cpr 2013 handout
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CPR 2013 !
CPR 2013
Overview Guideline CPR 2010 What s new since 2010 Post resuscitation care Coronary angiography & PCI in Cardiac arrest
Chain of Survival
Basic Life Support
Advanced Cardiac Life Support
Summary of Key BLS Components "
>8 1-8
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Quality of CPRPush fast & hard
AHA: Depth>5cm & rate>100/minERC: Depth upto 6 cm & rate upto120/min
Decrease hand-off time
Near -infrared spectroscopy "
Monitoring of regional cerebral oxygenation during CPRusing portable near -infrared spectroscopy "
Airway
Lower Esophageal SphincterTone During Cardiac Arrest
20 mmHg 5mmHg
1/3 of OHCA have aspiration
Regurgitation of gastric content
Tracheal intubation
No study has shown a survival benet fortracheal intubation after cardiac arrest "
chest compression " Unrecognized esophageal intubation "
Waveform capnography "
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Supraglottic Airway Devices "Esophageal-tracheal "
combitube "Laryngeal mask airway "
(LMA)"i-Gel "
Waveform Capnography "
1. Proof a correct position of ET "When tracheal intubation is undertaken
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Mechanical chest compressions devices "
AutoPulse Lucas
ACLSCardiac ArrestAlgorithm
Drugs in CPR
Epinephrine Alpha and beta adrenergic effect
myocardial & cerebral blood flow duringCPR
Used in - cardiac arrest - symptomatic bradycardia - severe hypotension - anaphylaxis Dose CPR : 1 mg q 3-5 min. bolus flush
with 20 ml fluid or 10 mg+ Nss or D 5W 100ml IV
Vasopressin
Anti-diuretic hormone High dose -> non-adrenergic peripheral
vasoconstrictor T 10-20 min alternative for epinephrine in shock-refractory VF
patient Dose 40 U iv push x 1
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Vasopressin vs Epinephrine
Vasopressin for cardiac arrest: asystematic review and meta-analysis. ArchIntern Med. 2005;165:1724.
Aung K, Htay T. no statistically significant differences
between vasopressin & epinephrine for ROSC, 24-hour survival, or survival tohospital discharge.
CPR 2008 CPR 2008
Epinephrine 1mg +Vasopressin40iu vs Epinephrine 1 mg
the combination of vasopressin & epinephrine during ACLS for out-of-hospital cardiac arrest does not improve outcome
New Eng J Med 2008
Vasopressin, Epinephrine, and Corticosteroids for In-HospitalCardiac Arrest "
Combined vasopressin- epinephrine and methyl-prednisolone duringresuscitation and stress-dose hydrocortisone in post-resuscitation shockimproved survival in refractory in-hospital cardiac arrest "
Arch Intern Med. 2009;169(1):15-24 "
Vasopressin (20 IU /CPR cycle) + epinephrine (1 mg per resuscitation cycle)+methylprednisolone sodium succinate (40 mg) On the rst resuscitation cycle "
Amiodarone
Used in : VT/VF +/- arrest (FIRST CHOICE)
Dose Cardiac arrest : 300 mg in 20-30 ml
DW iv repeat once if necess 150mgiv
non-arrest : 150 mg in 10 min. Maintainance : then 1 mg/min x 6h and
0.5 mg/min later
Extracorporeal Life Support "
Observational studies showedhigher rate of survival discharge & 1year survival
Chen, Y. S. et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitationin adults with in-hospital cardiac arrest: an observational study and propensity analysis. Lancet 372, 554561 (2008). "
Percent of patients alive at various time points
Time pointCPR + extracorporeal
life support (%) CPR alone (%)24 h 65.2 41.3
3 d 52.2 34.8
14 d 37.0 23.9
30 d 34.8 17.4
6 mo 32.6 15.2
1 y 19.6 13.0
Chen Y-S et al. Lancet; published online before print July 7, 2008.
CPR with assisted extracorporeal life-support versusconventional CPR in adults with in hospital cardiac arrest:
an observational study and propensity analysis.
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Care After CardiacArrest
The greatest drop-off in survivaloccur in hospital "
J AC C : C AR D I O V A S C U L AR I N T E R V E N T I O N S , V O L . 5 , N O . 6 , 2 0 1 2 J U N E 2 0 1 2 : 5 9 7 6 0 5 "
Cause of Death
Out-of-hospital cardiac arrest = Neurologicalinjury
In-hospital cardiac arrest = Cardiovascular +
multiple organ failure
Post cardiac arrest syndrome "1.Precipitating pathology !
2.Neurologic dysfunction secondary to
anoxic brain injury !
3.Myocardial stunning and
dysfunction, !
4.Systemic ischemia/ reperfusion
response !
(1) Persistent precipitatingpathology
Pathophysiology Clinical Manifestation Potential Treatments
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 causebut complicatedby concomitant PCAS
Disease-specificinterventionsguided by patientconditionand concomitant PCAS
Post-Resuscitation Care
That Improve Outcome " Mild Therapeutic hypothermia after
cardiac arrest
Coronary angiography & PCI aftercardiac arrest
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Improvement in 1 year survival after implement of standardpost-resuscitation care emphasis on therapeutic hypothermiaand early coronary angiography for possible PCI "
J AC C : C AR D I O V A S C U L AR I N T E R V E N T I O N S , V O L . 5 , N O . 6 , 2 0 1 2 J U N E 2 0 1 2 : 5 9 7 6 0 5 "
Rate of Coronary Occlusion isfrequent in OHCA "
Studies " Rate of Coro occlusion "
Spaulding C et al " 67% "
Davies MJ et al. " 73.3 "
Farb A et al. " 57 "
Lo YS et al. " 33 "
Spaulding C et al, N Engl J Med, 1997; 336: 1629-33 "Davies MJ et al, Circulation 1992;85:119-24 "Farb A et al, Circulation 1995;92:1701-9 "Lo YS et al AHJ 1988; 115:781-5 "
January 2003-December 2008: 714OHCA with ROSC
No obvious extra-cardiac cause435
Obvious extra-cardiac cause279
ST segment elevation
134 (31%)
No ST segment elevation
301 (69%)
Successful PCI99 (74%)
No or failed PCI35 (26%)
Successful PCI78 (26%)
No or failed PCI223 (74%)
Dumas F et al , Circ Inter 2010: 3;
Ravascularization after successful "resuscitation for OHCA ""
"" What is the value of post-ROSC clinical and ECG data "" "for predicting coronary artery occlusion as a cause of "" "OHCA? "" " " ECG is often difcult to analyze in this setting, "" " " "predictive value of ECG is poor and lack of ST !! ! ! !segment elevation does not exclude acute !! ! ! !coronary occlusion or unstable lesions which can "
" " " "be treated by PCI !
When should a coronary angiogram be performed? !
Circulation. 2008 ;118:2452-83
ILCOR Consensus Statement
In summary, patients resuscitated from cardiacarrest who have electrocardiographic criteria for ST-elevation myocardial infarction should undergoimmediate coronary angiography, with subsequentPCI if indicated. Furthermore, given the highincidence of ACS in patients with out-of-hospitalcardiac arrest and limitations of electrocardiography-
based diagnosis , it is appropriate to consider immediate coronary angiography in all post cardiacarrest patients in whom ACS is suspected .
Circulation. 2008 ;118:2452-83
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Does PCI improve the prognosis of "
"survivors of OHCA? !
PROCAT
Dumas F et al , Circ Interv 2010; 3:
PROCAT Predictor of survival "
Dumas F et al , Circ Interv 2010; 3:
Time from BLS to ROSC
Time from Collapse to BLS
Diabetes Mellitus
Age>59 yrs
Initial arrest rhythm: Asystole/PEA
Blood lactate
ST segment elevation
Successful PCI
Better Prognosis "
19 Clinical Reportsof CoronaryAngiography AfterResuscitation "From CardiacArrest "
J AC C : C AR D I O V A S C U L AR I N T ER V E N T I O N S , V O L . 5 , N O . 6 , 2 0 12 J U N E 2 0 1 2 : 5 9 7 6 0 5 "
Post Cardiac Arrest Coma
cath ? " In OHCA patients with STEMI or new LBBB onECG after ROSC, early angiography and PPCIshould be considered. Out-ofhospital cardiac arrestpatients are often initially comatose but this should not be a contraindication to consider immediate angiography and PCI . It may bereasonable to include cardiac catheterization in astandardized post-cardiac-arrest protocol as part ofan overall strategy to improve neurologically intactsurvival in this patient group "
2010 American Heart Association Guidelinesfor Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care Science !
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No differences in survival-to-discharge or favorableneurological function among survivors were seenbetween those with or without ST-segment elevationon their post-resuscitation electrocardiograms "
J Am Coll Cardiol Intv 2013;6:11525 !
Thammasat Data 2007-2012 "45 OHCA /IHCA & angiography "
Normal/ "minor coro ds "
18"(1PE) "
Signicant Coronary stenosis = 27 "
1vessel "5"
2vessel "8"
3vessel "5"
LMCA+2VV"
2"
LMCA"+3VV"
7"(1postCABG) "
Revascularization = 26 "
"3 PCI "
"8 PCI "
3 PCI "2 CABG "
"2 PCI "
"6"
4PCI "2CABG "
"
Thammasat Data 2007-2012 "
45 OHCA /IHCA & angiography "
1827
(2) Post cardiac arrest braininjury
Pathophysiology Clinical Manifestation Potential Treatments
Impaired
cerebrovascular
autoregulation
Cerebral edema
(limited)
Postischemic
neurodegeneration
Coma
Seizures
Myoclonus
Cognitive dysfunction
Persistent vegetative
state
Secondary Parkinsonism
Cortical stroke
Spinal stroke
Brain death
Therapeutic hypothermia
Early hemodynamic
optimization
Airway protection and
mechanical ventilation
Seizure control
Controlled reoxygenation
(SaO2 94% to 96%)
Supportive care
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Therapeutic HyPothermia
The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome aftercardiac arrest. NEJM 2002;346:549-556
Out-of-hospital VFcool to 32-34 C
for 12-24 hrstart minutes-hors
after ROSC
Maximize Recovery of Brain Function
Hypothermia Optimize cerebral perfusion
Control seizure Control metabolic-blood glucose
(3) Postcardiac arrestmyocardial dysfunction
Pathophysiology Clinical Manifestation Potential Treatments
Global hypokinesis
(myocardial stunning)
ACS
Reduced cardiac
output
Hypotension
Dysrhythmias
Cardiovascular
collapse
Early revascularization
of AMI
Early hemodynamic
optimization
Intravenous fluid
Inotropes
IABP
LVAD
ECMO
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(4) Systemic ischemia/reperfusionresponsePathophysiology Clinical Manifestation Potential Treatments
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
Early hemodynamic
optimization
Intravenous fluid
Vasopressors
High-volume
hemofiltration
Temperature control
Glucose control
Antibiotics for
documented
infection
General Goal-directed therapy
MAP of 65 to 100 mm Hg Central venous pressure of 8 to 12 mm Hg ScvO2 70% urine output 0.5-1 mL / kg/ h1 normal or decreasing serum or blood
lactate level hemoglobin concentration?- 30% O2 Sat 94-96%
CPR 2008
Prognostication
Multimodal approach Neurological examination
Electrophysiological investigation
Delay until 72 hr after return tonormothermia
Prevention of Cardiac Arrest "
IHCA: 80% Vital
sign
"
Rapid responsesystem "
Kause, J. et al. the ACADEMIA study. Resuscitation 62, 275282 (2004). "Muller, D et al. How sudden is sudden cardiac death? Circulation 114, 11461150 (2006). "
OHCA: warningsign "
Typical angina was presentfor a median duration of 2 hin 25% of 274 patients withwitnessed OHCA "
In-Hospital " Out-Hospital "