Intraoperative myocardial protection by potassium arrest and local cardiac hypothermia

The combined modalities of potassium arrest and local cardiac hypothermia were used for myocardial protection in 82 patients. The cardioplegic solution used was Ringer's lactate to which potassium chloride and sodium bicarbonate were added so that the final solution had a pH of 7.5 and 30 meq/liter potassium. The myocardium was cooled externally by cold Ringer's lactate at 4 °C and through coronary circulation by cold cardioplegic solution at 8 °C. The myocardial temperature was continuously monitored and kept between 12 and 18 °C. Moderate systemic hypothermia was used (26 to 30 °C). Eighty-two patients have been operated upon using this technique. Eighteen patients had single or double valve replacements, 4 had valve replacements with coronary bypass, and 60 had coronary bypass procedures. The operating conditions have been excellent and the myocardial protection offered by this technique has been good. Perioperative myocardial infarctions, as diagnosed by ECG and CPK (MB isoenzymes) and myocardial scans, were seen in 6 patients. In conclusion the combined modalities of potassium arrest and local cardiac hypothermia give excellent myocardial protection during cardiac surgery.     

Out-of-hospital cardiac arrest in high-rise buildings: delays to patient care and effect on survival

Background:

The increasing number of people living in high-rise buildings presents unique challenges to care and may cause delays for 911-initiated first responders (including paramedics and fire department personnel) responding to calls for out-of-hospital cardiac arrest. We examined the relation between floor of patient contact and survival after cardiac arrest in residential buildings.

Methods:

We conducted a retrospective observational study using data from the Toronto Regional RescuNet Epistry database for the period January 2007 to December 2012. We included all adult patients (≥ 18 yr) with out-of-hospital cardiac arrest of no obvious cause who were treated in private residences. We excluded cardiac arrests witnessed by 911-initiated first responders and those with an obvious cause. We used multivariable logistic regression to determine the effect on survival of the floor of patient contact, with adjustment for standard Utstein variables.

Results:

During the study period, 7842 cases of out-of-hospital cardiac arrest met the inclusion criteria, of which 5998 (76.5%) occurred below the third floor and 1844 (23.5%) occurred on the third floor or higher. Survival was greater on the lower floors (4.2% v. 2.6%, p = 0.002). Lower adjusted survival to hospital discharge was independently associated with higher floor of patient contact, older age, male sex and longer 911 response time. In an analysis by floor, survival was 0.9% above floor 16 (i.e., below the 1% threshold for futility), and there were no survivors above the 25th floor.

Interpretation:

In high-rise buildings, the survival rate after out-of-hospital cardiac arrest was lower for patients residing on higher floors. Interventions aimed at shortening response times to treatment of cardiac arrest in high-rise buildings may increase survival.More than 400 000 out-of-hospital cardiac arrests occur annually in North America.^1,2 Despite considerable effort to improve resuscitation care, survival to hospital discharge in most communities remains below 10%.² Rapid defibrillation and high-quality cardiopulmonary resuscitation (CPR) are essential for survival, with an absolute decrease in survival of 7% to 10% for each 1-minute delay to defibrillation.^3–5Recently, there has been a dramatic increase in the number of people living in high-rise buildings (e.g., a 13% relative increase in Toronto from 2006 to 2011^6,7). As more high-rise buildings are constructed in urban centres across Canada, the number of 911 calls for emergency medical services in high-rise buildings will also continue to increase. Furthermore, over 40% of homeowners over the age of 65 years reside in high-rise buildings.⁸ These older residents have higher risks for a number of serious medical conditions, including cardiac arrest. Cardiac arrests that occur in high-rise buildings pose unique challenges for 911- initiated first responders. Building access issues, elevator delays and extended distance from the location of the responding vehicle on scene to the patient can all contribute to longer times to patient contact and, ultimately, longer times to initiation of resuscitation. Previous research has shown that longer 911 response times result in decreased patient survival after cardiac arrest,^9,10 but response times are traditionally measured from the time a call is received by the 911 dispatch centre to when the response vehicle arrives on scene. This measure fails to take into account the time required for 911-initiated first responders to make patient contact once they arrive on scene. This interval can contribute substantial delays to patient treatment, in some cases more than 4 minutes, and can account for up to 28% of the total time from the 911 call to arrival of the first responders at the patient’s side.^11–14There is a lack of literature describing the delay to patient contact during out-of-hospital cardiac arrests in high-rise buildings, where time-sensitive, life-saving interventions matter most. Furthermore, the effect on survival of vertical delay to patient contact is unknown. As the number of high-rise buildings continues to increase and as population density rises in major urban centres, is important to determine the effect of delays to patient care in high-rise buildings on survival after cardiac arrest and to examine potential barriers to patient care in this setting.The primary objective of this study was to compare the rate of survival to hospital discharge after out-of-hospital cardiac arrest at different vertical heights in residential buildings, specifically higher floors (≥ 3 floors) relative to lower floors (< 3 floors), with adjustment for standard Utstein variables.¹⁵The secondary objectives were to determine the delay to patient contact by 911-initiated first responders for cardiac arrests occurring on higher floors and to examine the use of automated external defibrillators by bystanders in private residences.     

Myocardial flow distribution. II : Empty beating heart, ventricular fibrillation and cardiac arrest

Myocardial oxygen consumption (MVO2) and coronary blood flow (CBF) distribution were studied in 21 isolated, metabolically supported dog hearts. Measurements of MVO2 and CBF distribution were carried out in three different experimental conditions : empty beating heart (EBH), ventricular fibrillation (VF) and high potassium-induced cardiac arrest (CA). MVO2 was approximately the same in EBH and VF (4.09 +/- 0.77 and 4.28 +/- 0.68 ml O2 min-1 100 g-1 respectively), and significantly lower in the group with CA (2.40 +/- 0.18 ml O2 min-1 100 g-1, P less than 0.05). Total CBF showed no significant differences among the three groups (84 +/- 7 ml/min in EBH; 78 +/- 7 ml/min in VF and 83 +/- 7 ml/min in CA). Subendocardial CBF per unit of tissue mass was significantly lower in hearts with VF (0.43 +/- 0.01 ml/min-1 g-1, P less than 0.05) when tested against the other two groups of experiments (0.69 +/- 0.03 ml min-1 g-1 in EBH and 0.65 +/- +/- 0.04 ml min-1 g-1 in CA). This was also reflected in the endo/epi ratio, that was significantly lower in VF (1.41 +/- 0.07, P less than 0.05) with respect to the other two groups (2 +/- 0.09 in EBH and 2.21 +/- 0.07 in CA). From data presented here we can conclude that cardioplegia, even in absence of hypothermia, is a method that will assure myocardial protection providing : (1) a lower subendocardial MVO2; (2) a higher subendocardial CBF, which helps for a prompt recovery during reperfusion.     

Inhibition of microglial activation contributes to propofol‐induced protection against post‐cardiac arrest brain injury in rats

It has been suggested that propofol can modulate microglial activity and hence may have potential roles against neuroinflammation following brain ischemic insult. However, whether and how propofol can inhibit post‐cardiac arrest brain injury via inhibition of microglia activation remains unclear. A rat model of asphyxia cardiac arrest (CA) was created followed by cardiopulmonary resuscitation. CA induced marked microglial activation in the hippocampal CA1 region, revealed by increased OX42 and P2 class of purinoceptor 7 (P2X7R) expression, as well as p38 MAPK phosphorylation. Morris water maze showed that learning and memory deficits following CA could be inhibited or alleviated by pre‐treatment with the microglial inhibitor minocycline or propofol. Microglial activation was significantly suppressed likely via the P2X7R/p‐p38 pathway by propofol. Moreover, hippocampal neuronal injuries after CA were remarkably attenuated by propofol. In vitro experiment showed that propofol pre‐treatment inhibited ATP‐induced microglial activation and release of tumor necrosis factor‐α and interleukin‐1β. In addition, propofol protected neurons from injury when co‐culturing with ATP‐treated microglia. Our data suggest that propofol pre‐treatment inhibits CA‐induced microglial activation and neuronal injury in the hippocampus and ultimately improves cognitive function.