scispace - formally typeset
Search or ask a question
Author

William Stezoski

Bio: William Stezoski is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Clinical death & Resuscitation. The author has an hindex of 19, co-authored 67 publications receiving 1721 citations.


Papers
More filters
Journal ArticleDOI
TL;DR: Postischemic neurological deficit is at least partially due to impaired reperfusion and can be ameliorated or prevented by blood flowing-promoting therapy by therapy enhanced constriction of pupils and normalization of the electroencephalogram.
Abstract: To determine the efficacy of cerebral microcirculation promoting therapy in postischemic brain failure, 11 dogs awakening from methohexital sodium anesthesia were subjected to 12 minutes of reversible circulatory arrest by ventricular fibrillation. Physiological variables were controlled for six hours after resuscitation, and the dogs were observed for seven days. Six dogs without the special postresuscitative therapy did not awaken, and either died within 36 hours or remained comatose for seven days. In five dogs, a combination of the following measures was applied: (1) mean arterial pressure was raised to 150 to 180 mm Hg with norepinephrine for six hours; (2) heparinization; (3) rapid intra-aortic injection of dextran 40 (10 ml/kg body weight); and (4) normovelemic hemodilution with dextran 40 to a hematocrit reading of 25% to 30%. All five treated dogs awakened within 24 hours and appeared normal on the seventh day. Therapy enhanced constriction of pupils and normalization of the electroencephalogram (P less than .05). Postischemic neurological deficit is at least partially due to impaired reperfusion and can be ameliorated or prevented by blood flowing-promoting therapy.

241 citations

Journal ArticleDOI
TL;DR: In this article, the long-term effects of deliberate hypotension in the treatment of uncontrolled hemorrhage were evaluated in 40 rats by a preliminary bleed (3 mL per 100 g) followed by 75 percent tail amputation.

240 citations

Journal Article
TL;DR: Attempts to achieve normal MAP during uncontrolled bleeding increased blood loss, hemodilution and mortality, andHypotensive resuscitation resulted in less acidemia and improved long-term survival.
Abstract: BACKGROUND Recent studies have challenged current guidelines for prehospital fluid resuscitation. However, long-term studies evaluating the consequences of fluid restriction in uncontrolled hemorrhagic shock are lacking. This study was done to examine the long-term effects of 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 percent tail amputation. Experimental design consisted of three phases: a "prehospital phase" (90 minutes of uncontrolled bleeding with or without treatment with lactated Ringer's [LR] solution), followed by a "hospital phase" (60 minutes, 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 consisted of 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 mm Hg with LR, and group 4 had prehospital resuscitation to MAP of 80 mm Hg with LR. Groups 2, 3, and 4 received fluid and blood to MAP of 80 mm Hg and hematocrit of 30 percent in the hospital phase. RESULTS All rats in group 1 (untreated) died within 2.5 hours. Five rats in group 2 (no prehospital FR) survived 90 minutes; however, only one survived three days. In group 3, all ten rats survived 2.5 hours and six survived three days. In group 4, eight rats died within 90 minutes, 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.

237 citations

Journal ArticleDOI
TL;DR: It is documented that a calcium entry blocker, given after cardiac arrest, can ameliorate late postischemic neurologic deficit (ND) and ND scores improved consistently through the 96-h observation period in the lidoflazine-treated dogs.
Abstract: Calcium entry blockers can ameliorate postischemic cerebral hypoperfusion, protect the myocardium against ischemia, and may protect against early postischemic neurologic deficit. This study documents that a calcium entry blocker, given after cardiac arrest, can ameliorate late postischemic neurologi

161 citations

Journal ArticleDOI
TL;DR: It is concluded that, in this model, immediate postinsult hypothermia of 31 degrees C for 5 hours prevents a rise in IVP and significantly decreases cerebral tissue damage, but does not prevent brain herniation during rewarming.
Abstract: A canine model of temporary epidural cerebral compression and standardized intensive care was developed to evaluate the effect of resuscitative (postinsult) moderate systemic hypothermia. A balloon was inflated over the temporal region to maintain contralateral intraventricular pressure (IVP) at 62 mm Hg for 90 minutes. For a 66-hour period after initiation of brain compression, the intubated dogs received controlled ventilation and standard intensive care. From 66 to 90 hours postinjury, the extubated dogs were evaluated as to functional outcome. Morphological brain damage was evaluated at 90 hours or earlier if brain death occurred. Eight dogs in a control group were maintained at a body of temperature of 38 degrees C. Eight treated dogs had core body temperature reduced by surface cooling starting 15 minutes after balloon inflation, first to 31 degrees C for 5 hours and then to 35 degrees C from 5 to 62 hours after insult. Intraventricular pressure increased to 20 mm Hg or greater in the control group at a mean of 2.9 hours (range 2 to 4 hours) following the insult, and in the hypothermic group at a mean of 14.8 hours (range 5 to 30 hours)--that is, during the time period when the body temperature was 35 degrees C, not 31 degrees C (p = 0.01). There was no difference in peak pressures between the two groups. Brain death occurred in four of the eight dogs in the normothermic group at 18, 24, 24, and 48 hours (mean +/- standard deviation 28 +/- 13 hours) and in three of the eight in the hypothermic group at 27, 42, and 45 hours (mean 38 +/- 10 hours) (not significant). The animals surviving 90 hours (four in the normothermic and five in the hypothermic group) were neurologically near normal. The total mean macroscopically damaged brain volume was 2584 +/- 1890 cu mm in the normothermic versus 765 +/- 611 cu mm in the hypothermic group (p = 0.03). The mean necrotic volume was 741 +/- 599 cu mm in the normothermic versus 263 +/- 346 cu mm in the hypothermic group (p = 0.07). Microscopically, the damaged regions consisted of ischemic neurons, reactive glia, edema, vascular endothelial hypertrophy, and erythrocyte extravasation. It is concluded that, in this model, immediate postinsult hypothermia of 31 degrees C (not 35 degrees C) for 5 hours prevents a rise in IVP and significantly decreases cerebral tissue damage, but does not prevent brain herniation during rewarming.

92 citations


Cited by
More filters
Journal ArticleDOI
TL;DR: The goal of immediate post-cardiac arrest care is to optimize systemic perfusion, restore metabolic homeostasis, and support organ system function to increase the likelihood of intact neurological survival.
Abstract: There is increasing recognition that systematic post–cardiac arrest care after return of spontaneous circulation (ROSC) can improve the likelihood of patient survival with good quality of life. This is based in part on the publication of results of randomized controlled clinical trials as well as a description of the post–cardiac arrest syndrome. 1–3 Post–cardiac arrest care has significant potential to reduce early mortality caused by hemodynamic instability and later morbidity and mortality from multiorgan failure and brain injury. 3,4 This section summarizes our evolving understanding of the hemodynamic, neurological, and metabolic abnormalities encountered in patients who are initially resuscitated from cardiac arrest. The initial objectives of post–cardiac arrest care are to ● Optimize cardiopulmonary function and vital organ perfusion. ● After out-of-hospital cardiac arrest, transport patient to an appropriate hospital with a comprehensive post–cardiac arrest treatment system of care that includes acute coronary interventions, neurological care, goal-directed critical care, and hypothermia. ● Transport the in-hospital post–cardiac arrest patient to an appropriate critical-care unit capable of providing comprehensive post–cardiac arrest care. ● Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest.

2,590 citations

Journal ArticleDOI
TL;DR: This poster presents a poster presented at the 2016 International Congress of the American College of Vascular Surgery (ICS) entitled “Cardiology and Vascular Surgeons: Foundations of Cardiac Rhythm Management, 2nd Ed.”

1,291 citations

Journal ArticleDOI
TL;DR: This scientific statement outlines current understanding and identifies knowledge gaps in the pathophysiology, treatment, and prognosis of patients who regain spontaneous circulation after cardiac arrest to provide a resource for optimization of post–cardiac arrest care.
Abstract: The contributors to this statement were selected to ensure expertise in all the disciplines relevant to post–cardiac arrest care. In an attempt to make this document universally applicable and generalizable, the authorship comprised clinicians and scientists who represent many specialties in many regions of the world. Several major professional groups whose practice is relevant to post–cardiac arrest care were asked and agreed to provide representative contributors. Planning and invitations took place initially by e-mail, followed a series of telephone conferences and face-to-face meetings of the cochairs and writing group members. International writing teams were formed to generate the content of each section, which corresponded to the major subheadings of the final document. Two team leaders from different countries led each writing team. Individual contributors were assigned by the writing group cochairs to work on 1 or more writing teams, which generally reflected their areas of expertise. Relevant articles were identified with PubMed, EMBASE, and an American Heart Association EndNote master resuscitation reference library, supplemented by hand searches of key papers. Drafts of each section were written and agreed on by the writing team authors and then sent to the cochairs for editing and amalgamation into a single document. The first draft of the complete document was circulated among writing team leaders for initial comment and editing. A revised version of the document was circulated among all contributors, and consensus was achieved before submission of the final version for independent peer review and approval for publication. This scientific statement outlines current understanding and identifies knowledge gaps in the pathophysiology, treatment, and prognosis of patients who regain spontaneous circulation after cardiac arrest. The purpose is to provide a resource for optimization of post–cardiac arrest care and to pinpoint the need for research focused on gaps in knowledge that would potentially improve outcomes …

1,222 citations

Journal ArticleDOI
TL;DR: A randomized, controlled trial compared the effects of moderate hypothermia and normothermia in 82 patients with severe closed head injuries and found thatHypothermia may limit some of the deleterious metabolic responses of traumatic brain injury.
Abstract: Early reports of therapeutic hypothermia for severe traumatic brain injury can be traced back to the first half of the 20th century. It is only within the last two decades that clinical studies have demonstrated that therapeutic moderate hypothermia for brief durations can improve patient outcomes following brain injury. The historical background, recent clinical experience, and mechanisms of action of moderate hypothermia are reviewed.

1,212 citations