Background: The likelihood of neurologically favorable survival declines with prolonged resuscitation. However, the ability of extracorporeal cardiopulmonary resuscitation (ECPR) to modulate this decline is unknown. Our aim was to examine the effects of resuscitation duration on survival and metabolic profile in patients who undergo ECPR for refractory ventricular fibrillation/ventricular tachycardia out-of-hospital cardiac arrest. Methods: We retrospectively evaluated survival in 160 consecutive adults with refractory ventricular fibrillation/ventricular tachycardia out-of-hospital cardiac arrest treated with the University of Minnesota (UMN) ECPR protocol (transport with ongoing cardiopulmonary resuscitation [CPR] to the cardiac catheterization laboratory for ECPR) compared with 654 adults who had received standard CPR in the amiodarone arm of the ALPS trial (Amiodarone, Lidocaine, or Placebo Study). We evaluated the metabolic changes and rate of survival in relation to duration of CPR in UMN-ECPR patients. Results: Neurologically favorable survival was significantly higher in UMN-ECPR patients versus ALPS patients (33% versus 23%; P =0.01) overall. The mean duration of CPR was also significantly longer for UMN-ECPR patients versus ALPS patients (60 minutes versus 35 minutes; P <0.001). Analysis of the effect of CPR duration on neurologically favorable survival demonstrated significantly higher neurologically favorable survival for UMN-ECPR patients compared with ALPS patients at each CPR duration interval <60 minutes; however, longer CPR duration was associated with a progressive decline in neurologically favorable survival in both groups. All UMN-ECPR patients with 20 to 29 minutes of CPR (8 of 8) survived with neurologically favorable status compared with 24% (24 of 102) of ALPS patients with the same duration of CPR. There were no neurologically favorable survivors in the ALPS cohort with CPR ≥40 minutes, whereas neurologically favorable survival was 25% (9 of 36) for UMN-ECPR patients with 50 to 59 minutes of CPR and 19% with ≥60 minutes of CPR. Relative risk of mortality or poor neurological function was significantly reduced in UMN-ECPR patients with CPR duration ≥60 minutes. Significant metabolic changes included decline in pH, increased lactic acid and arterial partial pressure of carbon dioxide, and thickened left ventricular wall with prolonged professional CPR. Conclusions: ECPR was associated with improved neurologically favorable survival at all CPR durations <60 minutes despite severe progressive metabolic derangement. However, CPR duration remains a critical determinate of survival.
Multi-system organ failure is ubiquitous but treatable with adequate hemodynamic support. Neurologic recovery was prolonged requiring delayed prognostication. Immediate 24/7 availability of surgical and medical specialty expertise was required to achieve 48% functionally intact survival.
Introduction: While early enteral nutrition is generally preferred in critically ill patients, the optimal timing of feeding among refractory cardiac arrest patients is unknown. We examined the association between timing of enteral nutrition and patient survival and safety outcomes in patients with refractory out-of-hospital cardiac arrest (OHCA) who were treated with extracorporeal cardiopulmonary resuscitation (ECPR).Methods: We performed a retrospective analysis of 142 consecutive patients presenting with OHCA due to ventricular fibrillation or ventricular tachycardia treated with ECPR and targeted temperature management (TTM). Neurologically favorable survival and clinical outcomes were compared between patients who received early enteral nutrition (<48 h after admission to the intensive care unit) and patients receiving delayed enteral nutrition (initiated >48 h after admission).Results: Enteral nutrition was initiated in 90/142 (63%) patients. Early enteral nutrition was provided in 34/90 (38%) while delayed nutrition occurred in 56/90 (62%). In adjusted analysis including patients who received nutrition, delayed enteral feeding was associated with increased odds of neurologically favorable survival (29 vs 54%, CI 1.04À7.25, p = 0.04). There were no significant differences in the incidence of pneumonia (18 vs 27%, p = 0.16), gastrointestinal bleeding (5.9 vs 3.6%, p = 0.42), intestinal ischemia (5.9 vs 5.4%, p = 0.90), ileus (12 vs 11%, p = 0.98), or need for tracheostomy (15 vs 20%, p = 0.81) between early and late feeding groups. Conclusion:In patients with refractory OHCA treated with ECPR and TTM, delayed enteral nutrition was associated with improved neurologically favorable survival. Adverse events related to enteral feeding were not associated with timing of feeding initiation.
Studies were made on isolated and intact dog kidneys provided with a controlled renal arterial perfusion pressure. Renal function tests were performed for a period of 1–2 hours. Creatinine and PAH extraction ratios, clearance rates and TmPAH values were calculated. A procedure was devised for the calculation of renal clearances from simultaneously occurring values which obviated errors due to urinary dead space and permitted the measurement of rapid changes in extraction rates. Renal blood flows and urine flows were measured. After administration of endotoxin PAH extraction ratios and extraction rates declined. TmPAH values temporarily fell but within an hour returned to pre-endotoxin levels. Creatinine extraction ratios and rates and urine flow showed irregular changes after endotoxin. Renal hyperemia was observed if the arterial pressure was maintained and especially when smaller injections of endotoxin were administered. It is concluded that the effect of endotoxin on the kidney is primarily a vascular one. There is no evidence for the poisoning of renal tubule cells, and renal vascular occlusion is not observed.
Our recent work has been concerned with hemodynamic changes in animals f ollcwing lethal injections of endotosin( 1-6). Similarity between vascular actions of histamine and endotoxin has been noted (4-7), suggesting that hemodynamic changes in endotoxin shock may be brought about by release of histamine. Our aim in this study was (a) to estimate changes in whole blood and plasma histamine following lethal injections of endotoxin, and (b) to determine if changes in vascular reactivity to histamine may result following endotoxin administration. Our findings suggest a prominent role of histamine in shock produced by endotoxin. Methods.Histamine estimations were made with chemical procedure utilizing paper chromatography. Blood samples from catheterized femoral vessels of dogs, anesthetized with soditrm pentobarbital (30 mg/kg) , were collected directly into 4 volumes of acetone. Plasma samples were obtained frcm chilled centrifuged blood containing 1.7% potassium oxalate( 8 ) , plasma then added to acetone as above. Samples were refrigerated 12 hours, filtered until clear and evaporated to dryness, by warming and later by lyophilization. Dried residue was extracted with water and evaporated to standard volume -< 1 ml.Equal aliquots of final solutions were placed on Whatman #1 paper and run for 10-16 hours in a solvent of n-butano1:acetic acid: water (4: 1 : 5) , using descending paper chromatography. Pauly reagent, followed by sodium carbonate overspray was used for color development ( 9 ) . Rf's ranged between 0.10-0.14. and recoveries were 90-95*% complete. Other procedures( 1 0 , l l ) were used for comparison with present technic and re-sults were in close agreement. Changes in histamine concentration were estimated by comparisons of area X density of spots to pre-endotoxin values. Absolute concentrations of blood histamine were also estimated by comparisons to known standard concentrations, and all values before and after endotoxin ranged between 0.03 and 2.20 pg/ml. E. coli endotoxin (Difco), 2 mg/kg, was administered intravenously to anesthetized adult dogs. In second series, hindlimbs of dogs were perfused with heparinized blood continuously obtained from adult anesthetized dogs, as previously described ( 12). Intra-arterial injections of histamine (1 p g ) were made in the isolated limb before and after intravenous injection of E . coli endotoxin (2 mg/kg, Difco) into the intact dog. Limbs were suspended on strain gauge weighing device and perfused a t highest flow compatible with the isogravimetric state, flow remaining constant until termination of experiments.Results. In Fig. 1 mean changes in plasma and whole blood histamine are shown following lethal injections of endotoxin. Within 2 minutes after injection there is a marked fall in whole blood histamine and a rise in plasma histamine. Plasma histamine remains
Experiments were performed on isolated perfused dog kidneys to determine relationships between tissue pressure, vascular volume, ‘over-all’ and ‘intraorgan’ vascular resistances. Results indicate that autoregulation of renal blood flow is brought about by disproportionately large increases in extravascular pressure. Since extravascular and intravascular pressures are opposing forces there is progressively less vascular distention with increases in arterial pressure as the increments in extravascular pressures approach the increments in intravascular pressures. The effective propellent force of blood flow through the kidney is thought to be the difference between the renal artery pressure and extravascular pressure. Vascular resistances calculated on this basis showed no significant changes throughout the range of autoregulation in four of the six experiments. It is proposed that the extravascular pressure within Bowmans capsule may exceed the renal interstitial pressure, and when the effects of renal extravascular pressures within and without Bowman's capsule are taken into account in the calculation of intrarenal vascular resistance, the pressure-flow relations of the kidney will be similar to those of other vascular beds.
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