Cuidados Post PCR

Cuidados post PCR
adultos
Pablo Aguilera F
Instructor adjunto
Programa Medicina de Urgencia
Curso de Reanimación 2012
www.urgenciauc.cl
Cadena de sobrevida
Cuidados post PCR=
Síndrome post PCR
Introducción
• ¿Sirve de algo reanimar personas en PCR?
• Mayores costos, baja sobrevida, escases de
recursos.
• Evolución en el tiempo...
• Nuevas terapias específicas en sindrome
post PCR
Introducción
• “Enfermedad post reanimación”.
• Acuñado por Dr.Vladimir Negovsky 1970
• 2008 nace término SPPCR guías ILCOR
• “No sólo ROSC es importante sino
secuelas funcionales”
• Conceptos de reanimación cardiocerebral
o CCR
Reanimación
Cardiocerebral (CCR)
• Representa una serie de de terapias
específicas destinadas para mejorar la
perfusión durante RCP.
• Implementado en Wisconsin año 2003.
• Particularmente útil en pacientes con PCR
presenciado: Reserva funcional de O2
ordingly, is a
U.S., as a cause
ths combined
in 1974 (19),
elines in 1992
(7) for emerCLS, with rare
HCA remains
rvival rates in
90; and in Los
gher than 1%,
l futility (22).
e who receive
ose with rapid
ea et al. (29),
with witnessed
ed their EMS
mmediate chest
alysis of postrecommended
% (29).
CPR has herent pathophysiin which the
arrest who receive prompt bystander resuscitation efforts.
Most bystanders who witness a cardiac arrest are willing to
alert EMS but are not willing to initiate bystander rescue
efforts because they are not willing to perform mouth-tomouth ventilation. Training and certification in basic life
Pilares CCR
Three Pillars of Cardiocerebral Resuscitation
Table 1
Three Pillars of Cardiocerebral Resuscitation
1. CCC (compression-only cardiopulmonary resuscitation) by anyone who
witnesses unexpected collapse with abnormal breathing (cardiac arrest).
2. Cardiocerebral resuscitation by emergency medical services (arriving during
circulatory phase of untreated ventricular fibrillation [e.g., !5 min])
a. 200 CCCs (delay intubation, second person applies defibrillation pads and
initiates passive oxygen insufflation).
b. Single direct current shock if indicated without post-defibrillation pulse
check.
c. 200 CCCs prior to pulse check or rhythm analysis.
d. Epinephrine (intravenous or intraosseous) as soon as possible.
e. Repeat (b) and (c) 3 times. Intubate if no return of spontaneous circulation
after 3 cycles.
f. Continue resuscitation efforts with minimal interruptions of chest
compressions until successful or pronounced dead.
3. Post-resuscitation care to include mild hypothermia (32°C to 34°C) for
patients in coma post-arrest. Urgent cardiac catheterization and percutaneous
coronary intervention unless contraindicated.
CCC " continuous chest compression.
n
Cardiocerebral resuscitation was begun in November 2003
in Tucson, Arizona, and by 2007 was being used throughout
the majority of the state. In 2005, the AHA updated their
guidelines and incorporated some of the changes made with
CCR (52). In 2008, the AHA published a science advisory
statement supporting chest compressions only for bystander
response to adult cardiac arrest (71). Table 3 compares
current aspects of CCR with the AHA 2005 guidelines and
their 2008 advisory statement.
Uninterrupted perfusion to the heart and brain by CCC
prior to defibrillation during cardiac arrest is essential to
JACCneurologically
Vol. 53, No. 2, normal
2009 survival. The low incidence of
bystander-initiated
resuscitation efforts in patients with cardiac
January
13, 2009:149–57
arrest is a major public health problem. We have long advocated CCC CPR by bystanders as a solution to this critical
issue because eliminating mouth-to-mouth “rescue breathing”
will go a long way toward increasing the incidence of
bystander-initiated resuscitation efforts. It is exciting to see that
a technique (chest compression–only CPR) that had not been
heretofore formally taught results in the same or better neurologically normal survival rates than those achieved with techniques taught for decades. CCR also changes the approach of
those delivering ACLS. These changes resulted in dramatic
(250% to 300%) improvement in survival of patients most
likely to survive: those with witnessed cardiac arrest and
shockable rhythm. More aggressive post-resuscitation care,
including hypothermia and emergent cardiac catheterization
and PCI, is required to save even more victims of sudden
cardiac arrest.
Por qué cambiar
conceptos?...
) oxygen (3). This is referred
n.
ned in Figure 1.
and Walworth counties in
2004 (3). Using a historical
rs following the 2000 AHA
atic increase in neurologically
he mean survival to hospital
c function was 15% in the 3
year when CCR was provided
all number of witnessed arrests
ieve, suggesting a significant
m et al. (5) 3-year experience
ted. Neurologic intact survival
40% (including 1 patient who
s, there may well have been a
the first year. Nevertheless, in
essed cardiac arrest and shockaramedics, there was dramatic
Reprint requests and correspondence: Dr. Gordon A. Ewy,
University of Arizona Sarver Heart Center, University of Arizona
College of Medicine, Tucson, Arizona 85724. E-mail: gaewy@
aol.com.
Figure 2
Neurologically Normal Survival of
Patients With Witnessed Out-of-Hospital
REFERENCES
Cardiac Arrest and a Shockable Rhythm
1. Ewy G. Cardiocerebral resuscitation: the new cardiopulmonary resusThis figure contrasts the percent of patients with witnessed out-of-hospital
car- 2005;111:2134 – 42.
citation. Circulation
2.
Kern
KB,
Valenzuela
TD, Clark LL, et al. An alternative approach to
diac arrest and a shockable electrocardiographic rhythm upon arrival of emeradvancing resuscitation science. Resuscitation 2005;64:261– 8.
gency medical services (EMS) who survived neurologically intact
before MJ, Kennedy KW, Ewy GA. Cardiocerebral resuscitation
3. Kellum
survival of patients with out-of-hospital cardiac arrest. Am J
(cardiopulmonary resuscitation [CPR]) and after the institution ofimproves
cardiocerebral
Med 2006;119:335– 40.
resuscitation (CCR). Of note is the fact that only 1 patient in the CCR group
received hypothermia therapy post-resuscitation. The approach used by EMS
during the CPR period was that of the 2000 American Heart Association and
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
Fisiopatología
• Componentes del SPPCR
– Daño Cerebral post PCR
– Disfunción Miocárdica post PCR
– Respuesta Sistémica a isquemia/reperfusión
– Persistencia de Patología precipitante de PCR
Isquemia global y reperfusión
10
Neumar et al
6-12 hours
Immediate
Early
Intermediate
Prognostication
72 hours
Rehabilitation
Rehabilitation
Recovery
Disposition
Prevent Recurrence
20 min
Goals
Limit ongoing injury
Organ support
ROSC
Phase
Figure. Phases of post– cardiac arrest syndrome.
51 children who survived out-of-hospital cardiac arrest had
either pediatric CPC 1 to 2 or returned to their baseline
neurological state.20 The CPC is an important and useful
outcome tool, but it lacks the sensitivity to detect clinically
Post–Cardiac Arrest Syndrom
from 8% to 16%.22,23 Although this is clearly a po
these patients can and should be considered
donation. A number of studies have reported no d
transplant outcomes whether the organs were ob
appropriately selected post– cardiac arrest patie
other brain-dead donors.23–25 Non– heart-beating
tion has also been described after failed resuscitat
after in- and out-of-hospital cardiac arrest,26,27 bu
generally been cases in which sustained ROSC
achieved. The proportion of cardiac arrest patie
the critical care unit and who might be suitable
beating donors has not been documented.
Despite variability in reporting techniques,
little evidence exists to suggest that the in-hospi
rate of patients who achieve ROSC after cardia
changed significantly in the past half-century. T
artifactual variability, epidemiological and in
post– cardiac arrest studies should incorporate w
standardized methods to calculate and report mo
at various stages of post– cardiac arrest care,
long-term neurological outcome.16 Overriding th
a growing body of evidence that post– cardiac
impacts mortality rate and functional outcome.
IV. Pathophysiology of Post–Car
Arrest Syndrome
The high mortality rate of patients who initia
ROSC after cardiac arrest can be attributed t
pathophysiological process that involves mult
Although prolonged whole-body ischemia init
global tissue and organ injury, additional dam
during and after reperfusion.28,29 The unique
post– cardiac arrest pathophysiology are often su
on the disease or injury that caused the cardiac ar
as underlying comorbidities. Therapies that focus
ual organs may compromise other injured organ s
Objetivos generales del
manejo
• Mantener adecuada oxigenación.
• Mantener perfusión de órganos
• Soporte de sistemas dañados
• Resolución de causa de base
Global ischemia-reperfusion
injury
post-resuscitation disease
Ischemia
VF = ventricular fibrillation
ROSC= return of spontaneous circulation
13
Table 1.
Post–Cardiac Arrest Syndrome: Pathophysiology, Clinical Manifestations, and Potential Treatments
Syndrome
Post– cardiac arrest brain
injury
Pathophysiology
●
●
●
Post–cardiac arrest myocardial
dysfunction
●
●
Impaired cerebrovascular
autoregulation
Cerebral edema (limited)
Postischemic
neurodegeneration
Global hypokinesis
(myocardial stunning)
ACS
Clinical Manifestation
●
●
●
●
●
●
●
●
●
Coma
Seizures
Myoclonus
Cognitive dysfunction
Persistent vegetative state
Secondary Parkinsonism
Cortical stroke
Spinal stroke
Brain death
●
●
●
●
Reduced cardiac output
Hypotension
Dysrhythmias
Cardiovascular collapse
Potential Treatments
●
●
●
●
●
●
●
●
●
●
●
●
●
Systemic ischemia/reperfusion
response
●
●
●
●
●
●
Persistent precipitating
pathology
●
●
●
●
●
●
●
Systemic inflammatory
response syndrome
Impaired vasoregulation
Increased coagulation
Adrenal suppression
Impaired tissue oxygen
delivery and utilization
Impaired resistance to
infection
●
●
●
●
●
●
●
Ongoing tissue hypoxia/ischemia
Hypotension
Cardiovascular collapse
Pyrexia (fever)
Hyperglycemia
Multiorgan failure
Infection
Cardiovascular disease
(AMI/ACS,
cardiomyopathy)
Pulmonary disease
(COPD, asthma)
CNS disease (CVA)
Thromboembolic disease
(PE)
Toxicological (overdose,
poisoning)
Infection (sepsis,
pneumonia)
Hypovolemia
(hemorrhage,
dehydration)
●
Specific to cause but complicated
by concomitant PCAS
●
●
●
●
●
●
●
●
Therapeutic hypothermia177
Early hemodynamic
optimization
Airway protection and
mechanical ventilation
Seizure control
Controlled reoxygenation
(SaO2 94% to 96%)
Supportive care
Early revascularization of
171, 373
AMI
Early hemodynamic
optimization
Intravenous fluid97
Inotropes97
IABP13,160
LVAD161
ECMO361
Early hemodynamic
optimization
Intravenous fluid
Vasopressors
High-volume hemofiltration374
Temperature control
Glucose control223,224
Antibiotics for documented
infection
Disease-specific interventions
guided by patient condition
and concomitant PCAS
AMI indicates acute myocardial infarction; ACS, acute coronary syndrome; IABP, intra-aortic balloon pump; LVAD, left ventricular assist device; EMCO, extracorporeal
membrane oxygenation; COPD, chronic obstructive pulmonary disease; CNS, central nervous system; CVA, cerebrovascular accident; PE, pulmonary embolism; and
PCAS, post– cardiac arrest syndrome.
excitotoxicity, disrupted calcium homeostasis, free radical
Prolonged cardiac arrest can also be followed by fixed or
Daño cerebral post PCR
• Causa frecuente de morbi-mortalidad de
pacientes.
• En algunos trabajos es la causa de un 70%
de mortalidad.
• Causa: Mala tolerancia a la isquemia y
respuesta a la reperfusión.
Daño cerebral post PCR
• Mecanismos involucrados complejos:
•
Toxicidad por neuromediadores
•
Dis-regulación de la homeostasis del calcio
•
Formación de radicales libres
•
Activación de cascadas de proteasas
•
Activación de mecanismos apoptóticos
Daño cerebral post PCR
• Se altera la auto-regulación de flujo
cerebral.
• Infartos e isquemia en regiones cerebrales.
• Trombosis microvascular.
• Más significativo si PCR es prolongado
• Reperfusión hiperémica como causal de
daño y edema.
FSC (ml/100gr/min
Hipotenso
Rango de
perfusión
normal
Edema
Hipertenso
Isquemia
PAM (mm Hg)
Brain injury after cardiac arrest
4 min
4-10 min
> 10 min
Duration of CA
Electrical Circulatory Metabolic
Electrical & Circulatory reduction of the
duration of global ischemia (primary brain
injury)
Metabolic attenuation of post-resuscitation
disease due to reperfusion injury (secondary
brain injury)
4
Hypothermia after cardiac arrest
Hipotermia
terapéutica
Hypothermia
cardiac arrest
a treatment that after
works
!
a treatment that works !
number needed to treat : 6
Curr Opin Crit Care, 2003;9:205
Crit Care Med, 2005;33(2):414
number needed to treat : 6
Curr Opin Crit Care, 2003;9:205
Crit Care Med, 2005;33(2):414
30
30
Hipotermia terapéutica
• Trabajos RCT 2002
• Australiano y Europeo
• Hipotermia Leve ( 32-34 grados).
36
36
Crit Care Med 2004
25
Enfermedad post
Reanimación
hipotermia
26
Hypothermia after cardiac arrest
a treatment that works !
*
*
*
*
*
*
529529
patients
involved
in 6 studies
pacientes
en 6 estudios
29
Therapeutic hypothermia
duration of cardiac arrest
Irrespective to the presence of shock or the
initial rhythm, the predicted benefit of
hypothermia is strongly dependent on
the duration of cardiac arrest
Oddo M, Crit Care Med, 2006;34(7):1865
27
Protocolo Hipotermia UC
Protocolo0de0Hipotermia0Inducida
Medicina0de0UrgenciaV0Unidad0de0Cuidados0Intensivos0PUC
Nombre:
Hora0Inicio:
Fecha:
Rut: Rut:
•Paro Cardiorrespiratorio (cualquier ritmo, cualquier lugar)
Lugar0inicio0de0hipotermia:00UCI0000000000000URGENCIA
Criterios0de0Inclusión0(debe0cumplir0todos)
Post0PCR0(cualquier0ritmo0como0causa0es0eligible)
0Duración0maniobras0menos0300min0hasta0
recuperación0pulso.
Menos0de060horas0desde0recuperación0pulso0hasta0el0
minuto.
Comatoso0(0no0obedece0órdenes)
PAM0>0650con0no0más0de0un0vasopresor.
en paciente mayores 15 años.
Criterios0de0Exclusión
•Duración maniobras resucitación < 45 minutos.
Orden0de0no0reanimar,0status0basal0pobre,0enfermedad0
terminal
Hemorragia0intracerebral0acRva
PCR0de0eRología0traumáRca
Crioglobulinemia
Embarazo0(relaRva/0consulta0gineVobs)
Cirugía0Mayor0reciente0(relaRva)
Sepsis0como0causa0PCR0(0relaRva)
•Retorno a circulación espontanea (RCE)
Evaluar
Criterios
Exclusión
•Paciente en coma
(En Hoja
Protocolo)
Ingresar en
carpeta
Hipotermia
Paciente candidato Hipotermia
Examen0neurológico
Apertura(ocular((((((((((((((((Verbal(((((((((((((((((((((((((((((((((((Motor(((((((((((((((((((((((((((((Troncoencéfalo
Espontánea0…..000*00000000000Orientado………000*00000000000000Obedece…….000000000000000000Pupilas0reacRvas0000000000000000SI00000000NO000000000000000
Voz……………….0 0*00000000000Confuso…………00.0*00000000000000Localiza……….00000000000000000Corneales0000000000000000000000000000SI00000000NO0
Dolor0……………0 00000000000000Inapropiada……00000000000000000000ReRra………….00000000000000000Respiración0espontánea000SI00000000NO0
Ninguna………..00000000000000000Sonidos…………..0000000000000000000DecorRca…….00000000000000000Ojos0de0Muñeca0000000000000000SI00000000NO0
0
00000000000000Ninguno…………..000000000000000000Descerebra…
0
00000000000000Intubado0………..0000000000000000000Ninguno………
Registrar Historia Clínica
Discutir
Protocolo Con
Familiares
Monitorización
(según
-Avisar a equipo
Hipotermia
protocolo)
Exámenes iníciales
- Solicitar cama UCI
ROT00000000000000000000000000000000000Bicipital00I000D0000000000000000000000000Rotuliano00000I0000000D000000000Aquiliano00000000000I000000D
Indicar0fármacos0sedantes0o0Relajantes0musculares0al0momento0del0examen
Item(que(presente((*)(excluye(paciente(de(protocolo
Protocolo
Iden>ficar(caso(elegible.(Ac>var(equipo(hipotermia(UrgenciaEUCI.
1. DiscuRr0caso0con0residente0de0UCI0o0staff0(0deben0estar0de0acuerdo0con0la0hipotermia0y0debe0haber0cama0de0UCI0disponible0en0las0
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
0
siguientes0horas)0.0Evaluar0causas0eRológicas0PCR0,0evaluar0necesidad0de0acRvación0hemodinamia.
ECG0y00eventual0Ecocardiograca00por0cardiología.
Hora0discusión:0______________0.0Si0paciente0no0es0elegible0por0UCI,00indique0razón0_____________________________000
Enviar0exámenes0de0sangre0con:0ELPV0CELLDYNV0COAGULACIÓNV0LACTATO0VENOSOV0GASES0VENOSOSV0ENZIMAS0CARDÍACASV0LIPASAV0
AMILASAVCLASIFICACIÓN
20Vías0venosas0periféricas0gruesas
Foley0y0medir0diuresis0
Exponer0paciente0completamente
Preparar0para0monitoreo0hemodinámico0invasivo0en0servicio0de0urgencia
Registrar0temperatura0corporal0rectal0o0esofágica:0_______________
Preparar0sedación0con0midazolam0–fentanyl.0Para0SAS0score001V2
Inicio0infusión0de0SF00,9%0a04°C0.0Máximo0bolo030cc/kg0.0Velocidad0infusión00~1000ml/min0con0apuradores0de0suero0.0Hora0_______
Si0temperatura0inicial0es00<34°C,0mantener0a033°C0
Si0paciente0inicia0calofríos,0Vecuronio00,10mg/kg0x010vez
Traslado0a0UPCV00en0caso0de0no0contar0con0cama0disponible
La0temperatura0a0lograr0es033°C.0Luego0de0terminada0la0infusión.0Bolos02500cc00SF0frío00
Solicitar0equipo0coolgard®0a0UCI0para0hipotermia0intravascular
Fijar0temperatura0a033°C0y0programar0máquina0a0enfriamiento0máximo.
Vol.0total0de0cristaloides0infundidos0_________________________0000Hora0que00paciente0logra00temperatura033°C______________
Si0paciente0presenta00sangrado0significaRvo0o0inestabilidad0hemodinámica0severa,0considerar0recalentar.
Hora0de0recalentamiento0_______________________000000Causa0que0moRvó0recalentamiento________________________0
Mantener0PAM0>0800Rtular00con0norV0adrenalina__________________________0000Dosis0máxima0:_______________________
Notas:
Notas:
Traslado
UCI
Inicio de Hipotermia
Sedación y
relajo
Muscular
Temperatura
central 33°C
Control
laboratorio
según protocolo
Aguilera, Alvizú et al
Disfunción Miocárdica post
RCP
• “Stunning” miocárdico
• Disfunción transitoria
• IC menor a 2
• 48- 72 horas de duración
• Enfermedad coronaria asociada
• Reperfusión precoz en todos los pacientes
Reperfusión Miocárdica
•
•
•
•
•
•
•
Protocolo intervencional
Hipotermia + angiografía precoz
Ewy and Kern
Cardiocerebral Resuscitation
JACC Vol. 53, No. 2, 2009
January 13, 2009:149–57
68 pacientes
28. Bohm K, Rosenqvist M, Herlitz J, Hollenberg J, Svensson L. Survival
is similar after standard treatment and chest compression only in
out-of-hospital bystander cardiopulmonary resuscitation. Circulation
2007;116:2908 –12.
29. Rea TD, Helbock M, Perry S, et al. Increasing use of cardiopulmonary
resuscitation during out-of-hospital ventricular fibrillation arrest: survival implications of guideline changes. Circulation 2006;114:2760 –5.
30. Steen S, Liao Q, Pierre L, Paskevicius A, Sjöberg T. The critical
importance of minimal delay between chest compressions and subsequent defibrillation: a haemodynamic explanation. Resuscitation 2003;
58:249 –58.
31. Becker L, Berg R, Pepe P, et al. A reappraisal of mouth-to-mouth
ventilation during bystander-initiated cardiopulmonary resuscitation. A
statement for healthcare professionals from the Ventilation Working
Group of the Basic Life Support and Pediatric Life Support Subcommittees, American Heart Association. Circulation 1997;96:2102–12.
32. Standards and guidelines for cardiopulmonary resuscitation (CPR) and
emergency cardiac care (ECC). JAMA 1986;255:2905– 89.
33. SOS-KANTO Study Group. Cardiopulmonary resuscitation by bystanders with chest compression only (SOS-KANTO): an observational study. Lancet 2007;369:920 – 6.
34. Ewy GA. Cardiac arrest— guideline changes urgently needed. Lancet
2007;369:882– 4.
35. Abella BS, Aufderheide TP, Eigel B, et al. Reducing barriers for
implementation of bystander-initiated cardiopulmonary resuscitation. A
15 vivos
50. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give
basic cardiopulmonary resuscitation to patients with out-of-hospital
ventricular fibrillation: a randomized trial. JAMA 2003;289:1389 –95.
51. Wik L, Kramer-Johansen J, Myklebust H, et al. Quality of cardiopulmonary resuscitation during out-of-hospital cardiac arrest. JAMA
2005;293:299 –304.
52. International Liaison Committee on Resuscitation. 2005 international
consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation
2005;67:181–341.
53. Aufderheide T, Sigurdsson G, Pirrallo R, et al. Hyperventilationinduced hypotension during cardiopulmonary resuscitation. Circulation 2004;109:1960 –5.
54. Aufderheide TP. The problem with and benefit of ventilations: should
our approach be the same in cardiac and respiratory arrest? Curr Opin
Crit Care 2006;12:207–12.
55. Schoenenberger RA, von Planta M, von Planta I. Survival after failed
out-of-hospital resuscitation. Are further therapeutic efforts in the
emergency department futile? Arch Intern Med 1994;154:2433–7.
56. Sunde K, Pytte M, Jacobsen D, et al. Implementation of a standardised
treatment protocol for post resuscitation care after out-of-hospital
cardiac arrest. Resuscitation 2007;73:29 –39.
57. Hypothermia after Cardiac Arrest Study Group. Mild hypothermia to
improve the neurologic outcome after cardiac arrest. N Engl J Med
2002;346:549 –56.
96% tenían lesiones coronarias
82% con lesiones criticas
OR 27
157
Respuesta sistémica a
isquemia/reperfusión
• Estado de Shock más severo
• RCP suple la necesidad de manera parcial y
muchas veces precaria.
• Se activan cascadas inmunológicas y de
coagulación que incrementan las
infecciones y disfunciones.
Respuesta sistémica a
isquemia/reperfusión
• Micro trombosis
• SIRS post ROSC
• Terapia orientada por metas
Persistencia de patología
precipitante de PCR
•
•
•
•
•
•
•
SCA
Enfermedades pulmonares
Hemorragia
Sepsis
Toxidromes
Alteraciones HEL
Otras
Estrategias terapéuticas
• Monitoreo estricto
• Optimización hemodinámica precoz guiada
por metas.
• Oxigenación
• Ventilación
• Soporte Circulatorio.
• Manejo SCA
Estrategias terapéuticas
• Sedación y RNM
• Manejo de convulsiones
• Control glicemia
• Neuroprotección farmacológica.
• Disfunción Adrenal.
• Falla Renal
Cuidados post PCR en
situaciones especiales
• Post hipotermia
• Post trombolisis
• Etc etc etc etc.
Pronósticos
• No existen protocolos de pronósticos
establecido
• Predicción Multimodal pareciera ser lo
mejor.
• No es útil los criterios clásicos
Neumar et al
6-12 hours
Immediate
Early
Intermediate
Prognostication
72 hours
Rehabilitation
Rehabilitation
Recovery
Disposition
Prevent Recurrence
20 min
Goals
Limit ongoing injury
Organ support
ROSC
Phase
Figure. Phases of post– cardiac arrest syndrome.
51 children who survived out-of-hospital cardiac arrest had
either pediatric CPC 1 to 2 or returned to their baseline
neurological state.20 The CPC is an important and useful
outcome tool, but it lacks the sensitivity to detect clinically
Post–Cardiac Arrest Syndrom
from 8% to 16%.22,23 Although this is clearly a po
these patients can and should be considered
donation. A number of studies have reported no d
transplant outcomes whether the organs were ob
appropriately selected post– cardiac arrest patie
other brain-dead donors.23–25 Non– heart-beating
tion has also been described after failed resuscitat
after in- and out-of-hospital cardiac arrest,26,27 bu
generally been cases in which sustained ROSC
achieved. The proportion of cardiac arrest patie
the critical care unit and who might be suitable
beating donors has not been documented.
Despite variability in reporting techniques,
little evidence exists to suggest that the in-hospi
rate of patients who achieve ROSC after cardia
changed significantly in the past half-century. T
artifactual variability, epidemiological and in
post– cardiac arrest studies should incorporate w
standardized methods to calculate and report mo
at various stages of post– cardiac arrest care,
long-term neurological outcome.16 Overriding th
a growing body of evidence that post– cardiac
impacts mortality rate and functional outcome.
IV. Pathophysiology of Post–Car
Arrest Syndrome
The high mortality rate of patients who initia
ROSC after cardiac arrest can be attributed t
pathophysiological process that involves mult
Although prolonged whole-body ischemia init
global tissue and organ injury, additional dam
during and after reperfusion.28,29 The unique
post– cardiac arrest pathophysiology are often su
on the disease or injury that caused the cardiac ar
as underlying comorbidities. Therapies that focus
ual organs may compromise other injured organ s
Post-Cardiac Arrest Syndrome Management
Who needs this?
Resuscitated patients with:
GCS Motor score < 6
No other reason for coma
Not DNR B/C or DNI status
Getting Started:
Algoritmo propuesto!
Use 2 liters of 4 C saline
(peripheral IV preferred) if
initiating TH
500 ml IVF over 5 min q 20
min until CVP > 8
If no CHF, continue IVF to get
MAP > 80, CVP > 8, but < 20
PA catheter if CVP >15 or > 5
liters IVF or CHF or
significant vasopressor need
Stat ECG, echocardiogram, & cardiology consult (Please see TH
protocol for instructions regarding Stat ECG, Echo & Cards consult)
Stat head CT if deemed medically necessary
Initiate therapeutic hypothermia (TH) & place radial or femoral a-line
Insert PreSep® CVC in subclavian or internal jugular vein
Notify Super SAR for ICU bed and EEG fellow for EEG
If pregnant, consult Ob/Gyn
< 80
> 100
MAP
CVP > 8
> 80
< 80
Start IV NTG at 10 mcg/min. Titrate to
MAP < 100. Assure adequate CVP
Consider Furosemide if CHF
If tachycardic or ACS* w/ normal EF &
Scv02 then consider Esmolol
If EF is normal, use Norepinephrine (1-20 mcg/min)
If EF, start Dobutamine (2.5-20 mcg/kg/min); If
MAP , add Norepinephrine
Ongoing hypotension, consider 2nd vasopressor
If severe hypotension-> IABP
80-100
(Consider > 65 if ACS*, CHF, Shock)
Yes
ScvO2
65%
No
If evidence of shock is present:
Optimize CVP if not already done (up to 20)
Transfuse PRBC’s if hemoglobin 10 mg/dL
Dobutamine if not already initiated
Consider RHC if CVP>15 or escalating vasopressors
No
MAP, CVP, ScvO2 goals achieved
Monitor serial lactate to rule out
inadequate organ perfusion
ScvO2<65%
w/ shock?
Yes
Re-evaluate to achieve goal
Consider IABP
* ACS=Acute coronary syndrome
Updated 07/2010