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Journal Latinoamericano de Medicina Veterinaria de Emergencia y Cuidados
Intensivos
Use of Vasopressors and Whole Blood in Hemorrhagic Shock in Swine
Autor:
Martins,A.R.C
1
*; Voorwald, F
2
; Nani, R.S
3
; Rocha Filho, J.A
3
1 - PhD student in anesthesiology at FM-USP
2 - PhD student in surgery at UNESP-Jaboticabal
3 - Medical Research at Medical Research Laboratory of Liver Transplantation, FM-USP.
*doutorevet@usp.br
JLAVECC ISSN 1688-6100 3(3) 2011, pp 261-265
Fecha: 2011-08-01
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Resmenes Comunicaciones Cientficas y Casos Clnicos en Medicina de Emergencia y Cuidados Intensivos en Animales de
Compaa presentados en el 4 Congreso Latinoamericano de Emergencias y Cuidados Intensivos, LAVECCS
Abstract
Hemorrhagic shock (HS) is the second leading cause of early mortality in trauma, accounting for 40% of
deaths. The ideal strategy for resuscitation in HS is yet undetermined but it is recognized that this
should include the prevention of cardiac arrest, the progression to refractory shock and rescue of prolonged
shock1-3. Patients with HS are exposed to pathophysiologic processes and therapeutic interventions,
particularly blood transfusion, that may predispose to hyperkalemia (hiperK), one of the most lethal electrolyte
disturbances4. The aim of the study was to compare the hemodynamic and microcirculatory states after using
a rapid infusion of whole blood associated with vasopressors.
The conclusion of this experimental work was that blood transfusion should be administered at a low constant
rate in order to prevent an acute increase of blood K. Moreover, both whole blood and vasopressors are
indicated to prevent the harmful effects of HS over the organs.

Material and Methods
Twelve pigs were anesthetized and mechanically ventilated whose were submitted to surgical resection of the
liver or for autologous transplant, the animals selected for this study were the ones that presented hemorrhagic
shock. The shock was determined by the following criteria: blood loss ! 40% of total blood volume, central
venous oxygen saturation (SvO2) <70%, mean arterial pressure (MAP) " 50 mmHg and decreased cardiac
output (CO) 50% from baseline. After shock the animals were randomly divided into two groups: one
group were treated with vasopressin (0.01 IU/Kg/min), norepinephrine (0.3 mg/Kg) and Ringer's lactate (RL)
(20 mL/Kg aliquots of 20 minutes) to reach MAP values ! 60 mmHg (GI) or treatment with vasopressin and
norepinephrine in the same scheme, including blood transfusion stored for 10 days in a volume corresponding
to half of the lost in an infusion time of 20 minutes (GII). The animals were monitored for hemodynamic data,
through the femoral artery catheterization to measure blood pressure and blood sampling for blood gas
analysis and introduction of the Swan Guanz cateter 7.5 F for DC analysis, pulmonary artery pressure(PAP),
central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). The arterial blood and
central venous blood were analyzed at baseline (T0), at observation of the shock (T1), through every 15
minutes during treatment (T2, T3, T4, T5 and T6) and finally to 120 minutes after treatment (T7). Statistical
analysis was based on Student's t test and differences were considered significant when p <0.05.
RESULTS
Both groups showed a significant decrease in MAP, CO, PAP and SvO2 during hemorrhagic shock and a
significant increase in lactate levels (T1) compared toT0, no significant differences between groups. After
treatment, GI symptoms improved in all parameters that remained standard until the end of observation
period. However, the GII had improvement on parameters only until t3. During t4 GII observed a significant
increase in K levels, lactate and SvO2, while the CO, MAP and PAP decreased significantly when compared
to T0 (p <0.01) and when compared to G1.Following treatment the animals that received
blood showed a strong increase of the T wave, followed by ventricular fibrillation and death. The mortality
rate was 50% for group II, whereas in animals of GI there were no deaths within the first 3 hours.
Discussion - In a retrospective study of 138 pediatric cardiac arrest comparing patients who received blood
transfusions to those who have not, they found levels of serum potassium during cardiac arrest of 8.2 mEq/L
in transfused patients vs. 5.6 mEq/L in non-transfused. The data from their study showed that hiperK during
cardiac arrest could be explained as a consequence of transfusion of packed red blood cells in patients with
hipovolemic hypotension5. We believe that the behavior of potassium in acute HS is responsible
for hyperkalemia's characteristic and silent way to explain the little attention directed to this
14/03/12 20:07 Journal Laveccs
Pgina 2 de 3 http://www.journal.laveccs.org/full.php?id=294
for hyperkalemia's characteristic and silent way to explain the little attention directed to this
complication. The hiperK can't be seen in those who die early during resuscitation, as well as those
who regresses immediately resuscitation is successful, as demonstrated by some studies
6
.
Parameter Group T0 T1 T2 T3 T4
CO (L/min) G1
G2
3.6 0.4
4.0 0.4
1.3 0.3
1.5 0.5
3.2 0.2
3.5 0.3
3. 0 0.4
3.0 0.4
3.3 0.1
1.1 0.2*a
MAP (mmHg) G1
G2
86 10
84 8
48 10
44 5
90 5
86 4

88 6
80 3
85 8
40 4*a
SVO 2 (%) G1
G2
75 3.0
73 3
58 5
57 3
78 1
72 2
76 1
65 4a
75 2
89 1*a
PAP (mmHg G1
G2
18 2
20 3
8 3
10 2
29 4
28 4
29 5
18 4a

30 5
9 2*a
K (mmol/L) G1
G2
3.5 0.4
4.0 0.2
4.0 0.3
4.3 0.3
3.8 0.2
5.0 0.1a
3.9 0.1
6.1 0.8a
3.7 0.1
7.3 0.3*a
Lactate (mg/dL) G1
G2
19 8
20 10
47 8
50 8
40 3
45 6
35 5
47 3a
34 3
60 5*a
Table 1. Hemodynamic and metabolic parameters (meansd); CO: cardiac output; MAP: mean arterial pressure; SvO2: mixed
venous oxygen saturation; PAP: pulmonary artery pressure; K: potassium; *: different from T0; : different from T2; : different
from T3; a: different from group G1; p<0,05.

CONCLUSION
It is possible to conclude that replacement of blood in animals in HS should be slow and steady to avoid the
effects of high concentrations of K administration for a short period. These therapeutic interventions are
indicated to prevent the effects of HS on the organs.
Introduo
Choque hemorrgico (CH) constitui a segunda causa de mortalidade precoce no trauma, correspondendo a
40% dos bitos. A estratgia ideal de ressuscitao no CH ainda est para ser determinada, mas
reconhecido que esta deva incluir a preveno da parada cardaca, da progresso para o choque refratrio e
resgate do choque prolongado 1-3 . Pacientes com CH esto exposto processos fisiopatolgicos e
intervenes teraputicas, principalmente transfuso sangunea, que predispem hiperpotassemia (hiperK),
um dos distrbios eletrolticos mais letais 4 . O objetivo do estudo veio para comparar o estado hemodinmico
e microcirculatrio aps o uso de infuso rpida de sangue total associado a vasopressores.
Material e Mtodos- Foram anestesiados e ventilados mecanicamente doze porcos, submetidos resseco
cirrgica do fgado ou transplante autlogo, foram selecionados para este estudo os animais que
apresentaram choque hemorrgico. O choque foi determinado pelos seguintes critrios: perda de sangue !
40% do volume de total de sangue; saturao venosa central de oxignio (SvO2) <70%, presso arterial
mdia (PAM) "50 mmHg e diminuio do dbito cardaco (Dc) de 50% em relao ao basal. Aps o choque,
os animais foram divididos aleatoriamente em dois grupos: sendo que um grupo foi tratado com vasopressina
(0,01 UI / kg / min), noradrenalina (0,3 mg / kg) e soluo de Ringer lactato (RL) (20 mL / kg em alquotas de
20 minutos) at MAP alcanar valores ! 60 mmHg (GI) ou o tratamento com vasopressina e noradrenalina no
mesmo esquema, mas com a transfuso de sangue total armazenados por 10 dias num volume
correspondente a metade do volume perdido em um tempo de infuso de 20 minutos (GII). Os animais foram
monitorados por dados hemodinmicos, por meio da cateterizao da arteria femoral para aferio da
presso arterial e coleta de sangue para gasometria e introduo do cateter de Swan Guanz 7,5F para
analise do Dc; presso da arteria pulmonar (PAP); presso venosa central (PVC) e presso da artria
pulmonar ocluida (PAPo). A coleta do sangue arterial e venoso central foram analisados no momento basal
(T0), na constatao do choque (T1), e a cada de 15 minutos durante o tratamento (T2, T3, T4, T5 e T6) e,
finalmente, aos 120 minutos aps o tratamento (T7 ). A anlise estatstica baseou-se em t de Student e as
diferenas foram consideradas significativas quando P <0,05.
Resultados
Ambos os grupos mostraram uma diminuio significativa na PAM, Dc, PAP e SvO2 durante o choque
hemorrgico e um aumento significativo dos nveis de lactato (T1) em relao ao T0, sem diferenas
significativas entre os grupos. Aps o tratamento GI apresentou melhora em todos os parmetros que se
manteve normalizado at o final do perodo de observao. No entanto, para o GII a melhora dos parmetros
foi verificada somente at t3. Durante t4 do GII foi observado um aumento significativo nos nveis de K, lactato
e SvO2, enquanto o Dc, PAM e PAP diminuiu significativamente quando comparadas ao T0 (p <0,01), e em
relao ao G1. Na sequncia do tratamento os animais que receberam sangue mostraram um forte aumento
da onda T, seguido de fibrilao ventricular e morte. A taxa de mortalidade foi de 50% para os animais do GII,
enquanto que nos animais de GI no houve mortes dentro das primeiras 3 horas.
Discusso
Em estudo retrospectivo de 138 paradas cardacas peditricas comparando pacientes que receberam
transfuso sangunea com os que no receberam, encontraram nveis de potssio srico durante a parada
cardaca de 8,2 mEq/L nos pacientes transfundidos versus 5,6 mEq/L nos no transfundidos. Os dados de
seu estudo demonstraram que a hiperK durante a parada cardaca poderia ser explicada como conseqncia
da transfuso de concentrado de hemcias em pacientes com hipotenso hipovolmica
5
. Acreditamos que ao
comportamento agudo do potssio na do CH seja responsvel pela caracterstica silenciosa da
hiperpotassemia e possa forma explicar a pouca ateno direcionada a esta complicao. A hiperK pode no
ser percebida naqueles que morrem precocemente durante a ressuscitao, assim como regride
imediatamente naqueles que tem a ressucitao bem sucedida, conforme demonstrado por alguns estudos
6
.
Concluso
possvel concluir que a reposio de sangue nos animais em CH deve ser lenta e constante para evitar os
efeitos de altas concentraes de K administrao durante curto perodo. Essas intervenes teraputicas
14/03/12 20:07 Journal Laveccs
Pgina 3 de 3 http://www.journal.laveccs.org/full.php?id=294
efeitos de altas concentraes de K administrao durante curto perodo. Essas intervenes teraputicas
so indicadas para evitar as consequncias do CH sobre os rgos.
Referencias
1. Liberman M, Roudsari BS. Prehospital trauma care: what do we really know? Curr Opin Crit Care
2007;13:691-696;
2. Peruski AM, Cooper ES. Assessment of microcirculatory changes by use of sidestream dark field
microscopy during hemorrhagic shock in dogs. Am J Vet Res 2011;72:438-445;
3. Moochhala S, Wu J, Lu J. Hemorrhagic shock: an overview of animal models. Front Biosci 2009;14:4631-
4639;
4. Hall TL, Barnes A, Miller JR, et al. Neonatal mortality following transfusion of red cells with high plasma
potassium levels. Transfusion 1993;33:606-609;
5.Brown KA, Bissonnette B, MacDonald M, et al. Hyperkalaemia during massive blood transfusion in
paediatric craniofacial surgery. Can J Anaesth 1990;37:401-408;
6.Rocha Filho JA, Nani RS, D'Albuquerque LA, et al. Hyperkalemia accompanies hemorrhagic shock and
correlates with mortality. Clinics (Sao Paulo) 2009;64:591-597.

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