Biomedical subjects

A C Krismer

Publications and source records attributed to A C Krismer.

27 records · Page 2Linked to original sources

PubMed2000

Survival with full neurologic recovery and no cerebral pathology after prolonged cardiopulmonary resuscitation with vasopressin in pigs.

OBJECTIVES: We sought to determine the effects of vasopressin and saline placebo in comparison with epinephrine on neurologic recovery and possible cerebral pathology in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). BACKGROUND: It is unknown whether increased cerebral blood flow during CPR with vasopressin is beneficial with regard to neurologic recovery or detrimental owing to complications such as cerebral edema after return of spontaneous circulation. METHODS: After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive every 5 min either vasopressin (0.4, 0.4 and 0.8 U/kg; n = 6), epinephrine (45, 45 and 200 microg/kg; n = 6) or saline placebo (n = 5). The mean value +/- SEM of aortic diastolic pressure was significantly (p < 0.05) higher 90 s after each of three vasopressin versus epinephrine versus saline placebo injections (60 +/- 3 vs. 45 +/- 3 vs. 29 +/- 2 mm Hg; 49 +/- 5 vs. 27 +/- 3 vs. 23 +/- 1 mm Hg; and 50 +/- 6 vs. 21 +/- 3 vs. 16 +/- 3 mm Hg, respectively). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve return of spontaneous circulation. RESULTS: All the pigs that received epinephrine and saline placebo died, whereas all pigs on vasopressin survived (p < 0.05). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait in all vasopressin-treated animals; after 96 h, magnetic resonance imaging revealed no cerebral pathology. CONCLUSIONS: During prolonged CPR, repeated vasopressin administration, but not epinephrine or saline placebo, ensured long-term survival with full neurologic recovery and no cerebral pathology in this porcine CPR model.

Animals↗

PubMed2000

Cardiopulmonary resuscitation during severe hypothermia in pigs: does epinephrine or vasopressin increase coronary perfusion pressure?

UNLABELLED: The American Heart Association does not recommend epinephrine for management of hypothermic cardiac arrest if body core temperature is below 30 degrees C. Furthermore, the effects of vasopressin administration during hypothermic cardiac arrest are totally unknown. This study was designed to assess the effects of vasopressin and epinephrine on coronary perfusion pressure in a porcine model during hypothermic cardiac arrest cardiopulmonary resuscitation (CPR). Pigs were surface-cooled until their body core temperature was 26 degrees C. After 30 min of untreated cardiac arrest, followed by 3 min of basic life support CPR, 15 animals were randomly assigned to receive, at 5-min intervals, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 5), epinephrine (45, 45, and 200 microg/kg; n = 5), or saline placebo (n = 5). Compared with epinephrine, mean +/- SEM coronary perfusion pressure was significantly higher (P < 0.05) 90 s and 5 min after the first (35+/-4 vs 22+/-3 mm Hg and 37+/-2 vs 16+/-2 mm Hg) and the second vasopressin administration (40+/-5 vs 26+/-5 mm Hg and 36+/-5 vs 18+/-2 mm Hg, respectively). After the third drug administration, coronary perfusion pressure in the epinephrine group increased dramatically and was comparable to vasopressin. In the saline placebo group, coronary perfusion pressure was significantly lower (P < 0.05) than in the vasopressin and epinephrine groups. Six animals treated with epinephrine or vasopressin had transient return of spontaneous circulation, whereas all placebo animals died (P < 0.05). During CPR in severe hypothermia, administration of both vasopressin and epinephrine resulted in significant increases in coronary perfusion pressure when compared with placebo. IMPLICATIONS: Our study was designed to assess the effects of vasopressin and epinephrine in a porcine model simulating cardiac arrest during severe hypothermia. This study demonstrates that the administration of both emergency drugs results in an increased perfusion pressure in the heart.

Animals↗

PubMed2000

The effects of repeated doses of vasopressin or epinephrine on ventricular fibrillation in a porcine model of prolonged cardiopulmonary resuscitation.

This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n = 5) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively, n = 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0. 8 units/kg, respectively, n = 5) or epinephrine (late epinephrine: 45 and 200 microg/kg, n = 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 +/- 1.5 Hz vs 7. 0 +/- 0.7 Hz (P < 0.001), mean amplitude was 0.65 +/- 0.26 mV vs 0. 21 +/- 0.14 mV (P < 0.001, and coronary perfusion pressure was 27 +/- 9 mm Hg vs 8 +/- 4 mm Hg (P < 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survived 1 h (P < 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation.

Animals↗

PubMed2000

Vasopressin improves survival after cardiac arrest in hypovolemic shock.

UNLABELLED: Survival after hypovolemic shock and cardiac arrest is dismal with current therapies. We evaluated the potential benefits of vasopressin versus large-dose epinephrine in hemorrhagic shock and cardiac arrest on vital organ perfusion, and the likelihood of resuscitation. In 18 pigs, 35% of the estimated blood volume was withdrawn over 15 min and ventricular fibrillation was induced 5 min later. After 4 min of cardiac arrest and 4 min of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 7), 0.8 unit/kg vasopressin (n = 7), or saline placebo (n = 4) was administered in a blinded, randomized manner. Defibrillation was attempted 2.5 min after drug administration, and all animals were subsequently observed for 1 h without further intervention. Spontaneous circulation was restored in 7 of 7 vasopressin animals, in 6 of 7 epinephrine pigs, and in 0 of 4 placebo swine. At 5 and 30 min after return of spontaneous circulation, median (minimum and maximum) renal blood flow after epinephrine was 2 (0-31), and 2 (0-48) mL. 100 g(-1). min(-1), respectively; and after vasopressin 96 (12-161), and 44 (16-105) mL. 100 g(-1). min(-1), respectively (P: <.01 between groups). Epinephrine animals developed a profound metabolic acidosis by 15 min after return of spontaneous circulation (mean arterial pH, 7.11 +/- 0.01), and by 60 min all epinephrine-treated animals had died. The vasopressin pigs had (P: = 0.015) less acidosis (pH = 7.26+/-0. 04) at corresponding time points, and all survived > or =55 min (P: < 0. 01). In conclusion, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital organ perfusion, less metabolic acidosis, and prolonged survival. Based on these findings, clinical evaluation of vasopressin during hypovolemic cardiac arrest may be warranted. IMPLICATIONS: The chances of surviving cardiac arrest in hemorrhagic shock are considered dismal without adequate fluid replacement. However, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital organ perfusion and prolonged survival in an animal model of suspended infusion therapy.

Animals↗

PubMed2000

Intraosseous blood gases during hypothermia: correlation with arterial, mixed venous, and sagittal sinus blood.

OBJECTIVE: Especially in pediatric patients with severe hypothermia, intraosseous access may be more readily available than intravascular access during an early phase of treatment and therefore, may be helpful to optimize management. The purpose of this study was to determine whether intraosseous blood gases are comparable with arterial, mixed venous, and sagittal sinus blood gases during different degrees of hypothermia. DESIGN: Prospective, descriptive laboratory investigation using a porcine model. SETTING: University hospital laboratory. SUBJECTS: Twelve anesthetized, 12- to 16-wk-old domestic pigs weighing 30-35 kg. INTERVENTIONS: Volume-controlled ventilated animals were instrumented with arterial, pulmonary artery, sagittal sinus, and 16-gauge intraosseous catheters. Blood samples were obtained from each site every 15 mins during surface cooling with crushed ice until mean +/- SEM core temperature decreased from 38.5+/-0.1 degrees C [101.3+/-0.2 degrees F] to 27+/-0.5 degrees C [80.5+/-0.9 degrees F] over 2 hrs. MEASUREMENTS AND MAIN RESULTS: Intraindividual correlation of Pco2 and pH values were determined as the difference (delta) between intraosseous and reference blood samples. With hypothermia, absolute values of Pco2 decreased and pH increased in samples from all sites. At 27 degrees C, intraosseous--arterial delta P(CO2) and delta pH (mean +/- 95% confidence intervals) were 2.6+/-10.6 torr [0.35+/-1.4 kPa] and -0.11+/-0.07 units; intraosseous - mixed venous were 0.4+/-12.2 torr [0.05+/-1.6 kPa] and -0.06+/-0.08 units; and intraosseous - sagittal sinus were -7.3+/-16 torr [-0.97+/-2.1 kPa] and 0.001+/-0.14 units, respectively. Intraosseous Pco2 was not comparable to end-tidal values (deltaP(CO2) 17.4+/-14.6 torr [2.3+/-1.9 kPa]), and intraosseous lactate did not correlate with arterial, mixed venous, or sagittal sinus values. CONCLUSIONS: During hypothermia, intraosseous P(CO2) values were predictable for mixed venous Pco2 and arterial P(CO2). Intraosseous pH values also correlated with mixed venous and sagittal sinus blood samples. Accordingly, interpretation of blood gas values obtained from bone marrow aspirates may be helpful to adjust ventilation and optimize fluid and drug therapy during the early treatment of patients with severe hypothermia.

Animals↗

PubMed2000

Comparison of epinephrine and vasopressin in a pediatric porcine model of asphyxial cardiac arrest.

OBJECTIVE: This study was designed to compare the effects of vasopressin vs. epinephrine vs. the combination of epinephrine with vasopressin on vital organ blood flow and return of spontaneous circulation in a pediatric porcine model of asphyxial arrest. DESIGN: Prospective, randomized laboratory investigation using an established porcine model for measurement of hemodynamic variables, organ blood flow, blood gases, and return of spontaneous circulation. SETTING: University hospital laboratory. SUBJECTS: Eighteen piglets weighing 8-11 kg. INTERVENTIONS: Asphyxial cardiac arrest was induced by clamping the endotracheal tube. After 8 mins of cardiac arrest and 8 mins of cardiopulmonary resuscitation, a bolus dose of either 0.8 units/kg vasopressin (n = 6), 200 microg/kg epinephrine (n = 6), or a combination of 45 microg/kg epinephrine with 0.8 units/kg vasopressin (n = 6) was administered in a randomized manner. Defibrillation was attempted 6 mins after drug administration. MEASUREMENTS AND MAIN RESULTS: Mean +/- SEM coronary perfusion pressure, before and 2 mins after drug administration, was 13 +/- 2 and 23 +/- 6 mm Hg in the vasopressin group; 14 +/- 2 and 31 +/- 4 mm Hg in the epinephrine group; and 13 +/- 1 and 33 +/- 6 mm Hg in the epinephrine-vasopressin group, respectively (p = NS). At the same time points, mean +/- SEM left ventricular myocardial blood flow was 44 +/- 31 and 44 +/- 25 mL x min-(1) x 100 g(-1) in the vasopressin group; 30 +/- 18 and 233 +/- 61 mL x min(-1) x 100 g(-1) in the epinephrine group; and 36 +/- 10 and 142 +/- 57 mL x min(-1) x 100 g(-1) in the epinephrine-vasopressin group (p < .01 epinephrine vs. vasopressin; p < .02 epinephrine-vasopressin vs. vasopressin). Total cerebral blood flow trended toward higher values after epinephrine-vasopressin (60 +/- 19 mL x min(-1) x 100 g(-1)) than after vasopressin (36 +/- 17 mL x min(-1) x 100 g(-1)) or epinephrine alone (31 +/- 7 mL x min(-1) x 100 g(-1); p = .07, respectively). One of six vasopressin, six of six epinephrine, and four of six epinephrine-vasopressin-treated animals had return of spontaneous circulation (p < .01, vasopressin vs. epinephrine). CONCLUSIONS: Administration of epinephrine, either alone or in combination with vasopressin, significantly improved left ventricular myocardial blood flow during cardiopulmonary resuscitation. Return of spontaneous circulation was significantly more likely in epinephrine-treated pigs than in animals resuscitated with vasopressin alone.

Adrenergic Agonists↗

PubMed2000

Survey of effects of anesthesia protocols on hemodynamic variables in porcine cardiopulmonary resuscitation laboratory models before induction of cardiac arrest.

OBJECTIVE: An advantage of animal models in cardiopulmonary resuscitation (CPR) research is the possibility to control confounding variables that may be impossible to standardize in clinical trials. A neglected effect of the anesthesia protocol in porcine CPR studies may be its impact on hemodynamic variables before induction of cardiac arrest. Accordingly, the purpose of the study reported here was to evaluate published CPR reports with regard to their anesthesia protocol. METHODS: Of 100 articles that reported on laboratory models simulating cardiac arrest between 1987 and 1997 in peer-reviewed journals, 25 met inclusion criteria and were analyzed for values of coronary perfusion pressure, mean arterial pressure, heart rate, temperature, and cardiac index before induction of cardiac arrest. Subsequently, mean values for all animals in a given report were calculated and corrected for group size; statistical analysis was not performed since this was a survey only. RESULTS: Different anesthesia protocols resulted in a widely distributed pattern of hemodynamic variables prior to induction of cardiac arrest. Ranges compared with reference values were: heart rate, 100 to 122 beats/min versus 105+/-11 beats/min; mean arterial pressure, 68 to 130 mm Hg versus 102+/-9 mm Hg; coronary perfusion pressure, 55 to 114 mm Hg (no reference value); cardiac index, 69 to 152 ml/kg/min versus 147+/-22 ml/kg/min; body temperature, 37 to 38.5 degrees C versus 38.5+/-0.7 degrees C. CONCLUSION: The anesthesia protocol may have an impact on hemodynamic variables before induction of cardiac arrest in CPR studies.

Anesthesia↗

PubMed1999

Repeated administration of vasopressin but not epinephrine maintains coronary perfusion pressure after early and late administration during prolonged cardiopulmonary resuscitation in pigs.

BACKGROUND: It is unknown whether repeated dosages of vasopressin or epinephrine given early or late during basic life support cardiopulmonary resuscitation (CPR) may be able to increase coronary perfusion pressure above a threshold between 20 and 30 mm Hg that renders defibrillation successful. METHODS AND RESULTS: After 4 minutes of cardiac arrest, followed by 3 minutes of basic life support CPR, 12 animals were randomly assigned to receive, every 5 minutes, either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 U/kg, respectively; n=6) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively; n=6). Another 12 animals were randomly allocated after 4 minutes of cardiac arrest, followed by 8 minutes of basic life support CPR, to receive, every 5 minutes, either vasopressin (late vasopressin: 0.4 and 0.8 U/kg, respectively; n=6), or epinephrine (late epinephrine: 45 and 200 microg/kg, respectively; n=6). Defibrillation was attempted after 22 minutes of cardiac arrest. Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after early vasopressin compared with early epinephrine (50+/-4 versus 34+/-3 mm Hg, P<0.02; 42+/-5 versus 15+/-3 mm Hg, P<0.0008; and 37+/-5 versus 11+/-3 mm Hg, P<0. 002, respectively). Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after late vasopressin compared with late epinephrine (40+/-3 versus 22+/-4 mm Hg, P<0.004, and 32+/-4 versus 15+/-4 mm Hg, P<0.01, respectively). All vasopressin animals survived 60 minutes, whereas no epinephrine pig had return of spontaneous circulation (P<0.05). CONCLUSIONS: Repeated administration of vasopressin but only the first epinephrine dose given early and late during basic life support CPR maintained coronary perfusion pressure above the threshold that is needed for successful defibrillation.

Animals↗

PubMed1999

Effect of small-dose dopamine on mesenteric blood flow and renal function in a pig model of cardiopulmonary resuscitation with vasopressin.

UNLABELLED: Vasopressin (antidiuretic hormone) seems a promising alternative to epinephrine for cardiopulmonary resuscitation (CPR) in cardiac arrest victims, mediating a pronounced blood flow shift toward vital organs. We evaluated the effects of small-dose dopamine on splanchnic blood flow and renal function after successful resuscitation with this potent vasoconstrictor in an established porcine CPR model. After 4 min of cardiac arrest and 3 min of CPR, animals received 0.4 U/kg vasopressin and were continuously infused with either dopamine 4 microg x kg(-1) x min(-1) (n = 6), or saline placebo (n = 6). Defibrillation was performed 5 min after drug administration; all animals were observed for 6 h after return of spontaneous circulation. During the postresuscitation phase, average mean +/- SD superior mesenteric artery blood flow was significantly (P = 0.002) higher in the dopamine group compared with the placebo group (1185+/-130 vs 740+/-235 mL/min), whereas renal blood flow was comparable between groups (255+/-40 vs 250+/-85 mL/min). The median calculated glomerular filtration rate had higher values in the dopamine group (70-120 mL/min) than in the placebo group (40-70 mL/min; P = 0.1 at 0 min and P = 0.08 at 360 min). We conclude that small-dose dopamine administration may be useful in improving superior mesenteric artery blood flow and renal function after successful resuscitation with vasopressin. IMPLICATIONS: Long-term survival after cardiac arrest may be determined by the ability to ensure adequate organ perfusion during cardiopulmonary resuscitation and in the postresuscitation phase. In this regard, small-dose dopamine improved postresuscitation blood flow to the mesenteric bed when vasopressin was used as an alternative vasopressor in an animal model of cardiac arrest.

Animals↗