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Treatment of septic shock with human monoclonal antibody HA-1A: A randomized, double-blind, placebo-controlled trial
Literature
of resuscitation /Resuscitation
diopulmonary resuscitation time of >20 min. Of the 774 patients, 27% recovered good neurologic function. There was no statistically significant difference in neurologic recovery rates by age. Multivariate analysis showed that independent predictors of g,ood neurologic recovery were: no history of diabetes mellitus; a cardiac cause of arrest, short arrest time, and short cardiopulmonary resuscitation time. Conclusion: Increasing age was a factor in postresuscitation mortality, but was not an independent predictor of poor neurologic outcome.
30 (1995) 79-85
81
and survived the l-h observation period. Conclusions: We conclude that administration of vasopressinleads to a significantly higher coronary perfusion pressureand myocardial blood flow than epinephrine during closed-chest CPR in a pig model of ventricular fibrillation. Cm ecntral vemms oxygen saturatiao monitoriog es M adjunet in tba treatment of cardiec arreet Md sbocl: Prillcipks dprnctioe
Ander DS, Rivers EP, l&George FT, Rady MY Vrsopressin improvee vital organ blood flow during closed-chest eardiopldnloMry realdtatioll in pigs
Department of Emergency Medicine, Henry Ford Health Systems, 2799 West Grand Boulevard, Detroit, MI 48202, USA
Lindner KH, Prengel AW, Pfenninger EG, Lindner IM, Strohmenger H-U, Georgieff M, Lurie KG
Clin Intensive Care 1994;5/5; 232-240 Background The Emergency Physician is frequently faced with haemodynamically unstable patients with presentations ranging from cardiac arrest to various forms of shock. Current resuscitative efforts are guided by vital signs (blood pressure and heart rate) and central venous pressure.Despite normalisation of these haemodynamic variables tissue hypoxia may still persist. Ill-recognition and under treatment of tissue hypoxia in the early stagesof the initial insult have been implicated in the increasedincidence of organ failure and death. Concepts: Continuous mixed venous oxygen saturation monitoring (SvG2) dynamically reflects changesin tissue oxygen delivery and consumption. Vital signs may correlate poorly with these haemodynamic and oxygen transport variables. Measurement of SvG2 requires placement of a pulmonary artery catheter which is not feasible in most Emergency Departments due to added risk, time constraints, monitoring requirements and manpower demand. Following similar trends, a continuous central venous oxygen saturation monitor (SCvod can provide the Emergency Department physician with similar information. Methods: Cannulation of the central venous system for monitoring of central venous pressureswith the addition of a tibre-optic bundle via a central venous oximetric catheter (Resuscicathregistered trademark sign) for continuous SCvoz monitoring. Conclusion: Diagnostically, continuous SCvos monitoring can detect unrecognised tissue hypoxia and indicate impending haemodynamic compromise. This can aid in the appropriate triage and disposition of resuscitatedpatients. Therapeutically, continuous SCvo, monitoring provides the clinician with a meansof optimising systemicoxygen delivery and consumption through earlier and more sensitive detection of tissue hypoxia. Earlier resolution of tissue hypoxia decreasesthe accumulation of oxygen debt which may potentially improve outcome.
Universitatsklinik Anasthesiologie, Klinikum Urn. Sleinbovelstr 9, 89075 Ulm, Germany
&r
Universitat
Circulation 1995;91/l; 215-221 Background: This study was designed to compare the effects of epinephrine with those of vasopressin on vital organ blood flow during closed-chestcardiopulmonary resuscitation (CPR) in a pig model of ventricular fibrillation. Methods and Results: Vasopressin was compared with epinephrine by randomly allocating 28 pigs to receive either 0.2 mg&g epinephrine (n = 7) 0.2 U/kg vasopressin (low dose) (n = 7), 0.4 U/kg vasopressin (medium dose) (n = 7), or 0.8 U/kg vasopressin (high dose) (n = 7) after 4 min of ventricular fibrillation and 3 min of closed-chest CPR. Left ventricular myocardial blood flow, determined by use of radiolabeled microspheres during CPR, before and then 90 s and 5 min after drug administration was 17 f 2, 43 f 5, and 22 * 3 ml - min-’ - 100 g-’ (mean * S.E.M.) in the epinephrine group; 18 l 2, 50 f 6, and 29 f 3 ml - min-’ * 100 g-’ in the low-dose vasopressin group; 17 f 3, 52 f 8, and 52 f 6 ml - min-’ - 100 g-’ in the medium-dose vasopressin group; and 18 f 2, 95 f 9, and 57 f 6 ml - min-’ - 100 g-’ in the high-dose vasopressin group (P < 0.001 at 90 s and 5 min between epinephrine and high-dose vasopressin, and P < 0.01 at 5 min between epinephrine and medium-dosevasopressin).At the same times, calculated coronary systolic perfusion pressures were 12 * 2, 36 f 5, and 18 f 2 mmHg in the epinephrine group; 10 f 1, 39 f 6, and 26 f 5 mmHg in the low-dose vasopressin group; 11 f 2, 49 & 6, and 38 * 5 mmHg in the medium-dose vasopressin group; and 10 f 2, 70 f 5, and 47 f 6 mmHg in the high-dose vasopressin group (P < 0.01 at 90 s and 5 min between epinephrine and high-dose vasopressin); and calculated coronary diastolic perfusion pressureswere 15 * 2, 24 + 2, and 19 f 2 mmHg in the epinephrine group; 13 f 1, 25 f 2, and 20 f 1 mmHg in the low-dose vasopressin group; 13 f 2, 25 f 2, and 21 f 2 mmHg in the medium-dose vasopressin group; and 13 f 2, 35 f 3, and 24 f 2 mmHg in the high-dose vasopressin group (P < 0.05 at 90 s between epinephrine and high-dose vasopressin). Total cerebral blood flow was significantly higher after high-dose vasopressin than after epinephrine (P < 0.05 at 90 s and P < 0.01 at 5 min between groups). Five animals in the epinephrine, 5 in the lowdose vasopressin, 7 in the medium-dose vasopressin, and 6 in the high-dose vasopressingroups were successfullyresuscitated
Treatmeot of septic shock witb boman moooclooal antibody HA1A: A randomized, doable-blind, placebo-controlled trial
McCloskey RV, Straube RC, SandersC, Smith SM, Smith CR Clinical Research, Centocor Inc., Nx) Great Valley Parkway, Malvern, PA 19355, USA
Ann Intern Med 1994; 121/l; I-5 Objective: To compare the effectivenessof 100mg of HA-IA and placebo in reducing the 14day all-cause mortality rate in patients with septic shock and gram-negative bacteremia in the Centocor: HA-IA Efficacy in Septic Shock (CHESS) trial, and to assessthe safety of 100mg of HA-IA given to patients with
82
Literature of resuscitation /Resuscitation
septic shock who did not have gram-negative bacteremia. Design: Large, simple, group-sequential, randomized, doubleblind, multicenter, placebo-controlled trial. Setting: 603 investigators at 513community and university-affiliated hospitals in the United States.Patients: Within 6 h before enrohnent, the patients had been in shock with a systolic blood pressureof less than 90 mmHg after adequate fluid challenge or had received vasopressors to maintain blood pressure. These episodes of shock began within 24 h of enrolment. A presumptive clinical diagnosis of gram-negative infection as the cause of the shock episodeand a commitment from the patients’ physicians to provide full supportive care were required. Measurements: Blood cultures were obtained within 48 h of enrolment, and death at day 14after treatment was recorded. Adverse events occurring within 14 days after enrolment were also tabulated. Results: 2199patients were enrolled; 621 (28.2%)met all enrolment criteria, received HA-IA or placebo, and had confirmed gramnegative bacteremia. Mortality rates in this group were as follows: placebo, 32% (95 of 293) and HA-IA, 33%(109 of 328) (p = 0.864, Fisher exact test, two-tailed; 95% CI for the difference, -6.2% to 8.6%). Mortality rates in the patients without gram-negative bacteremia were as follows: placebo, 37% (292 of 793)and HA-lA, 41% (318 of 785) @ = 0.073, Fisher exact test, one-tailed; CI, -0.8% to 8.8%). Conclusions: In this trial, HA1A was not effective in reducing the M-day mortality rate in patients with gram-negative bacteremia and septic shock. These data do not support using septic shock as an indication for HA1A treatment. If HA-IA is effective in reducing the mortality rate in patients dying from endotoxemia, thesepatients must be identified using other treatment criteria. An esophageal and gastric approach to ventricular pacing
Ccchrane DJ, McEneaney DJ, Dempsey GJ, Anderson JM, Adgey AAJ Regional Medical Cardiology Cenire, Royal Victoria Hospital, Be&xi BTI2 6BA, UK
Pace Pacing Clin Electrophysiol 1995; 18/l; I 28-33 Using a unipolar esothoracic pacing system (where current passesfrom a point source positioned in the distal esophagus to a chest wall pad) and pulse duration of 50 msec,satisfactory 1:1 ventricular capture was obtained in 57 (86%) of 66 patients, with a mean threshold current of 27.7 mA at an optimal depth of 40.3 cm from the lower lip. When the unipolar esothoracic and bipolar transesophageal ventricular pacing systems were compared, the bipolar system was associatedwith a lower success rate and higher threshold current. When unipolar esothoracic pacing and gastrothoracic pacing (where current passesfrom a point source positioned in the stomach to a chest wall pad) were compared in 23 patients with bradyarrhythmia, ventricular capture was achieved using gastrothoracic pacing in 22 patients (96%) and esothoracic pacing in 21 (91%): gastrothoracic pacing required less current (16.0 mA f S.D.7.2 vs. 25.8 mA f S.D.8.6). Optimal ventricular capture occurred using a unipolar gastrothoracic pacing electrode inserted to an average depth of 44.3 cm together with a high impedance chest pad (250 Omega) placed in the fourth interspace at the left sternal edge, with 50-ms current pulses and a mean threshold of
30 (1995) 79-85
16.0mA. Thus, using a gastroesophagealelectrode system,ventricular pacing can be achieved successfully,and the availability of such a systemcould play a major role in resuscitation of patients from severebradyarrhythmias. Improved outcome witb floid restriction io treatment of onconbollcd hcmurrhagic shwk
Capone AC, Safar P, Stezoski W, Tisherman S, Peitzman AB Presbyterian University Hospital, Pittsburgh, PA 15213, USA
J Am Coil Surg 1995; 180/l; 49-56 BACKGROUND: Recent studies have challenged current guidelines for prehospital fluid resuscitation. However, longterm studies evaluating the consequencesof fluid restriction in uncontrolled hemorrhagic shock are lacking. This study was done to examine the long-term effectsof deliberate hypotension in the treatment of uncontrolled hemorrhage. STUDY DESIGN: Uncontrolled hemorrhagic shock was produced in 40 rats by a preliminary bleed (3 ml per 100 g) followed by 75% tail amputation. Experimental design consistedof three phases: a ‘pre-hospital phase’ (90 min of uncontrolled bleeding with or without treatment with lactated Ringer’s [LR] solution), followed by a ‘hospital phase’ (60 mitt, including control of hemorrhage and fluid resuscitation including blood), and a three day observation phase. Forty rats were studied in four treatment groups (ten rats per group). Group 1 consistedof untreated controls (no resuscitation). Group 2 had no fluid during the prehospital phase. Group 3 had prehospital resuscitation to a mean arterial pressure (MAP) of 40 mmHg with LR, and group 4 had prehospital resuscitation to MAP of 80 mmHg with LR. Groups 2, 3, and 4 received fluid and blood to MAP of 80 mmHg and hematocrit of 30% in the hospital phase. RESULTS: All rats in group 1 (untreated) died within 2.5 h. Five rats in group 2 (no prehospital FR) survived 90 min; however, only one survived three days. In group 3, all ten rats survived 2.5 h and six survived three days. In group 4, eight rats died within 90 min, but none survived long-term. Blood loss (ml per 100 g) for each group was 3.75 0.6 for group 1, 3.35 0.1 for group 2, 4.15 0.8 for group 3, and 8.45 0.6 for group 4, (p < 0.05, group 4 compared with groups 1, 2, and 3). CONCLUSIONS: Attempts to achieve normal MAP during uncontrolled bleeding increased blood loss, hemodilution and mortality. Hypotensive resuscitation resulted in less acidemia and improved long-term survival. EQb atria1 natrioretic peptide concentrations blunt tbe pressor response du&g cardiopulmonary resnscitrtioo in humaos
Paradis NA, Wortsman J, Malarkey WB, Martin GB, Goetting MG, Feingold M, Nowak RM 48 Remsen Street, Brooklyn, NY 11201-4106. USA
Crit Care Med 1994;22/2 (213-218) Objective: To determine the relationship of circulating atria1 natriuretic peptide concentrations to the pressor response to high-doseepinephrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest. Design: Prospective study. Patients: Fourteen normothennic, adult, prehospital and emergency department patients suffering unexpected cardiac arrest. Intervention: Patients received high-dose epinephrine
of resuscitation /Resuscitation
diopulmonary resuscitation time of >20 min. Of the 774 patients, 27% recovered good neurologic function. There was no statistically significant difference in neurologic recovery rates by age. Multivariate analysis showed that independent predictors of g,ood neurologic recovery were: no history of diabetes mellitus; a cardiac cause of arrest, short arrest time, and short cardiopulmonary resuscitation time. Conclusion: Increasing age was a factor in postresuscitation mortality, but was not an independent predictor of poor neurologic outcome.
30 (1995) 79-85
81
and survived the l-h observation period. Conclusions: We conclude that administration of vasopressinleads to a significantly higher coronary perfusion pressureand myocardial blood flow than epinephrine during closed-chest CPR in a pig model of ventricular fibrillation. Cm ecntral vemms oxygen saturatiao monitoriog es M adjunet in tba treatment of cardiec arreet Md sbocl: Prillcipks dprnctioe
Ander DS, Rivers EP, l&George FT, Rady MY Vrsopressin improvee vital organ blood flow during closed-chest eardiopldnloMry realdtatioll in pigs
Department of Emergency Medicine, Henry Ford Health Systems, 2799 West Grand Boulevard, Detroit, MI 48202, USA
Lindner KH, Prengel AW, Pfenninger EG, Lindner IM, Strohmenger H-U, Georgieff M, Lurie KG
Clin Intensive Care 1994;5/5; 232-240 Background The Emergency Physician is frequently faced with haemodynamically unstable patients with presentations ranging from cardiac arrest to various forms of shock. Current resuscitative efforts are guided by vital signs (blood pressure and heart rate) and central venous pressure.Despite normalisation of these haemodynamic variables tissue hypoxia may still persist. Ill-recognition and under treatment of tissue hypoxia in the early stagesof the initial insult have been implicated in the increasedincidence of organ failure and death. Concepts: Continuous mixed venous oxygen saturation monitoring (SvG2) dynamically reflects changesin tissue oxygen delivery and consumption. Vital signs may correlate poorly with these haemodynamic and oxygen transport variables. Measurement of SvG2 requires placement of a pulmonary artery catheter which is not feasible in most Emergency Departments due to added risk, time constraints, monitoring requirements and manpower demand. Following similar trends, a continuous central venous oxygen saturation monitor (SCvod can provide the Emergency Department physician with similar information. Methods: Cannulation of the central venous system for monitoring of central venous pressureswith the addition of a tibre-optic bundle via a central venous oximetric catheter (Resuscicathregistered trademark sign) for continuous SCvoz monitoring. Conclusion: Diagnostically, continuous SCvos monitoring can detect unrecognised tissue hypoxia and indicate impending haemodynamic compromise. This can aid in the appropriate triage and disposition of resuscitatedpatients. Therapeutically, continuous SCvo, monitoring provides the clinician with a meansof optimising systemicoxygen delivery and consumption through earlier and more sensitive detection of tissue hypoxia. Earlier resolution of tissue hypoxia decreasesthe accumulation of oxygen debt which may potentially improve outcome.
Universitatsklinik Anasthesiologie, Klinikum Urn. Sleinbovelstr 9, 89075 Ulm, Germany
&r
Universitat
Circulation 1995;91/l; 215-221 Background: This study was designed to compare the effects of epinephrine with those of vasopressin on vital organ blood flow during closed-chestcardiopulmonary resuscitation (CPR) in a pig model of ventricular fibrillation. Methods and Results: Vasopressin was compared with epinephrine by randomly allocating 28 pigs to receive either 0.2 mg&g epinephrine (n = 7) 0.2 U/kg vasopressin (low dose) (n = 7), 0.4 U/kg vasopressin (medium dose) (n = 7), or 0.8 U/kg vasopressin (high dose) (n = 7) after 4 min of ventricular fibrillation and 3 min of closed-chest CPR. Left ventricular myocardial blood flow, determined by use of radiolabeled microspheres during CPR, before and then 90 s and 5 min after drug administration was 17 f 2, 43 f 5, and 22 * 3 ml - min-’ - 100 g-’ (mean * S.E.M.) in the epinephrine group; 18 l 2, 50 f 6, and 29 f 3 ml - min-’ * 100 g-’ in the low-dose vasopressin group; 17 f 3, 52 f 8, and 52 f 6 ml - min-’ - 100 g-’ in the medium-dose vasopressin group; and 18 f 2, 95 f 9, and 57 f 6 ml - min-’ - 100 g-’ in the high-dose vasopressin group (P < 0.001 at 90 s and 5 min between epinephrine and high-dose vasopressin, and P < 0.01 at 5 min between epinephrine and medium-dosevasopressin).At the same times, calculated coronary systolic perfusion pressures were 12 * 2, 36 f 5, and 18 f 2 mmHg in the epinephrine group; 10 f 1, 39 f 6, and 26 f 5 mmHg in the low-dose vasopressin group; 11 f 2, 49 & 6, and 38 * 5 mmHg in the medium-dose vasopressin group; and 10 f 2, 70 f 5, and 47 f 6 mmHg in the high-dose vasopressin group (P < 0.01 at 90 s and 5 min between epinephrine and high-dose vasopressin); and calculated coronary diastolic perfusion pressureswere 15 * 2, 24 + 2, and 19 f 2 mmHg in the epinephrine group; 13 f 1, 25 f 2, and 20 f 1 mmHg in the low-dose vasopressin group; 13 f 2, 25 f 2, and 21 f 2 mmHg in the medium-dose vasopressin group; and 13 f 2, 35 f 3, and 24 f 2 mmHg in the high-dose vasopressin group (P < 0.05 at 90 s between epinephrine and high-dose vasopressin). Total cerebral blood flow was significantly higher after high-dose vasopressin than after epinephrine (P < 0.05 at 90 s and P < 0.01 at 5 min between groups). Five animals in the epinephrine, 5 in the lowdose vasopressin, 7 in the medium-dose vasopressin, and 6 in the high-dose vasopressingroups were successfullyresuscitated
Treatmeot of septic shock witb boman moooclooal antibody HA1A: A randomized, doable-blind, placebo-controlled trial
McCloskey RV, Straube RC, SandersC, Smith SM, Smith CR Clinical Research, Centocor Inc., Nx) Great Valley Parkway, Malvern, PA 19355, USA
Ann Intern Med 1994; 121/l; I-5 Objective: To compare the effectivenessof 100mg of HA-IA and placebo in reducing the 14day all-cause mortality rate in patients with septic shock and gram-negative bacteremia in the Centocor: HA-IA Efficacy in Septic Shock (CHESS) trial, and to assessthe safety of 100mg of HA-IA given to patients with
82
Literature of resuscitation /Resuscitation
septic shock who did not have gram-negative bacteremia. Design: Large, simple, group-sequential, randomized, doubleblind, multicenter, placebo-controlled trial. Setting: 603 investigators at 513community and university-affiliated hospitals in the United States.Patients: Within 6 h before enrohnent, the patients had been in shock with a systolic blood pressureof less than 90 mmHg after adequate fluid challenge or had received vasopressors to maintain blood pressure. These episodes of shock began within 24 h of enrolment. A presumptive clinical diagnosis of gram-negative infection as the cause of the shock episodeand a commitment from the patients’ physicians to provide full supportive care were required. Measurements: Blood cultures were obtained within 48 h of enrolment, and death at day 14after treatment was recorded. Adverse events occurring within 14 days after enrolment were also tabulated. Results: 2199patients were enrolled; 621 (28.2%)met all enrolment criteria, received HA-IA or placebo, and had confirmed gramnegative bacteremia. Mortality rates in this group were as follows: placebo, 32% (95 of 293) and HA-IA, 33%(109 of 328) (p = 0.864, Fisher exact test, two-tailed; 95% CI for the difference, -6.2% to 8.6%). Mortality rates in the patients without gram-negative bacteremia were as follows: placebo, 37% (292 of 793)and HA-lA, 41% (318 of 785) @ = 0.073, Fisher exact test, one-tailed; CI, -0.8% to 8.8%). Conclusions: In this trial, HA1A was not effective in reducing the M-day mortality rate in patients with gram-negative bacteremia and septic shock. These data do not support using septic shock as an indication for HA1A treatment. If HA-IA is effective in reducing the mortality rate in patients dying from endotoxemia, thesepatients must be identified using other treatment criteria. An esophageal and gastric approach to ventricular pacing
Ccchrane DJ, McEneaney DJ, Dempsey GJ, Anderson JM, Adgey AAJ Regional Medical Cardiology Cenire, Royal Victoria Hospital, Be&xi BTI2 6BA, UK
Pace Pacing Clin Electrophysiol 1995; 18/l; I 28-33 Using a unipolar esothoracic pacing system (where current passesfrom a point source positioned in the distal esophagus to a chest wall pad) and pulse duration of 50 msec,satisfactory 1:1 ventricular capture was obtained in 57 (86%) of 66 patients, with a mean threshold current of 27.7 mA at an optimal depth of 40.3 cm from the lower lip. When the unipolar esothoracic and bipolar transesophageal ventricular pacing systems were compared, the bipolar system was associatedwith a lower success rate and higher threshold current. When unipolar esothoracic pacing and gastrothoracic pacing (where current passesfrom a point source positioned in the stomach to a chest wall pad) were compared in 23 patients with bradyarrhythmia, ventricular capture was achieved using gastrothoracic pacing in 22 patients (96%) and esothoracic pacing in 21 (91%): gastrothoracic pacing required less current (16.0 mA f S.D.7.2 vs. 25.8 mA f S.D.8.6). Optimal ventricular capture occurred using a unipolar gastrothoracic pacing electrode inserted to an average depth of 44.3 cm together with a high impedance chest pad (250 Omega) placed in the fourth interspace at the left sternal edge, with 50-ms current pulses and a mean threshold of
30 (1995) 79-85
16.0mA. Thus, using a gastroesophagealelectrode system,ventricular pacing can be achieved successfully,and the availability of such a systemcould play a major role in resuscitation of patients from severebradyarrhythmias. Improved outcome witb floid restriction io treatment of onconbollcd hcmurrhagic shwk
Capone AC, Safar P, Stezoski W, Tisherman S, Peitzman AB Presbyterian University Hospital, Pittsburgh, PA 15213, USA
J Am Coil Surg 1995; 180/l; 49-56 BACKGROUND: Recent studies have challenged current guidelines for prehospital fluid resuscitation. However, longterm studies evaluating the consequencesof fluid restriction in uncontrolled hemorrhagic shock are lacking. This study was done to examine the long-term effectsof deliberate hypotension in the treatment of uncontrolled hemorrhage. STUDY DESIGN: Uncontrolled hemorrhagic shock was produced in 40 rats by a preliminary bleed (3 ml per 100 g) followed by 75% tail amputation. Experimental design consistedof three phases: a ‘pre-hospital phase’ (90 min of uncontrolled bleeding with or without treatment with lactated Ringer’s [LR] solution), followed by a ‘hospital phase’ (60 mitt, including control of hemorrhage and fluid resuscitation including blood), and a three day observation phase. Forty rats were studied in four treatment groups (ten rats per group). Group 1 consistedof untreated controls (no resuscitation). Group 2 had no fluid during the prehospital phase. Group 3 had prehospital resuscitation to a mean arterial pressure (MAP) of 40 mmHg with LR, and group 4 had prehospital resuscitation to MAP of 80 mmHg with LR. Groups 2, 3, and 4 received fluid and blood to MAP of 80 mmHg and hematocrit of 30% in the hospital phase. RESULTS: All rats in group 1 (untreated) died within 2.5 h. Five rats in group 2 (no prehospital FR) survived 90 min; however, only one survived three days. In group 3, all ten rats survived 2.5 h and six survived three days. In group 4, eight rats died within 90 min, but none survived long-term. Blood loss (ml per 100 g) for each group was 3.75 0.6 for group 1, 3.35 0.1 for group 2, 4.15 0.8 for group 3, and 8.45 0.6 for group 4, (p < 0.05, group 4 compared with groups 1, 2, and 3). CONCLUSIONS: Attempts to achieve normal MAP during uncontrolled bleeding increased blood loss, hemodilution and mortality. Hypotensive resuscitation resulted in less acidemia and improved long-term survival. EQb atria1 natrioretic peptide concentrations blunt tbe pressor response du&g cardiopulmonary resnscitrtioo in humaos
Paradis NA, Wortsman J, Malarkey WB, Martin GB, Goetting MG, Feingold M, Nowak RM 48 Remsen Street, Brooklyn, NY 11201-4106. USA
Crit Care Med 1994;22/2 (213-218) Objective: To determine the relationship of circulating atria1 natriuretic peptide concentrations to the pressor response to high-doseepinephrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest. Design: Prospective study. Patients: Fourteen normothennic, adult, prehospital and emergency department patients suffering unexpected cardiac arrest. Intervention: Patients received high-dose epinephrine