Beneficial effects of vasopressin in prolonged pediatric cardiac
arrest: a case series
Keith Mann
a, Robert A. Berg
b, Vinay Nadkarni
c,*
aDepartment of Pediatrics,Thomas Jefferson Uni6ersity School of Medicine,A.I.duPont Hospital for Children,1600Rockland Road,
Wilmington,DE19899,USA
bSteele Memorial Children’s Research Center,The Uni6ersity of Arizona College of Medicine,1501N.Campbell A6enue,P.O.Box245073,
Tucson,AZ85724-5073,USA
cDepartment of Pediatrics,Thomas Jefferson School of Medicine,Department of Anesthesia and Critical Care,
A.I.duPont Hospital for Children,P.O.Box269,1600Rockland Road,Wilmington,DE19899,USA Received 17 August 2001; received in revised form 31 August 2001; accepted 31 August 2001
Abstract
Children who suffer cardiac arrest have a poor prognosis. Based on laboratory animal studies and clinical data in adults, vasopressin is an exciting new vasopressor treatment modality during cardiopulmonary resuscitation (CPR). In particular, vasopressin has resulted in short term resuscitation benefits as a ‘rescue’ pressor agent in the setting of prolonged out-of-hospital CPR for ventricular fibrillation in adults. This retrospective series presents the first evidence for resuscitation benefit of bolus vasopressin therapy in the specific setting of pediatric cardiac arrest. All episodes of CPR initiated in a 120-bed tertiary care children’s hospital over a three-year period (1997 – 2000) were reviewed. Four children in the pediatric ICU received vasopressin boluses as rescue therapy during six cardiac arrest events, following failure of conventional CPR, advanced life support, and epinephrine vasopressor therapy. Return of spontaneous circulation for greater than 60 min occurred in three of four patients (75%) and in four of six CPR events (66%) following vasopressin administration. Two of four vasopressin recipients survived\24 h; one survived to hospital discharge and one had withdrawal of supportive therapies following family discussion. Our observations are AHA level 5 (retrospective case series) evidence that vasopressin administration may be beneficial during prolonged pediatric cardiac arrest. Such reports should pave the way for prospective clinical trials comparing vasopressor medications in the setting of pediatric cardiac arrest. © 2002 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Vasopressin; Resuscitation; Cardiac arrest; Cardiopulmonary resuscitation (CPR); Children; Pediatric; Epinephrine; Vasopressor therapy
www.elsevier.com/locate/resuscitation
1. Introduction
Children who suffer cardiac arrest have a poor prog-nosis, particularly when cardiac arrest is prolonged or refractory to more than two doses of epinephrine [1 – 6]. Recent AHA International Consensus Pediatric Resus-citation Guidelines recommend vasopressors for
pedi-atric cardiac arrest, although most pharmacologic agents have little data to support their use [1,7 – 9]. Many of the AHA recommendations for pediatric re-suscitation are based on data extrapolated from studies in adults, animal laboratory experiments, and studies of pediatric resuscitation medications in the non-arrest setting. This experience is supplemented by anecdotal retrospective clinical reports during cardiopulmonary resuscitation (CPR) in children. Lack of data and the continuing dismal outcomes of pediatric arrest drive the search for improved pharmacotherapy of pediatric car-diac arrest [8].
In the recent AHA International Guidelines for Car-diopulmonary Resuscitation and Emergency
PII of linked article: S0300-9572(01)00496-8
* Corresponding author. Present address: Director, Pediatric Criti-cal Care Fellowship Program, Department of Anesthesia and CritiCriti-cal Care, Children’s Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, PA 19104-4309. Tel.: + 1-215-590-1868; fax: +1-215-590-4327.
E-mail address:nadkarni@email.chop.edu(V. Nadkarni).
0300-9572/02/$ - see front matter © 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S 0 3 0 0 - 9 5 7 2 ( 0 1 ) 0 0 4 7 0 - 1
vascular Care, vasopressin is recommended as an alter-native vasopressor for shock refractory ventricular fibrillation cardiac arrest in adults (Class IIB) [1]. This recommendation was based on extensive animal labora-tory data and promising initial out-of-hospital human data in adults in the setting of prolonged CPR and advanced life support. However, no survival benefits were demonstrated in a randomized controlled com-parison of early vasopressin versus epinephrine in an adult in-hospital setting with rare ventricular fibrilla-tion, early CPR, early ALS, and early pressor adminis-tration [10]. Vasopressin has been reported to exert pressor effects in infants and children in the non-car-diac arrest settings of circulatory shock [11] and during brain death evaluation [12]. However, there are no reports of vasopressin benefit or harm in the specific setting of pediatric cardiac arrest. On the basis of these data, the AHA pediatric recommendation for vaso-pressin in the setting of cardiac arrest is classified as ‘Indeterminate’ [1].
The purpose of this retrospective case series is to report successful return of spontaneous circulation after the rescue administration of vasopressin following pro-longed cardiac arrest and failure of conventional CPR, advanced life support and epinephrine therapy in chil-dren. This clinical series applies evidence of beneficial vasopressin pressor effect extrapolated from laboratory animal studies, adult clinical trials, and pediatric non-arrest settings to the specific setting of pediatric cardiac arrest. Such reports should pave the way for prospec-tive clinical trials comparing vasopressor medications in the setting of pediatric cardiac arrest.
2. Methods
All documented episodes of CPR initiated in a 120-bed tertiary care children’s hospital from 1997 to 2000 were reviewed for vasopressin administration during CPR with advanced life support. Cardiac arrests with CPR initiated in the pre-hospital setting were excluded. Process and outcome variables were recorded and ana-lyzed using the operational definitions from the in-hos-pital Utstein style guidelines, modified in accordance to the pediatric Utstein style and pediatric International Liaison Committee on Resuscitation (ILCOR)
recom-mendations [2,7,9]. Cardiopulmonary resuscitation
events triggering review by investigators were defined according to Utstein and AHA National Registry of CPR criteria [2,13]: either chest compressions and as-sisted ventilation provided because of cardiac arrest, or chest compressions provided because of bradycardia
with poor perfusion. Cardiac arrest is defined as the
cessation of cardiac mechanical activity, determined by the inability to palpate a central pulse, unresponsive-ness, and apnea. The major outcome variables included
any return of spontaneous circulation (ROSC), ROSC
for \20 min, ROSC for \60 min, survival for \24 h
and survival to hospital discharge. The ‘end of arrest’ time was documented, but the exact time that the first spontaneous pulse or blood pressure occurred was not universally documented. This time was extrapolated from nursing notes, progress notes, and the code blue record. Vasopressin was assumed to relate to ROSC only when it was the last medication given before documented ROSC.
The patients in this series all received standard AHA CPR and pediatric advanced life support [1] including immediate assisted and invasive ventilation, continuous electrocardiogram (ECG) monitoring, invasive arterial blood pressure monitoring, exhaled CO2 monitoring during resuscitation, immediate intravascular access, and early medication interventions with standard
epinephrine dosing (10 mcg/kg) repeated every 3 min.
Reversible causes of arrest (e.g. hypoxemia,
hypov-olemia, hypothermia, hypokalemia, hyperkalemia,
toxin or metabolic cause, severe acidosis, tension pneu-mothorax, tamponade, thromboembolus) were treated if present, early in resuscitation. A board certified pedi-atric intensive care physician was present and directing care throughout the resuscitation. Vasopressin was ad-ministered late in resuscitation as an ‘intervention of last resort’ at the discretion of the attending physician. In this hospital, standardized pediatric advanced life support protocols are practiced weekly in supervised multidisciplinary mock code scenarios throughout the
hospital. Synthetic 8-L-arginine vasopressin (American
Regent pharmaceuticals, 20 U/ml, 1 ml/vial) is available
on all code carts. Transthoracic defibrillation is
pro-vided with an Agilent/HP Codemaster defibrillator
de-livering a standard damped sinusoidal, monophasic waveform. Peak energy is manually set by protocol to 2
J/kg for initial shocks, and to 4 J/kg for subsequent
shocks. A designated in-hospital code blue team re-sponds to arrests with immediate supervision by a board certified pediatric critical care or emergency medicine attending physician. All variables and out-come measures reported are routinely recorded for continuous quality improvement purposes and partici-pation in the AHA National Registry of CPR [13], and families sign consent for use of such data for research review.
3. Results
All 70 in-hospital cardiopulmonary resuscitation
events documented during the three-year period from 1997 to 2000 were reviewed by two authors
indepen-dently. Vasopressin was provided in six cardiac arrests
among four children. All cardiac arrests in this case
pedi-atric ICU. Vasopressin was only administered after failure to respond to initial conventional CPR and advanced life support, including at least two doses of intravenous epinephrine.
The characteristics, interventions and outcomes of the six cardiac arrest events are reported in Table 1. The initial cardiac arrest rhythm was a form of
pulse-less electrical activity in all six cardiac arrests (ECG=
wide complex with rate B50 per minute in three
events, narrow complex with rate B50 per minute in
two events and wide complex with rate \150 per
minute in one event). At the time of vasopressin admin-istration, arrest ECG rhythm was asystole in four events, pulseless ventricular tachycardia in one event, and ventricular fibrillation in one event. The mean duration of CPR was 28.3 min in these six cardiac arrests with vasopressin administration, with a range of 12 – 55 min, and a median of 24 min.
ROSC occurred in three of four patients (75%), and in four of six cardiac arrests with vasopressin adminis-tration (66%). All cardiac arrest victims who responded
to vasopressin with ROSC sustained ROSC for \60
min. Two of the four vasopressin recipients (50%)
survived \24 h. One survived to hospital discharge
with neurologic function close to baseline level of neu-rologic function on admission (see Section 4). The other 24-h survivor died following family decision to limit and then withdraw ICU technological support.
In three of four events where vasopressin resulted in
ROSC \60 min, the ROSC occurred after the second
0.4 U/kg dose of vasopressin. In the five events where
more than one dose of vasopressin was administered, the mean time between first and second doses of vaso-pressin was 9.8 min with a range of 3 – 20 min and a median of 6 min. In the four events where vasopressin administration was associated with ROSC, the mean time from the last dose of vasopressin to ROSC was 2 min with a range of 1 – 3 min and a median of 2 min.
4. Case example
A 5-year-old with cerebral palsy, developmental de-lay, seizure disorder controlled by ketogenic diet, and nephrolithiasis was admitted with sepsis syndrome. On the third day of hospital admission she developed acute respiratory failure, shock and profound hypotension. Following tracheal intubation, mechanical ventilation, fluid boluses and support with IV epinephrine and dopamine infusions, she was transferred to the pediatric ICU.
Fifteen hours later, after stabilization on infusions of
central venous epinephrine (1 mcg/kg/min) and
do-pamine (5 mcg/kg/min), she developed pulseless
electri-cal activity: narrow complex bradycardia without pulses. Immediate effective ventilation via tracheal tube
and chest compressions guided by arterial pressure
waveform was initiated. Two bolus doses of
epinephrine (10 mcg/kg), one dose of atropine (0.02
mg/kg), two doses of high dose epinephrine (100 mcg/
kg), an attempt at transcutaneous pacing, calcium
glu-conate (50 mg/kg) and a dose of 0.4 U/kg of central
venous6asopressindid not restore effective spontaneous
circulation at 10 min into the resuscitation. ECG rhythm appeared as fine ventricular fibrillation without detectable pulse and was refractory to defibrillation
attempts and magnesium sulfate (50 mg/kg). A second
dose of 0.4 U/kgVasopressinwas given via central vein
and circulated by CPR for 1 min, followed by success-ful transthoracic defibrillation. ROSC occurred 16 min after the initiation of chest compressions, with a sinus
rhythm at a rate of 102/min and blood pressure of
80/52 mmHg. Over the next 5 days she was stabilized
and weaned from pressors. She remained on mechanical ventilator dependent secondary to airway obstruction from oral secretions and poor swallowing function. She required tracheostomy and returned close to her
devel-opmentally delayed neurologic baseline within 3
months after the arrest.
5. Discussion
Cardiopulmonary arrest in children often occurs as a terminal event in the course of a prolonged illness rather than as a primary cardiac event [2 – 9]. Although nearly two-thirds of children attain ROSC after in-hos-pital pediatric CPR and approximately one-third sur-vive for 24 h, only 10 – 18% sursur-vive an entire year [5,6]. Cardiac arrest is also uncommon in children. It has been reported that less than 2% of children admitted to
a pediatric ICU setting require CPR for \2 min, with
survival to hospital discharge following cardiac arrest reported at 13.7% [4]. Despite international consensus pediatric resuscitation guidelines and improvements in pediatric critical care, children who suffer cardiac arrest continue to have a poor prognosis [1 – 7,14].
There are currently a limited number of medications used in pediatric cardiac arrest and very limited data to support their use [1,8,9]. Although many pharmacologic agents have been proposed, little data exists to support their use in the specific setting of cardiac arrest in children. Much of the data is extrapolated from studies in animal laboratories, adult clinical trials, and usage of these medications in pediatric non-arrest settings. To some extent, this information is often supplemented by anecdotal retrospective clinical case series during CPR in children. The lack of data and the continuing dismal outcomes of pediatric arrest drive the search for im-proved pharmacotherapy of pediatric cardiac arrest. Following the implementation of the 1992 AHA guide-lines [15], the major international resuscitation councils
Table 1 Characteristics, interventions a nd outcomes o f four cardiac arrest patients c 1 c 2 c 3 c 4 Patient Age 5 years 3 m onths 7 m onths 1 8 m onths Male Female Male Female Sex Co-morbidities Septic shock; Adult respiratory distress syndrome; Disseminated intravascular Viral pneumonitis; Chronic Tracheal narrowing; GE Septic shock, Delayed lung disease, GE re fl ux; re fl ux; 3 h after cardiac development, Seizures coagulopathy; Renal failure arrest at home Prior cardiac arrest at home c 1 c 1 c 1 c 2 c 3 c 1 Arrest c Wide complex bradycardia, Narrow complex Wide complex tachycardia, Narrow complex Initial rhythm Wide complex Wide complex bradycardia, PEA bradycardia, PEA bradycardia, PEA bradycardia, PEA No pulse PEA Wide complex tachycardia, Asystole Ventricular fi brillation Asystole Asystole Asystole Rhythm a t time No pulse of VP dose Epinephrine a, A tropine, Epinephrine a, Epinephrine a, Epinephrine a, Epinephrine a, Epinephrine a, A tropine, Bolus medication Epinephrine a, Epinephrine a, E pinephrine a, B icarbonate, interventions C alcium, B icarbonate, Epinephrine a, A tropine, Calcium, EPINEPHRINE a, Epinephrine a, Atropine, Bicarbonate, Atropine, Epinephrine a, Steroids, Epinephrine a, Bicarbonate, Calcium, Bicarbonate, Calcium, Bicarbonate, Calcium, EPINEPHRINE a, Bicarbonate, Calcium, Bicarbonate, EPINEPHRINE a, Vasopressin , Vasopressin Bicarbonate, Calcium, Epinephrine a, C alcium, Epinephrine a, A tropine, Epinephrine a, Vasopressin , B icarbonate, Calcium, EPINEPHRINE a, C alcium, Bicarbonate, Vasopressin , Vasopressin , Glucagon EPINEPHRINE a, A tropine, Magnesium, Vasopressin , Magnesium, Lidocaine, Vasopressin Vasopressin Bicarbonate, Vasopressin , Vasopressin Amiodarone, Vasopressin 16 min 15 min 1 2 m in 40 min Arrest duration 32 min 5 5 m in No Yes Y es Yes ROSC \ 20 min N o Yes 2m in N / A 2 3m in 6m in 5m in Time from 1st N / A VP to ROSC 3m in 1m in N / A 2 m in N / A N / A Time from 2nd VP to ROSC No Yes Y es Yes ROSC \ 60 min Y es No Yes ROSC \ 24 h Yes No No No No Died Died after 23 days b Died Li 6 ed Hospital discharge ( DNAR ) outcome Abbreviations: VP, vasopressin; ROSC, Return of Spontaneous C irculation; PEA, Pulseless Electrical Activity; GE re fl ux; G astro-Esophageal Re fl ux; DNAR, Do Not Attempt Resuscitation. aEpinephrine: dose o f 1 0 m cg / kg IV; EPINEPHRINE: high dose of 100 mcg / kg IV. bTwenty-three days following ROSC, the family decided to establish DNAR orders and withdraw technological support.
developed ILCOR advisory statements reflecting con-sensus recommendations based on existing resuscitation guidelines, practical experience, and debate of an inter-national resuscitation database [7,9]. Recently, the AHA and ILCOR modified an evidence based review template and applied it to key resuscitation issues in order to update the PALS guidelines, assign classes of recommendations where possible, and objectively at-tempted to link the class of recommendation to the identified level of evidence [16]. This international evi-dence based review of advanced life support therapies for cardiac arrest resulted in AHA recommendations for vasopressin as Class IIB in adults and Indetermi-nate in children for shock refractory ventricular fibrilla-tion cardiac arrest [1].
Vasopressin is an endogenous hormone that acts at specific receptors to cause vasoconstriction. There are three different receptors involved, V1a, V1b, and V2. V1a receptors are localized to the vasculature and,
when stimulated, cause vasoconstriction [17,18]. Inlab
-oratory animal in6estigations using swine cardiac arrest
models have established that vasopressin administration during CPR shunts more blood flow to the heart and brain and away from less vital organs, when compared with epinephrine administration [19,20]. Concerns have been raised about the decreased splanchnic blood flow during CPR after vasopressin and worse post-resuscita-tion myocardial funcpost-resuscita-tion [21]. Nevertheless, short- and long-term survival in these animal models is consis-tently superior after vasopressin [22 – 27]. Recent animal studies indicate that vasopressin is well absorbed via the intravenous, intraosseous or endobronchial routes during CPR. Importantly, the same dose by either of these routes is as effective as an intravenous dose [28,29]. These experimental findings are especially rele-vant for pediatric resuscitation where intravenous ac-cess can be problematic.
Data from swine models of pediatric cardiac arrests and asphyxial cardiac arrests are more complex,
per-haps due to developmental differences and/or
mecha-nistic differences from adult ventricular fibrillation induced cardiac arrest models. In a piglet model of prolonged cardiac arrest after asphyxia, vasopressin alone during CPR was less effective than epinephrine alone, whereas vasopressin plus epinephrine was as effective as epinephrine alone [30]. Similarly, in a swine model of adult asphyxial cardiac arrest, the combina-tion of vasopressin plus epinephrine resulted in superior coronary perfusion pressure and superior survival when compared with epinephrine alone or vasopressin alone [31]. Finally, in a pediatric porcine model of ventricular
fibrillation, the combination of vasopressin and
epinephrine resulted in higher left ventricular blood flow than either vasopressin alone or epinephrine alone, and both vasopressin plus epinephrine and vasopressin alone resulted in superior cerebral blood flow compared
with epinephrine alone [32]. It is important to note that all of the pediatric patients in this case series received the combination of both vasopressin and epinephrine (i.e. vasopressin rescue following epinephrine failure); none received vasopressin alone.
In reported adult cardiac arrest experience, initial
evidence of acute beneficial vasopressin pressor effect during CPR for adult cardiac arrest is very encouraging when CPR or advanced life support interventions are delayed or prolonged. In an initial in-hospital case series, ROSC was attained following prolonged CPR in eight patients with rescue vasopressin treatment of ven-tricular fibrillation refractory to defibrillation attempts and epinephrine. Three of these eight survived to hospi-tal discharge [33]. In a randomized, controlled out-of-hospital trial, 40 adults with delayed CPR, advanced life support interventions, and shock refractory ventric-ular fibrillation received either 1 mg of epinephrine or
40 U of intravenous vasopressin. Seventy percent (14/
20) of vasopressin treated patients versus 35% (7/20) of
epinephrine treated patients survived to hospital
admis-sion (P=0.06). Sixty percent (12/20) of the vasopressin
treated patients versus 20% (4/20) of the epinephrine
treated patients survived 24 h (PB0.02) [34]. In
con-trast, there were no differences in outcome from a larger, randomized, controlled in-hospital study com-paring early vasopressin versus epinephrine during CPR for adult cardiac arrest. In distinction from the out-of-hospital study, these patients received early CPR, early advanced life support and early vasopressor therapy [10]. Whether vasopressin therapy is beneficial in the setting of adult or pediatric cardiac arrest is still in question.
In thenon-cardiac arrest setting, clinical use of
vaso-pressin infusions as an effective vasopressor agent in infants and children is well established [11,12]. One retrospective case-control series analyzed 63 critically ill children during brain death evaluation and organ re-covery; 34 received very low dose vasopressin infusion for treatment of diabetes insipidus. Children who re-ceived vasopressin infusions maintained higher average mean arterial pressures on fewer vasopressor agents than carefully matched controls [12]. Pressor effects of vasopressin were likewise demonstrated in 11 pediatric post-operative cardiac patients with vasodilatory hy-potension refractory to high dose pressor infusion ther-apy [11]. Thus, vasopressin is an effective vasopressor in children, and by extrapolation, may be beneficial in some pediatric cardiac arrest settings.
To our knowledge, this is the first case series describ-ing the use of vasopressin durdescrib-ing cardiac arrest in children. After high doses of epinephrine and early, appropriate advanced life support interventions had failed to restore spontaneous circulation, the immediate effects of this ‘rescue medication’ were quite remark-able. Despite the historically poor outcomes following
prolonged in-hospital cardiac resuscitation efforts, three of these four patients treated with rescue vasopressin
responded with initial ROSC (\60 min). Two of the
four patients survived 24 h despite very prolonged CPR, including multiple doses of epinephrine. These encouraging hemodynamic and short-term benefits of vasopressin are consistent with data from laboratory animal studies, adult human clinical trials and pediatric non-cardiac arrest experience.
Although temporal relationships to outcome can be inferred, no single intervention in this in-hospital ICU setting is likely to be solely responsible for successful resuscitation or intact neurologic survival. All cardiac arrests occurred in a pediatric ICU setting where imme-diate and effective CPR and invasive advanced life support interventions were provided and continuous monitoring was available. Despite this, there was lim-ited response to conventional advanced life support interventions and CPR duration was prolonged. It is difficult to extrapolate this data to a much less con-trolled, pre-hospital setting. However, it is important to note that vasopressin appeared to exert some beneficial effect, even when administered very late into resuscita-tion efforts and for rhythms other than ventricular fibrillation.
Several limitations are acknowledged. As with all retrospective chart reviews, documentation was occa-sionally less than optimal and exact time intervals are suspect. Where exact time intervals were not specifically documented, data was extrapolated from each chart by two investigators independently. The ‘end of arrest’ time was always documented, but the exact time that the first spontaneous pulse or blood pressure occurred was necessarily extrapolated from progress notes, nurs-ing documentation, and code blue data sheets. In addi-tion, case series cannot control for, but can only emphasize the importance of, controlling for potential confounding variables such as duration of arrest, re-sponse intervals for CPR and advanced life support interventions, time to first vasopressor, concurrent vasopressor medications, dose, dose interval, and se-quence of vasopressor administration. It will be impor-tant for future clinical trials to carefully account for these resuscitation variables. Finally, case series only serve as AHA level of evidence 5 (Table 2) [1] or preliminary evidence for intervention effect in cardiac arrest research, and caution regarding enthusiasm for widespread use of vasopressin during cardiac arrest is warranted.
6. Conclusions
This case series is the first to report the beneficial effects of vasopressin during pediatric cardiac arrest, in the setting of prolonged in-hospital resuscitation with
Table 2
Summary of AHA-emergency cardiovascular care levels of evidence overview
Level 1 Positive RCTs: prospective, randomized clinical trials or meta-analyses of multiple clinical trials with substantial treatment effects
Level 2 Neutral RCTs: prospective, randomized clinical trials with smaller or less significant treatment effects Prospective cohort studies: non-randomized, Level 3
prospective observational study of a group: must have a control group for comparisons
Retrospective observational studies with controls; Level 4
historic, non-randomized, cohort or case-control studies
Le6el5 Case series:patients compiled in serial fashion,lacking a control group
Level 6 Animal studies or mechanical model studies (sub-level A indicates study higher quality and better design than sub-level B)
Extrapolations from existing data collected for other Level 7
purposes, theoretical analyses and quasi-experimental designs
Rational conjecture (common sense); no evidence of Level 8
harm, common practices accepted before evidence-based guidelines
Abbreviation: RCT, Randomized Controlled Trial.
aggressive CPR and advanced life support. Our obser-vations suggest that vasopressin administration can contribute to successful return of spontaneous circula-tion in children when convencircula-tional advanced life sup-port and pressor therapy have failed. Preliminary evidence, like this case series, are important to pave the way for controlled, prospective study of vasopressin in the specific setting of pediatric cardiac arrest.
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Portuguese Abstract and Keywords
As crianc¸as que sofreram paragem cardı´aca teˆm um mau progno´stico. Baseados em estudos animais laboratoriais e em dados clı´nicos de adultos, a vasopressina surgiu como uma nova modalidade de terapia vasopressora durante a reanimac¸a˜o cardiopul-monar (RCP). A utilizac¸a˜o da vasopressina resultou em efeitos bene´ficos na reanimac¸a˜o a curto prazo em casos de paragem cardı´aca por fibrilhac¸a˜o ventricular em adultos fora do hospital. Esta se´rie retrospectiva representa a primeira evideˆncia dos efeitos bene´ficos da terapeˆutica com a vasopressina no caso especı´fico da paragem cardı´aca pedia´trica. Foram revistos todos os casos de RCP iniciados num hospital pedia´trico tercia´rio de 120 camas durante um perı´odo de 3 anos (1997 – 2000). Quatro crianc¸as na UCI (Unidade de Cuidados Intensivos Pedia´trica) receberam bolus de vasopressina como terapeˆutica de ‘salvamento’ durante seis episo´dios de paragem cardı´aca depois de as manobras convencionais de RCP, suporte avanc¸ado de vida e terapeˆutica vasopressora com epinefrina, terem falhado. O retorno de circulac¸a˜o espontaˆnea por mais de 60 minutos ocorreu em treˆs de
quatro doentes (75%) e em quatro de seis episo´dios de RCP (66%) apo´s a administrac¸a˜o de vasopressina. Dois de quatro receptores de vasopressina sobreviveram mais de 24 horas; um sobreviveu a` alta hospitalar e num outro foram suspensas as medidas terapeˆuticas de suporte apo´s discussa˜o com a famı´lia. Estas observac¸o˜es sa˜o nı´vel 5 da AHA (Uma se´rie de casos retrospectivos) que evidenciam que a administrac¸a˜o de vasopressina pode ser bene´fica durante paragens cardı´acas pedia´tricas prolongadas. Estes relatos devem abrir o caminho para a realizac¸a˜o de estudos clı´nicos prospectivos comparando medicamentos vasopressores no contexto de paragem cardı´aca pedia´trica.
Pala6ras cha6e: Vasopressina; Reanimac¸a˜o; Paragem cardı´aca; Reanimac¸a˜o cardiopulmonar (RCP); Crianc¸as; Pediatria; Epinefrina; Terapeˆutica vasopressora
Spanish Abstract and Keywords
Los nin˜os que sufren paro cardı´aco tienen un prono´stico pobre. En base a estudios de laboratorio y datos clı´nicos en adultos, la vasopresina es una nueva modalidad de tratamiento vasopresor durante la resucitacio´n cardiopulmonar (CPR). En particular, la vasopresina ha resultado en beneficios a corto plazo en la resucitacio´n como un agente presor ‘de rescate’ en la escena de fibrilacio´n ventricular en adultos con CPR extrahospitalaria prologada. Esta serie retrospectiva presenta la primera evidencia para los beneficios de terapia con bolos de vasopresina en el caso especı´fico de paro cardı´aco pedia´trico. Se revisaron todos los episodios de CPR ocurridos en un perı´odo de tres an˜os (1997 – 2000) en un hospital pedia´trico de cuidados terciarios con 120 camas. Cuatro nin˜os en la unidad de cuidados intensivos (ICU) recibieron bolos de vasopresina como terapia de rescate durante seis eventos de paro cardı´aco, despue´s del fracaso de la CPR convencional, soporte vital avanzado, y terapia vasopresora con adrenalina. Hubo retorno a circulacio´n esponta´nea despue´s de la administracio´n de vasopresina en tres de cuatro pacientes (75%) y en cuatro de seis eventos de CPR (66%). Dos de cuatro receptores de vasopresina sobrevivieron \24 horas; uno sobrevivio´ al alta y a uno se le suspendieron las terapias de soporte despue´s de discusio´n con la familia. Nuestras observaciones son evidencia de nivel 5 de la AHA (series de casos retrospectivas) que apoya que la administracio´n de vasopresina puede ser beneficiosa durante el paro cardı´aco pedia´trico prolongado. Estos reportes allanan el camino para ensayos clı´nicos prospectivos comparando la medicacio´n vasopresora en paro cardı´aco pedia´trico.
Palabras cla6e: Vasopresina; Resucitacio´n; Paro Cardı´aco; Resucitacio´n cardiopulmonar (CPR) R6CP; nin˜os; Pediatrico; Adrenalina; Terapia vasopresora