ventilation de l'arrêt cardiaque : contre par nicolas peschanski

CHU_ Hôpitaux de Rouen - page 1

Nicolas PESCHANSKI SAU Adultes GHUEP

Hôpital Tenon Paris

CHU_Hôpitaux de Rouen - page 2

Liens d’intérêts avec l’industrie

 Membre d’un Conseil ScienDfique  VYGON SA (Sonde Boussignac®, B-‐Card®)

  IntervenDons lors de Congrès  SMITHS Medical (Sondes d’intubaCon, Cricoïdotomie)  VERATHON (GlideScope®)  Wienmann (Respirateurs)

  InvitaDons Congrès  VYGON SA  VERATHON


Que disent les sociétés savantes ?


ILCOR 2010

Travers A H et al. CirculaDon 2010;122:S676-‐S684  Chaîne de survie…

  Le chaînon manquant ?  … ou le maillon faible ?


RecommandaDons fortes dans le but d’améliorer la survie

OpDmiser les compressions thoraciques durée des compressions profondeur des compressions

Améliorer la circulaDon coronaire et cérébrale

la survie la qualité de la survie

J.P. Nolan et al. ResuscitaDon 81 (2010) 1219–1276


RecommandaDons faibles car pas de preuve d’amélioraDon de la survie

IntubaDon oro-‐trachéale Uniquement par opérateurs entraînés

En moins de 10’’ Si possible sans arrêt MCE

Pas d’amélioraDon pronosDque !

la survie nombre de pauses MCE

C.D. Deakin et al. ResuscitaDon 81 (2010) 1305–1352


Place de la venDlaDon dans l’AC

Mise au point. Revue Médicale Suisse, 2013


Qualité de prise en charge de l’AC

 Dépend de 4 facteurs péjoraDfs idenDfiés  Fréquence de compression thoracique trop faible

 Pauses dans le massage cardiaque

 Profondeur des compressions insuffisantes

 HypervenDlaDon

Travers A H et al. CirculaDon 2010;122:S676-‐S684


HypervenDlaDon

 Dépend de la pression posiDve exercée…  Soit par vos mains (ou votre souffle)

 Soit par vos ouCls


CirculaDon 2004;109:1960-‐65

  ObjecDf : évaluer le degré d’hypervenClaCon durant la prise en charge de l’AC extra-‐hospitalier

  Inclusions : 13 adultes en arrêt cardiaque extra-‐hospitalier

  Données : durée et fréquence de la venClaCon

  Résultats : hypervenClaCon très fréquente   Comparaison expérimentale animale

  Paramètres hémodynamiques évalués chez le porc   AugmentaCon de la pression intrathoracique   Baisse de la perfusion coronaire   DiminuCon de la survie

Quid de l’hypervenDlaDon dans l’AC


CirculaDon 2004;109:1960-‐65

results, animal studies were performed to determine thepotential hemodynamic and survival rate consequences ofexcessive ventilation rates.

MethodsClinical Observational StudyThis study was performed with an exception from informed consentrequirements for emergency research (21 §CFR Part 50.24) aftercommunity consultation and public notification. It was part of butunrelated to another study for which the Food and Drug Adminis-tration had approved an investigational device exemption. TheHuman Research Review Committee at the Medical College ofWisconsin approved the study.The clinical observational study was performed in the City of

Milwaukee, where basic life support and advanced life support EMSpersonnel respond in a tiered manner. Care is provided according toAHA guidelines. For the study, an additional research team includinga physician and paramedic were dispatched to the scene of eachpatient. Entry criteria for the study were (1) adult patients (presumedor known to be !21 years) believed to be in cardiac arrest ofpresumed cardiac cause and (2) patients who were successfullyintubated with an endotracheal tube who were undergoing CPR at thetime of scene arrival of the research team. A portable pressuremonitor (Propaq, Welch Allyn Protocol, Inc) was used for electronicmeasurement of airway pressures, a surrogate for intrathoracicpressures. After arrival at the scene and after patient intubation, theresearch team connected the noninvasive intrathoracic pressuresensor between the endotracheal tube and the bag-valve resuscitator.Ventilations were then continuously recorded until resuscitationattempts were discontinued or the patient was resuscitated. There area variety of factors that may affect ventilation rate throughout theresuscitation efforts, including the practice of hyperventilating im-mediately before and after intubation. For this reason, we sought todetermine the maximum ventilation rate, defined as the highestventilation rate recorded during CPR over a 16-second periodoccurring at least 2 minutes after intubation. The ventilation fre-quency, duration, and percentage of time in which a positive pressurewas recorded in the lungs were then calculated with a digital caliper.The first 7 consecutive cases constitute group 1. After recognizing

that rescuers were consistently hyperventilating patients in cardiacarrest, investigators immediately retrained all EMS personnel toprovide ventilations at a rate of 12 breaths per minute during CPRafter establishment of a secured airway. The duration of eachventilation was not addressed during retraining. The subsequent 6consecutive cases (after retraining) constitute group 2. Data werealso analyzed by combining groups 1 and 2 (group 3). Differencesbetween the means of groups 1 and 2 were statistically analyzed byANOVA. A probability value of !0.05 was considered statisticallysignificant. All data are expressed as mean"SEM.

Results: Clinical Observational StudyThe average age of the 13 consecutive patients (6 women, 7 men)was 63"5.8 years (range, 34 to 96); 3 patients had an initial rhythmof ventricular fibrillation (VF), 5 had pulseless electrical activity, and5 had asystole. Overall, the maximum ventilation rate was observedan average of 18.8"11.9 minutes after intubation (range, 2 to 39minutes). No patient survived. The average maximum ventilationrate for group 1 patients was 37"4 breaths per minute (range, 19 to49), ventilation duration was 0.85"0.07 seconds/breath, and thepercentage of time in which a positive pressure was recorded in theairway was 50"4% (Table 1). After retraining, 3 of 6 group 2patients had ventilation rates !26 breaths per minute. The ventila-tion rate for these 6 patients was slower than in group 1 patients, at22"3 breaths per minute (range, 15 to 31). However, ventilationduration was significantly longer than in group 1 patients (1.18"0.06versus 0.85"0.07 seconds/breath, respectively, P!0.05). As a result,the percentage of time in which a positive pressure was recorded inthe airway was similar in group 2 and group 1 patients (44.5"8.2%versus 50"4%, respectively) (P#NS). Combining groups 1 and 2

(group 3), the ventilation rate for all 13 patients was 30 breaths perminute (twice the AHA-recommended rate).Individual recordings provide insight into the rate and duration of

ventilations provided by professional rescuers. Figure 1A representsdelivery of CPR relatively close to AHA guidelines. Only one suchcase was observed. Figure 1, B, C, and D illustrate representativeexamples of hyperventilation observed in the majority of casesbefore retraining. After retraining, slower ventilation rates were seenin group 2 patients, but ventilation duration was more prolonged(Figure 1E). As a result, the percentage of time in which a positivepressure was recorded in the airway was not significantly differentbetween groups 1 and 2.

Animal StudiesThe porcine hemodynamic and survival studies were approved by theCommittee of Animal Experimentation at the University of Minne-sota. The animals received care in compliance with the 1996 Guidefor the Care and Use of Laboratory Animals by the NationalResearch Council. The animal preparation and surgical techniqueshave been previously described in detail.3 Briefly, each animalreceived 10 mL (100 mg/mL) of intramuscular ketamine HCl forinitial sedation, followed by intravenous propofol (2.3-mg/kg bolusand then a constant intravenous infusion of 165 "g/kg per minute).During the preparatory phase, animals were ventilated with room airby a positive-pressure ventilator (Harvard Apparatus Co). The rateand tidal volume were adjusted to maintain an arterial carbon dioxide(PaCO2) at 40 mm Hg and oxygen saturation $90%, based onanalysis of arterial blood gases (IL Synthesis, InstrumentationLaboratory).Central aortic and right atrial pressures were recorded continu-

ously using a micromanometer-tipped catheter (Mikro-Tip Trans-ducer, Millar Instruments). All animals were treated with heparin(100 U/kg IV) as a single bolus once catheters were in place.Intrathoracic pressures were measured continuously with a micro-manometer-tipped catheter positioned within the trachea, 2 cm belowthe tip of the endotracheal tube at the level of the carina. End-tidalcarbon dioxide (ETCO2) was recorded continuously (CO2SMO Plus,Novametrix Medical Systems).

Resuscitation ProtocolsVentricular fibrillation was induced by using a 5F bipolar pacingcatheter (St Jude Medical Corp) placed into the right ventricle, withalternating current at 7 V and 60 Hz. As soon as VF was induced, thepositive-pressure ventilator was disconnected from the animal. After6 minutes of untreated VF, closed-chest standard CPR was per-formed continuously with a pneumatically-driven automatic pistondevice (CPR Controller, AMBU International).3 The compressionrate was 100 per minute with a 50% duty cycle, and the compressiondepth was 25% of the anterior-posterior diameter of the chest wall.After each compression, the chest wall was allowed to recoilcompletely and without any impedance from the compressiondevice. Pressure-controlled, synchronous ventilations were per-formed with a semiautomatic ventilator (Demand Valve ModelL063–05R, Life Support Products Inc) at a constant flow rate of 160L/min. Ventilation was initiated during the decompression phase ofCPR, and each breath was delivered over a 1-second period of time.

TABLE 1. Clinical Observational Study: Maximum VentilationRate, Duration, and Percentage of Time in Which a PositivePressure Was Recorded in the Lungs (Mean!SEM)

GroupVentilation Rate

(Breaths per Minute)Ventilation Duration

(Seconds per Breath)% PositivePressure

Group 1 37"4* 0.85"0.07† 50"4%

Group 2 22"3* 1.18"0.06† 44.5"8.2%

Group 3 30"3.2 1.0"0.7 47.3"4.3%

*P!0.05; †P!0.05; group 1, first 7 consecutive cases; group 2, subsequent6 consecutive cases (after retraining); group 3, groups 1 and 2 combined.

Aufderheide et al Hyperventilation-Induced Hypotension During CPR 1961

by guest on November 25, 2012http://circ.ahajournals.org/Downloaded from

Pression posiDve > 50 cmH2O retour veineux !

Résultats en % de Pression PosiDve


CirculaDon 2004;109:1960-‐65

Limites…

  Etude clinique uniquement observaDonnelle

  Effecteurs : EMS technicians et EMS (Paramedics)

  Inclusions : 13 adultes en arrêt cardiaque extra-‐hospitalier   Données non comparables à nos PEC

  RaCo Compression/VenClaCon non conforme aux recommandaCons actuelles   Pas de venClaCon mécanique   Pas d’insufflaCon conCnue

  Comparaison expérimentale animale ?


Do we hypervenDlate cardiac arrest paDents?

  Clinical observaConal study   12 paCents OHCA

O’Neill J.F, Deakin C.D, Resuscitation 2007

> 20

Autre étude… mêmes résultats !

O’Neill J.F, Deakin C.D, ResuscitaDon 2007


Donc… hypervenDlaDon dans l’AC

 Courante (voire fréquente)  par fréquence trop élevée  plutôt que par volume courant excessif

 RetenDssement contre-‐producDf  effet délétère sur le flux sanguin  …et le remplissage coronaire

 effets bien connus (recommandaCons),

 mais ne sont pas pris en compte par les effecteurs


Soyons minimalistes…

Rea TD et al. N Engl J Med 2010:363;5


Endotracheal intubaCon versus supraglodc airway inserCon in out-‐of-‐hospital cardiac arrest. ResuscitaCon 2012

  Effect of out-‐of-‐hospital pediatric endotracheal intubaCon on survival and neurological outcome: a controlled clinical trial. JAMA 2000

  InterrupCons in cardiopulmonary resuscitaCon from paramedic endotracheal intubaCon. Ann Emerg Med 2009

  Field intubaCon of paCents with cardiac arrest: a dying art or just a quesCon of Cming? Emerg Med J 2011

  AssociaCon of prehospital advanced airway management with neurologic outcome and survival in paCents with out-‐of-‐hospital cardiac arrest. JAMA 2013

Soyons réalistes…


Ne pas arrêter les compressions !

VenDlaDon > FaDgue > Analyses du rythme


InterrupCng chest compressions for rescue breathing can adversely affect hemodynamics during CPR for VF

Adverse Hemodynamic Effects of InterrupDng Chest Compressions for Rescue Breathing During CPR for Ventricular FibrillaDon Cardiac Arrest

Berg et al. CirculaDon. 2001;104:2465 !

Pourquoi ?


Chest Compressions & Coronary Perfusion Pressure

15:2 RaDo

20 mmHg

40 mmHg

20 mmHg

5:2 RaDo

Pourquoi ?

CHU_Hôpitaux de Rouen - page 20 L. Wik et al. JAMA. 2005;293:299-‐304

Quelques raisons de s’inquiéter…

”Chest compressions were not delivered half of the Dme,(...) and

most compressions were too shallow”



Ideal CPR

71%

19%



Real CPR

58% 42%


Revenons aux recos !

Travers A H et al. CirculaDon 2010;122:S676-‐S684

 A propos de la venDlaDon « à la française… » « Once an advanced airway is in place, the compressing provider should give con8nous chest compression at a rate of at least 100 per minute,

without pauses for ven8la8on »


Conclusions

  La venDlaDon est délétère durant la RCP   Car elle interrompt les compressions thoraciques

  Elle uClise des volumes courants trop importants

 Durant la RCP spécialisée   L’intubaCon entraîne un arrêt du MCE

  Et les venClateurs ne sont pas adaptés

  Elle est néanmoins absolument nécessaire !   Synchroniser la venClaCon au MCE ?

  InsufflaCon conCnue ?


Pour vous convaincre définiDvement


Phénomène de Lazare

CHU_Hôpitaux de Rouen - page 28 28 XXème siècle XXIème siècle

Merci de votre ayenDon

RCP du XXI° siècle

ventilation de l'arrêt cardiaque : contre par nicolas peschanski

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