedian Aortic Fund; Hewlett Foundation; Mardigian Foundation; UM Faculty Group Practice; Ann &amp; Bob Aikens

Toward a new cold and warm nondepolarizing, normokalemic arrest paradigm for orthotopic heart transplantation

Currently, the safe human heart preservation time is limited to around 4 to 5 hours of cold ischemic storage. Longer arrest times can lead to donor heart damage, early graft dysfunction, and chronic rejection. The aim of this study was to examine a new nondepolarizing, normokalemic preservation solution with adenosine and lidocaine for as long as 6 hours of arrest at cold and warmer storage temperatures. Isolated perfused rat hearts (n = 87) were switched from working to Langendorff (nonworking) mode and arrested at 37 degrees C with 200-micromol/L adenosine and 500-micromol/L lidocaine in Krebs-Henseleit buffer (10-mmol/L glucose, pH 7.7, 37 degrees C) or with Celsior (Sangstat Medical Corp, Fremont, CA). Hearts were removed and placed in static storage at 4 degrees C for 2 and 6 hours or remained on the apparatus and were intermittently flushed at 37 degrees C every 20 minutes for 2 minutes at 68 mm Hg (average arrest temperature 28 degrees -30 degrees C) for 2 and 6 hours. We further investigated the effect of the warmer adenosine-lidocaine solution supplemented with 1- or 5-mmol/L pyruvate. Adenosine-lidocaine solution arrested hearts in 16 +/- 2 seconds (n = 32), whereas Celsior did so in 39 +/- 4 seconds (n = 23). After 2 hours of cold static storage, there were no functional differences between the adenosine-lidocaine and Celsior groups, with approximately 70% return of cardiac output. In contrast, after 6 hours of 4 degrees C storage, adenosine-lidocaine hearts had significantly higher functional recoveries (68% +/- 5% cardiac output) than Celsior hearts (47% +/- 14% cardiac output) during 60 minutes of reperfusion. In addition, Celsior hearts took 5 minutes longer to reanimate and showed early reperfusion arrhythmias. At warmer temperatures after 2 hours of arrest, adenosine-lidocaine and Celsior hearts were not significantly different, despite a 43% higher cardiac output in adenosine-lidocaine hearts (80% +/- 3% vs 56% +/- 12%). After 6 hours, adenosine-lidocaine hearts had recovered 55% +/- 3% of prearrest cardiac output, which increased significantly to 75% +/- 4% with addition of 1-mmol/L pyruvate. Adenosine-lidocaine with 1-mmol/L pyruvate hearts spontaneously recovered 106% heart rate, 93% to 105% developed pressures, 70% aortic flow, and 81% coronary flow. Coronary vascular resistance increased 1.7- to 1.9-fold during the 6-hour arrest. In contrast, Celsior hearts did not have return of aortic or coronary flow after 6 hours in these warmer conditions. A new nondepolarizing, normokalemic adenosine-lidocaine arrest solution in Krebs-Henseleit buffer with 10-mmol/L glucose was versatile at both 4 degrees C and 28 degrees C to 30 degrees C relative to Celsior, and the addition of 1-mmol/L pyruvate significantly improved cardiac output at warmer arrest temperatures. This new arrest paradigm may be useful in the harvest, storage, and implantation of donor hearts.

Survival from prehospital cardiac arrest is critically dependent upon response time

This study correlated the delay in initiation of bystander cardiopulmonary resuscitation (ByCPR), basic (BLS) or advanced cardiac (ACLS) life support, and transport time (TT) to survival from prehospital cardiac arrest. This was a secondary endpoint in a study primarily evaluating the effect of bicarbonate on survival. Prospective multicenter trial. Patients treated by urban, suburban, and rural emergency medical services (EMS) services. Eight hundred and seventy-four prehospital cardiac arrest patients. This group underwent conventional ACLS intervention followed by empiric early administration of sodium bicarbonate noting resuscitation times. Survival was measured as the presence of vital signs on emergency department (ED) arrival. Data analysis utilized Student's t-test and logistic regression (p<0.05). Survival was improved with decreased time to BLS (5.52 min versus 6.81 min, p=0.047) and ACLS (7.29 min versus 9.49 min, p=0.002) intervention, as well as difference in time to return of spontaneous circulation (ROSC). The upper limit time interval after which no patient survived was 30 min for ACLS time, and 90 min for transport time. There was no overall difference in survival except at longer arrest times when considering the primary study intervention bicarbonate administration. Delay to the initiation of BLS and ACLS intervention influenced outcome from prehospital cardiac arrest negatively. There were no survivors after prolonged delay in initiation of ACLS of 30 min or greater or total resuscitation and transport time of 90 min. This result was not influenced by giving bicarbonate, the primary study intervention, except at longer arrest times.

Interaction of temperature with hematocrit level and pH determines safe duration of hypothermic circulatory arrest

Objective Previous studies have demonstrated that both hematocrit level and pH influence the protection afforded by deep hypothermic circulatory arrest. The current study examines how temperature modulates the effect of hematocrit level and pH in determining a safe duration of circulatory arrest. The study also builds on previous work investigating the utility of near-infrared spectroscopy as a real-time monitor of cerebral protection during circulatory arrest. Methods Seventy-six piglets (9.3 ± 1.2 kg) underwent circulatory arrest under varying conditions with continuous monitoring by means of near-infrared spectroscopy (hematocrit level of 20% or 30%; pH-stat or alpha-stat strategy; temperature of 15°C or 25°C; arrest time of 60, 80, or 100 minutes). Neurologic recovery was evaluated daily by a veterinarian, and the brain was fixed in situ on postoperative day 4 to be examined on the basis of histologic score in a blinded fashion. Results Multivariable analysis of total histologic score revealed that higher temperature, lower hematocrit level, more alkaline pH, and longer hypothermic circulatory arrest duration were predictive of more severe damage to the brain ( P < .01). Regression modeling revealed that higher temperature exacerbated the disadvantage of a lower hematocrit level and longer arrest times but not pH strategy. Normalized oxyhemoglobin nadir time, derived from near-infrared spectroscopy, was positively correlated with neurologic recovery on the fourth postoperative day and with total histologic injury score ( P < .0001). Conclusion Hematocrit level and pH, as well as temperature, determine the safe duration of hypothermic circulatory arrest. Near-infrared spectroscopy is a useful real-time monitor of safe duration of circulatory arrest.

Safety of prolonged ischemic arrest using hypothermic cardioplegia

An evaluation was carried out of 200 consecutive patients undergoing elective cardiac operations. Hypothermic potassium (25 mEq/L) crystalloid cardioplegia was used for myocardial preservation during ischemic arrest. The purpose of this study was to determine if the length of cardioplegic arrest correlated with any parameter of myocardial injury, operative morbidity, or mortality. There were 154 patients undergoing coronary revascularization (CBG) and 46 valve replacement of repair (VR/R). The duration of cardioplegic arrest varied from 17 to 187 minutes. Eighteen patients (12%) in the CBG group and 11 (24%) in the VR/R group had arrest times of greater than 2 hours. In the CBG group, serum enzyme measurements, the incidence of inotropic support, perioperative myocardial infarction, and operative mortality rate did not correlate with the duration of ischemic arrest. In the VR/R group, however, the CPK-MB level increased in proportion to the duration of ischemia; none of the other parameters changed significantly. Myocardial infarction was diagnosed in 3.7% of the coronary bypass (CBG) patients having cardioplegic arrest times of less than 120 minutes and in none of the 18 patients having longer arrest times. Three operative infarcts occurred in the VR/R group, two between 60 and 90 minutes of arrest and one between 120 and 150 minutes. The only clinical manifestation of prolonged cardioplegic arrest in the CBG patients was an increase in the incidence of postoperative arrhythmias. The results of this study support the safety of prolonged (3 hour) cardioplegic arrest under appropriate hypothermic conditions in the CBG group, but not necessarily in the VR/R group, where increased myocardial enzyme generation was noted. The proper reduction of myocardial temperature in the use of multidose cardioplegia is considered essential for optimal preservation.